PMC4008090_01
Chest leads electrocardiogram showing ST-segment elevations in V2, V3, and V4.
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fig1
The initial ECG showed ST-elevation in the precordial leads from V2 to V4 (Figure 1).
Coronary angiogram minor disease in the left anterior descending artery but no other coronary artery disease.
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fig2
Coronary angiogram, however, showed some atherosclerotic coronary artery disease, but no significant stenosis (Figure 2).
LV angiogram in diastole (a) and systole (b) in right anterior oblique projection demonstrating wall-motion abnormality characteristic of stress cardiomyopathy. At end systole, LV chamber adopts distinctive "short neck with round flask" configuration in which distal (apical) portion is akinetic/hypokinetic, whereas in contrast, the remaining proximal (basal) segment is hypercontractile. Left panel, angiogram after 4 days.
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fig3
Left ventriculography demonstrated typical apical ballooning with a globally reduced ejection fraction estimated at 35% (Figure 3).
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 (46 to 130 mmHg) increase in gradient. This phenomenon, known as the Brockenbrough-Braunwald-Morrow sign, is part of the classical description of hypertrophic obstructive cardiomyopathy. Ao: aorta; ECG: electrocardiogram; LV: left ventricle; PVC: premature ventricular complex.
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fig4
Pressure tracings showed no pressure gradient between the LV and the aorta (Figure 4).
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 (46 to 130 mmHg) increase in gradient. This phenomenon, known as the Brockenbrough-Braunwald-Morrow sign, is part of the classical description of hypertrophic obstructive cardiomyopathy. Ao: aorta; ECG: electrocardiogram; LV: left ventricle; PVC: premature ventricular complex.
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fig5
On day four, a second invasive hemodynamic evaluation was performed, confirming a simultaneous pressure gradient between the LV and aorta of 45 mmHg at rest that increased to 70 mmHg after Valsalva maneuver (Figure 5).