2019 Vol. 16, No. 12
Objective To examine whether cardiovascular disease (CVD) is associated with depression status. Methods 29,328 participants from baseline of Canadian Longitudinal Study for Aging were categorized into four groups of depression status. Group 1: no depression (reference); Group 2: currently with depression symptom (CES-D10 score ≥ 10, negative self-reported depression); Group 3: self-reported depression with no current symptom (CES-D10 score i.e., heart related disorders (HRD) including heart disease, myocardial infarction, and angina; and peripheral/vascular related disorders (PRD) including hypertension, stroke, and peripheral vascular disease. Adjusted odds ratios (ORs) were used to evaluate the associations between depression and CVDs. Results 17.3% of participants had self-reported depression, 15.3% were with current depression symptom, 10.5% were with HRD and 34.4% were with PRD. After adjusting for variables of demographics, sex, lifestyles, and comorbidities, compared to reference, people in Group 2 had a slightly increased odds, but most of them were not statistically significant; the ORs (95% CI) were 1.36 (1.18–1.58, P P P P Conclusions Seniors with self-reported depression are associated with an increased risk of CVDs, the association varies by depression status, sex and age.
Background Increasing research suggests that mitochondrial defect plays a major role in pulmonary hypertension (PH) pathogenesis. Mitochondrial dynamics and quality control have a central role in the maintenance of the cell proliferation and apoptosis balance. However, the molecular mechanism underlying of this balance is still unknown. Methods To clarify the biological effects of hypoxic air exposure and hypoxia-inducible factor-1α (HIF-1α) on pulmonary arterial smooth muscle cell (PASMC) and pulmonary arterial hypertension rats, the cells were cultured in a hypoxic chamber under oxygen concentrations. Cell viability, reactive oxygen species level, cell death, mitochondrial morphology, mitochondrial membrane potential, mitochondrial function and mitochondrial biosynthesis, as well as fission-and fusion-related proteins, were measured under hypoxic conditions. In addition, rats were maintained under hypoxic conditions, and the right ventricular systolic pressure, right ventricular hypertrophy index and right ventricular weight/body weight ratio were examined and recorded. Further, we assessed the role of HIF-1α in the development and progression of PH using HIF-1α gene knockdown using small interfering RNA transfection. Mdivi-1 treatment was performed before hypoxia to inhibit dynamin-related protein 1 (Drp1). Results We found that HIF-1α expression was increased during hypoxia, which was crucial for hypoxia-induced mitochondrial dysfunction and hypoxia-stimulated PASMCs proliferation and apoptosis. We also found that targeting mitochondrial fission Drp1 by mitochondrial division inhibitor Mdivi-1 was effective in PH model rats. The results showed that mitochondrial dynamics were involved in the pulmonary vascular remodeling under hypoxia in vivo and in vitro. Furthermore, HIF-1α also modulated mitochondrial dynamics in pulmonary vascular remodeling under hypoxia through directly regulating the expression of Drp1. Conclusions In conclusion, our data suggests that abnormal mitochondrial dynamics could be a marker for the early diagnosis of PH and monitoring disease progression. Further research is needed to study the signaling pathways that govern mitochondrial fission/fusion in PH.
Objective To determine the association between the irregularity of carotid plaque surface using multidimensional magnetic resonance imaging (MRI) of ipsilateral acute cerebral infarction (ACI) cases. Methods Patients with recent cerebrovascular symptoms (stroke or transient ischemic attack Results A total of 217 included subjects (mean age: 60.7 ± 10.2 years, 149 men) were recruited and 89 (41.0%), 88 (40.6%) and 118 (54.4%) of them exhibited irregular plaque surface on axial, oblique and multidimensional MR images, respectively. The OR of irregularity of the plaque surface was determined by multidimensional MRI to be 5.88 (95% CI: 3.16–10.96, P P P Conclusions The irregular plaque surface was determined by multidimensional MRI as an independent indicator for ipsilateral acute cerebral infarction.
