Poor outcomes after acute myocardial infarction in systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is associated with higher risk for acute myocardial infarction (MI); but the post-infarction outcomes among these patients are unknown. Our objective was to compare post-acute MI outcomes in patients with SLE to those with diabetes mellitus (DM) and those with neither condition. METHODS: We analyzed the risk for prolonged hospitalization and in-hospital mortality following acute MI in the 1993-2002 US Nationwide Inpatient Sample. We used logistic regression to calculate odds ratios (OR) for prolonged hospitalization and Cox proportional hazards regression to calculate hazard ratios (HR) for in-hospital mortality with and without adjustments for age, sex, race/ethnicity, socioeconomic status, and presence of congestive heart failure. RESULTS: For the SLE (n = 2192), DM (n = 236,016), SLE/DM (n = 474), and control (n = 667,956) groups, the in-hospital mortality rates were 8.3%, 6.2%, 5.7%, and 4.7%, respectively. In multivariable regression models, all 3 disease groups had higher adverse outcome risk compared to control. The OR for prolonged hospitalization was higher for those with SLE (OR 1.48, 95% CI 1.32-1.79) compared to those with DM (OR 1.30, 95% CI 1.28-1.32). A similar pattern was observed for hazard ratios for in-hospital mortality as well (SLE, HR 1.65, 95% CI 1.33-2.04; DM, HR 1.11, 95% CI 1.07-1.14). CONCLUSION: SLE, like DM, increases risk of poor outcomes after acute MI. These patients need to be triaged appropriately for aggressive care.

Coronary, peripheral and cerebrovascular disease: a complex relationship.

Atherosclerosis is a diffuse process that may affect different vascular beds with considerable overlap between coronary, cerebrovascular and peripheral arterial disease. These conditions are related to similar predisposing risk factors and genetic predisposition. Presence of atherosclerosis at one arterial site should prompt the clinician to assess for an involvement, symptomatic or asymptomatic, at other arterial distributions. Patients with peripheral or cerebrovascular disease often receive less than optimal secondary preventive therapy than those with coronary artery disease. It is imperative that these individuals with noncoronary atherosclerotic disease be also treated aggressively to reduce the high adverse cardiovascular event rate reported in these patients.

Pulmonary artery pressure changes during ethanol embolization procedures to treat vascular malformations: can cardiovascular collapse be predicted?

PURPOSE: Ethanol has been used for embolization of vascular malformations. Cardiovascular collapse, although rare, has been reported, occurring immediately to a few hours after ethanol embolization. The pathophysiology has been theoretically attributed to direct toxicity to the cardiac conduction system or pulmonary artery (PA) vasospasm leading to cardiovascular collapse. Because of cardiovascular collapse in one patient at the authors' institution, it was standard of care at the time of this study to monitor the pulmonary artery pressures during ethanol embolization. This study was conducted to clarify the effect of ethanol on the PA pressure during these procedures. METHODS: Data from 92 ethanol embolization procedures performed on 56 patients with vascular malformations between May 2001 and May 2003 are reported. PA and noninvasive cuff systemic pressures were recorded before and after each injection and also before and after the entire procedure. Upper limit for volume of ethanol used during these procedures was drawn at 1 mL/kg. Simple and multiple linear regression analyses were done to study factors affecting changes in PA and systemic blood pressure. RESULTS: For each injection, ethanol volume averaged 3.1 mL per injection. The systolic systemic and PA systolic pressures increased by 2.3 and 1.0 mm Hg, respectively. Amount of ethanol injected and systemic blood pressure changes were predictive of change in PA blood pressure. During the entire procedure, systemic systolic blood pressure increased by an average of 11.6 mm Hg, and PA systolic blood pressure by 5 mm Hg. Change in systemic blood pressure was a strong predictor of, and volume of ethanol was a weak predictor of, change in PA blood pressure. CONCLUSION: The mild rise in PA blood pressure in the patients during ethanol embolization correlated strongly with minor elevation in systemic blood pressure throughout the procedure, which the authors believe is related to pain from the ethanol injection causing sympathetic stimulation, even when patients are under general anesthesia. The minimal rise in PA blood pressure during these procedures does not elucidate the cause of the rare complication of cardiovascular collapse during ethanol embolization.