Stroke complicating percutaneous coronary revascularization

Absolute late loss of luminal diameter was defined as the difference between the postangioplasty and followup lesion diameters. Relative late loss was the absolute loss normalized to normal arterial diameter. Values are presented as mean + SD. A t test was used to compare 2 subgroups, and the relations between continuous variables were assessedusing the Pearson correlation coeficient. Table I summarizes the clinical, angiographic and biochemical variables for the patients studied. Lipid levels were not significantly different from those measured in 380 elective patients who underwent angiography or angioplasty, or both, in our laboratory and are not included in this report.8 The correlation coeficients between the absolute late loss of luminal diameter, and cholesterol and high-density lipoprotein cholesterol levels were 0.01 and 0.05, respectively. Similar low, nonsignificant correlation coejicients were found for the other lipoprotein subfraction when examined separately for men and women, and when relative loss of luminal diameter was used instead of absolute loss. Using clinical dichotomous definitions of restenosis(>50% diameter stenosis), the restenosis rate was not signtjicantly difSerent between patients with high-density lipoprotein cholesterol > or <40 mgldl (46 and 39%, respectively). Conflicting results have been published relating the association of lipoproteins and coronary artery restenosis after angioplasty. Austin et al5 did not show a significant correlation between the different lipoprotein subfractions and restenosis,and Arora et al9 could not predict restenosisbased on cholesterol levels at the time of angioplasty. More recently, Reis et al4 concluded that baseline and follow-up cholesterol/high-density lipoprotein ratio were strongly associatedwith clinical restenosis, and Shah and Amin suggestedthat low high-density lipoprotein cholesterol is associatedwith a higher

Stroke Complicating

Percutaneous

David L. Brown, MD, and Eric J. Topol,

restenosis rate. In both those studies,3,4angiographic data were incomplete because patients without clinical restenosis did not have angiographic follow-up. In the present angiographic study, there was no relation between any measuredlipoprotein and restenosis.The explanation for the differencesin the results of these stu’dies is not clear, but it may be related to the detinition of restenosis,the time of measurementof plasma lipids, or the inclusion of different patient groups. We did not study the effect of modifying the lipid profile on the rate of restenosis;conflicting published results have appeared,loJ1and this issue is currently being investigated in a multicenter trial.‘2

1. Ross R. The pathogen.& of atherosclerosis-an update. N Engl J Med 1986; 314:488-500. 2. Liu MW, Roubin GS, King SB. Restenosis after coronary angioplasty. Potential biologic determinants and role of intimal hyperplasia. Circulation 1989;79: 137&1387. 3. Shah PK, Amin J. Low high density lipoprotein level is associated with increased restenosis rate after coronary angioplasty. Circulan’on 199285: 1279-1285. 4. Reis GJ, Kuntz RE, Silverman DI, Pastemack RC. Effect of serum lipid levels on restenosis after coronary angioplasty. Am J Cardiol 1991;68:1431-1435, 5. Austin GE, Hollman J, Lynn MJ, Meyer B. Serum lipoprotein levels fail to predict postangioplasty recurrent coronary artery stenosis. Clew Clin J Med 1989;56: 509-5 14. 6. Blankenhom DH, N&m SA, Johnson RL, Sanmarco ME, Azen SP, CashenHemphill L. Beneficial effects of combined colestipol-niacin therapy on coronary atherosclerosis and coronary venous bypass grafts. JAMA 1987;257:3233-3240. 7. Kane JP, Malloy MKJ, Ports TA, Phillips NR, Diehl JC, Have1 RJ. Regression of coronay atherosclerosis during treatment of familial hypercholesterolemia with combined drug regimens. JAMA 1990;264:3007-3012. 8. Luria MH, Erel J, Sapo.znikov D, Gotsman MS. Cardiovascular risk factor cluswring and ratio of total cholesterol to high-density lipoprotein cholesterol in angiographically documented coronaq artery disease. Am J Cardiol 1991;67:31-36. 9. Arora RR, Konrad K, Badhwar K, Hollman J. Restenosis after transluminal coronary angioplasty: a risk factor analysis. Cather Cardiovasc Diagn 1990; 19~17-22. 10. Austin GE. Lipids and vascular restenosis. Circularion 1992;85:1613-1615. 11. Sahni R, Maria A, Gerard0 V, Vidya B. Prevention of restenosis by lovastatin after successful coronary angioplasty. Am Heart J 1991;121:160&1608. 12. Weitraub WS, Bcccwzi SJ, Brown CL, Cohen CL, Hirsch LJ, King SB, Alexrvder RW. Background and methods for the lovastatin restenosis trial after percotaneous transluminal coronary angioplasty. Am J Cmdiol 1992;70:293-299,

