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Article

Hepatitis C Infection Is Not a Cardiovascular Risk Factor in Young Adults

by
Paweł Rajewski
1,2,*,
Małgorzata Pawłowska
3,
Dorota Kozielewicz
3,
Dorota Dybowska
3,
Anita Olczak
3 and
Jakub Cieściński
1
1
Department of Internal and Infectious Diseases, Provincial Infectious Disease Hospital, 85-030 Bydgoszcz, Poland
2
Faculty of Health Sciences, University of Health Sciences in Bydgoszcz, 85-067 Bydgoszcz, Poland
3
Department of Infectious Diseases and Hepatology, Faculty of Medicine, Collegium Medicum Bydgoszcz, Nicolaus Copernicus University, 87-100 Torun, Poland
*
Author to whom correspondence should be addressed.
Biomedicines 2024, 12(10), 2400; https://doi.org/10.3390/biomedicines12102400
Submission received: 28 September 2024 / Revised: 15 October 2024 / Accepted: 17 October 2024 / Published: 20 October 2024
(This article belongs to the Special Issue Cardiac and Vascular Diseases: Pathogenesis, Pharmacological Treatments, Advances in Therapies (2nd Edition))
Versions Notes

Abstract

:
Background: Cardiovascular diseases are one of the leading causes of hospitalization and death in Poland and around the world and are still an ongoing problem for modern medicine. Despite advances in diagnosis and treatment, both conservative and invasive, the prevention of cardiovascular disease directed at reducing risk factors remains a problem. The main classical risk factors for the development of cardiovascular disease in Poland include hypertension, lipid disorders, obesity, diabetes and smoking. A new non-classical risk factor is HCV infection. Most of the studies on the impact of HCV infection on cardiovascular disease involve elderly populations with long-term infections and advanced liver fibrosis. Methods: Hence, we set out to analyze the prevalence of risk factors and cardiovascular disease in a population of young adults under 45 years of age infected with HCV, according to gender, HCV genotype and the duration of infection. The study group consisted of 217 patients of both sexes aged 21 to 45 years (mean age 36 years). Results: No cardiovascular disease was found among the young adults infected with HCV in the study group. The most common risk factor was cigarette smoking, which affected 20.7% of the subjects, followed by hypertension (12%) and diabetes mellitus (5.5%); the prevalence was lower than in the general population. Most of the patients were characterized as overweight, with a mean BMI of 26.39 kg/m2. The mean values of other metabolic parameters—total cholesterol, LDL, HDL, uric acid and glucose—were within the population norm. The mean value of CRP was 1.43, which may indicate a moderate cardiovascular risk. Conclusions: Based on the conducted research, it was found that HCV infection in young individuals was not a risk factor for cardiovascular diseases, and the prevalence of risk factors was similar to that in the general population. The effect of HCV on the increase in C-reactive protein requires further study. The early detection of HCV infection and treatment can be considered as a prevention of cardiovascular disease.

1. Introduction

Atherosclerosis-related cardiovascular disease (ASCVD, atherosclerotic cardiovascular disease), which includes ischemic heart disease, ischemic stroke or peripheral vascular disease, is the most common and important cause of morbidity, hospitalization and mortality in Poland and worldwide [1,2,3,4,5,6,7,8,9,10].
The main risk factors for the development of cardiovascular disease in Poland include hypertension, lipid disorders, obesity, diabetes and smoking (Table 1) [6,7,8,9,10].
Chronic hepatitis C is one of the leading causes of chronic liver disease worldwide and one of the most common causes of cirrhosis and hepatocellular carcinoma, contributing to a reduced quality of life and life expectancy.
It is estimated that there are 71 million patients with chronic hepatitis C worldwide (0.5–2.3% of the population). In Poland the percentage of people with positive anti-HCV antibodies is about 1% of the population and with confirmed infection is 0.6%; however, these figures may be underestimated, due to the lack of screening. The risk of HCV is due to years of sparse or asymptomatic courses, low detection rates and lack of immunizations [11,12,13,14,15,16].
Studies in recent years show that HCV infection also leads to the development of metabolic disorders, which play an important role as a risk factor for the development of cardiovascular disease [17,18,19,20,21,22].
The noticeable effect of HCV on the development of obesity, insulin resistance, the development of pre-diabetes, diabetes, lipid disorders or hepatic steatosis has led to the metabolic disorders in the course of HCV infection being called “metabolic-viral syndrome” by some authors and hepatic steatosis being described is as an organ form of metabolic syndrome [19,20,21,22].
The observed increased incidence of cardiovascular disease in patients with hepatitis C has also contributed to HCV being considered in recent years as a new, non-classical risk factor for cardiovascular disease and the complications that occur in this regard as an extrahepatic manifestation of HCV infection. The potential role of HCV as a risk factor for the development of cardiovascular disease is complex. On the one hand, the infection directly leads to chronic inflammation, contributing to the development of atherosclerosis and vascular endothelial dysfunction; on the other hand, it leads to the development of the aforementioned metabolic disorders, which have been recognized as classic cardiovascular risk factors for years [17,18,19,20,21,22,23,24,25,26].
Most of the studies evaluating the impact of HCV infection on the development of metabolic disorders and cardiovascular disease involve adult and elderly populations with long-standing chronic hepatitis C, so we decided to examine the impact of HCV infection on the development of these conditions in a population of young adults under 45 years of age [19,22].

Purpose of the Work

The aim of this study was to analyze the prevalence of selected cardiovascular risk factors and the incidence of cardiovascular disease among young adults up to 45 years of age with chronic hepatitis C and to assess their association in relation to gender, age, the duration of infection, progression of liver fibrosis and HCV genotype.

2. Material and Methods

The study group consisted of 217 patients, 96 women and 121 men (58% male and 42% female) aged between 21 and 45 years (mean age 36 years) diagnosed with chronic hepatitis C qualified for and starting HCV treatment with drugs that act directly on the virus under the state drug program for chronic hepatitis C treatment. The patients were hospitalized at the Regional Observational and Infectious Diseases Hospital in Bydgoszcz from 2022 to 2024.
The patients’ medical records were analyzed for cardiovascular risk factors: total cholesterol, LDL (low-density lipoprotein), HDL (high-density lipoprotein), triglycerides, glucose, uric acid, BMI (body mass index), blood pressure, GFR (glomerular filtration rate), CRP (C-reactive protein) and smoking. Also analyzed were the degree of liver fibrosis and steatosis, HCV genotype and the time from the detection of the infection to the inclusion of treatment.
Each patient’s medical history was analyzed for cardiovascular diseases: hypertension, chronic coronary syndrome, myocardial infarction, history of coronary angioplasty, past coronary artery bypass grafting (CABG), stroke or TIA (transient ischemic attack), peripheral vascular disease (carotid atherosclerosis, lower limb atherosclerosis, previous lower limb artery angioplasty and aortic aneurysm), metabolic disease, diabetes and dyslipidemia.
The degree of liver fibrosis and steatosis was assessed by liver elastography performed by fibroscan with the FibroScan Expert 630 and Compact 530 (Echosens, Paris, France) instruments. The assessed parameters were the LSM by VCTE—the liver stiffness measurement by vibration-controlled transient elastography—expressed in kPa and the CAP-controlled attenuation parameter expressed in dB/m. These were respectively converted to the degree of fibrosis and steatosis using Echosens’ validation for HCV infection.
The determination of the HCV RNA and HCV genotype was performed in standardized laboratories by PCR and nucleic acid hybridization methods.
The conducted study had limitations in the comprehensive assessment of the cardiovascular risk in the examined group, as the evaluation of the cardiovascular diseases was based on the medical history collections and the assessment of cardiovascular risk factors through laboratory tests, including blood pressure measurement and BMI. The limitations included the lack of a waist circumference measurement, non-HDL cholesterol levels and apolipoproteins A (apoA) and B (apoB), a carotid artery Doppler ultrasound, coronary artery CT, or coronary angiography to detect the subclinical features of cardiovascular diseases. However, since the patients did not report clinical symptoms, these tests were not performed, and this study was a retrospective review of their medical histories. The medical histories were reviewed for smoking habits, but the use of electronic cigarettes and alcohol consumption were not assessed. Due to the age of the patients, the SCORE—the systematic coronary risk estimation—for assessing cardiovascular death over 10 years and the SCORE2 for assessing the risk of death, myocardial infarction and/or stroke, scales commonly used for this purpose, were not used to assess cardiovascular risk.

