Objective. The most important step in the treatment of ST elevation myocardial infarction is to sustain myocardial blood supply as soon as possible. The two main treatment methods used today to provide myocardial reperfusion are thrombolytic therapy and percutaneous coronary intervention. In our study, reperfusion arrhythmias were investigated as if they are indicators of coronary artery patency or ongoing ischemia after revascularization. Methods. 151 patients with a diagnosis of acute ST elevation myocardial infarction were investigated. 54 patients underwent primary percutaneous coronary intervention and 97 patients were treated with thrombolytic therapy. The frequency of reperfusion arrythmias following revascularization procedures in the first 48 hours after admission was examined. The relation between reperfusion arrhythmias, ST segment regression, coronary artery patency, and infarct related artery documented by angiography were analyzed. Results. There was no statistically significant difference between the two groups in the frequency of reperfusion arrhythmias (P = 0.355). Although angiographic vessel patency was higher in patients undergoing percutaneous coronary intervention, there was no significant difference between the patency rates of each group with and without reperfusion arrythmias. Conclusion. Our study suggests that recorded arrhythmias following different revascularization procedures in acute ST elevation myocardial infarction may not always indicate vessel patency and reperfusion. Ongoing vascular occlusion and ischemia may lead to various arrhythmias which may not be distinguished from reperfusion arrhythmias.

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BackgroundAcute myocarditis (AM) can be defined as an inflammatory disease of the myocardium and characterized by large heterogeneity of clinical presentation. Myocarditis is becoming increasingly recognized as a contributor to unexplained mortality, and is thought to be a major cause of sudden cardiac death in the first two decades of life. The present study aimed to search the assessment of repolarization dispersion measured from the 12-lead surface electrocardiogram (including Tp-e interval, Tp-e/QT and Tp-e/QTc ratios) in AM patients.MethodsTotally 56 patients (mean age was 22 ± 3.7 years and 67% of the patients were male) with AM and 56 control subjects (23 ± 4.7 years and 64% of the patients were male) were enrolled. Tp-e intervals, Tp-e/QT and Tp-e/corrected QT (QTc) ratios were calculated from 12-lead electrocardiogram.ResultsHeart rate, QT and QTc values were similar between groups. QRS interval was lower in AM group compared to the control group (p <  0.001). Tp-e, Tp-e/QT and Tp-e/ QTc were significantly higher in AM group (p <  0.001, p <  0.001, p = 0.03 respectively) and they were significantly correlated with high troponin and high sensitive C reactive protein levels. In hospital follow-up time was 6 ± 2 days. Four patients have non sustained ventricular tachyarrhythmias and 1 patient dead because of cardiac arrest.ConclusionsOur study demonstrated that Tp-e intervals, Tp-e/QT and Tp-e/QTc ratios were higher in patients with AM than control subjects. The increased frequency of ventricular arrhythmias can be clarified by increased indexes of ventricular repolarization parameters in patients with AM.

Takotsubo cardiomyopathy (TTC) is primarily regarded as a form of acute and transient myocardial disease with a variety of characteristic wall-motion abnormalities. Importantly, a significant portion of TTC cases generally present with variable degrees of acute left ventricular (LV) dysfunction with or without clinical HF. On the other hand, LV dysfunction in the setting of TTC has been universally and exclusively considered as a synonym for systolic dysfunction, potentially overlooking other forms of myocardial pathologies, including transient diastolic dysfunction, in this setting. More interestingly, recent observations suggest that TTC, despite its macroscopic recovery, may not always manifest as a fully reversible phenomenon, suggesting persistence of microscopic changes at the cellular level to some degree. In clinical practice, these residual changes might largely account for the evolution of certain pathologies, including persistent diastolic dysfunction and subclinical LV dysfunction with variable symptomatology (particularly those arising during high levels of myocardial workload, including exercise, etc.) among TTC survivors. Within this context, the present review aims to highlight various clinical patterns and implications of LV dysfunction in the setting of TTC, and to provide basic information regarding morphological and mechanistic characteristics of wall-motion abnormalities in this setting.