Coronary Revascularization

MD

ercutaneous techniques have become an important P method of myocardial revascularization. Although percutaneous transluminal coronary angioplasty was originally used in healthy patients with focal stenosisof 1 coronary artery, the indications have now expandedto include those with multivessel disease, older patients, and those with acute myocardial infarction (including those in cardiogenic shock), chronic severe impairment of left ventricular function, and obstructed bypass grafts.’ There has been a marked expansion in the indications for percutaneous revascularization and in the array of devices with which a lesion may be treated.Previous reports on complications associatedwith percutaneous revascularization generally focused on untoward events after standard balloon angioplasty of the instruFrom Desk F25, Department of Cardiology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195. Manuscript received February 25, 1993; revised manuscript received and accepted May 25, 1993.

mented vessel (in particular, abrupt closure).* Little attention has been given to stroke, which although a welldocumented complication of coronary artery bypass grafting3-5 is a rarely reported complication of angioplasty.*JjTherefore, we report, for the iirst time, the incidence, clinical characteristicsand outcome of stroke in a large, single-centerpopulation undergoing various percutaneousrevascularization techniques. All patients undergoing coronary intervention at the Cleveland Clinic Foundation are’ prospectively entered in a computerized data base and monitored throughout hospitalization for complications that are also entered in the data base. Any patient with a new neurologic dejcit after a procedure is coded as having had a cerebrovascular accident. The medical records of all patients coded as having a cerebrovascular accid(ent after a coronary intervention betweenMay 1,1991 and October 31, 1992 were reviewed. For the purpose of this study, stroke was defined as the occurrence at any BRIEF REPORTS

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TABLE I Preprocedural Characteristics Patients

Variable Age (years) Men/women (%) Hypertension (%) Diabetes mellitus (%) Hypercholesterolemia (%) Left ventricular dysfunction None-mild (%I Moderate-severe (%f Prior coronary bypass (%)

of Control and Stroke

Control Patients (n = 2,670)

Stroke Patients (n = 9)

62 73127 1,415 (53) 640 (24) 1,402 (60)

68 44156 5 (55) 4 (44) 3 (33)

2,323 (87) 347 (13) 694 (26)*

6 (66) 3 (33) 6 (66)*

*p = 0.01.

TABLE II Incidence of Stroke After Percutaneous and Surgical Coronary Revascularization

Technique PTCA* PTCA6 Multiple Percutaneous CABG” CABG3 CABG5

Year Published

Stroke incidence (%)

NHLBI Emory Cleveland Clinic

1983 1985 1993

0.06 0.03 0.3

Cleveland Clinic Johns Hopkins William Beaumont

1983 1985 1992

5.2 1.7 1.3

Institution

CABG = coronary artery bypass grafting; NHLBI = National Heart, Lung, and Blood Institute; PTCA = percutaneous transluminal coronary angioplasty.

time during hospitalization of a new neurologic deficit that persisted for >24 hours after an intervention, unless an intervening procedure was per$ormedthat in the opinion of the neurology consultant was responsiblefor the stroke. All patients underwent consultation by the neurology service and had either computed tomography or magnetic resonance imaging of the brain to confirm the diagnosis. Based on the imaging and the neurologist’s clinical impression, strokes were classtjied as ischemic or hemorrhagic. Ischemic strokes were further classified as embolic if the scan showed multiple new parenchymal defectsor a nonlacunar infarct, there was relative absence of carotid disease, there was no prolonged episode of hypotension, and there was no other explanation for the stroke.7The control population comprised all patients during the same time period who did not have a stroke (n = 2,670). Patients undergoing intervention were pretreated with 325 mg of oral aspirin and 10,000 to 15,000 units of intravenous heparin. Additional heparin was administered in doses suficient to maintain the activated clotting time at >300 seconds.In uncomplicated cases, heparin was discontinued at the end of the procedure. In procedures complicated by dissection or thrombus, heparin was continued generally for 18 hours. In vessels containing thrombus before intervention or in those developing a large thrombus burden during the procedure, intracoronary urokinase therapy was considered as either a bolus injection (250,000 to 500,000 units) or by continuous infusion (150,000 unitslhour), together with intravenous heparin, according to the preference 1208