Statistical Methods

The results were presented as the mean ± standard deviation for the quantitative data and as counts expressed in numbers and percentages for the qualitative data. The normal distribution of the data was checked using the Shapiro–Wilk test, while the homogeneity of variance was checked using the Brown–Forsyth test. When the data met the assumptions of parametric analysis for comparing two dependent variables, Student’s t-test for the dependent samples and the Wilcoxon paired rank–order test was used when the data did not have a natural distribution and/or a homogeneous variance. Pearson’s chi2 test was used to compare abundances. On the other hand, the quantitative data were subjected to a correlation analysis using Pearson’s correlation coefficient for the data with a normal distribution or Spearman’s rank correlation coefficient for the data that did not meet the assumption of normality of distribution. A linear regression and analysis of covariance (ANOVA/ANCOVA) were used in the statistics to account for confounding factors. The level of statistical significance was taken as p < 0.05. The statistical analysis was performed using STATISTICA 12.0, StatSoft, Inc. (Tulsa, USA) (2014), www.statsoft.com (StatSoft Poland, Krakow, Poland).

3. Results

The study enrolled 217 patients, 96 women and 121 men, representing 42% and 58%, respectively, aged 21 to 45 years (mean age 36 years). Among the subjects, there were 22 patients (10.1%) aged 20–30, 135 (62.2%) aged 30–40 and 60 (27.6%) aged 40–45.
The study group was dominated by genotype 1b (59.45%), genotype 4 (11.52%), genotype 3 (9.68%) and genotype 1a (6.91%), while no genotype was determined (not marked) in 12.44% of the group.
The time from the diagnosis of an HCV infection to the start of treatment in 62.21% of the patients was up to 5 years, between 5 and 10 years in 14.75% and more than 10 years in 18.43%, and in 4.61% of respondents it was not possible to determine the exact time of the detection of the infection.
In the study group, the mean value of liver elasticity was 9.44 kPa (SD = 9.87), corresponding to fibrosis at the F2 level according to the Metavir scale. The level of hepatic steatosis, on the other hand, averaged 222.88 dB/m, corresponding to steatosis at the S0 level according to the Brunt scale.
Based on the analysis of the medical records in the study group, among both men and women, there was no history of burdened cardiovascular diseases: coronary artery disease, myocardial infarction, history of coronary intervention or CABG, stroke or TIA or peripheral artery disease.
Among the subjects, the most common cardiovascular risk factor was cigarette smoking, which was present in 20.7% of the subjects, more often in the age group of 20–30 years and more often in men. Hypertension was present in 12%, in the 20–30 age group in 3 people (13.6%), in the 30–40 age group in 11 people (8.1%) and in the 40–45 age group in 12 people (20%). Hypertension was more common in men.
Diabetes was diagnosed in 5.5% of the patients in the study group, with no cases of diabetes in the 20–30 age range, 3.7% in the 30–40 age range and 11.7% in the 40–45 age range. Diabetes was more common in men. The mean fasting glucose level in the study group was 96.28 mg/dL (SD = 15.69 mg/dL), the mean total cholesterol was 171.09 mg/dL (SD = 36.963 mg/dL), the LDL fraction was 86.32 mg/dL (SD = 26.00 mg/dL), the HDL fraction was 53.24 mg/dL (SD = 16.57 mg/dL) and the TG was 117.49 mg/dL (SD = 51.80 mg/dL).
In the study group, most patients were overweight, with a mean BMI of 26.39 kg/m2 (SD = 4.98 kg/m2), a minimum of 16.70 and a maximum of 39.91 kg/m2.
The mean uric acid value in the study group was 5.14 (SD = 1.52 mg/dL).
The mean concentration of CRP was 1.43 mg/L (SD = 1.81 mg/L). The renal function determined by glomerular filtration rate (GFR) showed an average of 108.46 mL/min/1.73 m2 (SD = 23.13 mL/min/1.73 m2) (Table 2, Table 3, Table 4 and Table 5).
The study group showed a significant positive relationship between the subjects’ age and glucose. The r-Pearson coefficient r = 0.313, p < 0.001 indicates a moderate association in the absolute range |0.3–0.5|, meaning that glucose levels increase with age.
In addition, a significant positive association was found between the subjects’ age and BMI. The r-Pearson coefficient r = 0.188, p < 0.006 indicates a weak relationship in the absolute range |0.0–0.3|, meaning that BMI levels increase with age.
There was a significant negative association between the subjects’ age and GFR. The r-Pearson coefficient r = −0.149, p < 0.001 indicates a weak association in the absolute range |0.0–0.3|, meaning that GFR levels decrease with age.
In addition, there was a significant positive association between the subjects’ age and liver fibrosis expressed in kPa on the liver elastography by fibroscan. The r-Pearson coefficient r = 0.228, p < 0.001 indicates a weak association in the absolute range |0.0–0.3|, indicating that the level of kPA-fibrosis increases with age, and a significant positive association between the age of the subjects and the CAP parameter indicates hepatic steatosis in the fibroscan liver elastography. The r-Pearson coefficient r = 0.211, p < 0.025 indicates a weak association in the absolute interval |0.0–0.3|, indicating that CAP increases with age (Table 4).

