Low or Even Zero CAC may not be Warranted as Safe in Thai Officers: A 10-year prospective

Main Article Content

Lertlak Chaothawee
Gumpanart Veerakul
Pongpan Poonsawas
Sucharath Warutama
Sruangpat Sitakalin
Supaporn Krisneepaiboon

Abstract

OBJECTIVES: CAC has been widely accepted as a strong independent event predictor in asymptomatic moderate risk in the western population. However, the role of coronary artery calcium (CAC) has not been established in the Thai population yet. Thus, we conducted a 10-year prospective study to verify the predictive role of CAC in asymptomatic Thai participants.
 
MATERIAL AND METHODS: A total of 239 asymptomatic officers were voluntarily enrolled and consented to take part. We excluded participants aged < 35 or > 60 years, prior cardiovascular diseases (CVD), pregnant and those not willing to sign an informed consent of participation. The population underwent an exercise stress test (EST) to screen for occult coronary artery disease (CAD). Coronary angiography was performed if there is an evidence of exercise-induced myocardial ischemia within 7 METS. All the studied population underwent a 256-slide multidetector computed tomography (MDCT) scan to obtain a CAC scoring. CAC volume was measured by Agaston method which defines CAC as a mass of HU 130 or more. The studied population were divided into two groups,CAC = 0 and CAC > 0. All of them received medication, education for lifestyle modification and were followed up annually for ten consecutive years (2006-2016). Primary end points were fatal or non-fatal acute coronary syndrome (ACS) and any types of stroke. Secondary end point was all causes of mortality. Student t test and Pearson’s Chi-square were used to compare the difference and the p value of < 0.05 was considered statistically significant.

RESULT: Most candidates were men (96.7%) and had a mean age of 52.4 ± 4.8 years. The common coronary risk factors were elevated low density lipoprotein cholesterol (LDL-C) >130 mg/dl (66.9%), elevated triglyceride (TG) > 150 mg/dl (53.1%), systolic blood pressure (SBP) > 140 mmHg (39.7%), impaired fasting glucose > 100 mg/dl (34.5%), cigarette smoking (32.2%) and low high-density lipoprotein cholesterol (HDL-C) < 40 mg/dl, (12.6%). Ten cases (4.2%) had ischemic exercise test (EST) response and 50% of them had severe coronary stenosis requiring revascularization or aggressive medication. The other half also had documented causes of exercise-induced ischemia including coronary slow flow, vasospasm and myocardial bridging. Thus, all of these cases were excluded for outcome measurement, therefore we had total of 229 cases, half (51.5%) of them had no detectable calcified coronary plaque using the Agaston-130 method (CAC = 0). There was no statistical difference in age, gender, SBP, fasting blood sugar (FBS), total serum cholesterol (T. Chol), serum TG, HDL-C and cigarette smoking between candi- dates with absent or present CAC, except the mean LDL-C which was statistically significantly higher in the group with no CAC, 154.7 vs 143.7 mg/dl, p = 0.036. After ten years, there were 23 CVD events including 3 ACS cases, 9 strokes (all ischemic type) and 11 deaths (91% were non-CVD causes). There was no statistically significant difference between these events in the two groups, CAC = 0 (n = 121) vs CAC > 0 (n = 108) regarding to; ACS 0.8% vs 1.9% (p = 0.603), stroke 5% vs 2.8% (p = 0.506), death 2.5% vs 7.4% (p = 0.121) and the combined outcome (ACS + stroke + death): 8.3% vs 12% (p = 0.384). The mean CAC in CVD victims was quite low, 32.76 (0 - 53.1) for three ACS cases and 23.75 (0 - 180.9) for nine strokes.



CONCLUSION: While the small number and the prominent male gender of candidates were the major limitations and precluded extrapolation to others, this study was the first 10-year cohort that reported different results from western studies, low or even zero CAC might not be safe in asymptomatic Thai people. Thus, we should be skeptical to use CAC as a CVD risk predictor in our population. Whether or not Thai men had low prevalence of calcified coronary plaque or had a different pathophysiologic mechanisms, further study in a larger population is mandatory.

Article Details

How to Cite
1.
Chaothawee L, Veerakul G, Poonsawas P, Warutama S, Sitakalin S, Krisneepaiboon S. Low or Even Zero CAC may not be Warranted as Safe in Thai Officers: A 10-year prospective. BKK Med J [Internet]. 2020 Feb. 25 [cited 2024 Dec. 22];16(1):1. Available from: https://he02.tci-thaijo.org/index.php/bkkmedj/article/view/239965
Section
Original Article

References

Hobbs FDR, Hoes AW, Cowie MR. The epidemiology of cardiovascular disease. In R. Hobbs, B. Arroll ed. Cardiovascular Risk Management, Wiley-Blackwell publishing 2009:1-7.

