Original Article
Prognostic Implications of Echocardiographically Determined Left Ventricular Mass in the Framingham Heart Study
N Engl J Med 1990; 322:1561-1566May 31, 1990
- Abstract
- Abstract
A pattern of left ventricular hypertrophy evident on the electrocardiogram is a harbinger of morbidity and mortality from cardiovascular disease. Echocardiography permits the noninvasive determination of left ventricular mass and the examination of its role as a precursor of morbidity and mortality. We examined the relation of left ventricular mass to the incidence of cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes in 3220 subjects enrolled in the Framingham Heart Study who were 40 years of age or older and free of clinically apparent cardiovascular disease, in whom left ventricular mass was determined echocardiographically.
During a four-year follow-up period, there were 208 incident cardiovascular events, 37 deaths from cardiovascular disease, and 124 deaths from all causes. Left ventricular mass, determined echocardiographically, was associated with all outcome events. This relation persisted after we adjusted for age, diastolic blood pressure, pulse pressure, treatment for hypertension, cigarette smoking, diabetes, obesity, the ratio of total cholesterol to high-density lipoprotein cholesterol, and electrocardiographic evidence of left ventricular hypertrophy. In men, the risk factor—adjusted relative risk of cardiovascular disease was 1.49 for each increment of 50 g per meter in left ventricular mass corrected for the subject's height (95 percent confidence interval, 1.20 to 1.85); in women, it was 1.57 (95 percent confidence interval, 1.20 to 2.04). Left ventricular mass (corrected for height) was also associated with the incidence of death from cardiovascular disease (relative risk, 1.73 [95 percent confidence interval, 1.19 to 2.52] in men and 2.12 [95 percent confidence interval, 1.28 to 3.49] in women). Left ventricular mass (corrected for height) was associated with death from all causes (relative risk, 1.49 [95 percent confidence interval, 1.14 to 1.94] in men and 2.01 [95 percent confidence interval, 1.44 to 2.81] in women).
We conclude that the estimation of left ventricular mass by echocardiography offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors. An increase in left ventricular mass predicts a higher incidence of clinical events, including death, attributable to cardiovascular disease. (N Engl J Med 1990; 322:1561–6.)
Media in This Article
Figure 1
Four-Year Age-Adjusted Incidence of Cardiovascular Disease, According to Left Ventricular Mass (Corrected for Height).Figure 2
Four-Year Age-Adjusted Rate of Death from All Causes, According to Left Ventricular Mass (Corrected for Height).Article Activity
- Article
LEFT ventricular hypertrophy, although infrequently noted on the electrocardiogram, imparts a substantial risk of morbidity and mortality.1 2 3 Echocardiography has permitted the reliable, noninvasive estimation of left ventricular mass4 5 6 7 and has proved a more sensitive tool for the detection of left ventricular hypertrophy than other techniques previously available. The Framingham Heart Study has developed sex-specific criteria for left ventricular hypertrophy, based on the distribution of left ventricular mass in a healthy reference population.8 The application of these criteria to a large, free-living population studied with echocardiography has documented a prevalence of left ventricular hypertrophy of 15 to 20 percent in adults9; this value is considerably higher than the prevalence of electrocardiographically demonstrated left ventricular hypertrophy in the same population.10
Recent reports have documented an increased risk of the sequelae of cardiovascular disease in subjects with echocardiographic evidence of left ventricular hypertrophy.11 12 13 14 In a study of more than 1000 elderly men and women, we found an association between echocardiographically determined left ventricular mass and the incidence of coronary heart disease; this association persisted after adjustment for traditional cardiac risk factors.14 The present investigation was undertaken to extend this smaller study by examining the relation of left ventricular mass, determined echocardiographically, to the four-year risk of cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes in a much larger group of middle-aged and elderly subjects enrolled in the Framingham Heart Study.
