title: Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM.
abstract: The determinants of left ventricular mass in normal control subjects and subjects with non-insulin-dependent 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. Measurements of erythrocyte sodium-lithium counter-transport, 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.l-1.h-1; 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 counter-transport compared to only seven (19%) of those without (p < 0.05). 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; F1.55 = 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.
authors.affiliation: Department of Medicine, University College London Medical School, Whittington Hospital, UK.
authors.forename: M J
authors.initials: MJ
authors.lastname: Sampson
authors.forename: E
authors.initials: E
authors.lastname: Denver
authors.forename: W J
authors.initials: WJ
authors.lastname: Foyle
authors.forename: D
authors.initials: D
authors.lastname: Dawson
authors.forename: J
authors.initials: J
authors.lastname: Pinkney
authors.forename: J S
authors.initials: JS
authors.lastname: Yudkin
mesh_terms: D000328:Adult; D000368:Aged; D000419:Albuminuria; D000804:Angiotensin II / Q000032:analysis; D017920:Antiporters / Q000097:blood*; D001794:Blood Pressure; D015992:Body Mass Index; D016009:Chi-Square Distribution; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D018619:Echocardiography, Doppler, Pulsed; D004837:Epinephrine / Q000097:blood; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006339:Heart Rate; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D008094:Lithium / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D012044:Regression Analysis; D012964:Sodium / Q000097:blood*
chemical_list: D000804:Angiotensin II; D017920:Antiporters; D004837:Epinephrine; D006442:Glycated Hemoglobin; D007328:Insulin; D008094:Lithium; D009638:Norepinephrine; D012964:Sodium; C045885:sodium-lithium countertransporter