Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 30  |  Issue : 3  |  Page : 818-822

Hepatitis C as a risk factor for coronary artery disease in silent myocardial ischemia


1 Department of Internal Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Cardiology, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Date of Submission30-Jan-2016
Date of Acceptance08-May-2016
Date of Web Publication15-Nov-2017

Correspondence Address:
Ramy M Omar
Department of Cardiology, Faculty of Medicine, Menoufia University, Shibein El-Kom 32511, Menoufia
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_106_17

Rights and Permissions
  Abstract 

Objective
The aim of the present study was to evaluate the relationship between seropositivity of hepatitis C virus (HCV) and the severity of coronary artery disease in silent myocardial ischemic patients.
Background
Silent myocardial ischemia is defined as an objective evidence of myocardial ischemia occurring in the absence of symptoms. HCV was found to have a positive association with carotid artery plaque.
Patients and methods
We investigated 50 patients with silent myocardial ischemia. Patients were divided into two groups (group A included 25 HCV-seropositive patients and group B included 25 HCV-seronegative patients). Patients were subjected to history taking, clinical examination, and investigations such as 24-h Holter monitoring, complete blood count, liver and renal function tests, and random blood glucose, lipid profile, viral marker tests. Abdominal ultrasonography, echocardiography, and coronary angiography were carried out for all patients. The SYNTAX score was calculated.
Results
Fifteen patients of group A had left anterior descending disease versus seven of group B (P = 0.013). Thirteen patients of group A had left circumflex disease versus six of group B (P = 0.013). Fourteen patients of group A had right coronary artery disease versus six of group B (P = 0.0023).The SYNTAX score of group A was 15.76 ± 6.75, whereas the score for group B was 11.36 ± 7.64 (P = 0.0.036).
Conclusion
There was a positive relationship between HCV and number of diseased coronary vessels, and there was a positive relationship between HCV seropositivity and complexity of coronary lesions in the light of SYNTAX score as well.

Keywords: coronary artery disease, hepatitis C, risk factors


How to cite this article:
Dala AG, Hamed WA, Badr MH, Omar RM. Hepatitis C as a risk factor for coronary artery disease in silent myocardial ischemia. Menoufia Med J 2017;30:818-22

How to cite this URL:
Dala AG, Hamed WA, Badr MH, Omar RM. Hepatitis C as a risk factor for coronary artery disease in silent myocardial ischemia. Menoufia Med J [serial online] 2017 [cited 2020 Apr 8];30:818-22. Available from: http://www.mmj.eg.net/text.asp?2017/30/3/818/218249


  Introduction Top


Coronary artery disease (CAD) is the most common form of heart disease with multifactorial etiology with atherosclerosis being the principal cause. Although CAD has been viewed as a dyslipidemic degenerative disease, it is now considered a dynamic process with a strong inflammatory characteristic [1]. The inflammation theory postulates that the initiation and progression of lesions are represented by inflammatory and fibroproliferative processes. This process is responsible for progression and destabilization of atherosclerotic plaques [2].

Hepatitis C virus (HCV) is a small, single-stranded virus, and it is a major healthcare concern worldwide but more so in developing countries [3]. There is a positive association between HCV infection and carotid artery plaque independent of other risk factors for atherosclerosis [4]. Silent myocardial ischemia is defined as an objective evidence of myocardial ischemia occurring in the absence of symptoms in a patient who has either CAD or spasms [5],[6]. It can be detected by transient ischemic ECG abnormalities that occur without symptoms during exercise testing [7]. Moreover, reversible left ventricular wall motion abnormalities without symptoms can be detected by radionuclide angiography or two-dimensional echocardiography [8].

The aim of the present study was to evaluate the relationship between seropositivity for HCV and the severity of CAD in silent myocardial ischemic patients.


  Patients and Methods Top


This cross-sectional hospital-based study was carried out at Menoufia University Hospital and the Egyptian National Heart Institute in the period between May 2015 and May 2016. The study included 50 patients with silent myocardial ischemia who underwent coronary angiography for evaluation of myocardial ischemia.

  1. written informed consent after thorough explanation of the technique and possible procedural risks and benefits was obtained from all patients
  2. The study was approved by the Ethics Committee of Menoufia Faculty of Medicine.


Study design

Patients were classified into two groups:

  1. Group A included 25 HCV-seropositive patients (study group)
  2. Group B included 25 HCV-seronegative patients (control group). Patients of the control group were matched with patients of the study group with respect to demographic data and risk factors.


Patients included in this study fulfilled the following criteria.

Inclusion criteria

Patients diagnosed as having silent myocardial ischemia by transient ischemic electrocardiographic abnormalities using 24-h Holter monitoring, without the presence of anginal pain at the same time as mentioned by the patients using a diary in which they recorded how they felt, were included.

