Published online Oct 15, 2019. doi: 10.4239/wjd.v10.i10.490
Peer-review started: May 20, 2019
First decision: May 31, 2019
Revised: September 25, 2019
Accepted: September 25, 2019
Article in press: September 25, 2019
Published online: October 15, 2019
Processing time: 154 Days and 10.8 Hours
The prevalence of type 2 diabetes (T2D) has increased worldwide and doubled over the last two decades. It features among the top 10 causes of mortality and morbidity in the world. Cardiovascular disease is the leading cause of complications in diabetes and within this, heart failure has been shown to be the leading cause of emergency admissions in the United Kingdom. There are many hypotheses and well-evidenced mechanisms by which diabetic cardiomyopathy as an entity develops. This review aims to give an overview of these mechanisms, with particular emphasis on metabolic inflexibility. T2D is associated with inefficient substrate utilisation, an inability to increase glucose metabolism and dependence on fatty acid oxidation within the diabetic heart resulting in mitochondrial uncoupling, glucotoxicity, lipotoxicity and initially subclinical cardiac dysfunction and finally in overt heart failure. The review also gives a concise update on developments within clinical imaging, specifically cardiac magnetic resonance studies to characterise and phenotype early cardiac dysfunction in T2D. A better understanding of the pathophysiology involved provides a platform for targeted therapy in diabetes to prevent the development of early heart failure with preserved ejection fraction.
Core tip: Altered myocardial metabolism and impaired metabolic flexibility are key mechanisms implicated in diabetic cardiomyopathy. Glucotoxicity, lipotoxicity, coronary microvascular dysfunction and suboptimal substrate utilisation are examined in detail. The mechanisms implicated and the impact on myocardial structure and function have been scrutinised within this review.