Non-ST-segment elevation myocardial infarction in the setting of sexual intercourse following the use of cocaine and sildenafil.

Acute myocardial infarction (MI) in the setting of sexual intercourse following the concomitant use of cocaine, alcohol, and sildenafil has not been previously reported. We present a case of a middle-aged patient with no previous history of angina pectoris or coronary artery disease who presents with severe ischemic chest pain and an MI induced by cocaine, alcohol, sildenafil, and sexual intercourse.

Predictors of cardiac hepatopathy in patients with right heart failure.

BACKGROUND: Some patients with right heart failure develop cardiac hepatopathy (CH). The pathophysiology of CH is thought to be secondary to hepatic venous congestion and arterial ischemia. We sought to define the clinical and hemodynamic characteristics associated with CH. MATERIAL/METHODS: A retrospective cross sectional analysis was performed in which subjects were identified from our institutional cardiology database if echocardiography showed either right ventricular (RV) hypokinesis or dilatation, and was performed within 30 days of right heart catheterization. A chart review was then performed to identify patient clinical characteristics and to determine if the patients had underlying liver disease. Subjects with non-cardiac causes for hepatopathy were excluded. RESULTS: In 188 included subjects, etiology for right heart dysfunction included left heart failure (LHF), shunt, pulmonary hypertension, mitral- tricuspid- and pulmonic valvular disease. On multivariate analysis, higher RV diastolic pressure and etiology for RV dysfunction other than LHF were both associated with CH. Low cardiac output was associated with CH only amongst those without LHF. CONCLUSIONS: CH is most often seen in subjects with elevated RV diastolic pressure suggesting a congestive cause in most cases. CH associated with low cardiac output in patients without LHF suggests that low flow may be contributing to the patophysiology in some cases.

Left ventricular torsional mechanics in uncomplicated pregnancy.

BACKGROUND: Alterations in left ventricular (LV) twist (torsion) and untwist have been described for a variety of physiologic and pathologic conditions. Little information is available regarding changes in these parameters during normal pregnancy. HYPOTHESIS: Pregnancy is associated with significant changes in LV torsional mechanics. METHODS: Left ventricular twist and untwist was measured in 32 pregnant females (mean gestation 199 ± 48 d) and 23 nonpregnant controls using speckle-tracking echocardiography. RESULTS: Left ventricular ejection fraction (68 ± 5% vs 66 ± 5%) was similar between the groups (P not significant). There was a significant increase in peak LV twist from nonpregnant controls (9.4 ± 3.7 degrees) to second-trimester (12.0 ± 4.2 degrees) and third-trimester subjects (12.6 ± 5.9 degrees, all P<0.05). Peak LV twist velocity was also increased in second- and third-trimester groups compared with controls (94 ± 24 degrees/sec and 93 ± 30 vs 64 ± 21 degrees/sec, respectively, both P<0.05). Both peak untwist velocity and time to peak untwist velocity were not significantly different between groups (P not significant). Multiple regression analysis indicate that only systolic blood pressure (r = 0.394, P = 0.005) was an independent predictor for increased LV torsion. CONCLUSIONS: There are significant changes in LV torsional indices during the course of pregnancy, whereas untwist parameters remain unchanged. Blood pressure is independently associated with increased torsion during pregnancy.