[Peri-myocarditis during urinary tract infection by Escherichia coli]. / Peri-miocardite durante infezione delle vie urinarie da Escherichia coli.

We report a case of acute myocarditis associated with pericarditis in a patient hospitalized for urinary tract infection due to Escherichia coli. To the best of our knowledge, there are no prior descriptions of acute myocarditis associated with pericarditis during Escherichia coli infections in the absence of sepsis. In our patient, myocardial damage has been accurately documented by electrocardiography, echocardiography and magnetic resonance imaging. Inclusion of magnetic resonance imaging allows detection of myocardial inflammatory lesions that otherwise would have remained undiagnosed. The basic mechanisms of myocardial damage during Escherichia coli infection are unclear. Endotoxins might cause inflammatory reactions in the myocardium leading to myocyte damage. After initiation of antibiotic therapy, there was a rapid improvement of contractile function, with concomitant normalization of clinical and biochemical abnormalities. We discussed our findings in the context of the limited information available from the literature.

[Hypokinetic cardiac arrest and hypereosinophilia: a case of Kounis or Churg-Strauss syndrome?] / Arresto cardiaco ipocinetico ed ipereosinofilia: sindrome di Kounis o sindrome di Churg-Strauss?

Ischemic heart disease can be caused by multiple factors. However, epidemiological studies have evidenced an association between hypereosinophilia and acute coronary syndrome, most frequently observed in the Kounis and Churg-Strauss syndromes. We here report the case of a 37-year-old man, who was admitted to our hospital for acute coronary syndrome, complicated by hypokinetic cardiac arrest with severe hypereosinophilia.

Cystatin C and risk of mortality among patients undergoing percutaneous coronary intervention.

AIMS: We tested the prognostic value of cystatin C in patients with documented coronary artery disease (CAD) who underwent percutaneous coronary artery intervention (PCI). We also tested the hypothesis that the incremental predictive value of cystatin C on all-cause mortality was superior to that of glomerular filtration rate (GFR) by the Modification of Diet in Renal Disease (MDRD) formula. METHODS AND RESULTS: Included in the study were 2,757 patients (mean age 63 years, 77% men). Blood samples for cystatin C levels were collected immediately before PCI. During a median follow-up of two years, 114 patients died. In multivariable Cox analyses, after adjustment for several confounders, GFR (p=0.004) and cystatin C concentration (p<0.0001) were independent predictors of all-cause death. Cystatin C predicted all-cause death (c-statistic: 0.794) better than GFR estimate based on creatinine (c-statistic: 0.776, p=0.008 for comparison), and significantly reclassified 15% of patients into categories that reflected their actual likelihood of death more accurately (p=0.005). Adding cystatin C and GFR in the same multivariable survival model, only cystatin C level was a significant predictor of death. CONCLUSIONS: This study presents for the first time the incremental predictive value of cystatin C over the creatinine-based MDRD formula on all-cause mortality for CAD patients undergoing PCI.

Echocardiographic left ventricular hypertrophy in hypertension: marker for future events or mediator of events?

PURPOSE OF REVIEW: To discuss the most relevant studies on the prognostic impact of echocardiographic left ventricular hypertrophy in hypertension. RECENT FINDINGS: There is abundant evidence from epidemiological studies that increased left ventricular mass identifies hypertensive patients at increased risk of major cardiac and cerebrovascular events. Looking at the geometric patterns of the left ventricle, concentric remodelling and concentric left ventricular hypertrophy carry the highest risk for adverse events. Patients with left ventricular hypertrophy reversal as an effect of treatment are exposed to a lesser risk of events as compared with patients with persistence of left ventricular hypertrophy. Reversal of concentric remodelling predicts a lesser risk of adverse events compared with persistence of remodelling. Experimental evidence is accumulating that several haemodynamic and nonhaemodynamic factors which are able to promote progression of atherosclerosis through plaque growth and destabilization may also induce left ventricular hypertrophy by acting on myocyte and interstitium. Increased left ventricular mass may also be a causative factor for reduced pumping performance and arrhythmias. SUMMARY: Increased left ventricular mass is a marker of cardiovascular risk because it reflects and integrates the long-term level of activity of factors inducing progression of atherosclerosis. Increased left ventricular mass may also mediate myocardial ischaemia with potential evolution towards heart failure and arrhythmias.