Metformin treatment may be associated with decreased levels of NT-proBNP in patients with type 2 diabetes.

PURPOSE: Individuals with type 2 diabetes (T2DM) are at increased risk of cardiovascular disease, including heart failure (HF). In patients with T2DM elevated serum concentrations of the N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) correlate with cardiovascular morbidity and mortality. We aimed to identify predictors of increased serum NT-proBNP levels in patients with T2DM. METHODS: The study included 185 patients with T2DM treated with either oral antidiabetic agents (49.7%) or insulin (17.8%), or both (32.5%). We divided the patients into two groups: with high (>200 pg/mL) and low (≤200 pg/mL) NT-proBNP concentrations. RESULTS: We found differences between the patients with high and low NT-proBNP levels including age, prevalence of dyslipidemia and HF, history of previous myocardial infarction (MI), heart rate, hemoglobin level, platelet count, creatinine, urea and uric acid concentrations, use of beta-blockers, loop diuretics, metformin and insulin. In a multivariate analysis metformin was a negative predictor of increased NT-proBNP concentration. Age, history of HF and decreased estimated glomerular filtration rate (eGFR) were positive predictors. We found no correlation between NT-proBNP serum concentration and insulin treatment or history of coronary artery disease or MI. CONCLUSION: Metformin correlates with lower concentrations of NT-proBNP in patients with T2DM.

Genetic determinants of platelet reactivity during acetylsalicylic acid therapy in diabetic patients: evaluation of 27 polymorphisms within candidate genes.

AIMS: Decreased platelet responsiveness to acetylsalicylic acid (ASA) reported previously in diabetic patients could be attributed to patient-based, clinical, genetic and cellular factors. The objective of the present study was to investigate the effect of the genomic polymorphism on the platelet reactivity in diabetic patients treated with ASA. METHODS AND RESULTS: The study cohort consisted of 295 Caucasians with diabetes type 2 who had been taking ASA tablets at the dose of 75 mg per day for at least 3 months for primary or secondary prevention of myocardial infarction (MI). Platelet reactivity analyzes were performed using VerifyNow ASA and PFA-100 assays. Genotyping for the selected 27 single nucleotide polymorphisms (SNPs) within 19 genes was performed using a Sequenom iPLEX platform. The results indicate that the statistically significant differences in platelet reactivity were observed in the PFA-100 assay for SNPs in following genes: TXBA2R (rs1131882), ADRA2A (rs4311994), PLA2G7 (rs7756935) and 9p21.3 (rs10120688) (P = 0.02, P = 0.03, P = 0.02, P = 0.03, respectively, all significance levels corrected for multiple comparisons). When using the VerifyNow ASA test, a weak nominal statistical significance (i.e. before multiple comparison testing) was observed for two SNPs in the GPVI gene: rs1671152 and rs1613662 [P = 0.025 (0.5) for both SNPs, corrected for multiple comparisons test]. CONCLUSIONS: The results from the present study suggest that the four analyzed genes may contribute to platelet reactivity measured with the PFA-100 assay in the diabetic population treated with ASA.

Gene expression profiling in peripheral blood nuclear cells in patients with refractory ischaemic end-stage heart failure.

Functional analysis of up- and down-regulated genes might reveal whether peripheral blood cells may be considered as a material of diagnostic or prognostic value in patients with end-stage heart failure (HF). The aim of the present study was to compare the transcriptomic profile of peripheral blood nuclear cells from 6 male patients with ischaemic end-stage HF with those of 6 male patients with asymptomatic cardiac dysfunction. The expression of genes in peripheral blood nuclear cells in both groups of patients was measured using whole-genome oligonucleotide microarrays utilizing 35 035 oligonucleotide probes. Microarray analyses revealed 130 down-regulated genes and 15 up-regulated genes in the patients with end-stage HF. Some of the down-regulated genes belonged to the pathways that other studies have shown to be down-regulated in cardiomyopathy. We also identified up-regulated genes that have been correlated with HF severity (CXCL16) and genes involved in the regulation of expression of platelet activation factor receptor (PTAFR, RBPSUH, MCC, and PSMA7). In conclusion, the identification of genes that are differentially expressed in peripheral blood nuclear cells of patients with HF supports the suggestion that this diagnostic approach may be useful in searching for the molecular predisposition for development of severe refractory HF in patients with post-infarction asymptomatic abnormalities and remodelling of the left ventricle. These results need further investigation and validation.

