Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1971;44:446-455

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by FROHLICH, E. D.
Right arrow Articles by DUSTAN, H. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by FROHLICH, E. D.
Right arrow Articles by DUSTAN, H. P.

(Circulation. 1971;44:446.)
© 1971 American Heart Association, Inc.


Clinical-Physiological Correlations in the Development of Hypertensive Heart Disease

EDWARD D. FROHLICH M.D.1; ROBERT C. TARAZI M.D.1; HARRIET P. DUSTAN M.D.1

1 From Research Division, Cleveland Clinic, Cleveland, Ohio, and the Department of Medicine, the University of Oklahoma Medical Center, Oklahoma City, Oklahoma.

In order to understand more precisely the progression of ventricular dysfunction in hypertension prior to development of ventricular failure, 25 normal volunteer subjects and 97 untreated essential hypertensive patients (21 of whom had coronary arteriography and failed to show significant atherosclerosis) were classified into three groups: (I) normal-sized hearts, 54 patients; (II) left atrial enlargement (ECG criteria), 20 patients; and (III) left ventricular enlargement (ECG and chest X-ray criteria), 23 patients. Heart rate was elevated (P < 0.001) in all three groups; total peripheral resistance and arterial pressure increased progressively from group I to II to III (P < 0.001); cardiac index was reduced only in group III (P < 0.001). However, despite normal cardiac index in group II, left ventricular ejection rate was impaired (P < 0.01), and tension-time index and pressure-time per beat were greater than in patients with normal-sized hearts (P < 0.001). Thus, left atrial enlargement provided the initial evidence of left ventricular dysfunction. Later, when left ventricular hypertrophy became clinically apparent (always associated with left atrial abnormality) further impairment of left ventricular function was evident. Since these hemodynamic changes were observed in patients with normal coronary arteries, presence of left atrial and ventricular enlargement should provide useful criteria for classifying functional impairment in hypertensive heart disease.


Key Words: Arteriography • Left atrial abnormality • Essential hypertension • Left ventricular hypertrophy • Hemodynamics of hypertension

Submitted on February 8, 1971
Accepted on May 11, 1971




This article has been cited by other articles:


Home page
HypertensionHome page
E. Gerdts, K. Wachtell, P. Omvik, J. E. Otterstad, L. Oikarinen, K. Boman, B. Dahlof, and R. B. Devereux
Left Atrial Size and Risk of Major Cardiovascular Events During Antihypertensive Treatment: Losartan Intervention for Endpoint Reduction in Hypertension Trial
Hypertension, February 1, 2007; 49(2): 311 - 316.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
M. H. Drazner, J. E. Rame, E. K. Marino, J. S. Gottdiener, D. W. Kitzman, J. M. Gardin, T. A. Manolio, D. L. Dries, and D. S. Siscovick
Increased left ventricular mass is a risk factor for the development of a depressed left ventricular ejection fraction within five years: The Cardiovascular Health Study
J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2207 - 2215.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
E. D. Frohlich
Left ventricular hypertrophy: a "factor of risk": Mass is reversible, but is the risk?
J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2216 - 2218.
[Full Text] [PDF]


Home page
HypertensionHome page
E. Gerdts, L. Oikarinen, V. Palmieri, J. E. Otterstad, K. Wachtell, K. Boman, B. Dahlof, and R. B. Devereux
Correlates of Left Atrial Size in Hypertensive Patients With Left Ventricular Hypertrophy: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study
Hypertension, March 1, 2002; 39(3): 739 - 743.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
E. D. Frohlich
Risk Mechanisms in Hypertensive Heart Disease
Hypertension, October 1, 1999; 34(4): 782 - 789.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
F. G. Dunn and M. A. Pfeffer
Left Ventricular Hypertrophy in Hypertension
N. Engl. J. Med., April 22, 1999; 340(16): 1279 - 1280.
[Full Text]


Home page
ANGIOLOGYHome page
R. Fariello, M. Crippa, G. Damiani, I. Notaristefano, R. Costa, E. Boni, L. Corda, E. Chiari, and A. Zaninelli
Ventricular Arrhythmias in Normotensive Subjects and in Mild Hypertensive Patients
Angiology, February 1, 1998; 49(2): 99 - 103.
[Abstract] [PDF]


Home page
HypertensionHome page
A. Elhendy, R. T. van Domburg, J. R. T. C. Roelandt, M. L. Geleijnse, M. M. Ibrahim, and P. M. Fioretti
Safety and Feasibility of Dobutamine-Atropine Stress Testing in Hypertensive Patients
Hypertension, June 1, 1997; 29(6): 1232 - 1239.
[Abstract] [Full Text]


Home page
HypertensionHome page
S. M. Vaziri, M. G. Larson, M. S. Lauer, E. J. Benjamin, and D. Levy
Influence of Blood Pressure on Left Atrial Size : The Framingham Heart Study
Hypertension, June 1, 1995; 25(6): 1155 - 1160.
[Abstract] [Full Text]


Home page
CirculationHome page
B. D. Hoit, Y. Shao, M. Gabel, and R. A. Walsh
Disparate Effects of Early Pressure Overload Hypertrophy on Velocity-Dependent and Force-Dependent Indices of Ventricular Performance in the Conscious Baboon
Circulation, February 15, 1995; 91(4): 1213 - 1220.
[Abstract] [Full Text]


Home page
ANGIOLOGYHome page
E. D. Frohlich
High Cardiac Output Hypertensions
Angiology, July 1, 1976; 27(7): 475 - 485.
[PDF]