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Case 3: A Patient With Systemic Hypertension and Left Ventricular Hypertrophy Robert A. Kloner, MD, PhD, and Vincent E. Friedewald, Jr., MD Interactive Grand Rounds is designed to provide health care providers with the opportunity to earn CME credit by accessing the Internet at www. CardiovascularEd.com. The program features a clinical case accompanied by a discussion of the case.
CLINICAL CASE
he patient is a 65-year-old African-American who was reT ferred to you because of an abnormal electrocardiogram. He is asymptomatic but has a family history of hypertension and heart failure. His blood pressure at rest is 160/100 mm Hg in both arms. Cardiac examination is positive for a left ventricular heave at the left 5th intercostal space in the midclavicular line at the apex, an accentuated A2, and an S4. An electrocardiogram shows sinus rhythm, left atrial enlargement, and left ventricular hypertrophy (LVH). An echocardiogram shows concentric LVH. From the Heart Institute, Good Samaritan Hospital and University of Southern California, Los Angeles, California; and Baylor College of Medicine, Houston, Texas. This section is supported by an unrestricted educational grant from Pfizer, New York, New York. Dr. Kloner’s address is: The Heart Institute, Good Samaritan Hospital, 1225 Wilshire Blvd., Los Angeles, California 90017. Manuscript received December 20, 1999; revised manuscript received and accepted December 21, 1999. This CME activity was planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the A. Webb Roberts Center for Continuing Education of Baylor Health Care System, Dallas, Texas, and American Medical Communications, Inc. The A. Webb Roberts Center for Continuing Education of Baylor Health Care System, Dallas, is accredited by the ACCME to provide continuing medical education for physicians and takes responsibility for the content, quality and scientific integrity of this CME activity.
522
SUMMARY Hypertension is often referred to as the “silent killer” because most hypertensive patients are asymptomatic until cardiovascular sequelae such as stroke, myocardial infarction, heart failure, or renal failure occur. LVH is a common finding in patients with hypertension, especially African-Americans.1,2 Data from the Framingham Heart Study indicate that LVH is an independent risk factor for major cardiovascular events.3 In the Amlodipine Cardiovascular Community Trial,4 37% of 124 hypertensive patients screened by means of echocardiography had LVH at baseline. Although there was no difference in the prevalence of LVH by gender or age, AfricanAmerican patients were nearly twice as likely to have LVH than white patients (64% vs 34%, p ⬍0.05). Hence, aggressive therapy to reach target goals outlined in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) is especially important in this group of patients.5 Even lifestyle modifications such as weight reduction and limitation of salt intake, if sufficiently aggressive, can lead to regression of LVH, as demonstrated by results of the Treatment of Mild Hypertension Study (TOMHS).6 Most classes of antihypertensive drugs are effective in causing regression of LVH.7 Vasodilators, such as minoxidil and hydralazine, do not have an effect on regression, possibly because reflex tachycardia and stimulation of catecholamines and the renin-angiotensin system associated with these agents may negate the benefit of reduced afterload. There is some controversy re-
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 85 February 15, 2000
garding the ability of the angiotensin receptor blockers to reduce LVH. In some studies, these agents were associated with regression, whereas in others they were not.8,9 Whether targeting LVH as the primary treatment goal in hypertensive patients will have long-term benefits on outcome above and beyond simply reducing blood pressure is not clear. 1. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114:345–352. 2. Liao Y, Cooper RS, McGee DL, Mensah GA, Ghali JK. The relative effects of left ventricular hypertrophy, coronary artery disease, and ventricular dysfunction on survival among black adults. JAMA 1995;273:1592–1597. 3. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990;322: 1561–1566. 4. Kloner RA, Sowers JR, DiBona G, Gaffney M, Wein M. Effects of amlodipine on left ventricular mass in the Amlodipine Cardiovascular Community Trial. J Cardiovasc Pharmacol 1995;26:471– 476. 5. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157: 2413–2446. 6. Neaton JD, Grimm RH Jr, Prineas RJ, Stamler J, Grandits GA, Elmer PJ, Cutler JA, Flack JM, Scheonberger JA, McDonald R, et al. Treatment of Mild Hypertension Study. Final results. Treatment of Mild Hypertension Study Research Group. JAMA 1993;270:713–724. 7. Devereux RB. Do antihypertensive drugs differ in their ability to regress left ventricular hypertrophy? Circulation 1997;95:1983–1985. 8. Cheung B. Increased left-ventricular mass after losartan treatment. Lancet 1997;349:1743–1744. 9. Thurmann PA, Kenedi P, Schmidt A, Harder J, Rietbrock N. Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension. Circulation 1998; 98:203–2042.
