The beneficial impact of cardiac rehabilitation on obstructive sleep apnea in patients with coronary artery disease.

STUDY OBJECTIVES: To assess the impact of cardiac rehabilitation for decreasing sleep-disordered breathing in patients with coronary artery disease. METHODS: The study included 121 patients aged 60.01 ± 10.08 years, 101 of whom were men, with an increased pretest probability of OSA. The cardiac rehabilitation program lasted 21-25 days. The improvement in cardiorespiratory fitness was assessed using the changes in peak metabolic equivalents, the maximal heart rate achieved, the proportion of the age- and sex-predicted maximal heart rate, and the Six-Minute Walk Test distance. Level 3 portable sleep tests with respiratory event index assessments were performed in 113 patients on admission and discharge. RESULTS: Increases were achieved in metabolic equivalents (Δ1.20; 95% confidence interval [CI], 0.95-1.40; P < .0001), maximal heart rate (-Δ7.5 beats per minute; 95% CI, 5.00-10.50; P < .0001), proportion of age- and sex-predicted maximal heart rate (Δ5.50%; 95% CI, 4.00-7.50; P < .0001), and the Six-Minute Walk Test distance (Δ91.00 m; 95% CI, 62.50-120.00; P < .0001). Sleep-disordered breathing was diagnosed in 94 (83.19%) patients: moderate in 28 (24.8%) patients and severe in 27 (23.9%) patients, with a respiratory event index of 19.75 (interquartile range, 17.20-24.00) and 47.50 (interquartile range, 35.96-56.78), respectively. OSA was dominant in 90.40% of patients. The respiratory event index reduction achieved in the sleep-disordered breathing group was -Δ3.65 (95% CI, -6.30 to -1.25; P = .003) and was in parallel to the improvement in cardiorespiratory fitness in the subgroups with the highest effort load and with severe sleep-disordered breathing: -Δ6.40 (95% CI, -11.40 to -1.90; P = .03) and -Δ11.00 (95% CI, -18.65 to -4.40; P = .003), respectively. CONCLUSIONS: High-intensity exercise training during cardiac rehabilitation resulted in a significant decrease in OSA, when severe, in parallel with an improvement in cardiorespiratory fitness in patients with coronary artery disease.

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.

Transcriptional activity of genes encoding Transforming Growth Factor beta and its receptors in peripheral blood mononuclear cells from patients with acute coronary syndromes.

BACKGROUND: Recent data report altered gene expression of numerous pro- and anti-inflammatory factors involved in pathology of acute coronary syndromes (ACS). Transforming growth factor beta (TGFbeta) signaling is engaged in a wide range of processes. Its effect on vessels seems to be protective due to its anti-inflammatory and anti-atherogenic action. However, it also seems to be engaged in such negative effects as neointima formation and fibrosis. The aim of the study was to assess the expression of the genes encoding TGFbeta and its receptors (type I, II, and III) in patients with ACS. METHODS: The study was carried out on 24 patients with acute coronary syndrome (7 with unstable angina [UA] and 17 with myocardial infarction [MI]) and 10 age-matched healthy subjects (control). To evaluate gene expression of TGFbeta and its receptors total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR). RESULTS: MI and UA patients demonstrated significantly lower TGFbeta gene expression compared to control (2789+/-418 c/microg vs. 20262+/-2548 c/microg; p<0.001, and 3390+/-518 c/microg vs. 20262+/-2548 c/microg; p<0.001, respectively), as well as noticeably lower transcriptional activity of genes encoding its type I (3295+/-447 c/microg vs. 12859+/-1929 c/microg; p<0.001, and 3258+/-721 c/microg vs. 12859+/-1929 c/microg; p<0.01, respectively) and type II receptors (2364+/-346 c/microg vs. 19003+/-2357 c/microg; p<0.001, and 2680+/-522 c/microg vs. 19003+/-2357 c/microg; p<0.01, respectively). Also, gene expression of the type III receptor was inferior in the studied group compared to the control, although the difference was significant only for the UA group vs. control. Expressions of the studied genes did not differ between patients with MI and those with UA. CONCLUSION: Our report shows that the decreased activity of TGFbeta in patients with ACS is at least partly due altered transcriptional activity of genes encoding both TGFbeta and its receptors, what may be responsible for the evolution of atherosclerotic lesions.