Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM

Abstract

SummaryThe determinants of left ventricular mass in normal control subjects and subjects with non-insulindependent diabetes (NIDDM) are ill-defined. We therefore recorded M-mode and pulsed Doppler echocardiograms and 24-h ambulatory blood pressure in 57 normotensive subjects, 34 with NIDDM and 23 matched non-diabetic control subjects 9 Measurements of erythrocyte sodium-lithium countertransport, plasma angiotensin II, plasma and platelet catecholamines and fasting plasma insulin were also made. Six control subjects (26 %) and 15 diabetic subjects (44 %) had some degree of left ventricular hypertrophy. Subjects with left ventricular hypertrophy (n = 21) had an elevated mean rate of sodium-lithium countertransport (0.40 + 0.13 vs 0.31 + 0.09 mmol. 1-1 9 h-l; p < 0.01), parallel differences being observed in both the diabetic and control groups. Twelve of the subjects with left ventricular hypertrophy (57 %) had elevated rates of sodium-lithium countertransport compared to only seven (19 %) of those without (p < 0.05) 9 There was no consistent difference between those with and without left ventricular hypertrophy in any other clinical or biochemical variable. Multivariate analysis, with the presence or absence of left ventricular hypertrophy as the dependent variable, demonstrated that the maximal rate of sodium-lithium countertransport was the only variable that independently contributed to left ventricular hypertrophy (partial r= 0.35; F~.ss = 7.74; p = 0.007). This study demonstrates for the first time an association between left ventricular hypertrophy and erythrocyte membrane cation transport that is independent of hypertension, is present in both diabetic and non-diabetic groups, and may represent a link between elevated rates of membrane sodium transport and cardiovascular risk. [Diabetologia (1995) non-insulin-dependent diabetes (NIDDM) suffer from cardiovascular disease at a rate in excess of that predicted by known cardiovascular risk factors [5], and there is some limited evidence that NIDDM is independently associated with an increased left ventricular mass [6].Age, body mass index and blood pressure all contribute to population variability in left ventricular mass [7], but the potential contributions of the renin-angiotensin system [8], plasma catecholamines [9], insulin and insulin resistance [10] and membrane cation transport [11] are well recognised, at least in hypertensive populations. NIDDM patients and non-diabetic subjects differ in many of these variables, but whether this contri-

The effect of valsartan on regression of left ventricular hypertrophy in type 2 diabetic patients

“…Left ventricular hypertrophy (LVH) is an ominous prognostic sign and is an independent factor for sudden death, ventricular arrhythmia, myocardial ischaemia, coronary heart disease and heart failure [5]. LVH is often present in type 2 diabetic patients [6–8], and its reversal reduces the cardiovascular risk in patients with essential hypertension and LVH [9,10]. A meta‐analysis of LVH studies has suggested that angiotensin‐converting enzyme (ACE) inhibitors are currently the most effective drugs that can cause regression of LVH [11,12].…”