Clinical and angiographic risk factors associated with adverse outcomes after percutaneous coronary intervention (PCI) have been included in previous validated risk scores. Complications after PCI are known to increase mortality and morbidity but have not been included in any model. Records of 6,932 consecutive patients who underwent PCI from 2000 to 2005 were reviewed. Patients presenting with cardiogenic shock were excluded. Logistic regression and bootstrap methods were used to build an integer risk score for estimating risk of death at 1 year after PCI using baseline, angiographic, and procedural characteristics and postprocedural complications. This risk score was validated in a set of consecutive patients who underwent PCI from 2006 to 2007. The following 8 variables were significantly correlated with outcome: older age, history of diabetes mellitus, chronic renal failure, heart failure, left main coronary artery disease, lower baseline hematocrit, greater hematocrit decrease after PCI, and Thrombolysis In Myocardial Infarction grade <3 flow after PCI. In the validation population (n = 973), average receiver operating characteristic curve area was 0.836. In conclusion, we developed and validated a simple integer risk score, including postprocedural variables that closely predict long-term mortality after PCI. This model emphasizes the significant impact of complications occurring after PCI on long-term outcomes.
Several statistical models have been developed and validated to predict adverse outcomes and complications after percutaneous coronary intervention (PCI). To simplify the process of risk prediction, risk scores provide useful information from corresponding logistic regression models to clinicians. All these models include baseline clinical, angiographic, and procedural characteristics in patients presenting with acute myocardial infarction (MI) and in unselected populations undergoing PCI. Postprocedural complications such as slow coronary flow after PCI, bleeding, and renal failure have been reported to negatively affect outcomes, most significantly by increasing mortality. We recently reported the value of hematocrit before and after PCI as a strong predictor for long-term outcome. However, none of the previously validated risk scores has included postprocedural complications to assess the negative impact of such adverse events. The goals of the present study were to (1) identify preprocedural, clinical, angiographic, and procedural characteristics and postprocedural risk factors associated with long-term mortality in a consecutive series of patients undergoing contemporary PCI; (2) construct a simple risk score for prediction of long-term mortality after PCI using pre- and postprocedural risk factors; and (3) internally validate this risk score with an independent cohort of patients undergoing PCI.
Methods
An ongoing registry of catheter-based coronary procedures is maintained at our institution. For data analysis and risk score construction, we included consecutive patients who underwent PCI and completed 1-year follow-up from January 1, 2000 to December 31, 2005. Patients in cardiogenic shock before PCI were excluded from the study, because it is already known this population has a very poor prognosis. Internal validation was performed using patients who underwent PCI from January 1, 2006 to December 31, 2007. This study was approved by the institutional review board at Washington Hospital Center and MedStar Research Institute (Washington, DC).
In all cases, the interventional strategy was at the discretion of the responsible physician. Periprocedural anticoagulation was ensured using bivalirudin or unfractionated heparin to achieve an activated clotting time >250 seconds in all patients. Glycoprotein IIb/IIIa inhibitor administration was also at the operator’s discretion. All patients received aspirin 325 mg and continued this regimen indefinitely. All patients received a clopidogrel loading dose of 300 to 600 mg, followed by a maintenance dose of 75 mg indefinitely. Independent research personnel blinded to the objectives of the study conducted clinical follow-up by telephone contact or office visits. In case of hospitalization, data were obtained by systematic review of source documents. All clinical events were adjudicated by independent physicians who were not involved in the procedures.
The outcome of interest was death at 1 year. Death was defined as all-cause mortality. MI was defined as the association of ≥1 clinical and ≥1 biological criteria: acute onset chest pain and/or typical changes on electrocardiogram (ST or T-wave changes or new left bundle branch block) and an increase of troponin >99th percentile of the upper reference limit. Chronic renal insufficiency was defined as the presence of previously documented renal failure and/or a baseline serum creatinine >2.0 mg/dl. Heart failure was defined as objective evidence of fluid retention due to cardiac causes before admission. Angiographic lesions were designated as A, B or C using the American College of Cardiology/American Heart Association classification. Angiographic flow immediately after PCI was classified using Thrombolysis In Myocardial Infarction (TIMI) criteria. Hematocrit decrease was defined as the baseline value minus the nadir hematocrit level after PCI. Indications for PCI were classified as stable angina pectoris, unstable angina pectoris (defined as pain at rest or prolonged episodes of pain associated with objective evidence of ischemia), and acute MI.
