(Circulation. 1999;100:e66.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
C-Reactive Protein After First-Ever Ischemic Stroke
Department of Neurology and Neurorehabilitation, Villa Pini d'Abruzzo, Casa di Cura, Chieti, Italy
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To the Editor:
We would like to compliment Paul Ridker and colleagues on the interesting study published in Circulation1 regarding the role of inflammation in secondary prevention after myocardial infarction and add further observations. In their study, Ridker and colleagues1 found an intriguing association between evidence of inflammation after myocardial infarction and an increased risk of recurrent coronary events. Though the mechanism responsible for this increased risk was unclear, the authors' recommendation to stratify postinfarction patients into relatively high- and low-risk groups according to inflammation levels sounds appropriate considering that the relevance of inflammation in cardiovascular disease is not completely established,2 and it encourages us to study the role of C-reactive protein (CRP) levels in short-term prognosis after first-ever ischemic stroke.
We studied 30 ischemic stroke patients (10 men and 20 women) between 49 and 90 years of age (mean±SD 72±10 years) within 4 weeks of their qualifying event who were prospectively included in the Villa Pini Stroke Data Bank, Chieti, Italy. To avoid confounding factors, no patients with evidence of acute infection were included in the series. CRP samples were collected a median of 14 days from stroke event. The mean±SD Canadian Neurological Stroke Scale score was 9.0±2.7.
Increased CRP levels were detected in all examined patients. There was a notable difference in the mean level of CRP between patients and our healthy control subjects (3.8 mg/dL [95% CI 1.4 to 6.1] versus 0.3 mg/dL [95% CI 0 to 0.5]). Higher CRP levels also correlated with a significant neurological deficit (P=0.01) and a relevant disability (P=0.05), assessed with the Canadian Neurological Scale (Pearson correlation coefficient, r=-0.6) and the Barthel Index (r=-0.4), respectively. Patients with the highest CRP levels (>5.0 mg/dL) at study entry died (n=2), had severe complications after stroke (n=1; pulmonary embolism), or had no evidence of recovery (n=3) during the 2-month follow-up.
In conclusion, CRP was increased in patients with cerebral ischemia and appears to provide additional information regarding prognosis after ischemic stroke, as it appears to do after myocardial infarction. We believe that the role of CRP after ischemic stroke is far more complicated than perhaps we realize. CRP may be primarily an indicator of other vascular risk factors that are themselves related to prognosis. In our patients, CRP levels were correlated with serum ferritin levels (r=0.7; P=0.002), suggesting that the effect of CRP may rely on a positive association with serum ferritin. Iron overload may elevate the risk of atherosclerotic disease and has been identified as a risk factor and an outcome predictor in recent studies.3 4
The overall benefit of a preliminary study of CRP levels in all patients with cerebral ischemia is still undetermined, but this marker appears to provide additional information and should be included in future investigations of prognostic factors in stroke.
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1. Ridker PM, Rifai N, Pfeffer MA, Sacks FM, Moye LA, Goldman S, Flaker GC, Braunwald E, for the Cholesterol and Recurrent Events (CARE) Investigators. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Circulation. 1998;98:839–844.
2.
Tracy RP. Inflammation in
cardiovascular disease: cart, horse, or both?
Circulation. 1998;97:2000–2002.
3.
Salonen JK, Nyssönen K, Korpela H, Tuomilehto J,
Seppänen R, Salonen R. High stored iron levels are associated
with excess risk of myocardial infarction in eastern Finnish men.
Circulation. 1992;86:803–811.
4. Dàvalos A, Fernandez-Real JM, Ricart W, Soler S, Molins A, Planas E, Genís D. Iron-related damage in acute ischemic stroke. Stroke. 1994;25:1543–1546.[Abstract]
Response
Brigham and Women's Hospital, Harvard Medical School, Boston, Mass
Children's Hospital Medical Center Boston, Mass
University of Texas School of Public Health Houston, Tex
Veterans Administration Medical Center Tucson, Ariz
University of Missouri Columbia, Mo
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Inflammatory parameters may be elevated among individuals with diabetes mellitus, and Drs Choudhury and Leyva hypothesize on this basis that the elevations of C-reactive protein (CRP) and serum amyloid A (SAA) we observed among post–myocardial infarction (MI) patients in the CARE trial might be confounded by this factor. However, as described in our original article,1 adjustment for diabetes had minimal impact on risk estimates. Specifically, in logistic regression analyses, the crude relative risk (RR) of recurrent coronary events for those with SAA levels above the 90th percentile was 1.61 (P=0.03), whereas the RR after adjustment for diabetes was 1.54 (P=0.04). Similarly, the crude RR associated with baseline CRP levels above the 90th percentile was 1.62 (P=0.03), whereas the RR after adjustment for diabetes was 1.58 (P=0.04). Thus, at least among the 782 participants evaluated, we found no important differences between diabetic and nondiabetic subjects with regard to either SAA (0.29 versus 0.30 mg/dL) or CRP (0.36 versus 0.38 mg/dL). Our data do not, however, address whether or not diabetes has an important effect on inflammatory parameters among those without a prior history of MI.
The role of CRP and other inflammatory markers as risk factors for ischemic stroke is less well established. However, in the prospective Physicians' Health Study of apparently healthy men, those with elevated baseline levels of CRP had a 2-fold increase in the risk of developing thromboembolic stroke over an 8-year follow-up period (RR=1.9, 95% CI 1.1 to 3.3).2 Similar risk estimates have been reported for apparently healthy women.3 Thus, the data provided from Drs Di Napoli, Di Gianfilippo, and Bocola regarding CRP levels among patients with acute stroke syndromes add to our understanding of the role of inflammation in cerebral thrombosis.
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References |
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TopIntroductionReferencesIntroduction References |
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1. Ridker PM, Rifai N, Pfeffer MA, Sacks FM, Moye LA, Goldman S, Flaker GC, Braunwald E, for the Cholesterol and Recurrent Events (CARE) Investigators. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Circulation. 1998;98:839–844.
2.
Ridker PM, Cushman M, Stampfer MJ, Tracey RP,
Hennekens CH. Inflammation, aspirin, and the risk of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.
3.
Ridker PM, Buring JE, Shih J, Matias M, Hennekens CH.
Prospective study of C-reactive protein and the risk of future
cardiovascular events among apparently healthy women.
Circulation. 1998;98:731–733.
This article has been cited by other articles:
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  M. Di Napoli, F. Papa, and V. Bocola C-Reactive Protein in Ischemic Stroke : An Independent Prognostic Factor Stroke, April 1, 2001; 32(4): 917 - 924. [Abstract] [Full Text] [PDF]
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M. Di Napoli, F. Papa, and V. Bocola Prognostic Influence of Increased C-Reactive Protein and Fibrinogen Levels in Ischemic Stroke Stroke, January 1, 2001; 32(1): 133 - 138. [Abstract] [Full Text] [PDF]
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