Methods
Study Population
In 1948, residents of Framingham, Massachusetts, who were between the ages of 28 and 62 were enrolled in a prospective epidemiologic study. The selection criteria and study design have been described previously.15 , 16 In 1971, children of the original study population and the spouses of those children were enrolled in the Framingham Offspring Study.17 From 1979 to 1983, the surviving members of the original cohort underwent their 16th biennial examination and subjects in the Offspring Study underwent their second examination; these examinations routinely included 12-lead resting electrocardiography, measurements of resting blood pressure, anthropometric measurements, determinations of blood glucose levels, and echocardiography. Electrocardiograms were examined for evidence of definite left ventricular hypertrophy (increased voltage plus a "strain" pattern).1 Diabetes was indicated by any one of the following: a fasting blood glucose level ≥7.77 mmol per liter (140 mg per deciliter), a random nonfasting blood glucose level ≥11.11 mmol per liter (200 mg per deciliter), or the use of insulin or an oral hypoglycemic agent. Data regarding cigarette smoking and measurements of plasma total cholesterol and high-density lipoprotein cholesterol were obtained from the 15th biennial examination of the members of the original cohort and the second examination of subjects in the Offspring Study (index examination).
Outcome Events
To be eligible for inclusion in this study, subjects in the Offspring Study and members of the original study cohort had to be free of clinically apparent cardiovascular disease. Because of the low incidence of morbidity and mortality from cardiovascular disease in young subjects, the present study was restricted to the original cohort and their children or children's spouses who were 40 years of age or older at the index examination. At each examination, interim cardiovascular disease events were identified by medical history, physical examination, 12-lead electrocardiography, and review of hospital records. Medical records were routinely obtained for participants who did not appear for an examination and were evaluated for evidence of incident cardiovascular disease. All suspected cardiovascular disease events were reviewed by three physicians who evaluated the pertinent records. The cardiovascular disease events included in this study were coronary heart disease, congestive heart failure, stroke or transient ischemic attack, and intermittent claudication. Coronary heart disease events included angina pectoris, coronary insufficiency, myocardial infarction, and sudden or nonsudden death attributed to coronary heart disease. Criteria for the various cardiovascular disease events have been reported previously.18 The echocardiogram was not used to determine the presence or absence of cardiovascular disease.
All deaths were evaluated similarly, and the probable cause was established by a committee of three physicians after a review of the hospital records, autopsy findings, death certificates, and interviews with family members. Deaths in this study were classified as due to cardiovascular or noncardiovascular causes. Deaths from cardiovascular disease included deaths due to coronary heart disease, stroke, and other cardiovascular causes. Deaths from coronary heart disease included both sudden and nonsudden deaths. A death that might have been sudden but was not witnessed was assigned to other causes of death. A witnessed death that occurred more than one hour after the onset of symptoms suggestive of myocardial infarction was classified as a nonsudden death from coronary heart disease.
Echocardiographic Methods
The echocardiographic methods used in this study have been described previously.8 The subjects were studied with M-mode echocardiography. Measurements of the internal diameter and wall thickness of the left ventricle were made at end-diastole, according to the methods of Devereux and Reichek.4 Left ventricular mass was calculated with the following formula: left ventricular mass (in grams) = 1.04[(LVID + VST + PWT)3 − (LVID)3] − 13.6, where LVID denotes the left ventricular internal diameter, VST the ventricular septal thickness, and PWT the posterior wall thickness. To correct for differences in heart size in subjects of different body size, the left ventricular mass (in grams) was divided by the height (in meters), because of the association observed between left ventricular mass and height in a previously defined healthy reference group of 864 subjects (r = 0.39, P<0.001 in men; r = 0.23, P<0.001 in women).8 Unless otherwise specified, all values reported here for left ventricular mass have been corrected for height. Left ventricular hypertrophy was defined as a left ventricular mass 2 SD or more above the mean for the healthy reference group. The cutoff values for left ventricular hypertrophy were 143 g per meter in men and 102 g per meter in women.8
Statistical Analysis
The follow-up period in this study was four years. Separate analyses were performed for men and women. The outcome events studied were cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes. The four-year incidence of these outcome events was examined both as a function of increments in left ventricular mass (corrected for height) and as a function of the presence or absence of left ventricular hypertrophy. Age-adjusted rates of the outcome events were calculated by the direct method.
