Although cardiovascular disease is a universally prominent reason for morbidity and mortality, it is a gradually progressive disease from subclinical atherosclerosis to acute major cardiac events. Consequently, immense concentration was established for the primary prevention and risk modification of cardiovascular disease.[13, 14] The measurement of CACS has implications for the discovery of premature atherosclerosis and the exploration of its sequences; therefore, it is strongly assumed to be valuable in preventing cardiac events. [15]
Therefore, the current study was based on the CACS effect for determining the degree of CAD and cardiovascular events during the 2 years of follow-up. The mean age of the patients in group II was higher than that of group I, which was in line with the Pereira et al. study [16] and reinforced by the results of McClelland et al. [17], both of which showed an increase in CACS with increasing age. The majority of participants in group II were male, representing about 60.5%, though males represented only 49.5% in group I. Accordingly, multiple studies done on the CACS assessment showed the high prevalence of males relative to females. [15, 17, 18] Regarding the risk factors that highly impact CAD, hypertension involved 62 patients in group I (28.2%) and increased significantly to affect 80 patients in group II (37.2%). Nicoll et al. [19], Turner et al. [20], and Liaquat et al. [21] discovered a strong relationship between systolic hypertension and the degree of CACS. Also, the obesity ratio was higher in group II patients (44.2%) than in group I patients (34.5%). The Jensen et al. [22] study was in parallel with our findings, as it observed that the CACS increased significantly in overweight and obese patients.
In addition, the current study's positive family history of CVD exemplified about 33.5% of patients with higher calcium scores. Nasir et al. [23] studied the relationship between the family history of IHD and coronary artery calcification, and their results demonstrated the intense correlation between a family history of premature coronary heart disease and CAC with a higher prevalence of 64%. Moreover, in our study, the Framingham risk score in individuals with CACS ≥ 400 was 9.74 ± 5.87% compared to 7.86 ± 4.85% in those with CACS ˂400. Okwuosa et al. [24] observed that with a higher Framingham risk score, the possibility of having a CACS ≥ 300 drastically increased; e.g., the patients with a Framingham risk score of 15.1–20% represented about 24% of patients with a CACS ≥ 300 while those with 2.6-5% Framingham risk score represented only 4.4%.
In the current study, the incidence of LAD lesions was significantly higher in group II (47.9%) compared with group I (38.2%) and was also higher than other coronary vessel lesions in the same group. Likewise, Almasi et al. [25] revealed the predominant affection of LAD was 15.4% in comparison with left circumflex 4.5% and right coronary artery 12.4% in patients with a CACS > 400. Furthermore, regarding the segmental analysis of coronary lesions, our study data showed a significant upsurge in the proximal lesions in the group with high CACS ≥ 400 (41.9%) relative to the other group (32.7%), which was in agreement with Ferencik et al.[26], who clarified that the proximal lesions increased proportionally with the increase of the CAC score in comparison with other segments. In addition, Bergström et al.,[27] studied subclinical atherosclerosis in a huge number of populations using MSCT-CA and CACS and revealed a penchant for allocation at the proximal segments rather than the other segments with indifference to age or sex.
Regarding MACE, there was a substantial rise in patients with CACS ≥ 400 who experienced unstable angina, MI, revascularization utilizing PCI, and heart failure during a two-year period of follow-up. Carr et al. [28] discovered within 12.5 years of follow-up of middle-aged patients that CAC was linked with an initial increase of 8.9% for any cardiac events and aggressively increased with the elevation of CACS, which buttressed the current study outcomes. Liu et al. [29] proved that increased CACS was directly proportionate to an increase in coronary heart disease and cardiovascular events. Furthermore, Javaid et al. [30] studied patients less than 50 years old with a negative history of cardiovascular disease and observed during 11 years of follow-up that a higher CACS was obviously linked to a higher risk of MACE and overall mortality.
Multivariate regression analysis revealed that increasing age ≥ 55 years, Framingham risk score > 10, CACS ≥ 400, BMI ≥ 30, and proximal segment lesions were the independent predictors of clinical outcomes. In concordance with this finding, age ≥ 60 years, CACS ≥ 400, and BMI ≥ 23 were highly characteristic of MACE occurrence and increased mortality incidence in Limpijankit et al.,[31] study on 8687 patients with chronic stable angina. Similarly, Jensen et al., [22] established the relationship between BMI, CACS, and cardiac outcomes by studying 36509 patients and found that patients with BMI ≥ 30 kg/m² had a higher prevalence of CACS ≥ 400 and were at a greater risk of IHD, CVD, and all-cause mortality in comparison with those with normal BMI. Moreover, Nugroho et al. [32] conducted a study on 110 healthy volunteers to ascertain the relationship between the Framingham risk score and different categories of CACS, They found a strong positive association (P < 0.001) that subsequently had a critical impact on cardiovascular events. Additionally, combining the CACS with the Framingham risk score generated a high-level estimation of upcoming cardiac events in ischemic stroke patients with no chest pain. [33]
In parallel with the current results, which confirmed that CACS ≥ 400 was a strong independent predictor influencing the CVD outcomes, Peng et al., [34] compared the hazards of different CACS proportions and showed that the hazard ratios for all CVD event types rose with increasing CACS. Furthermore, in the Hollenberg et al., [35] study, patients with a CACS ≥ 400 revealed a disproportionate expansion of about 15.7 fold in a calcified plaque compared to non-calcified plaque with rated growth in CVD event risk of 3.3% for zero CACS to 21.9% for CACS ≥ 400 (P < 0.001), which was consistent with the current result and supported by the cardiovascular computed tomography society recommendations for the use of the CACS in patients with coronary heart disease and at atherosclerotic cardiovascular disease risk.[36] Tummala et al.,[37] found that having proximal CAC was associated with a higher risk of MACE than not having it (P = 0.009); this finding was highlighted in the current study. That was explained by Bax et al.,[38] who found that the proximal plaques progressed more rapidly with a higher volume than distal plaques, making them more liable to impending plaque rupture and cardiac events.