Ventricular unloading and improvement in left ventricular function after angiotensin converting enzyme inhibition with enalapril in patients with chronic congestive heart failure
Naganuma, F.; Kubota, S.; Hirahara, N.; Imai, K.; Kamiyama, H.; Iizuka, T.; Imai, S.; Murata, K.; Suzuki, T.
Japanese Circulation Journal 58(1): 34-42
1994
ISSN/ISBN: 0047-1828 PMID: 8139090 DOI: 10.1253/jcj.58.34
Accession: 009721967
To clarify how angiotensin converting enzyme inhibition affects left ventricular function through ventricular unloading, ventricular wall stress, ventricular volumes, and other cardiac indices and exercise tolerance were evaluated in 17 patients with mild to moderate chronic congestive heart failure before and after 3 months of treatment with enalapril. Echocardiographic examination revealed that treatment with this angiotensin converting enzyme inhibitor resulted in significant reductions in end-systolic wall stress (117 +- 25 to 89 +- 2 8 g/cm-2, p lt 0.01) and left ventricular volume indices (end-diastolic: 163 +- 56 to 143 +- 60; end-systolic 99 +- 51 to 77 +- 57 ml/m-2 p lt 0. 0 1). Ejection fraction (42 +- 11 to 48 +- 13%, p lt 0.01) and systolic blood pressure/end-systolic volume (SBP/ESV; 1.06 +- 0.30 to 1.33 +- 0.48 mmHg/ml, p lt 0.01) were both increased. By radionuclide ventriculography, ejection fraction and peak ejection rate (2.30 +- 0.74 to 2.80 +- 0.76 EDV/sec, p lt 0.01) were increased, while time to peak ejection, time to peak filling, and peak filling rate were unchanged. Heart rate and double product at exercise were decreased and AEF was significantly increased (-1.4 +- 4.1 to 1.6 +- 4.4%, p lt 0.02). The decrease in end-systolic wall stress was consistently related to both the increase in ejection fraction and SBP/ESV, while the decrease in end-diastolic volume was related only to SBP/ESV and not to ejection fraction. Furthermore, there was a direct relationship between the decrease in systolic wall stress and the decrease in end-diastolic volume. These results suggest that the improvement of left ventricular contractility due to angiotensin converting enzyme inhibition was produced through a parallel reduction of both afterload and preload. Afterload reduction had a greater effect on the improvement of left ventricular ejection fraction than preload reduction.