Periodontal destruction is associated with coronary artery disease and periodontal infection with acute coronary syndrome.

BACKGROUND: Coronary artery disease (CAD) is a highly prevalent disease with significant morbidity and mortality. Periodontal disease has been suggested to influence this disease and has been associated with CAD in some epidemiologic studies. However, this relation is still controversial. This study aimed to determine the relationship between periodontal disease measures and CAD and acute coronary syndromes (ACSs). METHODS: Two hundred one patients presenting with stable angina or ACS referred for coronary angiography underwent a periodontal assessment including evaluation of periodontal pathogens. Severity of CAD was determined by the number of obstructed coronary arteries. RESULTS: Patients with severe CAD defined by multiple vessel disease had significantly more periodontal destruction than those with mild CAD, as shown by mean clinical attachment level, a measure of chronic periodontal disease (CAL; 5.43 +/- 1.8 versus 4.85 +/- 1.6; P = 0.02), percentage of teeth with CAL >or=5 mm (82.1 +/- 23.4 versus 70.4 +/- 26.9; P = 0.002), and number of missing teeth (8.75 +/- 6.6 versus 6.76 +/- 6.6; P = 0.03). Logistic regression analysis showed that percentage of teeth with CAL >or=5 mm was significantly associated with CAD severity. Patients with ACS had significantly higher plaque scores, gingival index, and Porphyromonas gingivalis counts than stable patients. Logistic regression analysis showed that either plaque score or percentage of P. gingivalis was significantly associated with ACS. CONCLUSION: Periodontal destruction measures are significantly correlated with CAD severity, whereas periodontal infectious measures are significantly associated with clinical cardiac status.

Combined role of the Lewis antigenic system, Chlamydia pneumoniae, and C-reactive protein in unstable angina.

OBJECTIVES: The goal of this study was to assess the prognostic role of the Lewis antigenic system, Chlamydia pneumoniae (CP) seropositivity (CP+), and C-reactive protein (CRP) levels in unstable angina (UA). BACKGROUND: The role of CP infection in acute coronary syndromes is contradictory. The Lewis antigenic system, a genetically determined blood group system associated with infections and several disorders, including ischemic heart disease, might influence the susceptibility to CP infection, inflammatory response, and risk of cardiac ischemic events. METHODS: The CRP levels, Lewis antigens, and CP+ were measured in 54 patients with Braunwald's class IIIB UA. All patients were followed up for one year, and the occurrence of new coronary events (coronary death, myocardial infarction, and recurrence of instability) were recorded. RESULTS: Twenty-five coronary events occurred during follow-up. At univariate analysis CRP >3 mg/l (CRP+) (p = 0.0056), Lewis antigen b (Leb+) (p = 0.028), and the combination of Leb+ and CP+ (p = 0.006) and of CRP+ and Leb+ (p = 0.003) were associated with new coronary events, while CP+ alone was not. At multivariate analysis, CRP+ (p = 0.008) and combined Leb+CP+ (p = 0.03) were independent predictors of worse outcome. The event rate was 64% in CRP+ patients, 67% in Leb+CP+ patients, and 86% in CRP+Leb+CP+ patients. Combined Leb+CP+, but not Leb+ and CP+ alone, was related to CRP levels (p = 0.03). Among CP+ patients, CRP levels were higher in Leb+ than Leb- (p = 0.028). CONCLUSIONS: Our data demonstrate that in UA the Lewis antigenic system plays an important role, probably determining individual susceptibility to the detrimental effects of CP infection and by determining an enhanced inflammatory response.

Presence of Chlamydia pneumoniae DNA in the artery wall--biomarker of coronary artery disease.

