A 60-year-old male was admitted for a 2-day history of newly documented repeated severe chest pain lasting 10–15 min.

choose ALL correct answerS
EXPLANATION
There exist four stages of pericarditis :
Stage 1 – diffuse concave ST elevation and PR depression in all leads (reciprocal ST depression and PR elevation in aVR),  
Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks),  
Stage 3 – flattened T waves become inverted (3 to several weeks) and
Stage 4 – ECG returns to normal or persistence of T-wave inversions (several weeks onwards). Spodick’s

How can you differentiate between Pericarditis and STEMI:  
1) STE in pericarditis are concave; in AMI - convex or horizontal,  
2) STE in pericarditis - diffuse; in AMI - localised,  
3) Pericarditis - PR depression; AMI - Q waves,  
4) Pericarditis - inversion of T waves appear after normalising of ST segment; AMI - T wave inversion appears with STE ECG manifestation.
EXPLANATION
There exist four stages of pericarditis :
Stage 1 – diffuse concave ST elevation and PR depression in all leads (reciprocal ST depression and PR elevation in aVR),  
Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks),  
Stage 3 – flattened T waves become inverted (3 to several weeks) and
Stage 4 – ECG returns to normal or persistence of T-wave inversions (several weeks onwards). Spodick’s

How can you differentiate between Pericarditis and STEMI:  
1) STE in pericarditis are concave; in AMI - convex or horizontal,  
2) STE in pericarditis - diffuse; in AMI - localised,  
3) Pericarditis - PR depression; AMI - Q waves,  
4) Pericarditis - inversion of T waves appear after normalising of ST segment; AMI - T wave inversion appears with STE ECG manifestation.
EXPLANATION
There exist four stages of pericarditis :
Stage 1 – diffuse concave ST elevation and PR depression in all leads (reciprocal ST depression and PR elevation in aVR),  
Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks),  
Stage 3 – flattened T waves become inverted (3 to several weeks) and
Stage 4 – ECG returns to normal or persistence of T-wave inversions (several weeks onwards). Spodick’s

How can you differentiate between Pericarditis and STEMI:  
1) STE in pericarditis are concave; in AMI - convex or horizontal,  
2) STE in pericarditis - diffuse; in AMI - localised,  
3) Pericarditis - PR depression; AMI - Q waves,  
4) Pericarditis - inversion of T waves appear after normalising of ST segment; AMI - T wave inversion appears with STE ECG manifestation.
EXPLANATION
There exist four stages of pericarditis :
Stage 1 – diffuse concave ST elevation and PR depression in all leads (reciprocal ST depression and PR elevation in aVR),  
Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks),  
Stage 3 – flattened T waves become inverted (3 to several weeks) and
Stage 4 – ECG returns to normal or persistence of T-wave inversions (several weeks onwards). Spodick’s

How can you differentiate between Pericarditis and STEMI:  
1) STE in pericarditis are concave; in AMI - convex or horizontal,  
2) STE in pericarditis - diffuse; in AMI - localised,  
3) Pericarditis - PR depression; AMI - Q waves,  
4) Pericarditis - inversion of T waves appear after normalising of ST segment; AMI - T wave inversion appears with STE ECG manifestation.
EXPLANATION
There exist four stages of pericarditis :
Stage 1 – diffuse concave ST elevation and PR depression in all leads (reciprocal ST depression and PR elevation in aVR),  
Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks),  
Stage 3 – flattened T waves become inverted (3 to several weeks) and
Stage 4 – ECG returns to normal or persistence of T-wave inversions (several weeks onwards). Spodick’s

How can you differentiate between Pericarditis and STEMI:  
1) STE in pericarditis are concave; in AMI - convex or horizontal,  
2) STE in pericarditis - diffuse; in AMI - localised,  
3) Pericarditis - PR depression; AMI - Q waves,  
4) Pericarditis - inversion of T waves appear after normalising of ST segment; AMI - T wave inversion appears with STE ECG manifestation.
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Incorrect. SVT is characterized by a rapid heart rate originating above the ventricles.

Incorrect. It is an irregular rhytm. The pathogenesis of multifocal atrial tachycardia is not well understood; however, multiple discrete P-wave morphologies with variable PR intervals suggest atrial pacemaker activity originating from multiple ectopic foci within the atria.

Correct! This condition is typically seen in elderly patients with a variety of underlying conditions, the most common of which is a chronic obstructive pulmonary disease (COPD). Multifocal atrial tachycardia is most commonly associated with underlying pulmonary disease, cardiac disease, electrolyte abnormalities (mainly hypokalemia, hypomagnesemia), drugs and chronic renal failure.

Incorrect. Presyncope and syncope are less common, and tend to be associated with presentation in older individuals. Older patients usually are more symptomatic with dizziness, presyncope, and syncope. Most of the time patients complain of palpitations.

Correct! This response can be seen in sinus tachycardia, focal atrial tachycardia and junctional ectopic tachycardia

Correct! This response can be seen in AVNRT or AVRT. This is caused by interrupting the re-entry circuit in AVNRT and AVRT by acting on the AVN that is part of the circuit.

Correct! No response can be caused by inadequate stimulation or if it's a high septal VT.

Correct! This response can be seen in atrial flutter, micro-re-entrant focal AT. Atrial electrical activity can thus be unmasked, revealing typical ECG pattern.

Incorrect. Synchronized direct-current cardioversion is recommended for hemodynamically unstable patients with narrow QRS tachycardia. The reason for this is electrical discharge synchronized with R oscillation prevents induction of ventricular tachycardia.

Incorrect. 3 mg dose of adenosine is not recommended for termination of SVT. Recommended starting dose of adenosine is 6mg, with a maximum of 18mg. Adenosine should be given in a bolus becase of its very short halftime.

Correct! In case of no or insufficient response to pharmacological treatment, it is recommended to proceed to electrical cardioversion for termination of supraventricular tachycardia in patients in absence of established diagnosis

Correct! CAVE: I.v. beta blockers are contraindicated in the presence of decompensated HF.

Incorrect. Atrial fibrillation is a micro reentry tachycardia.

Correct! Atrial flutter is a macro reentry tachycardia which is divided into two groups: typical atrial flutter and atypical atrial flutter (isthmus independent atrial flutter). Typically is located around cavotricuspid isthmus, on the other hand isthmus independent can be located around vena cava inferior/superior, pulmonary veins and scar tissue e.g. after radiofrequency ablation.

Correct. Electrical impulse in AVRT is circling as a macro reentry between the atria and the ventricles. Arrhytmia is usually triggered by ventricular or atrial extrasystole.The rate in AVRT is usually around 170-250/min.

Incorrect. In MAT several theories have been proposed, including re-entry, abnormal automaticity and triggered activity, but no theory has yet been demonstrated conclusively. The theory of re-entry centers upon the idea that automaticity foci with different exit pathways or electrical circuits with abnormal intra-atrial conduction could produce tachycardia with several discrete P wave morphologies. The theory of abnormal automaticity focuses on an increase in the ability of atrial myocytes to spontaneously depolarize and trigger an action potential. This theory is supported by many of the underlying conditions associated with this arrhythmia. Pulmonary diseases, like COPD, can result in hypoxia, hypercapnia, acidosis, and increased adrenergic stimulation, all of which are known to increase automaticity. The theory of triggered activity involves spontaneous action potentials generated from afterdepolarizations due to myocardial cell membrane instability. According to this theory, a normal stimulus, such as an action potential generated by the sinoatrial node, gives rise to afterdepolarizations due to changes in membrane potential that can achieve threshold and “trigger” spontaneous action potentials.