THE AMERICAN JOURNAL OF CARDIOLOGY

VOLUME 72

of the primary operator. Patients who received a metallic stent within a native coronary or vein graft, in addition to oral aspirin and intravenous heparin, were treated with dipyridamole, wafarin and intravenous dextran. The stroke and control groups were compared using a paired t testfor age, and Fisher’s exact testfor other variables. The comparison of stroke incidence between patients who received thrombolytic therapy and those who did not was also obtained with Fisher’s exact test. A p value ~0.05 was considered signiJicant. In the 18-month period of the study, 2,679 percutaneous revascularization procedures were pegormed. These procedures comprised 3,208 balloon angioplasties, 460 directional and 276 rotational atherectomies, 80 transluminal extractions and 10.5 intracoronary stent placements. Intracoronary or intravenous urokinase was administered to 183 patients in combination with 21 percutaneous therapy. The data base contained 17 patients coded as having a postprocedural cerebrovascular accident. Review of the records of these patients resulted in the exclusion of 8. Four patients developed a neurologic deficit after coronary bypass surgery that was peqormed 1 to 14 days after a percutaneous procedure. Two patients developed seizures without focal neurologic dejicits. One patient was thought to have metabolic encephalopathy.One patient had massive bilateral subarachnoid hemorrhages found incidentally at autopsy, together with an acute infarction and right ventricular rupture, 11 days after bypass surgery and 10 after angioplasty. The remaining 9 patients form the basis of this report. The incidence of stroke after percutaneous intewention was 0.3%. In comparison with the 2,670 patients who did not develop a stroke, the 9 with stroke did not direr regarding age, gender, left ventricular&nction, or the presence of hypertension, diabetes or hypercholesterolemia (Table I). There was a trend toward an increase in strokes in women and diabetic patients. Sixtysix percent of stroke patients previously underwent bypass surgery compared with 26% of control subjects (p = 0.01) (Table I). Native vesselswere treated in 6 patients with stroke, saphenous vein grafts in 2, and both a native coronary and vein graft in 1. The procedure in patients with stroke was angioplasty alone in 7, angioplasty and directional atherectomy in 1, and angioplasty, directional atherectomy and transluminal extraction in 1. Urokinase was infused continuously overnight in the vein grafts of 2 patients with stroke. Urokinase as a bolus in the catheterization laboratory was administered in the vein graft of 1 patient and in a native coronary artery of another The incidence of stroke in patients treated with thrombolytic therapy (2.1%) was signtficantly higher than in those undergoing intervention without thrombolytic therapy (0.3%) (p
heparin infusion had an ischemic stroke due to hypotension induced by bleeding from the site of femoral access.The stroke in the other patient treated by urokinase bolus was considered to be embolic. The 5 patients with stroke who did not receive thrombolytic therapy developed strokes of ischemic origin, I of which was caused by air emboli. Symptomsfirst occurred in the catheterization laboratory in 2 of 9 patients. In 6 patients, symptoms began within 24 hours of leaving the laboratory. Symptomsin the patient with the groin hemorrhage and hypotension-induced stroke began 3 days after the procedure. Four of 9 strokes (1 hemorrhagic and 3 ischemic) resulted in in-hospital deaths. During the time of this study, 58 patients died from complications of percutaneous interventions. Thus, 7% of procedural related deaths during this period were due to stroke. Four patients needed transfer to rehabilitation facilities, because of persistent, severe neurologic impairment. Only 1 patient with a mild residual hemiparesis was su.ciently well to be discharged home. Stroke is an infrequently reported complication of percutaneouscoronary intervention. The National Heart, Lung, and Blood Institute registry of 1,500 angioplasties documented only 1 stroke for an incidence of 0.06%? In the Emory University angioplasty experience, only 1 stroke occurred in 3,500 proceduresfor an incidence of 0.03%.6We report a 0.3% incidence of stroke, which is 5 to 10 times greater than that of the aforementionedseries (Table II). A likely partial explanation for this increase is a shift in patient selection toward older patients, and those with more extensive coronary and vein graft disease,worse left ventricular function, and more unstable symptoms and hemodynamics. In the National Heart, Lung, and Blood Institute series, the average patient age was 52.5 years compared with 62.5 in this series. Only 9% of patients in the earlier series, but 26% of our patients had previous bypass surgery. Furthermore, unstable angina was present at the time of intervention in 40% of patients in the National Heart, Lung, and Blood Institute series,50% in the Emory series,and 70% of those in the Cleveland Clinic treated during the period of this study.6 It is not clear why previous bypass surgery predisposed patients to stroke. These patients may have more extensive and complex aortic atheroma that embolize during catheter or guide wire manipulations. Similarly, the explanations for the sevenfold increase in stroke in