Many authors have shown an association between Chlamydia pneumoniae (CPn) infection and coronary artery disease (CAD). However, whether CPn infection demonstrated by CPn DNA presence in the artery wall plays an important role in pathogenesis of CAD and acute coronary events (i.e. unstable angina) remains to be elucidated. One hundred and fifteen consecutive patients with CAD (51 with unstable angina and 64 with stable angina) were compared with 52 control subjects with aortic valve disease without angiographic evidence of CAD. The presence of CPn DNA in the aortic wall was assessed with nested polymerase chain reaction (PCR), and the IgM, IgG and IgA anti-CPn titres were assessed with microimmunofluorescence test. CPn DNA presence in the artery (i.e. aortic) wall was associated with 3.7-fold increased risk of CAD (95% CI 1.2-11.3, P < 0.01); however, no statistically significant difference in CPn DNA presence was demonstrated between unstable and stable angina (17.6% vs. 25%). In the CPn DNA positive group more often than in the CPn DNA negative group, serological signs of chronic infection (55.2% vs. 27%, P = 0.004) were demonstrated, whereas no statistically significant differences were demonstrated in prevalence of either acute infection (9.3% vs. 0%) or reinfection (0% vs. 0%). In conclusion, CPn DNA presence in the artery (i.e. aortic) wall was associated with CAD, therefore may be used as a biomarker for CAD. Moreover, no statistically significant differences in CPn DNA presence in the artery wall and in serology were present between unstable and stable angina; therefore, CPn infection does not seem implicated in triggering an acute coronary event.

Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials.

CONTEXT: Although Chlamydia pneumoniae infection has been associated with the initiation and progression of atherosclerosis, results of clinical trials investigating antichlamydial antibiotics as adjuncts to standard therapy in patients with coronary artery disease (CAD) have been inconsistent. OBJECTIVE: To conduct a meta-analysis of clinical trials of antichlamydial antibiotic therapy in patients with CAD. DATA SOURCES: The MEDLINE and Cochrane Central Register of Controlled Trials databases were searched from 1966 to April 2005 for English-language trials of antibiotic therapy in patients with CAD. Bibliographies of retrieved articles were searched for further studies. Presentations at major scientific meetings (2003-2004) were also reviewed. Search terms included antibacterial agents, myocardial infarction, unstable angina, and coronary arteriosclerosis. STUDY SELECTION: Eligible studies were prospective, randomized, placebo-controlled trials of antichlamydial antibiotic therapy in patients with CAD that reported all-cause mortality, myocardial infarction, or unstable angina. Of the 110 potentially relevant articles identified, 11 reports enrolling 19,217 patients were included. DATA EXTRACTION: Included studies were reviewed to determine the number of patients randomized, mean duration of follow-up, and end points. End points of interest included all-cause mortality, myocardial infarction (MI), and a combined end point of MI and unstable angina. DATA SYNTHESIS: Event rates were combined using a random-effects model. Antibiotic therapy had no impact on all-cause mortality among treated vs untreated patients (4.7% vs 4.6%; odds ratio [OR], 1.02; 95% confidence interval [CI], 0.89-1.16; P = .83), on the rates of MI (5.0% vs 5.4%; OR, 0.92; 95% CI, 0.81-1.04; P = .19), or on the combined end point of MI and unstable angina (9.2% vs 9.6%; OR, 0.91; 95% CI, 0.76-1.07; P = .25). CONCLUSION: Evidence available to date does not demonstrate an overall benefit of antibiotic therapy in reducing mortality or cardiovascular events in patients with CAD.

[Previous infection with Chlamydia pneumoniae and long-term prognosis in patients with acute coronary syndrome with non-ST segment elevation]. / Infección previa por Chlamydia pneumoniae y pronóstico a largo plazo en pacientes con síndrome coronario agudo sin elevación del segmento ST.

BACKGROUND AND OBJECTIVE: Contradictory data exists from case-control studies and in patients with stable coronary artery disease on the association of prior exposure to Chlamydia pneumoniae and cardiovascular events. We underwent a prospective study to investigate the prognostic value of C. pneumoniae seropositivity in patients with acute coronary syndromes. PATIENTS AND METHOD: In a prospective cohort of 259 consecutive patients (194 men and 65 women), mean age 65 (10 years) with non-ST elevation acute coronary syndromes, we measured serum levels of IgG antibodies directed against C. pneumoniae. RESULTS: After a mean follow-up of 28 (25, 29) months, the incidence of cardiovascular death or myocardial infarction was of 15% in seropositive patients versus 13% in seronegatives at IgG titers (1:64 (p=0.58); of 14% versus 14% at IgG titers > or = 1:128 (p=0.96); and of 14% versus 15% at IgG titers (1:256 (p=0.82). The relative risks (RR, 95% CI) of these major cardiac events adjusted for possible confounding factors were 1.11 (0.52-2.40); 1.01 (0.52-1.96); and 0.94 (0.48-1.87) respectively. CONCLUSIONS: Chlamydia pneumoniae IgG seropositivity is not associated with a higher incidence of death or myocardial infarction in patients with non-ST segment elevation acute coronary syndromes.

