Association of Chlamydia trachomatis, C. pneumoniae, and IL-6 and IL-8 Gene Alterations With Heart Diseases.

Atherosclerosis is a progressive disease characterized by chronic inflammation of the arterial walls, associated with genetic and infectious factors. The present study investigated the involvement of Chlamydia trachomatis and Chlamydia pneumoniae infections and immunological markers (C-reactive protein, CRP, TNF-α, IL-6, IL-8, and IL-10) in the process of atherosclerosis. The evaluation included 159 patients for surgical revascularization (CAD) and 71 patients for surgical heart valve disease (HVD) at three hospitals in Belém, Brazil. The control group (CG) comprised 300 healthy individuals. Blood samples collected before surgery were used for antibodies detection (enzyme immunoassay), CRP (immunoturbidimetry) and IL-6 levels (enzyme immunoassay). Tissue fragments (atheroma plaque, heart valve and ascending aorta) were collected during surgery and subjected to qPCR for detection of bacterial DNA. Promoter region polymorphisms of each marker and relative quantification of TNF-α, IL-8, and IL-10 gene expression were performed. Demography and social information were similar to the general population involved with both diseases. Antibody prevalence to C. trachomatis was 30.6, 20.3, and 36.7% (in the CAD, HVD, and CG, respectively) and to C. pneumoniae was 83.6, 84.5, and 80.3% (in the CAD, HVD, and CG, respectively). C. trachomatis cryptic plasmid DNA was detected in 7.4% of the samples. Frequency of IL6-174G>C polymorphism was higher in CAD and HVD than in CG regardless of previous exposure to Chlamydia. Previous C. trachomatis infection showed involvement in HVD and CAD. Significant association between disease and previous C. pneumoniae infection was found only among HVD. GG genotype of IL6-174G>C is apparently a risk factor for heart disease, whereas AT genotype of IL8-251A>T was mainly involved in valvulopathies, including patients with prior exposure to C. pneumoniae.

Association of antiphospholipid antibodies with valvulopathy in systemic lupus erythematosus: a systematic review.

Over the last few years, several studies in patients with systemic lupus erythematosus (SLE) have demonstrated an association between valvulopathy, including Libman-Sacks endocarditis (LS) and the presence of antiphospholipid antibodies (aPL), suggesting a role of these antibodies in the pathogenesis of the lesions. On the other hand, other studies found no such association. The aim of the present study is to analyze, by means of a systematic review, the existent evidences about the association between aPL and valvular lesions, including LS endocarditis, in patients with SLE. The information was obtained through searches for articles in the MEDLINE (1966 to 2010), SciELO, and LILACS databases, using the following key words: "Libman-Sacks endocarditis", "antiphospholipid and Libman-Sacks", "antiphospholipid and valvular heart disease", "antiphospholipid and verrucous endocarditis", "antiphospholipid and heart", "antiphospholipid and valvular vegetations", "anticardiolipin antibodies" and the corresponding translations in Portuguese. Twenty articles were found, which evaluated the association between the presence of aPL and valvulopathy. Thirteen of these studies evaluated the association of aPL with the LS lesion. Of the 20 articles, 15 demonstrated a positive association between aPL and valvular lesions, whereas 5 articles demonstrated that there was no association. Evidence of an association between the presence of aPL and valvular lesion was demonstrated in the majority of studies. Nevertheless, the possible role of these antibodies in the etiopathogenesis of the lesion has not yet been proved.

The Heart and APS.

The heart is a target organ in antiphospholipid syndrome (APS). Endocardial disease, intracardiac thrombosis, myocardial involvement including coronary heart disease and microvascular thrombosis, as well as pulmonary hypertension have all been described in APS patients. Valvular involvement is the most common manifestation with a prevalence of 82% detected by transesophageal echocardiography. Symmetrical, nodular thickening of the mitral and/or aortic valves is characteristic. Anticoagulant/antiplatelet treatment is ineffective in terms of valvular lesion regression. Some patients require cardiac valve replacement. However, patients with APS have shown an increased perioperative morbidity and mortality. Intracardiac thrombosis, although a rare complication, can cause pulmonary and systemic emboli. Differential diagnosis with myxoma may be very difficult.