Exclusion criteria

Patients with recent acute coronary syndrome, heart failure, acute pulmonary embolus, noncardiac disorders that may preclude exercise performance (e.g., infection, renal failure, thyrotoxicosis, etc.), acute myocarditis or pericarditis, stenotic valvular heart disease, electrolyte abnormalities, tachyarrhythmias or bradyarrhythmias, patients with liver cell failure, or HBsAg seropositive patients were excluded.

Patients were subjected to the following: full history taking; thorough clinical examination and investigations such as 12-lead resting ECG, 24-h Holter monitoring, and complete blood count; tests to determine levels of alanine transaminase, aspartate transaminase, bilirubin, urea, creatinine, serum electrolytes, random blood glucose, lipid profile, and viral markers for HCV and hepatitis B virus; and PCR for HCV-positive patients. Echocardiography was performed using an echocardiographic machine (GE Vivid 6, Davis Medical Electronics, Inc., California, USA), with a 5-s probe of 2.2–5 MHz for both two-dimensional and Doppler imaging in all patients, for detecting atrial, ventricular, and septal diameters and dimensions, ejection fraction, fractional shortening, and wall motion abnormalities. Abdominal ultrasonography was performed for all patients.

Coronary angiography was performed for all patients, and all coronary angiograms were analyzed. The cineframe was digitalized on a video monitor. The coronary artery tree was divided into segments. For each lesion, an end-diastolic frame was selected with identical angulations that best showed the stenosis at its most severe degree with minimal foreshortening and branch overlap. For each patient, we analyzed each artery including branches and site and significance of lesions, number of lesions, and number of diseased vessels. The SYNTAX score is defined as an anatomy-based risk score that takes into account features such as bifurcations, total occlusions, thrombus, calcification, and small vessels.

Statistical analysis

All statistical analyses were performed using statistical package for the social sciences (SPSS) version 17 (SPSS Inc., Chicago, Illinois, USA). For quantitative data, the mean and the SD were calculated. Comparison between the studied groups was performed using the Student t-test, with P value less than 0.05 considered statistically significant. For qualitative data, correlation between variables was evaluated using Pearson's correlation coefficient.


  Results Top


There were no statistically significant differences between both groups with regard to age and sex.

There was no statistically significant differences between both groups regarding the mean left ventricular ejection fraction [Table 1].
Table 1: Baseline clinical data in the study and control groups

Click here to view


There were no significant differences between both groups regarding hemoglobin level, white blood cell count, serum creatinine, lipid profile, total bilirubin, albumin, and the international normalized ratio [Table 2].
Table 2: Baseline laboratory data in the studied groups

Click here to view


There was no statistically significant difference between both groups with regard to hypertension [21 (84%) patients of group A were hypertensive vs. 20 (80%) patients of group B], diabetes mellitus [16 (64%) patients of group A were diabetic vs. 15 (60%) patients of group B], smoking [14 (56%) patients of group A were smokers vs. 13 (52%) patients of group B], or dyslipidemia [12 (48%) patients of group A were dyslipidemic vs. 13 (52%) patients of group B] [Table 3].
Table 3: Comparison between both groups according to risk factors

Click here to view


Left anterior descending coronary artery findings

A statistically significant difference was found regarding left anterior descending coronary artery (LADCA) affection as 15 (60%) patients of group A had LADCA lesions versus seven (28%) patients of group B. In addition, a statistically significant difference was found regarding proximal lesions, as 13 (52%) patients of group A had proximal lesions versus five (20%) patients of group B. No statistically significant differences were found regarding mid-segment, distal, or diagonal lesions.

Left circumflex coronary artery findings

A statistically significant difference was found regarding left circumflex coronary artery (LCCA) affection as 13 (52%) patients of group A had LCCA lesions versus six (24%) patients of group B. In addition, a statistically significant difference was found regarding proximal lesions as13 (52%) patients of group A had proximal lesions versus three (12%) patients of group B. No statistically significant differences were found regarding mid-segment, distal, or obtuse marginal lesions.

Right coronary artery findings

A statistically significant difference was found regarding right coronary artery right coronary artery affections: 14 (56%) patients of group A had right coronary artery lesions versus six (24%) patients of group B. In addition, a statistically significant difference was found regarding proximal lesion affection: 12 (48%) patients of group A had proximal lesions versus four (16%) patients of group B. No statistically significant differences were found as regarding mid-segment or distal lesions [Table 4].
Table 4: Comparison between both groups regarding site of coronary artery disease

Click here to view


SYNTAX score findings

There was a statistically significant difference between both groups regarding the SYNTAX score. It was 15.76 ± 6.75 in group A, whereas it was 11.36 ± 7.64 in group B.

