Dabek J

Percutaneous coronary intervention with stent implantation in haemophilic A patient with unstable angina.

Summary.  The prevalence of coronary artery disease (CAD) and acute coronary syndromes in patients with haemophilia is much lower than in general population and there is a lack of information regarding safe interventional or surgical treatment of CAD in haemophiliacs. This report presents a case of patient with moderate haemophilia A and unstable angina pectoris, who underwent successful coronary angioplasty. The patient was pretreated with factor VIII (before and after the procedure) and the incision site was sealed with vessel closure device. Additionally, the article discusses the issue of the safety of standard, postpercutaneous coronary intervention antiplatelet therapy in patients with haemophilia.

Expression of genes encoding kinin receptors in peripheral blood mononuclear cells from patients with acute coronary syndromes

Background:  Inflammation plays a critical role in all stages of atherogenesis, including plaque destabilization leading to the rupture and local thrombosis, clinically manifested as unstable angina (UA) or myocardial infarction (MI). Recent data report enhanced expression of numerous pro‐inflammatory genes in patients with acute coronary syndrome (ACS) both in plaque and in inflammatory cells. Kinins are peptides involved in vasodilation, vascular permeability, pain and inflammation. Their effects are mediated by two receptors, B1 and B2. As the role of kinins in ACS is not clear, the aim of the study was to assess the expression of the genes encoding kinin receptors in patients with ACS.

Gene expression of kinin receptors B1 and B2 in PBMC from patients with cardiac syndrome X

Introduction. Cardiac syndrome X (CSX) is defined by typical chest pain, ST segment depression on ECG and normal coronary angiography. Pathology of CSX may involve microvascular dysfunction related to inflammation and abnormal pain sensitivity. Kinins are labile peptides participating in vasodilation, inflammation and pain. Their effects are mediated by two receptors: B1 and B2. The aim of the study was to assess gene expression of kinin receptors in peripheral blood mononuclear cells (PBMC) from patients with CSX. Methods. The study was carried out in 34 patients with cardiac syndrome X, 13 with unstable angina and ten healthy subjects. Total mRNA was extracted from PBMC and the number of mRNA copies was assessed by quantitive reverse transcriptase polymerase chain reaction. Results and Conclusion. The study showed 7-fold higher transcriptional activity of B1R in CSX vs. control and 3.5 higher vs. UA. B2R expression was 2.5-fold higher in CSX group vs. control and UA, while in the letter two groups it was similar. Such disturbance in kinin signaling may participate in local vasoconstriction and may reflect disturbances in kinin signaling leading to nociceptive disturbances in these patients.

Altered transcriptional activity of gene encoding GAPDH in peripheral blood mononuclear cells from patients with cardiac syndrome X - an important part in pathology of microvascular angina?

Introduction Cardiac syndrome X (CSX) is characterized by anginal pain with ECG suggestive of ischaemia and normal coronary arteries at angiography. Pathology of CSX involves microvascular dysfunction and is possibly linked with metabolic syndrome. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an enzyme involved in glycolysis. The GAPDH gene is a “housekeeping” gene and is used for normalization in quantitative gene expression assays. The aim of the study was to evaluate GAPDH gene expression in CSX. Material and methods The study was performed in 35 CSX patients and 10 control subjects. mRNA was extracted from peripheral blood mononuclears and the mRNA was assessed by QRT-PCR. Results GAPDH gene expression was enhanced in CSX patients vs. controls (93022 ±23837 copies/μg vs. 1067 ±240 copies/μg respectively; p < 0.001). Moreover, transcriptional activity of the GAPDH gene was heterogeneous within the CSX group. Conclusions GAPDH gene expression is markedly enhanced in CSX, which reflects carbohydrate metabolism disturbances and makes the GAPDH gene unsuitable as an endogenous control in patients with CSX.

Changes in transforming growth factor β and its receptors' mRNA expression in monocytes from patients with acute coronary syndromes.

Introduction Transforming growth factor β (TGF-β) is thought to be a vasoprotective cytokine. Numerous reports confirm its significance in blood and plaques. There is, however, a lack of information on the molecular mechanisms involving TGF-β in circulating inflammatory cells in atherogenesis. sThe aim of the study was to assess gene expression of TGF-β and its receptors in monocytes from patients with acute coronary syndromes (ACS) and the effect of standard treatment on the studied genes. Material and methods The study was carried out in 32 patients with ACS and 15 healthy subjects. Gene expression of TGF-β and receptors TGF-βRI and TGF-βRII was evaluated on day 1 and 5 in the study group and once in controls. The number of mRNA copies isolated from monocytes was assessed by QRT-PCR. Results Monocytes of ACS patients showed slightly elevated transcriptional activity of TGF-β1 and its receptors RI and RII genes (0.29 ±0.043 vs. 0.08 ±0.020, p = 0.05; 0.071 ±0.022 vs. 0.036 ±0.023, p < 0.05; 0.134 ±0.020 vs. 0.048 ±0.016, p < 0.05, respectively). After 5-day standard treatment modest reduction of TGF-βRI expression was observed. The studied genes’ expression was unrelated to ejection fraction, myocardial necrosis markers, GRACE score, time from the onset of pain to percutaneous coronary intervention and angiographic findings. Among risk factors family history of CAD was associated with increased TGF-βRI expression. Moreover, the presence of 4 or more classic risk factors correlated with higher TGF-βRI expression. Conclusions Monocytes of ACS patients demonstrate overexpression of TGF-β1 and its receptors’ genes. Five-day standard treatment downregulated the TGF-βRI gene but did not affect TGF-β1 and TGF-βRII.