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CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY

Characteristics of cerebrovascular accidents after percutaneous coronary interventions

Srinivas Dukkipati, MD^*, William W. O'Neill, MD, FACC^*, Kishore J. Harjai, MD, FACC^*, William P. Sanders, MD, Datinder Deo, MD^*, Judith A. Boura, MS^*, Beth A. Bartholomew, MD^*, Michael W. Yerkey, MD^*, H. Mehrdad Sadeghi, MD^* and Joel K. Kahn, MD, FACC^*,*

^* Division of Cardiology, William Beaumont Hospital, Royal Oak, Michigan, USA
Department of Radiology, William Beaumont Hospital, Royal Oak, Michigan, USA

Manuscript received July 30, 2003; revised manuscript received October 30, 2003, accepted November 3, 2003.

^* Reprint requests and correspondence: Dr. Joel K. Kahn, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan 48073, USA.
jkahn{at}mhgpc.com

This study was presented in part as an abstract at the American College of Cardiology Scientific Sessions in Chicago, Illinois, in March 2003.

	Abstract

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OBJECTIVES: We sought to identify the incidence, predictors, and clinical implications of cerebrovascular accidents (CVAs) after percutaneous coronary interventions (PCIs).

BACKGROUND: Cerebrovascular accidents after PCI, although rare, can be devastating. Limited information exists regarding the characterization of this complication.

METHODS: The study population comprised 20,679 patients who underwent PCI between September 1993 and April 2002. A CVA was defined as a composite of transient ischemic attack (TIA) and stroke. The characteristics of those who had a periprocedural CVA were compared with those who did not.

RESULTS: A CVA occurred in 92 patients (0.30% of procedures). Of these, TIA occurred in 13 patients (0.04%) and stroke in 79 patients (0.25%). On multivariate analysis, patients with this complication more frequently had diabetes mellitus (adjusted odds ratio [OR] 1.8, 95% confidence interval [CI] 1.1 to 3.0; p = 0.013), hypertension (OR 1.9, 95% CI 1.1 to 3.3; p = 0.033), previous CVA (OR 2.3, 95% CI 1.3 to 4.0; p = 0.0059), and creatinine clearance 40 ml/min (OR 3.1, 95% CI 1.8 to 5.2; p < 0.0001). They underwent urgent or emergent procedures (OR 2.7, 95% CI 1.3 to 5.5; p = 0.0092) with more thrombolytic (OR 4.7, 95% CI 2.3 to 9.7; p < 0.0001) and intravenous heparin (OR 1.9, 95% CI 1.1 to 3.4; p = 0.030) use before PCI, and they more often required emergent intra-aortic balloon pump placement (OR 2.2, 95% CI 1.1 to 4.3; p = 0.028). On multivariate analysis, CVA was independently associated with in-hospital death (OR 7.8, 95% CI 4.2 to 14.7; p < 0.0001), acute renal failure (OR 2.8, 95% CI 1.4 to 5.7; p = 0.0042), and new dialysis (OR 3.73, 95% CI 1.01 to 13.8; p = 0.049) after PCI.

CONCLUSIONS: Cerebrovascular accidents after PCI, although rare, are associated with high rates of in-hospital death and acute renal failure, often requiring dialysis.

Abbreviations and Acronyms   CI = confidence interval   CVA = cerebrovascular accident   IABP = intra-aortic balloon pump   MI = myocardial infarction   NQMI = non–Q-wave myocardial infarction   OR = odds ratio   PCI = percutaneous coronary intervention   TIA = transient ischemic attack

	Methods

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Definition of CVA.   A CVA was defined as the onset of a new neurologic deficit that occurred anytime after PCI during the index hospitalization. If the duration of the deficit was <24 h, it was defined as a TIA. If the deficit persisted for a longer period, it was defined as a stroke. The diagnosis of CVA was made by experienced neurologists.

Study population.   The clinical, angiographic, and in-hospital outcomes of all patients who had PCI from September 1993 through April 2002 at the William Beaumont Hospital were stored prospectively in a database. The 334 PCI patients who also underwent coronary artery bypass grafting during the index hospitalization were excluded. None of the excluded patients suffered a CVA before surgery. The remaining 20,679 patients underwent 30,998 PCI procedures during this time period. In patients with multiple procedures, only data from the last visit were used in subsequent analyses. However, if a CVA occurred in a hospital stay other than the last one, then data from that visit were used instead. The clinical and angiographic features, as well as in-hospital outcomes of the patients who suffered an in-hospital CVA after PCI, were compared with those who did not.