4. Discussion

Recent studies have shown the association of chronic hepatitis C with an increase in the risk of cardiovascular diseases and their complications and a (1.65-fold) increase in the risk of death compared to the uninfected population. The increase in the risk of cardiovascular disease in patients with chronic hepatitis C is 1.75 times greater than in uninfected individuals when an additional risk factor, such as diabetes or hypertension, is present [17,19]. Based on observational studies from Taiwan, HCV has been shown to be an independent factor in stroke and to increase the risk of peripheral arteriosclerosis by 1.43 times. A reduction in the number of acute coronary syndromes and ischemic strokes has been shown in HCV patients treated for cause compared to untreated patients. An American observational study showed that patients with detectable HCV RNA were statistically more likely to have a coronary incident [17,19,25,26]. In the study group of young HCV-infected individuals under 45 years of age, there was no history of cardiovascular disease.
This may most likely be due to the young age of the subjects, which does not increase the risk of cardiovascular disease in the general population, and the low prevalence of other classic modifiable cardiovascular risk factors in the study group.
Patient age (>45 years for men and >55 years for women) is an independent risk factor for hypertension and cardiovascular disease in both the general population and HCV patients; in the study group, the patients were under 45 years old, and the majority of subjects—62.2%—were between 20 and 30 years old. A more advanced age reflects the likelihood of other risk factors. Old age potentially has a longer overlap of single cardiovascular risk factors-more cases of diabetes, hypertension and hyperlipidemia. Also, male gender is a non-modifiable risk factor for cardiovascular disease. In the study group of HCV-infected patients, men accounted for 58% of the subjects; this was unrelated to the increased risk of cardiovascular disease in this group [1,2,8,10].
In the general population, male gender is associated with a 3-fold increased risk of coronary incidents and a 4-fold increased risk of death from coronary causes. This is associated with the presence of other cardiovascular risk factors, such as smoking, elevated levels of total and LDL cholesterol, lower levels of HDL cholesterol and the presence of hypertension. The phenomenon of gender difference is explained by the protective role of estrogens in premenopausal women, estrogens that contribute to the regulation of carbohydrate metabolism, lipid parameters, vascular endothelial function and the homeostatic system. In women with HCV, endocrine disorders are also observed with the progression of liver fibrosis, endocrine disorders, including estrogen production, which are independent of age and may contribute to the occurrence of hypertension in this group of patients. In the group of young subjects analyzed, the women were premenopausal, with little liver fibrosis; the average liver fibrosis was at the F2 level according to Metavir [1,2,3,4].
Based on large Polish population-based surveys (WOBASZ, NATPOL and PolSenior2), it has been shown that hypercholesterolemia may affect 61% of the adult population, hypertension 35%, smoking 26%, diabetes 9% and obesity 22% [1,2,4,6,7,19].
In the study group of HCV-infected young adults, no patient was treated for hyperlipidemia. The mean concentration of total cholesterol in the men was 172.82 mg/dL and of the mean concentration of LDL 88.27 was mg/dL, and in the women the mean concentrations were 168.62 and 83.64 mg/dL, respectively, and they did not meet the criteria for a diagnosis of hypercholesterolemia. In contrast, the average concentration of HDL fraction cholesterol was 51.53 mg/dL in the men and 55.80 mg/dL in the women, which were also normal values. There were no statistically significant differences in the cholesterol levels according to HCV genotype and the duration of the HCV infection. The lower prevalence of lipid disorders in the study group of patients with HCV can be explained by the young age of the patients and the low prevalence of obesity and diabetes among the subjects, as well as the awareness of the application of an appropriate lifestyle, especially dietary recommendations, in patients with liver disease.
Hypertension in the study group occurred in 12% in patients, more often in men, and the frequency increased with age, as in the general population. Although HCV-infected patients have many risk factors that increase the likelihood of hypertension, the study group did not show an increase in its frequency compared to the general population. This may be related to the young age of the subjects, which is associated with a shorter exposure to HCV and thus a shorter time for inflammatory factors to affect the vasculatures, less liver fibrosis and less obesity among the subjects. The development of inflammation appears to be one of the factors contributing to atherosclerosis and vascular damage in HCV. Ceramides composed of long-chain saturated fatty acids contribute to the development of inflammation in HCV patients. The consequences of inflammation are the apoptosis of adipocytes, mobilization of macrophages, formation of inflammatory infiltrate, release of oxygen free radicals, TNF-alpha, FFA and PA I 3, which contribute to the development of hepatic steatosis, insulin resistance, obesity and consequently the development of atherosclerosis and hypertension. TNF-alpha deregulates post-receptor pathways for insulin, blocks the insulin receptor connection to IRS-1, inhibits phosphatidyl-inositol-3 kinase and deregulates glycogen, fat and protein synthesis. IL-6 reduces insulin receptor autophosphorylation and IRS-2 phosphorylation. Oxidative stress also appears to contribute to metabolic dysfunction, resulting in the development of atherosclerosis and increased blood pressure in HCV patients. It can result in insulin resistance due to the activation of the protein kinase c-JUN N-terminal kinase, which causes IRS degradation [17,19,23,27,28,29,30].
Also, a higher risk of developing hypertension is observed with the severity of liver fibrosis; in the study group of patients, liver fibrosis was insignificant and rated at an average of F2 according to Metavir [17,19,25]. The effect of HCV on the activity of cytokines produced by adipose tissue and the associated weight gain and development of obesity may be responsible for the increased incidence of hypertension in HCV patients.
HCV patients have reduced levels of adiponectin and leptin, and increased levels of resistin, ghrelin and vizfatin, contributing to inflammation, insulin resistance, lipid disorders and atherosclerosis and consequently to the development of hypertension and obesity [8,21,22].
In the general population of Poland, obesity occurs in 22% of people, while in the population of HCV patients, obesity occurs in 17–38% of patients; this is related to the abnormalities of the adipocytokines produced by the adipose tissue mentioned above [1,6,31,32,33,34].
In the study group, the average body mass index BMI was 26.39 kg/m2; in the women, it was 24.61, and in the men, it was 27.77 kg/m2. The BMI increased with age. However, there were no statistically significant differences related to HCV genotype or length of infection in the young adults.
Type 2 diabetes occurs in 9% of Polish adults [1,6,35,36]. Epidemiological data show an association between HCV infection and the development of carbohydrate disorders, including abnormal fasting glucose, glucose intolerance or diabetes. It is estimated that the prevalence of carbohydrate disorders in patients with chronic hepatitis C is four to ten times higher than in the population of healthy people and occurs in 14–30% of patients. Hence, HCV infection is now considered a risk factor for the development of diabetes, and diabetes is considered an extrahepatic manifestation of HCV infection. Based on long-term observations, it has been shown that risk factors for the development of diabetes in patients with HCV are older age, HCV genotype 3, markedly severe fibrosis or cirrhosis, a positive family history of diabetes and kidney or liver transplantation [8,20,22,37,38,39,40]. The increased risk of developing diabetes in HCV infections is associated with insulin resistance and a chronic inflammatory response due to an increased synthesis of pro-inflammatory cytokines, mainly tumor necrosis factor (TNF) alpha and interleukin-6 (IL-6) [27,41,42]. As a result of insulin resistance, there is an increase in the concentration of insulin, which is not used efficiently by tissues, and secondary hyperinsulinemia, followed by an increase in serum glucose and the development of carbohydrate disorders. Insulin resistance also enhances adipose tissue lipolysis and the availability of free fatty acids, consequently leading to hepatic steatosis. The phenomenon of insulin resistance affects all HCV genotypes; however, it is most pronounced in genotype 3 and coexists with a lower HOMA index value [20,38,40].
The development of insulin resistance has also been linked to the direct effects of the virus on the pathway insulin signaling. In HCV genotype 3, viral proteins can directly affect intrahepatic insulin signaling by downregulating the expression of the peroxisome proliferator-activated receptor alpha (PPAR alpha). It controls the gene expression of mitochondrial carnitine palmitoyltransferase-1 (CPT-1), which reduces mitochondrial beta-oxidation responsible for fatty acid catabolism and acetyl CoA oxidase (AOX). One mechanism of insulin resistance in patients with chronic liver disease is acquired growth hormone (GH-growth hormone) resistance, which is caused by an increase in pro-inflammatory cytokines, mainly TNF alpha. Acquired GH resistance consequently causes a decrease in insulin-like growth factor-1 (IGF-1) and a compensatory increase in GH, exacerbating insulin resistance secondarily [42,43,44,45]. Insulin resistance through the increased influx of free fatty acids (FFA) into the liver, hypertriglyceridemia and hyperinsulinemia exacerbates hepatic steatosis and fibrosis. Recent studies have shown that a decreased insulin receptor substrate-1 (IRS-1 insulin receptor substrate-1) and kinase B (PKB/Akt) phosphorylation plays an important role in the pathomechanism of insulinoproneness in HCV patients. In addition, HCV affects the insulin signaling pathway through SOCS-3 (suppressor of cytokines signaling proteins) regulatory proteins, which are directly stimulated by HCV core proteins and cause the degradation of IRS-1 AND IRS-2, inhibiting relay in the insulin signaling pathway. Chronic inflammation occurring in HCV infections is also associated with the increased expression of SOCS-1 and SOCS-3 in the liver, which is associated with a decreased response to antiviral treatment. SOCS-3 also stimulates the expression of sterol regulatory element response sequence binding protein 1 c (SREBP-1c), associated with fatty acid metabolism in the liver, causing steatosis. In HCV genotype 3, core proteins enhance the degradation of IRS-1 by the aforementioned reduction in peroxisome proliferator-activated receptor gamma- (PPAR-gamma) synthesis and stimulation of SOCS-7 regulatory protein synthesis. Insulin resistance is also associated with increased levels of pro-inflammatory cytokines, TNF alpha and IL-6 [46]. The presence of insulin resistance in metabolic steatosis is correlated with its severity and appears to be an unfavorable determinant of fibrosis progression. An increased risk of developing diabetes is also associated with increased leptin secretion, resistin and decreased adiponectin secretion by adipose tissue [22,25,39].
The mean glucose level in the study group of the young adults infected with HCV was 96.28 mg/dL, and glucose levels were shown to increase with age. In contrast, in the study group of the young HCV patients, the prevalence of diabetes was 5.5% and increased with age. There were no statistically significant differences according to HCV genotype as well as length of infection.
Another cardiovascular disease risk factor analyzed was cigarette smoking. In Poland, 26% of the adult population smokes cigarettes [1,6,47]. In the study group, 20.7% of the subjects smoked, more often men. The lower number of cigarette smokers in the study group may be due to awareness of the harmful effects of smoking on the body in HCV patients and the conscious cessation of smoking, as well as the decreasing prevalence of cigarette smoking in society, especially among young people, observed in the last several years [47,48,49].
Uric acid levels were also analyzed, which averaged 5.14 mg/dL and did not depend on HCV genotype or the duration of infection. It was also within the sex-specific normal range [1,50,51,52].
In the study group of HCV-infected patients under the age of 45, there was also no increased number of patients with chronic kidney disease as a cardiovascular risk factor, and the average glomerular filtration rate (GFR) was 108, 46 mL/min. This may be due to the young age of the patients, as well as the small number of patients in the study group with diabetes or hypertension. Renal extrahepatic manifestations of HCV infection such as glomerulonephritis were also not observed in the study group [1,3,24].
Studies in recent years have highlighted the role of inflammation, particularly low-grade chronic inflammation, in the pathogenesis of coronary artery disease. C-reactive protein is an inflammatory molecule that has demonstrated value as a predictive marker in cardiovascular risk assessments, both independently and in combination with other parameters. CRP, which is mainly synthesized in the liver under the influence of pro-inflammatory cytokines such as IL-6, IL-1β and TNF, plays a key role in the progression of atherosclerotic cardiovascular disease.
Most studies have shown no or a statistically insignificant impact of HCV infection on CRP levels [53]. Based on available studies determining the relationship between HCV infection and CRP levels, higher CRP values are observed in individuals with detectable HCV- RNA viremia compared to those with a negative HCV- RNA status, and higher levels are observed in individuals infected with HCV genotype 2 compared to genotypes 1 and 3, although this was not statistically significant [54]. However, other studies have observed that IL-6 levels, which play an important role in regulating the inflammatory response and stimulate CRP production, decrease in HCV infections, explaining this through the mechanism of so-called immune tolerance due to the continuous replication of the hepatitis C virus [55,56].
In the study group of HCV-infected young adults, the mean C-reactive protein value was within normal limits, averaging 1.43 mg/L, but in terms of cardiovascular risk, values > 1 suggest a moderate cardiovascular risk. Based on available studies, CRP values below 1 correspond to a low cardiovascular risk, while values above 3 correspond to a high risk [57,58,59,60].
Based on the analysis, there was no increased risk of cardiovascular disease in the population of young adults under 45 years of age with chronic hepatitis C, and the prevalence of individual risk factors was comparable or lower than in the general population. To date, HCV infection has been considered a new, non-classical risk factor for cardiovascular disease, and cardiovascular disease an extrahepatic manifestation of HCV, but most of the studies supporting this thesis have been in the population of adults aged 45 and older [17,19,22,26]. The different results obtained in this study, compared to other researchers, related to the lack of an increase in cardiovascular morbidity among young HCV patients, may indicate that the most important risk factor for cardiovascular disease in HCV-infected patients is the patient’s age and the long duration of an HCV infection, which is associated with the likelihood of other cardiovascular factors with age, including diabetes, hypertension, obesity and more severe liver fibrosis. In addition, in recent years, and especially among young people and young adults, there has been a noticeable shift to more health-promoting lifestyles, paying attention to healthy diets and regular physical activity, and a turn away from smoking, compared to the older generation.
These obtained results require further research and can be considered as a pilot study.
These results should encourage the testing of young people for HCV infection, which will contribute to rapid detection and treatment and may help reduce the incidence of cardiovascular disease in this population [25,26,61,62].