Cardiovascular diseases. World Health Organization News; May 2017.

The Ministry of Health. China Health Statistics Year Book 2005 (in Chinese). Beijing: Publishing House of Peking Union Medical College, 2005.

Zhang XH, Lu ZL, Liu L. Coronary heart disease in China. Heart 2008; 94:1126-31.

Division of Health Statistics Bureau of Health Policy and Planning. Public Health Statistics AD 2007-2014, Bangkok: Office of the Permanent Secretary, Ministry of Public Health 2014.

Suwanwela NC, Stroke Epidemiology in Thailand. J Stroke 2014;16(1):1-7

Goff DC Jr, Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63(25 Pt B):2935-59.

2016 European Guidelines on cardiovascular disease prevention in clinical practice. The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice. Eur Heart J 2016;37:2315-81.

Greenland P, Smith SC Jr, Grundy SM. Improving coronary heart disease risk assessment in asymptomatic people: role of traditional risk factors and noninvasive cardiovascular tests. Circulation 2001;104:1863-7.

Agatston AS, Janowitz WR, Hildner FJ, et al. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 1990;15: 827-32.

Greenland P, Alpert JS, Beller GA, et al. 2010 ACCF/AHA Guideline for assessment of cardiovascular risk in adults. A report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2010;56: e50-103.

Hecht H. Coronary Artery Calcium Scanning, Past, Present and Future. J Am Coll Cardiol Img 2015;8(5):579-96.

Detrano R, Guerci AD, Carr JJ, et al. Coronary calcium as a predictor of coronary events in four racial or ethnic groups. N Engl J Med 2008;358:1336-45.

Hermann DM, Gronewold J, Lehmann N, et al. Heinz Nixdorf Recall Study Investigative Group. Coronary artery calcification is an independent stroke predictor in the general population. Stroke 2013;44:1008-13.

Gibson AO, Blaha MJ, Arman MK, et al. Coronary artery calcium and incident cerebrovascular events in an asymptom- atic cohorts: the MESA study. J Am Coll Cardiol Img 2014;7:1108-15.

Leening MJG, Elias-Smale SE, Kavousi M, et al. Coronary calcification and the risk of heart failure in the elderly. The Rotterdam Study. J Am Coll Cardiol Img 2012; 5:874-80.

Veerakul G, Nootaro A, Damrongrat B, et al. Five Year Outcome of primary cardiovascular prevention in Air Force Officers. Asian Heart J 2012; 20;1-11.

Veerakul G, Khajornyai A, Wongkasai S et al. Predicting and Preventing Cardiovascular Events in Asymptomatic Patients: A 10-Year Perspective Study. BKK Med J 2017;13(1):1-12.

Vliegenthart R, Oudkerk M, Song B, et al. Coronary calcifica- tion detected by electron-beam computed tomography and myocardial infarction. The Rotterdam Coronary Calcification Study. Eur Heart J 2002.23:1596-603.

Arad Y, Goodman KJ, Roth M et al. Coronary calcification, coronary risk factors, and atherosclerotic cardiovascular events. The St. Francis Heart Study. J Am Coll Cardiol 2005; 46:158-65.

Becker A, Leber A, Becker C, et al. Predictive value of coronary calcifications for future cardiac events in asymptomatic individuals. Am Heart J 2008; 155:154-60.

Sarwar A, Shaw LJ, Shapiro MD, et al. Diagnostic and prog- nostic value of absence of coronary artery calcification. JACC Cardiovasc Imaging 2009;2:675-688.

Blaha M, Budoff MJ, Shaw LJ, et al. Absence of coronary artery calcification and all-cause mortality. JACC Cardiovasc Imaging 2009;2:692-700.

Valenti V, Ó Hartaigh B, Heo R, et al. A 15-year warranty period for asymptomatic individuals without coronary artery calcium: a prospective follow-up of 9,715 individuals. JACC Cardiovasc Imaging 2015;8:900-9.

AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/ APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation 2019; 139:e1082–e1143.

Lloyd-Jones DM, Braun LT, Ndumele CE, et al. Use of Risk Assessment Tools to Guide Decision-Making in the Primary Prevention of Atherosclerotic Cardiovascular Disease. A Special Report from the American Heart Association and American College of Cardiology. Circulation 2018; DOI: 10.1161/CIR.0000000000000638.