Multivariate analyses were performed for subjects for whom complete data on risk factors were available. The Cox proportional-hazards model19 was used to examine the relation between both left ventricular mass and left ventricular hypertrophy and the incidence of cardiovascular disease and death. The covariates in the multivariate Cox analyses were chosen because of their potential roles as risk factors for cardiovascular disease.20 They included age, diastolic blood pressure, pulse pressure (to account for levels of systolic pressure), antihypertensive treatment (those currently taking prescribed medication for the treatment of hypertension were assigned a value of 1, and all others were assigned a value of 0), number of cigarettes smoked per day, ratio of total to high-density lipoprotein cholesterol, diabetes (yes = 1; no = 0), obesity (as defined by the body-mass index [the weight in kilograms divided by the square of the height in meters]), and electrocardiographic evidence of definite left ventricular hypertrophy (yes = 1; no = 0).
Risk factor—adjusted relative-risk values (and 95 percent confidence intervals) for an outcome event were calculated for every increment of 50 g per meter in the left ventricular mass on the basis of the coefficients for left ventricular mass derived from the multivariate model.
Results
Study Population
Of the 4850 men and women above 40 years of age who were seen at the index examination, 4073 were free of cardiovascular disease, and 3220 had echocardiograms of adequate quality to measure left ventricular mass (Table 1Table 1
Population Studied and Incidence of Outcome Events.*). Complete risk-factor information was available for 3100 of those 3220 subjects (96 percent). The characteristics of the study population are summarized in Table 2Table 2
Characteristics of the Study Subjects.*.Echocardiograms of adequate quality to assess left ventricular mass could not be obtained for 366 of the 1769 men (20.7 percent) and 487 of the 2304 women (21.1 percent) who were free of cardiovascular disease at the index examination. The subjects with suboptimal studies were generally older than the subjects with adequate echocardiograms.21 The four-year age-adjusted rates for cardiovascular disease, death from cardiovascular disease, and death from all causes in the men with adequate echocardiograms, as compared with those without adequate studies, were 8.6 versus 11.8 percent, 2.1 versus 1.9 percent, and 5.6 versus 6.1 percent, respectively. The corresponding rates for women were 6.0 versus 7.9 percent, 0.9 versus 2.0 percent, and 3.6 versus 6.4 percent.
Cardiovascular Disease Events
A summary of incident cardiovascular disease events is provided in Table 1. There were 113 new cardiovascular disease events in men and 95 in women. Figure 1Figure 1
Four-Year Age-Adjusted Incidence of Cardiovascular Disease, According to Left Ventricular Mass (Corrected for Height). shows the four-year age-adjusted rates for cardiovascular disease according to levels of left ventricular mass. In men, the four-year incidence of cardiovascular disease increased from 4.7 percent in those with a left ventricular mass <90 g per meter to 12.2 percent in those with a left ventricular mass ≥140 g per meter. The corresponding values for women were 4.1 and 16.1 percent.Mortality
A summary of the deaths in the study population is provided in Table 1. During the follow-up period, 69 men died, 25 of them from cardiovascular disease. There were 55 deaths among women, including 12 from cardiovascular disease. The age-adjusted mortality rates from all causes ranged from 4.1 percent in men with a left ventricular mass <90 g per meter to 8.1 percent in those with values ≥ 140 g per meter; the corresponding values for women were 2.6 and 6.8 percent (Fig. 2Figure 2
