Patients with left ventricular apical aneurysms represent a unique patient subgroup in the broad clinical spectrum of hypertrophic cardiomyopathy (HC) associated with the risk for sudden death, heart failure, and peripheral thromboembolism. Routine chronic anticoagulation has not been a standard recommendation for these patients. We present a 36-year-old patient with HC with features of acute coronary syndrome, likely secondary to coronary thromboembolism as a complication of left ventricular apical aneurysm. Our experience with this patient raises consideration for prophylactic anticoagulant therapy for this unusual subset of patients with HC.
Patients with hypertrophic cardiomyopathy (HC) and left ventricular (LV) apical aneurysms represent an underappreciated subset within the heterogeneous clinical spectrum of HC but with important management implications. Among the adverse disease complications is the underrecognized risk for peripheral thromboembolism, potentially preventable with prophylactic anticoagulation therapy.
Case Report
A 36-year-old man with HC and LV apical aneurysm and a prophylactic implantable cardioverter–defibrillator presented with a clinical scenario consistent with acute coronary syndrome. He complained of jaw and chest pain, diaphoresis, and presyncope, triggered by running on a treadmill. Twelve-lead electrocardiogram showed diffuse deep T-wave inversion, most prominent in the lateral precordial leads. Cardiac troponin I was 0.69 ng/ml on admission and peaked at 0.84 ng/ml. Coronary arteriography and computed tomography angiogram (CTA) excluded obstructive atherosclerotic coronary narrowing and plaque rupture ( Figure 1 ). A thrombus was identified in the distal right coronary artery (posterolateral branch of the posterior descending artery) and was immediately removed by aspiration thrombectomy, followed by balloon angioplasty. An extensive hypercoagulable workup proved normal, including factor V Leidin, protein C and S, and homocysteine levels; anticardiolipin antibodies; dilute Russell viper venom time; and hexagonal-phase phospholipid neutralization assay.
Two-dimensional echocardiogram demonstrated anterior ventricular septal thickness of 14 mm. Systolic anterior motion of the mitral valve was absent and continuous-wave Doppler interrogation of the LV outflow tract yielded normal velocities of 1.2 m/s at rest and 1.4 m/s with Valsalva maneuver. Left atrial dimension was 39 mm; LV end-diastolic dimension was 50 mm and ejection fraction was 74%.
Cardiovascular magnetic resonance (CMR) imaging with intravenous contrast injection of gadolinium ( Figure 1 ) and CTA ( Figure 1 ) showed an LV apical aneurysm, 2 cm in transverse dimension, with transmural late gadolinium enhancement of the aneurysmal rim (consistent with myocardial scarring) extending into adjacent myocardium. An intraventricular clot was not identified by CTA, echocardiography, or CMR.
Histopathology of the aspirated clot showed alternating lines of red blood cells, platelets, and fibrin ( lines of Zahn ), diagnostic of a thrombus ( Figure 1 ), and without evidence of atherosclerotic plaque (i.e., absence of cholesterol clefts, foam cells, or calcification). The patient was discharged uneventfully on warfarin for prevention of stroke.
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