Association of peripheral mononuclear cells containing Chlamydia pneumoniae DNA with acute coronary syndrome and stable coronary artery disease in Japanese subjects.

To clarify the association of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells (PBMCs) with acute coronary syndrome (ACS) and stable coronary artery disease (CAD) in Japanese adults, touchdown-nested polymerase chain reaction was used to detect the presence of C. pneumoniae DNA. The prevalence of C. pneumoniae DNA in PBMCs was similar in a comparison of 88 patients (52.3%) with ACS, 164 patients (50.0%) with stable CAD, and 88 control subjects (50.0%). Temporal changes in the prevalence of C. pneumoniae DNA in PBMCs were also assessed every 3 months during a 1-year period (n=59). The prevalence was significantly higher in the first 3-month period (January through March) than in any of the other 3-month periods. In conclusion, the prevalence of C. pneumoniae DNA in PBMCs in patients with ACS or stable CAD was comparable to that in control populations. Furthermore, the presence of circulating C. pneumoniae was strongly associated with seasonal variability.

Chlamydia pneumoniae: inflammation and instability of the atherosclerotic plaque.

Coronary heart disease remains the most common cause of death in industrialized countries. Although atherosclerosis is generally asymptomatic in the early stages, progressive plaque development leads to arterial stenosis which is characterized by angina and may eventually lead to unstable angina, myocardial infarction and cardiac death. Evidence that the coagulation cascade is activated during acute coronary events has justified the use of antithrombotic agents such as aspirin, heparin and low molecular weight heparin (LMWH) in the standard management of acute coronary syndromes. The inflammatory process is also known to play a significant role in the pathogenesis of atherosclerosis, resulting in a cycle of continued inflammatory cell activation and ongoing cell recruitment. As the human leukocyte-associated antigen (HLA) system plays a key role in the regulation of the inflammatory process, the expression of HLA antigens in patients with symptomatic coronary heart disease has been investigated. These studies have demonstrated a relationship between the major histocompatibility complex (MHC) class II expression and the most severe pattern of angina refractory to conventional therapy, within the framework of a chronic infectious disease. A number of studies have documented an association between coronary heart disease and the presence of high titres of antibodies to Chlamydia pneumoniae, and this organism has been implicated in plaque instability. Such findings have stimulated interest in the role of C. pneumoniae in the pathogenesis of coronary heart disease, with a view to developing novel and effective treatment approaches. The ROXIS study showed a lower incidence of acute ischaemic events in patients with unstable angina treated with an antichlamydial antibiotic, roxithromycin.

Does chronic Chlamydia pneumoniae infection increase the risk of myocardial injury? Insights from patients with non-ST-elevation acute coronary syndromes.

BACKGROUND: Cumulative evidence suggests a positive association between Chlamydia pneumoniae (Cpn) infection and risk of future coronary events among patients with stable coronary artery disease. However, its prognostic role in unstable coronary syndromes is less well defined. Because Cpn immunoglobulin A (IgA) may be a more reliable indicator of chronic infection than immunoglobulin G (IgG), we speculated that in patients with non-ST-elevation acute coronary syndromes (ACS), this marker might serve as a more useful prognostic tool. Accordingly, we evaluated plasma samples acquired at presentation in 178 patients with ACS for a possible association between Cpn IgA titer and biochemical evidence of myocardial injury. METHODS: Cpn IgG (positive if > or =1:32), and IgA titers (positive if > or =1:16) were measured by use of the microimmunofluorescence technique in 70 patients with ACS in whom myocardial injury developed associated with their presenting events (elevated CK-MB and/or troponin I); and in 108 patients with ACS without such injury. The odds ratios (ORs) for myocardial injury associated with consecutive antibody titers were determined for each of Cpn IgG and IgA. Multiple logistic regression was applied to adjust for key baseline characteristics. RESULTS: Median age of subjects was 64 years; 63% were male and 33% were smokers. The median antibody titers among those with and without myocardial injury respectively were as follows: IgG (1:128 vs 1:128), IgA (1:32 vs <1:16, P =.2). The adjusted ORs for myocardial injury associated with consecutive IgA titers were as follows: IgA > or =1:16, adjusted OR 1.49 (P =.22); > or =1:32, OR 1.95 (P =.04); > or =1:64, OR 1.37 (P =.38); > or =1:128, OR 0.77 (P =.55). No significant trend was found for any IgG titer. CONCLUSIONS: Among patients with non-ST-elevation ACS, a Cpn IgA > or =1:32 at presentation was associated with a significantly higher risk of myocardial injury complicating the presenting event.

