The process of atherosclerotic plaque formation starts from early childhood and progresses gradually over the years. Clinical symptoms of CVD and angina occur only when coronary arteries have narrowed to the extent that they result in the limitation of coronary blood flow or due to the formation of thrombus on a pre-existing plaque that suddenly ruptures or gets eroded. Although a clinical CVD event doesn’t occur in all the individuals with atherosclerotic plaque, the risk for future cardiovascular events is directly proportional to the extent of subclinical atherosclerosis. The identification of asymptomatic patients with elevated risk for CVD and the presence of atherosclerosis is paramount importance, as future CVD events and morbidity can be decreased by timely medical interventions.[6,8,13-16]
CVD risk can be further assessed by imaging arteries to identify and calculate the presence of subclinical vascular disease. It is of utmost importance that imaging modality for screening is affordable, safe, sensitive and guide to interventional options that can change the natural course of CVD favorably.
Measurement of CIMT with Ultrasound (B-mode) to calculate C-IMT is a sensitive, non-invasive, and reproducible method for identification and quantification of atherosclerotic burden and CVD risk. As a research tool, it is well verified and is used in clinical practice in abundance.[13,17-22]
CVD risk can be further assessed by imaging arteries to identify and calculate the presence of subclinical vascular disease. It is of utmost importance that imaging modality for screening is affordable, safe, sensitive and guide to interventional options that can change the natural course of CVD favorably. Measurement of CIMT with Ultrasound (B-mode) to calculate C-IMT is a sensitive, non-invasive, and reproducible method for identification and quantification of atherosclerotic burden and CVD risk. As a research tool, it is well verified and is used in clinical practice in abundance.[13,17-22]
Numerous studies in middle-aged (40-65) have shown that the major risk factor for CHD (which includes cholesterol level, Blood Pressure, and cigarette smoking) is predictive of long term outcomes in these age groups. However, equally compelling data from observational studies are almost non existing in young adults.[2]
Autopsy studies showed that atherosclerosis of coronary arteries can start in the second decade of life and a recent study found severely stenotic coronary arteries (narrowing >40%) in 19% of men in their early 30s.[42] Based on national cholesterol education programmed recommended cholesterol screening in all adults 20 years of age or older. Similarly, JNC-VI on identification, prevention, and management of high blood pressure recommends screening for HTN in person 18 years or older.
However, guidelines in the prevention of CAD in young adults have not been uniformly accepted, in part because data on risk prediction and prevention of CVD is scarce in individuals less than forty years of age.[2]
Therefore, we conducted a cross-sectional study with 120 cases with no obvious symptoms suggestive of CAD. Most cases of CAD become clinically apparent in patients aged 40 years or older, that’s why we included patients having a mean age of 32±10.74 years. The mean ages of male patients were 31±9 and that of females was 34±8 years.
The mean CIMT in male patients who were involved in this study were 0.84±0.16 and that of female were 0.83±0.1.5 mm. The mean FA-IMT for male patients was 1.2±0.4 and that of female patients was 0.90±0.40.[23,24]Salonen and Salonen documented that a single measurement of the maximum CCA-IMT >1mm was predictive of future acute MI over a 1 month to 3 years period.[25]) Belcaro and colleagues also documented that 1-time IMT measurement of carotid and femoral arteries of >1 mm in asymptomatic patients was able to successfully predict CVD events over a period of 6 years.[26] In our study, there was a clear male preponderance (64.17%) which is in agreement with the previous studies suggesting that CAD is predominately a disease of men.[27]
In our study hypertension was present in 23.33%, DM 20.83%, Smoking 58.33%, Dyslipidemia 55%, and family history of CAD in 30% patients respectively. The diabetic patients had the highest abnormal CIMT and in smokers, abnormal FA-IMT was highest. This is in contrast to previous studies that showed hypertensive patients had greater IMT in the carotid artery. As observed in the previous studies there was an increased degree of IMT in tobacco consumers, our study found similar results.[28]
The CIMT and FA-IMT in male patients were more as compared to female patients. The mean CIMT in male patients was 0.84±0.14 and in female patients was 0.83±0.15.
While in FA mean IMT in male and female patients was 1.2±0.4 and 0.90±0.40 respectively. Twelve studies (case-control) showed that median IMT was comparable (0.83-1.05 mm) and in the 06 studies (cohort),(0.73-1.08 millimeter). The meta-analysis of these studies showed that with advanced age, screening may become less reliable. But David S Wald and Jonathan P Bestwick weren’t able to confirm this pattern and there is a likelihood that results of screening can be better.[29]
It clearly shows that IMT is a primarily a surrogate parameter for the inherent process of atherogenesis and therefore appear to be approximate means of identifying and possibly monitoring of young healthy adults at significantly high risk of future vascular events.[30]
The angiographic analysis revealed that 23.33% of patients had SVD, 48.34% had DVD and 19.16% had TVD, and 9.17% of patients had normal angiography. The involvement of LM was 4.17%, LAD was seen in 39.17%, LCX in 29.17%, and RCA in 18.33% patients. The results are in contrast to another study which showed the involvement of LAD as 42%, LCX 26%, and RCA 22%.[31,32] In our study, the majority of patients suffered from DVD disease. i.e. 48.34% and single-vessel disease 23.33%. Sridevis et al reported 27.4% and Akanda et al have reported 42.1% that majority of patients have TVD.[31,32]
The frequency of Left Mainstem disease was 4.17% while Soleimani A et al showed that LM disease to be 3.6-6.4%.[33] The published literature showed that LAD is the most commonly affected artery which is similar to our study. The normal angiogram in our study was 9.17% which is contrary to MAK Akanda et al who reported 25% normal angiograms. The reported difference in our study is that LCX is the second most commonly affected artery as compared to RCA in Previous studies.[31] The severity of stenosis observed in our study was mild 14.1%, moderate in 20.83%, and severe in 55.83% patients.
The prognostic importance of CIMT and FA-IMT was significantly linked to the hazard of development of CAD as compared to patients who had normal IMT. CVD events or MI are linked to the formation of thrombus after erosion or rupture of plaque& there is an increasing body of evidence that those plaques which look less stenotic on angiographic views are more susceptible to progress or rupture as compared to more stenotic lesions at the time of revascularization. Outcomes from pathoanatomic studies have shown that during the early stages of coronary atherosclerosis, vessels may undergo compensatory enlargement.[28]
Due to a strong body of evidence that CVD events and IMT are co-related, FDA has accepted two-dimensional ultrasound as a tool to quantify the degree of atherosclerosis. Ludwig M et al proposed the utilization of Duplex Ultrasound for the quantification of IMT and to detect the presence of plaques and stenosis.[34]