Advice and Guidance

In editing the Red Book every attempt is made to ensure that statements are fully compatible with the advice given by the British National Formulary, the Drug and Therapeutics Bulletin, the various professional bodies however the advice is meant to be pragmatic and practice and useful for the General Practitioner working in primary care and trying to manage cardiac patients and interpret the large volume of cardiac investigations which are available, The aim is to give advice and to explain the evidence behind that advice. The topics chosen for inclusion have been derived from common questions asked on Advice and Guidance however the editor is happy to receive suggestions for further additions to the guide and these should be forwarded to the email address below:

Editorial: Richard Bogle ([email protected])

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Arrhythmia

Common abnormalities on continuous ECG monitoring

To understand the significance of abnormalities found on continuous ECG recordings it is important to know what is normal for the population in which the recording is done. This is not contained in reports which provide no context of what is acceptable and what is abnormal and requires further evaluation by cardiology.

Community based studies in health populations using continuous ECG recording tell us what you would normally expect to see when you perform ECG monitoring in people. This then helps to understand what is acceptable and what requires further evaluation. It is also important to be aware of the patient age when evaluating any ECG changes since arrhythmia is more common in older patients and the threshold for further evaluation and treatment is different.

Patients <55 years old: In a younger population (mean age 45 years) whilst SVE and VE are common (61% and 43%) they are of low frequency (<50/24h) and are generally unifocal. Second degree AV block Mobitz type 1 is not uncommon (2.5%) as are pauses <3 seconds (4%). Therefore, younger patients with if anything other than low frequency ectopics, nocturnal pauses of <3 seconds, second degree AV block, Mobitz type 1 or occasional dropped beats.

Patients > 55 years: In healthy older adults (mean age 75 years) about 45% women and 52% men will have >100 PAC/24h, 29% of women and 30% of men will have >100 PVC per 24h. About 85% of people will have any SVT (defined as ≥4 PACs in a row), 90% will have bradycardia of <60bpm. These things are common, usually asymptomatic and do not need any specific action or referral.

In older patients the following require evaluation by Cardiology initially through Advice and Guidance:

· Atrial ectopics >60/hour (more than 1500/24h)

· Runs of supraventricular tachycardia >15s

· Atrial fibrillation

· Ventricular ectopics (>5%)

· Ventricular tachycardia >10 beats

· Heart rate <40 bpm

· High-grade AV block (Second degree, Mobitz type 2 or complete heart block)

· Pauses >3 sec

Arrhythmia detected on wearable devices (iWatch)

A single lead electrocardiogram (iECG) can be recorded. Rhythm analysis is reported after 30s of recording and classifies an iECG as sinus rhythm, atrial fibrillation (AF) or inconclusive.

ECG algorithm performance is limited in classifying other arrhythmias. Unclassified rhythms such as second or third-degree AV block, bigeminy, frequent ectopy, junctional rhythm and low and high heart rate (outside 50–150 bpm) and paced rhythms may not be accurately identified by iECG.

In an Apple sponsored multi-center study of 70 AF and 70 sinus rhythm patients the ECG app generated waveform had morphologic equivalence to Lead I ECG for 98.4% of AF and 100% of SR patients; only 0.8% were excluded for analysis due to artefact. Therefore, Apple Watch iECG recordings are reliable, have high fidelity and high performance.

Sensitivity and specificity of the rhythm classification algorithm were evaluated in 602 individuals. Presence or absence of AF was determined by the ECG obtained at the time of enrolment. There were 301 and 287 participants in the AF and SR cohorts, respectively. With appropriate placement of the watch and arm positioning, iECGs via the ECG app and conventional 12 ECGs were recorded simultaneously. In paired strips generated by the ECG app and 12 lead ECG rhythm strips, 80.5% of strips were classifiable (excluding unreadable and unclassified rhythms). The ECG app algorithm classification showed sensitivity of 95.5% and specificity of 97.1%. Other devices such as Fitbit do not record an ECG but use PPG for the detection of the pulse and heart rate. In a study of 455 699 participants enrolled (median age 47 years, 71% female, 73% White) between May 6 and October 1, 2020. IHRDs occurred for 4728 (1%) participants, and 2070 (4%) participants aged ≥65 years during a median of 122 (interquartile range, 110–134) days at risk for an IHRD. Among 1057 participants with an IHRD notification and subsequent analysable ECG patch monitor, AF was present in 340 (32.2%). Of the 225 participants with another IHRD during ECG patch monitoring, 221 had concurrent AF on the ECG and 4 did not, resulting in an IHRD positive predictive value of 98.2% (95% CI, 95.5%–99.5%). For participants aged ≥65 years, the IHRD positive predictive value was 97.0% (95% CI, 91.4%–99.4%). Our advice therefore is that irregular HR or AF detected on wearable devices should prompt further evaluation of the patient since these devices have a highly positive prediction for the detection of this arrhythmia.

References: Fitbit Heart Study. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.122.060291

Atrial Ectopics on 12 lead ECG

If atrial ectopics (AE) are detected on a 12-lead ECG we recommend doing a 24h ECG monitor to assess their frequency. In healthy older adults (mean age 75 years) about 45% women and 52% men will have >100 PAC/24h. About 85% of people will have any SVT (defined as ≥4 PACs in a row).

Atrial Ectopics on Implantable or Continuous Cardiac Monitors

AE are commonly seen in people over 65 years who have continuous or implantable ECG monitors often with atrial couplets, triplets and short runs of AE for a few beats. About 45% women and 52% men will have >100 PAC/24h. About 85% of people will have any SVT (defined as ≥4 PACs in a row). These short episodes may be referred to as atrial high-rate events (AHRE). The presence of AHRE predict an increased risk of atrial fibrillation (AF). When there are AHRE which are irregular, no P waves and which last 30 seconds or more they should be referred to as AF.

Generally, AE or AHRE do not need treatment unless they are symptomatic. There is no evidence for benefit of anticoagulation in patients with AE or AHRE. However, they are associated with AF patients should be evaluated further to look for evidence of AF when the frequency of AE or AHRE is >2% or 2,000 per 24h.

When AE are detected on short term monitoring (e.g. 24 - 48h) in patients with a CHADSVASC score of 1 (male) or 2 (female) we assess further if the frequency of AE is >2%. We recommend echo to assess cardiac structure and function, check TSH and CV risk factors. We perform ECG monitoring (7 days) to look for AF and if this is detected we consider offering a OAC (see Anticoagulation in atrial fibrillation with a CHADSVASC score of 1).

Premature Ventricular Complexes (PVC) also known as Ventricular ectopic beats

First determine if the patient is at risk of complications from the PVC or if there is underlying structural heart disease.

Evaluate PVC morphology: Left bundle branch block pattern with an inferior axis usually originate from the RV outflow tract and are generally a common benign cause. PVC of right bundle branch block morphology generally originate from the left ventricle and are more commonly seen in patients with ischaemic or structural heart disease.

All patients should have a 48h period of ECG monitoring to assess the frequency of ectopics. If the PVC are multifocal or of right bundle branch block morphology the patient should have an echocardiogram as well.

People with >10% PVC burden, impaired LV function (EF<50%), structural cardiac or electrical conduction system disease or a history of syncope, chest pain, or dyspnoea should be referred to a cardiologist.

People with a moderate burden of PVC >2% and <10% should have an echocardiogram and be discussed with cardiology via Advice and Guidance.

Patients with a low burden of PVCs (<2%), no or mild PVC symptoms and no high-risk factors (see above) should be reassured by their GP that the arrhythmia is usually self-limiting, rarely life-threatening, and in most cases.

Eliminating possible triggers is appropriate and there is no clear evidence that PVC suppression or elimination with drugs or ablation improves overall survival in patients who have no symptoms, no heart disease, and no sustained ventricular arrhythmias. In low-risk patients with noticeable symptoms in a quiet environment, such as at night while lying in bed, counselling them to move around and increase their heart rate may alleviate symptoms and provide reassurance.

Explaining the natural history of PVC to patients is an important part of reassurance. In a prospective cohort study of 100 untreated patients (52 years old, 57% female) the median PVC burden of 18% reduced to <1% in 44% of patients at median follow-up of 15.4 months. Recurrence was uncommon (9.1%). This may allow an appropriate period of watchful waiting. Patients with significant and/or persistent PVC-related symptoms can be treated to reduce the PVC burden.

Treatment is beta blockers (1st line – Bisoprolol 2.5mg od), CCB (2nd line – Diltiazem or Verapamil – especially PVC of fascicular origin (relatively narrow QRS, right bundle branch block-like, left axis deviation).

After treatment patients should be evaluated for PVCs burden with periodic ECG monitoring for 24 hours. If symptoms and PVC burden have been reduced and are not high, treatment should be continued. If a patient prefers to stop or reduce their medications, a trial of weaning and/or stopping may be done after 6 to 12 months.

Atrial flutter

There are four major issues that must be considered in the management of atrial flutter:

1. Control of the ventricular rate

2. Reversion to sinus rhythm

3. Maintenance of sinus rhythm

4. Prevention of systemic embolization

Rate control in atrial flutter: Rate control usually involves the administration of a diltiazem/verapamil or a beta blocker. Digoxin is used less often because its major action is an enhancement of vagal tone, which is offset during exertion and its main indication is concurrent heart failure when it can be given with a beta-blocker.

We find that it is is more difficult to affect rate control in atrial flutter, as compared with atrial fibrillation. While up-titration of atrioventricular (AV) nodal blocking agents typically lowers the mean rate in atrial fibrillation, patients with atrial flutter are frequently "stuck" at 2:1 AV conduction. Rarely, amiodarone may also be also as a rate control agent, particularly in acutely ill patients, but is not generally used long term due to the risk of potential side effects.

Reversion to normal sinus rhythm: Due to the high rate of recurrence of atrial flutter in patients without a correctable cause, and because of its high success rate with low rate of complications, definitive treatment with radiofrequency catheter ablation is the preferred treatment for most patients. It is less preferable for most patients to consider antiarrhythmic drugs because of potential for side effects and we suggest avoiding Class IA and IC drugs since they increase the likelihood of causing rapidly conducted atrial flutter.

For hemodynamically stable patients who will not require urgent catheter ablation, watchful waiting under anticoagulation and rate control medicines may be reasonable, as atrial flutter may convert to sinus rhythm spontaneously. DC Cardioversion is also reasonable if the patient has had no prior episodes of atrial flutter, or if they choose to decline ablation as an invasive first-line strategy. Usual precautions should be taken with regard to anticoagulation or transesophageal echocardiography (TEE) if the duration of atrial flutter is beyond 24 to 48 hours or of unknown duration.

Maintenance of normal sinus rhythm — The rate of recurrence of atrial flutter is more than 50% over 2-3 years in patients without a correctable cause. Radiofrequency catheter ablation is generally preferable to long-term pharmacologic therapy in patients with typical atrial flutter because it is highly effective. A meta-analysis of 21 studies demonstrated an ablation success rate for a single procedure of 92% and for multiple procedures of 97%.

