Cause of Acute Myocardial Angioplasty
Infarction After Successful Coronary
Richard Kerensky, MD, Michael Kutcher, MD, Michael Mumma, William c. Little, MD ercutaneous transluminal coronary angioplasty is now accepted as effective therapy for selected patients with coronary artery disease.’ It has been suggested that patients with complete revascularization after coronary angioplasty have a lower incidence of subsequent myocardial infarction than those with incomplete revasculariiation. However, it is not known whether myocardial infarction after angioplasty is due to occlusion at the angioplasty site, at the site of an undilated stenosis or at the site of a previously nonobstructive lesion. In patients treated medically2$3 or with bypass surgery,4 subsequent myocardial infarction frequently occurs owing to occlusion at a site that previously had I80 with MB fraction, or the need for in-hospital coronary artery bypass graft surgery). Thirty-four patients had had 3.5 myocardial infarctions >2 weeks after successful angioplasty and had undergone another coronary angiogram within 2 days of myocardial infarction. In each case, myocardial infarction was documented by prolonged chest pain, followed by an elevated serum creatine kinase-MB. New electrocardiographic changes of myocardial infarction or new left ventricular wall motion abnormalities by ventriculography, or both, were present in all cases.
P
From the Cardiology Section, Department of Medicine, School of Medicine, Wake Forest University, Medical vard, Winston-Salem, North Carolina 27157-1045. supported in part by the Wuliger Angioplasty Research Salem, North Carolina. Manuscript received April manuscript received June 14, 1991, and accepted June
Bowman Gray Center BouleThis study was Fund, Winston1, 1991; revised 15.
MD, Robert
J. Applegate,
MD, and
Selected coronary angiograms were obtained in multiple projections. The angiogram obtained after myocardial infarction was used to determine the site of obstruction (culprit site) causing the myocardial infarction. In each patient, a new total or subtotal coronary artery occlusion was identified, corresponding to the location of the electrocardiographic abnormalities or of the new wall motion abnormality on contrast left ventriculography, or both. The coronary angiograms that had been obtained immediately before and after angioplasty were then reviewed. If the culprit site was in the same vessel as the angioplasty site and was not >2 cm proximal or distal to the angioplasty site, the myocardial infarction was classified as occurring at the angioplasty site. If the culprit site was in a different artery than the angioplasty site, or was >2 cm proximal or distal to the angioplasty site, the culprit site was classified as a nonangioplasty site. The severity of the stenosis at the culprit site after angioplasty, and at the angioplasty site before and after angioplasty was determined as a % diameter stenosis using the angiographic view in which the stenosis appeared most severe. Calipers were used to measure the stenotic area, and comparison was made with the nearest adjacent normal arterial segment. Angiograms were reviewed to determine the degree of revascularization. Complete revascularization was defined as the dilitation of all stenoses >.50%. Incomplete revascularization was defined as successful dilitation of 1 or more stenoses, but with 1 or more remaining stenoses >.50%. Data were expressed as mean f standard deviation. Comparison of groups was performed with Fischer’s exact or Student’s t test. Thirty-four patients were identified who had acute myocardial infarcts after successful angioplasty. One patient who had a myocardial infarction on 2 separate occasions after 2 successful angioplasties was evaluated twice, for a total of 35 patients. The indications for angioplasty were culprit lesion of recent myocardial infarction in 22 patients (63%), unstable angina in 11 (31%) and chronic stable angina in 2 (6%). Six patients in the group with recent myocardial infarction had received thrombolytic therapy. One-vessel angioplasty was performed in 34 patients and 2-vesse1 angioplasty in 1. Angioplasty was performed on the left anterior descending artery in 13 cases, the BRIEF
REPORTS
967
right coronary artery in 1.5, the left circumflex artery with incomplete revascularization, 5 had myocardial in 7 and a saphenous vein bypass graft in 1. infarction due to occlusion of an angioplasty site, 7 Twenty patients (57%) had complete revascularhad occlusion at the site of a previously nonobstrucization after angioplasty. Fifteen patients (43%) had tive lesion and only 3 had occlusion at the site of an incomplete revascularization after angioplasty. Inundilated stenosis (Figure 2). Myocardial infarctions complete revascularization was due to a chronic total due to occlusion at an angioplasty site occurred earliocclusion in 4 patients. The remaining 11 patients er (128 f I65 days) than those due to occlusion at a with incomplete revascularization had 1 or more 50% nonangioplasty site (646 f 511 days; p
Infarction After Successful Coronary
Richard Kerensky, MD, Michael Kutcher, MD, Michael Mumma, William c. Little, MD ercutaneous transluminal coronary angioplasty is now accepted as effective therapy for selected patients with coronary artery disease.’ It has been suggested that patients with complete revascularization after coronary angioplasty have a lower incidence of subsequent myocardial infarction than those with incomplete revasculariiation. However, it is not known whether myocardial infarction after angioplasty is due to occlusion at the angioplasty site, at the site of an undilated stenosis or at the site of a previously nonobstructive lesion. In patients treated medically2$3 or with bypass surgery,4 subsequent myocardial infarction frequently occurs owing to occlusion at a site that previously had I80 with MB fraction, or the need for in-hospital coronary artery bypass graft surgery). Thirty-four patients had had 3.5 myocardial infarctions >2 weeks after successful angioplasty and had undergone another coronary angiogram within 2 days of myocardial infarction. In each case, myocardial infarction was documented by prolonged chest pain, followed by an elevated serum creatine kinase-MB. New electrocardiographic changes of myocardial infarction or new left ventricular wall motion abnormalities by ventriculography, or both, were present in all cases.
