Background. The timing of cardiac surgery after stroke in infective endocarditis (IE) remains controversial. We examined the relationship between the timing of surgery after stroke and the incidence of in-hospital and 1-year mortalities. Methods. Data were obtained from the International Collaboration on Endocarditis–Prospective Cohort Study of 4794 patients with definite IE who were admitted to 64 centers from June 2000 through December 2006. Multivariate logistic regression and Cox regression analyses were performed to estimate the impact of early surgery on hospital and 1-year mortality after adjustments for other significant covariates. Results. Of the 857 patients with IE complicated by ischemic stroke syndromes, 198 who underwent valve replacement surgery poststroke were available for analysis. Overall, 58 (29.3%) patients underwent early surgical treatment vs 140 (70.7%) patients who underwent late surgical treatment. After adjustment for other risk factors, early surgery was not significantly associated with increased in-hospital mortality rates (odds ratio, 2.308; 95% confidence interval [CI], .942–5.652). Overall, probability of death after 1-year follow-up did not differ between 2 treatment groups (27.1% in early surgery and 19.2% in late surgery group, P = .328; adjusted hazard ratio, 1.138; 95% CI, .802–1.650). Conclusions. There is no apparent survival benefit in delaying surgery when indicated in IE patients after ischemic stroke. Further observational analyses that include detailed pre- and postoperative clinical neurologic findings and advanced imaging data (eg, ischemic stroke size), may allow for more refined recommendations on the optimal timing of valvular surgery in patients with IE and recent stroke syndromes.

We describe the first case of Moraxella lacunata definite native valve endocarditis in a patient with previously normal mitral valves. The disease was complicated with embolizations of the brain and spleen. After 6 weeks of antimicrobial treatment, valvular replacement was performed. The clinical course and diagnostic findings suggest that Moraxella lacunata possesses high aggressiveness leading to progressive valvular destruction and embolizations.

During acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and ATPase activity are decreased in the myocardium, and the subsequent elevation in Ca2+ levels activates protease I (caplain I), leading to the proteolytic degradation of troponins. Concurrently, the levels of apelin and APJ expression are increased by limiting myocardial injury. In this prospective observational study, 100 consecutive patients with ST-elevation acute myocardial infarction were included. Patients meeting the following criteria were included in our study: (1) continuous chest pain lasting for >30 min, (2) observation of ST-segment elevation of more than 2 mm in two adjacent leads by electrocardiography (ECG), (3) increased cardiac troponin I levels, and (4) patients who underwent reperfusion therapy. We evaluated the levels of apelin-12 and troponin I on the first and seventh days after reperfusion therapy in all patients. Apelin-12 was inversely correlated with troponin I levels (Spearman’s correlation = −0.40) with a p value 2.2 for the association of apelin with MACE was determined, and the AUC was 0.71 (95% CI, 0.58–0.84). Survival analysis using the Kaplan-Meier method showed a lower rate of MACE among patients with apelin levels >2.2 (p = 0.002), and the ROC curve analysis showed a statistically significant difference in the area under the curve (p = 0.004). The influence of apelin levels on troponin levels in the acute phase of STEMI is inversely correlated, whereas in the non-acute phase, low apelin values were associated with a high rate of MACE.

Background: Increased level of high‐sensitivity C‐reactive protein (hs‐CRP) is associated with no‐reflow phenomenon. Therefore, even when timely coronary revascularization is performed through the primary percutaneous coronary intervention (pPCI), the process can induce reperfusion injury. Purpose: We evaluated the influence of hs‐CRP level on the no‐reflow phenomenon in patients with ST‐segment elevation myocardial infarction (STEMI). Methods: In this study, we included one hundred and eighty‐two consecutive patients with STEMI of onset < 12 h, who underwent pPCI. The levels of creatine kinase (CK), the MB fraction of creatine kinase (CK‐MB), troponin I, hs‐CRP, and other routine laboratory parameters were measured. Measurement of hs‐CRP was done on the day of admission by Cobas assay (particle‐enhanced immunoturbidimetric assay) on Cobas c501 (Roche). Thereafter, patients were divided in two groups according to the thrombolysis in myocardial infarction (TIMI) flow grade. Results: From a total of 182 STEMI patients who underwent pPCI, the median value of hs‐CRP of the patients with TIMI grade flow 3 (successful reperfusion) was 8.5 (0.4–268) and of the patients with no‐reflow phenomenon (unsuccessful reperfusion, TIMI flow grade ≤ 2) was 37.90 (1.8–271.20), p < 0.0001. Receiver operating characteristics (ROC) curve of hs‐CRP plots the true positive rate against the false positive rate at different cutoff points, AUC = 0.73 (95% CI, 0.64–0.81), and the cutoff value for the hs‐CRP was 18.0 mg/L, p = 0.0001. Conclusions: hs‐CRP may be associated with no‐reflow phenomenon in STEMI patients. The cutoff value for hs‐CRP may be used to identify patients at risk for reperfusion injury.