The prevalence of Chlamydia pneumoniae in the aortic wall and in peripheral blood of patients scheduled for coronary artery bypass grafting.

Some reports confirm a potential role of Chlamydia pneumoniae (ChP) in atherogenesis. In order to explore possible association between ChP and atherosclerosis, investigations were carried out in which the frequency of ChP in the arterial wall and peripheral blood was assessed in a group of patients with chronic coronary artery disease (CAD). Fifty-seven patients were enrolled in the study, 13 women and 44 men aged 61.8±6.5 (47-74), with previously diagnosed CAD, scheduled for planned coronary artery bypass grafting due to clinical indications. Vessel specimens retrieved from the ascending aorta (as a part of routine proximal venous graft development procedure) and peripheral blood mononuclear cells (PBMCs) from venous blood were evaluated for the presence of ChP DNA. Genomic DNA was extracted from PBMCs and vessel specimens. Quantitative real-time polymerase chain reaction (qPCR) was performed to detect ChP DNA. A statistically more frequent occurrence of ChP was observed in aortic tissues compared to blood samples (70.2% vs 56.1%, respectively). Similarly, the number of ChP DNA genomic copies [n/1µg genomic DNA] was significantly higher in tissue specimens compared to blood samples (89±91 vs 41±77, respectively; p=0.0046). In patients without ChP in blood specimens, we observed significantly higher amounts of ChP in tissue specimens compared to patients with ChP in blood specimens (156±71 vs 107±88, respectively; p=0.0453). No correlation was found between the number of ChP DNA copies [n/1µg genomic DNA] in blood and in aortic specimens. The infection of ChP in the aortic wall was connected with hypercholesterolemia (p=0.029) and diabetes (p=0.03). We conclude that Chlamydia pneumoniae is a pathogen frequently occurring in the aortic wall of patients with CAD. The occurrence of ChP DNA in the aortic tissue is related to classic CAD risk factors such as diabetes and dyslipidemia.

The Correlation of PPARα Activity and Cardiomyocyte Metabolism and Structure in Idiopathic Dilated Cardiomyopathy during Heart Failure Progression.

This study aimed to define relationship between PPARα expression and metabolic-structural characteristics during HF progression in hearts with DCM phenotype. Tissue endomyocardial biopsy samples divided into three groups according to LVEF ((I) 45-50%, n = 10; (II) 30-40%, n = 15; (III) <30%, n = 15; and control (donor hearts, >60%, n = 6)) were investigated. The PPARα mRNA expression in the failing hearts was low in Group (I), high in Group (II), and comparable to that of the control in Group (III). There were analogous changes in the expression of FAT/CD36 and CPT-1 mRNA in contrast to continuous overexpression of GLUT-4 mRNA and significant increase of PDK-4 mRNA in Group (II). In addition, significant structural changes of cardiomyocytes with glycogen accumulation were accompanied by increased expression of PPARα. For the entire study population with HF levels of FAT/CD36 mRNA showed a strong tendency of negative correlation with LVEF. In conclusion, PPARα elevated levels may be a direct cause of adverse remodeling, both metabolic and structural. Thus, there is limited time window for therapy modulating cardiac metabolism and protecting cardiomyocyte structure in failing heart.

[Genetic changes and clinical management in familial hypertrophic cardiomyopathy]. / Zmiany genetyczne a obraz kliniczny rodzinnej kardiomiopatii przerostowej.

Hypertrophic cardiomyopathy (HCM) is phenotypically and genotypically heterogeneous disease of heart. Nine chromosomal loci responsible for this condition have been identified: beta-myosin heavy chain, essential and regulatory myosin light chains, troponin T and I subunits, alpha-tropomosin, cardiac myosin binding protein C, cardiac actin and titin. These genes code for proteins involved in the contraction mechanism or in the control of contraction, therefore HCM has been classified as a disease of cardiac sarcomere. Over 107 mutations have been identified. More then half of them have been detected in the beta-myosin heavy chain gene (beta-MHC). Some mutations in beta-MHC gene are associated with a benign prognosis, other are associated with high incidence of sudden cardiac death (SCD) and severe hypertrophy. Mutations in myosin binding protein C are associated with mild, delayed expression of cardiac hypertrophy and benign prognosis. Mutations in cardiac troponinT are associated with a mild degree of hypertrophy but a high incidence of SCD. Study of genes responsible for HCM will assume role in the context of clinical management of HCM, in particular regarding diagnosis and prognosis patients and families with HCM.