Objectives: Increased homocysteine (HCY) levels are associated with an increased risk of cardiovascular disease. Plasma HCY is increased in chronic heart failure (CHF) patients, and previous studies suggest that hyperhomocysteinemia causes adverse cardiac remodeling and affects pump function. We aimed to evaluate the HCY levels in patients with diastolic heart failure with preserved left ventricular ejection fraction (LVEF). Methods: We prospectively studied 68 patients (39 females and 29 males) who were hospitalized for symptomatic heart failure, as well as 40 age- and sex-matched healthy subjects who comprised the control group. CHF was diagnosed in all cases based on Framingham diagnostic criteria. CHF with preserved LVEF was defined as cases with CHF with an LVEF of 50% or more. Patients with regional left ventricular wall motion abnormalities, atrial fibrillation, and renal failure were excluded. Results: The mean age was 65.5 ± 9.6 years in the heart failure group and 65.2 ± 9.7 years in the control group. The mean LVEF was 59.8 ± 5.3 in the heart failure group and 61.4 ± 5.2 in the control group. The mean total fasting HCY concentrations were significantly higher in patients with heart failure (16.9 ± 5.27 µmol/l vs. 10.15 ± 3.49 µmol/l, respectively; p < 0.001). Multiple regression analysis indicated that NT-proBNP, hs-CRP, E/A ratio, and HbA1C were independently associated with hyperhomocysteinemia. Conclusions: Our results suggest that hyperhomocysteinemia is prevalent in heart failure with preserved ejection fraction. Larger scale studies are needed to clarify its pathogenic mechanisms and effects on the natural history of heart failure.
Introduction. Subclinical hypothyroidism (SCH) is defined as a serum thyroid-stimulating hormone (TSH) level above the upper limit of normal despite normal levels of serum free thyroxine. There is growing evidence that SCH is associated with increased cardiovascular risk. We tried to investigate prevalence of SCH in acute myocardial infarction patients. Methods and Results. We evaluate free T3, free T4, and TSH levels of 604 patients (age 58.4) retrospectively, who have been admitted to the coronary intensive care unit between years 2004–2009 with the diagnosis of ST elevation (STEMI) or non-ST elevation acute myocardial infarction (NSTEMI). Mild subclinical hypothyroidism (TSH 4.5 to 9.9 mU/l) was present in 54 (8.94%) participants and severe subclinical hypothyroidism (TSH 10.0 to 19.9 mU/l) in 11 (1.82%). So 65 patients (10.76%) had TSH levels between 4.5 and 20. Conclusions. In conclusion, 65 patients (10.76%) had TSH levels between 4.5 and 20 in our study, and it is a considerable amount. Large-scale studies are needed to clarify the effects of SCH on myocardial infarction both on etiologic and prognostic grounds.
Cytochrome P450 (CYP) 1A2 gene polymorphisms are thought to be involved in the metabolism of theophylline (TP). We aimed to investigate the effect of CYP1A2*1C, CYP1A2*1D, CYP1A2*1E, and CYP1A2*1F polymorphisms of the CYP1A2 on TP metabolism by PCR-RFLP in 100 Turkish patients with chronic obstructive pulmonary disease (COPD) receiving TP. One hundred and one healthy volunteers were included as control group. The genotype frequencies of the CYP1A2*1D and CYP1A2*1F were found to be significantly different in the patients compared to the controls. The "T" allele at -2467 delT and the "C" allele at -163 C > A in the CYP1A2 displayed association with a significantly increased risk for COPD. "T" allele at -2467 delT was also associated with a high risk of disease severity in COPD. In conclusion, our data suggest that genetic alterations in CYP1A2 may play a role both in the pharmacogenetics of TP and in the development of COPD.[BMB reports 2010; 43(8): 530-534]
In rural hospital settings, clinical resources and transfer facilities are limited. Therefore, improvement of early transfer and prehospital fibrinolysis capabilities should decrease mortality.
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