Prevention of systemic embolization — Sustained atrial flutter carries an elevated thromboembolic risk and should be treated as for anticoagulation in atrial fibrillation. Risk stratification using the CHA2DS2-VASc scoring system should be completed prior to deciding on the use of oral anticoagulation. Four weeks after successful ablation of isolated typical atrial flutter (ie, no prior atrial fibrillation history) anticoagulation is discontinued. In a meta-analysis of 48 studies (between 1996 and 2015) of patients undergoing catheter ablation for typical atrial flutter, who were followed for an average of 2.5 years, those without prior atrial fibrillation had a 23 percent incidence of new atrial fibrillation diagnosis. Those with prior history of paroxysmal atrial fibrillation undergoing atrial flutter ablation had a much higher recurrence rate of 52 percent, highlighting the need for individualized risk assessment for long-term anticoagulation and in patients with prior atrial fibrillation history, anticoagulation should be continued long term based on the CHA2DS2-VASc scoring system.

Rate control in atrial fibrillation

Some studies of rate control for AF suggest that beta-blockers are inferior to diltiazem, verapamil and digoxin. Other studies indicate that lenient rate control up to 110 bpm is non-inferior to stricter rate control (<80bpm)

The only RCT is the RATE-AF trial which compared Bisoprolol (mean 3.2mg) to Digoxin (mean 161mcg) in older patients with permanent AF and breathlessness (NYHA class 2 or higher). The primary endpoint was patient-reported quality of life at 6 months as measured by the physical component of the SF-36 questionnaire. Heart rate responses were nearly identical in the two groups. For the primary outcome at 6 months there were no significant difference between digoxin and beta-blockers.

In consideration of the lack of evidence from large outcomes studies and the availability of alternative agents, beta-blockers may be overused in AF and the data suggest that the adverse effect of beta-blockers is most pronounced in patients with a normal ejection fraction and low heart rates, typified by patients with paroxysmal AF on high maintenance doses of beta-blockers that markedly suppress the sinus rate.

Diltiazem or verapamil, have a pharmacological advantage over beta-blockers since they preferentially bind to activated calcium channels making their effect on heart rate use dependent. In other words, they have little effect at lower heart rates, while exerting a robust dromotropic effect at rates encountered with fast conducting atrial fibrillation and thus provide protection from tachycardia-induced cardiomyopathy when it is most needed. By extension, these calcium-channel blockers have little effect on sinus rate, filling pressures, and wall stresses to explain why the progression towards permanent atrial fibrillation they may be slower and why are better tolerated than beta-blockers.

Sinus rate lowering in patients with a normal ejection fraction increases the risk for atrial fibrillation. Two large, randomized hypertension trials provided a better understanding of the effects of beta-blockers on the incidence of atrial fibrillation in patients with predominantly normal ejection fractions. The LIFE hypertension trial compared atenolol with losartan and there was a >30% higher risk of subsequent AF in those treated with atenolol. The safe effect was seen in the ASCOT hypertension trial of amlodipine vs. atenolol. These trials also showed beta-blockers increase stroke risk and they were down-graded from preferred to second-line antihypertensive agents.

Suppression of the sinus rate plays a key role in these outcomes. The SIGNIFY trial with ivabradine vs. placebo in patients with CAD and normal LV function at baseline showed that ivabradine reduced the HR by 10 bpm and increased the RR for heart failure by 20% and AF by 40%. Lowering HR prolongs diastolic filling time and leads to higher filling pressures as the additional blood volume must overcome the increasing resistance of the expanding ventricle. Higher filling pressures raise left atrial and ventricular wall stress and increased atrial afterload impairs atrial function and triggers atrial remodelling and dilation. Thus, by reducing the heart rate below normal, beta-blockers create a reversible state of intracardiac congestion reflected in attendant increases in natriuretic peptide levels, a biomarker of wall stress that predicts both heart failure and AF. This mechanism is further compounded by the load-induced activation of the Frank–Starling mechanism to increase stroke volumes and central arterial pressures which are further augmented by superimposed reflected peripheral pressure waves. These mechanisms combine to raise the risk for atrial fibrillation and heart failure with a preserved ejection fraction.

Rhythm control in paroxysmal atrial fibrillation

The recurrence rate of AF is high with 70-80% of patients experiencing a recurrence annually. Whilst this is modified by drug treatment the drugs have limited effectiveness. In primary care we recommend that beta blockers be the only agent which should be routinely used for the maintenance of sinus rhythm in patients with PAF. We recommend bisoprolol (1.25-10mg). However, prescribers should note that although safe to use beta blockers are relatively ineffective in maintaining sinus rhythm in atrial fibrillation with limited data with 2 studies only and most of these patients were young with a short history of atrial fibrillation and structurally normal hearts. It is seen that whilst there may be some effect of beta blockers in this population it is relatively small, and this was a short-term study which is difficult to translate this to the general population of patients we see.

An advantage of using a β-blocker for the maintenance of sinus rhythm is the conduction-slowing effect of the compound on the atrioventricular node. If atrial fibrillation recurs, the ventricular rate is usually well controlled. This contrasts with findings with class I antiarrhythmic drugs.

Other drugs for paroxysmal AF are class 1C (Propafanone, Flecanide) and Class III (Amiodarone and (+/-) Sotalol in doses of 240mg daily or above). All of these have increased potential for adverse effects and their prescription should be initiated and followed up by a cardiologist. Virtually all studied anti-arrhythmics showed increased pro-arrhythmic effects. This may be sinus bradycardia which is relatively benign or more dangerous arrhythmia such as torsade des points (Sotalol & Amiodarone), flutter with 1:1 conduction (Class 1C). There is high‐certainty evidence from five trial indicating that sotalol is associated with a 2.23-fold increase in all‐cause mortality rate with a number needed to treat to cause 1 additional death per year of 100. Of all the treatments available catheter ablation is the most effective with an annual recurrence rate of 32.3% compared to 42-65% with antiarrhythmic drugs and 72-81% with placebo.

Drug	ARR % Placebo	ARR % Drug	ARR % Ablation	NNT	RR, 95% CI
Amiodarone	81.2	42.3	-	3	0.52 [0.46-0.58] n=6
Flecanide	69.8	45.5	-	4	0.65[0.55-0.77], n=4
Propafenone	73	48.9	-	4	0.67[0.61-0.74], n=5
Sotalol	78.8	65.4	-	7	0.83[0.80-0.87], n=14
Metoprolol	72	59.7	-	-	0.83[0.60-1.02], n=2
Ablation	-	53	32.3	5	0.62[0.51-0.74], n=6
Non DHB CCB		46
ARR = Annual rate of recurrence

Manging atrial fibrillation with high and low ventricular response

This is not an uncommon problem in older patients when there is a mixture of sinus node disease, conduction system disease and paroxysmal AF and cannot tolerate rate slowing agents because of bradycardia yet without these they have a heart rate which is not controlled.

Basically, there are 4 strategies:

· Restoration of sinus rhythm with cardioversion

· Restoration of sinus rhythm with ablation

· Backup pacemaker with rate control agents

· AV node ablation with pacemaker

Restoration of sinus rhythm with cardioversion may be successful but the patient may well end up back in AF and so the problem repeats. It is often difficult to use anti-arrhythmic drugs to try to prevent the AF recurrence due to sinus node disease and slow heart rates. Similar provisos apply to ablation although this is likely to be more successful than ablation and there is no need to use anti-arrhythmic drugs.

The other options are acceptance of AF and either control the rate with drugs but have a pacemaker as a backup to stop the rate being too low or accept the AF, ablate the AV node and then make the patient pacemaker dependent but with complete control. All these things need hospital cardiology input and therefore referral to an arrhythmia clinic is the most appropriate route.

Sometimes what is seen is slowing of HR on Holter monitors in patients with paroxysmal AF and then the question is whether to change or reduce the patients medication. It is likely that non dihydropyriine calcium channel blockers are preferred over beta blockers in this situation as they have less propensity to cause bradycardia. In a recent study a total of 4060 patients were enrolled in the AFFIRM trial with mean age was 70±9 years, 39% were women were studied. They focused on 1112 patients who were in sinus rhythm at baseline and used either non-dihydropyridine channel blockers or beta-blockers. Of them, 474 had AF during follow-up while remaining on the same rate control drugs, 218 (46%) on calcium channel blockers and 256 (54%) on beta-blockers. A resting heart rate <110 beats per min during AF was achieved in 92% of patients using calcium channel blockers and 92% of patients using beta-blockers (p=1.00). Bradycardia during sinus rhythm occurred in 17% of patients using calcium channel blockers vs 32% using beta-blockers (p<0.001). After adjusting for patient characteristics, calcium channel blockers were associated with a reduction in bradycardia during sinus rhythm (OR 0.41, 95% CI 0.19 to 0.90). So it is likely that the CCB are better tolerated in this situation. So in patients with non-permanent AF, calcium channel blockers instituted for rate control were associated with less bradycardia during sinus rhythm compared with beta-blockers.

Anticoagulation prior to electrical or chemical cardioversion

Patients with AF of more than 48 hours or of unknown duration should receive at least four weeks of therapeutic anticoagulation prior to cardioversion and four weeks of anticoagulation after cardioversion. In this setting, this treatment regimen can reduce the risk of thromboembolism during the four weeks after cardioversion from 6% to <1%. For patients in whom there is a reason to not wait four weeks, an option for management is pre-cardioversion therapeutic anticoagulation in conjunction with a screening TEE to guide early cardioversion. While the TEE approach shortens the pre-cardioversion duration of anticoagulation, it does not change our recommendation for four weeks of anticoagulation after cardioversion or the need to be therapeutically anticoagulated at the time of the cardioversion due to the risk associated with post-cardioversion atrial appendage stunning. Prospective studies have shown that the risk of clinical stroke or systemic embolism ranges from 0 to 0.9 percent if preceded by four weeks of therapeutic anticoagulation with warfarin (target international normalized ratio [INR] 2.0 to 3.0) or one of the DOACs, or shorter-term anticoagulation with TEE-guided approach discussed directly above. Retrospective data demonstrated that the thromboembolism risk is 4 to 7 percent in non-anticoagulated patients.

DOAC versus Warfarin

For most patients with AF with an indication for anticoagulation, we recommend a direct oral anticoagulant (DOAC) rather than vitamin K antagonist (VKA, e.g. warfarin). For patients with AF who have been treated with warfarin with an annual TTR of at least 70%, we suggest switching to a DOAC however, it is also reasonable to continue a VKA in these patients. Exceptions to this general preference for DOAC in patients with AF is for patients with a mechanical heart valve of any type and location, patients with rheumatic mitral stenosis that is severe or clinically significant (mitral valve area ≤1.5 cm2) and patients for whom the DOAC agents are avoided due to drug interactions (e.g. those receiving P-glycoprotein drug efflux pump inducers which can decrease the anticoagulant effect of DOACs and chronic antiviral agents, which may increase the anticoagulant effect of DOACs). Clinical settings in which VKA is reasonable or preferable to DOAC include patients who are not likely to comply with the twice daily dosing of dabigatran or apixaban and who are unable to take once-a-day rivaroxaban or edoxaban due to intolerance. For patients with severe CKD (creatinine clearance by Cockcroft-Gault equation < 25-30 mL/min), a VKA is generally preferred, although some clinicians prescribe apixaban for selected patients in this setting.

Combining anticoagulation with antiplatelet therapy

First assess the indication for anticoagulation with an oral anticoagulant (OAC). Most often this is AF and the OAC should be continued long-term. The issue of whether an antiplatelet should be taken as well has is based on expert opinion not trials. Therefore, there will be differences in approach between different cardiologists with some stopping anti-platelets after 6- or 12-months others continuing it long term with DOAC. Clopidogrel is recommended as the anti-platelet agent of choice when combined with anticoagulation because it is not associated with gastrointestinal irritation.

