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J Am Coll Cardiol, 2003; 41:33-38 © 2003 by the American College of Cardiology Foundation |
* Cardiac Catheterization Laboratory of the Zena & Michael A. Wiener Cardiovascular Institute, Mount Sinai Hospital, New York, New York, USA
Manuscript received March 27, 2002; revised manuscript received July 18, 2002, accepted September 20, 2002.
* Reprint requests and correspondence: Dr. Samin K. Sharma, Mount Sinai Hospital, Box 1030, One Gustave Levy Place, New York, New York 10029-6574, USA.
samin.sharma{at}msnyuhealth.org
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Abstract |
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BACKGROUND: Chest pain after PCI occurs frequently even in the absence of procedural events and is considered to be due to vasospasm or coronary artery stretch. The short- and long-term significance of PPCP after otherwise successful stenting is not clear.
METHODS: We analyzed 1,362 patients undergoing coronary stenting for PPCP, procedural and in-hospital events, 30-day major adverse cardiac events, and target vessel revascularization (TVR) at 6 to 9 months.
RESULTS: There were 488 patients with PPCP and, of these, 312 patients were excluded due to procedural events. The remaining 176 patients with PPCP were compared with 874 patients without PPCP. Creatine kinase-MB isoenzyme elevation occurred in 25.6% of the PPCP group versus 9.6% of the no PPCP group (p < 0.001). Despite similar reference vessel diameter, the PPCP group had larger postprocedure minimum lumen diameter, higher stent-to-vessel ratio, and higher inflation pressure versus the no PPCP group (p < 0.01). At 30 days, the emergency room visits and repeat catheterization (16% vs. 2.7%; p < 0.001) were higher in the PPCP group versus the no PPCP group, but repeat intervention was similar. At 6- to 9-month follow-up, the TVR was significantly higher in the PPCP group compared with the no PPCP group (29.5% vs. 16.6%; p < 0.01).
CONCLUSIONS: Our analysis suggests micromyonecrosis and vessel stretch as causes of PPCP. Postprocedure chest pain is associated with similar short-term outcome as no PPCP, but has higher restenosis, perhaps mediated by deep vessel wall injury. Therefore, PPCP may identify patients at high risk for restenosis.
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Methods |
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Definitions
Postprocedure chest pain was defined as varying degrees of typical or atypical chest pain starting after PCI. Creatine kinase-MB isoenzyme measured by the Mass technique was considered normal if <16 U/l and elevated if 
16 U/l further subdivided in 1 to 3 x (16 to 48 U/l), 3 to 5 x (49 to 80 U/l), and >5 (>81 U/l) normal. Troponin I of 2.0 ng/ml was considered elevated. Significant ECG changes were ST-segment depression 1.0 mm or any ST-segment elevation. Nonspecific ECG changes were ST-segment depression <1.0 mm or T-wave changes. Procedural events were defined as transient or persistent acute closure, coronary vasospasm, side-branch occlusion of >1.0-mm size, coronary dissection type C, thromboembolism or air embolism, slow-flow or no flow, perforation, and/or prolonged hypotension. Stent-to-vessel ratio was calculated by dividing the nominal size of the maximum final stent or postdilation balloon to the reference vessel size. Angiographic lesion morphology was classified in the usual manner, including complex/thrombotic (irregular, ulcerated, haziness, or visible filling defect), calcified, and American College of Cardiology/American Heart Association (ACC/AHA) classification. Major adverse cardiac events were defined as death, Q-wave MI or large non–Q-wave MI with CK-MB >8x normal, or urgent revascularization.
Statistics
Data were entered in the interventional database (Access-based program), and the required data retrieved in Microsoft Excel format and transferred to the statistical program for analysis. Pearson’s chi-squared test was used for analysis of cross-tabulation of the categorical variables. Fisher exact test was used for 2 x 2 cross-table analysis. Student t test was used for continuous variables. Continuous variables were presented as mean ± SD. Stepwise logistic regression technique (forward logistic regression method) was employed to obtain multivariate predictors for restenosis (entry probability 0.05; removal probability 0.20). All analysis was performed using SAS/JMP (SAS Institute, Cary, North Carolina) and SPSS 10.0 (SPSS Inc., Chicago, Illinois). A p value of <0.05 was considered statistically significant.