5. Conclusions

  • HCV does not increase cardiovascular risk in young adults up to the age 45.
  • The prevalence of cardiovascular risk factors in young adults infected with HCV is not increasing.
  • HCV genotype has no effect on the prevalence of cardiovascular factors in young adults.
  • HCV infection may cause an increase in CRP levels, which is associated with an increased cardiovascular risk, but this requires further research.
  • Age, the duration of HCV infection and the severity of liver fibrosis appear to be the most significant risk factors for cardiovascular disease in HCV-infected patients.
  • The early detection of HCV infection and its early treatment can provide the prevention of cardiovascular disease.

Author Contributions

Conceptualization, P.R.; Methodology, P.R.; Software, P.R. and A.O.; Validation, P.R.; Formal analysis, P.R., D.K. and D.D.; Investigation, P.R.; Data curation, D.K., D.D., A.O. and J.C.; Writing—original draft, P.R.; Writing—review & editing, M.P. and J.C.; Visualization, J.C.; Supervision, M.P.; Project administration, M.P. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The patients were not exposed to any experimental interventions nor did the study intervene with the clinical managment of the patients. This study only collected information from patients’ medical records. The analysis included routine examinations and tests performed in patients treated within the therapeutic program of the National Health Fund. The data were originally collected to assess the treatment efficacy and safety in individual patients, not for scientific purposes. The study was approved by the ethical committee in January 2024 (The Bioethics Committee Nicolaus Copernicus University in Torun at the Collegium Medicum. Ludwik Rydygier in Bydgoszcz).. The study was not conducted on animals.

Informed Consent Statement

Patient consent was waived due to the retrospective design of the study.

Data Availability Statement

Data are contained within the article.

Conflicts of Interest

The authors declare no conflicts of interest.

