Ann Thorac Surg 1998;66:492
© 1998 The Society of Thoracic Surgeons
Original articles: cardiovascular
Invited commentary
Frank W. Sellke, MDa
a Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, Boston, MA 02215, USA
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Invited commentary
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The renin–angiotensin system traditionally has been thought to be involved in blood pressure regulation and fluid homeostasis. Although to a large extent this remains true, it is now recognized that the renin–angiotensin system is involved in the regulation of many more physiologic and pathologic processes. In the past decade, many investigators have concentrated on modulating the renin–angiotensin system with the use of angiotensin-converting enzyme (ACE) inhibitors and have studied their effects on patient mortality, improvement in cardiac function, and myocardial remodeling after acute myocardial infarction. In general, the use of ACE inhibitors in this setting has resulted in improved patient outcome. Angiotensin-converting enzyme inhibitors are now a first-line therapy for patients having suffered myocardial infarction, especially for those patients with reduced ventricular function.
Because cardiovascular surgeons deal with altered myocardial contractility on a daily basis and ACE inhibitors have been found to improve myocardial function, the notion that ACE inhibitors may improve patient outcome after cardiac operations seems plausible. In this article, Lazar and colleagues examined the effects of the ACE inhibitor enalaprilat on ischemic damage after coronary occlusion followed by cardioplegia and reperfusion, a scenario similar to what may occur during emergency coronary artery bypass grafting. Lazar and colleagues found that pigs treated acutely with enalaprilat had less ventricular irritability, improved regional wall motion, and less myocardial infarction than pigs receiving saline-vehicle alone.
Enalaprilat and other ACE inhibitors may decrease superoxide generation and reduce oxidative stress by inhibiting angiotensin II production [1]. In addition, synthesis of nitric oxide and prostacyclin appear to be increased in blood vessels of hearts treated with ACE inhibitors. This may contribute to the beneficial effects observed in the setting of myocardial ischemia by lowering afterload and inhibiting neutrophil adherence. However, the use of ACE inhibitors during cardiopulmonary bypass requires a word of caution. Some studies have determined that chronic treatment with ACE inhibitors before cardiopulmonary bypass is associated with significantly greater need for pressor agents to maintain blood pressure [2], whereas other studies have demonstrated no effect or actually improved renal perfusion during cardiopulmonary bypass. In addition, ACE is also known as kininase II, which catalyzes the degradation of bradykinin, a very potent vasodilator and mediator of vascular permeability. Thus, the use of ACE inhibitors (especially acute administration) during cardiopulmonary bypass may considerably increase systemic inflammation and increase fluid requirements postoperatively. Although the acute administration of ACE inhibitors during cardiopulmonary bypass may on a theoretical basis improve myocardial protection, it is not without risk, and their use needs to be weighed against their possible adverse effects on systemic vasomotor tone, permeability, and overall patient outcome.
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References
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- Rajagopalan S., Kurz S., Munzel T., et al. Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. J Clin Invest 1996;97:1916-1923.[Medline]
- Tuman K.J., McCarthy R.J., O’Connor C.J., Holm W.E., Ivanovich A.D. Angiotensin-converting enzyme inhibitors increase vasoconstrictor requirement after cardiopulmonary bypass. Anesth Analg 1995;80:473-479.[Abstract]
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Invited commentary
References