A retrospective chart review of all CVA patients was performed to obtain information that was unavailable in the computer database. The information collected in this manner consisted of presenting with neurologic deficits, time of onset after PCI, neurologists' clinical diagnosis, type and location of CVA, duration of deficits, and disposition at hospital discharge. Most patients had computed tomography or magnetic resonance imaging studies of the brain performed and interpreted at the time of hospitalization by independent neuroradiologists. Based on their reports, another experienced neuroradiologist retrospectively classified the stroke type (ischemic or hemorrhagic) and location (e.g., frontal, parietal). If the findings reported by the independent neuroradiologists were questionable or negative, the imaging studies were reviewed again for confirmation and classification of CVA.

Other definitions.   The baseline creatinine clearance was calculated using the Cockcroft-Gault equation (7). Urgent PCI was defined as PCI in hemodynamically stable patients during hospitalization for unstable angina or non–Q-wave myocardial infarction (NQMI). Emergent PCI was defined as immediate PCI for acute ST-segment elevation myocardial infarction (MI) or a hemodynamically unstable acute coronary syndrome. Post-PCI NQMI was defined as the presence of two of the following three criteria: prolonged chest pain, elevation of serum creatine kinase 3 times the upper limit of normal, or electrocardiographic (ECG) changes suggesting ischemia. Q-wave MI after PCI was defined as the presence of two of the three aforementioned criteria and the appearance of new pathologic Q waves on 2 contiguous ECG leads. Acute renal failure after PCI was defined as 1 mg/dl elevation in serum creatinine above the baseline value before PCI.

Statistics.   All statistical analyses were performed using SAS version 8.0 software (Cary, North Carolina). Continuous variables are expressed as the mean value ± SD. Comparisons between groups were performed using the Student t test. Categorical variables are expressed as counts and percent frequencies and were compared using the chi-square test. Comparisons between the three types of CVA were made using a Kruskal-Wallis test for continuous variables and a chi-square test for categorical variables, if appropriate (expected frequency >5). Otherwise, the Fisher exact test was used. Step-down multivariate logistic regression analysis was performed to identify independent predictors of in-hospital CVA. Variables with a univariate relation (p 0.05) with CVA or thought to be important were included in the model. The C statistic was used to determine the discriminatory power of the model. The C statistic is a rank-correlation index that measures the association between predicted probabilities and observed responses. A perfect correlation would be 1. The adjusted odds ratio (OR) and 95% confidence interval (CI) were calculated for each variable in the final model. Furthermore, we performed multiple logistic regression to assess the independent impact of in-hospital CVA on clinical outcomes (death, renal insufficiency, and new dialysis).

	Results

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Baseline patient characteristics.   In-hospital CVA after PCI occurred in 92 of 20,679 patients (0.30% of procedures). Of these, a TIA occurred in 13 (0.04%) patients and stroke in 79 (0.25%) patients. The incidence of CVA after PCI was significantly higher in the period before 1998 compared with 1998 and after (0.39% vs. 0.22%, p = 0.0075). The baseline clinical differences between patients who had a periprocedural CVA and those who did not are shown in Table 1. Patients with a CVA were older females with a smaller body surface area. Those with CVA more often had a history of hypertension, diabetes mellitus, congestive heart failure, previous CVA, peripheral vascular disease, and worse baseline renal function, as measured by creatinine clearance. Cardiac catheterization was more often urgent or emergent in the CVA group, with a significantly greater prior use of intravenous heparin and thrombolytics.

View larger version (15K): [in this window] [in a new window]   Figure 1 Characteristics of cerebrovascular accidents (CVAs) after percutaneous coronary interventions (PCIs). CT = computed tomography; MRI = magnetic resonance imaging; TIA = transient ischemic attack.