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Table 1. Classic risk factors for cardiovascular disease.
Table 1. Classic risk factors for cardiovascular disease.
Modifiable FactorsNon-Modifiable Factors
  • Improper diet;
  • Smoking;
  • Reduced physical activity;
  • Hypertension;
  • Increased serum levels of total cholesterol, LDL fraction and triglycerides;
  • Reduced serum levels of HDL fraction cholesterol;
  • Diabetes and prediabetic condition
  • Obesity;
  • Metabolic syndrome;
  • Chronic kidney disease;
  • Increased serum levels of C-reactive protein, fibrinogen and homocysteine.
  • Age ≥ 45 in men and ≥55 in women;
  • Male gender;
  • A loaded family history in men < 55 years of age and in women < 65 years of age;
  • History of cardiovascular disease;
  • Genetic factors.
Table 2. Total results. (1) Total results by gender. (2) Results by age group. (3) Results by age group and gender.
Table 2. Total results. (1) Total results by gender. (2) Results by age group. (3) Results by age group and gender.
AverageMedianStandard DeviationMinimumMaximum
Total cholesterol mg/dL171.09174.0036.96385.00265.00
LDL mg/dL86.3185.5026.0148.00133.00
HDL mg/dL53.2453.0016.5726.00103.00
TG mg/dL117.49110.0051.8047.00260.00
CRP mg/L1.430.701.810.0016.20
Uric acid mg/dL5.144.801.522.0010.90
GFR mL/min/1.73 m2108.46106.0023.1324.00232.00
LSM by VCTE
(kPa)		9.446.109.872.8074.60
CAP (dB/m)222.88217.0049.03105.00400.00
BMI kg/m226.3925.704.9816.7039.91
Glucose mg/dL96.2895.0015.6969.00199.00
(1)
Gender M/WTotal Cholesterol mg/dLLDL mg/dLHDL mg/dLTG mg/dLCRP mg/L
WomenN96
Average168.6683.6455.80108.940.96
Median167.0077.0054.50100.500.59
Standard deviation39.6827.4417.64342.190.82
Minimum106.0051.0032.0047.000.00
Maximum265.00125.00103.00260.005.80
MenN121
Average172.8288.2751.53124.171.75
Median176.0091.0047.00111.000.90
Standard deviation35.2625.7015.7857.842.20
Minimum85.0048.0026.0050.000.60
Maximum260.00133.0089.00256.0016.20
Statistics
Gender M/WUric Acid mg/dLGFR mL/min/1.73 m2LSM by VCTE
kPa		CAP
dB/m		BMI kg/m2Glucose mg/dL
WomenAverage4.25106.097.190214.6124.6093.70
Median4.40103.005.75203.0023.1094.00
Standard deviation0.9421.144.2951.885.0210.40
Minimum2.00243.00105.0016.7070.00
Maximum7.1016923.50400.0038.28126.00
MenAverage5.87110.3611.22229.6927.7798.32
Median6.00106.006.50228.5027.4095.00
Standard deviation1.5324.52812.3945.874.50918.65
Minimum2.0064.002.80144.0018.5069.00
Maximum10.90232.0074.60333.0039.91199.00
(2)
Age in RangesUric Acid
mg/dL		GFR
mL/min/1.73 m2		LSM by VCTE(kPa)CAP (dB/m)BMI
kg/m2		Glucose
mg/dL
Age 20 to 30N22
Average5.85113.767.06216.6025.4988.05
Median5.00114.005.55208.0025.8087.00
Standard deviation2.2817.124.7553.634.558.72
Minimum3.9085.003.80105.0018.7070.00
Maximum10.90149.0022.70301.0035.80105.00
Age 30 to 40N13572.00135.00135.0070.00131.00135.00
Average5.06108.988.51217.9626.0894.35
Median4.75106.005.80215.0025.5093.00
Standard deviation1.4421.888.9744.174.8813.80
Minimum2.0069.003.50137.0016.7069.00
Maximum9.1023274.60294.0038.80195.00
Age 40 to 45N60
Average5.13105.4512.40238.5727.38103.63
Median5.45103.007.07232.0025.9098.50
Standard deviation1.4727.2612.3656.175.2618.78
Minimum2.2024.002.80144.0018.8785.00
Maximum7.70207.0072.60400.0039.91199.00
Age in RangesTotal Cholesterol
mg/dL		LDL
mg/dL		HDL
mg/dL		TG
mg/dL		CRP
mg/L
Age 20 to 30Average149.5670.3348.2290.783.159
Median146.0067.0046.0078.001.400
Standard deviation22.2821.2015.7128.254.78
Minimum121.0051.0026.0054.000.60
Maximum178.0093.0069.00123.0016.20
Age 30 to 40Average177.8991.1455.95121.411.257
Median178.0095.5055.00106.000.590
Standard deviation40.4728.8516.9353.771.191
Minimum85.0048.0027.0047.000.60
Maximum265.00133.00103.00260.005.80
Age 40 to 45Average166.7184.1150.13120.961.34
Median170.5080.0045.00114.000.800
Standard deviation31.4622.5215.8653.851.35
Minimum106.0057.0032.0056.000.00
Maximum230.00118.0078.00256.006.60
(3)
Age in RangesGender M/FTotal CholesterolLDLHDLTGCRP
Age 20 to 30WomenN10
Average151.0067.0050.3389.671.04
Median146.0067.0054.0078.001.20
Standard deviation22.91 15.8229.300.4152
Minimum1316733680.60
Maximum17667641231.40
MenN12
Average148.8372.0047.1791.335.282
Median148.5072.0045.0091.502.600
Standard deviation24.1329.7017.0630.546.32
Minimum121.0051.0026.0054.000.60
Maximum178.0093.0069.00123.0016.20
Age 30 to 40WomenN65
Average175.2486.0058.47110.050.92
Median174.0091.0055.0095.000.59
Standard deviation42.4534.1819.2346.770.923
Minimum120.0051.0034.0047.000.60
Maximum265.00125.00103.00260.005.80
MenN70
Average180.3094.0053.96133.351.52
Median178.00100.0055.50128.000.750
Standard deviation39.3827.2514.9959.091.32
Minimum85.0048.0027.0050.000.60
Maximum260.0133.0089.00256.004.70
Age 40 to 45WomenN21
Average158.0084.6051.50113.251.01
Median158.5077.0054.50114.500.59
Standard deviation35.8125.2414.6134.7180.64
Minimum106.0057.0032.0061.000.00
Maximum210.00118.0074.00156.002.2
MenN37
Average171.0683.5049.40125.071.49
Median174.0080.0043.00111.000.85
Standard deviation29.2922.4116.9462.461.56
Minimum116.0060.0033.0056.000.60
Maximum230.00114.0078.00256.006.60
BMI, body mass index; CAP, controlled attenuation parameter; CRP, C-reactive protein; GFR, glomerular filtration rate; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LSM by VCTE, liver stiffness measurement by vibration-controlled transient elastography; TG, triglycerides.
Table 3. Results by sex, time of infection and HCV genotype.
Table 3. Results by sex, time of infection and HCV genotype.
Gender M/FHCV GenotypeTime of Infection
Years		Total Cholesterol
mg/dL		LDL
mg/dL		HDL mg/dLTG mg/dLCRP mg/L
WomenNo data availableUp to 5 yearsN 12
Average199.25 64.67125.750.59
Median199.00 65.00128.500.59
Standard deviation25.73 0.5827.500.00
Minimum176.00 64.0090.000.60
Maximum223.00 65.001560.60
Between 5 and 10 yearsN 0 00000
Over 10 yearsN 0 00000
1aUp to 5 yearsN 4
Average148.00 56.00156.000.99
Median148.00 56.00156.000.99
Standard deviation 0.57
Minimum148.00 56.00156.000.60
Maximum148.00 56.00156.001.40
Between 5 and 10 yearsN 2
Average131.0067.0054.0068.00
Median131.0067.0054.0068.00
Minimum131.0067.0054.0068.00
Maximum131.0067.0054.0068.00
Over 10 yearsN 4
Average215.00 44.00121.500.59
Median215.00 44.00121.500.59
Standard deviation70.71 0.0048.79
Minimum165.00 44.0087.000.60
Maximum265.00 44.00156.000.60
1bUp to 5 yearsN 32 9
Average165.33108.0057.67127.890.86
Median156.00115.0046.00115.000.59
Standard deviation32.1421.3420.9256.950.43
Minimum128.0077.0032.0062.000.60
Maximum227.00125.0088.00260.002.00
Between 5 and 10 yearsN 8
Average158.50103.0058.5096.500.47
Median158.50103.0058.5096.500.59