In AF patients with ACS or PCI there are differing risks of ischaemic stroke/systemic embolism, coronary ischaemic events, and antithrombotic treatment-related bleeding. These factors therefore should be considered when deciding the duration of use of combined antithrombotic therapy. Dual therapy with OAC and Clopidogrel is associated with significantly less major bleeding than triple therapy (OAC, Clopidogrel and Aspirin). Dual therapy with OAC and Clopidogrel is recommended for the first 12 months after PCI for ACS, or 6 months after PCI in patients with stable angina. After that OAC monotherapy should be continued provided there were no recurrent ischaemic events in the interim. In stable AF patients with CAD and no PCI, OAC monotherapy is recommended. There are some situations where risk of stent thrombosis is higher such as chronic renal failure, type 2 diabetes, long stent length or stenting of last remaining coronary artery. So, there will be some discretion in this decision which should be made by the responsible cardiologist.

Can I use a DOAC in a patient with LV thrombus?

Left ventricular thrombi (LVTs) increase the risk of stroke, systemic embolism, and subsequent death. Current guidelines recommend vitamin K antagonists (VKAs) as first-line treatment for LVT. Direct oral anticoagulants (DOACs) are increasingly used as alternatives to warfarin for the treatment of LVT. However, the efficacy and safety of DOACs versus VKAs remain controversial. The most comprehensive data comes from an updated meta-analysis of DOACs versus VKAs for LVT treatment. The meta-analysis included 12 cohort studies and 3 randomized controlled trials with a total of 2334 patients. They found that DOACs had a lower risk of clinically significant bleeding than VKAs (RR = 0.6; 95% CI, 0.39 to 0.90; P = 0.01; I2 = 0%). There was no difference in LVT resolution (RR = 1.01; 95% CI, 0.93 to 1.09; P = 0.48; I2 = 0%), stroke and/or systematic embolic events (RR = 0.87; 95% CI, 0.11 to 1.55; P = 0.2; I2 = 30%), and all-cause mortality (RR = 0.9; 95% CI, 0.58 to 1.4; P = 0.65; I2 = 0%).

So overall, DOACs are non-inferior to warfarin in LVT treatment but have a lower risk of clinically significant bleeding and the results suggest that DOACs might be better alternatives to warfarin for LVT treatment. The DOACs are not licenced for this indication but my view is that their use based on the evidence provided above is entirely reasonable and that they can be recommended.

rbAnticoagulation in atrial fibrillation with a CHADSVASC score 1

The most challenging patients with regards to risk are people with AF and non-sex related CHADSVASC 1 scores. Baseline stroke risk is low, and guidelines generally recommend that clinicians consider anti-coagulation.

Recent studies have informed the balance of risk and benefit and may be useful to clinicians. In a large study of one million plus individuals and 34,000 patients with AF followed for 8 years the 1-year incidence rates of stroke was estimated. In people with AF, the ischemic stroke incidence rate was 0.51%/person year in OAC users and 1.05%/person year in non-users (HR 0.47, 95% CI 0.37-0.59). Intracranial haemorrhage incidence (ICH) rate was 0.28%/person year in OAC users and 0.19%/person year in non-users (HR 1.23 [0.88–1.72]). OAC use was associated with an increased risk of major bleeding (HR 1.37 [1.16–1.63]) but lower risk of the combined outcome of ischemic stroke, major bleeding, and mortality (HR 0.57 [0.51–0.63]). Non-anticoagulated individuals with AF had higher risk of ischemic stroke compared with individuals without AF but with the same CHADSVASC risk profile (HR 2.47 [2.17–2.81]).

So, a yearly stroke rate of 1% with AF and no OAC versus 0.5% risk on OAC which is a 53% reduction with not much cost in terms of ICH. Whilst major bleeding was increased by 37% the higher rate of nuisance bleeding was swamped by lower rates of stroke. Importantly the rate of stroke on those CHADVASC 1 patients not on OAC was 2.5 times greater than for those similar risk patients without AF. So, AF is a significant modifiable risk factor in these patients and therefore we recommend anticoagulation for a CHADSVASC1 patient without bleeding risk.

Anti-coagulation in people with short episodes of paroxysmal AF detected on intracardiac devices or continuous ECG monitoring?

AF is increasingly being detected on continuous ECG monitors or implantable cardiac devices. This has led to shorter episodes of AF being detected. In these patients the risk/benefit of anticoagulation is less certain.

Recent trials in patients with subclinical atrial fibrillation detected by an implanted pacemaker, defibrillator, or cardiac monitor, with at least one episode lasting 6 mins or longer but no episodes lasting longer than 24h show that the absolute stroke risk is low (1 to 1.24% per year). This risk is lower than people with persistent AF and CHADS2VASC score 2 where the stroke risk is 2.2% per year but slightly higher than people with CHADSVASC score of 1 (0.6% per year).

People with short episodes of AF on monitoring have roughly a stroke risk of someone with a CHADSVASC score of 1 therefore the benefit of anticoagulation is more limited.

There have been 2 trials in this group of patients evaluating anticoagulants:

The NOAH-AFNET 6 [Edoxaban v Placebo] trial was stopped early due to excess bleeding [HR 2.1] although there was a stroke reduction [HR 0.65]. The ARTESiA [Apixaban v Aspirin] showed a similar significant reduction in stroke [HR 0.63] and increased major bleed (1.71% vs. 0.94% per person-year; HR 1.80). Fatal bleeding occurred in 5 patients in the apixaban group and 8 patients in the aspirin group.

In July 2024 an analysis was published of the ARTESiA which grouped patients by CHADSVASC score (<4, 4 and >4). Only the CHADSVASC > 4 group had a lower HR for stroke but there was an increase in bleed risk in all groups.

Thus there is a heterogeneous effect for stroke but not bleeding.

CHADSVASC of >4 gives the patient a 2.2% risk of stroke per year and the benefit of Apixaban is greater than the risk. We therefore advise clinicans to assess the CHADSVASC score in patients with device detected AF and offer anticoagulation to patients with CHADSVASC of > 4.

CHADSVASC	Apixaban Stroke Rate	Aspirin Stroke Rate	Number stroke prevented per 100 patient years	Number of major bleeds per 100 patient years
<4 (1578 patients)	0.85%	0.97%	0.12	0.33
4 (1349 patients)			0.32	0.28
>4 (1085 patients)	0.98%	2.25%	1.28	0.68

An analysis of the ARTESiA trial shows stroke risk is not dependent on the duration of AF (<1h, 1-6h or >6h) and concluded that in device detected AF the duration of the AF episode does not provide information that is helpful for stroke risk prediction. We would therefore advice that decisions are not made on the basis of duration of AF episode. https://esc365.escardio.org/EHRA-Congress/sessions/10668.

This does not address the question of what to do with patients where there is AF detected of more than 30s but <6 minutes. This is unclear at the moment but the risk for these patients is likely to be similar or lower than that of the group with >6 minutes and therefore the same principles should be applied.

Atrial fibrillation discovered prior to non-cardiac surgery

A new diagnosis of AF may be made at preoperative evaluation and our approach to these patients is generally like that in patients with new onset AF not related to non-cardiac surgery.

AF diagnosed preoperatively may arise in the setting of a risk factor such as hypertension or from an underlying systemic disorder such as severe hyperthyroidism. Both the AF and the underlying disorder may be a source of perioperative risk unless recognized and managed. For these reasons, we suggest that newly discovered AF be treated as a potentially unstable condition that should preclude elective non-cardiac surgery and be referred to a cardiologist for further evaluation.

For patients presenting for a minor surgical procedure, typically of limited duration and complexity (e.g., monitored anaesthesia care using local anaesthetics with minimal anticipated blood loss), it may be reasonable to safely proceed despite new onset AF, if the patient is asymptomatic and hemodynamically stable.

If a patient presents for emergent or urgent surgery and is found to have a new diagnosis of AF prior to surgery, in most cases, we do not attempt restoration of sinus rhythm, with either electrical or chemical cardioversion, prior to emergency surgery. The most common indication for doing so would be hemodynamic instability. We believe that most patients will benefit from a ventricular rate in AF that is less than 140 bpm. In many patients, we attempt to slow the rate to 100 to 110 bpm unless this leads to hypotension. Rate control can typically be achieved effectively and rapidly with beta blocker such as bisoprolol 2.5mg daily or diltiazem MR 120mg BD. In most cases, the initiation of anticoagulation can be deferred until after surgery. We do not recommend urgent transoesophageal echocardiography prior to surgery to screen for left atrial appendage thrombus.

For other patients rate control and anticoagulation should be considered. Patients presenting in AF should have the rate adequately controlled to avoid rapid ventricular rates and the possibility of ensuing cardiac ischemia. We do not suggest cardioversion in the preoperative period because this would mandate uninterrupted systemic anticoagulation for a minimum of four weeks after restoration of sinus rhythm, which may increase the risk of bleeding during the surgical procedure or be contraindicated. Major adverse cardiac events in AF patients undergoing non-cardiac surgery may be due to inadequate rate control and attendant cardiac ischemia during the perioperative period. Rate control is most often achieved pharmacologically, with beta blockers, non-dihydropyridine calcium channel blockers, or digoxin. Prior to surgery, heart rates between 50 and 100 beats per minute (bpm) are reasonable as long as the patient is asymptomatic. Postoperatively, in our experience, heart rates as high as 120 bpm are reasonable given the stressors of pain or hypovolemia, if these increased heart rates do not cause hemodynamic instability or myocardial ischemia

Many AF patients receive long-term oral anticoagulation to reduce the risk of embolism. While some surgical procedures can be performed safely on patients who are systemically anticoagulated interruption of anticoagulation during the perioperative period is required in others where the perioperative bleeding risk is high. For those patients who will have their anticoagulation interrupted, thromboembolic risk and estimation of bleeding risk should be weighed to determine duration of anticoagulation cessation. Longer interruption will increase risk of systemic thromboembolism. Decisions about the timing and duration of anticoagulation interruption require communication between the surgical and anaesthesia teams and the physicians managing the patient's anticoagulation.

Managing anticoagulation in patients requiring procedures or surgery

Most AF patients receive long-term oral anticoagulation to reduce the risk of embolic events such as stroke and systemic embolization.Some surgical procedures can be performed safely on patients who are systemically anticoagulated interruption of anticoagulation during the perioperative period is required in others where the perioperative bleeding risk is high. For those patients who will have their anticoagulation interrupted, thromboembolic risk and estimation of bleeding risk should be weighed to determine duration of anticoagulation cessation. Longer interruption will increase risk of systemic thromboembolism. We find Thrombosis Canada’s Perioperative Anticoagulation Management tool to be helpful in providing a bespoke plan for a patient.

https://thrombosiscanada.ca/hcp/practice/clinical_tools?calc=perioperativeAnticoagulantAlgorithm

The following are suggestions regarding anticoagulation cessation:

Patients at highest risk of left atrial thrombus formation or embolization should undergo the shortest duration of anticoagulation cessation possible and bridging therapy with low molecular weight heparin may be indicated.

Examples of such patients include those with CHA₂DS₂-VASc Score of ≥7, recent thromboembolic stroke or systemic embolism, recent cardioversion, or echocardiogram showing left atrial thrombus. If there has been an intracranial haemorrhage or major bleed in the prior three months, however, bridging may have more risk than benefit.