Four-Year Age-Adjusted Rate of Death from All Causes, According to Left Ventricular Mass (Corrected for Height).).Echocardiographic Evidence of Left Ventricular Hypertrophy
The echocardiographic criteria for left ventricular hypertrophy were fulfilled in 218 men (15.5 percent) and 382 women (21.0 percent). Among men, left ventricular hypertrophy was related to all the outcome events we studied (Table 3Table 3
Four-Year Age-Adjusted Incidence of Outcome Events, According to the Presence or Absence of Echocardiographic Evidence of Left Ventricular Hypertrophy (LVH).). The four-year age-adjusted rates for cardiovascular disease, death from cardiovascular disease, and death from all causes in the men with left ventricular hypertrophy, as compared with those without left ventricular hypertrophy, were 12.1 versus 6.8 percent (P<0.001), 4.8 versus 1.0 percent (P<0.0001), and 9.1 versus 4.0 percent (P<0.01), respectively. In women, left ventricular hypertrophy was associated with an increased incidence of cardiovascular disease (the four-year age-adjusted rate was 7.4 percent, as compared with 4.2 percent for women without left ventricular hypertrophy [P<0.05]).Multivariate Analyses
The results of the multivariate analyses are shown in Table 4Table 4
Relative Risk of Outcome Events, Adjusted for Age and Risk Factors.*. Left ventricular mass was significantly associated with the risk of cardiovascular disease, death from cardiovascular disease, and death from all causes in both sexes after adjustment for age, diastolic blood pressure, pulse pressure, antihypertensive treatment, number of cigarettes smoked per day, diabetes, body-mass index, ratio of total to high-density lipoprotein cholesterol, and electrocardiographic evidence of left ventricular hypertrophy. Age was the only variable other than left ventricular mass that showed consistent and strong relations to the incidence of all three outcome events in both sexes.The risk factor—adjusted relative risk of cardiovascular disease for each increment of 50 g per meter in left ventricular mass was 1.49 (95 percent confidence interval, 1.20 to 1.85) in men and 1.57 (95 percent confidence interval, 1.20 to 2.04) in women. The corresponding values for death from cardiovascular disease were 1.73 (95 percent confidence interval, 1.19 to 2.52) in men and 2.12 (95 percent confidence interval, 1.28 to 3.49) in women. The relative risk of death from all causes was 1.49 (95 percent confidence interval, 1.14 to 1.94) in men and 2.01 (95 percent confidence interval, 1.44 to 2.81) in women.
Additional Analyses
The results of the multivariate analyses were nearly identical when left ventricular mass corrected for body-surface area was substituted for left ventricular mass corrected for height. In this population, electrocardiographic evidence of left ventricular hypertrophy was not statistically significant in any of the analyses in which echocardiographically determined left ventricular mass was entered as a covariate.
An examination of the risk of sudden cardiac death was undertaken because of earlier experience with electrocardiographically demonstrated left ventricular hypertrophy in the Framingham Heart Study.2 Although there were too few sudden deaths among women to permit meaningful analyses, there were 15 sudden deaths among men, 8 of which occurred in subjects with echocardiographically demonstrated left ventricular hypertrophy. The four-year age-adjusted rates of sudden death in men with and without left ventricular hypertrophy were 2.7 and 0.6 percent, respectively. The risk factor—adjusted relative risk of sudden death was 1.70 (95 percent confidence interval, 1.02 to 2.83) for each increment of 50 g per meter in left ventricular mass.
