727-2 Changes in Left Ventricular Mechanics and Energetics in Canine Microembolization Model of Heart Failure

• Published in: Journal of the American College of Cardiology 1995-02, Vol.25 (2), p.133A-133A
• Main Authors: Todaka, Koji, Zhu, Shu-Ming, Gu, Anguo, Stemett, Richard, Burkhoff, Daniel
• Format: Article
• Language: English
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/0735-1097(95)92005-P

Myocardial mechanics and energetics have been shown previously to be markedly abnormal in a canine model of pacing induced heart failure. However, whether those abnormalities pertain to other, more clinically relevant forms of heart failure is unknown. To investigate this question, heart failure was created by ischemic damage in 6 dogs (CHF group) that underwent repeated coronary microsphere injections over 2 months resulting in afinal area ejection fraction (aEF) of 34±4%. A control group of 6 normal dogs had an aEF of 46±8%, Hearts of these animals were isolated, cross-perfused and balloons placed in the LV to control volume. We measured the LV endsystolic (ESPVR) and end-diastolic (EDPVR) pressure-volume relations and the relationship between oxygen consumption (mVO2) and pressure-volume area (PVA). β-responsiveness of the CHF group was significantly depressed compared to control as assessed by the increased amount of isoproterenol required to increase peak isovolumic LV pressure by 40% (72±36 vs. 29±14pg/min, p<0.05) providing pharmacologic evidence of the heart failure state, CHF hearts had a depressed and dilated LV as assessed by the ESPVR slope, Ees, and volume axis intercept, Vo, (both normalized to LV mass) compared to control (TABLE). EDPVR of CHF hearts was shifted to the right compared to control. Systolic and diastolic stress-strain relationships. estimated from the pressure-volume relations. were similar in the two groups. These data suggest that with the degree of chronic ischemic damage achieved, there was systolic LV chamber dysfunction and chamber remodeling but not myocardial property changes in surviving muscle. The mVO2-PVA relation in CHF hearts had smaller mVO2-intercept (B)than control with no change in the slope (A)(TABLE). This contrasts with a previous report using a rapid pacing CHF model in which myocardial strength was decreased, Awas decreased and Bwas unchanged. These data suggest that 1) in spite of the notable structural and functional changes in chamber mechanics, energetic aspects of the failing heart remained unaltered in this model and 2) conclusions about myocardial energetics in CHF are model dependent.ESPVR: Ees mmHg/ml.l00gVo ml/l00gmVO2-PVA:AmlO2/mmHg/mlBmlO2/beat/l00gCHF3.9±1.2*6.9±5.3**(1.3±04)×10-50.030±0.005**Control47±1.90.5±2.9(1.3±0.6)×10-50.036±0.004*p<0.05.**p<0.01 vs. Control by ANCOVA