Correct! Calcium channel blockers and beta blockers are of value with premature ventricular contractions. Beta blockers are effective at reducing PVC (premature ventricular contraction) symptoms. This is because beta blockers reduce the post-extrasystolic potentiation via the Starling mechanism (increased inotropy related to the increased stroke volume) associated with the PVC. Beta blockers can also prevent PVC recurrence. Beta blockers are most likely to suppress PVCs that result from excess sympathetic stimulation or are catecholamine sensitive.

Correct! The thrombo-embolic risk of atrial flutter, although lower than that of atrial fibrillation(AF), is still significant. These recommendations extend to the acute setting for cardioversion when flutter lasts for >48 hours. Anticoagulation is also given prior to and after cardioversion, as it is in patients with AF.

Incorrect. Electrical cardioversion is more effective than pharmacological treatment, but less energy is required for its termination. DC-synchronized shock (50 J) is indicated in all urgent situations (e.g. hemodynamic compromise). The success rate is between 95-100%. Alternative non-pharmacologic treatment by atrial overdrive pacing (transvenous or transoesophageal) has a success rate of 82% and is especially used during the post-operative period in cardiac surgery. Recently published LADIP trial showed a 100% success rate of radiofrequency ablation as first line treatment.

Correct! Catheter ablation is the most effective therapy to maintain sinus rhythm, and is clearly superior to amiodarone. Ablation of CTI (cavotricuspid isthmus) with confirmed bidirectional conduction block results in a <10% rate of recurrence.

Incorrect. This form compromises 90 to 95% of the reentrant tachycardia and can be initiated by PAC or PVC. Principle of orthodromic AVRT: Physiologically, the P wave originates from the SA node and passes through the AV node to the ventricles. Ventricular extrasystole depolarizes ventricles earlier than SA node. The impulse from the ventricular extrasystole propagates retrogradely along the accessory pathway, not via the AV node because it is in the refractory period. The atria are activated through the accessory pathway, causing a negative p wave morphology. Therefore, In orthodromic AVRT ventricles are depolarized through AV node and atria by a retrograde depolarization through the accessory pathway.

Incorrect. In antidromic AVRT, QRS complexes are wide, as the ventricles are depolarized through the accessory pathway. Atria are depolarized by retrograde conduction through the AV node causing a retrograde P wave after QRS complex.

Correct! AVRT, or atrioventricular reentrant tachycardia, is a type of macro reentrant tachycardia where electrical impulses propagate through an accessory pathway either anterogradely (from atria to ventricles) or retrogradely (from ventricles to atria).

Incorrect. AVRT, or atrioventricular reentrant tachycardia, is a type of macro reentrant tachycardia where electrical impulses propagate through an accessory pathway either anterogradely (from atria to ventricles) or retrogradely (from ventricles to atria).

Incorrect. AVNRT is a narrow complex tachycardia.

Correct! This is one of the most typical ECG finding for AVNRT. Atria are activated along the fast pathway and creating pseudo r' and s'. Pseudo s' is located in inferior leads II,III,aVF and pseudo r' in V1. This is due to the direction of depolarization.

Incorrect. Delta wave is typically found in presence of an accessory pathway causing a pre-excitation of the ventricular myocardium.

Incorrect. In most cases, an ECG will show heart rate between 140 and 280 beats per minute (bpm), and in the absence of aberrant conduction, a QRS < than 120 milliseconds.

Correct! A recent randomized clinical trial that compared catheter ablation as first line treatment with antiarrhythmic drugs demonstrated a significant decrease in arrhythmia related hospitalisations. Furthermore catheter ablation for SVT in general and AVNRT in particular is the current treatment of choice for symptomatic patients, because it substantially improves quality of life.

Correct! The majority of pediatric electrophysiologists prefer cryoablation over RF for ablation of SVT, particularly AVNRT, in children. This may be for its relative safety and higher long-term success rate. Cryoablation has an ability to demonstrate the functionality of prospective ablation sites without inducing permanent injury.

Correct! Most modern ICDs have sophisticated discrimination algorithms to differentiate atrial and ventricular arrhythmias. While ventricular arrhythmias are recognized and treated with precision, atrial arrhythmias can be misdiagnosed and lead to an inappropriate shock therapy.

Incorrect. The procedure using high frequency electrical current is called radiofrequency ablation.

Correct! Acessorry pathway may manifest as preexcitation on the ECG.

Correct! Corrected: Accessory pathways (APs) crossing the tricuspid or mitral annulus are remnants of early atrioventricular (AV) connections. These aberrant pathways occur due to incomplete embryological development of AV annuli and the failure of fibrous separation between the atria and ventricles. Catheter ablation has become a preferred treatment for patients manifesting a left anterior AP.

Incorrect. Approximately 60% are located along the mitral valve and are referred to as left free wall accessory pathways (APs).

Incorrect. The most common tachycardia associated with accessory pathways (APs) is atrioventricular reentrant tachycardia (AVRT).

Incorrect. Paroxysmal atrial fibrillation is the second most common tachycardia observed in patients with Wolff-Parkinson-White syndrome.

Incorrect. Pre-excited atrial fibrillation usually occurs in young patients with no structural heart disease.

Correct! Atrial fibrillation with a fast ventricular response over the accessory pathway with a short anterograde refractory period is a potentially life-threatening arrhythmia in patients with Wolff-Parkinson-White syndrome, due to the potential for degeneration into ventricular fibrillation.

Correct! Intravenous amiodarone may not be as safe as previously thought due to its potential to decrease atrioventricular (AV) node conduction and the associated risk of ventricular fibrillation.

Correct! The risk of stroke after carotid sinus massage is greater if there is a preexisting carotid stenosis or carotid plaques. In patients who have had a stroke, it is advisable to specify etiology of the stroke, if the stroke was due to carotid artery disease, carotid sinus massage should not be approached, because of the risk of loosening another part of the plaque resulting in a stroke.

Incorrect. Mitral regurgitation does not increase the risk of stroke associated with carotid massage.

Correct! Massage of the carotid sinus is contraindicated in patients with carotid artery disease because of the risk of stroke. Carotid artery disease may present as unilateral murmur over carotids.

Correct! Carotid massage might significantly decrease patient's blood pressure causing a severe hypotension. Vagal manoeuvres stimulate receptors in the internal carotid artery causing a reflex stimulation of the vagus nerve, which results in the release of acetylcholine, which may in turn slow the electrical impulse through the AV node and slow the heart rate. Carotid sinus massage is performed with the patients neck in an extended position, with the head turned away from the side to which the pressure is applied. It should always be unilateral and limited to 5 seconds. The patient should be monitored.

Correct! SVT can manifest for the first time during pregnancy, particularly in the third trimester or peri-partum, according to comprehensive discharge data from hospitals. Hemodynamic changes in pregnancy lead to an increased heart rate of at least 20% during the third trimester due to the decrease in systemic vascular resistance. High levels of estrogen have a significant impact on the excitability of cardiac tissue at the molecular level. The substantial increase in circulating catecholamine levels results in additional adrenergic stimulation potentially leading to arrhythmias.

Incorrect. The management of SVT in pregnancy, although remarkably similar, varies slightly based on the trimester of pregnancy and some medications are contraindicated.

Incorrect. Use of amiodarone is not recommended. Amiodarone used in pregnant women may increase the risk of fetal adverse effects as for example, neonatal hypo- and hyperthyroidism, neonatal bradycardia, neurodevelopmental abnormalities, preterm birth, and fetal growth restriction.

Incorrect. Catheter ablation is the most effective treatment of SVT, even in the first trimester of pregnancy. This modality is generally reserved for treatment of refractory cases or when pharmacological treatments are contraindicated or refused. Non-fluoroscopic ablation must be used in order to prevent any harm to the fetus. Non-fluoroscopic ablation can be achieved using three-dimensional electroanatomical mapping or intracardiac echocardiography.

