Abstract
Independent of the severity of coronary artery disease, diabetic patients have an increased risk of developing heart failure. This clinical entity has been considered to be a distinct disease process referred to as ‘diabetic cardiomyopathy’. Experimental studies suggest that extensive metabolic perturbations may underlie both functional and structural alterations of the diabetic myocardium. Translational studies are, however, limited and only partly explain why diabetic patients are at increased risk of cardiomyopathy and heart failure. Although a range of diagnostic methods may help to characterize alterations in cardiac function in general, none are specific for the alterations in diabetes. Treatment paradigms are very much limited to interpretation and translation from the results of interventions in non-diabetic patients with heart failure. This suggests that there is an urgent need to conduct pathogenetic, diagnostic and therapeutic studies specifically in diabetic patients with cardiomyopathy to better understand the factors which initiate and progress diabetic cardiomyopathy and to develop more effective treatments.
- diabetic cardiomyopathy
- diagnosis
- echocardiography
- molecular mechanism
- treatment
Abbreviations: 2D, two-dimensional; 3D, three-dimensional; AGE, advanced glycation end-product; ACE, angiotensin-converting enzyme; ARB, angiotensin II type 1 receptor blocker; CAC, coronary artery calcification; CAD, coronary artery disease; CAN, cardiac autonomic neuropathy; CHD, coronary heart disease; CI, confidence interval; CRP, C-reactive protein; CT, computed tomography; CVI, cyclic variation index; E/A ratio, ratio of early to late peak mitral filling wave velocities; ET, endothelin; HbA1c, glycated haemoglobin; HF, heart failure; HIF-1, hypoxia-inducible factor-1; IGF-1, insulin-like growth factor-1; LDL, low-density lipoprotein; LV, left ventricular; LVET, LV ejection time; LVH, LV hypertrophy; MFR, myocardial flow reserve; MHC, myosin heavy chain; MI, myocardial infarction; MPI, myocardial perfusion imaging; MRI, magnetic resonance imaging; NEFA, non-esterified fatty acid; NF-κB, nuclear factor κB; NO, nitric oxide; PEP, pre-ejection period; PKC, protein kinase C; PARP, poly(ADP-ribose) polymerase; PPAR, peroxisome-proliferator-activated receptor; RAS, renin–angiotensin system; ROS, reactive oxygen species; RR, relative risk; SERCA2a, sarcoplasmic/endoplasmic-reticulum Ca2+-ATPase 2a; SPECT, single photon emission CT; statin, hydroxymethylglutaryl CoA reductase inhibitor; SNS, sympathetic nervous system; TDI, tissue Doppler echocardiographic imaging; TZD, thiazolidinedione; VEGF, vascular endothelial growth factor
- The Biochemical Society
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December 2004
Volume: 107 Issue: 6
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