Association of peripheral neuropathy with subclinical left ventricular dysfunction in patients with type 2 diabetes

Diabetic cardiomyopathy is becoming increasingly prevalent that also acts as the leading cause of mortality of diabetes, for which there is an urgent requirement to develop an effective diagnostic method to identify this clinical entity at an early phase and to guide a targeted therapeutic intervention to manage people with diabetes and heart disease.1., 2. Based on the clinical investigations, diabetic cardiomyopathy is progressing insidiously and slowly, from an initial subclinical stage to clinically symptomatic cardiac dysfunction, and eventually to overt congestive heart failure.3., 4. As a multifactorial disease, it has become a silent factor that seriously impacts the life quality of patients, concentrated on patients with diabetes-related microangiopathy. Therefore, early and punctual attention to transformations in myocardial function in asymptomatic patients with type 2 diabetes is conducive to subclinical delay and prevention of those cardiac events. Recently, research has proposed that the occurrence of systole impairment at an initial stage of the diabetic cardiomyopathy process before ejection fraction (EF) variations become detectable, and recommended subclinical left ventricle (LV) systolic dysfunction as the first indicator in the development of early diabetic cardiomyopathy.5., 6. Under this context, the research on the evaluation of myocardial function could be more comprehensive, for which the decreased global longitudinal strain (GLS) assessed by speckle-tracking strain imaging has been demonstrated to reliably evaluate the global LV systolic function,7 through which the early variation in myocardium could be detected, followed by dynamic development. Furthermore, the concept of “common soil” theory suggests that diabetes-related microvascular malfunction significantly contributes to the adverse myocardium alterations.8 For instance, diabetic cardiac autonomic neuropathy (CAN), which may occupy 25 % to 75 % of patients with T2DM, has been demonstrated to be robustly correlated to cardiovascular events and mortality.9., 10. Similarly, diabetic peripheral neuropathy (DPN), a serious chronic complication resulting from diabetes, may affect up to 50 % of T2DM patients within 10 years of the disease.11 Persistent hyperglycemia will trigger microvascular ischemia, thus leading to peripheral nerve damage resulting from the vasoconstriction and microvasculopathy. A similar pattern of nerve injury12., 13. and the occurrence of microangiopathy14., 15. have even been reported in prediabetes. Despite the association with diabetic microvascular complications of GLS as some studies have suggested,16 the clinical data on GLS and DPN are still limited, especially for the unraveled exact association of GLS with peripheral nerve conduction. Therefore, the objective of this study was to investigate the correlation of GLS with DPN, followed by the evaluation of the relationship with nerve conduction parameters in T2DM patients with left ventricle ejection fraction (LVEF).

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