patients treated with thrombolytic agents are not obvious. The only hemorrhagic strokes occurred in patients who received prolonged thrombolytic therapy. No patient who received urokinase had a contraindication to thrombolytic therapy. However, the prolonged adrninistration of thrombolytic therapy has not been studied sufficiently and may lead to an increased risk of stroke. As more patients with advancedcoronary diseaseare considered for revascularization with percutaneoustech.niques rather than bypass surgery, careful attention should be given to the morbidity and mortality of th’e procedure. Stroke, although an infrequent complication of percutaneousprocedures,appearsto be increasing in frequency and accounting for a significant portion of the morbidity and mortality of coronary interventions. The incidence of stroke after coronary bypass surgery ranges from 4 to 17 times as frequent (1.3 to 5.2%) as that after percutaneous revascularization (Table II) and also appearsto be increasing as older patients with more extensive diseaseare treated surgically.3-5The mortality frorn stroke after bypass surgery in a comparable patient population (35%) is similar to that in the current series (44%): Thus, because the incidence of stroke is substantially lower and the mortality similar, percutaneous revascularization appearsto be associatedwith less overall cerebrovascularmortality than is surgical revascularization. More delinitive data comparing the 2 methodls of myocardial revascularization await the results of ongoing, prospective trials. 1. Dew?. K, Holubkov R, K&y S, Cowley M, Kent K, Williams D, Myler ‘R, Faxon D, Holmes D Jr, Bourassa M, Block P, Goss&n A, Bentivoglio L, Leatherman L, Dorros G, Kiig S IU, Galicbia J, Al-Bassam M, Leon M, Robertson T, Passamani E, and the Co-Investigators of the National Heart, Lung, and Blood Institute’s Percutaneous Translutninal Coronaq Angioplasty Registry. Percutaneous trans. luminal coronary angioplasty in 1985-1986 and 1977-1981: the National Heart, Lung, and Blood Institute Regishy. N Eng2 .I Med 1988;318:265-270. 2. Dorros G, Cowley MJ, Simpson J, Bentivoglio LG, Block PC, Bowassa M, Detre K, Go&ii AJ, Gruentzig AR, Kelsey SF, Kent KM, Mock MB, Mullin SM, Myler RK, Passamani ER, Statzer SH, Williams DO. Percutaneous tmnsluminal coronary angioplasty: report of complications from the National Hart, Lung, and Bldod Institute PICA Registq. Circulation 19X3$7:723-730. 3. Gardner TJ, Homeffer PJ, Manolio TA, Pearson TA, Gott VL, Baumgartner WA, Borkon AM, Watkins L Jr, Reitz EA. Stroke following coronary artery bypass mftim: a ten-war studv. Ann Thorac Sum 1985:40:574-581. i. Breker Ad, Furlan
Long-Term Outcome of Patients with Asymptomatic Restenosis After Percutaneous Transluminal Cdronary Angioplasty Patrick C. Chenu, MD, Erwin Schroeder,

MD,

Ren6 Krkmer,

estenosiswith recurrenceof symptomsafter percutaR neous transluminal coronary angioplasty (PTCA) is

treated in most casesby a second successfulPTCA. In

From the Department of Cardiology, University Hospital of MontGodinne, B-5530 Yvoir, Belgium. Manuscript received January 19, 1993; revised manuscript received and accepted May 25, 1993.

MD,

and Baudouin Marchandise,

MD

the caseof silent restenosisin a patient previously symlptomatic, the problem is less clear. Previous reports’” with a mean follow-up of ~18 months have suggested that the prognosis of these asymptomatic patients is favorable. Between 1982 and 1989, among 1,334 PTCA procedures, we retrospectivelyfound 56 patients who met the BRIEF REPORTS

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