Correct! Direct-current cardioversion has a higher success rate than medical therapy in converting supraventricular tachyarrhythmias to sinus rhythm and should be performed immediately in patients with hemodynamic instability

Incorrect. In atrial flutter, pharmacological cardioversion is even less successful than in atrial fibrillation. Therefore, in patients with rapid ventricular rate, we typically opt for rate control and electrical cardioversion.

Correct! Amiodarone is not superior to other antiarrhythmic drugs conventionally used for the pharmacological cardioversion of recent-onset atrial fibrillation. However, it is relatively safe in patients with structural heart disease and those with reduced left ventricular function. Therefore, amiodarone could be used particularly in patients with structural heart disease and left ventricular systolic dysfunction. On the other hand, the use of class Ic drugs such as propafenone and flecainide for cardioversion of atrial fibrillation is contraindicated in such patients.

Correct! Pharmacological cardioversion to sinus rhythm is an elective procedure indicated in hemodynamically stable patients. Its true efficacy is influenced by the spontaneous restoration of sinus rhythm within 48 hours of hospitalization in 76-83% of patients with recent-onset AF (10-18% within the first 3 hours, 55-66% within 24 hours, and 69% within 48 hours). Antiarrhythmics used for pharmacological cardioversion include propafenone, flecainide, and amiodarone. Some adverse effects of these antiarrhythmics are: Flecainide may induce mild widening of the QRS complex, while amiodarone may cause hypotension, bradycardia/atrioventricular block, and QT prolongation.

Incorrect. Amiodarone belongs to the class III antiarrhythmic drugs. Its primary mechanism involves the inhibition of potassium rectifier currents responsible for repolarizing the heart during phase 3 of the cardiac action potential. This potassium channel-blocking effect leads to increased action potential duration and a prolonged effective refractory period in cardiac myocytes. Consequently, myocyte excitability is reduced, thus hindering the continuation of tachyarrhythmias by preventing reentry mechanisms and ectopic foci.

Incorect. It is most commonly administered as a continuous intravenous infusion, during which it slows the heart rate, and conversion to sinus rhythm can be expected most often after several hours.

Correct! Amiodarone is associated with a relatively extensive range of drug-drug interactions, including medications such as clopidogrel, warfarin, atorvastatin, and trazodone. Concomitant use of amiodarone with other medications known to prolong the QT interval should be avoided or is contraindicated. Examples of these medications include citalopram, clarithromycin, and ondansetron.

Incorrect.Thyreotoxicosis is one of the main adverse effects of amiodarone. Therefore, the concentration of thyroid hormones should be checked in patients to whom amiodarone is administered. However, it is also necessary to assess the QT interval, as its prolongation may cause polymorphic ventricular tachycardia, such as Torsades de Pointes.

Incorrect. It is not recommended to apply more than three discharges due to the risk of myocardial damage. If the discharges are repeated, the interval between each discharge should be preferably after at least couple of minutes to allow a transient increase in thoracic impedance.

Correct! High-quality evidence has demonstrated that pre-treatment with amiodarone improves the restoration and maintenance of sinus rhythm after electrical cardioversion of AF. Short-term amiodarone is well-tolerated. This may particularly benefit patients with a combination of risk factors such as LA size, long AF duration, and patient age.

Correct! Low-energy electrical cardioversion is commonly used in cases of hemodynamic compromise or after the failure of previous actions, but it could be the first choice due to its high efficacy. Electrical cardioversion for atrial flutter is more effective, and less energy is required compared with AF.

Correct! Sinus bradycardia and sinus pauses, alone or in combination, occur in one-fifth of AF patients converting to SR. They are rapidly reversible, do not seem to be caused by concomitant medication, and can be regarded as benign in the absence of prior suspicion or documentation of sinus node dysfunction.

Correct! The aim of this score is to improve the stratification of risk of stroke in patients diagnosed with atrial fibrillation, by identifying patients who could safely do without oral anticoagulation therapy.

Incorrect. The CHA2DS2-VASc clinical stroke risk score helps to identify patients at 'low stroke risk' (CHA2DS2-VASc score = 0 in men, or 1 in women) who should not be offered anticoagulant therapy. Anticoagulation, especially using new oral anticoagulant agents, is recommended in patients with a significant risk of ischemic events (CHA2DS2-VASc score ≥ 2 in men and ≥ 3 in women), and should be initiated in patients with a CHA2DS2-VASc score of ≥ 1 in men and ≥ 2 in women, in the absence of major risk for severe bleeding.

Incorrect. 1 point in CHA2DS2-VASc score gains patients with congestive heart failure/LV dysfunction with EF<40%

Incorrect. The maximum score for the CHA2DS2-VASc clinical stroke risk score is 9.

Incorrect. It is necessary to anticoagulate patients for at least 3 weeks before electrical cardioversion. This time period is required for either NOACs or warfarin. Alternatively, a transesophageal echocardiogram (TEE) to exclude left atrial appendage thrombus (LAAT) could also be performed, followed by immediate electrical cardioversion and subsequent oral anticoagulation for at least 4 weeks.

Incorrect. The upper limit for safe cardioversion is considered to be an INR of 4.5.

Correct: Unless thrombi are very large and spreading to the body of the left atrium, they are hardly identified by means of TTE because the left atrium lies in the far field of the interrogating ultrasound beam. Often they reside between the trabeculae of the LAA( left atrial appendage). The ability of TTE to identify or exclude LA or left atrial appendage thrombi is limited, with a reported sensitivity of 40–60%, due largely to poor visualization of the LAA. In contrast, TEE provides detailed visualization of LA and LAA from multiple imaging planes, so offers superior assessment. It is the current gold standard diagnostic method.

Incorrect. We continue anticoagulation therapy for four weeks in all patients after pharmacological or electrical cardioversion (even in patients without evidence of TEE thrombi before cardioversion) because of the risk of new thrombus formation and possible thromboembolic events due to transient dysfunction of the left atrium and its orifice after cardioversion (atrial stunning), regardless of whether or not sinus rhythm has been restored.

Correct! The main disadvantage of mechanical valves is the need for lifelong anticoagulation. Warfarin is considered a standard treatment, but it is far from perfect. Direct oral anticoagulants (DOACs) are a new and more patient-friendly alternative to warfarin when anticoagulation is required, but they have not been approved for the indication of mechanical valves.

Incorrect. The efficacy of VKAs in stroke prevention may be similar to NOACs, whereas the relative safety benefit with NOACs is less affected by TTR (time in therapeutic range), with consistently lower rates of serious bleeding seen with NOACs compared to warfarin. Persistence with NOAC therapy is generally higher than with VKAs, facilitated by the better pharmacokinetic profile of NOACs and their favorable safety and efficacy, especially among vulnerable patients including the elderly, those with renal dysfunction, or previous stroke.

Incorrect. The dose reduction criteria for apixaban are two out of three of the following: 1) age ≥80, 2) serum creatinine above 133 umol/L, weight ≤ 60 kg.

Incorrect. For stroke risk assessment, a risk-factor-based approach is recommended, using the CHA2DS2-VASc clinical stroke risk score to initially identify patients at 'low stroke risk' (CHA2DS2-VASc score = 0 in men, or 1 in women) who should not be offered anticoagulant therapy. Moreover, treatment should be individualized based on net clinical benefit and consideration of patient values and preferences, particularly in patients with a CHA2DS2-VASc score of 1 in men or 2 in women.