Relation of Chlamydia pneumoniae infection in Taiwan to angiographically demonstrated coronary artery disease and to the presence of acute myocardial infarction or unstable angina pectoris.

Reports of the association of Chlamydia pneumoniae (C. pneumoniae) infection with coronary artery disease (CAD) are scarce in the Oriental population. We therefore conducted a case-control study to explore this issue in Taiwan. There were 242 consecutive subjects (166 men and 76 women) who underwent cardiac catheterization at the National Taiwan University Hospital Cardiac Catheterization Laboratory. Patients with CAD (n = 156) had > or = 1 coronary artery lesion of > 50% diameter stenosis on angiography. Controls (n = 86) had no demonstrable CAD angiographically. Antibodies to C. pneumoniae were tested by using an enzyme-linked immunosorbent assay. The prevalence of antibodies to C. pneumoniae was as follows: immunoglobulin-G (IgG), 50% (122 of 242 patients); immunoglobulin-A (IgA), 72% (176 of 242 patients); and either IgG or IgA, 79% (192 of 242 patients ). The odds ratio (OR) for CAD with either IgG or IgA was 1.4 (95% confidence interval [CI] 0.7 to 2.7, p = 0.31). After adjusting for the known CAD risk factors, the OR decreased to 0.8 (95% CI 0.3 to 2.1, p = 0.60). The OR for unstable angina or acute myocardial infarction with the presence of either IgG or IgA was 0.5 (95% CI 0.2 to 1.1, p = 0.08) and 0.4 ( 95% CI 0.1 to 1.0, p = 0.049) after adjusting for other risk factors. These results suggest a high prevalence of C. pneumoniae infection in Taiwan. However, C. pneumoniae infection is not associated with angiographically documented CAD, and, in contrast, is a negative predictor for the development of acute coronary syndromes.

Antibodies to chlamydial lipopolysaccharides in unstable angina pectoris.

Patients with coronary artery disease frequently have elevated antibody titers against Chlamydia pneumoniae, but whether antichlamydial antibody titers are correlated with prognosis in unstable angina remains unclear. We therefore investigated the sera of 1,096 patients with unstable angina regarding immunoglobulin (Ig) IgG, IgA, and IgM antibody titers against chlamydial lipopolysaccharides (LPS) and the concentrations of C-reactive protein (CRP) and troponin T (TnT). Anti-LPS IgG titers were increased in 45% of patients at enrollment and in 48% of patients at discharge (p <0.0001). Anti-LPS IgA titers were increased in 27% of patients at enrollment and in 33% of patients at discharge (p <0.0001). Patients who subsequently died had significantly lower IgM titers at enrollment than patients without events (p = 0.016). IgG, IgA, or IgM titers did not correlate with concentrations of CRP or TnT. In this large-scale study of patients with unstable angina, we frequently found elevated antichlamydial antibody titers. Patients with low IgM anti-LPS titers were at risk for subsequent death. However, there was no correlation between antichlamydial antibody titers and CRP or TnT.

Chlamydia pneumoniae exposure and inflammatory markers in acute coronary syndrome (CIMACS).