In those with a moderate risk of thromboembolism (CHA₂DS₂-VASc Score of 5 to 6 or prior thromboembolism >3 months prior), the bleeding risks of bridging will need to be balanced with risk of thromboembolism. Careful clinical decision making and discussion with the patient are encouraged. In general, if there is a high bleeding risk, bridging therapy should not be initiated. If the patient's bleeding risk is low and the patient has a history of a prior thromboembolic event, then bridging is encouraged. If there is a low bleeding risk and no prior thromboembolism, then bridging is not indicated.).

Patients at low risk of thromboembolic events (CHA₂DS₂-VASc Score of ≤4) may safely interrupt anticoagulation for longer periods than those at high thromboembolic risk.

Common ECG Abnormalities: Significance and Management

Non-specific ST-T wave changes

These are common and may be seen in any lead of the ECG. Changes may be seen in all or most of the leads (diffuse changes), or they may be present contiguous leads, such as the inferior, lateral, or anterior leads. The types of abnormalities are varied and include subtle straightening of the ST segment, actual ST-segment depression or elevation, flattening of the T wave, biphasic T waves, or T-wave inversion. In the absence of a clinical history or symptoms, T-wave abnormalities and flattened and depressed ST-segment changes are non-specific.

Some of the causes of these changes include:

· Functional and physiologic variants (e.g, postprandial)

· Myocardial ischemia, any cardiomyopathy, myocarditis, pericarditis, post-cardiac surgery

· Pulmonary emboli or intrinsic pulmonary disease

· Drugs such as digoxin

· Fever, anaemia, acidosis or alkalosis, electrolyte or other metabolic abnormalities, endocrine abnormalities, endogenous catecholamines, acute abdominal process, cerebrovascular accidents

Flat T waves and small ST-segment changes may also be seen in healthy individuals, including well-trained athletes, leading to mistaken diagnosis of heart disease. T-wave inversions, however, are more concerning for cardiomyopathy or another cardiac syndrome, depending on the clinical context.

Therefore, a careful clinical history is important. In the absence of any clear pointers further investigation with echocardiography may be appropriate to ensure there is no structural cardiac disease. If the patient is at significant risk of ischaemic heart disease functional testing may be appropriate.

Sinus bradycardia

For most patients with sinus bradycardia, the underlying cause can usually be determined from history and physical examination alone. The quantity of exercise performed, and level of fitness will determine the sinus node rate and common causes are exposure to medications and uncommonly systemic conditions (e.g. hypothyroidism). Symptoms may be subtle such as light-headedness, unexplained falls, or exertional dyspnoea due to chronotropic incompetence, or they may be pronounced such as syncope. These symptoms point to underlying sinus node disease. Therefore, it is important to establish if the patient can increase their heart rate to appropriate levels for their age. The maximum predicted heart rate is generally around 220-age. Sinus bradycardia in a healthy, athletic individual requires no further evaluation or intervention. On the other hand, sinus bradycardia in an older individual may indicate sinus node dysfunction and require further assessment. In young fit patients without cardiovascular symptoms and normal exercise capacity no action is needed.

Ectopic atrial rhythms

Ectopic atrial rhythm occurs when the dominant pacemaker is an ectopic focus in the atrium and not the sinus node. This may result from sinus node failure and the development of an escape atrial rhythm (generally at 30 - 60 bpm) or the acceleration of an ectopic atrial focus faster than the rate of the sinus node. In such cases, sinus node impulse generation is suppressed.

Ectopic atrial rhythm (EAR) is a common arrhythmia and represents that atrial ectopic electrical discharge replaces the sinoatrial node (SAN) with a continuous regular rhythm. EAR could result from different mechanisms. The ectopic atrial foci could serve as a subsidiary pacemaker to rescue the slow heart rate due to a diseased SAN. The diseased SAN might represent a common detrimental consequence due to pathological changes in the SAN and atria in various cardiovascular diseases. However EAR could be simply considered a transient benign phenomenon, while the hierarchy of the SAN might also be usurped by an accelerated ectopic focus and for this reason EAR is generally considered to be a benign arrhythmia,

Recent cohort studies of older patients show that ectopic atrial rhythm is associated with a 2-fold increase CV mortality and a 6-fold increase in the requirement for permanent pacemaker. For these patients we advise clinical assessment of any cardiovascular symptoms, an echocardiogram to assess for any underlying structural heart disease and a 24h period of continuous ECG monitoring. Referral to cardiology is required for further assessment if there are symptoms or significant abnormalities found on echo/continuous ECG.

Left axis deviation

This reflects a QRS axis of less than -30 degrees. Causes for left axis deviation include:

· Normal variation (physiologic, often with age)

· Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, abdominal tumor)

· Left ventricular hypertrophy

· Ischaemic heart disease

· Emphysema

First step is to look at the patients age and medical history. Those patients who are >75 years and with a history of hypertension LAD is commonly seen. In other patients an echocardiogram should be performed to look for LV hypertrophy, underlying structural heart disease or regional wall motion abnormalities. LAD itself does not need any treatment.

Left anterior fascicular block

This is present on the ECG when there is a significant left axis deviation (>-45 degrees) and S wave in the lateral leads. Prevalence ranges from 0.2% in younger adults to 8% in people > 90 years. In older patients LAFB is not associated with increased mortality but there is an increased risk of complete heart block and pacemaker placement. Any symptoms consistent with the development of cardiac disease (e.g., coronary heart disease, heart failure, atrial fibrillation) should be evaluated. It is associated with a greater risk for subsequent development of AF and HF so patients should be aware of symptoms attributable to these conditions, and they should consider further cardiac evaluation if there is any concerning history.

Patients with isolated LAFB are generally asymptomatic and do not require placement of a pacemaker or any other specific therapy or follow up up aside from routine care and management of cardiovascular risk factors. Pragmatically we undertake echocardiography in patients with LAFB and suggest referral to cardiology outpatients if there are significant structural abnormalities or symptoms suggestive of underlying heart disease. Our experience with younger patients (< 60 years old) who have LAFB is that there is often evidence of ischaemic heart disease and so investigation of these patients may be required and referral to cardiology is recommended.

Left bundle branch block

LBBB often occurs in patients with underlying heart disease and may be associated with progressive conducting system disease and impairment of left ventricular function and therefore patients should be evaluated for hypertension, coronary artery disease, heart failure and other cardiac disorders. In most patients, this can be accomplished with a careful history and physical examination combined with echocardiography and either ischaemic stress testing or CT coronary angiography. LBBB can occur without structural heart disease, ventricular dysfunction, or coronary artery disease is then associated with a low mortality and incidence of cardiomyopathy. In such patents the incidence of cardiomyopathy (EF<50%) was 0.71% at 10 years. This makes routine follow up echocardiography inappropriate. We therefore recommend referral of patients with LBBB to cardiology outpatients for further assessment.

Right Axis deviation

· Left posterior fascicular block

· Lateral myocardial infarction

· Right ventricular hypertrophy

· Chronic lung disease (e.g. COPD)

· Hyperkalaemia

· Sodium-channel blocker toxicity

· WPW syndrome

· Normal in children or thin adults with a horizontally positioned heart

Generally no action is needed for isolated right axis deviation. QRS axis is greatly dependent on age. It is rightward at birth and shifts leftward with age. In children and adolescents, the axis is still in transition and right-axis deviation is a common finding (reported prevalence as high as 20%). In older populations, right-axis deviation is rare and generally associated with pulmonary disease. Left-axis deviation occurs in 8% of healthy air crewmen and is the most common abnormal ECG finding in the 30 to 40s age group. Several large cohort studies have attempted to define normal axis for age. The largest of these studied 46,129 individuals with a low probability of cardiovascular disease and found that 95% of athletes <20 years of age had QRS axis 0 to 102° and 95% of athletes 20 to 29 years of age had QRS axis of -10 to 95°, in another study of a cohort 18 years of age and under 95% exhibited a QRS axis between 41and 113°.

Incomplete Right Bundle branch block pattern

Incomplete right bundle branch block (IRBBB), an entity undefined by a general consensus, can express a large pallet of both benign and pathological patterns. IRBBB is a common electrocardiogram (ECG) finding at all ages, more frequent in men and athletes. Usually, IRBBB does not need further evaluation; however, if abnormalities are found on the clinical exam, heart disease should be excluded. The RSR’ pattern and a QRS width below 100 ms define the crista supraventricularis (CSV) pattern. CSV is a right ventricular crest, one of the last structures to be depolarized by the Purkinje network. CSV pattern might result from posterior apex deviation, subpulmonic area delay, or late CSV activation. IRBBB can appear because of higher placement of electrodes V1 and V2 and pectus excavatum, in which P wave is negative, or in athletes, considered a benign pattern unless family history, symptoms, or left ventricular hypertrophy. It is necessary to differentiate IRBBB from pathological patterns such as type-2 Brugada ECG pattern, right ventricular enlargement, arrhythmogenic right ventricular cardiomyopathy, ventricular preexcitation—Wolf-Parkinson-White syndrome, and hyperkalemia. Examiners should be particularly alert to the splitting of the second heart sound because RBBB is a common finding in ostium secundum atrial septal defect. Therefore, clinicians need to be familiar with this ECG finding, which is not always a benign condition.

Right bundle branch block

Right bundle branch block (RBBB), a pattern seen on the surface electrocardiogram (ECG), results when normal electrical activity in the His-Purkinje system is interrupted with a resultant characteristic appearance on the ECG manifest by a widened QRS complex and changes in the directional vectors of the R and S waves. The prevalence of RBBB increases with age from 0.8% in subjects at age 50 to 11.3 % by age 80. There is no significant association with risk factors for, or the presence of, ischemic heart disease, myocardial infarction, or cardiovascular deaths, suggesting that RBBB is usually a marker of a slowly progressive degenerative disease that also affects the myocardium.RBBB can rarely occur in an otherwise normal heart, with a prevalence estimated between 1-2%. Patients with isolated chronic RBBB are generally asymptomatic and do not require placement of a pacemaker or any other specific therapy. However, a pacemaker may be needed if syncope occurs, particularly if other conduction disturbances are present, such as third-degree or type II second-degree AV block.In a patient with a new RBBB we advise a careful history focused on potential causes of RV stretch/strain (e.g., pulmonary hypertension, obstructive sleep apnoea, pulmonary embolism) and if there is suspicion of pulmonary disease potentially impacting the RV, an echocardiogram should be obtained for further evaluation. If there are symptoms of pre-syncope or syncope, then we advise further evaluation with echocardiogram and 24h continuous ECG monitoring.

First degree AV conduction delay

The diagnosis of first-degree AV block is made when the PR interval exceeds 200 msec. Asymptomatic patients with first-degree AV block do not require any specific therapy. The prognosis related to first-degree AV block remains uncertain. In a meta-analysis that included 400,000 patients first-degree AV block was associated with a higher risk of mortality (RR 1.2, 95% CI 1.0-1.5) as well as heart failure or left ventricular dysfunction (RR 1.4, 95% CI 1.2-1.7) and atrial fibrillation (RR 1.5, 95% CI 1.2-1.7) but was not associated with a higher risk of CV death, CHD, MI or stroke. Asymptomatic patients with incidental finding of first-degree AV block should be evaluated clinically for the presence of cardiac disease but do not need referral to cardiology. Echocardiography and continuous ECG monitoring are generally not required. Refer patients with first degree AV conduction disease associated with other ECG abnormalities such as bundle branch block or if there is suspicion of underlying cardiac disease.

