“…Hypertension, diabetes, and dyslipidemia were defined as previously reported. 28 HIV-seronegative participants received testing for HIV by immunoassay at every core visit and, if positive, confirmation by repeat immunoassay. Plasma HIV RNA was measured by commercial immunoassay (detection limit: 20 copies/mL).…”
“…Hypertension, diabetes, and dyslipidemia were defined as previously reported. 28 HIV-seronegative participants received testing for HIV by immunoassay at every core visit and, if positive, confirmation by repeat immunoassay. Plasma HIV RNA was measured by commercial immunoassay (detection limit: 20 copies/mL).…”
“…Current smoking was defined by self-report of any ongoing smoking, and heavy alcohol use as more than seven drinks/week. Hypertension, diabetes and dyslipidemia were defined as previously reported [26]. History of myocardial infarction was obtained by self-report.…”
Background: HIV and HCV have each been linked with cardiac dysfunction. Studies of HIV have often lacked appropriate controls and primarily involved men, whereas data for HCV are sparse.Methods: We performed repeat echocardiography over a median interval of 12 years in participants from the Women's Interagency HIV Study in order to evaluate the relationships of HIV and HCV with incident left ventricular (LV) dysfunction (systolic or diastolic).Results: Of the 311 women included (age 39 AE 9), 70% were HIV-positive and 20% HCV-positive. Forty three participants (13.8%) developed LV dysfunction, of which 79.1% was diastolic. Compared with participants with neither infection, the group with HIV-HCV coinfection showed a significantly increased risk of incident LV dysfunction after adjustment for risk factors [RR ¼ 2.96 (95% CI ¼ 1.05-8.31)], but associations for the HCV monoinfected and HIV monoinfected groups were not statistically significant [RR ¼ 2.54 (0.83-7.73) and RR ¼ 1.66 (0.65-4.25), respectively]. Comparison of HCVpositive and HCV-negative women showed a significantly increased risk independent of covariates [RR ¼ 1.96 (1.02-3.77)] but this was not the case for HIV-positive vs. HIVnegative women [RR ¼ 1.43 (0.76-2.69)]. There was no evidence of HCV-by-HIV interaction. A more restrictive definition of LV diastolic dysfunction led to fewer incident cases, but a similar, though nonsignificant, risk estimate for HCV.Conclusion: Among mostly middle-aged women, HCV but not HIV infection was associated with a pronounced risk of incident LV dysfunction. Although the influence of residual confounding cannot be excluded, these findings bolster the potential benefits that could be realized by adopting recent recommendations for expanding HCV screening and treatment.
“…Cardiac hypertrophy is an adaptive response to maintain cardiac function, but it ultimately becomes mainly maladaptive and leads to heart failure (HF). However, accumulated data provided evidence that CTRPs are highly associated with cardiometabolics, inflammatory response, and immunoregulatory function [ 53 , 54 , 55 ].…”
With continually improving treatment strategies and patient care, the overall mortality of cardiovascular disease (CVD) has been significantly reduced. However, this success is a double-edged sword, as many patients who survive cardiovascular complications will progress towards a chronic disorder over time. A family of adiponectin paralogs designated as C1q complement/tumor necrosis factor (TNF)-associated proteins (CTRPs) has been found to play a role in the development of CVD. CTRPs, which are comprised of 15 members, CTRP1 to CTRP15, are secreted from different organs/tissues and exhibit diverse functions, have attracted increasing attention because of their roles in maintaining inner homeostasis by regulating metabolism, inflammation, and immune surveillance. In particular, studies indicate that CTRPs participate in the progression of CVD, influencing its prognosis. This review aims to improve understanding of the role of CTRPs in the cardiovascular system by analyzing current knowledge. In particular, we examine the association of CTRPs with endothelial cell dysfunction, inflammation, and diabetes, which are the basis for development of CVD. Additionally, the recently emerged novel coronavirus (COVID-19), officially known as severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has been found to trigger severe cardiovascular injury in some patients, and evidence indicates that the mortality of COVID-19 is much higher in patients with CVD than without CVD. Understanding the relationship of CTRPs and the SARS-CoV-2-related damage to the cardiovascular system, as well as the potential mechanisms, will achieve a profound insight into a therapeutic strategy to effectively control CVD and reduce the mortality rate.
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