Incorrect. Amiodarone has antiarrhythmic effects such as prolongation of the action potential, which leads to a decrease in the flow of potassium into the cell. Moreover, amiodarone is the only recommended antiarrhythmic drug in the recent therapeutic guidelines for congestive heart failure (CHF) and can be used for both rhythm and rate control of atrial fibrillation (AF). The antianginal effect of amiodarone arises from a moderate decrease in peripheral vascular resistance and reduced heart rate, leading to lower oxygen consumption

Correct! This is stated for their rapid onset of action and effectiveness at high sympathetic tone.

Incorrect. Beta blockers are usually not administered in patients with acute HF (negative inotropic effect) and with a history of severe bronchospasm.

Esmolol or landiolol are higly beta-1 receptor selective and short acting beta blockers that can be potentially safely used in this cohort of patients.

Correct! Propafenon is a class Ic antiarrhytmic.

Correct! Propafenone is classified as a class IC antiarrhythmic drug, which means it has a potent sodium channel-blocking effect. By blocking sodium channels, propafenone decreases the influx of sodium ions into cardiac cells during depolarization, thereby reducing the conduction velocity and excitability of cardiac tissue.

Correct! Brugada syndrome results from mutations that decrease inward sodium or calcium currents or increase early outward potassium currents. These abnormalities lead to early loss of the action potential plateau, particularly in the epicardial cells of the right ventricular outflow tract, producing characteristic right precordial ECG changes and a propensity to ventricular tachyarrhythmias. Propafenone hydrochloride is an antiarrhythmic with membrane-stabilizing and sodium channel-blocking effects. This may exacerbate arrhythmias in patients with Brugada syndrome.

Incorrect. Propafenone prolongs the refractory phase of accessory pathways in patients with Wolf-Parkinson-White (WPW) syndrome, thus can be beneficial in supressing tachycardias including accessory pathways.

Correct! Amiodarone-induced pulmonary toxicity is the adverse effect of greatest concern. Suspected mechanisms of amiodarone lung toxicity include immunologic effects and direct cytotoxicity. Pulmonary toxicity from amiodarone may manifest as pulmonary fibrosis, chronic interstitial pneumonitis, and bronchiolitis obliterans. Another organ affected by long-term usage of amiodarone is the thyroid gland; these adverse effects may present in the form of hyperthyroidism or hypothyroidism.

Correct! Sotalol lengthens the QT/QTc interval but does not affect other ECG intervals. It increases the refractory period in the atria, ventricles, bypass tracts, and the His-Purkinje system while minimally slowing the heart rate. The potassium channel-blocking effect increases with increasing dose, and consequently, the risk of ventricular proarrhythmia (torsade de pointes) increases.

Incorrect. Sotalol is proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm) and left ventricular systolic dysfunction, and thus it is contraindicated in these settings.

Correct! Dronedarone is a congener of amiodarone, with the omission of its iodine molecule, developed with the intention of reducing the likelihood of toxic side effects, and it is consequently a safer alternative to amiodarone and was also a popular choice in EAST-AFNET 4.3 The only comparative randomized clinical trial (RCT) of these 2 drugs showed that dronedarone was better tolerated and had fewer side effects than amiodarone but was less effective in maintaining sinus rhythm. However Dronedarone is associated with increased mortality in patients with recent decompensated HF or permanent AF.

Correct! According to ESC guidelines for SVT verapamil or diltiazem is recommended in class IIa and should be considered in haemodynamically stable patients if vagal manoeuvres and adenosine fail. I.v. verapamil and diltiazem are contraindicated in the presence of hypotension or heart failure with reduced ejection fraction.

Incorrect. Due to numerous side effects, amiodarone is not routinely used as a first line agent to terminate narrow complex tachycardia in clinically stable patients.

Correct! According to ESC guidelines for SVT verapamil or diltiazem is recommended in class IIa and should be considered in haemodynamically stable patients if vagal manoeuvres and adenosine fail. I.v. verapamil and diltiazem are contraindicated in the presence of hypotension or heart failure with reduced ejection fraction.

Correct! According to ESC guidelines for SVT beta-blockers, e.g. esmolol and metoprolol are recommended in class IIa and should be considered in haemodynamically stable patients if vagal manoeuvres and adenosine fail. Beta-blockers are contraindicated in the presence of decompensated heart failure.

Incorrect. It is unlikely that caffeine consumption causes or contributes to AF. Habitual caffeine consumption might be associated with lower risk of AF, but caffeine intake may increase symptoms of palpitations unrelated to AF.

Correct. Autonomic dysfunction can also contribute to the development of AF in diabetic patients. Cardiac autonomic neuropathy caused by T2DM contributes to the downsizing of parasympathetic and upregulation of the sympathetic stimuli, resulting in an autonomic imbalance that can excite an arrhythmia, such as AF. Silent AF are favoured by concurrent autonomic dysfunction, thus suggesting an opportunity for routine screening for AF in diabetes mellitus patients.

Correct! The mechanisms facilitating AF include intermittent nocturnal hypoxemia/hypercapnia, intrathoracic pressure shifts, sympathovagal imbalance, oxidative stress, inflammation, and neurohumoral activation. Obstructive sleep apnoea has been shown to reduce success rates of AAD, electrical cardioversion and catheter ablation.

Incorrect. The incidence of AF appears to be increased among elite athletes, and multiple small studies reported a relationship between AF and vigorous physical activity, mainly related to long-term or endurance sport participation.

Correct. Use of apixaban for stroke prevention in patients with a mechanical aortic valve leads to a significantly higher rate of valve thrombosis and valve-related thromboembolic events compared with the use of warfarin.

Incorrect. Protamine sulfate is a reversal agent for heparin, while andexanet alfa serves as a reversal agent for direct Factor Xa inhibitors like rivaroxaban and apixaban. Andexanet alfa is approved for use in patients with life-threatening or uncontrolled bleeding associated with these medications. Its primary mechanism of action involves binding and sequestering Factor Xa inhibitors.

Correct: Warfarin significantly increased the risk of ICH in patients taking oral anticoagulants compared with 4 NOACs (dabigatran, edoxaban, apixaban, rivaroxaban) and aspirin. Apixaban is least likely to induce all-cause mortality.

Incorrect: a high bleeding risk score should not lead to withholding OAC as the net clinical benefit of OAC is even greater amongst such patients. However the formal assessment of bleeding risk informs management of patients taking OAC, focusing attention on modifiable bleeding risk factors that should be managed and reassessed at every patient contact.

Correct. Drugs influencing atrial remodeling process could prevent the onset of new atrial fibrillation (AF) by acting as non-conventional antiarrhythmic drugs (AAD). Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) have demonstrated promising results in preventing AF in preclinical studies. Retrospective analyses and studies where AF was a prespecified secondary endpoint suggest that ACEi/ARBs could prevent the onset of AF in patients with left ventricular dysfunction, left ventricular hypertrophy, or hypertension.

Correct. Drugs influencing atrial remodeling process could prevent the onset of new atrial fibrillation (AF) by acting as non-conventional antiarrhythmic drugs (AAD). Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) have demonstrated promising results in preventing AF in preclinical studies. Retrospective analyses and studies where AF was a prespecified secondary endpoint suggest that ACEi/ARBs could prevent the onset of AF in patients with left ventricular dysfunction, left ventricular hypertrophy, or hypertension.

Aspirin is an antiplatelet agent and has no direct nor indirect antiarrhytmic effect.

Statins are attractive candidates for upstream therapy, as the role of inflammation in AF is well established. Statins are highly effective and widely used lipid-lowering agents in clinical practice but they also display a number of pleiotropic properties beyond cholesterol lowering. These pleiotropic effects include anti-inflammatory, antioxidant, atrial remodeling attenuation, ion channel stabilization, and autonomic nervous system regulation.