Discussion
An appreciation of the morbidity and mortality associated with electrocardiographic evidence of left ventricular hypertrophy1 2 3 antedated the advent of echocardiography and its use in epidemiologic studies.21 Although left ventricular hypertrophy detected on the electrocardiogram is a harbinger of a multitude of adverse cardiovascular sequelae, it remains an uncommon finding, occurring in fewer than 1 percent of the subjects in the present study. In contrast, echocardiographic evidence of left ventricular hypertrophy is far more common, occurring in 16 percent of the men and 21 percent of the women in this study population. Only recently have the cardiovascular risks associated with increased left ventricular mass been appreciated.12 13 14 This study documents a significant relation between left ventricular mass and the incidence of cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes in subjects participating in the Framingham Heart Study. With the exception of age, left ventricular mass was the only variable that was consistently related to all three outcome events in this study population. These findings demonstrate that the echocardiographic assessment of cardiac structure offers prognostic information beyond that provided by the evaluation of traditional cardiac risk factors.
An earlier report from Framingham14 documented a strong association between echocardiographically determined left ventricular mass and the incidence of coronary heart disease in elderly men and women. In the present study we found that the adverse prognostic implications of increased left ventricular mass also applied to a population made up largely of middle-aged subjects. Recently, Casale et al.11 described the association of echocardiographically demonstrated left ventricular hypertrophy with the incidence of cardiovascular disease in hypertensive men. That report was based on a population of 140 men, of whom 14 had cardiovascular events. The present study confirms their findings in a much larger population, one less subject to selection bias, in which 208 cardiovascular disease events and 124 deaths occurred. It also extends their results to women, in whom the relation of left ventricular mass to the incidence of cardiovascular disease is similar to that observed in men. Discrepancies in the rate of cardiovascular disease between men and women were reduced when the subjects were stratified according to their base-line values for left ventricular mass (Fig. 1). Moreover, the present study suggests that the potential sequelae of increased left ventricular mass include death from cardiovascular disease and from all causes.
The mechanisms by which cardiac hypertrophy may promote cardiovascular morbidity and mortality are incompletely understood. Left ventricular hypertrophy increases myocardial oxygen consumption while reducing coronary blood-flow reserve. This supply—demand mismatch may predispose the patient to angina pectoris, myocardial infarction, and sudden death. The coronary blood supply may be impaired by atherosclerosis in persons with left ventricular hypertrophy, because factors associated with myocardial hypertrophy are atherogenic.9 In addition, there is evidence that coronary reserve is impaired in hypertrophied ventricles.22 , 23 Laboratory studies in animals with hypertensive left ventricular hypertrophy have demonstrated a threefold increased risk of sudden death as well as increased myocardial-infarct size after coronary occlusion24 , 25; these findings are consistent with the hypotheses described above.
Earlier studies of mortality in subjects with electrocardiographic evidence of left ventricular hypertrophy found an increased risk of sudden cardiac death.2 We found a similar relation between echocardiographic evidence of left ventricular hypertrophy and sudden death. Multivariate analyses document an association between left ventricular mass and the incidence of sudden cardiac death in men. The mechanism of sudden death is probably a ventricular arrhythmia to which subjects with cardiac hypertrophy are predisposed.12 , 26
Alternatively, left ventricular mass may simply be a marker of risk by serving as a sensitive indicator of cardiac end-organ damage. Subtle degrees of hypertrophy may reflect cumulative lifelong exposure to cardiovascular insults from hypertension and obesity9 or from coronary artery disease. Left ventricular mass, readily determined by echocardiography, may provide a better estimate of the extent of cardiac end-organ damage than is provided by casual measurements of blood pressure and body weight. Data from the Framingham Study and clinical studies11 suggest that the risk of morbidity and mortality associated with hypertension may be due in part to the effect of elevated blood pressure on left ventricular mass.
In subjects who were free of cardiovascular disease at base line, left ventricular mass remained significantly associated with all adverse outcomes even after electrocardiographically demonstrated left ventricular hypertrophy was taken into consideration. In this population, the electrocardiogram has proved to be an insensitive tool for detecting anatomical hypertrophy,27 raising questions about its usefulness in detecting left ventricular hypertrophy in population-based studies. New efforts to improve the accuracy of the electrocardiogram in the diagnosis of left ventricular hypertrophy are needed if it is to become a more useful and cost-effective screening tool.