SYNTAX score

This is an anatomy-based risk score that takes into account features such as bifurcations, total occlusions, thrombuses, calcifications, and small vessels [Table 5].
Table 5: Comparison between both groups regarding the SYNTAX score

Click here to view



  Discussion Top


Silent myocardial ischemia is defined as an objective evidence of myocardial ischemia occurring in the absence of symptoms. HCV was found to have a positive association with carotid artery plaques independent of other risk factors for atherosclerosis.

The present study found that the incidence of LADCA affection is higher in HCV-seropositive patients than in HCV-negative controls. This is concordant with the results of Satapathy et al. [9], who found that the incidence of LADCA affection is higher in HCV-positive patients than in HCV-negative controls.

The present study also found that the incidence of LCCA affection is higher in HCV-seropositive patients than in HCV-negative controls. In addition, the incidence of right coronary artery affection is higher in HCV-seropositive patients. This is in parallel with Asija et al. [10] whoinvestigated the association of HCV with angiographically documented obstructive CAD. They found that patients undergoing coronary angiography for chest pain have a significantly higher prevalence of obstructive CAD, obstructive three-vessel CAD, and obstructive two-vessel or three-vessel CAD if they are seropositive for HCV compared with patients seronegative for HCV.

In addition, Akhtar et al. [11] validated the hypothesis as to whether HCV seropositivity is associated with CAD or not. Their research showed that there is an unambiguous and clear association between HCV infection and complex CAD.

In addition, Satapathy et al. [9] found that the incidence of three vessel disease affection is higher in HCV-positive patients.

The present study revealed that there is a positive relationship between HCV seropositivity and severity of CAD, with respect to the SYNTAX score. The mean SYNTAX score of the HCV-positive group (group A) was 15.76 ± 6.75, whereas the mean SYNTAX score of the seronegative (control) group (group B) was 11.36 ± 7.64 (P = 0.0.036).

This is in agreement with Vassalle et al. [12], who evaluated whether seropositivity for HCV is associated with the occurrence of CAD; their results showed increased number of coronary artery affections in HCV-seropositive patients. In addition, the results showed that in addition to other conventional atherogenic risk factors (age, sex, smoking habits, diabetes, hypertension, and dyslipidemia), HCV was found to be associated with the presence of CAD. This is also in agreement with Alyan et al. [13], who studied the effect of chronic HCV infection on the extension and severity of CAD, and a modified Reardon scoring system was used to determine severity. The researchers found a higher Reardon severity score in HCV-seropositive patients and concluded that HCV infection is an independent predictor for increased coronary atherosclerosis.

Moreover, Ishizaka et al. [14] investigated the role of HCV core protein and carotid atherosclerosis and found a positive association between HCV core protein and carotid plaques. The associations between markers of HCV infection and CAD were stronger compared with the associations shown for all other established risk factors, including male sex, increasing age, hypertension, cholesterol, and smoking status.

Further confirmation was obtained from the study by Adinolfi et al. [15] who performed a prospective cohort study in Italy of consecutive HCV patients with and without hepatic steatosis. The HCV patients had significantly higher prevalence of carotid atherosclerosis than controls. In addition, when comparing HCV patients with steatosis with non-HCV controls with nonalcoholic fatty liver disease, significantly higher prevalence of carotid atherosclerosis was seen in the HCV group, suggesting that HCV itself may increase atherosclerotic risk independent of steatosis.

The study by McKibben et al. [16] evaluated the association of chronic HCV and coronary atherosclerosis. The study found that the prevalence of coronary artery calcification and the prevalence of noncalcified or mixed plaques were significantly higher among HCV-positive patients compared with HCV-seronegative patients and concluded that chronic HCV infection was associated with subclinical cardiovascular disease.

On the other hand, our study is discordant with the study by Arcari et al. [17] who investigated the association between HCV seropositivity and acute myocardial infarction. They did not support a relationship between HCV infection and coronary heart disease. It is also discordant withthe study by Bilora et al. [18] who assessed the progression of atherosclerosis in carotid and femoral arteries after a 5-year period using ultrasound in subjects with chronic hepatitis C. They concluded that chronic hepatitis C seems to cause a delay in the atherosclerosis process.


  Conclusion Top


There is a positive relationship between HCV and number of diseased coronary vessels, and there is also a positive relationship between hepatitis C seropositivity and complexity of coronary lesions with respect to the SYNTAX score.

Finally, HCV is an independent risk factor for silent myocardial ischemia and coronary heart disease.