Correct! The aim of AAD therapy is to improve AF-related symptoms. Hence, the decision to initiate long-term AAD therapy needs to balance symptom burden, possible adverse drug reactions, and patient preferences.

Incorrect. Proarrhythmia or extracardiac adverse effects are common with antiarrhythmic drugs (AAD). Various clinical, echocardiographic, and ECG criteria have been linked to a higher risk of proarrhythmia. Increasing age, female sex, impaired renal and/or liver function, and known coronary artery disease (CAD) have been identified as factors associated with a higher risk. Proarrhythmic events often occur shortly after initiating drug therapy, particularly with a loading dose or a change in dosage. Periodic ECG monitoring for signs of proarrhythmia has been successfully employed in recent AAD trials. Specifically, systematic ECG monitoring on days 1-3 was utilized for patients receiving flecainide, propafenone, or sotalol to identify those at risk of proarrhythmia.

Correct! Class Ia AAD (quinidine and disopyramide) and sotalol have been associated with increased overall mortality, therefore safety should dictate both the initiation and continuation of AADs.

Correct!

Correct! Structural changes in atria occur due to atrial fibrillation, leading to myocardial remodeling and mitochondrial dysfunction due to oxidative stress. Atrial activation rapidly leads to intracellular calcium accumulation due to the Na+/Ca2+ exchanger during atrial fibrillation. Flecainide inhibits intracellular Ca2+ accumulation, which reduces atrial remodeling and oxidative stress.

Correct! Flecainide exerts a negative inotropic effect and therefore is contraindicated in patients with congestive heart failure, coronary artery disease and reduced ejection fraction. Flecainide significantly reduces stroke volume index and left ventricle ejection fraction and increases right atrial and pulmonary capillary wedge pressures. Even in patients with normal ejection fraction, oral administration of flecainide can slightly reduce the ejection fraction.

Correct! Two major metabolites, the active meta-O-dealkylated flecainide and its inactive lactam, are produced by hepatic oxidative metabolism via cytochrome CYP2D6 and CYP1A2. Therefore CYP2D6 inhibitors prolong half time of flecainide. This can increase the risk of adverse effect, which in case of flecainide are proarrhythmic effect and reduction in ejection fraction. Examples of CYP2D6 inhibitors are fluoxetin, bupropion.

Correct! Flecainide is shown to block ryanodine receptor opening, which reduces calcium release from the sarcoplasmic reticulum resulting after depolarization and triggered activity, therefore indications for flecainide include catecholaminergic polymorphic ventricular tachycardia (CPVT)

Incorrect. Available evidence suggests that at least a short course of triple therapy (e.g. ≥ 1 week) would be desirable in some AF patients after a recent ACS or undergoing PCI, especially in those at increased risk of ischaemic event

Incorrect! Due to increased risk of bleeding, prasugrel and ticagrelor are contraindicated in patients with NOAC therapy. Patients need to be switchted to clopidogrel before discharge.

Incorrect. Use of prasugrel or ticagrelor has been associated with a greater risk of major bleeding compared with clopidogrel and should be avoided in ACS patients with AF.

​​Correct! Meta-analyses consistently showed a significant reduction in major bleeding with dual vs. triple and NOAC- vs. VKA-based therapies (NOAC-based treatments were also associated with a significant reduction in ICH)

Correct! This difference in ventricular repolarization appears at puberty, with a shortening of the QT interval in men that persists over time. Mechanism for this difference is not completely understood; the change is theorized to be related to androgen hormones. As discussed above, women have longer QT intervals at baseline, and this may affect their ability to tolerate antiarrhythmic medications, especially Class III antiarrhythmic drugs, which block potassium channels and prolong the QT interval.

Incorrect. Women with AF have a greater stroke severity and permanent disability than men with AF. Increasing evidence showed that female gender was an added risk factor for stroke. In 2010, the CHA2DS2-VASc risk scoring system, which added a female gender as a risk factor.

Correct! Women have a prolonged QT interval compared to men,on average by 10-20 ms and this may affect their ability to tolerate anitarrhythmic medication Class III anitarrhythmic drugs, which block potassium channels and prolong QT interval. Women tend to have more QT prolongation with the administration of Class III anitarrhytmics agents, sotalol and dofetilide. Examples of adverse effects are: bradyarrhytmias, Torsades de Pointes.

Correct! Atrial fibrosis has a strong association with atrial fibrillation, likely contributing to conduction abnormalities and creating a vulnerable substrate. Histologic studies show women with long-standing atrial fibrillation have increased atrial fibrosis compared to women without atrial fibrillation, a pattern not seen in men. MRI studies assessing delayed enhancement as a marker of atrial fibrosis show that female sex is a risk factor for delayed enhancement of both patients with and without atrial fibrillation. This difference in fibrosis may be a cause of the finding that women have more non-pulmonary vein triggers for atrial fibrillation and tend to have lower success rates for catheter ablation of atrial fibrillation.

Correct! Early arrhythmia recurrence after pulmonary vein isolation is often associated with inflammation and inhomogeneous scar tissue formation after ablation. Atrial remodeling refers to structural and functional changes in the atrial myocytes in response to internal or external stimuli. Atrial remodeling may also be described as a time-dependent adaptive regulation of cardiac myocytes in order to maintain homeostasis against external stressors. Atrial remodeling may also occur in response to volume/pressure overload such as in heart failure syndromes. Specific stressors, such as diastolic dysfunction, ischemia, and valvular diseases, e.g. mitral stenosis and mitral regurgitation, impose excess pressure and/or volume load on the atrial myocytes, which responds with a range of adaptive, as well as maladaptive, processes.

Correct! Atrial remodeling refers to structural and functional changes in the atrial myocytes in response to internal or external stimuli. Atrial remodeling may also be described as a time-dependent adaptive regulation of cardiac myocytes in order to maintain homeostasis against external stressors. The duration of atrial fibrillation is directly proportional to the structural changes in the atrium of the heart. These changes represent a negative factor to achieve successful pulmonary vein ablation and thus increase the incidence of atral fibrillation recurrence after pulmonary vein ablation. Descending risk from the highest to the lowest: longstanding persistent > persistent > paroxysmal.

Correct! Hypertension and AF often coexist and share common risk factors. Hypertension is associated with structural and electrical remodeling. Some studies show that up to 90% of patients with AF are hypertensive. Data from Framingham ranked hypertension after heart failure, aging, and valvular heart disease, but because of its higher prevalence in the population, hypertension was responsible for more cases of AF than other risk factors. The common mechanisms linking obstructive sleep apnoea and AF are complex and mediated by many mechanisms. Animal and human studies have demonstrated that the pathophysiologic changes brought on by sleep apnea, including changes in intrathoracic pressure, hypoxia, and hypercapnia may cause structural and electrical changes that predispose to arrhythmia including AF.

Correct! Age is related to structural and electrophysiological changes and increases the risk of onset of AF.

Incorrect. Complete isolation of pulmonary veins.

Correct! Subsequently, AADs may be weaned, ceased, or continued according to symptoms and rhythm status. Recent findings suggest that in AAD-treated patients remaining free of AF at the end of the blanking period, AAD continuation beyond the blanking period reduces arrhythmia recurrences.

Correct! Beyond this time, a decision to continue OAC is determined primarily by the presence of CHA2DS2-VASc stroke risk factors rather than the rhythm status.

Correct! Catheter ablation is the therapeutic method of choice in these patients.