Previous studies have shown higher levels of Chlamydia pneumoniae (C. pneumoniae, CP) antibody titers (CPIgG), C-reactive protein (CRP), and fibrinogen in patients with coronary artery disease. The role of these infectious and inflammatory markers in precipitating acute coronary syndrome (ACS) is unclear. We conducted a cross-sectional study on patients (n = 830, mean age 63 +/- 15 years, 57% male) admitted to the chest pain center of our institution. The differences in the CPIgG, CRP, and fibrinogen levels in patients who were diagnosed with ACS versus those who were not (non-ACS) were evaluated. CPIgG titers tended to be higher in the ACS group than in the non-ACS group. However, when different titers were used to define seropositivity, the difference achieved statistical significance only at the titer of > or =1:1,024 (35% vs 26%, p = 0.004). CRP (median 0.48 vs 0.33 mg/dl, p <0.0001), fibrinogen (median 317 vs 293 mg/dl, p <0.0001), and leukocyte count (median 7.7 vs 6.9 10(9)/L, p <0.0001) were higher in the ACS group. On multivariate analysis, CPIgG > or =1:1,024 (odds ratio [OR] 1.62), diabetes (OR 1.91), hypertension (OR 1.46), prior myocardial infarction (OR 1.78), smoking (OR 1.70), Caucasian race (OR 1.7), high-density lipoprotein (OR 0.98), and elevated troponin-T (OR 12.44) were the only factors independently associated with ACS. Thus, we found a strong association between high level seropositivity to CP and ACS. This may indicate recent re-infection or an exaggerated immune response to CP as an etiologic factor for ACS. This study also suggests that therapeutic interventions may need to be specifically targeted to these patients.

Infectious agents in coronary lesions obtained by endatherectomy: pattern of distribution, coinfection, and clinical findings.

BACKGROUND: Cytomegalovirus (CMV), Chlamydia pneumoniae (C. pneumoniae), and Helicobacter pylori (H. pylori) have been implicated in atherosclerosis and restenosis after angioplasty. The patterns of distribution within coronary lesions and possible coinfections of these pathogens in the coronary vasculature had not previously been evaluated. DESIGN: A prospective, observational clinical study. METHODS: Large coronary specimens (9-105 mm long) were obtained by endatherectomy of 53 patients undergoing aortocoronary bypass surgery. Samples were taken from two different sites of every lesion, resulting in a total of 106 probes. Presence of each pathogen was determined by polymerase chain reaction, subsequent hybridization, and DNA sequencing. RESULTS: Cytomegalovirus and C. pneumoniae were detected in 30 and 32% of the samples, respectively; H. pylori was not detectable. The pathogens were not homogeneously distributed. A concurrent infection with both pathogens was observed in five of 106 (5%) lesions and five of 53 (9%) patients. Restenotic lesions were more often found in specimens in which cytomegalovirus was detected (five of 16 versus two of 37). Patients with C. pneumoniae-positive coronary lesions more commonly presented with unstable angina. CONCLUSIONS: Inhomogeneous infections with cytomegalovirus and C. pneumoniae of coronary atherosclerotic lesions are found to be prevalent when serial analysis is performed. Concurrent infection with both pathogens occurs coincidentally; however, possible clinical implications of this new observation and the pathogenic impact on atherosclerosis need further investigation.

Thrombosis and coagulation abnormalities in the acute coronary syndromes.

The acute coronary syndromes, that include unstable angina, acute myocardial infarction, and many cases of sudden cardiac death, exact a considerable price on society in terms of mortality, morbidity, and health care costs. The coronary atherosclerotic lesion is often an indolent and progressive entity that can destabilize causing an acute syndrome with or without warning. The majority of acute coronary syndromes result from events such as rupture or disruption of the atherosclerotic plaque with intracoronary thrombosis and ischemia of the distal myocardium as a result. Advances in our understanding of the process underlying the acute coronary syndromes has allowed for the identification of targets and rational therapeutic strategies for the prevention and treatment of these syndromes. Many of these therapeutic strategies involve the reversal of prethrombotic forces that often coexist with coronary atherosclerosis. Even with recent advances in our approach to atherosclerosis, intracoronary thrombosis, and the resulting acute coronary syndromes, an unacceptably high event rate persists after these syndromes. Further advances in the prevention and treatment of coronary atherosclerosis and its thrombotic complications depends on a more thorough understanding of the biology of the atherosclerotic plaque and the factors which influence its stability.

Detection of Helicobacter pylori specific DNA in human atheromatous coronary arteries and its association to prior myocardial infarction and unstable angina.

