Major manifestations:Carditis (including subclinical evidence of rheumatic valve disease on echocardiograms)Polyarthritis or aseptic monoarthritis or polyarthralgiaChoreaSubcutaneous nodulesErythema marginatum.
Minor manifestations:FeverPolyarthralgia or aseptic monoarthritisESR ≥30 mm/hr or CRP ≥30 mg/LProlonged PR interval on ECG.
Treatment of ARF is benzathine penicillin G every four week, or every three week for high risk patients, for a minimum of 10 years after the last episode of ARF, or until aged 21 if no RHD or 35–40 if moderate–severe RHD.
ARF RHD Guideline [Internet]. Rheumatic Heart Disease Australia. 2019 [cited 19 August 2019]. Available from: https://www.rhdaustralia.org.au/arf‐rhd‐guideline
29. Answer: D
This patient's presentation and ECG changes are consistent with inferior and right ventricular (RV) myocardial infarction (MI). RV ischaemia complicates 30% to 50% of inferior MIs. Isolated RV myocardial infarction (RVMI) is rare. The coronary artery involved is usually an occluded right coronary artery (RCA). The proximal segment of the RCA supplies the sinoatrial (SA) node and the right atrial wall; the middle segment supplies the lateral and inferior right ventricle (RV); and the posterior portion of the left ventricle, the inferior septum, inferior left ventricular wall and atrioventricular (AV) node are perfused by the distal segment of the RCA. A few patients (10%) may have a right ventricle that is supplied by the circumflex artery.
Although the RVMI often shows good long‐term recovery, in the short term RVMI has a worse prognosis to uncomplicated inferior MI, with haemodynamic and electrophysiologic complications increasing in‐hospital morbidity and mortality. Acute RV shock has an equally high mortality to left ventricular (LV) shock.
Clinically, the triad of hypotension, elevated jugular venous pressure (JVP), and clear lung fields should raise the possibility of RVMI in patients with acute inferior MI. The classic 12 lead ECG provides information on the LV, but limited information on the electrical activity of the RV. Only lead V1 provides a partial view of the RV free wall. Right precordial leads are obtained by placing the precordial electrodes over the right chest in positions mirroring their usual arrangement. The presence of acute ST segment elevation, Q waves or both in the right precordial leads (V3R to V6R), is highly reliable in the diagnosis of RVMI. ST segment elevation 0.1 mV in the right precordial leads, especially V4R, is observed in 60–90% of patients with acute RVMI. ST elevation from the RV free wall may also be detected by ST elevation in lead III being more than that in lead II or by reciprocal ST depression in leads I and aVL. Echocardiogram should be performed in patient with or suspected RVMI. It may show RV dysfunction. Additional features of RV involvement include paradoxical septal motion due to increased RV end diastolic pressure, tricuspid regurgitation, and increased right heart pressure.
Cardiac MRI (CMR) can directly evaluate RV size, mass, morphology, and function in an accurate and reproducible manner. CMR is now considered the gold standard for non‐invasive assessment of RV function, particularly as it provides additional information on RV anatomy and myocardial mass.
It is important to recognise and diagnose RVMI, as the treatment is different to LVMI and inferior MI. Please see the following principles of the RVMI management.
1 Reperfusion therapyPrimary percutaneous coronary intervention preferable to thrombolysis, this should be performed as early as possible to preserve right heart function.
2 Optimise RV preloadAvoid morphine, diuretics, β‐blockers, nitrates, ACE inhibitorTrial of judicious fluid administration in the absence of pulmonary oedemaConsider intravenous fluid therapy to increase right sided preload in the absence of pulmonary oedema.
1 Reduce RV afterloadInotropes, pulmonary vasodilators (nitric oxide, prostacycline)Intra‐aortic balloon pump.
1 Maintain chronotropic competence and atrioventricular synchronyAvoid β‐blockers in patients with proximal right coronary artery occlusionConsider dual‐chamber temporary pacing.
Kakouros N, Cokkinos D. Right ventricular myocardial infarction: pathophysiology, diagnosis, and management. Postgraduate Medical Journal. 2010;86(1022):719–728.
https://www.ncbi.nlm.nih.gov/pubmed/20956396
30. Answer: D
Permanent pacing for sinus node dysfunction is only indicated in patients with symptoms directly attributable to bradycardia, irrespective of minimum heart rate or pause duration.
Sinus node dysfunction is most often related to age‐dependent progressive fibrosis of the sinus nodal tissue and surrounding atrial myocardium. It may lead to abnormalities of the sinus node, and atrial impulse formation and propagation, which will therefore result in various bradycardic or pause‐related syndromes. Less common causes include acute myocardial ischemia, atrial tachyarrhythmias, electrolyte abnormalities, hypothyroidism, medications, infections, and metabolic abnormalities. Evaluation for these potentially treatable or reversible causes can be performed non‐urgently in most cases.
Nocturnal bradycardias should prompt consideration of screening for sleep apnoea. Nocturnal bradycardias are common in patient with sleep apnoea. Treatment of sleep apnoea not only reduces the frequency of nocturnal bradycardias but also might offer cardiovascular benefits. The presence of nocturnal bradycardia is not in itself an indication for permanent pacing.
Kusumoto F, Schoenfeld M, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay. Circulation. 2018.
https://www.ahajournals.org/doi/abs/10.1161/CIR.0000000000000628
31. Answer: A
This patient has classical clinical features of Takotsubo (stress) cardiomyopathy which was first described in 1990. Its characteristic finding is the left ventricular apex ballooning. Presenting symptoms include chest pain, dyspnoea, and syncope and can be similar to those in patients with acute coronary syndrome (ACS). 80% of patients have elevated troponin levels and 80% of patients have ischaemic changes on ECG and most have elevated levels of NT‐pro BNP.
Diagnosis of Takotsubo cardiomyopathy does not preclude the diagnosis of ACS. Up to 15% of patients with Takotsubo cardiomyopathy have concurrent coronary artery disease on coronary angiography. Diagnostic criteria for Takotsubo cardiomyopathy includes the presence of a transient abnormality in left ventricular wall motion beyond a single epicardial coronary artery perfusion territory, the absence of obstructive coronary artery disease or angiographic evidence of acute plaque rupture, the presence of new ECG abnormalities or elevation in cardiac troponin levels, and the absence of pheochromocytoma and myocarditis. There are four types of Takotsubo cardiomyopathy: apical type (in most patients) followed by the midventricular type, the basal type, and the focal type.
Takotsubo cardiomyopathy has a higher incidence in patients with a past medical history of neurological and psychiatric disorders, such as epilepsy, stroke, subarachnoid haemorrhage, electroconvulsive therapy, anxiety, and depression. Previous studies suggest Takotsubo cardiomyopathy is associated with emotional triggers. Subsequent studies have found the condition may also occur with physical triggers