Continuous variables are presented as mean ± SD, and discrete variables are summarized as frequencies and percentages. Logistic regression analysis was used to estimate odds ratios and associated p values for the primary end point. Clinically relevant baseline angiographic, procedural, and postprocedural variables were included in the initial model: age, gender, history of diabetes mellitus, chronic renal failure, heart failure, previous MI, hematocrit at baseline, presentation with acute MI, left main coronary artery disease (≥50% stenosis), multilesion PCI (>1 lesion treated), American College of Cardiology/American Heart Association type C lesion treated, presence of TIMI grade <3 flow immediately after PCI, hematocrit decrease after PCI as a continuous variable, and creatinine increase after PCI ≥1.0 mg/dl from baseline value. The bootstrap method was then used to avoid overfitting the data. One thousand bootstrap samples were used. Backward selection with a p value <0.05 for statistical significance was used to remove variables in each sample. Variables selected ≥800 times (80%) in the overall sample were included in the final model. To construct a simple risk score, variables identified through the multivariable model were assigned an integer coefficient. Integers were chosen to be approximately proportional to the estimated continuous coefficient from the logistic model. Each risk factor’s corresponding coefficient was added to obtain a final risk score from 0 to 26. For the final score, 5 strata were defined (very low, 0 to 4; low, 5 to 8; moderate, 9 to 10; high, 11 to 14; and very high, ≥15) based on predicted event rates of each score. Observed and expected numbers of events were calculated within each group. Model adequacy of the scoring system was then evaluated with the Hosmer-Lemeshow goodness-of-fit test. For the validation set of procedures the estimated probability of death at 1-year follow-up was calculated using the integer risk score. The discriminatory capacity of the model was assessed using an area under the receiver operating characteristic (ROC) curve, and goodness-of-fit was tested with the Hosmer-Lemeshow statistic (p >0.05 considered to indicate lack of deviation between the model and the observed event rates). All statistical analysis was performed using SAS 9.1 (SAS Institute, Cary, North Carolina).
Results
A total of 6,932 patients who underwent PCI from January 1, 2000 to December 31, 2005 were included in the study. At 1-year follow-up there were 383 deaths (5.6%). Mean age was 65.1 ± 11.8 years, 65.6% were men, and unstable angina pectoris was the most common indication for PCI. This set of patients represented a high-risk population, with a high prevalence of co-morbidities, as listed in Table 1 . This population also had a high prevalence of high-risk angiographic findings; most patients had multivessel disease and complex coronary lesions requiring multilesion PCI. Stenting was used in most cases, with drug-eluting stents used in 60% of procedures. Univariable associations between covariables initially included in the bootstrapping sample and death at 1 year are presented in Table 2 .
| Clinical (n = 6,932) | |
| Age (years), mean ± SD | 65.1 ± 11.8 |
| Men | 4,544 (65.6%) |
| Diabetes mellitus | 2,387 (34.8%) |
| Previous myocardial infarction | 2,398 (36.8%) |
| Previous percutaneous coronary intervention | 1,988 (29.9%) |
| Previous coronary artery bypass grafting | 1,668 (24.3%) |
| Heart failure | 1,017 (15.7%) |
| Chronic renal failure | 872 (12.7%) |
| Stable angina pectoris | 2,700 (39.2%) |