Correct! Phrenic nerve paresis, likely from direct thermal injury, has been described after RF ablation, cryoablation, ultrasound, and laser ablation. The right phrenic nerve can be affected during ablation near the right superior PV or within the superior vena cava.The use of balloon technologies carries substantially higher risk of this complication, since the balloon has to be pressed inside the ostium and may prolapse deeper into the right superior PV and cause the damage. Left phrenic nerve is rarely affected during ablation within the LA appendage

Correct! Air embolism can occur mainly during introduction or flushing transseptal sheaths. The preferential localization for air emboli is right coronary artery territory due to the most superior position of the arterial ostium in the supine patient. Its clinical presentation is usually in form of acute inferior ischemia or heart block, which resolute in few minutes.

Correct! Atrio-esophageal fistula is the most serious potential complication. Although its occurrence is rare (0.1–0.25%), its mortality rate is higher than 80% and survivors of this complication are often left with disability from cerebrovascular events.Clinical manifestation of atrio-esophageal fistula occurs usually 2–4 weeks after the ablation procedure. The most common symptoms comprise dysphagia, odynophagia, septic fever, gastrointestinal bleeding and recurrent neurological events due to a massive air embolism

Correct! Current strategy of ablation at the pulmonary vein ostia significantly decreased the incidence of pulmonary vein stenosis. Symptoms usually develop several weeks to months after the procedure. Diagnosis can be confirmed by CT or MRI scans.

Correct! Vagal manoeuvres stimulate receptors in the internal carotid artery causing a reflex stimulation of the vagus nerve, which results in the release of acetylcholine, which may in turn slow the electrical impulse through the AVN and slow the heart rate. Carotid sinus massage is performed with the patients neck in an extended position, with the head turned away from the side to which the pressure is applied. It should always be unilateral and limited to 5 seconds. The patient should be monitored. The effectiveness, when correctly performed has been reported to be between 19 to 54%. AVRT is more likely to be terminated by vagal manouvres than AVNRT.

Correct! Adenosine is A1 receptor agonist which slows down conduction in sinoatrial (negative chronotropy) and atrioventricular node (negative dromotropy), at higher doses blocks the AV node, which is the main effect for SVT. This is caused by membrane hyperpolarization in SA and AV nodes. Due to this fact adenosine adverse effects are sinus bradycardia/sinus arrest and AV blocks.

Incorrect. Defibrillation involves delivering an unsynchronized electrical shock to stop a haemodynamically unstable heart rhythm, typically utilized in urgent situations such as ventricular fibrillation, pulseless ventricular tachycardia.

Correct! Cardioversion involves delivering a synchronized electrical shock to stop some SVTs. Immediate electrical cardioversion is recommended in haemodynamically unstable SVTs and is routinely used in restoring sinus rhytm in atrial fibrillation/atrial flutter/atrial tachycardia.

Correct! The relationship between atrial and ventricular events is 1:1 or greater (more atrial than ventricular beats) in most SVTs. Most VTs have a relationship <1:1 . (more QRS complexes than P waves).

Incorrect! In patients with SVT and aberrancy, the QRS axis is confined between -60 and +120. This is because SVTs often lie around the His-Purkinje network, extreme axis deviation (axis from -90 to ±180) is strongly indicative of VT, both in the presence of RBBB and LBBB.

Correct! The presence of negative chest lead concordance (all QRS complexes negative V1-V6) is almost diagnostic of VT, with a specificity >90%, but is only present in 20% of VTs. Positive concordance can be indicative of VT or an antidromic tachycardia utilising a left posterior or left lateral AP.

Correct! This pattern can suggest VT, however these criteria are not helpful for differentiating VT from SVT in specific settings, such as pre-excited SVT, or when class IC or class IA antiarrhythmic drugs are administered.

Correct! It is likely that chronic AF promotes electrical and structural remodelling, so that patients with chronic AF appear to have larger atria and are more resistant to ECV. The clinical implication is that patients with prolonged AF may be less likely to benefit from a rhythm‐control strategy. An AF duration >6 months has been shown to have a significant increase in AF recurrence, with no difference in recurrence between 6 months and 1 year, suggesting 6 months as a realistic cutoff for trial of ECV.

Correct! Increased LA size is strongly associated with lower SR rates following ECV in the short and longer term. Several studies have found an increased atrial diameter as a risk factor for AF recurrence, such as with left atrial diameter > 4.4 cm and 4.5 cm. Correction to body size with indexed LA volume is a stronger predictor of AF than simple measurement of LA diameter. This effect is most likely caused by atrial remodelling from stress on cardiac myocytes from volume/pressure overload or tachycardia leading to atrial fibrosis and electrophysiological predisposing to AF

Correct! It has been demonstrated that if achieving sinus rhythm was initially difficult (≥2 shocks), then the risk of recurrent AF was higher. It may be that the need for higher energy and multiple attempts could indicate more extensive cardiac structural and electrical remodelling, or that comorbidities such as COPD, HF, and high body mass index often require a higher amount of energy, although they found no difference in prevalence of these conditions between patients with 1 and multiple shocks

Correct! The prevalence of AF is higher in males than in females, at any given age. However, given that women live longer, there is a higher number of female patients with AF. Women also tend to be more symptomatic with AF and have a higher risk of recurrence of AF after successful ECV. Female AF patients are generally older with a higher prevalence of hypertension, thyroid disease, and valve regurgitation

Incorrect. Currently, all external defibrillators are delivering a biphasic discharge. Biphasic discharge passes through the myocardium in both directions in two phases and with a significantly lower peak value, therefore biphasic discharge is safer and more effective.

Incorrect. Application of electrical discharge in late systole has a higher probability of ventricular fibrillation at approximately 35% with a maximum probability of about 30 ms before the peak of the T wave. This is the reason why all accessible defibrillators have the possibility to set up synchronized discharge with R wave, apart from AED.

Correct! This statement is correct: Synchronization with R wave is mandatory to prevent resistant VF that could be induced by shock wave and T wave overlapping, called a vulnerable period, if a QRS complex appeared during electrical cardioversion.

Incorrect. AEDs are intended to be used only for termination of ventricular fibrillation.

Incorrect. Pulsed field ablation is a nonthermal technique used to ablate cells. In PFA, high electric field gradients are applied to cardiomyocytes using D.C. energy, which is rapidly pulsed. This process creates small pores in the cell membrane, known as electroporation, which makes the membrane more permeable. The strength of the electric field applied determines whether the effect is reversible or irreversible, with reversible electroporation repairing cell membranes and greater electric field application causing irreversible cell death through apoptosis or necrosis

Incorrect. Pulsed field ablation (PFA) employs ultrarapid electrical pulses to ablate myocardial tissue while preserving surrounding tissue. It has a lower threshold for dielectric cell membrane breakdown, resulting in necrosis of the myocardium with less impact on surrounding tissues, making it suitable for cardiac ablation. PFA has been shown to spare the esophagus, blood vessels, pericardium, and nerves, resulting in few major complications in both preclinical and clinical studies. Furthermore, deliberate ablation of collateral tissues with PFA in preclinical studies did not result in significant injury, and initial pilot human data have been promising. Unlike other energy sources, PFA allows for the adjustment of multiple parameters, leading to various lesion profiles and levels of efficacy.

Correct! Recent studies have demonstrated the success of MRI and CT image-guided ablation techniques. Improved imaging techniques and real-time guidance systems can help overcome this challenge.

Correct! Coronary vasospasm is not usually provoked during PFA at locations remote from coronary arteries, but when the energy is delivered adjacent to a coronary artery, PFA routinely provokes subclinical vasospasm. This phenomenon is attenuated by nitroglycerin, administered either post hoc to treat spasm or as prophylaxis.

Correct! Class I antiarrhythmic drugs should not be used in the absence of AV-blocking agents, because of the risk of slowing atrial rate, which may result in 1:1 AV conduction.

