Angiotensin-converting enzyme inhibitors: more different than alike? Focus on cardiac performance.
Development of an increased systemic vascular resistance and the concomitant increase in blood pressure are associated with significant changes in left ventricular structure and function. The plasma and tissue renin-angiotensin systems play an important, but variable, role in the regulation of blood pressure and systemic vascular resistance in normotensive and hypertensive patients. Non-angiotensin-mediated effects of angiotensin-converting enzyme (ACE) inhibitors and/or differential tissue specificities may result in a variable hemodynamic response to individual therapies. Using first-pass radionuclide cineangiography, the hemodynamic effects of captopril, lisinopril, and fosinopril were compared. Fosinopril induced a greater reduction in systemic vascular resistance than did equipotent hypotensive doses of captopril or lisinopril and was associated with an increase in cardiac output, left ventricular peak ejection rate, and left ventricular peak filling rate. Along with previously accumulated data, these results suggest that structural differences among ACE inhibitors may result in unique physiologic effects. Fosinopril appears to have a cardiotropic effect that causes improved left ventricular diastolic performance; this effect is unique among currently available ACE inhibitors. The clinical significance of the unique profiles of individual ACE inhibitors awaits assessment via comparative clinical investigations.[1]References
- Angiotensin-converting enzyme inhibitors: more different than alike? Focus on cardiac performance. Zusman, R.M. Am. J. Cardiol. (1993) [Pubmed]
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