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Ann Thorac Surg 1998;65:1571-1573
© 1998 The Society of Thoracic Surgeons
a Westmead and Royal Prince Alfred Hospitals, Sydney, Australia
Accepted for publication November 25, 1997.
Address reprint requests to Dr Paterson, Department of Cardiothoracic Surgery, Westmead Hospital, Hawkesbury Rd, Westmead NSW 2145 Australia
| Abstract |
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Methods. The case reports of 3 patients with similar presentations of ischemic heart disease and with severe manifestations of coronary artery spasm in the postoperative period are presented.
Results. All 3 patients were women aged 55 to 60 years. All had single-vessel coronary artery disease involving the left anterior descending artery and underwent a left internal mammary artery bypass graft. Severe manifestations of myocardial ischemia of abrupt onset developed approximately 7 hours postoperatively in each patient. One patient died of severe hemodynamic deterioration from which resuscitation was unsuccessful. Another sustained a large anterior myocardial infarction despite graft patency. The third patient was supported by an intraaortic balloon pump and made a full recovery.
Conclusions. The early diagnosis of coronary artery spasm is achieved by an awareness of the condition. The institution of early appropriate management may prevent its consequences.
| Introduction |
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| Patients |
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Patient 1, whose preoperative angiogram is typical of all 3 patients (Fig 1), became hypotensive with an elevated central venous pressure and associated ECG changes suggestive of anterior ischemia 8
hours after operation. Inotropic support was initiated and adequate hemodynamic parameters were maintained, but an anterior myocardial infarction occurred and the left ventricular ejection fraction declined to 0.32. Pulmonary edema refractory to diuretic therapy necessitated the use of mechanical ventilation for a further 20 days. Repeated angiography was not performed at this time but a spiral computed tomographic scan of the chest (Fig 2) confirmed graft patency 4 years later.
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hours after operation in patient 2. Resuscitation was commenced with the administration of inotropic agents and progressed to closed cardiac massage within 15 minutes. The sternotomy was reopened and internal cardiac massage was performed before resuscitation eventually was abandoned. An autopsy confirmed anastomotic patency and did not reveal the cause of death. Patient 3 was weaned from cardiopulmonary bypass with vigorous and healthy cardiac contractibility, but abrupt deterioration developed before the administration of protamine. This was associated with marked ST-segment changes on the ECG. Cardiopulmonary bypass was reinstituted and, based on a presumptive diagnosis of internal mammary artery insufficiency, an aortocoronary saphenous vein graft was performed to the left anterior descending artery. Anastomotic patency and excellent flow through the internal mammary artery were confirmed through the left anterior descending artery arteriotomy. The left anterior descending artery did not appear spastic. Cardiopulmonary bypass was discontinued again, with an identical result.
On both occasions, good cardiac contractibility returned after the reinstitution of cardiopulmonary bypass and the ECG normalized. However, on the second occasion, the ST-segment changes continued to occur and resolve spontaneously and at random despite the use of full cardiopulmonary bypass. Verapamil (2 mg) and glyceryl trinitrate (5 mg) were injected into the vein graft. The ECG stabilized and the ST-segment changes resolved. An intraaortic balloon pump was inserted prophylactically in view of the experience with patients 1 and 2. Cardiopulmonary bypass was discontinued without inotropic support and the patient clearly was not dependent on the intraaortic balloon pump. An intravenous infusion of glyceryl trinitrate (1 mg/h) was continued, along with a small titrated infusion of norepinephrine to maintain good systemic pressure.
At 7
hours after the procedure, abrupt hemodynamic deterioration occurred, with hypotension, mild bradycardia, ST-segment elevation, and obvious dependence on the intraaortic balloon pump. The hypotension was treated with metaraminol and an increase in the dosage of norepinephrine. An epinephrine infusion was commenced and the dosage of glyceryl trinitrate was increased to 2 mg/h. Inotropic support was discontinued after 90 minutes and hemodynamic stability persisted thereafter. The intraaortic balloon pump was removed 36 hours after the operation, but mechanical ventilation was continued for a further 5 days because of the presence of pulmonary edema that was refractory to diuretic therapy. Echocardiography demonstrated good left ventricular function and this was confirmed later by a gated heart pool scan after extubation. The patients recovery was uneventful thereafter.
The only preoperative medications common to all 3 patients were regular metoprolol and intermittent sublingual glyceryl trinitrate. All the internal mammary arteries were considered to have excellent caliber and flow, but this was not confirmed by objective measurement. No bolus medications were administered to any of the patients immediately before the coronary spasm events.
| Comment |
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Recently, the use of transesophageal echocardiography both during and after operation has provided more diagnostic information by identifying left ventricular segmental dysfunction. Segmental abnormalities may occur before the onset of ECG changes and usually are a more reliable indicator of the area of the coronary artery involved. When ischemia is localized to a grafted coronary system, the condition usually is attributed to graft or anastomotic problems, and this may or may not be confirmed by subsequent investigation. In most situations, this diagnosis is correct. Immediate postoperative myocardial dysfunction may be attributed to stunning (incomplete protection) or to a drug reaction (eg, protamine), particularly if there are no ECG changes suggestive of acute ischemia. Delayed myocardial failure or late-onset ECG changes suggestive of localized ischemia imply graft or anastomotic dysfunction in most cases. These complications should be excluded before a diagnosis of coronary artery spasm is made. Although there has been much discussion regarding internal mammary artery spasm, we believe it is a less common problem than coronary artery spasm.
When coronary artery spasm is identified, it can be treated most effectively with intracoronary vasodilators (eg, glyceryl trinitrate, papaverine, verapamil) administered through a bypass graft [5, 6] or during coronary angiography. Otherwise, intravenous medications have achieved variable success and should be instituted along with appropriate myocardial support and testing.
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