Correct! Sotalol is not recommended as a first-line antiarrhythmic drug as it is related to an increased risk of proarrhythmias and mortality. All antiarrhythmic drugs carry a proarrhythmic risk, and many patients with ACHD have underlying sinus node dysfunction or a predisposition for AVN disease. Antiarrhythmic drugs should therefore be used with particular caution, and are generally reserved for symptomatic patients after options for catheter ablation procedures and haemodynamic optimization. Beta-blockers should be considered in chronic therapy of SVTs in patients with congenital heart disease in adults for recurrent focal AT or atrial flutter, if ablation is not possible or successful.

Incorrect. AV nodal ablation with subsequent pacing (‘ablate and pace’), either biventricular or His- bundle pacing, is recommended if the tachycardia responsible for the TCM cannot be ablated or controlled by drugs.TCM is a reversible cause of impaired LV dysfunction due to persistent tachycardia or very frequent ventricular premature beats that can lead to HF. LV function frequently improves after 3 months of restoration of a normal heart rate.

Correct. It is well understood that drugs that slow atrioventricular nodal conduction like beta-blockers, calcium-blockers or adenosine, which are useful in many other supraventricular arrhythmias are to be avoided in this situation.In fact, the first documented conversion of atrial fibrillation to ventricular fibrillation occurred after the patient was treated with propranolol and digoxin. Current guidelines do not recommend using amiodarone because of reports of ventricular fibrillation in a few patients with administration of the drug. Amiodarone, especially when given intravenously, may have potent beta-blocking and calcium-channel blocking effects which can prove dangerous when atrial fibrillation conversion is not achieved. Therefore it is prudent to avoid the use of intravenous amiodarone in these patients.

Incorrect. Ventricular pre-excitation is a rare cause of sudden cardiac death in young athletes. Although many individuals with ventricular pre-excitation remain asymptomatic throughout their lives, symptomatic AVRT may occur. Patients with WPW may also develop other arrhythmias, such as AF, which could degenerate into ventricular fibrillation and sudden cardiac death.

Incorrect. Treatment of paroxysmal SVT with beta-blockers or sodium channel blockers is discouraged in athletes, because these drugs may reduce performance during sports and have limited ability to prevent arrhythmia recurrence during sports activity. Moreover, beta-blockers are listed by the World Anti-Doping Agency as prohibited drugs in particular sports. It is widely acknowledged that beta-blockers are beneficial to sports such as archery and shooting.

Correct! Hyperthyroidism directly affects the cardiovascular system, altering the heart's normal function and leading to high cardiovascular mortality. Excess thyroid hormones are associated with significantly increased risk and prevalence of cardiac arrhythmias, particularly atrial fibrillation (AF). Hyperthyreoidism has effect on heart by multiple mechanisms, as for example: increased protein synthesis, which chronically may lead to ventricular hypertrophy, vasodilation that decreased systemic vascular resistence and retrogradelly increases heart rate, last but not least increased symphatetic activity via B1 adrenergic receptors that have positive chronotropic and ionotropic effect. Coronary artery disease poses a risk for the development of SVT. This is due to the formation of scarred myocardial segments which represent a potential source for the development of ectopic electrical impulses that may lead to SVT arrhythmias.

Correct! Although the mechanism is not yet known. However athletes who participate in boxing, wrestling, weight-lifting also practice strenuous sport practices, but AF does not appear to be as prevalent in those groups. Pathophysiological mechanism of AF in athletes may be attributable to the interaction among these three factors. A specific trigger (atrial ectopy, sports supplements and illicit drug use) in the presence of a suitable substrate (genetic predisposition, inflammation, fibrosis and cardiac remodeling) and a modulator (autonomic activation, electrolyte abnormalities, acid reflux disease) remains the foundation in onset and maintenance of AF in athletes.

Incorrect. Tachycardia-induced cardiomyopathy (TCM), or more accurately arrhythmia-induced cardiomyopathy, is a reversible cause of impaired LV function due to persistent tachycardia or very frequent ventricular premature beats that can lead to HF and death. In TCM, LV function frequently improves after 3 months of restoration of a normal heart rate.

Correct! Long-term medical therapy with beta-blockers, and angiotensin- converting enzyme inhibitors or angiotensin II receptor blockers, is indicated before and after successful ablation for the known beneficial effects of these drugs on the LV remodelling process.

Correct! At the cellular level, the myocyte is the elemental component of the heart and is responsible for force generation. Translation of this force into mechanical pump performance is dependent on the relationship between the myocyte and extracellular matrix. The extracellular matrix ensures proper myocyte alignment during diastole, coordinates myocyte contraction during systole, and maintains capillary patency throughout the cardiac cycle. It has been found that chronic supraventricular tachycardia caused significant increase in myocyte length, and significant disruption of the sarcolemmal-basement membrane interface. This could reduce mechanical pump performance and impair ventricular function.

Catheter ablation is recommended for TCM due to SVT. This recommendation is a Class I in ESC Guideline for SVT.

Correct! Patients should preferably be referred to experienced centres with respect to complex MRATs and with access to advanced mapping systems as special expertise and knowledge of complex tachyarrhythmias and scar-related ablation procedures is required for a successful outcome.

Correct! Patients with severe congenital heart disease as for example patients with single ventricle or dextro-TGA [dextro transposition of great arteries] have poorer outcomes. Worse outcomes also have older aged patients due to worsening of structural abnormalities of the heart. However rapid evolution of electro-anatomical mapping systems with developments in computer technology and sophisticated ablation equipment have not only improved the mapping, but enhanced the understanding of specific arrhythmia mechanisms, appreciation of scar tissue and transmurality of ablation lesions.

Incorrect. Most macro re-entrant atrial tachycardia (MRATs) occurring in patients without prior closure of the ASD are CTI dependent and susceptible to catheter ablation.The ASD closure unlikely eliminates the atrial flutter and catheter ablation of the CTI is therefore the recommended approach. If the ASD mandates a closure, MRAT ablation prior to closure should be considered. Patients with unoperated significant ASD and arrhythmias should therefore undergo both ablation of the AT and closure of the ASD. The anatomical features of the ASD determine the most suitable choice between catheter and surgical treatment approach.

Correct! Accessory pathways are frequent (15–30 %), more often right sided and multiple in patients with ACHD than in other patients Catheter ablation of accessory pathways is challenging and associated with lower success rates (80 %) and higher recurrences (40 %) than in other patients, also depending on accessory pathway location. When surgical corrections are warranted and SVTs are present ablation is still recommended prior to surgery.

Correct. Macroreentrant atrial tachycardias are the most common (75 %) type of supraventricular tachycardia (SVT) in patients with adult congenital heart disease (ACHD).

Incorrect. MRATs are the most common type of supraventricular tachycardia (SVT) in patients with ACHD, occurring in 75 % of ACHD-associated SVT cases, most commonly in patients with Ebstein’s anomaly, Tetralogy of Fallot, single-ventricle Fontan procedures, transposition of the great arteries (TGA) or atrial septal defects (ASDs). Over 60 % of these MRATs involve the cavo-tricuspid isthmus (CTI) and are referred to as CTI-dependent atrial flutters, while the other MRATs are defined as non-CTI-dependent atrial flutters.

Incorrect. Majority of patients with Fallot tetralogy have a RBBB in sinus rhythm.

