Angiographic findings when chest pain recurs after successful percutaneous transluminal coronary angioplasty

AngiographicFindingsWhenChest Pain RecursAfter SuccessfulPercutaneous TransluminalCoronaryAngioplasty JOHN M. JOELSON, MD, ALBERT S. MOST, MD, and DAVID 0. WILLIAMS,

Angiographic and clinical characteristics of 102 consecutive patients who underwent coronary cineangiography for assessment of recurrent angiha pectoris after successful percutaneous transluminal coronary angioplasty (PTCA) were reviewed. Based on angiographic findings, patients were classified as havirig restenosis (n = 63), development of new, significant corotiary stenosis (n = 15), incomplete revascularization (n = 9) or no significant coronary artery disease (n = 15). Eighteen dlinical and technical characteristics of the study group were analyzed as predictors of angjographic outcome. The groups did not differ in terms of age, gender, num-

MD

ber of inflations performed, peak inflation pressure or in the pre- or post-PTCA stenosis or gradient. The time from PTCA. to onset of recurrent angina was the most powerful predictor of angiographic outcome. Patients in whom symptoms developed within 1 month of PTCA usually had incomplete revasculaiizatidn or no coronary narrowing. Restenosis was the mOst common explanation for chest pain 1 to 6 months after PTCA. Angina recurring more than 6 months after PTCA was usually due to development of new, significant coronary artery narrowings. (Am J Cardiol 1967;60:792-795)

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lthough percutaneous transluminal coronary angioplasty (PTCA) may be effective in relieving the manifestations of myocardial ischemia, angina recurs in many patients. Restenosis is often identified as the cause, yet other mechanisms may account for a significant proportion of patients having recurrent angina. We reviewed baseline characteristics and angiographic findings in consecutive patients who underwent coronary cineangiography to determine the causes of recurrent angina pectoris after successful PTCA.

was reduced to less than 50% of the luminal diameter and the patient did not have a myocardial infarction, undergo emergency coronary artery bypass g?afting or die during hospitalization. For the present study, consecutive patients in whom PTCA was successful’and who subsequently underwent coronary cineangiography for assessment of recurrent chest pain were identified and reviewed. Patients in whom chest pain developed in the first 48 hours after PTCA (i.e., during their hospitalization] were not included in the analy; sis. Thereafter, diagnostic cardiac catheterization was strongly recommended when patients sotight medical attention for recurrent symptoms suggestive of angina. The recurrence and timing of angina were documented through chart review or patient interview in each case. In patients undergoing 2 or more angiographic procedures for evaluation of chest pain after PTCA, only the first follow-up study was included in the analysis. Eligibility criteria were satisfied by 102 patients, who constitute the study group. Angioplasty procedure and adjunctive therapy: PTCA was accomplished using preformed gufding catheters via a percutaneous femoral appr0ach.l Dilatations were repeated until a satisfactorjr improvement of stenosis was achieved, with the concomitant aim of reducing the translesional gradient to less than 15 mm

Methods Patient selection: Since 1978, data of all patiehts undergoing PTCA at our institution have been prospectively entered into a computerized data bank. From February 1979 to December 1985, PTCA was attempted in 704 patients, with a success rate of 83%. Angioplasty was considered successful if the stenosis From the Division of Cardiology, Department of Medicine, Rhode Island Hospital, Brown University Program in Medicine, Providence, Rhode Island 02903. Manuscript received January 28.1987; revised manuscript received and accepted June 8,1987. Address for reprints: David 0. Williams, MD, Division of Cardiology, Rhode Island Hospital, Providence, Rhode Island 02903.

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TABLE I Variables Analyzed Angiographic Outcome

as Possible

Predictors

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Gender Male Female

Clinical variables Age, gender, history of hypertension, history of diabetes mellitus, number of diseased vessels, time from PTCA to recurrent angina, time from PTCA to follow-up angiography Procedure variables PTCA “case number,” PTCA location, number of PTCA sites, pre- and post-PTCA stenosis, pre- and post-PTCA translesional gradient, catheter type and diameter, total balloon inflation time, maximal inflation pressure

