Cardioplegic arrest in patients with previous Vineberg implants

Cardioplegic arrest in patients with previous Vineberg implants

J THORAC CARDIOVASC SURG 78:769-771, 1979 Cardioplegic arrest in patients with previous Vineberg implants During aortic cross-clamping for direct cor...

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J THORAC CARDIOVASC SURG 78:769-771, 1979

Cardioplegic arrest in patients with previous Vineberg implants During aortic cross-clamping for direct coronary operation in patients who previously had had internal mammary artery (Vineberg) implants, the heart may continue to beat or fibrillate. It may be important, therefore, to identify the mammary artery and temporarily snare it in order to achieve and maintain cardioplegic arrest.

Tomas A. Salerno, M.D., Fraser M. Keith, M.D., and Edward J. P. Charrette, M.D.,

Kingston, Ontario, Canada

More and more patients who previously had had a Vineberg procedure are undergoing repeat myocardial revascularization by direct coronary artery bypass grafting (CABO). The operative technique may prove difficult if cardioplegic arrest is used, since coronary flow via collaterals from the internal mammary artery (lMA) continues despite aortic cross-clamping, so that the cardioplegic solution is washed out and adequate myocardial protection is prevented. The present report delineates our surgical techniques in such cases and emphasizes the importance of noncoronary circulation in cardioplegic arrest.

IMA was occluded. There was no evidence of the presence of the omental graft. After cardiopulmonary bypass (CPB) was instituted, the aorta was cross-clamped and 350 cc of cardioplegic solution* was infused into the proximal compartment of the aorta. Surprisingly, the heart continued to beat. The IMA was then snared, and infusion of 100 cc of cardioplegic solution resulted in immediate arrest of the heart. Following quadruple CABG, the snare was removed from the IMA and CPB was discontinued uneventfully. Four additional patients who had had a Vineberg implant have been operated upon; one of these was similar to the patient just described. The other three patients had occluded IMA implants and posed no problems, since the heart immediately arrested with infusion of the cardioplegic solution.

Case report

Discussion

A 60-year-old man had undergone a double Vineberg procedure and a free omental graft in 1968 for angina caused by disease of the right coronary artery and left anterior descending artery (LAD). He remained well until 1977, when Class III angina symptoms developed and persisted despite intensive medical therapy. Results of the physical examination were unremarkable. At cardiac catheterization in November of 1978 the left ventricular end-diastolic pressure was 14 mm Hg. The right IMA was patent and, via collaterals, supplied the territory of the LAD (Fig. I) as well as the posterior descending coronary artery. There was a 50% stenosis of the left main coronary artery, total occlusion of the LAD, and a 60% narrowing of the circumflex coronary artery. Dense pericardial adhesions were found at operation. The right IMA measured 4 mm in diameter and was patent. The left

The importance of noncoronary collateral blood flow in normal hearts following chronic coronary artery occlusion and in hearts with left venticular hypertrophy has been previously demonstrated.' The source of noncoronary collaterals is known to be from the ventricular lumen-":' and from the pericardium and vasa vasorum leading to and from the myocardiurn.v " Nonluminal noncoronary flow is greatest during the period of cross-clamping. This explains the reason for continuation of heart action for a period of time following aortic cross-clamping. It is known that patients who have undergone Vineberg procedures may have patent IMA grafts. to Less well documented, however, is the amount of blood flow via such grafts. Should the flow be sufficient to perfuse the myocardium, one would expect that heart action would continue despite aortic cross-clamping

From the Department of Surgery, Queen's University, Kingston, Ontario, Canada. Supported by the Ontario Heart Foundation Grant 2-4. Received for publication March 16, 1979. Accepted for publication June 4, 1979. Address for reprints: Dr. T. A. Salerno, Department of Surgery, Queen's University, Kingston, Ontario, Canada.

*Cardioplegic solution: 500 ml of Ringer's lactate, 10 mEq of potassium chloride, 12.5 mEq of sodium bicarbonate, 12 ml of 2% lidocaine, 17 ml of 50% dextrose, 125 mg of Solu-Cortef, pH 7.7, and temperature 4 C.

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action ceased. Unfortunately, blood flow in the IMA grafts was not measured because of breakdown in our equipment. Therefore, no comment can be made as to the actual contribution of blood flow to the myocardium from the IMA or from other noncoronary collaterals. The fact that the three other hearts with an occluded IMA arrested immediately following cardioplegic infusion suggests that the predominant noncoronary flow was via the IMA in patients in whom it was patent, an extreme example of noncoronary collateral flow. We were unable to demonstrate the presence of the free omental graft during the operation, and no large collaterals were visualized between the pericardium and the heart. This communication emphasizes the importance of recognizing that patients who had Vineberg procedures may have patent IMA implants. Evidence from our two cases indicates that blood flow in the Vineberg implant was enough to maintain cardiac action following cross-clamping. Identification and preservation of the IMA and interruption of blood flow by a snare were important technical details necessary to achieve cardioplegic arrest and to facilitate the operation while protecting the myocardium. As a source of blood supply to the myocardium of ischemic hearts, noncoronary circulation (including the Vineberg implant) may playa greater role during cardioplegic arrest that is now appreciated. As we learn more about myocardial preservation it may become apparent that, for assurance of complete cardioplegic protection, noncoronary collateral flow may have to be minimized, interrupted, or counteracted. Manipulation of pump flow or blood viscosity or both appears to minimize the amount of noncoronary collateral flow. I Large noncoronary collaterals, such as the IMA, can be temporarily interrupted and preserved, as shown in our two cases. Obviously, periodic reinfusion of cardioplegic solution would be the simplest way of counteracting the deleterious effects of noncoronary collateral circulation during aortic cross-clamping in the cardioplegically arrested heart.

Fig. 1. Injection of the right subclavian artery demonstrating a patent Vineberg implant supplying the territory of the left anterior descending coronary artery. during the cardiac operation. This occurred in two of our patients in whom the IMA was found to be patent. Initial attempts to arrest the heart during cross-clamping and infusion of cardioplegic solution failed. It was only with subsequent snaring of the IMA that heart

REFERENCES Brazier 1, Hottenrott C, Buckberg G: Noncoronary collateral myocardial blood flow. Ann Thorac Surg 19:426, 1975

2 Moggio BA, Kabemba 1M, Hammond GL: Coronaryventricular lumen blood exchange demonstrated by 51 Cr-labelled erythrocytes. Am 1 Physiol 221:955, 1971 3 Moir TW: Study of luminal coronary collateralcirculation in the beating canine heart. Circ Res 24:735, 1969 4 Wearn JT, Mettier SR, Klumpp TG, Zschiesche LJ: The nature of the vascular communications between the coro-

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nary arteries and the chambers of the heart. Am Heart J 9:143, 1933 Bloor CM, Liebow AA: Coronary collateral circulation. Am J Cardiol 16:238, 1965 Halpern MH: Arterial supply to the nodal tissue in the dog heart. Circulation 9:547, 1954 Hudson CL, Moritz AR, Weam JT: The extracardiac anastomoses of the coronary arteries. Soc Exp Med 56:919, 1932 Kline JL, Stem H, Bloomer WE, Liebow AA: The appli-

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cation of an induced bronchial collateral circulation to the coronary arteries by cardiopneumonopexy, Am J Pathol 32:663, 1956 9 Sayen 11, Pierce G, Katcher AH, Sheldon WF: Correlation of intramyocardial electrocardiograms with polarographic oxygen and contractility in the non-ischemic and regionally ischemic left ventricle. Circ Res 9:1268, 1961 10 Vineberg AM: Medical News Section. JAMA 234:693, 1975

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