The TCB index (triglycerides × total cholesterol × body weight), a novel simply calculated nutritional index based on serum triglycerides (TGs), serum total cholesterol (TC), and body weight (BW), was recently reported to be a useful prognostic indicator in patients with coronary artery disease. Thus, this study aimed to investigate the relationship between TCBI and long-term mortality in acute decompensated heart failure (ADHF) patients. Patients with a diagnosis of ADHF who were consecutively admitted to the cardiac intensive care unit in our institution from 2007 to 2011 were targeted. TCBI was calculated using the formula TG (mg/dL) × TC (mg/dL) × BW (kg)/1000. Patients were divided into two groups according to the median TCBI value. An association between admission TCBI and mortality was assessed using univariable and multivariable Cox proportional hazard analyses. Overall, 417 eligible patients were enrolled, and 94 (22.5%) patients died during a median follow-up period of 2.2 years. The cumulative survival rate with respect to all-cause, cardiovascular, and cancer-related mortalities was worse in patients with low TCBI than in those with high TCBI. In the multivariable analysis, although TCBI was not associated with cardiovascular and cancer mortalities, the association between TCBI and reduced all-cause mortality (hazard ratio: 0.64, 95% confidence interval: 0.44–0.94, p = 0.024) was observed. We computed net reclassification improvement (NRI) when TCBI or Geriatric Nutritional Risk Index (GNRI) was added on established predictors such as hemoglobin, serum sodium level, and both. TCBI improved discrimination for all-cause mortality (NRI: 0.42, p < 0.001; when added on hemoglobin and serum sodium level). GNRI can improve discrimination for cancer mortality (NRI: 0.96, p = 0.002; when added on hemoglobin and serum sodium level). TCBI, a novel and simply calculated nutritional index, can be useful to stratify patients with ADHF who were at risk for worse long-term overall mortality.
Astaxanthin has strong antioxidant properties. We conducted a prospective pilot study on heart failure (HF) patients with left ventricular (LV) systolic dysfunction to investigate improvements in cardiac function and exercise tolerance in relation to suppression of oxidative stress by 3-month astaxanthin supplementation. Oxidative stress markers—serum Diacron reactive oxygen metabolite (dROM), biological antioxidant potential (BAP), and urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) concentrations, LV ejection fraction (LVEF), and 6-min walk distance (6MWD) were assessed before and after 3-month astaxanthin supplementation. Finally, the data of 16 HF patients were analyzed. Following 3-month astaxanthin supplementation, dROM level decreased from 385.6 ± 82.6 U.CARR to 346.5 ± 56.9 U.CARR (p = 0.041) despite no changes in BAP and urinary 8-OHdG levels. LVEF increased from 34.1 ± 8.6% to 38.0 ± 10.0% (p = 0.031) and 6MWD increased from 393.4 ± 95.9 m to 432.8 ± 93.3 m (p = 0.023). Significant relationships were observed between percent changes in dROM level and those in LVEF. In this study, following 3-month astaxanthin supplementation, suppressed oxidative stress and improved cardiac contractility and exercise tolerance were observed in HF patients with LV systolic dysfunction. Correlation between suppression of oxidative stress and improvement of cardiac contractility suggests that suppression of oxidative stress by astaxanthin supplementation had therapeutic potential to improve cardiac functioning.
In patients with heart failure (HF), the impact of the Geriatric Nutritional Risk Index (GNRI) on in-hospital mortality and length of hospital stay remains unclear. We aimed to identify the factors associated with increased in-hospital mortality and longer length of hospital stay considering the GNRI in acute decompensated HF with reduced and preserved ejection fraction (HFrEF and HFpEF, respectively). Patients with acute decompensated HF who were admitted to our institution between 2007 and 2011 were investigated. A total of 451 (201, HFrEF; 250, HFpEF) patients were divided into the following: patients with GNRI < 92 and ≥92. In HFrEF, there were no significant differences in in-hospital mortality and length of hospital stay between patients with GNRI < 92 and ≥92 (median (interquartile range), 24.0 (23.8) days and 20.0 (15.0) days, respectively, p = 0.32). In HFpEF, despite no differences in in-hospital mortality, patients with GNRI < 92 had significantly longer length of hospital stay than those with GNRI ≥ 92 (median (interquartile range), 20.0 (22.3) days and 17.0 (16.0) days, respectively, p = 0.04). In HFpEF, GNRI < 92, along with lower hemoglobin, higher B-type natriuretic peptide, and elevated C-reactive protein levels, were the independent factors for longer length of hospital stay. Among patients with acute decompensated HF, assessment of nutritional status with GNRI is useful for stratifying patients at high risk for longer length of hospital stay in HFpEF but not in HFrEF. These observations are particularly important when considering the increasing elderly population and prevalence of HFpEF.