Fasicular blocks – (Bi and tri-fasicular)

Interruptions in conduction with right bundle branch block (RBBB) and either left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB) is called bi-fascicular block (BFB). If there is also first-degree AV conduction delay, this is called tri-fascicular block (TFB).

Refer patients to a Cardiologist if they have cardiovascular symptoms such as syncope or pre-syncope, prior history of ischaemic heart disease or heart failure or if cardiac disease is strong suspected. These patients need to be assessed to see if they require a permanent pacemaker.

In asymptomatic people progression the progression to syncope or complete heart block is generally infrequent however risk depends on patient age and the type of block. The 10-year risk of syncope or complete heart block can be estimated from the chart below which is obtained from the Copenhagen Heart Study (Heart Rhythm Volume 19, Issue 2, February 2022, Pages 252-259):

We recommend referral to Cardiology if the risk of syncope or complete heart block is >10 percent over 10-years (i.e. > 1 percent per year). In those patients who are asymptomatic, with a 10-year risk of < 10 percent we suggest reviewing medication to identify any that slow cardiac conduction and if present if should be stopped, performing an echocardiogram and a 48h period of ECG monitoring. For those with a structurally normal heart and no higher degrees of block on ECG monitoring can be safely managed in primary care. If the patient subsequently develops symptoms of syncope they should be referred to Cardiology.

Septal q wave

First check that the leads have not been placed too high. If there is P wave flattening or inversion in V2 then this is likely to be the case and the ECG should be repeated. Otherwise, a septal q wave can be associated with septal infarction or as part of changes related to hypertension and therefore echocardiography is advised in the first instance.

T wave inversion

T wave changes are commonly seen in people with established structural or ischaemic heart disease and are usually secondary to those problems already identified. In people without established heart disease negative T waves could be a normal variant of the electrocardiogram in youth, an athlete’s heart adaptation to physical activity or a pathologic process such as right ventricular arrhythmogenic or hypertrophic cardiomyopathy. T-wave inversion in leads V1 to V3 is a relatively rare finding in middle-aged people it carries a normal prognosis in the absence of other features of heart disease. Although. In contrast, inverted T waves outside of V1 to V3 may imply cardiac pathology and is associated with increased cardiac mortality. We recommend further investigation when negative T waves are present beyond V1 or in the inferior-lateral leads to rule out cardiomyopathy. A TWI in these leads could be a benign finding but could also be the first sign of a pathologic condition not yet manifested. These patients should be referred to cardiology for further evaluation which would include echocardiography, possibly cardiac MRI in addition to other testing.

Reduced R wave progression on ECG

Poor R-wave progression (PRWP) is a common ECG finding that is often inconclusively interpreted as suggestive, but not diagnostic, of anterior myocardial infarction (AMI). PRWP is defined by R wave height ≤ 3 mm in V3. Possible causes are: Normal variant (38%), previous anteroseptal MI (35%); left ventricular hypertrophy (14%) and right ventricular hypertrophy (13%). It can also be caused by inaccurate lead placement (e.g. transposition of V1 and V3) and occasionally dilated cardiomyopathy. In a study of patients undergoing cardiac stress tests, only a small percentage of patients who met various criteria poor R wave progression had anterior MI and therefore conclusions about the presence of anterior MI solely on the basis of poor R wave progressio have little usefulness. In patients with normal cardiac autopsy who had poor R-wave progression on ECG recorded within 3 months of death it has been concluded that is not related to age, sex, height, weight, body surface area, obesity, thoracic skeletal abnormalities, diabetes mellitus, serum cholesterol level, or arterial BP.

Inferior Q waves on the ECG

Pathologic Q-waves are defined as duration of ≥ 30 ms and depth of ≥ 1 mm or QS-complex. While Q-waves in inferior leads, particularly lead III, can be regarded as a minor abnormality, it can also indicate the presence of myocardial scar. In studies the diagnostic value of pathologic inferior Q-waves (lead II, III, aVF) for detecting ischemic scars using a high-resolution cardiac magnetic resonance (CMR) has been examined. Q-waves in leads II + aVF and II + III + aVF show a high specificity (100% and 99.6%), positive predictive value (PPV) (80.0% and 86.7%), and negative predictive value (NPV) (82.6% and 84.3%) but low sensitivity (1.3% and 13.1%). These findings highlight the need for careful clinical assessment when pathologic Q-waves are present.

Kosum, P., Theerasuwipakorn, N., Srisuwanwattana, W. et al. Diagnostic values of inferior Q-waves for myocardial scar identification detected by 3.0 T cardiac MRI. Sci Rep 14, 16650 (2024). https://doi.org/10.1038/s41598-024-67908-8

QT prolongation on ECG

QT prolongation may occur with metabolic abnormalities such as hypokalemia and hypomagnesemia, impaired hepatic and/or renal function or medications. Patients with anorexia may be predisposed to a long QTc because of catabolic metabolism, electrolyte disturbances, psychotropic medications, or other physiologic changes. Ischemic QTc prolongation may be common during the early phase of ischemia.

Reversible causes of QTc prologation should first be sought and correct. Then the QT interval reassessed. If the QTc is <470 msec in males or <480 msec in females, then LQTS is unlikely, and referral is not required.

If QTc is ≥470 msec in males or ≥480 msec in females with personal or family history suspicious for LQTS, then the patient has high probability LQTS (estimated at >90% likelihood). These patients should be referred to an Inherited Cardiac Conditions clinic for further evaluation. If the patient QTc is ≥470 msec in males or ≥480 msec in females but <500 msec AND there is no personal or family history to suggest LQTS, the patient is graded as intermediate probability LQTS by the Schwartz score, this should not be viewed as definite LQTS. This means the patient has a small but definite chance (5 -20%) of having congenital LQTS. The background rate of genetic long QT syndrome is 1:2000 and therefore these individuals are at significantly higher risk and require referral to an Inherited Cardiac Conditions clinic for further specialist evaluation and genetic testing through the ERS – pathway of ICC/ICD and PICC.

Echocardiographic abnormalities

When valve regurgitation is graded on a scale from none –to- trace –to- trivial –to- mild –to- moderate –to- severe. Trace or trivial means barely detectable and is of no concern whatsoever. The tricuspid valve almost always has up to mild regurgitation. This is normally seen and should never be regarded as abnormal. This does not need any follow up or monitoring. For the aortic valve any degree of regurgitation is regarded as abnormal but when it is trivial, and the valve is tricuspid then this is of no cause for concern and does not need further follow up echocardiography nor any clinical monitoring. Echos are reported as to the probability of pulmonary hypertension from low to intermediate to high. When the probability is low this is normal, and no action is needed, I hope you will be able to apply this information to future cases you manage.

Grade 1 diastolic dysfunction

In someone over the age of 60 Grade 1 diastolic dysfunction is a normal finding since age is an important factor which defines the normal diastolic values. With the increasing stiffness of the ageing heart, diastolic impairment can be detected. Equalization of E and A velocities at approximately age 50 years and to a reversed E/A after that age and occurs independent of cardiovascular disease and other confounding physiologic variables making it essentially a normal finding. No specific treatment is needed for Grade 1 diastolic dysfunction apart from appropriate control of cardiovascular risk factors with lifestyle advice and medication. Patients do not need to be referred to cardiology. Patients <50 years old without obvious CV risk factors requiring treatment may be referred to cardiology for further assessment.

Aortic root dilatation

The ESC Guidelines on the diagnosis and treatment of aortic diseases tell us that AA dilatation is a common incidental finding in thoracic area imaging, especially in middle-aged and older male. They recommend patients be followed-up with annual imaging if the dilatation degree is <45 mm and every 6 months when the degree of dilatation is between 45 and 55 mm. However, these guidelines are now 10 years old and contemporary studies have indicated that the growth of AA is on average about 0.3mm/year with <40% of patients having any change in AA dimensions over a median of 3.4 years of follow up. This means the current guidelines are probably scanning too many people for which there will never be any significant change in AA and no need for intervention. Contemporary practice therefore in patients with a small AA (<45mm) and tricuspid aortic valve and no FH of AA disease and no genetic syndrome is to do a second echo at 1 year after the first and then if there is no significant change in the dimension to scan again after 3 years otherwise the frequency of echo is so high that the departments become overrun with these scans. If the dimensions are 45-55 then patient should be referred to cardiology.

Management of thoracic aortic aneurysm in adults

Based primarily on studies performed in Marfan patients, for patients with asymptomatic TAA who are being conservatively managed, we suggest blood pressure control primarily using beta blocker therapy with the aim of limiting further aortic expansion. While the theoretical benefit of anti-impulse therapy is widely accepted, no controlled studies have demonstrated a benefit. The goal systolic pressure is 105 to 120 mmHg, if tolerated. The adequacy of beta blockade is usually judged by the heart rate response. An angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) is an acceptable alternative for blood pressure control among those who do not tolerate beta blocker therapy. Statin therapy may provide a protective effect by inhibiting matrix metalloproteinases (MMPs) and plasminogen activator In one retrospective review of TAA patients, mortality rates were significantly lower among those taking statins compared with those who were not (20 versus 33 percent); this effect was independent of angiotensin blockade. Survival was attributed to a decreased need for surgical repair due to reduced aortic expansion. In another retrospective review, statin therapy was associated with a significant reduction in complications, including aortic dissection.

Ventricular septal bulge

Septal bulge is not an uncommon finding in older people on echocardiography and may occur as part of the cardiac remodelling associated with aging. Its prevalence increases with age, reaching 10% in people ≥70 years. Generally, it will not have any symptoms and is an incidental finding. There is no conclusive association= between hypertension and septal bulge. Due to the high prevalence of hypertension in the elderly, a history of it does not help in suggesting or ruling out the diagnosis.

The question is whether its presence is secondary to hypertrophic cardiomyopathy (HCM). It is a finding compatible with a diagnosis of HCM but only if the basal septal wall thickness measurement is increased. The presence of systolic anterior motion with septal contact resulting in an LVOT gradient (i.e, subaortic obstruction) strongly suggests a diagnosis of HCM in patients with is isolated sigmoid septal hypertrophy. A positive family history of HCM and/or sudden cardiac death and the presence of exertional symptoms usually support HCM, though they are less likely in older patients with HCM, and poorly investigated in individuals with VSB. A more severe hypertrophy and the presence of left ventricular outflow obstruction are considered diagnostic of HCM. Pragmatically we offer further evaluation in patients with a septal bulge who are younger (<65 years) or with other echocardiographic features of HCM described above or with a positive family history.

Patent foramen ovale

Patent foramen ovale (PFO) occurs in 25 to 30 percent of the general population. The prevalence of PFO is higher in patients with cryptogenic stroke, particularly those under age 55 years in whom PFO is more likely to play a causal role. An incidentally detected PFO generally requires no follow-up or treatment. Assessing clinical significance of PFO – Identification of PFO in a patient with an embolic event does not prove a causal relationship. The evaluation of patients with PFO with an embolic event should include careful assessment of the likelihood that the PFO is causally related to the event, including identification of other potential causes of thromboembolism and stroke and of potential sources of venous thromboembolism

Atrial Septal Aneurysm

An ASA is defined as redundant and mobile interatrial septal tissue in the region of the fossa ovalis with phasic excursion of at least 10 to 15 mm during the cardiorespiratory cycle. It is commonly associated with a patent foramen ovale which occurs in 25 to 30 percent of the general population.