We do not currently advocate the routine use of echocardiography for risk assessment or patient care, for several reasons. First, this study was carried out in a predominantly white population; thus, generalization of our findings to other racial groups may not be warranted. Second, although standardized methods have been proposed for echocardiography, they are not uniformly followed. Hence, the values used to define left ventricular hypertrophy may differ in other laboratories. Finally, the benefits of the primary prevention and secondary management of left ventricular hypertrophy remain largely unproved.
Our results implicate left ventricular hypertrophy as a harbinger of morbidity and mortality. The extent to which the prevention or regression of left ventricular hypertrophy can favorably affect the sizable risk of cardiovascular disease it carries remains unexplored. A growing body of evidence suggests that weight reduction in obese patients28 and blood-pressure control in hypertensive patients29 30 31 32 can promote the regression of left ventricular hypertrophy. An understanding of the mechanisms by which left ventricular hypertrophy contributes to the pathogenesis of cardiovascular disease may have important implications for the primary and secondary prevention of this country's leading cause of disability and death.
*Deceased, January 19, 1990.
We are indebted to Drs. Richard B. Devereux and Keaven M. Anderson for their reviews of the manuscript and to Sandra J. Anderson for her technical assistance.
Source Information
From the Framingham Heart Study, Framingham, Mass., and the Division of Epidemiology and Clinical Applications of the National Heart, Lung, and Blood Institute, Bethesda, Md. (D.L., R.J.G., W.P.C.), the National Center for Health Statistics, Hyattsville, Md. (D.D.S.); and the Department of Medicine and the Section of Preventive Medicine and Epidemiology, Boston University School of Medicine, Boston (W.B.K.). Address reprint requests to Dr. Levy at the Framingham Heart Study, 5 Thurber St., Framingham, MA 01701.
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Riccardo Pini, M.Chiara Cavallini, Francesca Bencini, Gabriella Silvestrini, Elisabetta Tonon, Walter De Alfieri, Niccolò Marchionni, Mauro Di Bari, Richard B Devereux, Giulio Masotti, Mary J Roman. (2002) Cardiovascular remodeling is greater in isolated systolic hypertension than in diastolic hypertension in older adults: the Insufficienza Cardiaca negli Anziani Residenti (ICARE) a Dicomano Study. Journal of the American College of Cardiology 40:7, 1283-1289
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Mikolaj Winnicki, Virend K. Somers, Valentina Accurso, Michal Hoffmann, Ryszard Pawlowski, Gianfranco Frigo, Pieralberto Visentin, Paolo Palatini. (2002) Alpha-Adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity. Journal of Hypertension 20:9, 1771-1777
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Fredrik Nyström, Karin Malmqvist, K. Peter Öhman, Thomas Kahan. (2002) Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study. Journal of Hypertension 20:8, 1527-1533
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Moto-o Date, Takashi Morita, Nobushige Yamashita, Kazuhiko Nishida, Osamu Yamaguchi, Yoshiharu Higuchi, Shinichi Hirotani, Yasushi Matsumura, Masatsugu Hori, Michihiko Tada, Kinya Otsu. (2002) The antioxidant N-2-mercaptopropionyl glycine attenuates left ventricular hypertrophy in in vivo murine pressure-overload model. Journal of the American College of Cardiology 39:5, 907-912
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Shelley A. Hall, Carlos G. Cigarroa, Lucille Marcoux, Richard C. Risser, Paul A. Grayburn, Eric J. Eichhorn. (1995) Time course of improvement in left ventricular function, mass and geometry in patients with congestive heart failure treated with beta-adrenergic blockade. Journal of the American College of Cardiology 25:5, 1154-1161
