146 research outputs found

    The relationship between Chlamydophila pneumoniae IgG titer and coronary atherosclerosis

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    Background: The role of Chlamydophila pneumoniae (CP) in the progression of atherosclerosis is controversial. Also no sufficient angiographic study is available about the impact of CP infection on severity and intensity of coronary atherosclerosis. We investigated the relation between CP IgG antibody titers and severity and intensity of coronary atherosclerosis Methods: The study population consisted of 516 consecutive patients who underwent a coronary angiography. The group included 353 patients who had coronary artery disease; a control group included 163 subjects with angiographically proven normal coronary arteries. Chlamydophila pneumoniae IgG antibody titers were measured by an enzyme immunoassay method in all patients. Gensini scores and extent scores were used to evaluate the angiographic extent and severity of atherosclerosis. Results: The mean value of IgG antibody titer was 44.3 &#177; 28.8 IU/mL in the patients and 39.8 &#177; 27.4 IU/mL in the control group (p = 0.14). There was no statistically significant correlation between the Gensini scores, extent scores and CP IgG titers (Gensini score: r = +0.103, p = 0.07, extent score: r = +0.110, p = 0.31). When we grouped the patients as high (> 50 IU/mL) and low (< 50 IU/mL) IgG antibody titers, the number of diseased coronary arteries was higher in patients with high IgG antibody titers (respectively: 2.6 &#177; 1.1 vs. 2.2 &#177; 0.8, p = 0.01). While the Gensini score was significantly higher in patients with high IgG antibody titers (7.5 &#177; 4.0 vs. 6.17 &#177; 4.0, p = 0.01), the extent score did not change with IgG titers (29.8 &#177; 15.9 vs. 25.8 &#177; 15.4, p = 0.08). Conclusions: In our study, we investigated the relation between CP infection and coronary atherosclerosis and found that CP IgG antibody titers are associated with the severity of coronary stenosis at higher antibody levels. However, there is no association between CP antibody titers and clinical presentation of coronary artery disease. We suggest that CP has limited effect on coronary atherosclerosis. (Cardiol J 2008; 15: 245-251

    Long term clinical outcomes of brachytherapy, bare-metal stenting, and drug-eluting stenting for de novo and in-stent restenosis lesions: Five year follow-up

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    Background: We aimed to investigate the effects of brachytherapy, drug-eluting stent (DES) and bare metal stent (BMS) applications in the treatment of coronary artery disease, on five- -year clinical outcomes and mortality. Methods: Two hundred and seventeen patients who were treated in our clinics between January 2000 and December 2003 with brachytherapy, DES, or BMS for both de novo and in- -stent restenosis lesions were included in this cohort study. Of these 217 patients, 69 received brachytherapy, 80 were given BMS and 68 were given DES. The clinical outcomes of the patients during hospitalization and over a long-term follow-up were evaluated. Cardiovascular events, revascularizations and mortality rates were compared among the three groups over a five-year follow-up. Results: The mean age was 60.1 &#177; 9.5 years in the brachytherapy group, 55.7 &#177; 9.2 years in the BMS group, and 58.9 &#177; 9.8 years in the DES group (p = 0.44). All-cause mortality rates were 20 (29%) brachytherapy patients, 22 (27.5%) BMS patients, and four (5.9%) DES patients (p = 0.01). Cardiovascular event was the cause of death for 14 (20.3%) brachytherapy patients, 16 (20%) BMS patients and four (5.9%) DES patients (p = 0.001). All-cause mortality rates were 20 (29%) brachytherapy patients, 22 (27.5%) BMS patients and four (5.9%) DES patients. All-cause and cardiovascular mortality rates were significantly lower in the DES group compared to both the BMS and the brachytherapy groups (p = 0.01 and p = 0.001, respectively). Conclusions: DES application for in-stent restenosis and de novo lesions was superior to brachytherapy and BMS application with respect to all-cause and cardiovascular mortalities. (Cardiol J 2011; 18, 6: 654&#8211;661

    Percutaneous coronary interventions for silent ischemia after myocardial infarction

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