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Abbreviation for angiotensin-converting enzyme inhibitors.
ACE inhibitorAngiotensin-converting enzyme inhibitor. Any of a family of drugs used to manage hypertension and reduce congestive heart failure (CHF)-related mortality and morbidity.
Bepridil, captopril, enalapril, lisionopril, losartan, quinapril, ramipril.
ACE inhibitor Effects in Heart Disease
• Restores balance between myocardial O2 supply and demand;
• Reduces left ventricular preload and afterload;
• Reduces left ventricular mass;
• Reduces sympathetic stimulation.
• Antiproliferative and antimigratory effects on smooth muscle and inflammatory cells;
• Antiplatelet effects;
• Improved arterial compliance and tone;
• Improved and/or restored endothelial function;
• Possible antiatherosclerotic effect.
ACEIs are cardioprotective and vasculoprotective; cardioprotective effects include improved haemodynamics and electric stability, reduce sympathetic nervous system (SNS) activity and reduce left ventricular mass; vasculoprotective benefits include improved endothelial function, vascular compliance and tone, and direct antiproliferative and antiplatelet effects. ACEIs also stimulate prostaglandin (PG) synthesis, reduce the size of MIs, and reduce reperfusion injury and complex ventricular arrhythmias.
ACEIs are the treatment of choice in CHF with systolic dysfunction; they are vasodilators which decrease preload and afterload. ACEI-induced reduction in angiotensin II inhibits the release of aldosterone, which in turn reduces sodium and water retention which, by extension, reduce preload; ACEIs improve haemodynamics of CHF by reducing right atrial pressure, pulmonary capillary wedge pressure, arterial BP, as well as pulmonary and systemic vascular resistance; ACEIs increase cardiac and stroke indices by the left ventricle and reduce the right ventricular end-diastolic volumes, thereby increasing cardiac output, while simultaneously reducing cardiac load and myocardial O2 consumption.
• Idiopathic—e.g., rashes, dysgeusia, BMsuppression.
• Class-specific—e.g., hypotension, renal impairment, hyperkaleamia, cough, angioneurotic oedema (the latter 2 of which are mediated by small vasoactive substances—e.g., bradykinin, substance P, and PG-related factors).