Cardiogenic shock due to dynamic left ventricular outflow tract obstruction in acute myocardial infarction

Sirs: Myocardial infarction (MI) may be complicated by life threatening cardiogenic shock (CS). Known reasons include severe ventricular dysfunction due to large myocardial necrosis or ongoing ischaemia, or severe arrhythmias. Acute mechanical complications may be caused by pericardial tamponade due to rupture of the ventricular free wall, or acute left-to-right shunting following rupture of the intraventricular septum, or papillary muscle dysfunction or rupture leading to severe mitral insufficiency [1]. Recently, dynamic left ventricular outflow tract obstruction (LVOTO) has been recognized as another reason for hemodynamic compromise and shock occurring in patients with MI, but without signs of hypertrophic obstructive cardiomyopathy (HOCM) [4–6]. In this case we describe diagnosis and management of this rare complication. A 61-year-old woman was admitted to another hospital for acute anterolateral MI. Immediate percutaneous coronary intervention (PCI) with stenting of the left anterior descending (LAD) coronary artery was performed. Eight hours later repeated coronary angiography with PCI was necessary for an acute instent thrombosis. Eptifibatide was given as infusion. After successful intervention, hypotension and oligo-anuria developed. Catecholamines and furosemide were instituted, but the patient deteriorated and was transferred to our hospital for planned renal support by hemofiltration and insertion of an intra aortic balloon pump (IABP). On admission the patient was responsive; heart rate (HR) was 115/min, blood pressure (BP) 90/50 mmHg. Her skin was slightly clammy; jugular veins were visible but not distended. Heart sounds were silent, with a grade 2/6 systolic murmur, but no friction rub. Lungs were clear. She received dobutamine (7 lg/kg/min) and noradrenaline (2.7 lg/kg/min) as well as eptifibatide and heparin, aspirin and clopidogrel. She was anuric. Her troponin was 190 lg/l (normal \ 0.3 lg/l). Initial CK level was 1,751 U/l (normal \ 170 U/l, maximum 3,043 U/l). SGOT was 7,235 U/l (normal \ 35 U/l, maximum 12,303 U/l on day 2), SGPT was 6,400 U/l (normal \ 35 U/l, maximum 8,070 U/l on day 2). BNP (brain natriuretic peptide) was 557 ng/l (normal \ 155 ng/l, maximum 1,463 ng/l on day 3). Lactate was 3.6 mmol/l (normal \ 2.0 mmol/l). Central venous oxygen saturation (CVSaO2) was 48.3%. Creatinine was 2.4 mg/dl (normal \ 1.1 mg/dl; maximum 2.8 mg/dl at day 2) ECG showed sinus rhythm with Q waves in leads V1 through V3 with ST elevation in V1 through V5. On immediate bedside transthoracic echocardiography (TTE) the apical and midventricular segment of the left ventricular anterior wall and the apical portion of the septum were akinetic. The basal segments of the lateral and inferior wall as well as the basal part of the septum showed hyperkinesis. Global left ventricular ejection fraction (LV-EF) was moderately reduced (45%), as estimated visually. There was a systolic anterior movement (SAM) with septal contact of the anterior leaflet of the mitral valve (see Fig. 1). Color Doppler examination revealed turbulent flow in the left ventricular outflow tract (LVOT) (see Fig. 2) and M. Moller (&) J. Volz R. Paliege C. Lenz D. Berger R. Gradaus J. Neuzner Department of Cardiology and Intensive Care, Klinikum Kassel, Monchebergstrase, 41-43, 34125 Kassel, Germany e-mail: michael.moeller@klinikum-kassel.de