BACKGROUND: Chronic infections have been proposed to play a role in the aetiology or progression of atherosclerotic plaques. Increased risk of coronary artery disease has been suggested in patients seropositive for Helicobacter pylori. AIM: To analyse coronary specimens in patients with severe (coronary artery disease) for Helicobacter pylori specific DNA. PATIENTS AND METHODS: Atherosclerotic plaques were obtained in 46 consecutive patients (9 female, 37 male, mean age 62.7+/-9.17 years) during coronary bypass procedures. Serum was analysed for IgG -/cagA-antibodies specific for Helicobacter pylori. Polymerase chain reaction and sequence analysis were used to identify bacterial DNA. Coronary artery biopsies from 19 autopsies without coronary artery disease were examined as a control group. RESULTS: Of the 46 coronary artery disease patients, 32 (69.6%) were Helicobacter pylori seropositive. Positive results for Helicobacter pylori DNA showed 18 seropositive and 4 seronegative (with anamnesis of eradication therapy). A total of 22 patients (47.8%) of the coronary artery disease group but none of controls revealed positive DNA. In the coronary artery disease group, a correlation between DNA presence and prior myocardial infarction (p=0.008) and unstable angina (p<0.001) was found. CONCLUSION: Identification of DNA in atherosclerotic plaques of patients with severe coronary artery disease supports the hypothesis that Helicobacter pylori infection may influence the development of atherosclerosis. Our results may indicate an direct involvement of Helicobacter pylori in the progression and instability of plaques in these patients.

Chlamydia pneumoniae in the atherosclerotic plaques of patients with unstable angina undergoing coronary artery bypass grafting: does it have prognostic implications?

OBJECTIVE: This study sought to evaluate the prognostic significance of the presence of DNA of Chlamydia pneumoniae in the coronary atherosclerotic lesions of patients with unstable angina. BACKGROUND: C. pneumoniae has been implicated in the pathogenesis of coronary artery disease by serological and pathological studies, but whether antichlamydial antibodies and the presence of this pathogen in the coronary atherosclerotic tissue are related to prognosis in unstable angina remains unclear. METHODS: A total 76 coronary specimens from 45 patients with unstable angina undergoing bypass surgery were subjected to nested polymerase chain reaction (PCR) for C. pneumoniae. Antichlamydial immunoglobulin G (IgG), A (IgA) and M (IgM) were also examined by an enzyme immunoassay. Patients were followed during a 2-year period to determine the incidence of adverse cardiovascular events. RESULTS: DNA of C. pneumoniae was detected in 57 (75%) of 76 atherosclerotic lesions: 39 patients showed a positive PCR result in at least one plaque. Of the 45 patients, 44 (97.7%) showed a positive serological result: IgG was positive in 39 (86.6%) patients, IgM in five (11.1%) patients and IgA in 42 (93.3%). Clinical characteristics and serologic results were similarly distributed in patients with and without infected lesions at enrollment. At least one adverse event occurred in 21 (46.6%) of the 45 patients at 2 years: death in nine (20%), recurrent angina in 12 (26.6%), revascularization in six (13.3%) and myocardial infarction in two (4.4%) patients. The composite endpoint of death, myocardial infarction, recurrent angina and revascularization at 2-year follow-up did not differ according to the PCR or serologic results. CONCLUSIONS: The presence of C. pneumoniae in coronary atherosclerotic plaques of patients with unstable angina undergoing coronary bypass grafting does not have prognostic significance. In addition, serology does not allow us to differentiate those patients with plaque infection by C. pneumoniae and also does not provide any prognostic information in these patients.

Chlamydia pneumoniae infection is associated with coronary artery disease but not implicated in inducing plaque instability.