Multivariate predictors of CVA.   Independent predictors of in-hospital CVA, with their respective adjusted OR and 95% CI, are shown in Figure 2. Included in the multivariate analysis were age >70 years, gender, body surface area, diabetes mellitus, hypertension, hypercholesterolemia, congestive heart failure, previous CVA or PCI, creatinine clearance 40 ml/min, peripheral vascular disease, urgent or emergent catheterization, thrombolytic or heparin use before PCI, fluoroscopy time, contrast amount, coronary perforations, no reflow, intervention to saphenous vein graft, planned or unplanned IABP use, and year prior to 1998. As there were changes in anticoagulation strategies with increasing glycoprotein IIb/IIIa use and decreasing postprocedural heparin use around 1998, this year was used to divide the study population. The C statistic for the model was 0.80, illustrating good discriminatory power. All of these variables and in-hospital CVA were used to determine the independent predictors of in-hospital death, acute renal failure, and new dialysis after PCI. A CVA was independently associated with in-hospital death (OR 7.8, 95% CI 4.2 to 14.7; p < 0.0001), acute renal failure (OR 2.8, 95% CI 1.4 to 5.7; p = 0.0042), and new dialysis (OR 3.73, 95% CI 1.01 to 13.8; p = 0.049). The C statistic was 0.91 for death, 0.92 for acute renal failure, and 0.94 for new dialysis.

View larger version (30K): [in this window] [in a new window]   Figure 2 Independent predictors of in-hospital cerebrovascular accidents (CVAs) after percutaneous coronary interventions (PCIs). CI = confidence interval; OR = odds ratio.

Discharge disposition.   Of 69 patients with CVA who survived the hospitalization, 72% had a persistent neurologic deficit at the time of hospital discharge. All of these deficits were in patients with ischemic or hemorrhagic strokes and not in TIA sufferers. Of these 69 patients, most were discharged home (43%) without any further care needed. However, skilled home care was needed in 26% of patients, nursing home or assisted living in 9%, and in-patient rehabilitation in 22%.

	Discussion

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Our study is the largest observational analysis of the incidence, predictors, and clinical implications of post-PCI CVA. In approximately 1 of 300 procedures, CVA complicates PCI. Patients with this complication had higher rates of hypertension, diabetes mellitus, previous CVA, and impaired renal function. They more frequently had cardiac catheterization for urgent or emergent reasons, with a greater prior use of thrombolytics and intravenous heparin. These patients underwent longer cardiac catheterization procedures with a greater use of contrast. Cerebrovascular events after PCI were associated with high rates of in-hospital complications, including an eight-fold adjusted risk of death, a three-fold risk of acute renal failure, and a four-fold risk of requiring dialysis. All of the deaths occurred in patients with an ischemic or hemorrhagic stroke, and TIA was associated with 0% mortality. However, the rates of acute renal failure and new dialysis were the same in all three groups. In the patients who survived the hospitalization, 72% had a persistent deficit at the time of discharge. All of the persistent deficits were once again limited to those with an ischemic or hemorrhagic stroke.

The incidence of TIA and stroke in our study is within the range reported in other studies (1,2). We found that hypertension, diabetes mellitus, impaired renal function, and a history of CVA are independently associated with periprocedural CVA. Hypertension and diabetes mellitus are both well-established risk factors for stroke (8). Although hypertension, diabetes mellitus, chronic renal dysfunction, and a history of CVA have been well established as risk factors for periprocedural stroke in patients undergoing coronary artery bypass grafting (9), they have not been reported in previous PCI studies (1,4–6,10,11). Rubenstein et al. (12) showed a borderline significant excess of stroke in those with baseline renal dysfunction, as compared with control subjects, after PCI. Patients with chronic renal insufficiency often have concomitant cardiovascular and cerebrovascular risk factors, such as diabetes mellitus and hypertension. In our analysis, even after adjusting for these risk factors, chronic renal insufficiency conferred an additional risk. The mechanism of stroke in these patients with advanced chronic renal insufficiency may be related to platelet dysfunction and bleeding diathesis, often present in this group (13).

We found that thrombolytic and intravenous heparin use before PCI was independently associated with periprocedural CVA. Thrombolytic therapy in the setting of an acute MI is a well-established risk factor for both hemorrhagic and nonhemorrhagic stroke (14,15). Even intracoronary thrombolytic therapy has been described as an independent risk factor for hemorrhagic stroke (16). However, the association between intravenous heparin and stroke is less clear. Although previous studies have found a borderline significant association, the observed differences are thought to be inconclusive because of the low number of patients involved in the studies (17–19).

