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This case underscores the continued importance of bedside physical examination in diagnosing hypertrophic obstructive cardiomyopathy, even in the era of advanced imaging techniques.
A 61-year-old man presented with exertional dyspnoea that resolved spontaneously with rest and had not progressed over time. The patient had hypertension and diabetes mellitus, which were well controlled with oral medication and diet. On physical examination, the apex beat showed a double apical impulse consisting of a high A-wave and sustained apical impulse (Figure 1A). On auscultation, the fourth sound was heard at the apex, and a mid-late systolic murmur (grade 3/6) was audible after an early systolic additional sound or pseudoejection sound (Figure 1B; see Supplementary material online, Sound 1). The systolic murmur did not radiate to the neck, increased with the Valsalva manoeuver and in the standing position, and decreased with squatting. The jugular venous pressure was not elevated, but the carotid pulse was notable for pulsus bisferiens or a spike-and-dome configuration (Figure 1C). All these physical findings were consistent with hypertrophic obstructive cardiomyopathy (HOCM). The remainder of the examination was normal. Echocardiography showed asymmetric septal hypertrophy with an interventricular septal thickness of 16 mm and systolic anterior motion (SAM) of the mitral valve (Figure 1DandE; see Supplementary material online, Video S1), resulting in a left ventricular outflow tract obstruction with a resting pressure gradient of 61 mmHg (Figure 1F) and mitral regurgitation (see Supplementary material online, Video S2). A diagnosis of HOCM was confirmed. Coronary angiography demonstrated showed two-vessel disease. The patient underwent coronary artery bypass grafting with extended myectomy of the ventricular septum. He has been doing well without any symptoms for >5 years after surgery. The apex cardiogram shows a high A-wave (A, arrow) and a high systolic plateau or a sustained apex beat (B, arrowhead) after the E-point, findings consistent with a double apical impulse. On the phonocardiogram obtained at the apex, an additional sound (B, arrow) before the first sound (S1) at a low frequency (L) but not at a lower-middle frequency (M1), higher-middle frequency (M2), or high frequency (H), findings consistent with the fourth sound. Note another additional systolic sound or pseudoejection sound (B, arrowheads), followed by a mid-late systolic murmur (B, asterisks) that ends before the second sound (S2). The carotid pulse tracing shows pulsus bisferiens: an initial sharp rise or spike (C, arrow) and a bump or dome (C, asterisk) before the dicrotic notch (C, arrowhead). An echocardiographic view of the parasternal long-axis view in mid-systole is notable for the systolic anterior motion of the mitral valve (D, arrow), as is the M-mode (E, arrow). A colour Doppler image shows a left ventricular outflow tract obstruction with a peak flow velocity of 3.9 m/s at rest (F). The underlying mechanisms of a high A-wave on the apical impulse and the fourth sound on auscultation remain unclear, but forceful atrial contraction into noncompliant ventricles may explain these unique physical findings.1 Since a pseudoejection sound has been reported to be associated with SAM on echocardiography,2 it is reasonable that a systolic ejection murmur would develop after the additional sound. The transient occlusion of the left ventricular outflow obstruction due to SAM also causes a mid-systolic dip in the aortic waveform, followed by a bump or dome before the dicrotic notch, in patients with HOCM. The present case underscores the need for clinicians to reaffirm the importance of bedside physical examination, even in the modern era of advanced imaging techniques. Supplementary material is available at European Heart Journal – Case Reports. None declared.
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Noguchi et al. (2023) studied this question.
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