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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.
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