Sex‐Specific Determinants of Increased Left Ventricular Mass in the Tecumseh Blood Pressure Study

BackgroundLeft ventricular hypertrophy (LVH) defined by either ECG or echocardiographic criteria is a risk factor for cardiovascular morbidity and mortality. A number of determinants of LVH have been described in previous studies, principally male sex, hypertension, obesity, and aortic valvular stenosis. We examined the distribution of LV mass (LVM) in a population of 18- to 42-year-old normotensive men and women who were free of valvular heart disease to establish sex-specific normal values for LVM index (LVMI) and to determine the correlates of LVMI. Methods and ResultsLVM was derived from measurements obtained by M-mode echocardiography. Average LVMI is significantly greater in men (102.9±0.7 g/m2) than women (88.2±0.7 g/m2). By defining LVH as an LVMI greater than the 90th percentile, we developed sex-specific criteria for LVH: men, >125.4 g/m2; women, >110 g/m2. We found that LVH in men is associated with indices of enhanced sympathetic nervous system reactivity and with elevated fasting insulin and triglyceride levels, which may be caused by insulin resistance. In women, LVH was associated with higher body weight and obesity. ConclusionsBefore the onset of hypertension, increased LVMI appears to have different determinants in men and women. We suggest that early LVH in young men is a manifestation of hyperkinetic borderline hypertension, a state previously shown to be associated with increased sympathetic nervous system activity and insulin resistance. The hyperkinetic state is less prevalent in young women, in whom increased adiposity seems to be the predominant factor associated with LVH.

[1]  J. Cutler,et al.  Hemodynamic Correlates of the Third Heart Sound During the Evolution of Chronic Heart Failure , 1993, Circulation.

[2]  R. Schieken,et al.  Sex Differences in the Determinants of Left Ventricular Mass in Childhood: The Medical College of Virginia Twin Study , 1992, Circulation.

[3]  P. Sugden,et al.  Stimulation of cardiac protein synthesis by insulin-like growth factors. , 1992, The Biochemical journal.

[4]  S. Julius,et al.  The interconnection between sympathetics, microcirculation, and insulin resistance in hypertension. , 1992, Blood pressure.

[5]  K. Light,et al.  Gender differences in left ventricular structure and function in young adults with normal or marginally elevated blood pressure. , 1992, American journal of hypertension.

[6]  N. Schork,et al.  Red Blood Cell Lithium‐Sodium Countertransport in the Tecumseh Blood Pressure Study , 1991, Hypertension.

[7]  R. DeFronzo,et al.  Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM, Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease , 1991, Diabetes Care.

[8]  N. Schork,et al.  Hyperkinetic borderline hypertension in Tecumseh, Michigan , 1991, Journal of hypertension.

[9]  Manyari De.  Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. , 1990 .

[10]  N. Schork,et al.  “White Coat” Versus “Sustained” Borderline Hypertension in Tecumseh, Michigan , 1990, Hypertension.

[11]  J. Loggie,et al.  Determinants of cardiac involvement in children and adolescents with essential hypertension. , 1990, Circulation.

[12]  N. Schork,et al.  The association of borderline hypertension with target organ changes and higher coronary risk. Tecumseh Blood Pressure study. , 1990, JAMA.

[13]  N. Schork,et al.  The Tecumseh Blood Pressure Study. Normative data on blood pressure self-determination. , 1990, Archives of internal medicine.

[14]  D. Levy,et al.  Association of echocardiographic left ventricular mass with body size, blood pressure and physical activity (the Framingham Study). , 1990, The American journal of cardiology.

[15]  E. Ogata,et al.  Increased sympathoadrenomedullary activity and left ventricular hypertrophy in young patients with borderline hypertension. , 1989, Journal of molecular and cellular cardiology.

[16]  M. Mancini,et al.  Adrenergic nervous system and left ventricular mass in primary hypertension. , 1989, European heart journal.

[17]  A. Buda,et al.  Laboratory Studies Neurogenic Pressor Episodes Fail To Cause Hypertension, But Do Induce Cardiac Hypertrophy , 1989, Hypertension.

[18]  W. White,et al.  Average daily blood pressure, not office blood pressure, determines cardiac function in patients with hypertension. , 1989, JAMA.

[19]  J. C. Christiansen,et al.  Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors. The Framingham Heart Study. , 2020, Annals of internal medicine.

[20]  J. Laragh,et al.  Relation of blood pressure and body build to left ventricular mass in normotensive and hypertensive employed adults. , 1988, Journal of the American College of Cardiology.

[21]  J. Laragh,et al.  Cost‐Effectiveness of Echocardiography and Electrocardiography for Detection of Left Ventricular Hypertrophy in Patients with Systemic Hypertension , 1987, Hypertension.