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CHARLES KINDER, PAUL TAMBURRO, DOUGLAS KOPP, JOHN KALL, BRIAN OLSHANSKY, DAVID WILBER. (1994) The Clinical Significance of Nonsustained Ventricular Tachycardia: Current Perspectives. Pacing and Clinical Electrophysiology 17:4, 637-664
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Dagnovar Aristizabal, Franz H. Messerli, Edward D. Frohlich. (1994) Disparate structural effects on left and right ventricles by angiotensin-converting enzyme inhibitors and calcium antagonists in essential hypertension. The American Journal of Cardiology 73:7, 483-487
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Edwin A. Rutsky, Stephen G. Rostand. (1994) Coronary Artery Bypass Graft Surgery in End-Stage Renal Disease: Indications, Contraindications, and Uncertainties. Seminars in Dialysis 7:2, 91-95
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David A. Orsinell, Gerard P. Aurigemma, Stephen Battista, Steven Krendel, William H. Gaasch. (1993) Left ventricular hypertrophy and mortality after aortic valve replacement for aortic stenosis. Journal of the American College of Cardiology 22:6, 1679-1683
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RICHARD W. ASINGER, CHARLES A. HERZOG, CANDACE D. DICK, LILLIAN MICHAUD. (1993) Echocardiography in the Evaluation of Cardiac Sources of Emboli:.. Echocardiography 10:4, 373-396
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KEVIN C. DELLSPERGER. (1993) Transthoracic Echocardiography for Evaluation of Hypertensive Heart Disease. Echocardiography 10:3, 295-302
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Fumiaki Nakamura, Masahiro Nagano, Jitsuo Higaki, Koichi Higashimori, Ryuichi Morishita, Hiroshi Mikami, Toshio Ogihara. (1993) THE ANGIOTENSIN-CONVERTING ENZYME INHIBITOR, PERINDOPRIL, PREVENTS CARDIAC HYPERTROPHY IN LOW-RENIN HYPERTENSIVE RATS. Clinical and Experimental Pharmacology and Physiology 20:3, 135-140
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Robert A. Kloner, Karin Przyklenk. (1993) Cardioprotection with angiotensin-converting enzyme inhibitors: Redefined for the 1990s. Clinical Cardiology 16:2, 95-103
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A. Zanchetti, J. P. Chalmers, K. Arakawa, I. Gyarfas, P. Hamet, L. Hansson, S. Julius, S. Macmahon, G. Mancia, J. Ménard, T. Omae, J. Reid, M. Safar. (1993) The 1993 Guidelines for the Management of Mild Hypertension: Memorandum from a WHO/ISH Meeting. Blood Pressure 2:2, 86-100
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A. Manolis, G. Athanasopoulos, G. Karatasakis, I. Gavras, M. Bresnahan, D. V. Cokkinos, H. Gavras. (1993) Pressor Hormone Profile During Stress in Hypertension: Does Vasopressin Interfere with Left Ventricular Hypertrophy?. Clinical and Experimental Hypertension 15:3, 539-555
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Karl T. Weber, Christian G. Brilla, John G. F. Cleland, Jay N. Cohn, Lennart Hansson, Anthony M. Heagerty, John H. Laragh, Stéphane Laurent, Jean-Pierre Ollivier, Paolo Pauletto, Hubert Pouleur, Jos F. M. Smits, Lip-Bun Tan. (1993) Cardioreparation and the Concept of Modulating Cardiovascular Structure and Function. Blood Pressure 2:1, 6-21
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Carlson Jan, Davies Robert, Ehlenz Klaus, Grunstein Ron, Hedner Jan, Podszus Thomas, Sinoway Lawrence, Stradling John, Telakivi Tiina, Zwillich Clifford. (1993) Obstructive Sleep Apnea and Blood Pressure Elevation: What is the Relationship?. Blood Pressure 2:3, 166-182
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Daniel Levy. (1993) A Multifactorial Approach to Coronary Disease Risk Assessment. Clinical and Experimental Hypertension 15:6, 1077-1086
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Richard B. Devereux, Giovanni de Simone, Antonello Ganau, Michael J. Koren, George A. Mensah, Mary J. Roman. (1993) Left Ventricular Hypertrophy and Hypertension. Clinical and Experimental Hypertension 15:6, 1025-1032
