The value of coronary calcium score in predicting clinical outcomes in patients with chronic coronary syndrome

Abstract

Background

Coronary artery atherosclerosis and calcification are the precursors to the development of coronary artery disease and its complications. Coronary artery calcium scoring (CACS) is useful as a risk-stratification tool in coronary artery disease.

Objective

The current study was designed to identify the relationship between CACS and major adverse cardiovascular outcomes in patients with stable coronary artery disease.

Methods

The study was conducted on 435 patients with stable ischemic heart disease. The patients were classified into two groups according to their coronary artery calcium score (CACS): group I (n = 220 patients), whose calcium score was mild to moderate (< 400), and group II (n = 215 patients), whose calcium score was high (≥ 400). All patients were closely monitored for two years to assess major adverse cardiovascular events (MACE).

Results

After 2 years of follow-up, MACE drastically increased in Group II in the form of unstable angina, myocardial infarction, demand for percutaneous coronary intervention, and heart failure. Multivariate regression analysis showed that age ≥ 55 years, Framingham risk score > 10, CACS ≥ 400, body mass index ≥ 30 kg/m2, and the proximal lesions of the vessels were the independent risk factors for major cardiac events.

Conclusion

The coronary calcium score is a distinct feature of coronary atherosclerosis, and a score of 400 or higher is a reliable, noninvasive predictor of the progression of coronary artery diseases and their consequences, including MACE.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12872-024-04157-7.

Introduction

Cardiovascular diseases (CVD) have the most widespread impact on morbidity and mortality. CVD continues to be asymptomatic while it invades gradually; thus, early detection of coronary artery disease plays a critical role in its prevention and management [1, 2]. Coronary vessel calcification is deeply linked with atherosclerosis expansion, which is the ancestor of CVD amplification [3]. Thus, coronary artery calcium (CAC) is a promoter of cardiovascular risk factors, and its measurement is considered a potential tool to enhance risk stratification and predict cardiac events [4]. Coronary artery calcium scoring (CACS) is a direct, individual assessment of patients’ coronary vessels that differs from other risk factors used in the assessment of cardiac risk stratification [5]. Furthermore, CACS was a precious tool for the anatomical assessment of atherosclerotic plaque burden [6]. Traditional risk factors, such as the Framingham risk score, clinical examinations, and stress testing, had limited ability to predict coronary artery disease (CAD) in patients at intermediate risk for CAD [7]. Therefore, multi-slice computed tomography-coronary angiography (MSCT-CA) was recommended for patients with an intermediate risk of CAD to establish a CAD diagnosis as well as early detection of subclinical coronary atherosclerosis. The MSCT-CA is a non-invasive modality with good anatomical visualization of coronary arteries and provides ample data on the morphology, distribution, and degree of stenosis of coronary plaques in addition to measuring the CAC score; hence, it is widely used in routine clinical practice [8]. The increased risk of cardiovascular morbidity and mortality has been correlated with the presence of coronary artery calcium and its amount [9]. Consequently, the current study was aimed at assessing the degree of CAC scoring, which has become an affordable, wide-world modality as a potent predictor for coronary artery disease progression, and its impact on clinical outcomes and adverse cardiovascular events.

Patients and methods

The current study was a prospective cohort study conducted on 435 consecutive adult patients who were presented to the outpatient clinic of the cardiology department at Tanta University Hospital between September 2019 and September 2020 with symptoms that suggested the presence of stable coronary artery disease, including Class I or II angina by the Canadian Cardiovascular Society or angina equivalents for a minimum of 2 months with no signs of instability involving heart failure, arrhythmia, or changes in degree, nature, frequency, or duration of their symptoms or asymptomatic with an already established diagnosis of CAD [10]. The diagnosis was confirmed upon the results of either functional non-invasive stress tests (electrocardiogram (ECG) or echocardiography) and/or anatomical tests (MSCT-CA or coronary angiography showed at least one atherosclerotic plaque). The patients were referred to the radiology department at Tanta University Hospital for an MSCT-CA and CAC score. After that, the patients underwent a follow-up for 2 years to evaluate their clinical outcomes and major adverse cardiovascular events (MACE). A signed informed consent was provided by all enrolled patients in the current study. In accordance with the principles of the Declaration of Helsinki II, the Ethical Committee of Tanta Medical School approved the current study under approval reference number 35,835/9/22.

The enrolled patients were divided into two groups based on their coronary calcium scores: Group I, patients with a mild to moderate CAC score < 400, and Group II, patients with a high CAC score ≥ 400. All patients underwent a thorough history assessment of their symptoms to identify cardiovascular risks, which included age, gender, obesity, the presence of diabetes, dyslipidemia, hypertension, smoking status, family history of ischemic heart disease (IHD), and a history of peripheral arterial and/or cerebrovascular diseases. In addition to their medications, which included nitroglycerine, antihypertensive, cholesterol-lowering, and antiplatelet therapy, a complete physical assessment and laboratory investigations were acquired, in addition to a baseline ECG and an echocardiogram at rest. Pre-test probability (PTP) was calculated and classified as low (< 15%), intermediate (15–65%), or high (> 65%) [11]. Furthermore, the Framingham risk score was calculated for all enrolled patients to estimate 10 years of risk. The 10-year CVD risk was categorized as (< 10%) low risk, (10–20%) intermediate risk, and (> 20%) high risk [12]. The Framingham risk score is the widely applicable method globally. While most studies agree that Framingham risk scoring is beneficial, it has poor predictive power for total cardiovascular events. Consequentially, CACS is an accurate predictor of coronary heart disease, outperforming Framingham risk variables [13].

