Association between the severity of newly diagnosed obstructive sleep apnea and subclinical carotid atherosclerosis in patients without overt cardiovascular disease.

OBJECTIVE: Obstructive Sleep Apnea (OSA) has been associated with both subclinical and accelerated atherosclerosis; however, it still remains unknown whether this association is unique or is mediated by the higher burden of co-existing cardio-metabolic disorders frequently seen in patients with OSA. PATIENTS AND METHODS: A total of 40 subjects without clinically diagnosed cardiovascular disease (CVD) referred for polysomnography test were included in the study. Subjects with apnea/hypopnea index (AHI > 15/h) were classified as moderate/severe OSA. Subclinical changes in carotid atherosclerosis were assessed using mean carotid intima-media thickness (cIMT) and presence of atheromatic plaques on both carotid arteries. The measurement was performed using B-mode ultrasonogram. Framingham risk score was used in the approximation of cardiovascular risk. RESULTS: The mean age of our cohort was 56.8 years, 70% (n = 28) of whom were males. Moderate/severe OSA was diagnosed in 21 subjects. Both groups were well matched in terms of clinical and demographic characteristics, and cardiovascular risk profile, as shown in their respective Framingham risk scores (10.4 ± 6.6 vs. 11.8 ± 8.8, p = NS). Patients with moderate/severe OSA had a higher mean AHI, 3% oxygen desaturation index, and lower minimum nocturnal oxygen saturation than controls. No significant differences were detected in terms of C-reactive protein levels. The two groups had similar cIMT (0.66 ± 0.17 vs. 0.75 ± 0.20 p = 0.33) and presence of atheromatic plaque (50% vs. 45%, p = 1.00). CONCLUSIONS: Our study suggests that among patients with similar cardiovascular risk profile and free of overt CVD, the severity of newly diagnosed OSA was not correlated with increased inflammation or subclinical carotid atherosclerosis.

Prognostic value of post-procedural aPTT in patients with ST-elevation myocardial infarction treated with primary PCI.

Unfractionated heparin is the most commonly used anticoagulant in ST-elevation myocardial infarction (STEMI) and its effect can be monitored with activated partial thromboplastin time (aPTT). However, the optimal aPTT range during heparin therapy after primary percutaneous coronary intervention (PCI) is yet to be defined. A mean aPTT was calculated of all aPTT measurements in the first 24 hours after pPCI in a total of 1,876 STEMI patients. Mean aPTT measurements were stratified into four categories; < 1.5 times the upper limit of normal (ULN), 1.5 - 2.0 times ULN (the therapeutic group), 2.01 - 3.99 times ULN, and ≥ 4 times ULN. Compared to patients with a therapeutic aPTT, patients with aPTTs < 1.5 times ULN had no increase in recurrent ischaemic events and had similar rates of bleeding complications. Patients with a mean aPTT ≥ 4 times ULN had higher rates recurrent ischaemic and haemorrhagic complications. After multivariable analyses, aPTT ratios ≥ 4 times ULN were no longer associated with recurrent ischaemic events, but remained a strong predictor of severe and moderate bleeding (hazard ratio [HR] 4.64, p = 0.016 and HR 2.27, p = 0.052). In conclusion, in 1,876 STEMI patients treated with pPCI, low aPTTs in the first 24 hours after PCI were not associated with an increase in ischaemic events, whereas high aPTT values were associated with more frequent bleeding complications. These results indicate no clear benefit as well as a safety concern with heparin treatment after primary PCI.

Common pathways for primary hypertrophic and dilated cardiomyopathy.

Testing the hypothesis that hypertrophic and dilated cardiomyopathy as well as viral myocarditis share a common mitogenic growth response pathway with mitotically competent cell types are the aims of this study. The expression of the c-fos, H-ras and c-myc genes was immunohistochemically determined in biopsies from 12 patients with dilated cardiomyopathy, 24 patients with hypertrophic cardiomyopathy, and 4 patients with myocarditis. Normal myocardium from 9 subjects was used as the control group. Staining results were correlated with patient's demographic data. C-fos, H-ras and c-myc protein overexpression was seen in 15 patients (62.5%) with primary hypertrophic and 4 patients (33.3%) with dilated cardiomyopathy. The majority of hypertrophic and dilated cardiomyopathy patients expressed at least one of the genes studied compared with the control group (p = 0.006). Primary cardiomyopathy patients also showed a statistically significant difference in the gene co-expression compared with the control group (p = 0.042). C-fos, H-ras, and C-myc protein expression did not differ substantially between patients with hypertrophic and dilated cardiomyopathy. Patients with myocarditis expressed only the C-fos protein (n = 2, 50%). C-fos, h-ras and c-myc genes are overexpressed in patients with cardiac hypertrophy and cardiac dilation. Cardiac myocytes respond to biomechanical stress by initiating several different processes. One of them is oncogene expression. This results in a hypertrophy of the myocytes proportional in length and width (hypertrophic cardiomyopathy or with a relatively greater increase in length than in the width (dilated cardiomyopathy).