Heart Disease in HCV+.......
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"the most relevant finding of this study is the evidence of a significant and direct correlation between HOMA and LVMI in patients with chronic HCV infection, similar to what observed in hypertensive patients.....HCV+ normotensive patients, in
comparison with healthy normotensive subjects, have a significant increase in echocardiographic
cardiac mass, totally similar to that observed in hypertensive patients.......IR/hyperinsulinemia HCV-related, by affecting
cardiac remodeling, suggests considering chronic HCV infection as a possible new factor in the global cardiovascular risk burden"
from jules: there is much discussion about extra hepatic manifestations for HCV+, earlier today i sent out email report of studies finding increased risk for HCV+ for heart disease, renal dysfunction, cancers etc. Here is another extra hepatic manifestation related to heart discussion. The authors appear to be suggesting I think that its important to address this health concern. Clearly I think the best way to address this health concern 7 all the others is to be treated for HCV & be cured.
"In conclusion, the most relevant finding of this study is the evidence of a significant and direct correlation between HOMA and LVMI in patients with chronic HCV infection, similar to what observed in hypertensive patients. Thus, IR/hyperinsulinemia HCV-related, by affecting cardiac remodeling, suggests considering chronic HCV infection as a possible new factor in the global cardiovascular risk burden. At this point arises the question whether it is necessary to treat IR in HCV+ patients not only to prevent progression to chronic fibrosis, T2DM and/or hepatocellular carcinoma and/or to improve the response to antiviral treatment, but also to prevent cardiac damage"
"The results of this study demonstrate, for the first time, that HCV+ normotensive patients, in comparison with healthy normotensive subjects, have a significant increase in echocardiographic cardiac mass, totally similar to that observed in hypertensive patients. These findings have clinical
relevance because contribute to expand previous knowledge about the pathogenetic mechanisms underlying the high prevalence of cardiovascular morbidity and mortality in this setting of patients.
In fact, there are consolidated evidences demonstrating that LVH [Left ventricular hypertrophy] is a powerful and independent
predictor of fatal and non-fatal cardiovascular events in general population , as well as in other clinical conditions [18,23,24]. Obviously, since cardiovascular events were not prospectively
evaluated in this study, our results do not consent to consider LVM as an independent predictor of cardiovascular events also in patients with liver disease."
HCV+ patients, with respect to healthy normotensive subjects, had an increased LVMI (100+23 vs 83+15 g/m2; P<0.0001), similar to that observed in HT group (103+25 g/m2) (Figure 1). In addition, regarding biochemical variables, HCV+ patients, in comparison with NT healthy subjects, had
higher triglyceride, creatinine, fasting insulin and HOMA. Of interest, no differences were found in HOMA values between HT and HCV+ (3.2+1.3 vs 3.3+1.3; P=0.651) patients. The mean value of HCV-RNA was 3868+2963 x 10 ^3 (UI/ml) in HCV+.
List of abbreviations
never-treated hypertensives (HT) and healthy subjects (NT)
LVH = Left ventricular hypertrophy
HCV = Hepatitis C Virus
LVM = Left ventricular mass
HOMA = homeostasis model assessment
LVMI = left ventricular mass index
IR = insulin resistance
T2DM = type-2 diabetes mellitus
BP = blood pressure
SBP = systolic blood pressure
DBP = diastolic blood pressure
LDL = low density lipoprotein
HDL = high density lipoprotein
CV = coefficient of variation
Chronic HCV Infection Affects Cardiac Mass in Normotensives
Journal of Hepatology Article in Press May 29, 2014
Perticone Maria, Miceli Sofia, Maio Raffaele, Caroleo Benedetto, Sciacqua
Angela, Tassone Eliezer Joseph, Greco Laura, Staltari Orietta, Sesti Giorgio,
Background and Aims
Left ventricular hypertrophy (LVH), is an independent predictor for cardiovascular events. We investigated if chronic hepatitis C virus (HCV) infection and the related insulin resistance (IR)/hyperinsulinemia could influence the increase of left ventricular mass (LVM).
We enrolled 260 outpatients matched for age, body mass index, gender, ethnicity: 52 with never-treated uncomplicated chronic HCV infection (HCV+), 104 never-treated hypertensives (HT) and 104 healthy subjects (NT). LVM was calculated according to the Devereux formula and indexed for body surface area. The following laboratory parameters were measured: fasting plasma glucose and insulin, total, LDL- and HDL-cholesterol, triglyceride, creatinine, e-GFR-EPI, HOMA. Quantitative HCV-RNA was assessed by PCR.
HCV+ patients with respect to healthy normotensive subjects had an increased LVMI (100+23 vs 83+15 g/m2; P<0.0001), similar to that observed in HT group (103+25 g/m2). Regarding biochemical variables, HCV+ patients, in comparison with normotensive healthy subjects, had higher triglyceride, creatinine, fasting insulin and HOMA (3.2+1.3 vs 2.5+1.0; P<0.0001). At linear regression analysis, the correlation between LVMI and HOMA was similar in HT (r= 0.528, P<0,0001) and HCV+ (r= 0.489, P<0,0001) groups. At multiple regression analysis, HOMA resulted the major determinant of LMVI in all groups, explaining respectively 21.8%, 27.8% and 23.9% of its variation in NT, HT and HCV+. At correlational analysis HCV-RNA and HOMA demonstrated a strong and linear relationship between them, explaining the 72.4% of their variation (P=0.022).
We demonstrated a significant and direct correlation between HOMA and LVMI in patients with chronic HCV infection, similar to that observed in hypertensives.
there are several evidences demonstrating that HCV infection is associated with some metabolic alterations, such as insulin resistance (IR) and new onset of type-2 diabetes mellitus (T2DM). In fact, several epidemiological and experimental data clearly demonstrates that HCV, operating by different pathogenetic mechanisms, is able to alter glucose metabolism [2-10]. In keeping with this, IR is already increased in the early stages of HCV-related liver disease . A possible explanation of this consists in the fact that HCV infection is able to alter glucose homeostasis through some direct and indirect mechanisms, leading to both hepatic and extra-hepatic IR [11,12]. Consequently, despite a favourable lipid profile, the cardiovascular risk of HCV+ 90 patients is moderately increased, as a consequence of the presence of subclinical atherosclerotic organ damage [6,13-16]. On the other hand, there are several evidences demonstrating that insulin signaling influences, through an interaction with the renin-angiotensin-aldosterone system [17-19], cardiac growth and the development of LVH [20-22] that is recognized as an independent predictor for cardiovascular events in such conditions as hypertension , diabetes , chronic kidney disease , as well as in general population .
At present, no information exists regarding a possible association between HCV infection and cardiac mass increase. Therefore, we designed the present study with the aim to investigate the effects of IR/hyperinsulinemia HCV-related on the development of cardiac hypertrophy in a group of subjects with a history of never-treated uncomplicated chronic HCV infection (HCV+100 ) in comparison with both never-treated hypertensives (HT) and healthy subjects (NT).