Objective Previous studies that evaluated cardiovascular risk factors considered age as a potential confounder. We aimed to investigate the impact of cardiovascular disease (CVD) and its risk factors on fatal outcomes according to age in patients with COVID-19. Methods A systematic literature review and meta-analysis was performed on data collected from PubMed and Embase databases up to 11 June 2020. All observational studies (case series or cohort studies) that assessed in-hospital patients were included, except those involving the paediatric population. Prevalence rates of comorbid diseases and clinical outcomes were stratified by mean patient age in each study (ranges: <50 years, 50–60 years and ≥60 years). The primary outcome measure was a composite fatal outcome of severe COVID-19 or death. Results We included 51 studies with a total of 48 317 patients with confirmed COVID-19 infection. Overall, the relative risk of developing severe COVID-19 or death was significantly higher in patients with risk factors for CVD (hypertension: OR 2.50, 95% CI 2.15 to 2.90; diabetes: 2.25, 95% CI 1.89 to 2.69) and CVD (3.11, 95% 2.55 to 3.79). Younger patients had a lower prevalence of hypertension, diabetes and CVD compared with older patients; however, the relative risk of fatal outcomes was higher among the former. Conclusions The results of the meta-analysis suggest that CVD and its risk factors (hypertension and diabetes) were closely related to fatal outcomes in COVID-19 for patients across all ages. Although young patients had lower prevalence rates of cardiovascular comorbidities than elderly patients, relative risk of fatal outcome in young patients with hypertension, diabetes and CVD was higher than in elderly patients. Prospero registration number CRD42020198152.

Background: As body fat composition and metabolism differ between men and women, we evaluated sex-related differences in the association among epicardial adipose tissue (EAT), secretome profile, and myocardial function of subjects with suspected metabolic syndrome. Methods: We evaluated 277 participants (men, n = 140; 56.1 ± 4.7 years) who underwent conventional echocardiography and two-dimensional speckle tracking from the Seoul Metabolic Syndrome cohort. EAT was measured from the right ventricular free wall perpendicular to the aortic annulus at end systole. Global longitudinal strain (GLS) was obtained from 18 apical segments. Apolipoprotein A1, apolipoprotein B, adiponectin, and high-sensitivity C-reactive protein (hs-CRP) levels were measured using immunoturbidimetry assay. Results: Mean age, body mass index, and hs-CRP level did not differ by sex. Waist circumference, fasting blood glucose level, and triglyceride/high-density lipoprotein cholesterol ratio were higher, and apolipoprotein AI and adiponectin levels were lower in men. No significant difference in mean EAT thickness was found (7.02 ± 1.81 vs. 7.13 ± 1.70 mm, p = 0.613). Men had a higher left ventricular (LV) mass index and lower GLS. EAT thickness was associated with hs-CRP level in men alone (ß = 0.206, p = 0.015). LV mass index (ß = 2.311, p = 0.037) and function represented by e′ (ß = − 0.279, p = 0.001) and GLS (ß = − 0.332, p < 0.001) were independently associated with EAT thickness in men alone. Conclusions: In middle-aged subjects with suspected metabolic syndrome, EAT was associated with inflammation represented by hs-CRP level, LV mass, and subclinical myocardial dysfunction only in men, suggesting that the inflammatory activity of EAT induced myocardial remodeling and dysfunction in middle-aged subjects but was attenuated in women. Trial registration NCT02077530 (date of registration: November 1, 2013)

Kim HD, et al. Int J Heart Fail. 2022 Jan;4:e5. https://doi.org/10.36628/ijhf.2021.0043

Abundant evidence indicates that oestrogen (E₂) plays a protective role against hypertension. Yet, the mechanism underlying the antihypertensive effect of E₂ is poorly understood. In this study, we sought to determine the mechanism through which E₂ inhibits salt-dependent hypertension. To this end, we performed a series of in vivo and in vitro experiments employing a rat model of hypertension that is produced by deoxycorticosterone acetate (DOCA)-salt treatment after uninephrectomy. We found that E₂ prevented DOCA-salt treatment from inducing hypertension, raising plasma arginine-vasopressin (AVP) level, enhancing the depressor effect of the V1a receptor antagonist (Phenylac¹,D-Tyr(Et)²,Lys⁶,Arg⁸,des-Gly⁹)-vasopressin, and converting GABAergic inhibition to excitation in hypothalamic magnocellular AVP neurons. Moreover, we obtained results indicating that the E₂ modulation of the activity and/or expression of NKCC1 (Cl⁻ importer) and KCC2 (Cl⁻ extruder) underpins the effect of E₂ on the transition of GABAergic transmission in AVP neurons. Lastly, we discovered that, in DOCA-salt-treated hypertensive ovariectomized rats, CLP290 (prodrug of the KCC2 activator CLP257, intraperitoneal injections) lowered blood pressure, and plasma AVP level and hyperpolarized GABA equilibrium potential to prevent GABAergic excitation from emerging in the AVP neurons of these animals. Based on these results, we conclude that E₂ inhibits salt-dependent hypertension by suppressing GABAergic excitation to decrease the hormonal output of AVP neurons.

Background: Although aldosterone has been demonstrated to induce left ventricular (LV) hypertrophy not only in primary aldosteronism but also in primary hypertension (HT), it can be affected by multiple factors, including age, and the effect of aldosterone on LV function is controversial. This study was to investigate the relationship of aldosterone to changes in LV geometry and function in young adults with never-treated HT. Methods: Seventy-five consecutive patients (age, 29.8 ± 6.3 years) with never-treated HT and 45 normal controls were enrolled. Echocardiographic values and LV global longitudinal strain (LVGLS) were obtained. Serum aldosterone concentration (SAC) and serum procollagen type III amino-terminal peptide (PIIINP) level were obtained in HT patients. Results: HT patients had higher LV mass index, higher relative wall thickness (RWT), and worse LV function than normal controls. LVGLS and e’ velocity were worse in HT patients with normal geometry than in normal controls. SAC was well correlated with LV mass index, RWT, e’ velocity, LVGLS, and PIIINP (all p < 0.05). LV geometry pattern was most related to SAC among clinical parameters (p = 0.019). LVGLS was most related to LV geometry and diastolic blood pressure. In contrast, e’ velocity was most related to PIIINP. Conclusion: Our findings may indicate that in young patients with never-treated HT, aldosterone significantly contributes to changes in LV geometry and functional impairment through its pro-hypertrophic and myocardial fibrosis effects beyond blood pressure.