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Table of Contents
ORIGINAL ARTICLE
Year : 2018  |  Volume : 19  |  Issue : 2  |  Page : 45-48  

Predictors of coronary artery disease progression among high-risk patients with recurrent symptoms


1 King Abdulaziz Cardiac Center, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs, Riyadh, Kingdom of Saudi Arabia
2 King Abdulaziz Cardiac Center, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs; King Saud bin Abdulaziz University for Health Sciences; King Abdullah International Medical Research Center, Riyadh, Kingdom of Saudi Arabia

Date of Web Publication26-Oct-2018

Correspondence Address:
Dr. Mouaz H Al-Mallah
King Abdulaziz Cardiac Center, King Abdulaziz Medical City for National Guard-Riyadh, Department Mail Code: 1413 P.O. Box 22490, Riyadh 11426
Kingdom of Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/HEARTVIEWS.HEARTVIEWS_23_17

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   Abstract 


Background: Despite the availability of new potent medical therapies, the rate of progression of angiographic coronary artery disease (CAD) is not well described. The aim of this analysis is to describe the rate and predictors of progression of CAD among patients with recurrent symptoms.
Materials and Methods: We reviewed 259 patients (mean age 61 ± 11 years, 70% males) who underwent two coronary angiograms between 2008 and 2013. Progressive CAD was defined as obstructive CAD in a previously disease-free segment or new obstruction in a previously nonobstructive segment. Patients who had coronary artery bypass surgery between these two angiograms were excluded from the analysis. Multivariate logistic regression was used to determine the independent predictors of progression of CAD.
Results: The included cohort had a high prevalence of coronary risk factors; hypertension (71%), diabetes (69%), and dyslipidemia (75%). Despite adequate medical therapy, more than half of the patients (61%) had CAD progression. Using multivariate logistic regression, a drop in the left ventricular ejection fraction (LVEF) by more than 5% was the predictor of CAD progression (adjusted odds ratio 5.8, P = 0.042, 95% confidence interval 1.1–31.2).
Conclusion: Among high-risk patients with recurrent symptoms, the short-term rate of progression of CAD is high. A drop in LVEF >5% is a predictor of CAD progression. Further studies are needed to determine the prognostic value of CAD progression in the era of potent medical therapy.

Keywords: Coronary artery disease progression, coronary artery disease risk factors, invasive coronary angiography, prediction of coronary artery disease


How to cite this article:
Farah I, Ahmed AM, Odeh R, Alameen E, Al-Khateeb M, Fadel E, Rabai R, Ali D, Bdeir B, Al-Mallah MH. Predictors of coronary artery disease progression among high-risk patients with recurrent symptoms. Heart Views 2018;19:45-8

How to cite this URL:
Farah I, Ahmed AM, Odeh R, Alameen E, Al-Khateeb M, Fadel E, Rabai R, Ali D, Bdeir B, Al-Mallah MH. Predictors of coronary artery disease progression among high-risk patients with recurrent symptoms. Heart Views [serial online] 2018 [cited 2018 Dec 19];19:45-8. Available from: http://www.heartviews.org/text.asp?2018/19/2/45/244184




   Introduction Top


Coronary atherosclerosis is the leading cause of mortality and morbidity.[1],[2] Coronary artery disease (CAD) progression may explain the severity of the progressive stenotic coronary arteries. Progressive stenotic lesions occur either in an initially normal coronary segment or previously diseased vessel. This is usually associated with rapid acute cardiac events leading to angina pectoris, acute myocardial infarction, and sudden cardiac death.[3],[4]

Coronary angiography, as a diagnostic invasive modality, allows for an accurate detection and exclusion of CAD. It demonstrates the coronary morphology, determines the lesion, and shows its severity.[5],[6] A significant group of patients undergoes a repeated coronary angiography during their life course. Repeated assessment of the coronaries provides an opportunity to study the progression of atherosclerosis over time.[7],[8] These changes were related to the severity of initial angiography, the coronary endothelial function, and ongoing pathophysiologic processes.[9],[10]

A series of risk factors including lifestyle, metabolic abnormalities, and other associated diseases has been associated with the incidence of CAD, but their role in the progression of CAD is not very clear.[11],[12]

In view of the limited knowledge about the predictors of CAD progression, the aim of this analysis is to describe the rate and predictors of progression of CAD in patients with recurrent symptoms.


   Materials and Methods Top


Study population

We conducted a retrospective study including 259 patients who had two clinically indicated coronary angiographies at least 1 year apart between 2008 and 2013. Patients with obstructive CAD at the baseline angiogram (more than 70% stenosis) or those who had coronary artery bypass grafting between the two angiograms were excluded from the study. Baseline characteristics (height, weight, and body mass index [BMI]), conventional cardiovascular risk factors (hypertension, diabetes, dyslipidemia, smoking, and prior history of peripheral vascular disease), echocardiographic parameters (ejection fraction, right ventricular systolic pressure, and presence of diastolic dysfunction), used mediations (beta-blockers, statins, clopidogrel, and angiotensin-converting enzyme inhibitors) and laboratory results (cholesterol, triglyceride, and high- and low-density lipoproteins) were collected. Most of patients were under regular follow-up in their specialized cardiac clinics during the period between the two angiographic studies.

