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Patients with peripheral artery disease (PAD) have higher cardiovascular event rates than patients with established coronary artery disease (CAD) and abnormal endothelial function predicts cardiovascular risk in PAD and CAD. We investigated the hypothesis that PAD is associated with a greater degree of impairment in vascular function than CAD. We used several non-invasive tests to evaluate endothelial function in 1320 men and women with combined PAD and CAD (n = 198), PAD alone (n = 179), CAD alone (n = 466), or controls aged > 45 years without CAD or PAD (n = 477). Patients with PAD had lower brachial artery flow-mediated dilation (5.1 ± 3.9% PAD and CAD, 5.9 ± 4.4% PAD alone) compared to patients with CAD alone (7.0 ± 4.5%) and no PAD or CAD (8.1 ± 5.1%, p < 0.0001). In multivariable models adjusting for clinical covariates and the presence of CAD, PAD remained associated with lower flow-mediated dilation (p < 0.0001). PAD was associated also with lower nitroglycerin-mediated dilation and reactive hyperemia. Patients with both PAD and CAD had a lower digital pulse amplitude tonometry (PAT) ratio in unadjusted models but not in adjusted models. Flow-mediated dilation was modestly associated with PAT ratio in patients with atherosclerotic disease (r = 0.23, p < 0.0001) but not among control participants (r = 0.008, p = 0.93). Our findings indicate that patients with PAD have greater impairment of vasodilator function and are consistent with the possibility that endothelial dysfunction may contribute to adverse cardiovascular prognosis in PAD.

Cocaine use is associated with increased cardiovascular mortality and can promote acute coronary syndrome (ACS). Use of beta-blockers is controversial in patients who use cocaine, and the safety and efficacy of these medications in ACS in patients actively using cocaine is unknown. We enrolled 90 patients with ACS and positive urine drug screen for cocaine. Patients received standard ACS therapy plus either labetalol (n = 60) or diltiazem (n = 30). Blood pressure and heart rate were measured at baseline and 48 hours. Levels of serum CD40 ligand, interleukin (IL)-6, and choline at baseline and 48 hours were determined. There were no baseline differences in hemodynamics or serum levels of inflammatory markers between the labetalol and diltiazem groups. Both groups experienced a significant and equivalent decrease in BP and HR at 48 hours compared with baseline. At 48 hours of treatment, there were significant decreases of 17% in CD40 ligand (P < .005) and 16% in IL-6 (P < .005) but no change in choline in the diltiazem group. Furthermore, in the labetalol group, there were significant differences of 30% in CD40 ligand (P < .005 time and group comparison), 22% in IL-6 (P < .005 time and group comparison), and 18% in choline (P < .005 time and group comparison). There were no adverse events during hospitalization in any patients who received labetalol. In conclusion, labetalol appears to be safe in cocaine-associated ACS. Furthermore, labetalol provides a beneficial hemodynamic response and, in comparison to diltiazem, potentiates an anti-inflammatory vascular response in this setting.

We report a case of an 81-year-old man with bacterial myocarditis presenting with elevated troponins and sepsis, who succumbed due to a ruptured ventricle. The infecting organism was found to be methicillin-resistant Staphylococcus aureus. Bacterial myocarditis is a rare occurrence when independent of infective endocarditis. Generally, this is a complication of bacteremia that is discovered post-mortem. Rarely, as in our patient, it causes significant necrosis of the myocardium leading to rupture of a ventricle. As with viral myocarditis, this disease can present with signs and symptoms of acute myocardial infarction, complicating the diagnosis. Much of the available data on bacterial myocarditis was collected before the development of many modern diagnostic tests and before antibiotics. Accordingly, the appropriate workup, diagnosis and treatment remain unclear. Our patient represents the first reported case of ventricular rupture due to methicillin-resistant S. aureus-associated bacterial myocarditis.