| Unstable angina pectoris | 3,433 (49.8%) |
| Acute myocardial infarction | 755 (11.0%) |
| Hematocrit (%), mean ± SD | 39.9 ± 11.9 |
| Angiographic (n = 12,411 lesions) | |
| Left main coronary artery disease | 215 (1.7%) |
| Type C–B target lesion | 10,847 (92.7%) |
| Left ventricular ejection fraction (%), mean ± SD | 48 ± 14 |
| Stenting | 10,522 (84.8%) |
| Drug-eluting stent | 7,372 (59.4%) |
| Postprocedural (n = 6,932) | |
| Number of narrowed coronary arteries, mean ± SD | 1.98 ± 0.88 |
| Multilesion percutaneous coronary intervention | 3,452 (47.5%) |
| Thrombolysis In Myocardial Infarction grade <3 flow | 264 (3.8%) |
| Hematocrit decrease (%), mean ± SD | 2.53 ± 3.5 |
| Creatinine increase >1 mg/dl | 162 (2.6%) |
| Odds Ratio | Confidence Interval | p Value | |
|---|---|---|---|
| Age (years) ⁎ | |||
| <50 | — | — | — |
| ≥50–<60 | 0.76 | 0.4–1.4 | 0.3 |
| ≥60–<70 | 1.46 | 0.9–2.5 | 0.2 |
| ≥70–<80 | 3.21 | 1.9–5.3 | <0.0001 |
| ≥80 | 4.35 | 2.6–7.4 | <0.0001 |
| Men | 0.74 | 0.59–0.92 | 0.008 |
| Diabetes mellitus | 2.44 | 1.95–3.05 | <0.0001 |
| Previous myocardial infarction | 1.85 | 1.47–1.87 | <0.0001 |
| Heart failure | 5.28 | 4.20–6.63 | <0.0001 |
| Chronic renal failure | 4.87 | 3.85–6.17 | <0.0001 |
| Presentation with acute myocardial infarction | 1.44 | 1.05–1.98 | 0.023 |
| Hematocrit at baseline (%) ⁎ | |||
| ≥40 | — | — | — |
| ≥35–<40 | 1.70 | 1.3–2.3 | 0.0002 |
| ≥30–<35 | 4.08 | 3.0–5.5 | <0.0001 |
| <30 | 5.27 | 3.4–8.1 | <0.0001 |
| Left main coronary artery disease | 2.89 | 1.88–4.45 | <0.0001 |
| Type C target lesion | 1.36 | 1.07–1.75 | 0.013 |
| Multilesion percutaneous coronary intervention | 1.20 | 0.9–1.6 | 0.16 |
| Thrombolysis In Myocardial Infarction grade <3 flow | 10.4 | 7.62–14.1 | <0.0001 |
| Hematocrit decrease (%) ⁎ | |||
| <5 | — | — | — |
| ≥5–<10 | 1.61 | 1.3–2.1 | 0.0002 |
| ≥10–<15 | 3.91 | 2.6–5.9 | <0.0001 |
| ≥15 | 6.19 | 3.4–11.4 | <0.0001 |
| Creatinine increase >1 mg/dl | 7.12 | 4.86–10.4 | <0.0001 |
⁎ Odds rates estimated point using the first category group as a reference for comparison.
Five clinical, 1 angiographic, and 2 postprocedural variables were selected in ≥80% of bootstrapping samples. Variables selected from the original model included presence of TIMI grade <3 flow after PCI, history of heart failure, left main coronary artery disease, chronic renal failure, diabetes mellitus, hematocrit decrease after PCI and hematocrit at baseline, and age ( Table 3 ). The data showed a lack of deviation from the model, as indicated by the Hosmer-Lemeshow test result (p = 0.43). Mean area under the ROC curve of the bootstrap samples was 0.818, indicating a good discriminatory capacity between patients who developed death at 1-year follow-up and those who did not.
| Variable | Integer Score | Model Coefficient | Odds Estimated | 95% Confidence Interval | p Value |
|---|---|---|---|---|---|
| Thrombolysis In Myocardial Infarction grade <3 flow | 7 | 2.035 | 7.65 | 5.3–10.9 | <0.0001 |
| Heart failure | 4 | 1.155 | 3.17 | 2.4–4.1 | <0.0001 |
| Left main coronary artery disease | 3 | 0.783 | 2.19 | 1.3–3.5 | 0.0001 |
| Chronic renal failure | 3 | 0.730 | 2.07 | 1.6–2.7 | <0.0001 |
| Diabetes mellitus | 2 | 0.527 | 1.69 | 1.3–2.2 | <0.0001 |
| Hematocrit decrease | 1 | 0.382 | 1.46 | 1.2–1.7 | <0.0001 |
| Hematocrit at baseline | 1 | 0.374 | 1.45 | 1.3–1.7 | <0.0001 |
| Age, number of decades after 40 years | 1 | 0.296 | 1.34 | 1.2–1.5 | <0.0001 |
| Intercept | N/A | −5.276 | N/A | N/A | N/A |
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