Coronary angiographic assessment

The two coronary angiograms were reviewed. Evaluation of the coronary arteries was per segment based using the 17 anatomical segments.[13] Segments were coded according to the degree of obstruction from normal, nonobstructive (<70% stenosis) to obstructive disease (>70% stenosis).

Definition of coronary artery disease progression

Progressive CAD was defined as new obstructive CAD in a previously disease-free segment or new obstruction in a previously nonobstructive segment on consecutive angiographic studies.

Statistical analysis

The continuous variables were reported as mean ± standard deviation, and the categorical variables were reported as frequencies and percentages. Chi-square test was used to assess the significance of the categorical data and independent sample t-test for the contentious data. Multivariate logistic regression was used to detect the predictors of CAD progression. Cofounders' selection was based on both univariate analysis and clinical judgment, including age, gender, hypertension, diabetes, dyslipidemia, ejection fraction on echocardiography, and diastolic dysfunction. The results considered significant with a significance level <0.05. The data analysis was done using SPSS, version 21 (IBM Statistics, IL, USA).


   Results Top


A total of 259 patients (mean age was 60 ± 11 years and 69.5% were male) had two clinically indicated angiographic studies. The mean duration between the two angiograms was 30 ± 14 months (12–64 months apart). In the initial angiogram, most patients had evidence of nonobstructive CAD with only 14 patients (5.4%) having disease-free coronary arteries. A total of 159 (61.4%) patients had evidence of progression of CAD. At the baseline, the mean ejection fraction on the echocardiography was 47 ± 10. One-third of patients had a systolic blood pressure more than 140 mmHg and BMI more than 30 kg/m2.

In univariate analysis, male patients, history of prior myocardial infarction, and patients with systolic heart failure have a higher prevalence of progressive CAD (75%, 20%, and 18% vs. 61%, 11%, and 4%, respectively). Most of study cohort had a control risk factors, (60%) had low-density lipoprotein (LDL) <100 mg/dl, (65%) had triglyceride <150 mg/dl, and (80%) had cholesterol <200 mg/dl [Table 1].
Table 1: Progressive and nonprogressive coronary artery disease; traditional cardiovascular risk factor distribution

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In a multivariate logistic regression, a drop in the left ventricular ejection fraction (LVEF) >5% was a predictor of CAD progression (adjusted odds ratio 5.8, 95% confidence interval 1.1–31.2, P = 0.042) [Figure 1].
Figure 1: Reduction of the left ventricular ejection fraction in the interval period between the two angiographies with rate <5 in difference has a good statistical relation with the progression of the coronary artery lesion that can be utilized as a predictor and useful on regular follow-up

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   Discussion Top


Our paper shows that the rate of progression among high-risk patients with recurrent symptoms is high. Our study demonstrated that a drop of the ejection fraction of more than five present using echocardiography in a symptomatic patient is a good predictor for the CAD progression.

Despite comprehensive risk factor intervention, progression of CAD was up to 77.9% in the SWISS II study.[14] Haft and Bachik[15] reported that the incidence of progression in symptomatic patients was 58.8%. Moise et al.[16] showed that a progression rate of 15% for patients with initially normal coronaries at baseline and 50% for those with initial minimal CAD at baseline. Our study progression rate lies in between. This can be approached by the differences in the current lifestyle, reliability in using medication, and appropriate management and risk factor.

The accuracy of the predictive investigation and the investigation used for evaluation of the coronary progression are the leading parts. We labeled progression in our study based on an angiographic assessment. Nissen et al.[17] used an intravenous ultrasound in the initial assessment. They got that intensive LDL cholesterol (LDL-C) lowering with high-dose statin therapy holds atheroma progression. Furthermore, other analysis achieved LDL-C levels <70 mg/dl with a regression on forming atheroma.[17] In our study, the significant results in predicting CAD progression were functional showed on echocardiographic finding. Besides, it gives a lightening pathophysiological process of the disease.

The crucial role of CAD risk factors in the pathogenesis of initial atherosclerotic cardiovascular diseases, some previous studies demonstrate that the intensive monitoring lipid profile and blood pressure, managing the causes through regular follow-up, and controlling lifestyle can decrease the rate of progression or even promote the atherosclerosis regression.[18] Other studies highlighted a direct relationship between reduction in LDL-C and cardiovascular morbidity and mortality.[19] Therefore, recent guidelines focus on stain therapy as a principal target for primary and secondary prevention of cardiovascular disease.[17]

Benefits and limitations

On the other hand, the coronary angiography assessment could underestimate the presence of the occluded CAD. These raised with small size coronaries, contrast dilution, or with technical complexities. Furthermore, the normal coronary segments could easily be missed in the diffuse nature of the CAD.


