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Dimorphic Cardiac Adaptation to Obesity and Arterial Hypertension

FRANZ H. MESSERLI, M.D.; KIRSTEN SUNDGAARD-RIISE, B.A.; EFRAIN D. REISIN, M.D.; GERALD R. DRESLINSKI, M.D.; HECTOR O. VENTURA, M.D.; WILLIE OIGMAN, M.D.; EDWARD D. FROHLICH, M.D.; and FRANCIS G. DUNN, M.D.
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▸Requests for reprints should be addressed to Franz H. Messerli, M.D.; Ochsner Clinic, 1514 Jefferson Highway; New Orleans, LA 70121.


New Orleans, Louisiana


© 1983 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1983;99(6):757-761. doi:10.7326/0003-4819-99-6-757
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Cardiovascular function and structure were evaluated by M-mode echocardiography and systemic hemodynamics in paired lean and obese patients, either hypertensive or normotensive. Compared to lean patients, obese patients had greater left atrial (p < 0.0001), ventricular (p < 0.001), and aortic root (p < 0.002) diameters; posterior and septal wall thickness (p < 0.001); and ventricular mass, cardiac output, stroke volume, and stroke work (all p < 0.0001). Hypertensive patients had increased posterior wall thickness, end diastolic wall stress, stroke work (p < 0.01), and a lower radius to posterior wall thickness ratio indicating concentric hypertrophy (p < 0.001) when compared to normotensive patients. Cardiac adaptation to obesity consists of left ventricular dilatation and hypertrophy (eccentric hypertrophy) irrespective of arterial pressure levels. In contrast, essential hypertension solely produces concentric hypertrophy. Both obesity and hypertension increase left ventricular stroke work by disparate hemodynamic mechanisms; their presence in the same patient will tax the heart and increase the long-term risk of congestive failure.

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