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Case Report: We report a case of biopsy proven myocardial damage after opiate-induced rhabdomyolysis. Myocardial biopsy showed focal lesions formed by small mononuclear inflammatory cells with a few neutrophils, associated with degenerated and necrolic myocardial fibers, interstilial edema and congestion of intrinsic blood vessels. These findings were similar to those seen with other drug overdoses if combined with strenuous muscular effort or hypoxic coma. We hypothesize that myocardial damage is a consequence of intracapillary myohypoxia associated with prolonged hypoxic coma following opiate overdose., INTRODUCTION Cardiac involvement with life threatening arrhythmias have been described in heroin overdose with rhabdomyolysis.[1] Electrocardiographic, echocardiographic and scintigraphic changes may also follow nontraumatic opiate-induced rhabdomyolysis in a minority of [...]

AbstractIn a 6-year-old child patient, transthoracic echocardiography revealed a large saccular structure (with anechogenic content) in the left atrium, near the fossa ovalis, and diagnosis of the left atrial septal pouch was made. The left atrial septal pouch is a kangaroo pouch-like structure on the left side of the interatrial septum, opened into the left atrial cavity without a connection between the left and right atria. It occurs when the foramen ovale is absent but the septum primum and septum secundum are only partially fused. The left atrial septal pouch is believed to be present in 47% of population. In many cases, the pocket on the atrial septum is small and it could not be detected by transthoracic echocardiography. Our description is uncommon because we diagnosed a very large septal pouch. Based on our knowledge, this is the youngest reported case of the left atrial septal pouch and the longest follow-up described in this type of congenital heart malformation.

Aims: Despite troponin assay being a part of the diagnostic work up in many conditions with acute chest pain, little is known about its frequency and clinical implications in acute aortic syndromes (AASs). In our study we assessed frequency, impact on diagnostic delay, inappropriate treatments, and prognosis of troponin elevation in AAS.Methods and results: Data were collected from a prospective metropolitan AAS registry (398 patients diagnosed between 2000 and 2013). Cardiac troponin test, using either standard or high sensitivity assay, was performed according to standard protocol used in chest pain units. Troponin T values were available in 248 patients (60%) of the registry population; the overall frequency of troponin positivity was 28% (ranging from 16% to 54%, using standard or high sensitivity assay respectively, p= 0.001). Troponin positivity was frequently associated with acute coronary syndromes (ACS)-like electrocardiogram findings, and with a twofold increased risk of long in-hospital diagnostic time (odds ratio (OR) 1.92, 95% confidence interval (CI) 1.05–3.52, p= 0.03). The combination of positive troponin and ACS-like electrocardiogram abnormalities resulted in a significantly increased risk of in-hospital delay/coronary angiography/antithrombotic therapy due to a misdiagnosis of ACS (OR 2.48, 95% CI 1.12–5.54, p= 0.02). However, troponin positivity was not associated with in-hospital mortality (OR 1.63, 95% CI 0.86–3.10, p= 0.131).Conclusions: Troponin positivity was a frequent finding in AAS patients, particularly when a high sensitivity assay was employed. Abnormal troponin values were strongly associated with ACS-like electrocardiogram findings and with in-hospital diagnostic delay but apparently they did not influence in-hospital mortality.