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 ≥1:32), and IgA titers (positive if ≥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 ≥1:16, adjusted OR 1.49 (P = .22); ≥1:32, OR 1.95 (P = .04); ≥1:64, OR 1.37 (P = .38); ≥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 ≥1:32 at presentation was associated with a significantly higher risk of myocardial injury complicating the presenting event. (Am Heart J 2002;144:987-94.)     

Chlamydia pneumoniae,and mycoplasma pneumoniae: Are they related to severe asthma in childhood?

Background: Mycoplasma pneumoniae and Chlamydia pneumoniae are frequent agents of acute respiratory diseases and they have been recognized as infectious triggers of asthma. Objective: To determine the frequency of these triggers and their relationship to severe asthma. Methods: 82 patients were enrolled in a prospective cross-sectional study from January 2007 to March 2013 and they were divided into three study groups: Group 1: 27 children with severe asthma, Group 2: 29 children with stable asthma and Group 3: 26 children which was the control group. Serological tests included IgG and IgM for both C. pneumoniae and M. pneumoniae. Results: Average age ± SD was 10.9 ± 2.5 for Group 1; 10.1 ± 2.9 for Group 2 and 9.9± 1.9 for Group 3 (p = 0.4). M. pneumoniae IgM was observed in 6/27 (22.2%) in Group 1, 2/29 (6.9%) in Group 2 and 0/26 in the Control Group (p = 0,01). C.pneumoniae IgM was present in 7/26 (26.9%) in Group 1, 2/29 (6.9%) in Group 2 and 0/26 in Group 3 (p = 0.005). No significant difference was observed between Group 2 and Group 3. M. pneumoniae IgG was observed in 7/27 (25.9%) in Group 1, 4/29 (13.7%) in Group 2 and 0/26 in the Control Group (p < 0,05). C.pneumoniae IgG was present in 8/26 (30.7%) in Group 1, 5/29 (17.2%) in Group 2 and 0/26 in Group 3 (p < 0,05). Conclusions: M. pneumoniae and C. pneumoniae may play a role in the development of severe asthma.     

Paraoxonase status in coronary heart disease: are activity and concentration more important than genotype?

Human serum paraoxonase (PON1) hydrolyzes oxidized lipids in low density lipoprotein (LDL) and could therefore retard the development of atherosclerosis. In keeping with this hypothesis, several case-control studies have shown a relationship between the presence of coronary heart disease (CHD) and polymorphisms at amino acid positions 55 and 192 of PON1, which we associated with a decreased capacity of PON1 to protect LDL against the accumulation of lipid peroxides, but some other studies have not. However, the PON1 polymorphisms are only 1 factor in determining the activity and concentration of the enzyme. Only 3 of the previous 18 studies directly determined PON1 activity and concentration. Therefore, we studied PON1 activity, concentration, and gene distribution in 417 subjects with angiographically proven CHD and in 282 control subjects. We found that PON1 activity and concentration were significantly lower in subjects with CHD than in control subjects (activity to paraoxon 122.8 [3.3 to 802.8] versus 214.6 [26.3 to 620.8] nmol. min(-1). mL(-1), P<0.001; concentration 71.6 [11.4 to 489.3] versus 89.1 [16.8 to 527.4] microg/mL, P<0.001). There were no differences in the PON1-55 and -192 polymorphisms or clusterin concentration between patients with CHD and control subjects. These results indicate that lower PON1 activity and concentration and, therefore, the reduced ability to prevent LDL lipid peroxidation may be more important in determining the presence of CHD than paraoxonase genetic polymorphisms.     

Lipid reduction in acute coronary syndrome: How much, when, and how?

The use of statins for secondary prevention after acute coronary syndrome is well established. In recent years, trials have investigated the dose of statins used and timing of administration. Initiation of statin therapy as early as 1 day after an acute coronary syndrome event has been shown to be effective in reducing major adverse cardiovascular events. The benefit of early statin use is linked to reduction in inflammation and increased compliance with therapy. In addition, intensive therapy further reduces events and inflammation, as reflected by decreased C-reactive protein. Given the findings of these recent studies, early and intensive lipid-lowering therapy with a statin is justified and safe.     

Platelet activating factor: A potential biomarker in acute coronary syndrome?

Platelet activating factor (PAF) is a potent pro‐inflammatory negotiator that shows distinct spectrum of biological and pharmacological effects. Importantly, it participates in a wide range of pathophysiological conditions. In cardiovascular system, PAF has been shown to have an important role in platelet and neutrophil aggregation, vascular permeability, microvascular leakage, thrombus formation, leukocyte adhesion to the endothelial cells, and initiation and progression of atherosclerosis. The purpose of this article was to review the PAF, a family of lipids that is associated with the pathology of coronary artery diseases due to their association with leading etiological mechanisms such as inflammation, endothelial dysfunction, oxidative and nitrosative stress, and platelet reactivity. This review further provides information about PAF and its potential role as a key contributor to the pathogenesis of cardiovascular disorders.     

Clinical trials versus registries in coronary revascularization: which are more relevant?

PURPOSE OF REVIEW: Clinical decision-making in coronary artery disease relies heavily on evidence-based medicine. Data from randomized controlled trials constitute the highest order of evidence and remain the standard for comparisons between therapies. While comprehensive, observational databases lack the scientific rigor of randomized controlled trials, they represent a more accurate accounting of everyday clinical care. Which data are more relevant to clinical practice?. RECENT FINDINGS: At least 11 randomized controlled trials and three meta-analyses comparing coronary artery bypass grafting and percutaneous coronary intervention exist, which all largely show no difference in death or myocardial infarction between the two treatments but more repeat revascularization with percutaneous coronary intervention. All these studies, however, are subject to the biases of trial design, which impact the external validity of the results. Analyses of four observational databases show a survival advantage in multivessel disease with coronary artery bypass grafting. Although these are reflective of real world clinical practice, they are subject to 'treatment bias', some of which can be corrected by risk adjustment. SUMMARY: Information from both randomized controlled trials and outcomes databases is necessary to determine appropriate strategy for individual patients. Reliance on data solely from either source is insufficient. It is incumbent on the treating physician to know not only the results of published studies, but also the limitations of that information.     

Is chest pain still the most important symptom of acute coronary syndrome?

BACKGROUND: Acute coronary syndrome (ACS) carries the risk of death due to electrical or haemodynamical disturbances. Thus, rapid in-hospital treatment is necessary. To achieve this, a patient, his family and his physician should correctly diagnose ACS, based mainly on clinical symptoms. AIM: To assess the symptomatology of ACS and to establish whether modern management of ischaemic heart disease did not change ACS clinical characteristics. METHODS: The study group consisted of 156 consecutive patients (96 males, mean age 65+/-15 years) admitted to hospital due to ACS. Physicians prospectively filled in a questionnaire addressing ACS symptomatology, including chest pain characteristics and clinical symptoms of painless ACS. RESULTS: Retrosternal chest pain was present in 119 (76%) patients, six (4%) patients had pain localised outside thorax (jaws or epigastric region) whereas 31 (20%) patients had painless ACS. In the latter group the most frequent symptoms were dyspnea and marked weakness. CONCLUSIONS: Chest pain remains the most frequent symptom of ACS and its prevalence is similar to that previously described in literature. Almost a quarter of patients have painless ACS; in those patients other intensive and sudden symptoms may suggest ACS.