Chlamydia pneumoniae, Antibiotic Treatment, and Early Atherosclerosis
Petru Liuba, MD, PhD and Erkki Pesonen, MD, PhDDivision of Pediatric Cardiology, Lund University Hospital, Lund, Sweden, Petru.Liuba@pedi.lu.se
Ilari Paakkari, MD, PhD
Department of Pharmacology, University of Helsinki, Helsinki, Finland
To the Editor:
Sander et al1 state that 30-day treatment with roxithromycin attenuates the thickening of carotid artery intima-media in Chlamydia pneumoniae (Cp)–seropositive patients aged >55 years. However, no benefit was observed in the combined incidence of stroke, myocardial infarction, and vascular death. Although the antibiotic therapy reduced C-reactive protein, no reduction in the Cp antibody titers was observed. The authors propose several explanations that might account for these discrepancies.
Another explanation is that Cp might simply have little impact on the arterial wall at this age. The multifactorial etiology of an acute event complicating an atherosclerotic plaque prevails in the elderly because of the potentially increased number of additional risk factors that accumulate with age and with which Cp may interact. We believe that a more effective approach to prevent the clinical manifestations of infection-related atherosclerotic disease is to address younger populations. The following arguments support our theory.
One fundamental issue is that atherosclerosis begins in childhood, and, as shown by serial angiographic studies, 2 proceeds in steps, with episodes of vascular growth followed by incomplete healing. This emphasizes the causative role of the repeated acute inflammatory stimuli, eg, acute infection, reinfection, and/or reactivation of a chronic infection, in the early arterial disease. Indeed, such infectious phenotype is commonly encountered in childhood. This also holds true for Cp, herpes viruses, and Helicobacter pylori, which are primarily acquired in childhood. Of note, experimental studies have shown that the arterial injury—particularly in relation to Cp—is greater in younger animals and correlates with the number of repeated exposures.3 Earlier autopsy studies documented the association of acute infections with coronary intimal thickening demonstrable during the first weeks and months of life.4 Residual arterial thickening may persist beyond an acute infectious episode, as was recently demonstrated in a carotid ultrasonography study of children with acute systemic infections. 5 Antibiotic treatment during the acute infection may lessen the postinfection thickening.5
References
- Sander D, Winbeck K, Klingelhöfer J, et al. Reduced progression of early carotid atherosclerosis after antibiotic treatment and Chlamydia pneumoniae seropositivity. Circulation. 2002; 106: 2428–2433.[Abstract/ Free Full Text]
- Bruschke A, Kramer J Jr, Bal E, et al. The dynamics of progression of coronary atherosclerosis studied in 168 medically treated patients who underwent coronary arteriography three times. Am Heart J. 1989; 117: 296–305.[Medline]
- O'Connor S, Taylor C, Campbell LA, et al. Potential infectious etiologies of atherosclerosis: a multifactorial perspective. Emerg Infect Dis. 2001; 7: 780–788. [Medline]
- Pesonen E, Paakkari I, Rapola J. Infection-associated intimal thickening in the coronary arteries of children. Atherosclerosis. 1999; 142: 425–429. [CrossRef][Medline]
- Liuba P, Persson J, Luoma J, et al. Acute infections in children are accompanied by oxidative modification of LDL and decrease of HDL cholesterol, and are followed by thickening of carotid intima-media. Eur Heart J. 2003; 24: 515–521.[Abstract/Free Full Text]