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Results |
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Clinical follow-up
At 30 days, the number of emergency room visits (9.1% vs. 1.4%; p < 0.001), readmissions (23.9% vs. 3.0%; p < 0.001), and repeat angiography (16.0% vs. 2.7%; p < 0.001) were higher in the PPCP group versus the no PPCP group (Table 1). However, repeat intervention, subacute thrombosis, death, re-MI, and 30-day MACE were not different between the two groups. The incidence of 30-day MACE was 2.5% in the atypical PPCP versus 3.0% in the typical anginal PPCP (p = 0.16). Clinically driven coronary angiography after 30 days occurred in 36% of the PPCP patients and 32% of no PPCP patients (p = NS). At 7.4 ± 1.2 months clinical follow-up, TVR was 29.5% in the PPCP group versus 16.6% in the no PPCP group (p < 0.01). Among the PPCP patients, TVR was 22.2% in the CK-MB elevation group compared with 32% in the no CK-MB elevation group (p = 0.20). For the entire group (both PPCP and no PPCP), the incidence of TVR was 17.8% in the CK-MB elevation group versus 18.9% in the no CK-MB elevation group (p = NS). The incidence of MI and mortality was not different between the two groups (2.2% vs. 1.5%; p = 0.20).
On multivariate analysis the predictors of TVR after stenting were PPCP (OR, 3.2; 95% CI, 1.9 to 4.6), diabetes mellitus (OR, 2.6; 95% CI, 1.5 to 3.8), and lesion length >10 mm (OR, 1.9; 95% CI, 1.2 to 2.8). Postprocedure MLD was not predictive of TVR once PPCP was entered in the multivariate model.
Procedural events registry
In 312 patients with some procedural events, 94% also had PPCP with CK-MB elevation of 69.9% (1 to 3 x normal = 37.8%, 3 to 5 x normal = 22.8%, and >5 x normal = 9.3%) and TnI elevation of 77.9%. In-hospital MACE and 30-day MACE were 2.2% and 4.8%, respectively; p < 0.02 versus the PPCP or the no PPCP group. The incidence of repeat angiography in-hospital or at 30 days was 5.1% and 11.5% (lower than PPCP group, but higher than no PPCP group). At 8.2 ± 1.8 months clinical follow-up, the incidence of death and MI was 6.7% (p < 0.01 vs. PPCP or no PPCP group), and TVR was 18.9% (p = 0.007 vs. PPCP and p = 0.32 vs. no PPCP).
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Discussion |
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Mechanism of PPCP and short-term events. Incidence of periprocedural CK-MB elevation after PCI varies (10% to 30%), mostly due to various procedural events including distal embolization of plaque and thrombus, and side-branch closure especially after stenting (6–8). To evaluate the exact mechanism of periprocedural CK-MB elevation, a recent report of contrast-enhanced magnetic resonance imaging, before and after PCI, in nine patients revealed side-branch closure in five of them (55%) and distal thromboembolism in four (45%) despite very high use of GPI (8). Several studies have shown that chest pain after coronary intervention correlates with procedural complications or ongoing ischemia as reflected by elevated CK-MB (2,3,7). In our study, the incidence of CK-MB and TnI elevation after PCI in the PPCP group with no identifiable procedural events was 25.6% and 55.7%, respectively, which we hypothesized to be due to micromyonecrosis caused by distal microthromboembolism. This hypothesis can be further substantiated by the fact that more patients with acute coronary syndrome and thrombotic lesions were seen in the PPCP group and were likely to be at high-risk for distal thromboembolism, despite a higher use of GPI. Markers of vessel stretch (high inflation pressure, high stent-to-vessel ratio) were higher in both CK-MB elevation and no CK-MB elevation patients in the PPCP group. This may implicate vessel stretch contributing to distal microembolization (13).