Background Permanent pacing is the therapy of choice for treating severe and/or symptomatic bradyarrhythmias. The number of very elderly patients receiving pacemakers is increasing and little is known about survival in this specific subgroup. This study is aimed at assessing the actual survival of patients requiring pacing therapy at age > 85 years and investigating variables associated with death. Methods Between 2010 and 2017, 572 patients aged ≥ 85 years underwent pacemaker implantation for conventional bradycardia indications in Department of Cardiology, S. Chiara Hospital, Italy. Results Thirty percent of patients were ≥ 90-year-old and comorbidities were frequent. Fifty-seven percent of patients required pacing for prognostic reasons (acquired atrioventricular block), and the remaining for relief of bradycardia symptoms. A dual-chamber pacemaker was implanted in 34% of patients. The 5-year survival was 45% (standard error: 3%), and the 8-year survival was 26% (standard error: 4%). The risk of death was similar in patients who received pacemaker for symptom relief and for prognostic reasons in the overall population (HR = 1.19, 95% CI: 0.93–1.52, P = 0.156), as well as in the ≥ 90-year-old group (HR = 1.39, 95% CI: 0.92–2.11, P = 0.102). At multivariate analysis, following variables were associated with death: higher age, lower ejection fraction, dementia/dysautonomia and diagnosis of cancer. The pacing indication and the implantation of a single chamber pacemaker were not associated with worse prognosis. Conclusions This study showed a good life expectancy in patients aged ≥ 85 years who received a pacemaker. Strong risk factors for all-cause death were non-cardiac. Pacemaker therapy seems a clinically effective therapeutic option to improve survival and to control bradyarrhythmia-related symptoms in very elderly patients.
Background Endogenous aldehyde damages DNA and potentiates an ageing phenotype. The aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism has a prevalence of 30%–50% in Asian populations. In this study, we aimed to analyze risk factors contributing to the development of heart failure with preserved ejection fraction (HFpEF) along with the genetic exposure in Chinese patients hospitalized with cardiovascular diseases (CVD). Methods From July 2017 to October 2018, a total of 770 consecutive Chinese patients with normal left ventricular ejection fractions (LVEF) and established CVD (hypertension, coronary heart diseases, or diabetes) were enrolled in this prospective cross-sectional study. HFpEF was defined by the presence of at least one of symptom (dyspnoea and fatigue) or sign (rales and ankle swelling) related to heart failure; N-terminal pro-B-Type natriuretic peptide (NT pro-BNP ≥ 280 pg/mL); LVEF ≥ 50%; and at least one criterion related to elevated ventricular filling pressure or diastolic dysfunction (left atrial diameter > 40 mm, E/E’ ≥ 13, E’/A’ Results Finally, among 770 patients with CVD, 92 (11.9%) patients were classified into the HFpEF group according to the diagnostic criteria. The mean age of the participants was 67 ± 12 years, and 278 (36.1%) patients were females. A total of 303 (39.4%) patients were ALDH2*2 variant carriers. In the univariate analysis, eight exposures were found to be associated with HFpEF: atrial fibrillation, ALDH2*2 variants, hypertension, age, anaemia, smoking, alcohol consumption and sex. Multivariable logistic regression showed that 4 ‘A’ variables (atrial fibrillation, ALDH2*2 variants, age and anaemia) were significantly associated with an increased risk of HFpEF. Atrial fibrillation was associated with a 3.8-fold increased HFpEF risk (95% CI: 2.21–6.61, P ALDH2*2 variant (OR = 2.41, 95% CI: 1.49–3.87, P P = 0.004), and anaemia (OR = 1.79, 95% CI: 1.05–3.03, P = 0.032). These four variables predicted HFpEF incidence in Chinese CVD patients (C-statistic = 0.745, 95% CI: 0.691–0.800, P Conclusions 4 A traits (atrial fibrillation, ALDH2*2 variants, age and anaemia) were associated with an increased risk of HFpEF in Chinese CVD patients. Our results provide potential clues to the aetiology, pathophysiology and therapeutic targets of HFpEF.