[22]  G Parati,et al.  Relationship of 24-hour blood pressure mean and variability to severity of target-organ damage in hypertension. , 1987, Journal of hypertension.

[23]  D. Levy,et al.  The spectrum of left ventricular hypertrophy in a general population sample: the Framingham Study. , 1987, Circulation.

[24]  J. Laragh,et al.  Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. , 1986, Annals of internal medicine.

[25]  E. Cerasi,et al.  Binding, degradation, and biological activity of insulin in vascular smooth muscle cells. , 1985, The American journal of physiology.

[26]  C. Kahn,et al.  Receptors and growth-promoting effects of insulin and insulinlike growth factors on cells from bovine retinal capillaries and aorta. , 1985, The Journal of clinical investigation.

[27]  J. Laragh,et al.  Standardization of M-mode echocardiographic left ventricular anatomic measurements. , 1984, Journal of the American College of Cardiology.

[28]  M. Pfeffer,et al.  Pharmacologic Regression of Cardiac Hypertrophy In Experimental Hypertension , 1984, Journal of cardiovascular pharmacology.

[29]  L. Elsas,et al.  Structural analysis and subunit interaction of insulin receptor from membranes of cultured embryonic chick heart cells. , 1984, Endocrinology.

[30]  M. Hartford,et al.  The relation between cardiac hypertrophy and hypertension. , 2009, Acta medica Scandinavica. Supplementum.

[31]  W. Kannel.  Prevalence and natural history of electrocardiographic left ventricular hypertrophy. , 1983, The American journal of medicine.

[32]  P. Simpson.  Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response. , 1983, The Journal of clinical investigation.

[33]  M. Motolese,et al.  Left ventricular wall thickness and plasma catecholamines in borderline and stable essential hypertension. , 1982, European heart journal.

[34]  N. Reichek,et al.  Left Ventricular Hypertrophy: Relationship of Anatomic, Echocardiographic and Electrocardiographic Findings , 1981, Circulation.

[35]  H. Ditschuneit,et al.  Insulin as a Cellular Growth Regulator of Rat Arterial Smooth Muscle Cells In Vitro , 1980, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.

[36]  A. Ooshima,et al.  Cardiac hypertrophy in early hypertension. , 1979, The American journal of cardiology.

[37]  J. Peuler,et al.  Simultaneous single isotope radioenzymatic assay of plasma norepinephrine, epinephrine and dopamine. , 1977, Life sciences.

[38]  S. Fajans,et al.  Insulin, proinsulin, glucagon and gastrin in pancreatic tumors and in plasma of patients with organic hyperinsulinism. , 1977, The Journal of clinical endocrinology and metabolism.

[39]  N Reichek,et al.  Echocardiographic Determination of Left Ventricular Mass in Man: Anatomic Validation of the Method , 1977, Circulation.

[40]  P. Freychet,et al.  Insulin Receptors in the Heart Muscle: Demonstration of Specific Binding Sites and Impairment of Insulin Binding in the Plasma Membrane of the Obese Hyperglycemic Mouse , 1975, Diabetes.

[41]  S. Julius,et al.  Altered Cardiac Responsiveness and Regulation in the Normal Cardiac Output Type of Borderline Hypertension , 1975, Circulation research.

[42]  R. Ross,et al.  Effect of Insulin on the Proliferation of Cultured Primate Arterial Smooth Muscle Cells , 1975, Circulation research.

[43]  R. Tarazi,et al.  Cardiac Hypertrophy in Spontaneously Hypertensive Rats , 1974, Circulation research.

[44]  F. Morady,et al.  Myocardial hypertrophy produced by chronic infusion of subhypertensive doses of norepinephrine in the dog. , 1973, Chest.

[45]  W. Kannel,et al.  Electrocardiographic left ventricular hypertrophy and risk of coronary heart disease. The Framingham study. , 1970 .

[46]  E. Haber,et al.  Application of a radioimmunoassay for angiotensin I to the physiologic measurements of plasma renin activity in normal human subjects. , 1969, The Journal of clinical endocrinology and metabolism.

[47]  W. Kannel,et al.  Left ventricular hypertrophy by electrocardiogram. Prevalence, incidence, and mortality in the Framingham study. , 1969, Annals of internal medicine.

[48]  J. Durnin,et al.  The assessment of the amount of fat in the human body from measurements of skinfold thickness , 1967, British Journal of Nutrition.

[49]  W. Kannel,et al.  Factors of risk in the development of coronary heart disease--six year follow-up experience. The Framingham Study. , 1961, Annals of internal medicine.

[50]  F. Grande,et al.  Effect of Intra‐arterial Insulin on Tissue Cholesterol and Fatty Acids in Alloxan‐Diabetic Dogs , 1961, Circulation research.

[51]  D. DuBois,et al.  A formula to estimate the approximate surface area if height and weight be known , 1989 .