[Effect of postinfarct left ventricular dysfunction on late occurrence of mitral regurgitation--two year experience]. / Wplyw pozawalowego uszkodzenia lewej komory na wystepowanie póznej niedomykalnosci mitralnej--obserwacja 2-letnia.

The aim of this study was to evaluate factors that might influence on the occurrence of mitral regurgitation (MR) in patients (pts) following myocardial infarction (MI) after fibrinolysis--two year experience. The study group comprised 118 pts: 40 women and 78 men (mean age: 58 +/- 9 years) following MI, who underwent Doppler echocardiography which revealed no MR 3 weeks after the MI. The second echocardiographic examination was performed after 2 years. We evaluated the following parameters: presence and stage of MR, left ventricular end-diastolic diameter (LVDD), left atrial diameter (LA), end-diastolic volume (EDV), wall motion score index (WMSI), asynergic area (AA) and ejection fraction (EF). Results after 2 years were as follows: 43 pts (36%) presented without MR, 45 (38%) MR I degree, 27 (23%) MR II degree, 3 (3%) MR III degree. Echocardiographic parameter comparison after 2 years demonstrated the following changes: LVDD increase from 5.0 +/- 0.5 cm to 5.3 +/- 4.6 cm (p < 0.005), LA increase from 3.7 +/- 0.4 cm to 4.3 +/- 0.4 cm (p < 0.00001), EDV increase from 130 +/- 29 ml to 147 +/- 39 ml (p < 0.005), WMSI increase from 1.37 +/- 0.23 to 1.45 +/- 0.21 (p < 0.05), AA increase from 23.5 +/- 10.1% to 27.8 +/- 7.9% (p < 0.005) and significant EF decrease 50.4 +/- 7.9% to 46.9 +/- 7.1% (p < 0.005). These results demonstrate that the occurrence of MR 2 years after the MI is caused by left ventricular remodelling, as well as segmental and global function deterioration.

Paroxysmal atrial fibrillation in a young female patient following marijuana intoxication--a case report of possible association.

Marijuana is one of the most popular drugs legally admitted for general sale in many countries. To consider it safe and unlikely to develop drug dependence is abusive. The use of marijuana as a herbal medication is being widely discussed in literature. The most promising effect of delta-9-etrahydrocannabinol seems to be observed in the case of nausea, following cancer chemotherapy. Despite its positive action on the human organism, marijuana smoking has been shown to exert adverse effects on the cardiovascular system causing well-tolerated tachycardia and/or hypotension. We also observed that marijuana abuse was associated with an increased risk of paroxysmal atrial fibrillation. The report presents a case of young healthy white subject suffering from paroxysmal atrial fibrillation following marijuana intoxication. The abuse of this substance was the most possible and identifiable risk factor for observed paroxysmal atrial fibrillation.

[Sulphonylurea derivatives and the cardiovascular system]. / Pochodne sulfonylomocznika a uklad krazenia.

Sulphonylurea derivatives (SUD) are a mainstay of treatment of type 2 diabetes but questions have been raised about the potential adverse effects of these drugs as far as cardiovascular functions are concerned. An early prospective study which examined the effects of glycaemic control with various agents on coronary heart disease was stopped in the 70-ies due to excess cardiovascular mortality in the group receiving SUD of first generation: tolbutamide. The discovery of ATP-sensitive potassium channels in the heart, their role in ischaemic heart disease and mechanisms of endogenous cardiac cell protection--preconditioning have brought back concerns of SUD safety. Recently, a new SUD--glimepiride--claimed as the first representant of III generation of these agents--has been introduced into clinical practice. Glimepiride appears to be devoid of vascular ATP-sensitive potassium channels binding properties. Postulated and confirmed in animal experimental studies cardioprotective features of glimepiride were evaluated in a randomised, placebo-controlled study with glimepiride and glibenclamide comparing effects of these drugs on ischaemic preconditioning during angioplasty of high grade coronary artery stenoses in patients with stable angina. Myocardial ischaemia was quantified by intracoronary electrocardiography and time to occurrence of angina during vessel occlusion was measured. The results of the study confirmed glimepiride effects of maintaining myocardial preconditioning. The article summarises current knowledge of SUD influence on cardiovascular system and discusses some differences in pharmacodynamics of glimepiride which appear to provide this agent with clinical advantages over conventional SUD at least in cardiovascular aspects.