After adjusting for prior treatment with thrombolytics and intravenous heparin, urgent or emergent catheterization conferred an additional risk for periprocedural CVA. Possible explanations for this include the greater propensity for hemodynamic compromise in these patients, which may increase the risk of ischemic stroke, and the less meticulous care in advancement of catheters through the aorta during urgent or emergent PCI, which increases the risk of scraping aortic plaque and increases the risk of embolization to the brain. Keeley and Grines (20) showed that scraping of aortic plaque occurs in more than 50% of percutaneous revascularization procedures. Furthermore, Eggebrecht et al. (21) showed that larger-caliber catheters scrape more aortic plaque than smaller catheters. Therefore, the increased risk of CVA after urgent or emergent procedures may reflect the scraping of more aortic plaque in these cases, thereby increasing the risk of emboli to the brain. Additionally, those with CVA also underwent longer procedures, thereby further increasing the likelihood of aortic plaque embolization. During cardiac catheterization, the amount of contrast agent used in those with CVA was significantly higher and was independently associated with this complication. This may relate to the previously described thrombogenic potential of some types of contrast agents (22). The association between IABP and periprocedural stroke has previously been reported (1,23).

We noted a temporal decrease in CVA when comparing interventions from 1998 to 2002 with those performed from 1993 to 1997 (0.22% vs. 0.39%, p = 0.0075). This trend may reflect improvement in instrumentation and techniques involved with coronary interventions over the years. Both arterial sheath and catheter sizes used in coronary interventions have decreased. Smaller catheters disrupt less aortic plaque, thereby diminishing the likelihood of embolization to the brain (20,21). Furthermore, heparin use after PCI has decreased, particularly after 1998, due to evidence for a lack of its benefit (24,25). These factors may have contributed to the observed temporal trend in CVA.

The increased rates of mortality and morbidity in patients with cerebrovascular complications after PCI are well known (1,6). However, the finding of high rates of acute renal failure and new dialysis in patients with periprocedural CVA has not previously been reported. After accounting for other baseline characteristics, including a history of baseline renal insufficiency and amount of contrast agent used, periprocedural CVA is independently associated with these adverse outcomes. Perhaps, periprocedural CVA is a marker of systemic embolization that occurs during cardiac catheterization, another manifestation of which is acute renal failure and possibly dialysis. In our study, patients who had a CVA were older and had higher rates of hypertension and peripheral vascular disease, which are both risk factors for atherosclerotic aortic plaque (26). Individuals with a higher atherosclerotic burden in the aorta have higher rates of systemic embolization, either spontaneously or from catheter manipulation (26–28). In an autopsy series of 29 patients who had cholesterol emboli to the brain, 55% also had emboli to their kidneys (29). The majority of the patients in this series underwent procedures involving manipulation of the aorta, and 10% of patients died due to complications of acute renal failure.

Study implications.   Few recommendations can be made regarding the prevention of CVA after PCI, as most risk factors are not modifiable, including a history of advanced renal insufficiency, diabetes mellitus, hypertension, and previous CVA. However, in patients with these risk factors who present with an acute MI, primary angioplasty should be favored over thrombolytics. During cardiac catheterization, careful attention should be made to minimize catheter manipulation and exchanges. The length of the procedure and amount of contrast used should also be minimized. Postprocedural anticoagulation with heparin should be eliminated in patients with uncomplicated coronary interventions. In patients who present with focal neurologic deficits soon after PCI, consideration should be given to immediate neuroimaging and percutaneous cerebral intervention.

Study limitations.   The retrospective, single-institution methodology and the absence of long-term follow-up are limitations of this study. Because the incidence of periprocedural CVA is very low, the study does not have the power to discriminate differences between TIA, ischemic stroke, and hemorrhagic stroke. The incidence of TIA is likely higher than that reported in our study, as transient neurologic deficits may not have come to the attention of physicians or may not have been identified. We recognize that the pathophysiology of CVA that occurred >48 h after the coronary intervention may not necessarily be related to the PCI. However, because a change in mental status was one of the presenting symptoms in 32% of CVA patients, this may have led to a delayed diagnosis. Furthermore, postprocedural anticoagulation may have contributed to delayed hemorrhage in CVA patients. Because of these factors, we have chosen to include all patients, regardless of the time frame of presentation.

Conclusions.   Cerebrovascular accidents complicating PCI are rare and have decreased in incidence as interventional techniques and instrumentation have improved. Many of the risk factors associated with this complication are not modifiable. With primary angioplasty replacing thrombolytics as the treatment of choice for acute MI, minimization of prolonged postprocedural anticoagulation, as well as continued improvement in interventional technology and techniques, we will likely continue to reduce this devastating complication.

	Acknowledgments

 
We thank Sue Glazier, Linda Mizejewski, and Linda McWilliams for their invaluable assistance in gathering and organizing the necessary patient information needed for the completion of this study. We also thank Sue Tomaszycki for her assistance with the illustrations in the manuscript.

	References

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