BACKGROUND: Many authors have shown an association between Chlamydia pneumoniae (C. pneumoniae) infection and coronary artery disease. However, whether C. pneumoniae infection plays an important role in triggering an acute coronary event remains to be elucidated. METHODS: Sixty-four consecutive patients with unstable angina (group A), 56 consecutive patients with stable exertional angina (group B) and 74 control subjects (group C) were studied. The IgM, IgG and IgA anti-C. pneumoniae titers were assessed (microimmunofluorescence test Labsystem), values > or =1:16, > or =1:32 and > or =1:16 being respectively considered positive. RESULTS: IgM antibodies were found in 10.9% of group A and 12.5% of group B patients, whereas no subject of group C showed IgM titers (A vs. B, p=ns; C vs. A and B, p<0.05). Positive IgG titers were found in 76.6%, 82% and 44.6% in groups A, B and C, respectively (A vs. B, p=ns; C vs. A and B, p<0.05). Positive IgA titers were found in 62.5%, 61% and 31.1% in groups A, B and C, respectively (A vs. B, p=ns; C vs. A and B, p<0.05). Acute infection was observed in 10.9% and 12.5% of patients in groups A and B, respectively (p=ns); reinfection in 17% and 11%; no patient of the control group had signs of acute infection or reinfection. Chronic infection was observed in 34.4% and 37.5% in group A and B, respectively (p=ns). CONCLUSION: C. pneumoniae infection is associated with coronary artery disease, but no difference in serology is present between unstable and stable angina. Therefore, it does not seem implicated in triggering an acute coronary event.

Prevalence of Chlamydia pneumoniae in the atherosclerotic plaque of patients with unstable angina and its relation with serology.

BACKGROUND: Chlamydia pneumoniae has been associated with coronary artery disease by both seroepidemiological studies, and by direct detection of the micro-organism in atherosclerotic lesions. This bacteria could play a potential role in the development of acute coronary events. We examined coronary arteries from patients with unstable angina in order to verify an endovascular presence of C. pneumoniae, and to determine if there is any relationship between serology of acute infection by this pathogen and its presence inside the atherosclerotic plaque of these patients. METHODS: We analysed a total of 76 atherosclerotic plaques obtained from 45 patients who underwent coronary artery bypass surgery. In all patients unstable angina was present within the prior 3 weeks. The presence of C. pneumoniae in the plaque was determined by nested polymerase chain reaction (PCR). Antichlamydial immunoglobulin G (IgG), A (IgA) and M (IgM) was examined by microimmunofluorescence and compared to the PCR result. FINDINGS: DNA of C. pneumoniae was detected in 57 (75%) of 76 atherosclerotic lesions. In most cases (74/76: 97%) a positive IgA, IgM or IgG result was seen. Seven (12%) and 54 (94%) of the 57 PCR positive plaques came from patients with a positive IgM and IgA result, respectively. There was no statistical significant difference between PCR positive and PCR negative plaques in patients with a positive or negative serological result. Clinical characteristics were similarly distributed in patients with and without infected lesions. INTERPRETATION: C. pneumoniae organisms are frequently found in the atherosclerotic lesions of patients undergoing coronary surgery for unstable angina. Neither serological results of acute or recent infection by C. pneumoniae nor clinical characteristics are useful in predicting the individual risk of harbouring C. pneumoniae in the coronary lesions of patients with unstable angina.

Seropositivity against Chlamydia pneumoniae in patients with coronary atherosclerosis.

BACKGROUND: Results of therapy in patients with unstable coronary syndromes with antibiotics directed against Chlamydia pneumoniae have been variable, perhaps due to the heterogeneity of patients in these trials. HYPOTHESIS: The aim of the present study was to correlate the severity of coronary artery disease (CAD) with seropositivity against C. pneumoniae prospectively. METHODS: We measured the frequency of seropositivity (IgG levels > or = 1/64 and IgA levels > or = 1/16 against Chlamydia pneumoniae) in 110 patients with CAD and in 49 controls. RESULTS: As expected, traditional CAD risk factors were seen more often in patients with CAD than in controls. Mean values of total cholesterol (184 +/- 52 and 166 +/- 44 mg/dl, respectively) and triglyceride (143 +/- 60 and 112 +/- 63 mg/dl, respectively) in serum were significantly higher in patients with CAD than in controls (both p < 0.04). There were no significant differences between the two groups in serum high-density lipoprotein cholesterol (34 +/- 13 and 32 +/- 14 mg/dl, respectively) and lipoprotein (a) (Lp(a):241 +/- 247 and 223 +/- 263 mg/l, respectively) levels. The rate of IgG seropositivity was 52% (28/54) in patients with stable CAD, 41% (23/56) in patients with unstable CAD, and 35% in controls (p = NS). The rate of IgA seropositivity was 25% (14/54) in patients with stable CAD, 12% (6/49) in patients with unstable angina, and 12% (6/49) in controls (all p = NS). CONCLUSIONS: Only a small percentage of patients with CAD demonstrate seropositivity against Chlamydia pneumoniae. Antibiotic therapy in these selected patients, but not in the remaining patients, may be considered rational. These considerations may underlie the failure to see consistent benefits of antibiotic therapy in patients with CAD.

