Geske, Jeffrey

A 34-year-old man was referred for progressive angina and exertional dyspnoea refractory to medical therapy, with a presumptive diagnosis of hypertrophic cardiomyopathy (HCM). Transthoracic echocardiography (TTE) revealed asymmetric septal hypertrophy without systolic anterior motion of the mitral valve leaflet and with no dynamic left ventricular outflow tract (LVOT) obstruction. However, the LVOT velocity was elevated at rest as well as with provocation, without the characteristic late peaking obstruction seen in HCM. Focused TTE to evaluate for suspected fixed obstruction demonstrated a subaortic membrane 2.2 cm below the aortic valve. Coronary CT angiography confirmed the presence of the subaortic membrane and was negative for concomitant coronary artery disease. Surgical resection of the subaortic membrane and septal myectomy resulted in significant symptomatic relief and lower LVOT velocities on postoperative TTE. This case reminds the clinician to carefully evaluate for alternative causes of LVOT obstruction, especially subaortic membrane, as a cause of symptoms mimicking HCM.

A 70-year-old man presented with recent onset, predominantly right-sided heart failure. Echocardiogram demonstrated features of hypertensive heart disease and was suggestive of, but non-diagnostic for, constrictive pericarditis (CP). CT demonstrated mild pericardial thickening. Right heart catheterisation showed elevation and equalisation of diastolic pressures in all cardiac chambers with early rapid filling, minimal ventricular interdependence, and no dissociation of intrathoracic and intracardiac pressures. While several features pointed towards CP, the minimal ventricular interdependence and no dissociation of intrathoracic and intracardiac pressures suggested other pathology. Diagnostic pericardiectomy was performed, after which the central venous pressure decreased from 22 to 12 mm Hg. Pathology revealed pericardial fibrosis. The patient experienced sustained resolution of his heart failure. A potential explanation for lack of CP criteria was the presence of hypertensive heart disease. CP needs to be considered when approaching patients with heart failure as diagnostic evaluation can be multifaceted and treatment curative.

A woman in her late 50s experienced a witnessed, sudden out of hospital cardiac arrest. Initial workup included coronary angiography, transthoracic echocardiogram and a CT scan of the chest to rule out pulmonary embolus. She was subsequently discharged home without an implantable cardioverter defibrillator (ICD) or a life vest. On follow-up at another facility, an ICD was placed and a Holter monitor showed no ventricular ectopy. Further transthoracic echocardiographic images were obtained, which were suggestive of apical hypertrophic cardiomyopathy. A limited transthoracic echocardiogram with contrast was performed, which did not elucidate the hypertrophy. However, eccentric left ventricular apical wall hypertrophy was visualised by a coronary CT scan.