Annabi M, Touboul E, Dahou A, et al. Dobutamine Stress Echocardiography for Management of Low‐Flow, Low‐Gradient Aortic Stenosis. Journal of the American College of Cardiology. 2018;71(5):475–485. https://www.sciencedirect.com/science/article/pii/S0735109717417785?via%3Dihub
5. Answer: D
There is an increased prevalence of AS in an ageing population. Severe AS is defined on transthoracic echocardiogram as a reduced aortic valve area (AVA) of < 1.0 cm2, peak velocity of > 4 m/s and a mean gradient of greater than 40 mmHg across the valve. Patients with less severe aortic stenosis may remain asymptomatic for years. Once the symptoms of syncope, angina, or heart failure develop, average survival reduces rapidly, with an increased risk of sudden cardiac death. Until transcatheter aortic valve implantation (TAVI) became available, the options to treat severe AS include medical (palliative management), surgical aortic valve replacement (SAVR), or a Ross procedure (where a diseased aortic valve is replaced by a patient's own pulmonary valve). SAVR involves a midline sternotomy, general anaesthetic, cardiopulmonary bypass, typically requires 24 to 48 hours stay in an intensive care unit (ICU) and 10 to 14 days as an inpatient for post‐op recovery and mobilisation, and an even longer hospital stay for rehabilitation in the frail and elderly. Patients who are greater than 75 years old have an increased morbidity and mortality associated with SAVR.
Since the advent of TAVI in 2002, elderly patients who were not suitable candidates for SAVR, can now be considered for TAVI if appropriate, provided they do not have severe COPD, debilitating stroke, active malignancy, and dementia indicating a survival of < 1 year.
The majority of TAVI procedures are performed with local anaesthetic and conscious sedation. In uncomplicated TAVI cases, patients can be mobilised 4 hours post‐procedure and do not require ICU admission and likely to be discharged within 48 hours after telemetry monitoring to rule out conduction disturbance. Patients usually require dual‐antiplatelets (aspirin and clopidogrel) for at least 3–6 months, with aspirin continued lifelong.
Adams H, Ashokkumar S, Newcomb A, et al. Contemporary review of severe aortic stenosis. Internal Medicine Journal. 2019;49(3):297–305.
https://www.ncbi.nlm.nih.gov/pubmed/30091235
6. Answer: D
A randomised non‐inferiority trial was terminated early due to safety concerns around the combination of rivaroxaban and anti‐platelets in patients with coronary artery disease (CAD) and intervention (percutaneous coronary intervention or bypass grafting) more than one‐year prior – or medically treated CAD. The primary efficacy measure of cardiovascular events or death from any cause was significantly lower in patients taking rivaroxaban alone compared to rivaroxaban plus aspirin. Bleeding was significantly lower in the monotherapy group, and the secondary outcome measure of death from any cause was significantly lower in the monotherapy group.
Yasuda S, Kaikita K, Akao M, Ako J, Matoba T, Nakamura M et al. Antithrombotic Therapy for Atrial Fibrillation with Stable Coronary Disease. New England Journal of Medicine. 2019;381(12):1103–1113.https://www.nejm.org/doi/full/10.1056/NEJMoa1904143
7. Answer: D
The anti‐anginal action of β‐blockers is predominantly through reduced heart rate, which results in a relative decrease in myocardial oxygen demand. This leads to decrease in angina symptoms. β‐blockade also results in decreased heart contractility, decreased atrioventricular conduction and nodal refractiveness, and competitive catecholamine inhibition to prevent cardiac remodelling.
Angina results from myocardial ischemia, due to a mismatch between myocardial oxygen demand and supply. Heart rate is the major determinant of oxygen consumption, and increased heart rate precedes most episodes of angina. Other determinants of myocardial oxygen demand include BP, myocardial wall tension, cardiac hypertrophy, and myocardial contractility. Coronary blood flow is the major determinant of myocardial oxygen supply, which is dependent on the pressure gradient across the coronary circuit, integrity of the coronary arteries, and oxygen carrying capacity of the blood. Typically, angina results from exercise or emotional stress precipitating further reduced coronary blood flow in patients with obstructive coronary artery disease (CAD). In a minority of patients, angina is secondary to functional alterations of coronary vessels, where coronary arteries can be angiographically normal, so called non‐obstructive CAD.
Treatment for stable angina includes lifestyle changes such as weight loss, exercise, smoking cessation, aspirin, moderate to high intensity statin therapy, and antianginal therapy as listed below. Heart rate should be targeted <70/min and BP <120/85 mmHg, with β‐blockers, calcium channel blockers, and/or nitrates, before considering newer agents.
1 Medications which reduce heart rate (reduce myocardial demand): β‐blockers, ivabradine, non‐dihydropyridine calcium antagonists.
2 Medications which induce coronary and vascular artery relaxation (increase myocardial supply): Dihydropyridine calcium channel blockers, nitrates, and nicorandil.
3 Medications which induce cellular tolerance to ischemia: Piperazine derivatives including trimetazidine, ranolazine.
Ohman E. Chronic Stable Angina. New England Journal of Medicine. 2016;374(12):1167–1176.https://www.nejm.org/doi/full/10.1056/NEJMcp1502240
8. Answer: C
Brugada syndrome (BS) is a rare inherited disease with ECG findings of coved type ST‐segment elevation (≥ 2mm) followed by a negative T wave in (≥ 1) the right precordial leads in V1 to V3 in patients with a structurally normal heart in patients with Type I BS.
ECG of Type II BS: The ST segments also have a high take‐off but the J amplitude of ≥ 2mV gives rise to a gradually descending ST elevation remaining ≥ 1mV above the baseline followed by a positive or biphasic T wave that results in a saddle back configuration. Type III BS ECG: Right precordial ST elevation of saddle‐back type or coved type.
BS is genetically transmitted as an autosomal dominant syndrome with incomplete penetrance and has a male predominance. Mutations of several genes have been reported to be linked to BS, with mutations of SCN5A gene the most common.
Presenting clinical symptoms include syncope, seizures, agonal breathing at night due to polymorphic ventricular tachycardia (PVTs), ventricular fibrillation and sudden cardiac death (SCD). Lethal arrhythmias are mainly observed during the night or at rest during the day suggesting a likely association with bradycardia or vagal events. Clinical manifestations are also noted in patients with fever, which requires prompt management with antipyretics to minimise the risks of arrhythmias.
The mainstay of management currently is to prevent SCD associated with arrhythmias with an implantable cardioverter defibrillator (ICD). More recently, radiofrequency epicardial catheter ablation has been suggested as to be a new therapeutic option for patients with BS.
Larkin D. Brugada Syndrome • LITFL • ECG Library Diagnosis [Internet]. Life in the Fast Lane • LITFL • Medical Blog. 2019 [cited 8 September 2019]. Available