A 79-year-old white woman with known hypertrophic obstructive cardiomyopathy (HOCM) presented with sudden-onset chest pain and no identifiable stressor. Examination suggested a new apical 3/6 systolic murmur and pulmonary edema. A 12-lead electrocardiogram showed anterolateral wall ischemia. The patient's peak troponin T level was 2.5 ng/mL. Echocardiography revealed a basalhypertrophied septum (Fig. 1) with a resting left ventricular (LV) outflow gradient ofapproximately 20 mmHg, severe mitral valve regurgitation, and apical akinesis. No obstruction of the coronary arteries was seen on arteriography. Simultaneous LV and aortic pressure tracing showed dynamic LV outflow tract (LVOT) obstruction as evidenced by the Brockenbrough-Braunwald-Morrow sign¹ (Fig. 2). Severe mitral regurgitation, anteroapical ballooning, and basal hyperkinesis with a low LV ejection fraction (LVEF, 0.25) were noted on ventriculography (Fig. 3). The patient was stabilized with oxygen, diuretics, and β-blockers, and she was discharged from the hospital on the 4th day. At her 2-month follow-up visit, the apical ballooning had completely resolved (LVEF, 0.65), and the dynamic LVOT obstruction was relatively less severe.

Fig. 1 Transthoracic echocardiogram (parasternal long-axis view) shows a thickened basal septum (22-mm, arrowheads) and systolic anterior motion of the mitral leaflet (arrow).

Fig. 2 Pressure tracings show a sharp rise in LV outflow gradient that follows the pause associated with PVC. A dynamic obstruction leads to a concomitant fall in aortic pressure and a disproportionate (12- to 50-mmHg) increase in gradient. This phenomenon, (more ...)

Fig. 3 End-diastolic (A) and end-systolic (B) ventriculograms (right anterior oblique view) show anteroapical akinesia or “ballooning” with basal hyperkinesis (arrows).

Apical ballooning syndrome is a newly described pattern of transient LV apical or midventricular wall motion abnormality that is commonly associated with physiologic or psychological stress in postmenopausal women and is believed to be catecholamine-mediated.² In patients with HOCM and LVOT obstruction, only 1 previously published report of apical ballooning syndrome appears in the medical literature.³ The mechanism of transient apical ballooning is difficult to explain in a patient who had HOCM, with pre-existing dynamic LVOT obstruction and the absence of a preceding stressor. It is possible that an aggravated dynamic LVOT obstruction led to a sympathetic surge and increased wall stress.^3,4 This, coupled with decreased coronary reserve and systolic coronary squeezing,^5,6 could have caused wall-motion abnormalities and electrocardiographic changes. Treatment of such a patient is mainly supportive, and a reversal of the dysfunction is likely.