Standard deviation45.96 21.9219.090.32
Minimum126.00103.0043.0083.000.00
Maximum191.00103.0074.00110.000.70
Over 10 yearsN 9
Average210.00 52.50104.501.24
Median210.00 52.50104.501.40
Standard deviation0.00 4.9554.450.674
Minimum210.00 49.0066.000.60
Maximum210.00 56.00143.002.20
3Up to 5 yearsN 6
Average137.0072.0063.6780.330.84
Median130.0068.0053.0085.000.84
Standard deviation35.0317.3535.2317.470.36
Minimum106.0057.0035.0061.000.60
Maximum175.0091.00103.0095.001.10
Between 5 and 10 yearsN 0 00001
Over 10 yearsN 2
Average126.00 38.0074.001.40
Median126.00 38.0074.001.40
Minimum126.00 38.0074.001.40
Maximum126.00 38.0074.001.40
4Up to 5 yearsN 7
Average146.3351.0066.0094.000.59
Median145.0051.0066.0090.000.59
Standard deviation27.02 15.5649.120.00
Minimum120.0051.0055.0047.000.60
Maximum174.0051.0077.00145.000.60
Over 10 yearsN 5
Average166.6751.0040.6781.332.09
Median146.0051.0034.0078.000.99
Standard deviation59.74 12.427.572.50
Minimum120.0051.0033.0076.000.60
Maximum234.0051.0055.0090.005.8
indefiniteBetween 5 and 10 yearsN 0
MenUp to 5 yearsN 3
Average121.00 33.00122.003.20
Median121.00 33.00122.002.10
Standard deviation 2.08
Minimum121.00 33.00122.001.90
Maximum121.00 33.00122.005.60
Over 10 yearsN 2
Average140.0074.0054.0077.001.64
Median140.0074.0054.0077.001.64
Standard deviation33.9436.779.9038.181.49
Minimum116.0048.0047.0050.000.60
Maximum164.00100.0061.00104.002.70
1Up to 5 yearsN 0
1aUp to 5 yearsN 1
Average124.0051.0065.0054.000.59
Median124.0051.0065.0054.000.59
Minimum124.0051.0065.0054.000.60
Maximum124.0051.0065.0054.000.60
Between 5 and 10 yearsN 4
Average161.50114.0039.00115.503.44
Median161.50114.0039.00115.504.10
Standard deviation9.19 7.077.782.09
Minimum155.00114.0034.00110.001.10
Maximum168.00114.0044.00121.005.10
Over 10 yearsN 1
Average192.00 33.00234.001.20
Median192.00 33.00234.001.20
Minimum192.00 33.00234.001.20
Maximum192.00 33.00234.001.20
1bUp to 5 yearsN 51
Average180.75103.0052.75101.461.46
Median178.00112.0056.0079.000.60
Standard deviation36.2435.3714.0955.671.49
Minimum116.0064.0027.0055.000.60
Maximum260.00133.0075.00256.006.60
Between 5 and 10 yearsN 11
Average185.0080.0056.00175.000.95
Median187.0080.0055.50171.500.70
Standard deviation4.69 9.4956.690.55
Minimum178.0080.0045.00111.000.60
Maximum188.0080.0068.00246.002.00
Over 10 yearsN 17
Average168.0090.5049.71150.671.587
Median168.0090.5040.00143.000.950
Standard deviation48.0521.9219.5659.691.33
Minimum85.0075.0033.0094.000.60
Maximum230.00106.0078.00256.004.30
3Up to 5 yearsN 11
Average169.5075.5048.00126.751.70
Median172.5075.5043.50126.500.80
Standard deviation41.6221.9212.9452.181.52
Minimum116.0060.0038.0065.000.60
Maximum217.0091.0067.00189.004.70
Between 5 and 10 yearsN 2
Average162.0080.0052.00190.001.19
Median162.0080.0052.00190.001.19
Standard deviation 0.86
Minimum162.0080.0052.00190.000.60
Maximum162.0080.0052.00190.001.80
4Up to 5 yearsN 8
Average184.50117.0059.75131.254.39
Median181.00117.0062.00139.50.59
Standard deviation37.85 28.9649.386.76
Minimum142.00117.0026.0066.000.60
Maximum234.00117.0089.00180.0016.20
Between 5 and 10 yearsN 5
Average173.0093.0069.0073.000.80
Median173.0093.0069.0073.000.80
Standard deviation 0.14
Minimum173.0093.0069.0073.000.70
Maximum173.0093.0069.0073.000.90
Over 10 yearsN 0
-Up to 5 yearsN 1
Average178.00 34.0078.001.30
Median178.00 34.0078.001.30
Minimum178.00 34.0078.001.30
Maximum178.00 34.0078.001.30
Gender M/WHCV GenotypeTime of InfectionUric AcidGFRFibroscan or SWE (kPa)Fibroscan (CAP)BMIGlucose
WomenUp to 5 years N 11
Average4.2099.006.62233.7825.2190.42
Median4.4099.005.45201.0022.2089.00
Standard deviation0.7111.644.3685.916.8213.65
Minimum3.0078.004.10105.0016.7070.00
Maximum4.80121.0020.00400.0037.24126.00
Between 5 and 10 yearsN 1
Average3.90115.005.30194.0018.7090.00
Median3.90115.005.30194.0018.7090.00
Minimum3.90115.005.30194.018.7090.00
Maximum3.90115.005.30194.018.7090.00
Over 10 yearsN 1
Average 80.006.20149.0020.0388.00
Median 80.006.20149.0020.0388.00
Minimum 80.006.20149.0020.0388.00
Maximum 80.006.20149.0020.0388.00
1Over 10 yearsN 1
Average5.20101.005.30203.0023.2084.00
Median5.20101.005.30203.0023.2084.00
Minimum5.20101.005.30203.023.2084.00
Maximum5.20101.005.30203.023.2084.00
1aUp to 5 yearsN 4
Average4.33108.755.87221.0021.2795.50
Median4.60115.505.60221.0019.2396.00
Standard deviation0.6421.411.5072.124.238.54
Minimum3.6078.004.60170.019.0085.00
Maximum4.80126.007.70272.0027.60105.00
Between 5 and 10 yearsN 2
Average 132.5014.10227.0023.3589.50
Median 132.5014.10227.0023.3589.50
Standard deviation 17.6812.162 3.463.54
Minimum 120.005.50227.020.9087.00
Maximum 145.0022.70227.025.8092.00
Over 10 yearsN 4
Average3.800112.006.2750238.00023.9975100.25
Median3.80109.006.25238.0024.79103.00
Standard deviation 18.461.135.662.9017.21
Minimum3.8093.005.30234.019.8378.00
Maximum3.80137.007.30242.026.57117.00
1bUp to 5 yearsN 32
Average4.46104.726.70195.4724.2094.22
Median4.40100.505.60198.0023.1595.00
Standard deviation1.15626.923.4837.893.6312.22
Minimum2.0024.003.50137.017.3072.00
Maximum7.10169.0018.10264.0031.20126.00
Between 5 and 10 yearsN 8
Average3.50106.256.62185.0025.4992.50
Median3.45101.505.70185.0022.8388.50
Standard deviation0.7120.192.6031.116.719.05
Minimum2.7083.003.80163.0018.8784
Maximum4.40141.0011.80207.038.28111.00
Over 10 yearsN 9
Average3.90107.566.80239.5028.4796.78
Median4.40108.006.10259.0030.2496.00
Standard deviation1.5112.651.6039.365.785.89
Minimum2.2090.005.30180.0020.2087.00
Maximum5.10134.009.60272.0035.20105.00
3Up to 5 yearsN 6
Average4.65109.1711.44249.5025.4398.50
Median4.65109.506.67249.5024.4098.00
Standard deviation0.9333.879.2554.454.953.89
Minimum3.6071.003.00211.0019.5094.00
Maximum5.70162.0023.50288.033.85103.00
Between 5 and 10 yearsN 1
Average 90.0012.40 38.00101.00
Median 90.0012.40 38.00101.00
Minimum 90.0012.40 38.00101.00
Maximum 90.0012.40 38.00101.00
Over 10 yearsN 2
Average4.60112.504.65 25.2293.50
Median4.60112.504.65 25.2293.50
Standard deviation 0.710.78 6.407.78
Minimum4.60112.004.10 20.7088.00
Maximum4.60113.005.20 29.7599.00
4Up to 5 yearsN 7
Average4.27107.009.33214.7523.3491.00
Median4.50109.006.40204.5020.7589.00
Standard deviation0.4915.255.4237.435.368.08
Minimum3.784.005.20184.0018.4383.00
Maximum4.6128.0018.40266.0031.24107.00
Over 10 yearsN 5
Average3.47109.005.22228.5022.2991.60
Median3.50103.004.60228.5020.7090.00
Standard deviation0.2514.780.9585.563.646.58
Minimum3.2092.004.40168.0018.0783.00
Maximum3.70126.006.40289.0026.70101.00
IndefiniteBetween 5 and 10 yearsN 1
Average5.30120.006.90205.0022.8586.00
Median5.30120.006.90205.0022.8586.00
Minimum5.30120.006.90205.0022.8586.00