Prevalence of PFO is higher in patients with cryptogenic stroke, particularly those under age 55 years in whom it is is more likely to play a causal role. No specific treatment is needed for incidentally discovered PFO and/or ASA in asymptomatic patients.

The available evidence from population-based studies suggests that PFO and large PFO are not independent risk factors for ischemic stroke in otherwise asymptomatic individuals. However, given the potential risk of paradoxical embolism in patients with PFO and ASA it is reasonable to educate the patient on how to prevent deep venous thrombosis by avoiding prolonged period of immobilization and dehydration.

PFO and Migraine:

PFO is a common abnormality present in about 25 to 30 percent of people but only detectable in about 5% people on echocardiography. A link was thought to occur between migraine with aura and PFO. Anecdotal evidence suggested that closure of the PFO led to resolution of the migraine. However, clinical trials have failed to show that PFO/ASD closure is beneficial for migraine.

The multicenter double-blind MIST trial enrolled 147 patients with a PFO who had frequent migraine with aura that was refractory to two types of preventive medication. At six months, there was no difference between PFO device closure and sham treatment for the primary end point of headache cure, which was achieved in each treatment group by three patients (4%). Furthermore, the PFO closure group experienced more serious adverse events than the sham group. The smaller open-label PRIMA trial, which was stopped prematurely due to slow recruitment, compared PFO device closure with medical management among subjects with migraine with aura. At one year, there was no difference between groups for reduction in monthly migraine days. In earlier reports, which were relatively small and largely retrospective, improvement in migraine after device closure of a PFO or an ASD was noted in some (but not all) studies. Most of the patients treated with shunt closure were selected because of prior cryptogenic stroke or paradoxical embolism. Most of the study patients were treated with aspirin and clopidogrel, which may have reduced migraine frequency. No action is needed from cardiology with regards to this finding on the echo.

Bicuspid aortic valve

The management of bicuspid aortic valve disease in adults includes surveillance, intervention for aortic valve disease and aortopathy, treatment of hypertension, measures to address the risk of infective endocarditis, counselling patients on physical activity and the management of risk if non-cardiac surgery is required.

The prevalence of BAV is about 1 in 100 in the general population with a 2:1 male to female ratio and 1 in 10 first degree relatives will have a BAV so they should be offered screening with echocardiography.

In a patient with a well-functioning bicuspid aortic valve with mild aortic regurgitation no significant stenosis and normal aortic root diameters echocardiography is recommended every three to five years. The patient does not require outpatient clinic follow up for this condition on a routine basis annually as if asymptomatic.

Patients with a bicuspid aortic valve with moderate valve dysfunction (stenosis or regurgitation) or a dilated aortic root (>40mm) should undergo annual echocardiography and cardiology outpatient review.

Aortic stenosis

Symptoms occur with severe aortic stenosis and include Dyspnoea on exertion or decreased exercise tolerance, Exertional dizziness (presyncope) or syncope and Exertional angina. It is not usual for patients to get symptoms from non-severe aortic stenosis and if they are other causes should be considered such as coronary artery disease, arrhythmia or lung disease.

Aortic valve disease is managed according to its stage:

Stage A: Asymptomatic patients with peak aortic velocity (AV) <2 m/s. These patients are at risk of aortic stenosis and AS are managed in primary care with an echo every 3-5 years.

Stage B: Asymptomatic progressive AS with mild AS or moderate AS. These patients can be managed in primary care with an echo every 2 years (mild) or annually (moderate).

Stage C: Asymptomatic severe AS. These patients should be referred to cardiology

Stage D, patients have symptomatic severe AS. These patients should be referred to cardiology

Biatrial dilatation

Echo measures LA volume, and it is commonly reported to be abnormal. LA volume indexed for BSA is measured as follows: Normal: 16–28 mild dilation: 29–33 moderate dilation: 34–39 Severe dilation: ≥40. In healthy individuals LA volume index is independent of age and attributable to the pathophysiologic changes associated with normal aging process as opposed to the result of normal aging itself. LA enlargement is mostly the result of pressure and/or volume overload. LA enlargement due to pressure overload is usually secondary to increase LA afterload in the presence of mitral stenosis or LV dysfunction. The relationship between LA enlargement and increased LV filling pressure has been shown in individuals with and without mitral valve disease. LA volume overload resulting from mitral valve regurgitation, arteriovenous fistula, left to right shunt, or high cardiac output state can also contribute to LA chamber remodelling.

LA volume predicts AF in elderly patients and is an independent predictor of first AF or atrial flutter, incremental to clinical and other echocardiographic parameters of AF or atrial flutter prediction. The association between LA size and new onset AF and the association of AF with increased risk of stroke have been noted, the relationship between LA size and stroke does not appear to invariably involve AF. Recently, in elderly patients without AF at baseline, LA volume index ≥32 was independently predictive of a first ischemic stroke. This association persisted even after patients who developed AF during the follow-up were deleted from consideration. LA volume is a sensitive barometer of LV filling pressure and reflects the burden of diastolic dysfunction in absence of severe valve disease and AF. LA volume index ≥32 was an independent predictor of first CHF. The European Society of Cardiology diagnosis of HF with normal LV ejection fraction considers LA volume index >40 to provide sufficient evidence of diastolic dysfunction when the E/E′ ratio is non-conclusive (15>E/E′>8) or when NTproBNP is elevated. Similarly, LA volume index <29 is proposed as a prerequisite to exclude HF with preserved systolic function.

Mitral regurgitation

Staging of chronic MR is based upon symptoms, valve anatomy, severity of MR, and hemodynamic consequences of MR as reflected by left atrial size, LV size and function, and pulmonary artery pressure. A goal of monitoring is to identify changes (which can occur with or without reported symptoms) for optimal timing of intervention. For individuals with mild MR, frequency of follow-up is based on the type and severity of mitral leaflet disease. Follow-up for patients with primary mitral valve disease and moderate to severe MR includes at least an annual history and physical examination. Serial TTE is performed to assess the severity of valve disease, LV size, LV ejection fraction (LVEF), and LV end-systolic dimension. The frequency of recommended follow-up varies with the severity of MR: For patients with primary mitral valve disease and mild MR and no evidence of LV enlargement, LV dysfunction, or pulmonary hypertension, echocardiography every three to five years is appropriate. Patients with primary mitral valve disease and moderate MR should undergo echocardiography every one to two years. Patients with severe MR should be seen every 6 to 12 months (sooner if symptoms occur) with a repeat TTE. The six-month interval is preferred if stability has not been documented, if there is evidence of progressive LV dilation, reduction in LV systolic function, or increase in pulmonary pressure, or if measurements are approaching values used in an indication for mitral valve surgery.

Heart failure

NT-proBNP measurement

BNP is useful as a component of the evaluation of suspected heart failure (HF) when the diagnosis is uncertain and the evaluation of undifferentiated patients with shortness of breath. It is important to understand when to measure this marker and how to interpret the results. ESTH uses NT-proBNP (referred to as BNP (pg/ml)) which is more stable in the plasma and therefore suitable for samples taken in primary care. BNP is not a specific test for heart failure and increases with structural heart disease, valve disease and age. Its main use is in ruling out heart failure since values <100 have a very high negative predictive value for HF as a cause of dyspnoea. Most dyspnoeic patients with HF have BNP values >400. In the range between 100 and 400 BNP is not very sensitive or specific for detecting or excluding HF. Age dependent cut offs can be considered also in patients aged <50 a BNP of 450 is optimal, 50 to 75 years, 900 optimal and >75 years, 1800 is optimal. So further evaluation of a patient with a BNP>400 is required but unless the BNP is greater than these values LV systolic impairment is still unlikely. After a patient has had an echocardiogram and the diagnosis made there is usually little point in measuring BNP again. Randomized trials studying the effect of BNP guided therapy on clinical outcomes have shown mixed results with the weight of evidence suggesting modest or no clinical benefit from use of BNP levels to aid optimization of HF drug doses.

Raised Cardiothoracic Ration on Chest X ray

Chest radiographs (CXR) are routinely used to assess the lungs and mediastinum. Cardiothoracic ratio (CTR) is a simple method to evaluate the heart size on chest radiographs. Despite having been introduced more than 100 years ago [1], it is still commonly reported nowadays, even though new imaging techniques have been developed. This is probably because CTR can be easily measured and simply interpreted on a widely available and inexpensive imaging study. Nevertheless, CTR depends on multiple technical and anatomic factors that can contribute to an inaccurate assessment of the real heart size. CTR is only considered reliable if calculated from a frontal upright postero-anterior (PA) chest radiograph. The supine position and any other antero-posterior (AP) projection overestimate cardiac size due to a magnification effect caused by the heart being closer to the imaging cassette. In addition, there are other cardiac and non-cardiac aspects such as sub-optimal inspiratory effort, patient’s or thoracic cage abnormalities that could influence the value of CTR.

CTR is defined as the ratio between the maximal horizontal cardiac diameter and the maximal horizontal inner thoracic cage diameter [2]. A CTR > 0.5 (or > 50%) is considered abnormal. In radiology reports, terms like “cardiomegaly” or “increased heart size” are commonly used to describe an increased CTR. Despite its broad use, some researchers have questioned the real value of this arbitrary cut-off point. For example, in a study with patients undergoing coronary angiography due to angina, a CTR between 42 and 49% was associated with a higher risk of all-cause mortality or major coronary event (death, non-fatal myocardial infarction) compared to patients with CTR < 42% A normal measurement is 0.42-0.50. A measurement <0.42 is usually deemed to be pathologic. A measurement >0.50 is usually taken to be abnormal although some radiologists feel that measurements up to 0.55 are "borderline". CTR correlates weakly with true chamber size assessed by gold standard cardiac MRI and has a weak discriminatory power. Thus, clinical decisions based on intermediate CTRs (45–55%) should be avoided. Large CTRs (> 55%) are likely indicative of true heart chamber enlargement. Low CTRs (< 45%) are likely indicative of normal heart size.

Guideline directed medical therapy for LV systolic dysfunction

For patients with an LVEF of <40% we recommend the following treatment:

1. ACE or ARB. Check the creatinine and potassium first and at 1-2 weeks after initiation. Generally start with Ramipril 1.25mg or Losartan 12.5mg daily. If the patient has significant fluid overload and in clinical heart failure watch for hypotension.

2. Beta blocker - Heart Failure specific such as Bisoprolol, Metorprolol CR or Carvedilol Generally start with Bisoprolol 1.25mg daily. Contraindications include bradycardia (HR <60 or evidence of heart block).

3. MRA - Generally Spironolactone 12.5 or 25mg daily depending on the blood pressure with a check of renal function and potassium within 10 days.

4. SGLT-2 inhibitor. Dapagliflozin 10mg daily. Well tolerated and simple to use.

So for this patient there is an indication for the medication described above which should be initiated in the absence of contraindications.

Heart failure with preserved ejection fraction

We use the H2FPEF Score for Heart Failure with Preserved Ejection Fraction was that combines easily obtained clinical and echocardiographic variables to determine the probability of HFpEF (H₂FPEF) in euvolemic patients with dyspnoea.

