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Effect of Calcium Antagonist Diltiazem on Renal Function in Open Heart Surgery FREE TO VIEW

Jun Amano; Akio Suzuki; Makoto Sunamori; Motohisa Tofukuji
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From the Department of Cardiothoracic Surgery, Tokyo Medical and Dental University, Tokyo, Japan, and the Department of Thoracic Surgery, Tohoku University, Sendai, Japan


1995 by the American College of Chest Physicians


Chest. 1995;107(5):1260-1265. doi:10.1378/chest.107.5.1260
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Abstract

Study objective: Acute renal failure, which is a serious complication following open heart surgery, has a high mortality rate. Previous reports have shown that the calcium antagonist diltiazem is beneficial either as an adjunct to cardioplegic solution or perioperative treatment for preservation of postoperative cardiovascular function. We studied the effects of diltiazem on renal function, plasma atrial natriuretic peptide levels, and the renin-angiotensin-aldosterone system in patients who had undergone coronary artery bypass grafting.

Patients and measurements: Diltiazem was administered, 0.1 mg/kg, in a bolus injection followed by continuous infusion at a rate of 2 µ/kg/min during surgery, and 30 mg through a nasogastric tube at every 8 h. Hemodynamics, renal function, and plasma hormone levels were measured in the diltiazem-treated group (n=13) and the nontreated group (n=10).

Results: Heart rate, mean arterial pressure, and systemic vascular resistance index in the diltiazem-treated group were significantly lower than those in the nontreated group following cardiopulmonary bypass. Urine volume, creatinine clearance, and free water clearance were well preserved in the diltiazem-treated group. However, plasma renin activity and aldosterone levels were significantly higher in the diltiazem-treated group with the same changes in plasma atrial natriuretic peptide levels.

Conclusion: Perioperative treatment with diltiazem has a beneficial effect on postoperative renal function, and reflex sympathetic activation induced by peripheral vasodilation activated the renin-angiotensin-aldosterone system.


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