P
From the Cardiology Section, Department of Medicine, School of Medicine, Wake Forest University, Medical vard, Winston-Salem, North Carolina 27157-1045. supported in part by the Wuliger Angioplasty Research Salem, North Carolina. Manuscript received April manuscript received June 14, 1991, and accepted June
Bowman Gray Center BouleThis study was Fund, Winston1, 1991; revised 15.
MD, Robert
J. Applegate,
MD, and
Selected coronary angiograms were obtained in multiple projections. The angiogram obtained after myocardial infarction was used to determine the site of obstruction (culprit site) causing the myocardial infarction. In each patient, a new total or subtotal coronary artery occlusion was identified, corresponding to the location of the electrocardiographic abnormalities or of the new wall motion abnormality on contrast left ventriculography, or both. The coronary angiograms that had been obtained immediately before and after angioplasty were then reviewed. If the culprit site was in the same vessel as the angioplasty site and was not >2 cm proximal or distal to the angioplasty site, the myocardial infarction was classified as occurring at the angioplasty site. If the culprit site was in a different artery than the angioplasty site, or was >2 cm proximal or distal to the angioplasty site, the culprit site was classified as a nonangioplasty site. The severity of the stenosis at the culprit site after angioplasty, and at the angioplasty site before and after angioplasty was determined as a % diameter stenosis using the angiographic view in which the stenosis appeared most severe. Calipers were used to measure the stenotic area, and comparison was made with the nearest adjacent normal arterial segment. Angiograms were reviewed to determine the degree of revascularization. Complete revascularization was defined as the dilitation of all stenoses >.50%. Incomplete revascularization was defined as successful dilitation of 1 or more stenoses, but with 1 or more remaining stenoses >.50%. Data were expressed as mean f standard deviation. Comparison of groups was performed with Fischer’s exact or Student’s t test. Thirty-four patients were identified who had acute myocardial infarcts after successful angioplasty. One patient who had a myocardial infarction on 2 separate occasions after 2 successful angioplasties was evaluated twice, for a total of 35 patients. The indications for angioplasty were culprit lesion of recent myocardial infarction in 22 patients (63%), unstable angina in 11 (31%) and chronic stable angina in 2 (6%). Six patients in the group with recent myocardial infarction had received thrombolytic therapy. One-vessel angioplasty was performed in 34 patients and 2-vesse1 angioplasty in 1. Angioplasty was performed on the left anterior descending artery in 13 cases, the BRIEF
REPORTS
967
right coronary artery in 1.5, the left circumflex artery with incomplete revascularization, 5 had myocardial in 7 and a saphenous vein bypass graft in 1. infarction due to occlusion of an angioplasty site, 7 Twenty patients (57%) had complete revascularhad occlusion at the site of a previously nonobstrucization after angioplasty. Fifteen patients (43%) had tive lesion and only 3 had occlusion at the site of an incomplete revascularization after angioplasty. Inundilated stenosis (Figure 2). Myocardial infarctions complete revascularization was due to a chronic total due to occlusion at an angioplasty site occurred earliocclusion in 4 patients. The remaining 11 patients er (128 f I65 days) than those due to occlusion at a with incomplete revascularization had 1 or more 50% nonangioplasty site (646 f 511 days; p
