OBJECTIVE: To focus on the cardioprotective role of angiotensin-converting enzyme (ACE) inhibitors in ischemic heart disease and to highlight some of the, as yet, unanswered questions about the relative merits of ACE inhibitors as cardioprotective drugs. DATA SOURCE: This review incorporates the data on this subject published in the available English literature up to June 1990. DATA SELECTION: The source material was analyzed and computed chronologically into two groups: experimental studies and clinical trials. DATA EXTRACTION: ACE inhibitors have gained access to the free world market for a variety of reasons. Their superiority in the management of hypertension and congestive heart failure is being recognized. Furthermore, recent experimental and limited clinical trials strongly indicate a role for ACE inhibitors in limiting myocardial ischemia-reperfusion-induced injury. Although the sulphydryl group (SH)-containing ACE inhibitor captopril has been extensively used for most studies, the cardioprotective role of non-SH-containing ACE inhibitors, particularly ramipril and enalapril, recently has been identified. ACE inhibitors reportedly limit infarct size, prevent ventricular remodelling and, more importantly, stabilize the electrical activity of the reperfused heart and prevent the occurrence of reperfusion arrhythmias. Preliminary clinical trials indicate an antianginal role for ACE inhibitors. ACE inhibition has also been reported to improve left ventricular performance in patients with long standing infarcts and ischemic failure. Although pharmacological effects of ACE inhibitors are well known, the mechanism of cardioprotection at the molecular and cellular levels is elusive. The role of ACE inhibitors in myocardial stunning and their free radical scavenging effects are still speculative. Furthermore, the effects of ACE inhibition during global myocardial ischemia-reperfusion are virtually unknown. CONCLUSIONS: The available data strongly indicates a role for ACE inhibitors in limiting myocardial ischemia-reperfusion-induced injury. However, more controlled studies, particularly multicentre clinical trials, are indicated to establish a therapeutic rationale for ACE inhibition in the management of ischemic heart disease.
OBJECTIVE: To focus on the cardioprotective role of angiotensin-converting enzyme (ACE) inhibitors in ischemic heart disease and to highlight some of the, as yet, unanswered questions about the relative merits of ACE inhibitors as cardioprotective drugs. DATA SOURCE: This review incorporates the data on this subject published in the available English literature up to June 1990. DATA SELECTION: The source material was analyzed and computed chronologically into two groups: experimental studies and clinical trials. DATA EXTRACTION: ACE inhibitors have gained access to the free world market for a variety of reasons. Their superiority in the management of hypertension and congestive heart failure is being recognized. Furthermore, recent experimental and limited clinical trials strongly indicate a role for ACE inhibitors in limiting myocardial ischemia-reperfusion-induced injury. Although the sulphydryl group (SH)-containing ACE inhibitor captopril has been extensively used for most studies, the cardioprotective role of non-SH-containing ACE inhibitors, particularly ramipril and enalapril, recently has been identified. ACE inhibitors reportedly limit infarct size, prevent ventricular remodelling and, more importantly, stabilize the electrical activity of the reperfused heart and prevent the occurrence of reperfusion arrhythmias. Preliminary clinical trials indicate an antianginal role for ACE inhibitors. ACE inhibition has also been reported to improve left ventricular performance in patients with long standing infarcts and ischemic failure. Although pharmacological effects of ACE inhibitors are well known, the mechanism of cardioprotection at the molecular and cellular levels is elusive. The role of ACE inhibitors in myocardial stunning and their free radical scavenging effects are still speculative. Furthermore, the effects of ACE inhibition during global myocardial ischemia-reperfusion are virtually unknown. CONCLUSIONS: The available data strongly indicates a role for ACE inhibitors in limiting myocardial ischemia-reperfusion-induced injury. However, more controlled studies, particularly multicentre clinical trials, are indicated to establish a therapeutic rationale for ACE inhibition in the management of ischemic heart disease.
Authors: Hsueh-Fu Wu; Chia-Wei Huang; Kanupriya R Daga; Ross A Marklein; Natalia Ivanova; Nadja Zeltner Journal: Clin Auton Res Date: 2022-01-29 Impact factor: 5.625