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Thomas J. Molloy, Peter M. Okin, Richard B. Devereux, Paul Kligfield. (1992) Electrocardiographic detection of left ventricular hypertrophy by the simple QRS voltage-duration product. Journal of the American College of Cardiology 20:5, 1180-1186
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Giovanni de Simone, Stephen R. Daniels, Richard B. Devereux, Richard A. Meyer, Mary J. Roman, Oreste de Divitiis, Michael H. Alderman. (1992) Left ventricular mass and body size in normotensive children and adults: Assessment of allometric relations and impact of overweight
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Janine Leandro, Jeffrey Forster Smallhorn, Lee Benson, Norman Musewe, John Williamson Balfe, John Daryl Dyck, Lori West, Robert Freedom. (1992) Ambulatory blood pressure monitoring and left ventricular mass and function after successful surgical repair of coarctation of the aorta. Journal of the American College of Cardiology 20:1, 197-204
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Lionel U. Mailloux. (1992) More Dialysis Leads to Better Survival: A Point of View. Seminars in Dialysis 5:3, 224-226
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Nathaniel Reichek. (1992) Patterns of left ventricular response in essential hypertension. Journal of the American College of Cardiology 19:7, 1559-1560
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Antonello Ganau, Richard B. Devereux, Mary J. Roman, Giovanni de Simone, Thomas G. Pickering, Pier Sergio Saba, Paolo Vargiu, Isabella Simongini, John H. Laragh. (1992) Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. Journal of the American College of Cardiology 19:7, 1550-1558
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Steven Sheingold, David Churchill, Norman Muirhead, Andreas Laupacis, Roberta Labelle, Ronald Goeree. (1992) The impact of recombinant human erythropoietin on medical care costs for hemodialysis patients in Canada. Social Science & Medicine 34:9, 983-991
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Jadwiga Szlachcic, Julio F. Tubau, Brian O'Kelly, Susan Ammon, Kim Daiss, Barry M. Massie. (1992) What is the role of silent coronary artery disease and left ventricular hypertrophy in the genesis of ventricular arrhythmias in men with essential hypertension?. Journal of the American College of Cardiology 19:4, 803-808
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Robert N. Foley, Patrick S. Parfrey, John D. Harnett. (1992) Left Ventricular Hypertrophy in Dialysis Patients. Seminars in Dialysis 5:1, 34-41
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Daniel Levy, Joanne M. Murabito, Keaven M. Anderson, Jane C. Christiansen, William P. Castelli. (1992) Echocardiographic Left Ventricular Hypertrophy: Clinical Characteristics. The Framingham Heart Study. Clinical and Experimental Hypertension a14:1-2, 85-97
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Karl T. Weber, Christian G. Brilla, Scott E. Campbell, Guoping Zhou, Luiz Matsubara, Eduardo Guarda. (1992) Pathologic Hypertrophy with Fibrosis: The Structural Basis for Myocardial Failure. Blood Pressure 1:2, 75-85
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Tord Ekbom, Björn Dahlöf, Lennart Hansson, Lars H. Lindholm, Anders Odén, Bengt Schersten, Per-Olov Wester. (1992) The Stroke Preventive Effect in Elderly Hypertensives Cannot Fully be Explained by the Reduction in Office Blood Pressure–Insights from the Swedish Trial in Old Patients with Hypertension (STOP-Hypertension). Blood Pressure 1:3, 168-172
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Michael S. Lauer, Keaven M. Anderson, Daniel Levy. (1992) Separate and joint influences of obesity and mild hypertension on left ventricular mass and geometry: The framingham heart study. Journal of the American College of Cardiology 19:1, 130-134
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