Hg.2,3 Calculation of the translesional gradient was performed in accordance with a previously described protocol.3 Treatment with antiplatelet drugs (aspirin, 325 mg, and dipyridamole, 75 mg, each 3 times daily] was initiated before the procedure and continued thereafter on an indefinite basis. Antianginal medications were not prescribed routinely. Angiographic evaluation: On the basis of findings at follow-up angiography, patients were classified as having restenosis, development of new, significant coronary stenosis, incomplete revascularization or no significant coronary artery disease. Restenosis was defined as recurrence of stenosis more than 50% in luminal diameter at the initial angioplasty site. New coronary artery disease was diagnosed if a new, significant (more than 50% luminal diameter] narrowing remote from the PTCA site was visualized on the follow-up angiogram. Incomplete revascularization was defined as the continued presence of a significant narrowing at follow-up angiography at a site that was not dilated. Finally, patients whose repeat angiograms revealed no significant coronary lesions were classified as having normal findings. In some cases, particularly those with multivessel narrowings, recurrent symptoms had more than 1 mechanism. For the purpose of this analysis, patients in whom revascularization was incomplete after successful PTCA but in whom recurrent stenosis developed at the PTCA site were classified as having restenosis [n = 8). In the 2 instances in which both restenosis and new significant disease was present, patients were excluded because we did not feel confident in identifying the mechanism of recurrent angina. Statistical analysis: Eighteen clinical and technical characteristics were analyzed as predictors of the 4 angiographic outcome groups [Table I). Univariate analysis was used initially. Chi-square analysis was used to assess differences among discrete variables. Analysis of variance was used.in assessing differences among continuous variables. A p value
WE

Voiume

60

793

(II = 102)

75% 25% 55.5 29% 6%

Age W History of hypertension History of diabetes mellitus No. of disease vessels One Two Three Time from PTCA to recurrent angina Time from PTCA to follow-up angiography Vessel dilated at PTCA LAD LGX RCA No. of PTCA sites One Two % stenosis Before PTCA After PTCA Translesional gradient Before PTCA After PTCA

63% 20% 8% 5.3 months 6.9 months

66 31 11 90 12 80.0% 25.7% 56.1 15.8

LAD = left anterior descending coronary artery; coronary artery; RCA = right coronary artery.

LCx = left circumflex

Results Baseline characteristics: Clinical and technical characteristics of the study population are listed in Table II. Mean age was 56 years; 75% were men. Onevessel coronary artery disease was present at initial angiographic evaluation in 64 patients (63%). Thirtyeight patients had multivessel narrowings. One lesion was dilated in 90 patients. Two lesions were dilated in 12 patients, with equal division between Z-vessel angioplasty and angioplasty of 2 sites within the same vessel. The mean interval from PTCA to recurrent chest pain was 5.3 months (range 1 week to 40 months). The mean interval from PTCA to follow-up angiography was 6.9 months. Angiographic outcome (Fig. 1): On the basis of findings at follow-up angiography, 63 patients (62%) were classified as having restenosis. Fifteen patients (15%] had new, significant coronary narrowings and 9 (9%] were characterized as having incomplete revascular0) 70 5 60 E 50 ;: L 0 2 2 ;

40 30 20 10 0

ANGIOGRAPHIC

FIGURE

1. Angiographic

outcome

OUTCOME

of the study

population.

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CHEST

PAIN AFTER

CORONARY

ANGIOPLASTY

TABLE III Relation Between Time from Angioplasty Recurrent Chest Pain and Angiographic Outcome Elapsed

Time

(mo)

6 Total

to

Re

New

IR

NL

1 60 2 63

0 2 13 15

6 2 1 9

5 5 5 15

IR = incomplete revascularization; New = new significant coronary lesions; NL = no significant lesions at the time of follow-up angiography; Re = restenosis.

ization. Fifteen patients (15%) had no significafit coronary narrowings at the time of follow-up angiography. Predictors of angiographic outcome: Univariate analysis revealed the following variables whose distribution across angiographic outcome group attained or approached statistical significance: time from PTCA to recurrent chest pain, time from PTCA to follow-up angiography, number of diseased vessels, PTCA l&ation and post-PTCA translesional gradient. After stepwise discriminant analysis was performed on these variables, only 2 characteristics retained significance: time from PTCA to recurrent chest pain and number of diseased vessels. The relation between time from PTCA to recurrent chest pain and angiographic outcome groups is shown in Table III. Of the 12 patients in whom recurrent chest pain developed within 1 month after angioplasty, all but 1 patient had incomplete revascularization or no significant coronary narrowing. In contrast, for recurrent angina between 1 and 6 months after PTCA, restenosis was the most common finding, present in, 60 of 69 patients (87%]. New disease and incomplete revascularization were each seen in only 3% of these patients. For patients with recurrent angina beginning more than 6 months after PTCA, new coronary artery disease was most often responsible. Restenosis in this group accounted for symptoms in only 2 of 21 patients. Angiographic outcome was also significantly related to the number of diseased vessels observed at baseline. Restenosis was the most common finding in patients with l-vessel and multivessel disease. As might be expected, patients with multivessel disease were more likely to show new disease or incomplete revascularization at follow-up. The difference was statistically significant in both univariate and multivariate analyses.