Saya S, Hennebry TA, Lozano P, et al. Coronary Slow Flow Phenomenon and Risk for Sudden Cardiac Death Due to Ventricular Arrhythmias. Clin Cardiol 2007; 31:352-5.

Wozakowska-Kaplon B, Niedziela J, Krzyzak P, et al. Clin- ical manifestations of slow coronary flow from acute coronary syndrome to serious arrhythmias. Cardiol J 2009; 16:462-8.

Veerakul G, Ounpothi, Satheeranate N, et al. Coronary slow flow phenomenon: A case report and literature review. BKK Med J 2015; 10: 22-6.

Maseri A, Mimmo R, Chierchia S, et al. Coronary spasm as a cause of acute myocardial ischemia in man. Chest 1975; 68: 625-33.

Ong P, Athanasiadis A, Hill S, et al. Coronary artery spasm as a frequent cause of acute coronary syndrome: the CASPAR (Coronary Artery Spasm in Patients with Acute Coronary Syndrome) study. J Am Coll Cardiol 2008; 52:523-27.

Myerburg RJ, Kessler KM, Mallon SM, et al. Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm. N Engl J Med 1992; 326:1451–55.

Bauters C, Chmait A, Tricot O, et al. Coronary thrombosis and myocardial bridging. Circulation 2002; 105(1):130.

Bergmark BA, Galper BZ, Shah AM, et al. Myocardial bridging in a man with non-ST-elevation myocardial infarction. Circulation 2015 131(11):e373-e374

Arjomand H, AlSalman J, Azain, et al. Myocardial bridging of left circumflex coronary artery associated with acute myocardial infarction. J Invasive Cardiol 2000;12(8):431-4.

Tio RA, Ebels T. Ventricular septal rupture caused bymyocardial bridging. Ann Thoracic Surg 2001; 72:1369-70.

Feld H, Guadanino V, Hollander G, et al. Exercise-induced ventricular tachycardia in association with a myocardial bridge. Chest 1991; 99:1295-6.

MCutler D, Wallace JM. Myocardial bridging in a young patient with sudden death. Clin Cardiol 1997; 20:581-3.

Douglas AE, Strong JP, McGill Jr HC. Coronary Calcification: relationship to clinically significant coronary lesions and race, sex and topographic distribution. Circulation 1965;XXXII: 948-55.

Bild DE, Detrano R, Peterson D, et al. Ethnic differences in coronary calcification: the Multi-Ethnic Study of Athero-sclerosis (MESA). Circulation 2005;111:1313-20.

Budoff MJ, Nasir K, Mao S, et al. Ethnic differences of the presence and severity of coronary atherosclerosis. Athero-sclerosis 2006; 187:343-350.

McClelland RL, Chung H, Detrano R, et al. Distribution of coronary artery calcium by race, gender, and age: results from the Multi- Ethnic Study of Atherosclerosis (MESA). Circulation 2006;113:30-37.

Nasir K, Shaw LJ, Liu ST, et al. Ethnic differences in the prognostic value of coronary artery calcification for all- cause mortality. J Am Coll Cardiol 2007; 50:953-960.

Lee JH, Han D, Park HE et al. Coronary artery calcification in the Asian population: an overview of the results from the Korea initiatives on coronary artery calcification registry. CVIA 2017;1(2):89-98.

Lee JH, Han D, Ó Hartaigh B, Rizvi A, et al. Warranty period of zero coronary artery calcium score for predicting all- cause mortality according to cardiac risk burden in asymptomatic Kore- an adults. Circ J 2016;80:2356-61.

Budoff MJ, McClelland L, Nasir K, et al. Cardiovascular events with absent or minimal coronary calcification: the Multi-Ethnic Study of Atherosclerosis (MESA). Am Heart J 2009; 158(4): 554–61.

Morrow JD, Frai B, Longmire AW, et al. Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers as a cause of oxidative damage. N Engl J Med 1995; 332:1198-03.

Binak E, Gunduz H, Sahin M, et al. The relation between glucose tolerance and slow coronary flow. Int J Cardiol 2006; 111:142-6.

De Caterina R, Massaro M, Libby P. Endothelial functions and dysfunctions. In Caterina RD, Libby P, ed. Endothelial Dysfunctions and Vascular Disease, Blackwell Futura 2007:3-25.

Blaha MJ, Mortensen MB2, Kianoush S, et al. Coronary Artery Calcium Scoring: Is It Time for a Change in Methodology? . JACC Cardiovas Imaging 2017;10:923-37