Limitations

  1. The relatively small number of the study population
  2. The onset of HCV infection was not assessed
  3. Atherosclerosis and CAD in general are progressive processes, and thus our estimation will be influenced by the stage at which the disease was discovered.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Mallat Z, Corbaz A, Scoazec A, Besnard S, Lesèche G, Chvatchko Y, et al. Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability. Circulation 2001; 104:1598–1603.  Back to cited text no. 1
    
2.
Ji Q, Zeng Q, Huang Y Shi Y, Lin Y, Y Lin, et al. Elevated plasma IL-37, IL-18, and IL-18BP concentrations in patients with acute coronary syndrome. Mediators Inflamm 2014; 665:742.  Back to cited text no. 2
    
3.
Younossi ZM, Stepanova M, Nader F, Elsheikh E. Associations of chronic hepatitis C with metabolic and cardiac outcomes. Aliment Pharmacol Ther 2013; 37:647–5.  Back to cited text no. 3
    
4.
Adinolfi LE, Restivo L, Guerrera B, Sellitto A, Ciervo A, Iuliano N, et al. Chronic HCV infection is a risk factor of ischemic stroke. Atherosclerosis 2013; 231:22–26.  Back to cited text no. 4
    
5.
Deedwania PC, Carbajal EV. Silent myocardial ischemia. A clinical perspective. Arch Intern Med 1991; 151:2373.  Back to cited text no. 5
    
6.
Di Franco A, Lanza GA, Valeriani M, A Villano, G Russo, Virdis D, et al. Impaired pain processing in patients with silent myocardial ischemia. Int J Cardiol 2015; 186:204–206.  Back to cited text no. 6
    
7.
Arenja N, Mueller C, Ehl NF, Mueller C, Ehl NF, Reichlin T, et al. Prevalence, extent, and independent predictors of silent myocardial infarction. Am J Med 2013; 126:515–522.  Back to cited text no. 7
    
8.
Park JI, Shin SY, Park SK, E Barrett-Connor. Usefulness of the integrated scoring model of treadmill tests to predict myocardial ischemia and silent myocardial ischemia in community-dwelling adults (from the Rancho Bernardo study). Am J Cardiol 2015; 115:1049–1055.  Back to cited text no. 8
    
9.
Satapathy SK, Yun J, Ashish K, Shifteh A, Bhansali R, Cerulli MA, et al. HCV infection may predict coronary artery disease. J Clin Exp Hepatol 2011; 3:186–191.  Back to cited text no. 9
    
10.
Asija A, Aronow WS, Ramdeen N, Chugh S. Patients undergoing coronary angiography because of chest pain with hepatitis c virus seropositivity have a higher prevalence of obstructive coronary artery disease than a control group. Chest. 2008; 134 (4_Meeting Abstracts):87002.  Back to cited text no. 10
    
11.
Akhtar B, Hanif A, Qureshi NUS, Hussain S, Siddique K, Khan BZ, et al. Hepatitis C virus (HCV) 'a possible independent risk factor' for coronary artery disease. Ann King Edward Med Uni 2010; 16:3.  Back to cited text no. 11
    
12.
Vassalle C, Masini S, Zucchelli GC. Evidence for association between hepatitis C virus seropositivity and coronary artery disease. Heart 2004; 90:565–566.  Back to cited text no. 12
    
13.
Alyan O, Kacmaz F, Ozdemir O. Hepatitis C infection is associated with increased coronary artery atherosclerosis defined by modified Rear don severity score system. Circ J 2008; 72:1960–1965.  Back to cited text no. 13
    
14.
Ishizaka Y, Ishizaka N, Takahashi E, Tooda E, Hashimoto H, E Tooda, et al. Association between hepatitis C virus core protein and carotid atherosclerosis. Circ J 2003; 67:26–30.  Back to cited text no. 14
    
15.
Adinolfi LE, Restivo L, Zampino R, Ciervo A, Iuliano N, B Guerrera, et al. Chronic HCV infection is a risk of atherosclerosis. Role of HCV and HCV- related steatosis. Atherosclerosis 2012; 221:496–502.  Back to cited text no. 15
    
16.
McKibben RA, Haberlen SA, Post WS, Brown TT, Budoff M, Witt MD, et al. A cross-sectional study of the association between chronic hepatitis C virus infection and subclinical coronary atherosclerosis among participants in the multicenter AIDS cohort study. J Infect Dis 2016; 213:257–265.  Back to cited text no. 16
    
17.
Arcari CM, Nelson KE, Netski DM, Krauss M, Gaydos C. No association between hepatitis C virus seropositivity and acute myocardial infarction. Clin Infect Dis 2006; 43:e53–e56.  Back to cited text no. 17
    
18.
Bilora F, Rinaldi R, Boccioletti V, Rossato A, Arzenton M, Petrobelli F. Chronic viral hepatitis: a prospective factor against atherosclerosis. A study with echo-color Doppler of the carotid and femoral arteries and the abdominal aorta. Gastroenterol Clin Biol 2002; 26:1001–1004.  Back to cited text no. 18
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Patients and Methods
Results
Discussion
Conclusion
References
Article Tables

 Article Access Statistics
    Viewed779    
    Printed5    
    Emailed0    
    PDF Downloaded70    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]