Stent implantation results in a larger postprocedure MLD, causing a higher degree of circumferential stretching resulting in irritation of sensory nerves located in adventitia and, thereby, can cause PPCP (5). This adventitial irritation can be a plausible explanation of PPCP in our study in patients without any postprocedure enzyme elevation. Both micromyonecrosis and vessel stretch contributed to the development of PPCP, but the exact extent of contribution of individual pathophysiologic process could not be established with certainty in the present study. In the current study, occurrence of PPCP in the absence of any obvious procedural complications was benign at short-term (30 days), not associated with higher revascularization or ischemic complications, but at the cost of higher health care resource utilization. Therefore, many times PPCP can be distinguished from ongoing ischemic pain by its nature, which is often atypical, continuous, and dull aching with fluctuation in severity.
PPCP as a predictor of clinical restenosis
Larger final MLD after various interventional devices has correlated with lower restenosis based on the "bigger is better" hypothesis (15). However, deep vessel wall injury, which may occur in a subset of patients due to overexpansion of stent causing adventitial irritation with resultant PPCP, has been shown to subsequently cause intense inflammation and exaggerated intimal hyperplasia by stent struts (11,12). This process of aggressive intimal hyperplasia after stenting may explain the higher incidence of TVR in the PPCP group in our study and even offset the advantage of a larger final MLD, as the final MLD was not associated with lower restenosis on multivariate analysis in this study. Also, PPCP was the strongest independent predictor of clinical restenosis (in addition to diabetes and lesion length), while other traditional risk factors like rest angina, thrombotic lesion, LAD location, and debulking were not predictors on multivariate analysis. Another interesting observation is that the majority of patients requiring follow-up angiography had clinical restenosis in the PPCP group versus the no PPCP group, perhaps due to more symptom recurrence.
Therefore, PPCP identifies a group of patients who are at risk of developing periprocedural enzyme elevation despite GPI use and no obvious procedural complications, but have a high incidence of clinical restenosis. As previously believed, patients developing PPCP without procedural events or significant ECG changes can be safely monitored without a need for repeat coronary angiography during the initial index hospitalization. Nevertheless, these patients need to be closely followed for symptoms of early restenosis.
Procedural events registry analysis
Similar to earlier reported observation, patients undergoing PCI complicated by procedural events are associated with high short- and long-term clinical events of death or MI compared with patients without procedural events, but not associated with a higher incidence of clinical restenosis (16). This could be explained by restenosis being clinically silent in these patients, the majority of whom have suffered periprocedural MI.
Study limitations
This is a nonrandomized study with clinical follow-up, but no routine follow-up angiography. Intravascular ultrasound was not routinely performed, which could have added in understanding the mechanism and probably confirmed the theory of "vessel stretch" in causing PPCP.
Study implications
Although PPCP in the absence of procedural events is not associated with short-term clinical events, the present study identifies these patients as high-risk for periprocedural enzyme elevation and clinical restenosis. While full stent expansion and optimum stent deployment have been shown to be important for late outcome (15), our data suggest that oversizing stents and very high inflation pressures could be detrimental because of deep wall injury, causing aggressive intimal hyperplasia and restenosis. Therefore, modifying procedural factors likely to cause PPCP such as high inflation pressure, oversize stents, and using appropriate debulking may result in lower clinical restenosis. This practice is now being routinely applied in our cath lab.
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This article has been cited by other articles:
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  J. Herrmann Peri-procedural myocardial injury: 2005 update Eur. Heart J., December 1, 2005; 26(23): 2493 - 2519. [Abstract] [Full Text] [PDF]
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 W.-H. Chen, P.-Y. Lee, W. Ng, H.-F. Tse, and C.-P. Lau Is aspirin resistance or female gender associated with a high incidence of myonecrosis after nonurgent percutaneous coronary intervention? Reply J. Am. Coll. Cardiol., February 15, 2005; 45(4): 636 - 636. [Full Text] [PDF]
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