Obesity (BMI >30 kg/m²; 2 points), atrial fibrillation (3 points), age >60 years (1 point), treatment with ≥2 antihypertensives (1 point), echocardiographic E/é ratio >9 (1 point), and estimated PASP >35 mmHg (1 point) are assessed and the score calculated. The assessment and probability calculation were based on data from 414 patients, all of whom underwent RHC. Patients were considered to have HFpEF if they had an elevated mean pulmonary capillary wedge pressure at rest (≥15 mmHg) or with exercise (≥25 mmHg).

The H₂FPEF score better discriminated those with dyspnoea from HFpEF from euvolemic patients with dyspnoea due to noncardiac causes (a score >7 is associated with a >95 percent chance of having HFpEF). This score can help more accurately identify those with HFpEF. #

Principles of management are treatment of any volume overload with loop diuretic therapy before initiating other therapies.

In patients with LVEF ≥50% and NYHA class II to III symptoms we recommend measuring NT-proBNP and if it is >300 pg/dL treat with both a sodium-glucose co-transporter 2 (SGLT2) inhibitor and a mineralocorticoid receptor antagonist (MRA).

We typically start the SGLT2 inhibitor first and then add the MRA two weeks later if the patient tolerates initial therapy. We do not withhold a second agent if HF symptoms resolve or if the BNP decreases in response to initial therapy.

Dapagliflozin and renal impairment

There is often concern about renal impairment in patients treated with SGLT2 inhibitors. In a large trial published in the NEJM among patients with chronic kidney disease, regardless of the presence or absence of diabetes, the risk of a composite of a sustained decline in the estimated GFR of at least 50%, end-stage kidney disease, or death from renal or cardiovascular causes was significantly lower with dapagliflozin than with placebo (N Engl J Med 2020;383:1436-1446 DOI: 10.1056/NEJMoa20248). Specially the least-squares mean estimated GFR slopes from baseline to 30 months in the dapagliflozin and placebo groups were –2.86±0.11 and –3.79±0.11 ml/min, respectively, resulting in a between-group difference of 0.93 ml/minute. During the first 2 weeks, there was a greater reduction in the estimated GFR in the dapagliflozin group than in the placebo group and thereafter the annual change in the mean estimated GFR was smaller with dapagliflozin than with placebo. This and other trials confirms that the kidney-protective effects of SGLT2 inhibitors extend to the broader population of persons with chronic kidney disease without type 2 diabetes, for whom ACE inhibitors are the only pharmacologic treatments that have been shown to prevent kidney failure. For clinicians in general practice a eGFR centric approach stopping these drugs when there are small changes in this parameter is likely to deny patients the proven benefits of these agents and therefore we recommend that they be continued.

Pulmonary hypertension

We use TR velocity and estimated PASP together with echocardiographic findings suggestive of RV hypertrophy/strain when evaluating the probability of PH

PH is suggested echocardiographically when the TRV is ≥2.8 m/s and/or when RV size, wall thickness, and function are abnormal, understanding that PH may still be present even in the absence of these findings. Peak TRV together with echocardiographic findings of PH is used to come up with a probability of PH., which should be interpreted together with clinical suspicion and signs of RV dysfunction to facilitate the decision about proceeding with additional testing for PH,

PH is likely if the TRV is >3.4 m/s and unlikely if the TRV is ≤2.8m/s and no other suggestive findings of PH on TTE. PH is possible if the TRV is >2.8 and ≤3.4, and there are findings suggestive of PH on TTE.

For those in whom the suspicion is low, the diagnostic evaluation should be directed toward alternative diagnoses. In this population, RHC is rarely performed unless their symptoms are unexplained by alternate diagnoses. For those in whom the clinical suspicion for PH is intermediate or high, progressing with an evaluation for PH that may involve RHC is appropriate.

When the probability of PH on echocardiography is intermediate or high, the underlying cause of PH needs to be assessed. Importantly, patients with evidence of severe PH and/or patients with significant symptoms should be referred to a PH centre for rapid evaluation.

The next step is to identify the presence of left heart disease (LHD) which would be sufficient to explain PH (ie, group 2 PH; LHD-PH). If there is no or insufficient LHD on echocardiography to explain PH, additional investigations targeted at other suspected aetiologies are necessary (ie, group 1, 3, 4, and 5 PH) and referral to a pulmonary hypertension centre is required.

Clinicians should determine whether there is enough LHD on the echocardiogram to explain the degree of estimated PH. Many patients in this category do not require further testing to confirm the diagnosis of LHD-PH (ie, group 2 PH).

The presence of significant LHD may be obvious in patients who have left atrial (LA) dilation in conjunction with severe left ventricular systolic dysfunction or severe mitral or aortic valve disease. However, the presence of heart failure with preserved ejection fraction (HFpEF) may be subtle on echocardiography and consequently missed.

Low probability of LHD– Patients <60 years old; no obesity, hypertension, dyslipidaemia, glucose intolerance, or diabetes; no previous cardiac intervention (coronary and valvular); no atrial fibrillation or structural LHD; and no signs of left heart abnormalities on ECG, echocardiography including assessment for diastolic function, These patients have insufficient LHD to explain PH discovered on echocardiography and should be investigated as such with referral to a PH centre.

Intermediate probability of LHD– Patients 60-70 years old; 1 or 2 of the following: obesity, hypertension, dyslipidaemia, glucose intolerance or diabetes; have no previous cardiac intervention, currently have paroxysmal atrial fibrillation; no structural LHD is present; have mild LVH on ECG; have not LA dilation with grade <2 diastolic dysfunction on echocardiography. The impact of LHD in this group is uncertain, and as such, most patients in this category should have an RHC, particularly when other risk factors for PH are present (eg, systemic sclerosis [SSC], thromboembolic disease), RV abnormalities are present, or dyspnea is unexplained.

High probability of LHD: Patients >70 years old; 2 of two of obesity, hypertension, dyslipidaemia, glucose intolerance, or diabetes; have previous cardiac intervention, atrial fibrillation (paroxysmal or persistent), and structural LHD is present; left bundle branch block or left ventricular hypertrophy (LVH) on ECG; LA dilation and tissue Doppler of elevated left heart filling pressure on echocardiography. These patients have sufficient disease to explain PH, and most do not need RHC for diagnostic purposes.

PH from HFpEF (diastolic dysfunction) is a growing group of patients who are being diagnosed with PH. Patients with obesity can also develop an extreme form of diastolic dysfunction sometimes referred to as an "obesity-associated restrictive cardiomyopathy It is characterized by fatty infiltration of cardiac myocytes, restrictive physiology, and marked elevation in left and right heart filling pressures. These patients can also progress to severe PH secondary to an occlusive vasculopathy of the small PAs and arterioles, like PAH. Echocardiographic signs of HFpEF can confirm the diagnosis of HFpEF, but they are imperfect and subject to limitations

Ischaemic heart disease

Evaluation of CVD Risk in patients without established CVD

We advise the use of a risk calculator to provide a 10 year estimated CVD risk although we note that age is a powerful risk factor and therefore

Aspirin in primary prevention of vascular disease

The decision to prescribe aspirin should be made on an individual basis through a process of shared decision making by the patient and health care provider after assessment of the benefit-to-risk profile of the patient.

Based on the totality of the clinical trial evidence the major potential benefit of long-term aspirin appears to be a reduction in the risk of myocardial infarction (MI) among a small number of individuals. This potential benefit needs to be balanced with the small number of individuals at increased risk for bleeding. For patients who receive aspirin for primary prevention, we recommend a dose of 75 to 100 mg daily. Whilst tools are available to calculate the risk of a cardiovascular event, none of these provides a risk-to-benefit calculation that takes into account risk of cardiovascular events, risk of the development of colorectal cancer, and risk of major bleeding with daily aspirin.

For all patients, whether low or high risk, the absolute benefit on MI approximated the absolute increase in the risk of major bleeding. Whatever the level of cardiovascular risk, patients considering primary prophylaxis may reasonably choose to use or not use aspirin. Although numerous trials have reported subgroup analyses for the benefit and harm of low-dose aspirin, results have been inconsistent. However, the risk/benefit ratio of aspirin for primary prevention appears to be less favourable among older adults.

In the ASPREE trial, the only trial enrolling only patients age 70 and above, there was no clear effect of aspirin in primary prevention of MI, stroke, or cardiovascular mortality and among patients treated with aspirin, the rate of major haemorrhage was higher compared with placebo (8.6 events per 1000 person-years versus 6.2; hazard ratio [HR] 1.38 95% CI 1.18-1.62). In the US Preventive Services Task Force (USPSTF) aspirin initiation provides a modest net benefit in life-years in those aged 40 to 59 years with 10% or more 10-year cardiovascular risk. In older patients, the impact varied according to age, sex, and cardiovascular risk. However, aspirin resulted in a loss of life years in men and woman aged 70 to 79.

Some individuals age 40 years or greater at high risk for developing cardiovascular disease (CVD) and without excess bleeding risks may conclude that the benefits of aspirin at a dose of 75mg daily for the prevention CVD events, colorectal cancer incidence, and overall mortality outweigh the risks. However, we suggest not initiating aspirin for primary prevention in patients over the age of 70. Patients already taking aspirin for primary prevention should re-discuss potential risks and benefits with their clinician upon reaching age 70.

Aspirin versus Clopidogrel for long term therapy

The evidence is that Clopidogrel may be a little more effective than Aspirin. The CAPRIE trial (1996) showed long-term administration of Clopidogrel to patients with atherosclerotic vascular disease is more effective than Aspirin in reducing the combined risk of ischaemic stroke, myocardial infarction, or vascular death. The overall safety profile of Clopidogrel is at least as good as that of medium-dose aspirin. However the detail shows that patients treated with Clopidogrel had an annual 5.32% risk of ischaemic stroke, myocardial infarction, or vascular death compared with 5.83% with aspirin. This translates into a number needed to treat of 196 for the prevention of 1 event using Clopidogrel versus Aspirin.

Incidental coronary artery calcification (CAC) on CT scans

Incidental CAC can be found on non-gated chest CT scans that are obtained for other reasons. The addition of CAC to the assessment of traditional risk factors should aid patient reclassification into more accurate risk groups, resulting in incremental clinical benefit through a change in patient behaviour and clinical management [3]. In a meta-analysis of 11,256 participants followed over 1.6–6 years, Gupta et al demonstrated significantly higher use of aspirin, lipid-lowering medication, antihypertensive medication, exercise, and dietary change in individuals with CACS > 0 compared to those with CACS = 0 [25]. In 950 individuals who met inclusion criteria for the use of statins in a preventive interventional clinical trial, the 5-year Number Needed to Treat (NNT) to prevent one CVD event varied from 124 for individuals with CACS = 0, to just 19 for those with CACS > 100 [26]. Similarly, the 10-year NNT to reduce ASCVD events by aggressive blood pressure regulation in patients with an intermediate risk of CAD and prehypertension or mild hypertension correlates to baseline CAC status, from 99 for CACS = 0 to only 24 for CACS > 100 [27]. The SCCT recommends prophylactic daily aspirin in those with CACS > 100, with studies showing a net benefit of aspirin therapy, regardless of risk factors in these cases [28, 29]. There remains a lack of clarity in therapeutic recommendations for Agatston CACS between 0 and 100; however, it may be prudent to initiate statin therapy in presence of any CAC [30].

