Kosuke Minai

The neutrophil-to-lymphocyte ratio (NLR) has emerged as a marker of systemic inflammation and a prognostic indicator in acute myocardial infarction (AMI). Simultaneously, infarct size (reflected by peak serum levels of creatine kinase (CK) and creatine kinase-myocardial band [CK-MB]) correlates with clinical outcomes in AMI. Given the inflammatory nature of infarction, elevated NLR at admission may contribute to larger infarct size and higher CK and CK-MB levels; however, this association has not been clearly established. We retrospectively analyzed data from 170 patients hospitalized for AMI. Univariate and multivariate linear regression analyses were conducted to examine associations between peak creatine kinase (peak CK) and CK-MB levels and clinical variables, including age, sex, body mass index, hemoglobin, creatinine, uric acid, B-type natriuretic peptide, albumin, C-reactive protein, mean blood pressure, NLR, and platelet-to-lymphocyte ratio at admission. Structural equation modeling was also employed to explore the relationship between NLR and infarct size. Multivariate analysis revealed a significant positive association between NLR at admission and both peak CK (β = 0.342, P = .002) and peak creatine kinase-myocardial band (β = 0.352, P = .001). Structural equation modeling confirmed these findings, showing significant correlations between NLR and peak CK (β = 0.342, P = .001) and CK-MB (β = 0.352, P < .001). Elevated NLR at admission is significantly associated with increased peak CK and CK-MB levels in patients with AMI, suggesting a potential link between systemic inflammation and infarct size. NLR may serve as an early, accessible predictor of infarct magnitude following AMI.

Diabetes may impair left ventricular (LV) contractility, but clear human evidence remains limited. This study investigated its impact in patients with aortic stenosis (AS), demonstrating that diabetes significantly reduces LV function. Clinically, our findings suggest that relying solely on pressure gradients may underestimate AS severity in patients with diabetes, highlighting the necessity for a more comprehensive assessment to ensure accurate evaluation and management of the disease.

Hypoxia leads to increased purine metabolism in tissues, resulting in increased serum uric acid levels, and may also cause impaired uric acid excretion in the kidneys and intestinal tract. However, the relationship between hypoxia and serum uric acid levels in patients with heart failure remains largely unexplored. Because mixed venous oxygen saturation is an acute indicator of systemic oxygenation, in this study, we investigated the relationship between mixed venous oxygen saturation and serum uric acid levels. This retrospective analysis included 386 patients with heart failure who underwent cardiac catheterization at our institution. The relationship between mixed venous oxygen saturation and serum uric acid levels was examined by single regression analysis. Stratified regression analysis, structural equation modeling, and partial correlation analysis were used to examine the effects of eight factors known to influence mixed venous oxygen saturation and serum uric acid levels. The single regression analysis showed a significant negative correlation between mixed venous oxygen saturation and serum uric acid levels (P<0.001). Significant negative correlations were also observed in many subgroups in the stratified analysis, in the path diagram based on structural equation modeling, and in the partial correlation analysis. These results suggest that there may be a direct relationship between mixed venous oxygen saturation and serum uric acid levels that is not mediated by any known factor.

BNP negatively regulates ACTH during a severe ischemic attack of ACS in which hypothalamic-pituitary-adrenal axis ought to be activated, indicating an important role of natriuretic peptides as a mechanism of adaptation to acute critical stress conditions in humans.

In the pathophysiology of acute coronary syndrome (ACS), platelet (PLT) and neutrophil (Neu) crosstalk may be important for activating coagulation and inflammation. It has been speculated that PLTs and Neu may affect each other’s cell counts; however, few studies have investigated this hypothesis. In this study, we measured changes in blood cell counts in 245 patients with ACS during treatment and investigated the mutual effects of each blood cell type. Path diagrams were drawn using structural equation modeling, and temporal changes in the count of each blood cell type and the relevance of these changes were analyzed. Throughout the treatment period, the numbers of all blood cell types (red blood cells [RBCs], leukocytes, and PLTs) were associated with each other before and after treatment. A detailed examination of the different cell types revealed that the PLT count at admission had a significant positive effect on the leukocyte (especially Neu) count after treatment. Conversely, the leukocyte (especially Neu) count at admission had a significant positive effect on the PLT count after treatment. During ACS, PLTs and leukocytes, especially Neu, stimulate each other to increase their numbers. The formation of a PLT-leukocyte complex may increase coagulation activity and inflammation, which can lead to a further increase in the counts of both blood cell types.

