Apical hypertrophic cardiomyopathy

Abstract

Apical hypertrophic cardiomyopathy (ApHCM) is a subtype of hypertrophic cardiomyopathy, which is clinically suspected by a characteristic giant negative T (GNT) wave on electrocardiogram (ECG) and diagnosed by demonstrating apical hypertrophy on ECG. However, GNT may not always be specific for ApHCM as in this report of apically displaced papillary muscle (ADPM). Methods and resultsBy retrospectively collecting 12-lead ECGs with a GNT wave and apical hypertrophy on 2D-ECG from 2008 to 2010, we identified 55 patients with both of these findings. ADPM was defined to be present when the base of the papillary muscle originated from the apical one-third of the left ventricle. A diagnosis of ApHCM in patients with apical hypertrophy but without evidence of ADPM was given otherwise. Careful evaluations of 2D-ECGs suggested that 20% (11/ 55) of all patients had an ADPM mimicking ApHCM. Baseline clinical and echocardiography data were not different between the two except for the maximal T wave on 12-lead ECG and apicoseptal hypertrophy, suggesting that the differentiation of these two groups may be subtle and difficult. In addition, patients with ADPM frequently showed abnormal insertion of papillary muscle into the left ventricular outflow tract or into the base of mitral valve leaflet. ConclusionThese findings suggest that ADPM may also be present with GNT on 12-lead ECG and emphasizes the careful evaluation of the left ventricular apex for proper diagnosis and discrimination of ApHCM.

Apical hypertrophic cardiomyopathy might lead to misdiagnosis of ischaemic heart disease

“…One proposed explanation for this finding is a diminished coronary vasodilator reserve in the region of hypertrophy [16]. This is supported by the demonstration of stress-induced reversible Thallium-201 perfusion defects in the apex in some patients [16]. AHCM might mimic ischaemic heart diseases via clinical properties and electrocardiographic findings as in our study.…”

“…Typical angina is frequent and can occur even in patients demonstrated to have normal coronary arteries by angiography. One proposed explanation for this finding is a diminished coronary vasodilator reserve in the region of hypertrophy [16]. This is supported by the demonstration of stress-induced reversible Thallium-201 perfusion defects in the apex in some patients [16].…”