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Chin Med J (Taipei) 1998;61:S102.

Ventricular-Arterial Coupling in Congestive Heart Failure

Che-Ping Cheng, M.D., Ph.D.

Wake Forest University School of Medicine, Winston-Salem, NC, USA


Abstract

Background. The function of the cardiovascular system is to provide for the perfusion of the tissues. This depends on the ability of the LV to produce both flow (stroke volume) (SV) and perfusion pressure (P) (arterial P). LV stroke work (SW) integrates both these parameters, and thus it provides a simple means of quantitating the performance of the cardiovascular system. The interaction of the LV and the arterial system, in addition to determining SW, also importantly influence the determinants of myocardial oxygen demand. Accordingly, we assessed the coupling between the LV and arterial system on SW and P-V area (PVA) in normal and CHF animals at rest and during exercise (EX).

Methods. The LV-arterial coupling was assessed in 8 conscious chronically instrumented animals before and after 2 levels of CHF produced by 3 and 5 weeks of rapid pacing at rest and during EX. The LV end-systolic P-V relation was determined by caval occlusions. Its slope (Ees) was compared to the arterial elastance (Ea), determined as Pes/SV. The efficiency of conversion of mechanical energy produced by LV to the external work was expressed as SW/PVA.

Results. Prior to CHF, the Ees (9.3 +/- 2.2 vs 11.9 +/- 3.9 mmHg/ml), and the Ea (8.9 +/- 2.9 vs 9.6 +/- 3.1 mmHg/ml) (p < 0.05) were all increased during EX. Ile ratio of Ees to Ea also increased from 1.0 +/- 0.2 to 1.2 +/- 0.2, (p < 0.05) during EX but remained within the range (Ees/Ea=0.8 to 1.2) in which we have previously found that SW was within 95% of the SW at optimal coupling when Ees/Ea=1.0. As the Ees/Ea ratio increased, the SW/PVA ratio, was improved (0.66 +/- 0.02 to 0.71 +/- 0.02) (p < 0.05). After moderate CHF, resting Ees decreased from 9.3 +/- 2.2 to 6.5 +/- 2.0 mmHg/ml, but Ea was increased from 7.6 +/- 1.6 to 10.3 +/- 1.3 mmHg/ml, thus reducing Ees/Ea to 0.64 +/- 0.2 (p < 0.05). At this coupling ratio, SW was reduced to 86% of the SW produced at optimal coupling, but the SW/PVA was significantly reduced to 0.50 +/- 0.08 (p < 0.05). Ees/Ea did not change during EX after moderate CHF (0.68 +/- 0.2, P=NS). When animals developed severe CHF and were not able to EX, Ees decreased to 4.8 +/- 1.6 mmHg/ml, while Ea was further increased to 11.3 +/- 2.1, greatly exceeded Ees. Thus, Ees/Ea fell to 0.42 +/- 0.1 (p < 0.05), where SW was substantially reduced to 75% maximum. SW/PVA was reduced to 0.39 +/- 0.06 ( p < 0.05). In this situation, SW was very sensitive to changes in Ea. Both SW and the ratio of SW`/PVA were markedly improved by a reduction in Ea with a vasodilator, losartan or nitroprusside.

Conclusions. The normally functioning LV and arterial system are nearly optimally coupled to produce SW both at rest and EX. During normal EX, as Ees/Ea increases, the SW/PVA was improved. After CHF, at rest, the LV-arterial coupling is adversely altered. When Ea greatly exceeds Ees, the SW falls substantially. As Ees/Ea decreases, the SW/PVA was also markedly reduced, but LV-arterial coupling is not further impaired during EX after moderate CHF.

Keywords: heart failure, stroke work, LV arterial coupling, LV end-systolic P-V relation.

[Chin Med J (Taipei) 1998;61:S102.]



Copyright: 1998, Chinese Medical Association (Taipei)