   Conclusion Top


Among high-risk patients with recurrent symptoms, the short-term rate of progression of CAD is high. A drop in LVEF >5% is the best predictor of progression of CAD. Further studies are needed to determine the prognostic value of CAD progression in the era of potent medical therapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Mintz GS, Painter JA, Pichard AD, Kent KM, Satler LF, Popma JJ, et al. Atherosclerosis in angiographically “normal” coronary artery reference segments: An intravascular ultrasound study with clinical correlations. J Am Coll Cardiol 1995;25:1479-85.  Back to cited text no. 1
    
2.
Libby P, Ridker PM, Hansson GK; Leducq Transatlantic Network on Atherothrombosis. Inflammation in atherosclerosis: From pathophysiology to practice. J Am Coll Cardiol 2009;54:2129-38.  Back to cited text no. 2
    
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McCready RA, Vincent AE, Schwartz RW, Hyde GL, Mattingly SS, Griffen WO Jr. Atherosclerosis in the young: A virulent disease. Surgery 1984;96:863-9.  Back to cited text no. 3
    
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Chan W, Stub D, Clark DJ, Ajani AE, Andrianopoulos N, Brennan AL, et al. Usefulness of transient and persistent no reflow to predict adverse clinical outcomes following percutaneous coronary intervention. Am J Cardiol 2012;109:478-85.  Back to cited text no. 4
    
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Kimbiris D, Iskandrian A, Saras H, Goel I, Bemis CE, Segal BL, et al. Rapid progression of coronary stenosis in patients with unstable angina pectoris selected for coronary angioplasty. Cathet Cardiovasc Diagn 1984;10:101-14.  Back to cited text no. 5
    
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Rafflenbeul W, Nellessen U, Galvao P, Kreft M, Peters S, Lichtlen P. Progression and regression of coronary sclerosis in the angiographic image. Z Kardiol 1984;73 Suppl 2:33-40.  Back to cited text no. 6
    
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Ben-Zvi J, Hildner FJ, Javier RP, Fester A, Samet P. Progression of coronary artery disease. Cinearteriographic and clinical observations in medically and surgically treated patients. Am J Cardiol 1974;34:295-301.  Back to cited text no. 7
    
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Houslay ES, Cowell SJ, Prescott RJ, Reid J, Burton J, Northridge DB, et al. Progressive coronary calcification despite intensive lipid-lowering treatment: A randomised controlled trial. Heart 2006;92:1207-12.  Back to cited text no. 8
    
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Sipahi I, Tuzcu EM, Schoenhagen P, Wolski KE, Nicholls SJ, Balog C, et al. Effects of normal, pre-hypertensive, and hypertensive blood pressure levels on progression of coronary atherosclerosis. J Am Coll Cardiol 2006;48:833-8.  Back to cited text no. 9
    
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Kataoka Y, Wolski K, Balog C, Uno K, Puri R, Tuzcu EM, et al. Progression of coronary atherosclerosis in stable patients with ultrasonic features of high-risk plaques. Eur Heart J Cardiovasc Imaging 2014;15:1035-41.  Back to cited text no. 10
    
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Trianti M, Xanthos T, Iacovidou N, Dagres N, Lekakis JP, Kyriakou F, et al. Relationship between individual cardiovascular risk factors and localization of coronary atherosclerotic lesions. Heart Lung 2011;40:201-7.  Back to cited text no. 11
    
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Bunch TJ, May HT, Bair TL, Crandall BG, Weiss JP, Osborn JS, et al. Trends in early and late mortality in patients undergoing coronary catheterization for myocardial infarction: Implications on observation periods and risk factors to determine ICD candidacy. Heart Rhythm 2011;8:1460-6.  Back to cited text no. 12
    
13.
Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WK, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation 2002;105:539-42.  Back to cited text no. 13
    
14.
Schoenenberger AW, Jamshidi P, Kobza R, Zuber M, Stuck AE, Pfisterer M, et al. Progression of coronary artery disease during long-term follow-up of the Swiss Interventional Study on Silent Ischemia Type II (SWISSI II). Clin Cardiol 2010;33:289-95.  Back to cited text no. 14
    
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Haft JI, Bachik M. Progression of coronary artery disease in patients with chest pain and normal or intraluminal disease on arteriography. Am Heart J 1984;107:35-9.  Back to cited text no. 15
    
16.
Moise A, Théroux P, Taeymans Y, Waters DD. Factors associated with progression of coronary artery disease in patients with normal or minimally narrowed coronary arteries. Am J Cardiol 1985;56:30-4.  Back to cited text no. 16
    
17.
Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: The ASTEROID trial. JAMA 2006;295:1556-65.  Back to cited text no. 17
    
18.
Chhatriwalla AK, Nicholls SJ, Wang TH, Wolski K, Sipahi I, Crowe T, et al. Low levels of low-density lipoprotein cholesterol and blood pressure and progression of coronary atherosclerosis. J Am Coll Cardiol 2009;53:1110-5.  Back to cited text no. 18
    
19.
Bayturan O, Kapadia S, Nicholls SJ, Tuzcu EM, Shao M, Uno K, et al. Clinical predictors of plaque progression despite very low levels of low-density lipoprotein cholesterol. J Am Coll Cardiol 2010;55:2736-42.  Back to cited text no. 19
    


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