Obstructive sleep apnea (OSA) is related to an increased risk of cardiovascular diseases, including coronary artery disease (CAD). We investigated the association between OSA and the severity of CAD by assessing coronary angiography findings. We retrospectively analyzed patients who underwent their first coronary angiography to evaluate CAD and polysomnography (PSG) to investigate the severity of OSA in our hospital from March 2002 to May 2015. The severity of CAD was determined based on coronary angiography findings using the SYNTAX score. The patients were divided into two groups according to the apnea-hypopnea index (AHI): mild OSA (AHI < 15/h) and moderate-to-severe OSA (AHI ≥ 15/h). Overall, 98 patients were enrolled. The SYNTAX score was significantly different between the two groups (p = 0.001). After adjustment for other risk factors, including age, sex, obesity, hypertension, hyperlipidemia, diabetes mellitus, smoking status, and family history of CAD, moderate-to-severe OSA significantly correlated to the SYNTAX score (partial correlations = 0.24, p = 0.039). These results suggest that the severity of CAD is related to moderate-to-severe OSA.
Whether malnutrition during the early phase of recovery from acute myocardial infarction (AMI) could be a predictor of mortality or morbidity has not been ascertained. We examined 289 AMI patients. All-cause mortality and composite endpoints (all-cause mortality, nonfatal stroke, nonfatal acute coronary syndrome, and hospitalization for acute decompensated heart failure) during the follow-up duration (median 39 months) were evaluated. There were 108 (37.8%) malnourished patients with GNRIs of less than 98 on arrival; however, malnourished patients significantly decreased to 91 (31.4%) during the convalescence period (p < 0.01). The incidence rates of mortality and primary composite endpoints were significantly higher in the malnourished group than in the well-nourished group both on arrival and during the convalescence period (All p < 0.05). Nutrition guidance significantly improved GNRI in a group of patients who were undernourished (94.7 vs. 91.0, p < 0.01). Malnourished patients on admission who received nutritional guidance showed similar all-cause mortality with well-nourished patients, whereas malnourished patients without receiving nutritional guidance demonstrated significantly worse compared to the others (p = 0.03). The assessment of GNRI during the convalescence period is a useful risk predictor for patients with AMI. Nutritional guidance may improve the prognoses of patients with poor nutritional status.
Hyperuricemia is influenced by diet and can cause gout. Whether it is a potential risk factor for cardiovascular disease (CVD) remains controversial, and the mechanism is unclear. Similar to CVDs, gout attacks occur more frequently in the morning and at night. A possible reason for this is the diurnal variation in uric acid (UA), However, scientific data regarding this variation in patients with CVD are not available. Thus, we aimed to investigate diurnal variations in serum levels of UA and plasma levels of xanthine, hypoxanthine, and xanthine oxidoreductase (XOR) activity, which were measured at 18:00, 6:00, and 12:00 in male patients with coronary artery disease. Thirty eligible patients participated in the study. UA and xanthine levels significantly increased from 18:00 to 6:00 but significantly decreased from 6:00 to 12:00. By contrast, XOR activity significantly increased both from 18:00 to 6:00 and 6:00 to 12:00. Furthermore, the rates of increase in UA and xanthine levels from night to morning were significantly and positively correlated. In conclusion, UA and xanthine showed similar diurnal variations, whereas XOR activity showed different diurnal variations. The morning UA surge could be due to UA production. The mechanism involved XOR activity, but other factors were also considered.