Impact of an angulated aorto-septal relationship on cardio-cerebrovascular outcomes in patients undergoing hemodialysis.

Aortic and valvular calcification are well-known risk factors for cardio-cerebrovascular events in patients undergoing hemodialysis. We investigated the clinical impact of an angulated aorto-septal angle as a result of aortic elongation due to aortic calcification on cardio-cerebrovascular outcomes in patients undergoing hemodialysis. We investigated 306 patients (mean age 65.4 years, 68% male) who underwent pre-scheduled routine echocardiography between April and September 2018. The angle between the anterior wall of the aorta and the ventricular septal surface (ASA) was quantified. We determined aortic and mitral valve calcification scores based on calcified cardiac changes; the aortic and mitral valve scores ranged between 0-9 and 0-6, respectively. The primary endpoint was a composite including cardio-cerebrovascular events and cardio-cerebrovascular death. The mean duration of dialysis among the patients in this analysis was 9.6 years. The primary endpoint was observed in 54 patients during the observational period (median 1095 days). Multivariable Cox proportional hazards analyses identified left ventricular ejection fraction (per 10% increase: hazard ratio [HR] 0.67; 95% confidential interval [CI] 0.53-0.84, P = 0.001), left ventricular mass index (per 10 g/m2 increase: HR 1.14; 95% CI 1.05-1.24, P = 0.001), ASA (per 10 degree increase: HR 0.69; 95% CI 0.54-0.88; P = 0.003), and aortic valve calcification score (HR 1.15; 95% CI 1.04-1.26, P = 0.005) as independent determinants of the primary endpoint. Kaplan-Meier analysis showed a higher incidence of the primary endpoint in patients with ASA <119.4 degrees than those with ASA ≥119.4 degrees (Log-rank P < 0.001). An angulated aorto-septal angle is an independent risk factor for cardio-cerebrovascular events and cardio-cerebrovascular death in patients undergoing hemodialysis.

Effectiveness of non-pharmacological interventions to prevent anemia in pregnant women: a quantitative systematic review protocol.

OBJECTIVE: This review aims to identify the effectiveness of non-pharmacological interventions in preventing iron deficiency anemia in pregnant women with a normal course of pregnancy. INTRODUCTION: The global prevalence of anemia among pregnant women is 36.5%, posing risks to women and fetuses. This underscores the need for effective prevention; however, the effectiveness of non-pharmacological approaches in preventing pregnancy anemia remains unclear. INCLUSION CRITERIA: This review will encompass experimental and quasi-experimental studies on the following approaches to prevent anemia during pregnancy: recommendations for dietary supplements, oral iron supplements (over the counter), provision of supplements to promote iron absorption, participation in anemia prevention education, and provision of information. There will be no restrictions on the duration or frequency of intervention, and longitudinal intervention studies will be included. In studies with a control group, the comparator may be usual care or pharmacological interventions; in studies without, it may involve no intervention, temporal comparisons, or baseline periods without non-pharmacological interventions. Evaluation of hemoglobin, hematocrit, and ferritin will be included as primary outcomes. Low birth weight, preterm birth, amount of blood loss at delivery, small for gestational age, and Apgar scores will be included as secondary outcomes. METHODS: A search will be conducted of MEDLINE (Ovid), Embase, CINAHL (EBSCOhost), Scopus, Australian New Zealand Clinical Trials Registry, Cochrane Central Register of Controlled Trials, and ICHUSHI-Web. Researchers will screen studies, extract data, assess the quality of studies, and analyze the data in accordance with the JBI guidance for systematic reviews of effectiveness. GRADE will be used to assess the certainty of the findings. REVIEW REGISTRATION NUMBER: PROSPERO CRD42022344155.

Predictors of congestive heart failure in patients on maintenance hemodialysis.

BACKGROUND: Cardiovascular disease is a major cause of death in patients on maintenance hemodialysis (HD). Predictors of congestive heart failure (CHF) events in patients on HD were investigated, focusing on left ventricular (LV) function. METHODS AND RESULTS: One hundred consecutive patients on HD were followed for at least 5 years after index examination performed 1 day after the last HD session. Tests included M-mode and Doppler echocardiography and plasma brain natriuretic peptide (BNP) and hemoglobin (Hb) concentration measurements. Patients with atrial fibrillation or poor echocardiographic images were excluded. Confounding factors included diabetes mellitus (DM), hypertension, age, HD duration, LV fractional shortening, E/A of transmitral flow velocity pattern, Tei index, LV mass index (LVMI), BNP level, Hb, and use of antihypertensive or antiarrhythmic drugs. Six CHF events occurred during 1,703+/-565 days. DM and Hb <10 g/dl were identified as independent predictors of CHF events in a stepwise Cox regression model after DM, LVMI, BNP, and Hb <10 g/dl were selected in the univariate analysis. The hazard ratio (confidence interval) was 10.96 (1.49-80.44) for DM, and 23.00 (2.41-219.76) for Hb <10 g/dl. The estimated hazard across time was constant (T_COV*DM; p=0.726, T_COV*Hb <10 g/dl; p=0.681) by time-dependent covariates analysis. CONCLUSION: In patients on maintenance HD, DM and anemia (Hb <10 g/dl), but not echo-derived cardiac function, predicted CHF events.

