Cardiovascular Endocrinology & Metabolism最新文献

The adaptive use of Janus kinase (JAK)-inhibitors has been suggested by rheumatology experts in the management of COVID-19. We recount the rationale behind their use in this setting, and the current evidence for and against their use in this review. JAK-inhibitors role in COVID-19 infection appears to be multifaceted, including preventing viral endocytosis and dampening the effect of excessive chemokines. This drug class may be able to achieve these effects at already preapproved dosages. Concerns arise regarding reactivation of latent viral infections and the feasibility of their use in those with severe disease. Most interestingly, JAK-Inhibitors may also have an additional advantage for diabetic and obese populations, where the dysregulation of JAK-signal transducer and activator of transcription pathway may be responsible for their increased risk of poor outcomes. Targeting this pathway may provide a therapeutic advantage for these patient groups.

There has been a recent increase in the use of testosterone supplementation among young adults in the United States, despite the controversy of testosterone replacement therapy (TRT) and cardiovascular safety. The lower testosterone levels and earlier age of TRT use in persons living with HIV (PLHIV) is of particular relevance for this population because cardiovascular disease (CVD) comorbidities are known to be increased among PLHIV. There is very limited data on TRT in PLHIV, as such, in this article, we sought to compile current evidence regarding the diagnosis and management of testosterone deficiency and its link to CVD risk including among PLHIV.

Background: There is conflicting data regarding the association between low levels of plasma vitamin D and ischemic heart disease. We aimed to investigate the relationship between plasma vitamin D levels and heart valve calcification in hospitalized patients with ischemic heart disease versus non-ischemic heart disease controls.

Methods: A prospective case-control study comprising two age and gender-matched groups. The study group included consecutive patients hospitalized due to acute coronary syndrome; the control group included consecutive non-ischemic heart disease patients hospitalized for noncardiac causes. Blood samples for 25-hydroxyvitamin D level were drawn. An echocardiogram was performed during the first 3 days of hospitalization and reviewed for presence and degree of valvular calcification.

Results: Forty patients with acute coronary syndrome and 40 controls (age 58 ± 11 years, 64% male in both groups) were included. Mean plasma 25-hydroxyvitamin D vitamin level in the entire cohort was 24.5 ± 8 ng/ml. Valve calcification rates were similar in acute coronary syndrome versus non-acute coronary syndrome group (28 vs. 21 had valvular calcification; 18 vs. 12 had aortic valve calcification; 21 vs. 14 had mitral valve calcification, respectively; P = NS for all). We found no significant relationship between vitamin D level and valvular calcification, aortic valve calcification, or mitral valve calcification rate or degree in the entire cohort and in each group alone (P = NS for all). There was a negative correlation between 25-hydroxyvitamin D levels and age in the acute coronary syndrome group (r = -0.399, P = 0.012).

Conclusions: We did not find a significant relationship between plasma vitamin D levels and the rate or degree of calcification of either aortic/mitral/both valves in hospitalized patients with or without ischemic heart disease.

A 24-year-old male patient came to the emergency room with melena, gum bleeding and nosebleeds. This patient has a history of mechanical prosthetic mitral valve replacement for severe mitral regurgitation (MR) and consumed warfarin irregularly, but did not come back for regular check-up. Investigations showed greatly increased thyroid function and international normalised ratio (INR) was 15.8. Patients were diagnosed with thyroid storm and bleeding due to prolongation of INR. His hyperthyroid state might have caused increased rate of degradation of vitamin K-dependent clotting factor thereby increased sensitivity to warfarin. Concomitant acute decompensated heart failure, thrombocytopenia and hypoalbuminemia also contributed to his risk of bleeding. Treatment included anti-thyroid therapy as well as warfarin reversal therapy by stopping warfarin, low-dose intravenous vitamin K due to his mechanical prosthetic valve and fresh frozen plasma. In conclusion, hyperthyroidism could increase the response to warfarin so close monitoring is needed to balance the risk of bleeding and thromboembolism.

Cardiovascular disease is one of the leading causes of morbidity and mortality in persons with cancer. The elevated risk is thought to derive from the combination of cardiovascular risk factors and direct cardiotoxicity from cancer therapies. Exercise may be a potential strategy to counteract these toxicities and maintain cardiovascular reserve. In this article, we review the evidence for the potential cardioprotective effects of exercise training in cancer patients before, during, and following treatment. We also propose a patient-tailored approach for the development of targeted prescriptions based on individual exercise capacity and cardiovascular reserve.

Background: Eukaryotes chromosomal ends are capped and protected by telomeres, which are noncoding DNA repeats synthesized by telomerase enzyme. The telomerase enzyme is a nucleoprotein encoded by TERC and TERT genes. Naturally, the length of the telomeres shortens with each cell cycle but the shortening is fastened in certain age-related diseases like hypertension (HTN) and type 2 diabetes mellitus (T2DM).

Materials and methods: Blood samples (n = 171) were obtained from Kuwaiti subjects with HTN, and HTN/T2DM comorbidity (HTN-DM) and healthy subjects. The leukocyte telomere length (LTL) was measured by SYBR green quantitative rtPCR, and plasma telomerase enzyme was measured by ELISA, in addition, three single nucleotide polymorphisms (SNPs) in telomere-related genes; TERC rs12696304GC, TERT rs2736100CA, and ACYP2 rs6713088GC were genotyped by real-time PCR.