Helicobacter pylori seropositivity in patients with unstable angina.

AIM: The pathogenesis of ischemic heart diseases has been correlated, on epidemiological and pathogenetic grounds, with infections by viruses and bacteria, including Helicobacter pylori (H. pylori). THE AIM: of this study were to investigate the association of unstable angina (UA) with anti-H. pylori seropositivity in a case-control study and to search for the classic cardiovascular risk factors in both infected and uninfected patients. METHODS: We studied 32 consecutive patients (20 males, 12 females), mean age 65 years (range 42-89), with final diagnosis of UA. A total of 64 subjects (40 males, 24 females, mean age 65 years, range 42-89) admitted to the Emergency Care Unit, age and sex-matched, served as controls. The presence of hypertension, serum levels of cholesterol and glucose, plasma levels of fibrinogen, smoking habit and social class were investigated in all patients. Cases and controls were inhabitants of NorthWestern Italy, and had similar socioeconomic status as based on working place and on instruction level. H. pylori seroprevalence was assessed by the presence of antibodies (IgG) against H. pylori by means of a commercial enzyme immunosorbent assay. RESULTS: Antibodies to H. pylori were found in 26/32 (81%) of the patients and in 34/64 (53%) of the controls (p=0.007); the odds ratio was 3.82 (95% confidence interval 1.27 to 12.04). Classical cardiovascular risk factors, such as socio-economic status, did not differ among patients with and without antibodies to H. pylori. CONCLUSION: Patients with unstable angina had a significantly higher seroprevalence of anti-H. pylori than the control population. Classical risk factors for ischemic heart disease, such as the indicators of socio-economic status, were equally distributed among infected or uninfected patients with UA.

[Serologic study of atherosclerosis and its vascular complications]. / Sérologické vysetrení u aterosklerózy a jejich cévních komplikací.

Chlamydia pneumoniae (C. p.) is very frequently cited as an important factor of the origin of atherosclerosis. To confirm the diagnostic value of the serological examination the following reactions have been used: microimmunofluorescence reaction (MIF) for estimating of antibodies against major outer membrane proteins C. p. (anti-MOMP) and ELISA for detecting antibodies against the lipopolysacharides of C. p. (anti-LPS), both in IgA and IgG immunoglobulin classes of the serum. The ELISA for the detection of the IgG antibodies against chlamydial heat shock protein (cHSP60) has been used. The sera of 155 patients suffering from acute myocardial infarction (AMI) and 69 patients with unstable angina pectoris (UAP) have been examined. The heart disease has been confirmed by anamnesis, electrocardiography and coronarography. As a control group the sera from 112 persons without sings of a heart disease were examined. The antibodies against the cHSP60 have been determined only in the sera 69 patients with UAP and 49 control sera. Statistically higher occurrence of the antibodies anti-MOMP C. p. in the IgA class sera of patients suffering from UAP has been noted compared with those found in the sera of the control group (chi 2 = 18.56; p < 0.01). In the globulin IgG class of the both groups no difference has been found. The anti-LPS C. p. antibodies in the IgA as well in IgG anti-LPS classes of the patients sera with UAP were present significantly more frequently than in the control group (chi 2 = 11.49; p < 0.01, chi 2 = 4.16; p < 0.05). Similarly the incidence of the anti-LPS C. p. antibodies in the IgA class sera of 155 patients suffering from AMI was significantly higher than in the control group (chi 2 = 8.55; p < 0.01). The anti-cHSP60 antibodies have been found in 41 out of 69 patients suffering from UAP (59.4%) and in 21 of 49 control individuals (42.9%). The results seem to confirm an important role of C. p. in atherogenesis. The monitoring of the antibodies against the C. p. may supplement the diagnostics in patients suffering from UAP and AMI and the efficacy of its therapy and prevention as well.