Tsunenori Nishijima

The endothelial nitric oxide synthase gene -786T/C polymorphism is a predictive factor for reattacks of coronary spasm.

Objective We previously found a -786T/C polymorphism in the 5′-flanking region of the endothelial nitric oxide synthase (eNOS) gene and reported that this polymorphism is strongly associated with coronary spasm. In this study, we examined whether the polymorphism is a prognostic marker in coronary spasm patients. Methods and results We examined the clinical courses of 201 consecutive patients with coronary spasm who were admitted to our institution: 146 patients with the -786T/T genotype; 50 patients with the -786C/T genotype; and five patients with the -786C/C genotype. The mean follow-up period was 76±60 months. All the patients took calcium channel blockers and/or nitrate during the follow-up period. In this study, no patients died due to a cardiac event. About 25 patients were readmitted owing to cardiovascular disease. Out of these 25 patients, 23 patients were readmitted owing to a reattack of coronary spasm. The -786C allele was significantly associated with readmission due to coronary spasm (P=0.0072, odds ratio: 3.37 in the dominant effect). Kaplan–Meier analysis revealed that the occurrence of readmission was significantly higher in the patients with the -786C allele than in the patients without the -786C allele (P=0.0079). Further, multiple logistic regression analysis revealed that the -786T/C polymorphism was an independent predictor for readmission due to reattack of coronary spasm (P=0.006; relative risk=3.590). Conclusions The eNOS -786C allele is an independent risk factor for readmission due to a recurrent attack of coronary spasm in patients with coronary spasm, even if the patients have taken calcium channel blockers and/or nitrate.

The synergistic combined effect of anemia with high plasma levels of B-type natriuretic peptide significantly predicts an enhanced risk for major adverse cardiac events

The prevalence of anemia in patients with heart failure (HF) increases according to disease severity as a consequence of renal insufficiency, cytokine production, plasma volume expansion, and/or malnutrition. B-type natriuretic peptide (BNP) has been recognized as a biochemical marker of ventricular dysfunction. The aim of this study was to evaluate the clinical significance of anemia in HF patients and furthermore, to investigate whether a significant correlation exists between anemia, BNP, and poor clinical outcomes in HF patients. We studied 185 consecutive HF patients. We assessed the occurrence of major adverse cardiac events (MACE) post hospital discharge. Anemia was defined as Hb concentrations <12.9 g/dl in men and <11.3 g/dl in women, respectively. Kaplan-Meier analysis revealed that anemia and high BNP levels (>259 pg/ml) were significantly associated with the occurrence of MACE. Multiple logistic analysis revealed that the most predictive independent risk factor for the occurrence of MACE was high BNP levels, followed by anemia (relative risk [RR] = 2.803 and 2.241, respectively). We divided the patients with or without anemia and high or low BNP levels into four groups according to their respective Hb and BNP levels. The hazard ratio for MACE in the group with anemia and high BNP levels was 10.3 in comparison to the group without anemia and with low BNP levels (P = 0.0002). Both anemia and high plasma levels of BNP are significantly and independently associated with the occurrence of MACE in HF patients; furthermore, the synergistic effect of anemia combined with high BNP levels significantly predicts an enhanced risk for MACE.

Clinical factors affecting serum potassium concentration in cardio-renal decompensation syndrome

BACKGROUND Renin-angiotensin-aldosterone system (RAAS) inhibitors are currently indispensable for the treatment of heart failure. It is well known that hyperkalemia is likely to occur in renal failure; however, it has not yet been clarified how the serum potassium concentration changes as heart failure progresses. Currently, the cardio-renal decompensation syndrome holds that the serum potassium concentration is altered similarly by both heart failure and renal failure; however, there are no definitive reports on this. In order to use RAAS inhibitors more safely and effectively in heart failure, it is necessary to understand the factors affecting serum potassium concentration in the clinical setting. METHODS AND RESULTS We examined the clinical factors affecting serum potassium concentration in 1035 consecutive patients with cardiovascular disease who were hospitalized in our institution. Multiple regression analysis showed that the independent factors associated with an elevated serum potassium concentration were renal insufficiency evaluated by estimated glomerular filtration rate (eGFR) (P<0.0001), diabetes mellitus evaluated by HbA(1c) (P=0.0005) and the use of RAAS inhibitors (P=0.0010). The independent factors associated with a decreased serum potassium concentration were mean blood pressure (P<0.0001), heart failure evaluated by log BNP (P=0.0164) and the use of diuretics (P=0.0232). CONCLUSIONS The serum potassium concentration decreases with the severity of heart failure if renal function is preserved. From the perspective of potassium homeostasis, we could use the RAAS inhibitors more aggressively in patients with heart failure who do not have renal failure.