Dynamic left ventricular outflow tract obstruction in the setting of acute anterior myocardial infarction: a serious and potentially fatal complication?

Dynamic left ventricular outflow tract (LVOT) obstruction was thought to be a hallmark of hypertrophic obstructive cardiomyopathy, especially in those cases with isolated asymmetric septal hypertrophy and systolic anterior motion (SAM) of the mitral valve. Recently, several authors described the occurrence of a dynamic LVOT obstruction during acute coronary insufficiency in ventricles without significant myocardial hypertrophy. The LVOT gradient was reported to disappear following resolution of the ischemic syndrome. Furthermore, it was reported that LVOT obstruction in the setting of acute myocardial infarction could predispose to cardiac rupture. We describe four cases with acute anterior myocardial infarction complicated with a dynamic LVOT obstruction documented by transthoracic Doppler echocardiogram. The detection of the dynamic LVOT obstruction allowed us to optimize the pharmacological treatment in each case. In spite of therapy, two of our patients worsened progressively to fatal cardiogenic shock and cardiac rupture. In conclusion, the development of a LVOT obstruction during acute anterior myocardial infarction has to be considered a serious and potentially fatal complication.

Modifications of Oxygen Saturation During Transesophageal Echocardiography.

The present study was designed: (1) to establish the effects of transesophageal echocardiography (TEE) on arterial oxygen saturation (SAO(2)%); (2) to verify the possible clinical consequences of this phenomenon; and (3) to study the possibility of predicting modifications of SAO(2)% by clinical or hemodynamic variables or by specific factors related to the TEE procedure. We prospectively studied 116 unselected patients, aged 61 +/- 12 years, who underwent diagnostic TEE for various clinical indications. Thirty-seven patients had mitral valve disease, 19 aortic valve disease, 14 combined mitroaortic disease, 8 congenital heart disease, and 38 other cardiovascular diseases. Eight patients were affected by chronic obstructive pulmonary disease. Ninety-seven patients were sedated by 4 +/- 2 mg of diazepam IV SAO(2)% (5-min average) (Ohmeda Biox 3700 pulse oxymeter finger probe), heart rate (HR), and blood pressure (BP) were considered during baseline transthoracic examination, after pharmacological sedation but before the introduction of the probe, and finally during TEE. Neither clinical complications nor major arrhythmias were observed. Baseline SAO(2)%, HR and BP were, respectively, 93.6 +/- 3.3%, 76 +/- 14 beats/min, and 129 +/- 20/75 +/- 10 mmHg. Pharmacological sedation did not modify SAO(2)%, HR, and BP (P > 0.1). During TEE a small but significant reduction in SAO(2)% by an average of 1.2 +/- 3.2% was observed (P < 0.005), as well as a small and significant increase in HR by an average of 3 +/- 10 beats/min (P < 0.01). BP did not change significantly (P > 0.1 for both systolic and diastolic). The changes of SAO(2)% and HR were not interrelated and were not related to the duration of the procedure and to any of the clinical and hemodynamic variables taken into consideration. TEE can induce a small but significant drop in SAO(2)% and a small increase in HR even without any clinical relevance. No clinical or hemodynamic variable or specific factors related to the TEE procedure were related to these changes.