A comparative serial echocardiographic analysis of cardiac structure and function in rats subjected to pressure or volume overload.
Heart failure is a leading cause of death that is reaching epidemic proportions. It is a clinical syndrome attributable to a multitude of factors that begins with a compensatory response known as hypertrophy, followed by a decompensatory response that eventually results in failure. Heart failure can be triggered when the heart is subjected to extended periods of pathological pressure overload (PO) or volume overload (VO). To date there have been no comparative serial echocardiographic studies outlining the progression of hypertrophy in PO versus VO rats. We hypothesized that PO or VO would induce differential cardiac remodeling leading to contractile dysfunction with subsequent heart failure. To address this hypothesis we used echocardiography to study the serial progression of heart structure and function in rat models of both PO- and VO-induced hypertrophy. PO or VO were induced by performing abdominal aortic banding or aortocaval shunt procedures, respectively, while cardiac structure and function were assessed in both models by M-mode and Doppler echocardiography at key time intervals. PO rats showed progressive wall thickening consistent with concentric hypertrophy, while VO rats showed marked left ventricular dilatation consistent with eccentric hypertrophy. Systolic dysfunction occurred early in VO compared to PO. Diastolic dysfunction was evident in PO, while VO showed signs of enhanced diastolic function. PO and VO induced differential changes in cardiac structure and function during the progression of compensated hypertrophy to decompensated heart failure.
Cantor
Elliott J F
EJ
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Department of Physiology, University of Manitoba, Winnipeg, Man., Canada R2H 2A6.
Babick
Andrea P
AP
Vasanji
Zainisha
Z
Dhalla
Naranjan S
NS
Netticadan
Thomas
T
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D006332:Cardiomegaly / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*; D003971:Diastole; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology; D006973:Hypertension / Q000150:complications; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013599:Systole