Association of left ventricular myocardial dysfunction with diabetic polyneuropathy.

Abstract

The pathogenesis of left ventricular (LV) dysfunction in diabetes has been attracting attention. It has been reported that LV longitudinal systolic myocardial function determined by speckle tracking echocardiography (STE) is associated with diabetic polyneuropathy (DPN). However, the relationship between the severity of peripheral neuropathy and LV myocardial dysfunction is unknown. This study examined the relationship between the severity of DPN and echocardiographic parameters as well as clinical features. The subjects were 166 patients (57 ± 14years old) with diabetes who had a normal LV ejection fraction (≥ 55%). To assess LV longitudinal systolic function, global longitudinal strain (GLS) was calculated by two-dimensional STE as the average peak strain of 18 LV segments in three standard apical views. A nerve conduction study (NCS) was performed in each subject to assess the severity of neuropathy based on the NCS Baba Classification (Grade 0: no apparent abnormalities-Grade IV: abolition). Three nerves in the lower extremity were examined: tibial nerve (F-wave latency, motor nerve conduction velocity, and amplitude), sural nerve (sensory conduction velocity and amplitude), and peroneal nerve (motor nerve conduction velocity and amplitude). Of the 166 subjects, 112 subjects (67.5%) were confirmed to have DPN, and all the subjects were divided into two groups according to the presence/absence of DPN. When multivariate analysis was performed using significant factors from univariate logistic regression analysis as explanatory variables, GLS was found to be an independent determinant of DPN (odds ratio: 0.55, p < 0.001). In multivariate analysis of NCS data, F-wave latency was the most important determinant of DPN (odds ratio: 1.43, p < 0.001). There was a significant negative correlation between F-wave latency and GLS (r = -0.43, p < 0.001). Regarding the relation between GLS and the severity of DPN, GLS was significantly lower in patients with Grade I or higher DPN than in patients without DPN, but showed no significant difference between the grades of neuropathy. In addition, GLS was significantly lower when 2-3 lower extremity nerves were affected by DPN than in patients without DPN. Patients with diabetes may already have subclinical LV myocardial dysfunction when DPN is Grade I. Assessment of LV longitudinal systolic function by GLS may be important in diabetic patients with DPN.