Dilated cardiomyopathy (DCM) is a myocardial disease with a high mortality rate. Approximately 40 genes have been found to be associated with DCM to date. Non-familial DCM can also be caused by gene mutations, suggesting that genetic factors were involved in the pathogenesis of DCM; therefore genetic testing is beneficial for the early diagnosis of DCM, which can facilitate the implementation of preventive measures by and within patient’s families. Here, we investigated the underlying genetic mutations involved in the cause of patients with DCM.
The aim of this study was to analyze the incidence and types of arrhythmia and their relationship with the severity and prognosis of chronic heart failure (CHF) in patients with dilated cardiomyopathy (DCM), and to investigate the therapeutic effect of torasemide versus furosemide on CHF and incidence of arrhythmia. DCM patients with NYHA cardiac function II-IV were continuously monitored using a 24-h dynamic electrocardiogram (Holter), and arrhythmia incidence was analyzed by computer automatic analysis combined with manual assessment.
ATP-sensitive potassium channels play an important role in myocardial electrical activity. Genetic disruption of these channels predisposes the myocardium to cardiac diseases. Herein we investigated whether two polymorphisms, E23K and I337V, located in the Kir6.2 subunit of ATP-sensitive potassium channels are associated with dilated cardiomyopathy (DCM) in a Chinese population. Blood was collected from DCM patients and controls. DNA was extracted for polymerase chain reaction, which was followed by DNA sequencing.