In cases of hypertrophic cardiomyopathy, the pathophysiologic role of the systolic pressure gradient across the left ventricular outflow tract is the subject of continued controversy. A patient with this disorder is described whose symptoms and provokable intraventricular gradient disappeared after inferior myocardial infarction. Diastolic left ventricular pressures were essentially unchanged, the isovolumic relaxation period became prolonged and the ejection fraction decreased from 0.77 to 0.61 after infarction. The peak ejection rate was unchanged, but the disappearance of systolic anterior motion of the mitral valve leaflet and obstructive manifestations may have resulted from enlarged mid to late systolic ventricular volumes. This case suggests a direct relation between symptoms and intraventricular pressure gradient in certain patients with hypertrophic cardiomyopathy.
Cardiology Figure 1. Electrocardiogram showed atrial fibrillation, QS in the anteroseptal leads, poor R-wave progression and nonspecific ST-T changes.An 87-year-old Caucasian female presented with symptoms of chest pain, progressive weakness and exertional dyspnea. She had a history of atrial fibrillation, well managed hypertension, and hyperlipidemia. Figure 1 shows her electrocardiogram on presentation.On the basis of the electrocardiogram (ECG), a diagnosis of septal infarct was entertained. The patient was referred for a gated single photon emission CT (SPECT) myocardial perfusion study with Tc-99m sestambi. Stress and rest tomographic images revealed an area of increased radiotracer activity within the left ventricular apex giving the appearance of a myocardial mass (Fig. 2). There was no evidence of myocardial ischemia or infarct. Selective coronary angiography showed no evidence of obstructive disease Cardiac magnetic resonance imaging (CMR) revealed hypertrophy of the left ventricular apex and distal septum, with iso-intense signal in the remaining myocardium (Fig. 3). No delayed hyper-enhancement suggestive of infarct was seen. Given the CMR findings, the patient was diagnosed with apical hypertrophic cardiomyopathy rather than a myocardial mass, and the patient was managed medically with beta-blockers.
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