Myocyte loss and left ventricular failure characterise the long term effects of coronary artery narrowing or renal hypertension in rats

• Published in: Cardiovascular research 1993-06, Vol.27 (6), p.1066-1075
• Main Authors: Li, Peng, Zhang, Xun, Capasso, Joseph M, Meggs, Leonard G, Sonnenblick, Edmund H, Anversa, Piero
• Format: Article
• Language: English
• Subjects: Animals; Arterial hypertension. Arterial hypotension; Arterial Occlusive Diseases - complications; Arterial Occlusive Diseases - pathology; Arterial Occlusive Diseases - physiopathology; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - physiology; cardiac failure; Cardiology. Vascular system; Cardiomegaly - etiology; Chronic Disease; Coronary Disease - complications; Coronary Disease - pathology; Coronary Disease - physiopathology; Experimental diseases; Heart Ventricles - pathology; Hypertension, Renal - complications; Hypertension, Renal - pathology; Hypertension, Renal - physiopathology; Hypertrophy, Left Ventricular - etiology; Hypertrophy, Left Ventricular - physiopathology; Male; Medical sciences; morphometry; myocyte hypertrophy; Rats; Rats, Sprague-Dawley; ultrasonic dimension crystals; wall and chamber remodelling; wall stress in vivo
• ISSN: 0008-6363; 1755-3245
• DOI: 10.1093/cvr/27.6.1066

Objective: The aim was to determine the effects of chronic coronary artery narrowing and two kidney, one clip renal hypertension alone and in combination on ventricular function and myocardial morphology. Methods: Left coronary stenosis and renal artery clipping were surgically induced in rats and pump dynamics, systolic and diastolic wall stress, cardiac anatomy, and the changes in number and size of left ventricular myocytes were examined 11-13 weeks later. Results: Ventricular failure evolved with each intervention: left ventricular end diastolic pressure was raised, whereas +dP/dt, −dP/dt, stroke volume, cardiac output, and cardiac index were reduced. Calculated ventricular systolic wall stress increased nearly 70% in the three experimental conditions. By contrast, diastolic wall stress was augmented 6.1-fold with coronary stenosis, 4.0-fold with hypertension, and 4.4-fold with combined treatment. These differences were due to variable preservations of wall thickness between the groups. Left ventricular weight expanded 26%, 35%, and 32% with stenosis, hypertension, and a combination of the two, whereas diastolic cavitary volume increased 57%, 35%, and 49%. Corresponding increases in systolic chamber volumes were 156%, 122%, and 154%. Finally, myocyte loss in the ventricle was 25%, 25%, and 37% in coronary narrowing, renal hypertension and a combination of the two with concomitant enlargements of the unaffected myocytes of 47%, 63%, and 65%. Conclusions: Decompensated eccentric ventricular hypertrophy developed as a result of coronary artery narrowing, renal hypertension, or the two in combination. Coronary artery narrowing, however, may have a greater maladaptive effect on ventricular function than systemic hypertension, and coronary stenosis and hypertension combined because of the more extensive chamber and wall remodelling which sustained greater increases in diastolic wall stress. Cardiovascular Research 1993;27:1066-1075