Case presentation: A 70-yearold white woman with a prior history of tobacco abuse, emphysema, and recent pneumonia presented to an outside emergency room with brief episodes of dull chest pressure recurring over 5 days. Because the current episode was not relieved after 4 hours, and because her ECG showed ST elevation up to 3 mm in V 2 through V 6 , she was given heparin and nitroglycerin infusions and was transferred to the University of Missouri. On admission to our hospital, she was painfree with stable vital signs. Her examination was remarkable for a grade 2/6 systolic ejection murmur in the left third intercostal space. An ECG showed Q waves in V 1 through V 3 . Echocardiography revealed significant left ventricular (LV) dysfunction, ejection fraction of 35% with systolic anterior motion (SAM) of the anterior mitral leaflet, and moderate mitral regurgitation (MR; Figure 1). LV outflow tract (LVOT) gradients were not quantified owing to MR Doppler contamination. Her maximum troponin was 5 ng/mL, and brain natriuretic peptide was 190 pg/mL. Catheterization showed normal coronaries with anteroapical akinesia and LV dysfunction with an ejection fraction of 30%.The patient became hypotensive after catheterization, with systolic pressures between 70 and 85 mm Hg. Dopamine infusion did not improve blood pressure, and the murmur increased to grade 3/6 intensity. Atrial fibrillation developed with a ventricular rate of 150 bpm. Dopamine was discontinued, and intravenous amiodarone converted the atrial fibrillation to sinus tachycardia at 115 bpm, but the hypotension and murmur persisted. Under close supervision, intravenous metoprolol was initiated. With reduction of heart rate to below 70 bpm, the murmur disappeared, and her blood pressure improved. Several hours later, a repeat echocardiogram showed no SAM or LVOT obstruction (LVOTO) and only mild MR.Numerous reports have highlighted the occurrence of dynamic LVOTO as a complication of ST-elevation myocardial infarction (STEMI). 1,2 LVOTO has also been detected in Ϸ20% of transient LV apical ballooning syndrome, also called Takatsubo cardiomyopathy. 3 The actual incidence of dynamic LVOTO is unclear, but it may be significantly underdiagnosed and can indeed mimic cardiogenic shock in an acute-care setting. 4
Mechanism of LVOTOStructural and functional factors contribute to the midsystolic development of gradients referred to as dynamic LVOTO. The asymmetrically hypertrophied septum, progressive narrowing of the LVOT during systole, and direction of the bloodstream cause drag forces and a Venturi effect on the anterior mitral leaflet, which results in SAM of the anterior mitral leaflet. This movement results in the anterior mitral leaflet contacting the septum for a period of systole, effectively obstructing the path of ventricular outflow. Failure of the anterior mitral leaflet to coapt with the posterior leaflet in systole results in MR. The degree and duration of mitral SAM determine the severity of the dynamic LVOTO gradients and MR. Although classically descr...