Mitral annular calcification on echocardiography

Mitral annular calcification (MAC) is most commonly an incidental finding requiring no specific treatment other than assessment and modification of cardiovascular risk factors. There is no established therapy to prevent progression of MAC. The most important intervention for most patients with MAC is evaluation and treatment of standard cardiovascular risk factors. MAC is strongly associated with atherosclerotic disease and adverse cardiovascular outcomes. Thus, presence of MAC should heighten clinical concern for concomitant coronary and atherosclerotic disease and serve as an opportunity to address potentially modifiable cardiovascular risk factors such as hypertension and dyslipidemia. Cardiovascular risk factors should be evaluated and treated according to standard recommendations.

Limited data are available for the natural history of MAC progression. A study from the University of Ottowa included 11,605 patients with MAC and at least two echocardiograms performed over a year apart between 2005 and 2019 and this showed among patients with initially mild or moderate MAC, 33 percent progressed to severe MAC at 10-year follow-up. Progression to severe MAC was more common in females and in patients with moderate MAC at baseline. At 10-year follow-up of all patients, severe MAC associated with mitral valve dysfunction was present in 10 percent, with higher rates in females and in patients with moderate or greater MAC at baseline.

Raised cholesterol

There is a significantly raised serum cholesterol at 7.7 mmol/L, with HDL cholesterol level 1.5 mmol/L and LDL cholesterol 5.5 mmol/L. When you come across a single isolated CV risk factor then you should treat it irrespective of the QRISK2 score which will generally always give a low risk for a female of this age and does not give you any sense of the lifetime risk for the patient. Treatment is relatively straightforward but I wonder if you should consider a diagnosis of familial hypercholesterolemia. This is suspected when there is:

-Elevated plasma LDL-C: An untreated LDL-C level of ≥4.9 mmol/L suggests FH. This value is greater than the 90th percentile for age and sex.

-A Family member with known FH or elevated cholesterol (6.2 mmol/L) in either parent.

-Cholesterol deposits in the patient or family members.

-Premature coronary heart disease in the patient or family member(s).

-Sudden premature cardiac death in a family member.

Miscellaneous

Pectus excavatum

Pectus excavatum (PE) can cause right heart compression and turbulent flow and patients with PE should be evaluated to estimate the severity of the deformity and whether there are associated anomalies especially if there are any cardiorespiratory symptoms. CT is the best way to quantify the severity of PE.

Evaluation with echocardiography and ECG is appropriate and this is a specialist are of cardiac/thoracic practice and I referral to Mr Ian Hunt, Thoracic Surgeon at St George's Hospital is recommended. Mr Hunt has extensive experience in this area and runs a Pectus clinic and can give the best possible advice on what to do, if anything, with regards to the chest abnormality.

The threshold for evaluation should b elow since the level of physical symptoms correlate poorly with severity of deformity on chest CT imaging. In other words, the patient’s symptoms are not a good guide. Pulmonary function testing for restrictive respiratory disease should be used combined with CPEX testing to assess for any cardiopulmonary limitation.

Fitness to fly for passengers with cardiovascular disease

General principles are hat there are few cardiovascular conditions that warrant the denial of fitness to fly as a passenger. Given the right aircraft, on-board equipment and appropriately qualified and experienced escort personnel, aircraft can act as flying intensive care units and carry extremely ill passengers. For those with cardiovascular disease who are not critically ill but who wish to fly on commercial aircraft, the aircraft environment does not pose a significant threat to their health. It is only when their underlying condition is associated with a significant risk of acute deterioration that reasonable restrictions should apply. For those at the more severe end of the spectrum of their specific cardiovascular condition, services exist to help make the journey more easily and safely. Most carriers and airport authorities provide assistance on the ground and in the air. Oxygen is available on most major carriers, although this is sometimes subject to a charge and at least 7 days’ notice is normally required. Passengers are advised to plan their arrival at the airport in plenty of time to avoid having to rush and to warn the carrier and/or airport authority of any requirements for assistance, including requirement for in-flight oxygen, well in advance of the date of departure. They are strongly advised to ensure they have an appropriate supply of their medication, a clear list of the medications and doses they take and a letter of explanation from their doctor regarding their condition, drugs, allergies and devices (eg, pacemaker).

Acute Coronary Syndromes: Passengers who have suffered an acute coronary syndrome can be reasonably divided into those at very low risk who may safely fly as early as 3 days after the event, those at medium risk who may fly from 10 days onwards and those at high risk or awaiting further investigation/treatment in whom flying should be deferred until a more stable situation is achieved.

Very low risk: age <65 years, first event, successful reperfusion, EF >45%, no complications and no planned investigations or interventions.

Low risk: EF >40%, no symptoms of heart failure, no evidence of inducible ischaemia or arrhythmia and no further investigations or interventions planned.

High risk EF: <40% with signs and symptoms of heart failure, those pending further investigation with a view to revascularisation or device therapy.

Stable angina: For patients with ischaemic heart disease the mild hypobaric hypoxaemia induced by commercial airline flight may be expected to have little or no effect in precipitating myocardial ischaemia in people without critical ischaemia at sea level. The available evidence suggests that it is unlikely that flying would precipitate acute myocardial ischaemia and no restriction should be applied. Passengers should be advised to allow plenty of time at either end of their journey to limit anxiety and haste. Passengers should be advised to seek assistance with personal transport at the airport if needed. They should also be advised to remember to take their medication in the usual way and at the usual times.

Arrhythmia: Hypoxia is unlikely to produce an increase in susceptibility to arrhythmia or to have any adverse effect on pacing threshold at cabin altitudes likely to be encountered during air travel. Flight itself does not appear to induce paroxysmal supraventricular tachycardia, atrial fibrillation or atrial flutter, and providing the passengers are symptomatically stable with a low frequency of events, there should be no restriction to flying.

Patients at risk of thrombosis: Commercial airline passengers breathe air with a reduced oxygen content which results in low blood oxygen saturations. The levels of blood oxygen saturations attained appear to have little or no adverse circulatory effects which would make the passenger more liable to myocardial ischaemia, myocardial infarction, left ventricular failure or arrhythmia. Passengers already at high risk may suffer additional risk from hypoxia during flight. This conclusion is supported by the available evidence and applies to short or medium length flights. There is no adequate information to indicate whether extended flying (>12 h) might have adverse effects.

Episodes of acute left ventricular failure may be caused by an acute coronary syndrome (see above) or provoked by anaemia or infection on the background of chronic left ventricular dysfunction. Once any precipitant is identified and treated, most cases should be stabilised within 6 weeks and should be safe to fly. Following an episode of acute heart failure, most patients should be stable within 6 weeks and be able to fly. With chronic heart failure there should be no restriction, although those with NYHA III and IV should consider airport assistance and request the availability of in-flight oxygen.

Chronic Heart failure: The available evidence suggests that, for patients with stable heart failure including NYHA grades III and IV, short-term (up to 1 h) hypoxia at rest produces no significant deleterious effects. Periods of up to 7 h are tolerated by those with mild to moderate stable heart failure (NYHA grade II). Passengers with stable chronic heart failure without recent changes in symptoms or medication are likely to be able to tolerate the mild hypoxia of the aircraft cabin environment even if they have severe heart failure.30–32 It is advisable that they take the precautions of avoiding physical exertion at the airport and making sure that they take their regular medication. It is probably prudent for passengers who are severely limited with NYHA class IV symptoms not to fly without special consideration and the availability of in-flight oxygen.

Renin Aldosterone: Who, what, why and when?

Renin is produced in the juxtaglomerular apparatus in response to sympathetic tone. It causes release of angiotensin I which is converted to angiotensin II and this causes vasoconstriction and release of aldosterone from the adrenal cortex which leads to sodium and water retention in the kidney. Hypertension is generally associated with either higher renin level (younger people aged <55 years and Caucasian) or lower renin levels (older people, African Caribbean origin). Drugs used for hypertension are either anti-renin (ACE, ARB, Beta blockers) or anti-volume (CCB, Diuretics, MRA).

Renin is measured either via a mass or an activity assay. It is assessed with aldosterone as the Aldosterone:Renin ratio. It is primarily used for the exclusion of Conn’s syndrome as a cause of hypertension. In this syndrome aldosterone is produce in excess either due to an adenoma in the adrenal or due to adrenal hyperplasia. The excess aldosterone causes sodium and water retention and this reduces the production of renin resulting in a high ARR of >200.

Many of the antihypertensive drugs alter renin. Generally ACE, ARB, CCB and diuretics increase renin levels, beta blockers reduce renin levels.

Antibiotics prophylaxis for endocarditis

Antibiotic prophylaxis is warranted for patients with cardiac conditions that confer the highest risk of adverse outcome from IE. This approach contrasts with the approach described in guidelines issued prior to 2007, which recommended prophylaxis for patients at moderate risk or high risk of IE

Conditions associated with highest risk of adverse outcomes from IE include:

Prosthetic cardiac valve or valve repair with prosthetic valve material.

-Prosthetic heart valve (surgical or transcatheter)

-Cardiac valve repair with prosthetic material (including annuloplasty rings or clips)

Durable mechanical circulatory support device (ventricular assist device or artificial heart).

Previous, relapsed, or recurrent IE.

Certain types of congenital heart disease including:

-Unrepaired cyanotic congenital heart disease (patients with palliative shunts and conduits are still considered unrepaired).

-Completely repaired congenital heart defect with prosthetic material or device (eg, septal closure device), during the first six months after surgical or transcatheter placement.

-Repaired congenital heart disease with residual defect at the site or adjacent to the site of a prosthetic patch or prosthetic device.

-Prosthetic pulmonary artery valve or conduit.

Hypertension in the Very Elderly

Topics to be added

DVLA Driving Assessment: Some particular issues

Assessment of hypertension

How to interpret a 24h ABPM

Renin Aldosterone measurements: Who, what, why and when?

Catecholamine interpretation

POTS

The relationship between stenosis and ischaemia and symptoms

How to interpret a pressure wire study

How to interpret a Coroventis study

Why intracoronary imaging is important

Which antiplatelet drug

Managing LVSD drugs such as SGLT-2 inhibitors and MRA antagnoists

Beta blockers in people with asthma

Hypertension in the Very Elderly

Dual Antiplatelet therapy post ischaemic stroke

For the vast majority of patients with ischemic strοke, the long-term use of DAPT with aspirin and clopidogrel does not offer greater benefit for strοke prevention than either agent alone but does substantially increase the risk of bleеԁiոg complications,

The MATCH trial of patients with stroke or TΙΑ who also had some additional "high-risk" feature, defined as prior ΜI, prior stroke (in addition to the index event), diabetes, angina, or symptomatic peripheral artery disease [randomly assigned people to the combination of clopidogrel (75 mg daily) plus aspirin (75 mg daily) or ϲlοрiԁоgrel (75 mg daily) alone. Follow-up was 18 months. Compared with ϲlοрidogrеl alone, аspiriո plus ϲlοpiԁοgrel treatment did not reduce the risk of major vascular events (relative risk reduction 6.4 percent, 95% CI -4.6 to 16.3 percent) but did result in more life-threatening bleeԁing complications, mainly intracranial and gastrointestinal. Over the 18-month trial period, there was an absolute excess of 1.3 percent for life-threatening hеmоrrhagе (95% CI 0.6-1.9) and an additional 1.3 percent for major hеmοrrhage in patients assigned combination therapy. Overall, treatment with aѕpirin and ϲlοрiԁogrel compared with ϲlοpiԁоgrеl alone might prevent 10 ischemic events per 1000 at the cost of 13 life-threatening hemorrhages per 1000 treated.

In this case therefore I would suggest to continue with monotherapy for both heart and stroke risk.