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Heat shock protein 60 (HSP60) is a mitochondrial protein constitutively expressed in the majority of cells, and its expression is up-regulated by a variety of stressors. In heart failure, HSP60 is released from cardiomyocytes. The authors speculate that increased serum HSP60 (sHSP60) may be related to the severity of heart failure. This investigation sought to assess the association between sHSP60 and the composite end point of death ⁄ readmission in patients with acute heart failure (AHF). A total of 132 consecutive patients were admitted for AHF. The independent association between sHSP60 and the end point was assessed with Cox regression. During a median follow-up of 7 months (interquartile range, 3–14), 35 (26.5%) deaths, 40 (30.3%) readmissions, and 65 (49.2%) deaths ⁄ readmission were identified. Patients who exhibited the outcome showed higher median sHSP60 values (6.15 ng ⁄ mL [8.49] vs 4.71 ng ⁄ mL [7.55] P=.010). A monotonic increase in the incidence of the composite end point was observed when moving from lower to higher tertile (4.74, 4.76, and 6.98 per 10 patients-years of follow-up, P for trend

Background: Data on the effect of revascularization on outcome in patients with high-risk non–ST-segment elevation acute coronary syndrome (NSTEACS) and significant comorbidities are scarce. Recently, a simple comorbidity index (SCI) including 5 comorbidities (renal failure, dementia, peripheral artery disease, heart failure, and prior myocardial infarction [MI]) has shown to be a useful tool for risk stratification. Nevertheless, therapeutic implications have not been derived. Hypothesis: We sought to evaluate the prognostic effect attributable to revascularization in NSTEACS according the SCI score. Methods: We included 1017 consecutive patients with NSTEACS. The effect of revascularization on a combined end point of all-cause mortality or nonfatal MI was evaluated by Cox regression according to SCI categories. Results: A total of 560 (55.1%), 236 (23.2%), and 221 (21.7%) patients showed 0, 1, and ≥2 points according to the SCI, respectively. Coronary angiography was performed in 725 patients (71.5%), and 450 patients (44.3%) underwent revascularization. During a median follow-up of 16 months (interquartile range, 12–36 months), 305 (30%) patients experienced the combined end point (202 deaths [19.9%] and 170 MIs [16.7%]). In multivariate analysis, a differential prognostic effect of revascularization was observed comparing SCI ≥2 vs 0 (P for interaction = 0.008). Thus, revascularization was associated with a greater prognostic benefit in patients with SCI ≥2 (hazard ratio [HR]: 0.51, 95% confidence interval [CI]: 0.29–0.89), P = 0.018), whereas no significant benefit was observed in those with 0 and 1 point (HR: 1.31, 95% CI: 0.88–1.94, P = 0.171 and HR: 1.11, 95% CI: 0.70–1.76, P = 0.651, respectively). Conclusions: In NSTEACS, the SCI score appears to be a useful tool for identifying a subset of patients with a significant long-term death/MI risk reduction attributable to revascularization. © 2011 Wiley Periodicals, Inc. This study was supported by a grant from the Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, RED HERACLES (FEDER) RD06/0009/1001 (Madrid, Spain). The authors have no other funding, financial relationships, or conflicts of interest to disclose.

Background: The diagnostic significance of a tilt table test (TTT) in patients with a suspected arrhythmic etiology for syncope and negative electrophysiologic study (EPS) has not been previously assessed comparing the TTT results with the findings of prolonged monitoring using an implantable loop recorder (ILR). We sought to assess the diagnostic yielding of TTT in patients with suspected arrhythmic syncope and negative EPS. Methods and Results: In 81 patients with suspected arrhythmic etiology for syncope and negative EPS, TTT was performed and an ILR implanted regardless the results of TTT. TTT was positive in 38 patients. During follow-up, syncope or presyncope recurred in 32 patients (39.5%). No differences were found in recurrence rates in patients with positive and negative TTT (31.5% vs 46.5%, P = ns). According to rhythm registered during ILR activation, mechanisms of syncopal events were classified as: arrhythmic (atrioventricular [AV] block and ventricular tachycardia; n = 18), neurally mediated (sinus bradycardia and sinus pause; n = 9), and indeterminate (normal sinus rhythm; n = 5). There was no statistical association between the results of TTT and the mechanism of syncope. Conclusions: In patients with a suspected arrhythmic etiology for syncope and a negative EPS, TTT is of little value to predict the mechanism of syncope and the ILR implantation seems to be a useful and safe diagnostic strategy.