Incorrect. Despite more modern surgical approaches, the incidence of atrial arrhythmia remains high. The most common AT in patients who have undergone a Fontan procedure is an MRAT (66 %), and CTI-dependent atrial flutter or AF can develop in up to 42 % of patients. Catheter ablation is often difficult due to multiple circuits and should be attempted only at experienced centres. When compared with other ACHD anomalies, both Fontan and Mustard repairs have been associated with less successful ablation results related not only to the low success rate of catheter ablation (54 % versus 83% for other CHDs), but also to a high recurrence rate (50 % versus 32 %) after an initial successful ablation procedure. The Fontan procedure is done for children who are born with heart problems like hypoplastic left heart syndrome (HLHS), tricuspid atresia, and double outflow right ventricle. Depending on the heart problem, children may need the Norwood procedure and Glenn procedure before the Fontan surgery.

Correct! Cardioversion seems safe in all phases of pregnancy as it does not compromise fetal blood flow, and has low risk of inducing fetal arrhythmias or initiating preterm labor. The fetal heart rate should be routinely controlled after cardioversion. Cardioversion between 50 J and 300 J applied at various pregnancy phases revealed negligible effects on the fetus, which means harmful electrical current may not reach the fetus.

Incorrect: In pregnancy selective beta-blockers, except for atenolol, can be used for the acute termination of SVT or control of ventricular rate. Atenolol crosses the placenta and reaches nearly identical concentrations in umbilical cord blood as in the mother's bloodstream. There is limited experience with atenolol use during the first three months of pregnancy, and the potential for fetal harm cannot be ruled out. Atenolol has been used to treat hypertension in the third trimester of pregnancy. Its administration to pregnant individuals with mild or moderate hypertension has been linked to intrauterine growth retardation.

Correct! SVT can manifest for the first time during pregnancy, particularly in the third trimester or peri-partum. Hemodynamic changes in pregnancy lead to an increased heart rate of at least 20% during the third trimester due to the decrease in systemic vascular resistance. High levels of estrogen have a significant impact on the excitability of cardiac tissue at the molecular level. The substantial increase in circulating catecholamine levels results in additional adrenergic stimulation potentially leading to arrhythmias.

Correct! Beta-blockers can be used in the first trimester in patients with SVT. All beta blockers can induce bradycardia and hypoglycemia in the fetus. As beta-1 selective beta blockers are less likely to impact uterine relaxation, they are preferred. Maternal use of beta blockers in the first trimester has not been linked to a significant increase in the risk of congenital malformations. However, the EUROmediCAT study reported an association between alpha/beta-adrenergic blocker use in the first trimester and multicystic renal dysplasia.

Correct! This is caused by activation of adenosine receptors found in vessels, causing vasodilation and increased skin perfusion.

Incorrect. Wolff-Parkinson-White syndrome is not an adverse effect. WPW syndrome involves the presence of an accessory pathway between the atria and ventricles. It is not recommended to use adenosine in patients with pre-excited atrial fibrillation as it can lead fo FBI tachycardia (fast-broad-irregular) by blocking the AV node conduction. Extreme caution is necessary when administering adenosine to any patient with supraventricular tachycardia (SVT) with an accessory pathway. Clinicians should avoid using adenosine in irregular or polymorphic wide-complex tachycardias, as it can lead to degeneration into ventricular fibrillation, which is a class III recommendation.

Correct! Adenosine stimulates potassium channels which leads to an increase in potassium efflux causing hyperpolarization of SA node and a decrease in the SA node rate or sinus arrest.

Correct! This usually is the desired effect of adenosine for terminating reentry circuits in AV node.

Incorrect. Multifocal atrial tachycardia is a rapid irregular atrial rhythm arising from multiple ectopic foci within the atria. It is most commonly seen in patients with severe COPD or congestive heart failure. Typical electrocardiographic features of multifocal atrial tachycardia are at least 3 distinct P-waves morphologies in the same lead, heart rate> 100 bpm, irregularly irregular rhythm with varying PP,PR and RR intervals.

Correct! This is a Class I recommendation. MAT is most commonly associated with lung diseases (such as COPD) in 60% of cases; other etiologies include electrolyte abnormalities (mainly hypokalemia, hypomagnesemia), or chronic renal failure. Treatment should focus on the underlying medical condition, after which most episodes of MAT resolve. If treatment is indicated, therapy should begin with first correcting underlying electrolyte abnormalities by repleting potassium to maintain levels greater than 4 mEq/L and magnesium greater than 2 mEq/L. Studies have shown that magnesium suppresses ectopic atrial activity and can be beneficial even if magnesium levels are within the normal range.

Incorrect. In MAT, the heart rate is > 100 bpm (usually 100-150 bpm).

Correct! These agents suppress atrial rate and decrease conduction through the AV node, thereby slow the ventricular rate. Studies have found an average reduction in the ventricular rate of 31 beats per minute, with 43% of patients reverting to sinus rhythm. Caution should be made in patients with preexisting heart failure or hypotension due to negative inotropic effects and peripheral vasodilation.

Incorrect. Anyone at any age can develop POTS, but it mainly affects women between the ages of 15 and 50. Some women report an increase in episodes of POTS before their menstrual periods. POTS often begins after pregnancy, major surgery, trauma, or a viral illness. It may render individuals unable to exercise because the activity brings on fainting spells or dizziness.

Incorrect. Postural orthostatic tachycardia syndrome can affect individuals of either sex at any age, but 75% to 80% are female. The prevalence of POTS is 0,2%.

Correct! Postural orthostatic tachycardia syndrome (POTS) is a chronic multisystem disorder characterized by orthostatic tachycardia as its cardinal feature. Patients with POTS experience symptoms of orthostatic intolerance that typically improve with recumbence. Girls and women are more commonly affected by POTS, with onset often occurring in puberty and persisting into early adulthood. The syndrome can lead to marked functional disability, frequently limiting work or schooling.

Correct! POTS can be typically diagnosed during stand test or HUTT (head-up-tilt-test).

Correct! Midodrine significantly reduces orthostatic tachycardia. It has a rapid onset with only minor effects and is typically administered three times daily. The drug should only be administered during daytime hours as it can cause supine hypertension. Non-pharmacological treatment should be attempted first in all patients. These include withdrawing medication that might worsen POTS, regular graduated exercise featuring aerobic conditioning with some resistance for the thighs. If non-pharmacological approaches prove ineffective, pharmacological therapies may be targeted.

Correct! Low-dose propranolol (10-20 mg per os) acutely lowers standing heart rate and improves symptoms in patients with POTS, while higher doses of propranolol are less well tolerated. Non-pharmacological treatment should be attempted first in all patients. These include withdrawing medication that might worsen POTS, regular graduated exercise featuring aerobic conditioning with some resistance for the thighs. If non-pharmacological approaches prove ineffective, pharmacological therapies may be targeted at specific aspects.

Correct! Pyridostigmin is a cholinergic agonist that works by inhibiting acetylcholinesterase, therefore can increase parasympathetic autonomic tone and lower the blood pressure. Non pharmacological treatment should be attempted first in all patients. These include withdrawing medication that might worsen POTS, regular, graduated exercise featuring aerobic reconditioning with some resistance for the thights. If non-pharmacological approaches prove ineffective pharmacological therapies may be targeted at specific aspects.

Correct! Ivabradine slows sinus rates without affecting blood pressure, and in an open-label study, 60% of patients with POTS had symptomatic improvement. Ideally, ivabradine should be administered with concomitant beta-blockers for long-term therapy. It can be opted as a second-line treatment in patients with POTS since beta-blockers are primarily used initially. In these scenarios, ivabradine can prove effective in abolishing the symptoms with uncommon or less severe side effects. Non-pharmacological treatment should be attempted first in all patients. These include withdrawing medication that might worsen POTS, regular graduated exercise featuring aerobic conditioning with some resistance for the thighs. If non-pharmacological approaches prove ineffective, pharmacological therapies may be targeted at specific aspects.