Diabetic Cardiomyopathy; Summary of 41 years

Patients with diabetes have an increased risk for development of cardiomyopathy, even in the absence of well known risk factors like coronary artery disease and hypertension. Diabetic cardiomyopathy was first recognized approximately four decades ago. To date, several pathophysiological mechanisms thought to be responsible for this new entity have also been recognized. In the presence of hyperglycemia, non-enzymatic glycosylation of several proteins, reactive oxygen species formation, and fibrosis lead to impairment of cardiac contractile functions. Impaired calcium handling, increased fatty acid oxidation, and increased neurohormonal activation also contribute to this process. Demonstration of left ventricular hypertrophy, early diastolic and late systolic dysfunction by sensitive techniques, help us to diagnose diabetic cardiomyopathy. Traditional treatment of heart failure is beneficial in diabetic cardiomyopathy, but specific strategies for prevention or treatment of cardiac dysfunction in diabetic patients has not been clarified yet. In this review we will discuss clinical and experimental studies focused on pathophysiology of diabetic cardiomyopathy, and summarize diagnostic and therapeutic approaches developed towards this entity.

The Presence of Fragmented QRS on 12-Lead Electrocardiography in Patients with Coronary Artery Ectasia

BACKGROUND AND OBJECTIVES: Coronary artery ectasia (CAE) is an angiographic finding characterized by dilation of an arterial segment with a diameter at least 1.5 times that of its adjacent normal coronary artery. Fragmented QRS (fQRS) complexes are electrocardiographic signals which reflect altered ventricular conduction around regions of a myocardial scar and/or ischaemia. In the present study, we aimed to evaluate the presence of fQRS in patients with CAE. SUBJECTS AND METHODS: The study population included 100 patients with isolated CAE without coronary artery disease (CAD) and 80 angiographically normal controls. fQRS was defined as the presence of an additional R wave or notching of R or S wave or the presence of fragmentation in two contiguous leads corresponding to a major coronary artery territory. RESULTS: The two groups were similar in terms of age, sex, hypertension, dyslipidemia, and family history of CAD. The presence of fQRS was significantly (p<0.05) higher in the CAE group than that in the normal coronary artery group (29% vs. 6.2%, p=0.008). Isolated CAE were detected most commonly in the right coronary artery (61%), followed by left anterior descending artery (52%), left circumflex artery (36%), and left main artery (9%). Multivariate stepwise logistic regression analysis showed that CAE {odds ratio (OR) 1.412; 95% confidence interval (CI) 1.085-1.541; p=0.003} and diabetes (OR 1.310; 95% CI 1.025-1.482; p=0.041) were independently associated with fQRS. CONCLUSION: The presence of fragmented QRS associated with increased risk for arrhythmias and cardiovascular mortality was significantly higher in patients with CAE than in patient with normal coronary artery. Further studies are needed to determine whether the presence of fragmented QRS is a possible new risk factor for patients with CAE.