Maximum5.30120.006.90205.0022.8586.00
MenUp to 5 yearsN 3
Average7.70111.3321.57266.0029.30100.33
Median6.10108.0020.20266.0027.4096.00
Standard deviation2.7726.162.54245.255.799.29
Minimum6.1087.0020.00234.0024.7094.00
Maximum10.90139.0024.50298.0035.80111.00
Over 10 yearsN 2
Average7.50105.508.37253.5024.0296.50
Median7.50105.508.37253.5024.0296.50
Standard deviation 44.553.4445.964.4216.26
Minimum7.5074.005.94221.020.9085.00
Maximum7.50137.0010.80286.027.15108.00
1Up to 5 yearsN 1 1=
Average 121.007.80 78.00
Median 121.007.80 78.00
Minimum 121.007.80 78.00
Maximum 121.007.80 78.00
1aUp to 5 yearsN 1
Average 114.007.00208.0023.40101.00
Median 114.007.70208.0023.40101.00
Minimum 114.007.70208.0023.40101.00
Maximum 114.007.70208.0023.40101.00
Between 5 and 10 yearsN 4
Average6.70111.505.62229.0028.4691.00
Median6.70109.005.45229.0028.1593.50
Standard deviation 15.970.64 2.817.62
Minimum6.7095.005.10229.0025.4080.00
Maximum6.70133.006.50229.0032.1497.00
Over 10 yearsN 1
Average6.10157.005.60 31.4986.00
Median6.10157.005.60 31.4986.00
Minimum6.10157.005.60 31.4986.00
Maximum6.10157.005.60 31.4986.00
1bUp to 5 yearsN 51
Average5.51110.6311.19221.0726.9099.37
Median5.50106.006.40212.0025.7397.00
Standard deviation1.3429.1212.5848.154.1718.42
Minimum3.0064.003.80144.018.5076.00
Maximum9.10232.0074.60333.038.80195.00
Between 5 and 10 yearsN 11
Average6.85105.828.95244.7529.85111.27
Median7.20101.005.90256.0030.0097.00
Standard deviation1.5821.537.2446.035.4136.17
Minimum4.2082.003.80181.0022.8969.00
Maximum8.80147.0026.10286.0039.91199.00
Over 10 yearsN 17
Average5.64108.0612.08246.0028.5396.41
Median5.95107.006.60250.0028.6991.00
Standard deviation1.2917.2611.0446.805.19014.74
Minimum3.8076.002.80156.0020.0085.00
Maximum7.70145.0034.60304.0037.04146.00
3Up to 5 yearsN 11
Average6.40104.5517.05223.1229.0694.73
Median6.40107.006.40234.5028.5091.00
Standard deviation0.1419.5322.5442.514.5613.42
Minimum6.3080.005.10155.0021.3680.00
Maximum6.50148.0072.60265.0036.80124.00
Between 5 and 10 yearsN 2
Average4.90102.509.850 32.0095.50
Median4.90102.509.85 32.0095.50
Standard deviation 17.682.90 8.480.71
Minimum4.9090.007.80 26.0095.00
Maximum4.90115.0011.90 38.0096.00
4Up to 5 yearsN 8
Average4.15103.005.59223.0025.3791.88
Median4.15103.005.10208.0025.5887.00
Standard deviation3.0410.021.3352.142.9615.60
Minimum2.0085.004.80180.0021.7974.00
Maximum6.30118.008.80281.0031.00126.00
Between 5 and 10 yearsN 5
Average5.97129.6014.72227.3326.3394.40
Median6.15124.006.50213.0025.8094.00
Standard deviation1.0930.8119.6567.653.613.65
Minimum4.5099.004.10168.0022.6090.00
Maximum7.10172.0049.70301.0030.2299.00
Over 10 yearsN 3
Average5.30124.006.93283.0031.41103.33
Median5.30132.007.40283.0031.00103.00
Standard deviation 23.062.93 1.7317.50
Minimum5.3098.003.80283.029.9286
Maximum5.30142.009.60283.0033.30121.00
-Up to 5 yearsN 1
Average 121.0012.10234.0030.2293.00
Median 121.0012.10234.0030.2293.00
Minimum 121.0012.10234.0030.2293.00
Maximum 121.0012.10234.0030.2293.00
BMI, body mass index; CAP, controlled attenuation parameter; CRP, C-reactive protein; GFR, glomerular filtration rate; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LSM by VCTE, liver stiffness measurement by vibration-controlled transient elastography; TG, triglycerides.
Table 4. Correlations with age.
Table 4. Correlations with age.
Correlations
Age
AgePearson correlation1
Total cholesterol
mg/dL		Pearson correlation0.007
Significance: twosided0.953
N77
LDL mg/dLPearson correlation0.125
Significance: twosided0.542
N26
HDL mg/dLPearson correlation−0.062
Significance: twosided0.595
N75
TG mg/dLPearson correlation0.123
Significance: twosided0.299
N73
Glucose mg/dLPearson correlation0.313
Significance: twosided<0.001
N217
BMI kg/m2Pearson correlation0.188
Significance: twosided0.006
N211
GFR mL/min./1.73 m2Pearson correlation−0.149
Significance: twosided0.028
N216
CRP mg/LPearson correlation−0.153
Significance: twosided0.083
N130
LSM by VCTE kPaPearson correlation0.228
Significance: twosided<0.001
CAP dB/mPearson correlation0.211
Significance: twosided0.025
BMI, body mass index; CAP, controlled attenuation parameter; CRP, C-reactive protein; GFR, glomerular filtration rate; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LSM by VCTE, liver stiffness measurement by vibration-controlled transient elastography; TG, triglycerides.
Table 5. Analysis of the prevalence of cardiovascular disease, hypertension, diabetes and smoking in the study group (N = 217). (1) Analysis of the prevalence of cardiovascular disease, hypertension, diabetes and smoking in the study group by age. (2) Analysis of the prevalence of cardiovascular disease, hypertension, diabetes and smoking in the study group by age and gender.
Table 5. Analysis of the prevalence of cardiovascular disease, hypertension, diabetes and smoking in the study group (N = 217). (1) Analysis of the prevalence of cardiovascular disease, hypertension, diabetes and smoking in the study group by age. (2) Analysis of the prevalence of cardiovascular disease, hypertension, diabetes and smoking in the study group by age and gender.
Cigarette Smoking,
N (%)		Diabetes,
N (%)		Chronic Coronary Syndrome /Heart Attack/Coronary Interventions-PTCA, CABG/Brain Stroke/TIA, N (%)Hypertension, N (%)
No171 (79.3%)205 (94.5%)217 (100%)191 (88.0%)
Yes45 (20.7%)12 (5.5%)0 (0%)26 (12.0%)
(1)
Age in RangesConditionCigarette Smoking,
N (%)		Diabetes, N (%)Hypertension,
N (%)
Age 20 to 30No16 (72.7%)22 (100.0%)19 (86.4%)
Yes6 (27.3%)0 (0.0%)3 (13.6%)
Total22 (100.0%)22 (100.0%)22 (100.0%)
Age 30 to 40No112 (83.0%)130 (96.3%)124 (91.9%)
Yes23 (17.0%)5 (3.7%)11 (8.1%)
Total135 (100.0%)135 (100.0%)135 (100.0%)
Age 40 to 45No44 (73.3%)53 (88.3%)48 (80.0%)
Yes16 (26.7%)7 (11.7%) 12 (20.0%)
Total60 (100.0%)60 (100.0%)60 (100.0%)
(2)
GenderAge in RangesConditionCigarette Smoking,
N (%)		Diabetes, N (%)Hypertension,
N (%)
WomenAge 20 to 30No8 (80%)10 (100%)10 (100%)
Yes2 (20%)0 (0%)0 (0%)
Total10 (100%)10 (100%)10 (100%)
WomenAge 30 to 40No56 (86.2%)65 (100%)62 (95.4%)
Yes9 (13.8%)0 (0%)3 (4.6%)
Total65 (100%)65 (100%)65 (100%)
WomenAge 40 to 45No17 (81%)19 (95.5%)15 (71.4%)
Yes4 (19%)2 (9.5%)6 (28.6%)
Total21 (100%)21 (100%)21 (100%)
MenAge 20 to 30No8 (66%)12 (100%)9 (75%)
Yes4 (33.3%)0 (0%)3 (25%)
Total12 (100%)12 (100%)12 (100%)
MenAge 30 to 40No55 (78.6%)65 (92,9%)62 (88.6%)
Yes14 (20%)5 (7.1%)8 (11.4%)
Total69 (98.6%)70 (100%)70 (100%)
MenAge 40 to 45No27 (69.2%)34 (87.2%)33 (84.6%)
Yes12 (30.8%)5 (12.8%)6 (15.4%)
Total39 (100%)39 (100%)39 (100%)
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MDPI and ACS Style

