Pheochromocytoma-Induced Takotsubo Cardiomyopathy.

Pheochromocytoma, a rare catecholamine-secreting tumor, typically manifests itself with paroxysmal hypertension, tachycardia, headache, and diaphoresis. Less often, symptoms related to substantial hemodynamic compromise and cardiogenic shock occur. We report the case of a 66-year-old woman who presented with abdominal pain. Examination revealed a large right adrenal mass, cardiogenic shock, and severe heart failure in the presence of normal coronary arteries. Within days, the patient's hemodynamic status and left ventricular ejection fraction improved markedly. Results of imaging and biochemical tests confirmed the diagnosis of pheochromocytoma-induced takotsubo cardiomyopathy. Medical therapy and right adrenalectomy resolved the patient's heart failure, and she was asymptomatic postoperatively. We recommend awareness of the link between pheochromocytoma and takotsubo cardiomyopathy, and we discuss relevant diagnostic and management principles.

Paraganglioma as a rare cause of left ventricular thrombus in the setting of preserved ejection fraction: discussing the literature.

Paragangliomas and pheochromocytomas are catecholamine-secreting tumours which if remain undiagnosed may cause severe morbidity and mortality. In rare circumstances these tumours can cause left ventricular (LV) thrombi to form by inducing cardiomyopathy and subsequent embolic complications. After a thorough literature review, six previous cases were found that presented the formation of an LV thrombus in the setting of a pheochromocytoma or paraganglioma. A majority of these cases were associated with significant wall motion abnormalities and their cardiac ejection fraction (EF) was compromised. This is a rare case of a patient developing LV thrombi in the setting of a paraganglioma with normal cardiac EF. We present this case to compare the similarities and differences of our case with previously reported cases and emphasise the importance of suspecting these LV thrombi in patients with these neuroendocrine tumours.

Thrombin-receptor antagonist vorapaxar in acute coronary syndromes.

BACKGROUND: Vorapaxar is a new oral protease-activated-receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. METHODS: In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization. RESULTS: Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan-Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P=0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P=0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P<0.001). Intracranial hemorrhage rates were 1.1% and 0.2%, respectively (hazard ratio, 3.39; 95% CI, 1.78 to 6.45; P<0.001). Rates of nonhemorrhagic adverse events were similar in the two groups. CONCLUSIONS: In patients with acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly reduce the primary composite end point but significantly increased the risk of major bleeding, including intracranial hemorrhage. (Funded by Merck; TRACER ClinicalTrials.gov number, NCT00527943.).

Active Lipid Management In Coronary Artery Disease (ALMICAD) study.

PURPOSE: Many providers have implemented specialized lipid clinics to more effectively identify, monitor, and treat hyperlipidemia in patients with coronary artery disease. The effectiveness of such a strategy is not known. We sought to investigate whether a specialized clinic achieves better lipid results and clinical outcomes than standard care. SUBJECTS AND METHODS: A total of 1233 patients who had coronary disease documented by coronary angiography were randomized to lipid clinic or standard care groups by their providers and followed for 2 years. The primary end point was a composite of death, myocardial infarction, repeat revascularization, and stroke. RESULTS: Lipid clinic (n=617) and standard care (n=616) groups had no significant baseline differences. After 2 years, the lipid clinic group had similar total cholesterol (166+/-42 mg/dL vs 166+/-41 mg/dL, P=.83), low-density lipoprotein cholesterol levels (84+/-32 vs 85+/-32, P=.28), and percentage of patients with low-density lipoprotein cholesterol less than 100 mg/dL (77.5% vs 77.6%, P=.97). There were no significant differences in the primary end point (12.3% vs 11.4%, P=.60) and mortality (7.6% vs 7.3%, P=.80) between the lipid clinic and standard care groups. CONCLUSIONS: In patients identified by diagnostic coronary angiography and managed within a single health care system, implementation of a specialized lipid clinic did not achieve greater attainment of hyperlipidemia treatment goals or improved cardiac outcomes.

Predictors and outcomes associated with gastrointestinal bleeding in patients with acute coronary syndromes.

BACKGROUND: Potent antiplatelet and anticoagulant agents along with early revascularization are increasingly used in patients hospitalized with acute coronary syndromes (ACS). An important complication associated with these therapies is gastrointestinal bleeding (GIB); yet, the predictors, optimal management, and outcomes associated with GIB in ACS patients are poorly studied. METHODS: We investigated the incidence, predictors, pathological findings, and clinical outcomes associated with GIB in patients with ACS hospitalized at a United States tertiary center between 1996 and 2001. RESULTS: Three percent (80/3,045) of ACS patients developed clinically significant GIB. Predictors of GIB were older age, female gender, non-smoking status, peak troponin I, and prior heart failure, diabetes, or hypertension. Patients with GIB were more critically ill with lower blood pressure and higher heart rates. GIB was associated with an increased need for transfusion, mechanical ventilation, and inotropes/pressors. In-hospital mortality was significantly higher in ACS patients with versus without GIB (36% vs. 5%, P < 0.001). Thirty patients (38%) with GIB underwent endoscopy with no procedural complications of death, arrhythmia, urgent ischemia, or hemodynamic deterioration. CONCLUSION: In patients with ACS, GIB is associated with older age, female sex, peak troponin I, non-smoking status, diabetes, hypertension, and heart failure. Hospital mortality is increased eightfold when ACS patients experience GIB. More studies are needed to establish the safety of and optimal timing of endoscopy in these patients.

Implications of elevated cardiac troponin T in ambulatory patients with heart failure: a prospective analysis.

BACKGROUND: Elevated concentrations of cardiac troponin T (TnT) have been reported in patients hospitalized for decompensated heart failure (HF). We assessed whether elevated TnT levels are associated with the severity, etiology, and prognosis of HF in stable, ambulatory patients. METHODS: From 1998-1999, we prospectively collected data from 136 ambulatory patients with HF, New York Heart Association functional class II to IV, ejection fraction < or =35%, and no recent unstable angina, myocardial infarction, surgery, or coronary revascularization. Blood was obtained and analyzed by immunoassay for TnT, and patients were followed for 14.0 +/- 4.3 months for death or HF hospitalization (primary end point) and other adverse cardiovascular outcomes. RESULTS: Thirty-three patients (24%) had an elevated TnT level (> or =0.02 ng/mL). Mean TnT concentration did not differ by etiology of HF (0.002 +/- 0.03 ng/mL vs 0.02 +/- 0.04 ng/mL for ischemic and nonischemic etiologies, P =.25). Compared with patients with normal (undetectable) levels of TnT, patients with elevated TnT were significantly older, had worse functional class, and had poorer renal function. Elevated TnT concentrations were associated with increased relative risks (RR) of death or HF hospitalization (RR 2.7, 95% CI 1.7-4.3, P =.001) and death alone (RR 4.2, 95% CI 1.8-9.5, P =.001) during follow-up. Elevated TnT and New York Heart Association class were significant, independent predictors of death or HF hospitalization. Increased age and serum creatinine concentrations were significant independent predictors of death alone. CONCLUSIONS: Nearly one fourth of ambulatory patients with chronic HF have ongoing myocardial necrosis as shown by abnormal TnT values, which are associated with increased mortality and morbidity.