Discussion Several reports have attempted to determine the incidence of restenosis after successful PTCA, and several risk factors for development of restenosis have been identified.2-8 Little attention, however, has been given to other mechanisms of recurrent angina. We considered only patients with recurrent chest pain after successful PTCA and examined a variety of possible angiographic outcomes. Angiographic analysis revealed 4 outcomes. Restenosis was the most common finding. The higher incidence of restenosis among

symptomatic patients at follow-up is consistent with results of early reports .4,5However, 38% of symptomatic patients in the present report did not have restenosis at follow-up. Most of these remaining patients had either new, significant coronary narrowings or persistence of a significant narrowing remote from the PTCA site. Surprisingly, many patients had no significant lesions detected at follow-up PTCA. Several of these latter patients described symptoms with features atypical of angina pectoris, yet symptoms were considered serious enough to warrant angiography. Although coronary spasm has been implicated as a cause of chest pain in patients after PTCA,6 ergonovine was not administered at the time of follow-up angiography in our study. Thus, we can neilher exclude nor confirm this as a mechanism of recurrent chest pain in patients without significant fixed coronary lesions. Of several clinical and technical variables evaluated by multivariate analysis, time from successful PTCA to the onset of recurrent angina was identified as the strongest predictor of angiographic outcome. Other studies report that restenosis is most often observed in the first few months after angioplasty.5 Our results show that among patients with recurrent symptoms, angiographic restenosis most often becomes clinically manifest in the first 6 months after successful angioplasty. However, restenosis was not usually observed when recurrent angina developed within 1 month after PTCA. In this group, knowledge of the completeness of revascularization at PTCA can help differentiate patients with incomplete revascularization from those without significant coronary lesions. Finally, late recurrence of angina was most frequently attributed to development of new coronary narrowings rather than to restenosis. A limitation of the present study is the number of patients in the analysis, particularly in the groups without restenosis. Given the sample size, a potentially important variable may reach or approach significance in the univariate analysis (e.g., PTCA location or final translesional gradient) yet not attain significance in multivariate analysis. Nevertheless, sample size considerations do not detract from the importance of the 2 variables identified by multivariate analysis as predictors of angiographic outcome. Regardless of other characteristics, patients who present with recurrent angina between 1 and 6 months after PTCA have such a high likelihood of restenosis that arrangements for repeat PTCA should be considered at the time of follow-up angiography. However, those in whom symptoms develop within 1 month or more than 6 months after the original PTCA appear to be at low risk of restenosis. Prediction of the mechanism of early recurrence of angina after angioplasty is influenced in large part by the completeness of revascularization at PTCA. Acknowledgment: We express our appreciation to Seth Michelson, PhD, for assistance in the statistical analysis, Steven Reinert and Paulette Lambert for help in the data collection and Christine Abatiello for secretarial assistance in preparing the manuscript.

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References 1. Griintzig AR, Senning A, Seigenthaler WE. Nonoperative dilatation of coronary artery stenosis. N Engl J Med 1979;306:61-68. 2. Leingruber PP, Roubin GS, Hollman J, Cotsonis GA, Meier B, Douglas JS, King SB, Gruentzig AR. Restenosis after successful coronary angioplasty in patients with single vessel disease. Circulation 1986;73:710-717. 3. Hodgson Jb, Reinert S, Most AS, Williams DO. Prediction of long-term clinical outcome with final translesional pressure gradient during coronary ongiopksty. Circulation 1986;74:563-566. 4. Levine S, Ewels CJ, Rosing DR, Kent KM. Coronary ongioplasty: clinical and angiographic follow-up. Am J Cardiol 1985;55:673-676. 5. Holmes DR Jr, Vlieistra RE, Smith HC. Restenosis after percutaneous

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transluminai coronary angiopiasty (PTCA): a report from the PTCA Registry of the National Heart, Lung, and Blood Institute. Am / Cardiol1984;53:77681C. 8. Hollman J, Austin GE, Gruentzig AR, Douglas JS, King SB. Coronary artery spasm at the site of angioplasty in the first z months after successful percutaneous transluminal coronary angioplasty. [ACC 1983;2:1039-1945. 7. Leingruber PP, Roubin GS, Anderson HV, Bredlau C, Whitworth HB. Douglas JS, King SB, Gruentzig AR. Influence of intimal dissection on restenosis after successful coronary angioplasty. Circulation 1966;72:530-535. 8. Mata LA, Bosch X, David PR, Rapold HJ, Corcos T, Bourassa MG. Clinical and angiographic assessment six months after double vessel percutaneous coronary angioplasty. JACC 1985;6:1239-1244.