Results: Marked LTL shortening in subjects with HTN and HTN-DM compared to healthy subjects, P = 0.043 and P < 0.001, respectively, was noticed. On the contrary, the plasma telomerase enzyme levels and minor allele frequencies and genotypes of the tested SNPs were comparable between the study groups, except for TERT (CA) genotype which was over-represented in HTN (P = 0.037). Furthermore, the comparisons between HTN and HTN-DM revealed significantly higher total cholesterol (P = 0.015) and LDL-C (P = 0.008) in HTN, while higher insulin levels (P < 001), HOMA-IR (P < 001), and BMI (P = 0.004) were observed in HTN-DM.

Conclusion: This study showed comparable LTL shortening in HTN and HTN-DM, irrespective of plasma telomerase enzyme levels or tested TERC, TERT, and ACYP2 gene polymorphisms, although HTN and HTN-DM differed in several metabolic markers. More studies are required to affirm these observations.

Objectives: Sirtuin 3 (SIRT3) can protect cardiomyocytes from oxidative stress-mediated cell damage and prevent cardiac hypertrophy development. The aim of this study was to evaluate whether a relationship existed between left ventricular mass index (LVMI) and serum SIRT3 levels in patients with hypertension.

Patients and methods: This study was conducted as a cross-sectional study of 83 patients between April 2018 and October 2018. The LVMI of all patients was calculated using the formula of the American Echocardiography Association and patients were divided into two groups according to results (increased LVMI and normal LVMI).

Results: Increased LVMI was determined in 37.3% of patients, whereas 62.7% had normal LVMI. There was no significant difference between serum SIRT3 levels between those with increased LVMI and normal LVMI (5.8 versus 5.4 ng/ml; P = 0.914). Serum pro-brain natriuretic peptide levels (69 versus 41 ng/ml; P = 0.019) were found to be higher in patients with increased LVMI than in those with normal LVMI. A positive correlation between SIRT3 levels and Sm (myocardial systolic) velocity was also determined (r = 0.338; P = 0.002).

Conclusion: The serum levels of SIRT3, a molecule which has been proposed to have protective properties against myocardial hypertrophy, were not found to be correlated with LVMI values; however, SIRT3 levels were found to be correlated with Sm velocity, which is accepted to be an indicator of myocardial early diastolic dysfunction.

Objectives: To demonstrate a magnitude of the cardiovascular benefits, concomitantly analyzing the safety outcomes of sodium-glucose cotransporter 2 inhibitor (SGLT2-I) comprehensively, as a class effect in a larger sample size combined from recent randomized control trials.

Methods: We searched electronic databases using specific terms and evaluated 6 efficacy and 10 safety outcomes. Odds ratios (ORs) and 95% confidence interval (CI) were used to compare two interventions.

Results: Five studies (n = 41 267) were included, among which 23 539 received SGLT2-I. The SGLT2-I group favored reduction in major adverse cardiovascular events (OR, 0.78; 95% CI, 0.62-0.98; P = 0.03), cardiovascular death (CVD) or heart failure hospitalization (OR, 0.60; 95% CI, 0.46-0.80; P = 0.0004), rate of hospitalization for heart failure (OR, 0.56; 95% CI, 0.44-0.72; P < 0.00001), CVD (OR, 0.68; 95% CI, 0.50-0.93; P = 0.01), all-cause mortality (OR, 0.67; 95% CI, 0.48-0.93; P = 0.02) and myocardial infarction (OR, 0.79; 95% CI, 0.64-0.99; P = 0.04) when compared to the placebo group. Safety analysis showed higher diabetic ketoacidosis (DKA) rate in SGLT2-I group (OR, 2.33; 95% CI, 1.40-3.90; P = 0.001); in contrast, major hypoglycemic events were significantly lower (OR, 0.79; 95% CI, 0.73-0.87; P < 0.00001). AKI was significantly higher in the placebo group (OR, 0.76; 95% CI, 0.65-0.88; P = 0.0004). There were no statistically significant effects on other outcomes.

Conclusion: In selected high-risk patients of cardiovascular disease, the SGLT2-I is a potential effective class of drugs for improving cardiovascular outcomes and all-cause mortality without an increased risk of all other major complications except DKA on this meta-analysis.

Introduction: Hypogonadism is associated with poorer glycaemic outcomes/increased all-cause and cardiovascular morbidity/mortality in type 2 diabetes mellitus (T2DM). Increasing CAG repeat number within exon-1 of the androgen receptor (AR) gene is associated with increased AR resistance/insulin resistance.

Methods: We determined in a long-term 14-year follow-up cohort of 423 T2DM Caucasian men, the association between baseline androgen status/CAG repeat number (by PCR then Sequenom sequencing) and metabolic/cardiovascular outcomes.

Results: Metabolic outcomes: Lower total testosterone was associated with higher BMI (kg/m²) at 14-year-follow-up: regression coefficient -0.30 (95% confidence interval -0.445 to -0.157), P = 0.0001. The range of CAG repeat number was 9-29 repeats. Higher CAG repeat number in exon-1 of the AR gene was associated with higher follow-up HbA1c2016 - each unit increase in CAG repeat-associated with an increment of 0.1% in HbA1C2016 (P = 0.04), independent of baseline testosterone. Cardiovascular outcomes and mortality: At an average of 14-year-follow-up, 55.8% of hypogonadal men had died vs 36.1% of eugonadal men (P = 0.001). There was a 'u' shaped relation between number of CAG repeats and mortality. Twenty-one CAG repeats were associated with an up to nearly 50% lower mortality rate than <21 CAG repeats and >21 CAG repeats - independent of baseline testosterone level.

Conclusion: A higher number of CAG repeats at the AR gene associates with higher future HbA1c. There was a 'u' shaped relation between CAG repeat number and mortality rate. Determination of CAG repeat number may become part of assessment of androgen status/its consequences for men with T2DM.