Rajewski, P.; Pawłowska, M.; Kozielewicz, D.; Dybowska, D.; Olczak, A.; Cieściński, J. Hepatitis C Infection Is Not a Cardiovascular Risk Factor in Young Adults. Biomedicines 2024, 12, 2400. https://doi.org/10.3390/biomedicines12102400

AMA Style

Rajewski P, Pawłowska M, Kozielewicz D, Dybowska D, Olczak A, Cieściński J. Hepatitis C Infection Is Not a Cardiovascular Risk Factor in Young Adults. Biomedicines. 2024; 12(10):2400. https://doi.org/10.3390/biomedicines12102400

Chicago/Turabian Style

Rajewski, Paweł, Małgorzata Pawłowska, Dorota Kozielewicz, Dorota Dybowska, Anita Olczak, and Jakub Cieściński. 2024. "Hepatitis C Infection Is Not a Cardiovascular Risk Factor in Young Adults" Biomedicines 12, no. 10: 2400. https://doi.org/10.3390/biomedicines12102400

APA Style

Rajewski, P., Pawłowska, M., Kozielewicz, D., Dybowska, D., Olczak, A., & Cieściński, J. (2024). Hepatitis C Infection Is Not a Cardiovascular Risk Factor in Young Adults. Biomedicines, 12(10), 2400. https://doi.org/10.3390/biomedicines12102400

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