VASCULAR

Full list of author information is available at the end of the articledeveloping and industrialized countries. Patients with T2DM are at increased risk of heart failure from diabetic cardiomyopathy [1], with the spectrum of disease ranging, in early stages, from diastolic dysfunction to overt systolic dysfunction during later stages. The pathogenesis of ven-tricular dysfunction in diabetic cardiomyopathy is multi-factorial, and independent of traditional cardiovascular risk factors such as hypertension, hyperlipidemia and perience prognosis and functional decline similar to pa-tients with heart failure and reduced ejection fraction. Evidence based management guidelines are limited for heart failure with preserved ejection fraction. Treatment is mainly directed towards symptomatic relief with loop di-uretics and treatment of associated conditions such as hypertension. Definitive treatment to halt disease progres-sion, improve prognosis and reverse the underlying patho-physiology is still lacking. Myocardial fibrosis has been suggested as one of the key mechanisms underlying myocardial dysfunction in T2DM [1]. Cardiac extracellular matrix (ECM) plays an activ