To participate in the management of the CME interactive case and to read the complete discussion, go to: www.CardiovascularEd.com
0002-9149/00/$–see front matter PII S0002-9149(99)00940-6
Case 3: A Patient With Systemic Hypertension and Left Ventricular Hypertrophy Robert A. Kloner, MD, PhD, and Vincent E. Friedewald, Jr., MD Interactive Grand Rounds is designed to provide health care providers with the opportunity to earn CME credit by accessing the Internet at www. CardiovascularEd.com. The program features a clinical case accompanied by a discussion of the case.
CLINICAL CASE
he patient is a 65-year-old African-American who was reT ferred to you because of an abnormal electrocardiogram. He is asymptomatic but has a family history of hypertension and heart failure. His blood pressure at rest is 160/100 mm Hg in both arms. Cardiac examination is positive for a left ventricular heave at the left 5th intercostal space in the midclavicular line at the apex, an accentuated A2, and an S4. An electrocardiogram shows sinus rhythm, left atrial enlargement, and left ventricular hypertrophy (LVH). An echocardiogram shows concentric LVH. From the Heart Institute, Good Samaritan Hospital and University of Southern California, Los Angeles, California; and Baylor College of Medicine, Houston, Texas. This section is supported by an unrestricted educational grant from Pfizer, New York, New York. Dr. Kloner’s address is: The Heart Institute, Good Samaritan Hospital, 1225 Wilshire Blvd., Los Angeles, California 90017. Manuscript received December 20, 1999; revised manuscript received and accepted December 21, 1999. This CME activity was planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the A. Webb Roberts Center for Continuing Education of Baylor Health Care System, Dallas, Texas, and American Medical Communications, Inc. The A. Webb Roberts Center for Continuing Education of Baylor Health Care System, Dallas, is accredited by the ACCME to provide continuing medical education for physicians and takes responsibility for the content, quality and scientific integrity of this CME activity.
522
SUMMARY Hypertension is often referred to as the “silent killer” because most hypertensive patients are asymptomatic until cardiovascular sequelae such as stroke, myocardial infarction, heart failure, or renal failure occur. LVH is a common finding in patients with hypertension, especially African-Americans.1,2 Data from the Framingham Heart Study indicate that LVH is an independent risk factor for major cardiovascular events.3 In the Amlodipine Cardiovascular Community Trial,4 37% of 124 hypertensive patients screened by means of echocardiography had LVH at baseline. Although there was no difference in the prevalence of LVH by gender or age, AfricanAmerican patients were nearly twice as likely to have LVH than white patients (64% vs 34%, p ⬍0.05). Hence, aggressive therapy to reach target goals outlined in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) is especially important in this group of patients.5 Even lifestyle modifications such as weight reduction and limitation of salt intake, if sufficiently aggressive, can lead to regression of LVH, as demonstrated by results of the Treatment of Mild Hypertension Study (TOMHS).6 Most classes of antihypertensive drugs are effective in causing regression of LVH.7 Vasodilators, such as minoxidil and hydralazine, do not have an effect on regression, possibly because reflex tachycardia and stimulation of catecholamines and the renin-angiotensin system associated with these agents may negate the benefit of reduced afterload. There is some controversy re-
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 85 February 15, 2000
garding the ability of the angiotensin receptor blockers to reduce LVH. In some studies, these agents were associated with regression, whereas in others they were not.8,9 Whether targeting LVH as the primary treatment goal in hypertensive patients will have long-term benefits on outcome above and beyond simply reducing blood pressure is not clear. 1. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114:345–352. 2. Liao Y, Cooper RS, McGee DL, Mensah GA, Ghali JK. The relative effects of left ventricular hypertrophy, coronary artery disease, and ventricular dysfunction on survival among black adults. JAMA 1995;273:1592–1597. 3. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990;322: 1561–1566. 4. Kloner RA, Sowers JR, DiBona G, Gaffney M, Wein M. Effects of amlodipine on left ventricular mass in the Amlodipine Cardiovascular Community Trial. J Cardiovasc Pharmacol 1995;26:471– 476. 5. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157: 2413–2446. 6. Neaton JD, Grimm RH Jr, Prineas RJ, Stamler J, Grandits GA, Elmer PJ, Cutler JA, Flack JM, Scheonberger JA, McDonald R, et al. Treatment of Mild Hypertension Study. Final results. Treatment of Mild Hypertension Study Research Group. JAMA 1993;270:713–724. 7. Devereux RB. Do antihypertensive drugs differ in their ability to regress left ventricular hypertrophy? Circulation 1997;95:1983–1985. 8. Cheung B. Increased left-ventricular mass after losartan treatment. Lancet 1997;349:1743–1744. 9. Thurmann PA, Kenedi P, Schmidt A, Harder J, Rietbrock N. Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension. Circulation 1998; 98:203–2042.
To participate in the management of the CME interactive case and to read the complete discussion, go to: www.CardiovascularEd.com
0002-9149/00/$–see front matter PII S0002-9149(99)00940-6