The relationship between variables of 123-I-metaiodobenzylguanidine cardiac imaging and clinical status of the patients with diastolic heart failure.

BACKGROUND: The status of cardiac sympathetic nerve activity in patients with diastolic heart failure has not been fully understood. 123-I-metaiodobenzylguanidine cardiac images are valuable for evaluating cardiac sympathetic nerve activity. METHODS: We obtained 123-I-metaiodobenzylguanidine cardiac images from 34 consecutive patients with moderate heart failure and an ejection fraction of > or = 45%. RESULTS: The decay-corrected washout rate of 123-I-metaiodobenzylguanidine correlated with each plasma concentration of brain natriuretic peptide (standardized correlation coefficient=0.305, p<0.05), New York Heart Association functional class (standardized correlation coefficient=0.364, p<0.02), and exercise capacity (standardized correlation coefficient=-0.388, p<0.04). A multiple regression analysis revealed that the washout rate independently predicted plasma concentration of brain natriuretic peptide (standardized regression coefficient=0.367, p<0.02). In a univariate regression, the washout rate did not significantly correlate with the presence of ischemic heart disease (p=0.254); in a multivariate regression, the presence of ischemic heart disease did not predict the washout rate. For the 14 patients with sinus rhythm, there was a marginal negative correlation between the E/A velocity ratio of the transmitral flow and washout rate (standardized correlation coefficient=-0.518, p<0.07). CONCLUSIONS: In diastolic heart failure, cardiac sympathetic nerve activity increases proportionally to severity of the disease.

Effects of carvedilol on plasma B-type natriuretic peptide concentration and symptoms in patients with heart failure and preserved ejection fraction.

Although the benefits of carvedilol in patients with heart failure and depressed ejection fraction (EF) have been elucidated, those in patients with preserved EF are not understood. We enrolled 40 patients with mild or moderate heart failure and EF >/=45%. They were randomly assigned to carvedilol (n = 19) or conventional therapy (n = 21). After 12 months of treatment, carvedilol significantly improved all end points (plasma concentration of B-type natriuretic peptide [BNP] from 175 (35 to 209) to 106 (52 to 160) pg/ml, mean (95% confidence interval) p <0.01; New York Heart Association functional class from 2.37 (2.13 to 2.61) to 1.56 (1.21 to 1.91), p <0.01; exercise capacity estimated with the Specific Activity Scale from 4.75 (4.50 to 5.00) to 5.68 (5.22 to 6.14) METs, p <0.02), whereas conventional therapy did not (plasma BNP concentration from 150 (114 to 186) to 174 (100 to 248) pg/ml; New York Heart Association functional class from 2.29 (2.08 to 2.50) to 2.11 (1.73 to 2.49); exercise capacity from 4.57 (4.34 to 4.80) to 4.72 (4.41 to 5.03) METs). Univariate regression analyses showed that only the use of carvedilol was correlated with the decrease in plasma BNP concentration (p <0.03). Multivariate analyses demonstrated that an ischemic cause of heart failure (p <0.02), high plasma concentration of BNP (p <0.02), left ventricular dilation (p <0.03), and use of carvedilol (p <0.04) at baseline were predictive of a decrease in plasma concentration of BNP. In conclusion, carvedilol potentially decreased neurohumoral activation, decreased symptoms, and increased exercise capacity in patients with heart failure and preserved EF.

Elevated white blood cell count as a risk factor of coronary artery disease: inconsistency between forms of the disease.

White blood cells (WBC) destabilize coronary artery plaques and an elevated WBC count is a risk factor of coronary artery disease (CAD). Nevertheless, the differences between the forms of CAD in the relationship with WBC count remain to be elucidated. To study these differences, we reviewed the health-checkup records from 1994 to 1999 for 6021 Japanese post office workers without any cardiovascular abnormalities. Baseline WBC counts of patients with acute coronary syndrome (ACS) were significantly higher than those of subjects free from coronary artery discase (mean +/- SD = 9210 +/- 2703/microL vs 6205 +/- 1635/microL, P<0.001), while the patients with stable angina pectoris (sAP) (6233 +/- 1528/microL) were similar to subjects without coronary artery disease in baseline WBC counts. Hypertension at the baseline was related to sAP (relative risk [95% CI] = 61.78 [17.29 to 78.66]) but not to ACS. Conversely, hypercholesterolemia and cigarette smoking were risk factors for ACS (relative risk [95% CI] = 11.48 [2.39 to 18.03] and 10.04 [3.00 to 12.12], respectively) but not for sAP. Multivariate logistic regression analysis found only WBC count (1000/microL) discriminated between ACS and sAP (P=0.038, odds ratio 2.049 [1.042-4.016]). We conclude that an elevated WBC count may be a risk factor of ACS but not sAP, and this finding is consistent with previous reports demonstrating the effects of WBCs in the destabilization of coronary artery plaques.