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(Circulation. 2004;109:e153.)
© 2004 American Heart Association, Inc.

Correspondence

C-Reactive Protein and Lesion Morphology

Dimitris Tousoulis, MD, PhD; Christos Pitsavos, MD; Christodoulos Stefanadis, MD

Cardiology Unit, Hippokration Hospital, Athens University Medical School, Athens, Greece, tousouli{at}med.uoa.gr

To the Editor:

Sano et al¹ in a recent work using intravascular ultrasound examined the relationship between lesion morphology and C-reactive protein (CRP) in patients with acute myocardial infarction. They found that elevated CRP is related to the presence of ruptured plaque, and this may reflect the inflammatory activity of the ruptured plaque.

The importance of stenosis morphology in predicting the high-risk stenoses that will progress to acute myocardial infarction has been recognized since 1988. Stenoses with an eccentric neck and multiple irregularities are often prone to rupture leading to an acute myocardial infarction.² Furthermore, these morphological types of stenoses showed increased vasoconstrictor responses to different stimuli such as acetylcholine, serotonin, etc.^3–4

The finding of Sano et al¹ that an inflammatory marker such as CRP is significantly increased in patients with myocardial infarction and ruptured plaques indirectly indicates activation of the systemic inflammatory process. This is consistent with recent data published from our group, indicating a thermal heterogeneity within human atherosclerotic coronary arteries. This heterogeneity is detected in vivo by application of a special thermography catheter, and correlates with the levels of CRP in the plasma.⁵ Therefore, plaques prone to acute coronary syndromes showed increased vasoconstriction and thermal heterogeneity, suggesting an active dynamic inflammatory process.

However, Sano et al¹ did not examine the inflammatory process locally within the ruptured plaque. Thus, pathological studies are needed to further elucidate the crucial relationship between the morphology of the ruptured plaque and the systemic and local inflammatory processes.

References

1. Sano T, Tanaka A, Namba M, et al. C-reactive protein and lesion morphology in patients with acute myocardial infarction. Circulation. 2003; 108: 282–285.[Abstract/Free Full Text]
   
2. Ambrose J, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol. 1988; 12: 56–62.[Abstract]
   
3. Tousoulis D, Davies G, McFadden E, et al. Coronary vasomotor effects of serotonin in patients with angina: relation to coronary stenosis morphology. Circulation. 1993; 88: 1518–1526.[Abstract/Free Full Text]
   
4. Tousoulis D, Crake T, Kaski JC, et al. Enhanced vasomotor responses of complex stenoses to acetylcholine in chronic stable angina pectoris. Am J Cardiol. 1995; 75: 725–728.[CrossRef][Medline] [Order article via Infotrieve]
   
5. Stefanadis C, Diamantopoulos L, Vlachopoulos C, et al. Thermal heterogeneity within human atherosclerotic coronary arteries detected in vivo: a new method of detection by application of a special thermography catheter. Circulation. 1999; 99: 1965–1971.[Abstract/Free Full Text]
   

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Response

Atsushi Tanaka, MD; Toshihiko Sano, MD; Masashi Namba, MD; Yoshiharu Nishibori, MD; Yukio Nishida, MD; Takahiko Kawarabayashi, MD

Department of Cardiology, Baba Memorial Hospital, Sakai, Japan

Daiju Fukuda, MD; Kenei Shimada, MD; Junichi Yoshikawa, MD

Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan

We are grateful to Dr Tousoulis and colleagues for their comments regarding our manuscript.¹ Dr. Tousoulis has reported that there is a thermal heterogeneity within the coronary plaque, that this heterogeneity correlates with CRP levels, and that it is suggestive of the inflammatory process.² We consider their findings to be in support of our own conclusions. As we also cited in our manuscript, Burke et al³ have previously reported that CRP may correlate with the number of thin-capped atheromas that can be considered vulnerable plaques using immunohistochemical staining for CRP in patients who have suffered sudden death with associated severe coronary artery disease. These pathological findings, too, support our findings.

References

1. Sano T, Tanaka A, Namba M, et al. C-reactive protein and lesion morphology in patients with acute myocardial infarction. Circulation. 2003; 108: 282–285.[Abstract/Free Full Text]
   
2. Stefanadis C, Diamantopoulos L, Vlachopoulos C, et al. Thermal heterogeneity within human atherosclerotic coronary arteries detected in vivo: a new method of detection by application of a special thermography catheter. Circulation. 1999; 99: 1965–1971.[Abstract/Free Full Text]
   
3. Burke AP, Tracy RP, Kolodgie F, et al. Elevated C-reactive protein values and atherosclerosis in sudden coronary death: association with different pathologies. Circulation. 2002; 105: 2019–2023.[Abstract/Free Full Text]
   

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