Obesity is believed to be one of the major risk factors for cardiovascular disease in Western countries. However, the effects of obesity should be continuously examined in the Japanese population because the average bodily habitus differs among countries. In this study, we collectively examined the significance of obesity and obesity-triggered risk factors including the low reactivity of B-type natriuretic peptide (BNP), for ischemic heart disease (IHD) in Japanese patients. The study patients consisted of 1252 subjects (IHD: n = 970; non-IHD: n = 282). Multiple logistic regression analysis revealed that dyslipidemia, hypertension, diabetes, and the low reactivity of BNP were significant risk factors for IHD, but body mass index (BMI) was not. A theoretical path model was proposed by positioning BMI at the top of the hierarchical model. Exploratory factor analysis revealed that BMI did not play a causative role in IHD (P = NS). BMI was causatively linked to other risk factors (P<0.001 for hypertension; P<0.001 for dyslipidemia; P<0.001 for HbA1c; P<0.001 for LogBNP), and these factors played a causative role in IHD (P<0.001 for hypertension; P<0.001 for dyslipidemia; P<0.001 for HbA1c; P<0.001 for LogBNP). The intrinsic power of the low reactivity of BNP induced by high BMI on the promotion of IHD was fairly potent. This study demonstrated that obesity per se is not a strong risk factor for IHD in Japanese patients. However, several important risk factors triggered by obesity exhibited a causative role for IHD. The low reactivity of BNP is a substantial risk factor for IHD.

Although the plasma B-type natriuretic peptide (BNP) level is a marker of heart failure, it is unclear whether BNP per se plays a pivotal role for pathogenic mechanisms underlying the development of ischemic heart disease (IHD). In this study, we retrospectively examined the plasma BNP levels in stable patients with IHD and compared to stable patients with cardiovascular diseases other than IHD. The study population was 2088 patients (1698 males and 390 females) who were admitted to our hospital due to IHD (n = 1,661) and non-IHD (n = 427) and underwent cardiac catheterization. Measurements of the hemodynamic parameters and blood sampling were performed. The plasma BNP levels were significantly lower in the IHD group than in the non-IHD group (pper se were significant explanatory variables. When the total study population was divided according to gender, the plasma BNP levels were found to be significantly lower in the IHD group than in the non-IHD group among males (p<0.001), but not females (p = NS). Furthermore, a multiple logistic regression analysis of IHD showed the logBNP value to be a significant explanatory variable in males (regression coefficient: −0.669, p<0.001), but not females (p = NS). The plasma BNP levels were relatively low in stable patients with IHD compared with those observed in stable patients with non-IHD; this tendency was evident in males. Perhaps, the low reactivity of BNP is causally associated with IHD in males. We hope that this study will serve as a test of future prospective studies.

Background: Although a decrease in serum potassium level has been suggested to be a fairly common observation in acute coronary syndrome (ACS), there have so far been no definitive reports directly demonstrating the transient potassium decrease (the potassium dip) during ischemic attack of ACS compared to stable phase in individual patients. To understand the pathophysiological significance of the potassium dip, we examined the changes in serum potassium level throughout ischemic attack and evaluated the clinical factors affecting it. Methods: The degree of the potassium dip during ischemic attack (as indicated by ΔK, ΔK = K at discharge − K on admission) was examined in 311 consecutive patients with ACS who required urgent hospitalization in our institution. Results: Serum potassium level during ischemic attack was significantly decreased compared to that during stable phase (P < 0.001). Multiple regression analysis revealed that plasma glucose level during attack was the sole factor which was positively correlated with ΔK (P < 0.01), while HbA1c level was negatively correlated (P < 0.05). The medication profiles and renal function had no impact on ΔK. A longer hospitalization period, higher incidence of myocardial infarction and higher peak creatine kinase level were observed in patients with a larger ΔK. Conclusions: We have clearly demonstrated that there is a transient decrease in serum potassium level during ischemic attack of ACS compared to stable phase. The degree of the potassium dip was tightly correlated with glucose level, which overwhelmed the diabetic condition, and it also indicates the disease severity. The present study therefore promotes awareness of the significance of monitoring potassium level in parallel with glucose level in patients with ACS.