MSCT-CA data acquisition

The multi-slice computed tomography-coronary angiography (MSCT-CA) examinations were performed using a 320-slice Aquilion One scanner (Toshiba Medical Systems, Otawara, Japan), which contains a detector width of 160 mm and 320 detector rows. Oral beta-blockers were used depending on heart rate (HR) one hour before data acquisition if HR exceeded 65 bpm. Initial, a triggered prospective coronary calcium scan was carried out, and then 60–90 ml of nonionic contrast medium (Ultravist 370 mg I/ml; Bayer HealthCare, Berlin, Germany) were injected via a peripherally inserted cannula using a dual-syringe mechanical power injector (Stellant D, Medrad, Indianola, PA, USA) at a flow rate of 5 ml/sec, followed by 50 ml of saline solution. Automatic bolus tracking was applied 10 to 15 s after contrast material injection, and the scan was initiated with a trigger threshold set at 230 HU obtained at the descending aorta at the mid-heart level. Before the examination ended, the image quality was reviewed. Images were reconstructed at a slice thickness of 0.5 mm and a 0.5 mm interval with smooth and sharp reconstruction kernels. A dedicated Vital Images workstation (Vitrea FX, Vital Images, USA) was used for post-processing.

The Agatston calcium score was used to report coronary artery calcium, which was divided into absent 0, mild 1-100, moderate 101–399, and severe 400 and above [14]. Coronary arteries were assessed utilizing thin-slab maximum intensity projection images in the standard planes as well as oblique and curved multiplanar reconstruction images. Coronary lesions were classified into non-obstructive lesions < 50% and obstructive lesions ≥ 50%. Patients with a high pre-test probability of coronary artery disease or a history of myocardial infarction (MI) and/or unstable angina and who underwent prior coronary revascularization, such as percutaneous coronary intervention (PCI) and/or coronary artery bypass grafting (CABG), extensive localized calcification, CACS above 1000, and coronary artery stenosis ≥ 50% were omitted. All enrolled patients were re-evaluated every 3 months for 2 years with the aim of recognizing the MACE incidence consisting of mortality, cardiac arrest, myocardial infarction, unstable angina, heart failure, arrhythmia, and the need for revascularization in the form of PCI or CABG.

Statistical analysis

Statistical analysis was performed using SPSS 23 (SPSS Inc., Released 2015; IBM Statistics for Windows, Version 23; Armonk, NY; IBM Corp.). Quantitative variables were expressed as mean ± standard deviation. An independent sample t-test was used for evaluating quantitative variables between the two groups. Qualitative variables were expressed as frequency and percentage. The Chi-square test (χ2) was used to assess two qualitative parameters. A P value < 0.05 was considered statistically significant. A multivariate logistic regression analysis was performed to assess the independent predictors affecting major adverse cardiovascular events.

Results

The current study included 435 patients with stable ischaemic heart disease who had undergone MSCT-CA. According to their Agatston score, 220 patients (50.6%) had a CACS < 400 and were enrolled in group I, while 215 (49.4%) had a CACS ≥ 400 and were enrolled in group II. Group II had a significantly higher median age than Group I (49.77 7.15 vs. 48.04 7.19 years, P = 0.012), with a male sex predominance of 60.5% versus 49.5% in Group I. Moreover, the prevalence of hypertension, obesity, and family history of IHD was greatly elevated in Group II, with no other significant variation between the two groups in basal characteristics and their medications. However, Framingham’s risk score was notably higher in group II (9.74 ± 5.87 vs. 7.86 ± 4.85, P = 0.001), and there was no considerable discrepancy in pretest probability between the two groups. No statistical difference in the clinical presentation or ECG was obtained between the patients of both groups, as illustrated in (Table 1).

Table 1.

Basal characteristics, and cardiovascular risk factors of all patients in both groups

	Group I (n = 220) Calcium score < 400	Group II (n = 215) Calcium score > 400	P value
Age, years	48.04 ± 7.19	49.77 ± 7.15	0.012*
Male gender, n (%)	109 (49.5%)	130 (60.5%)	0.022*
Smoking, n (%)	72 (32.7%)	59 (27.4%)	0.230
Hypertension, n (%)	62 (28.2%)	80 (37.2%)	0.045*
Diabetes, n (%)	80 (36.4%)	67 (31.2%)	0.252
Dyslipidemia, n (%)	85 (38.6%)	77 (35.8%)	0.543
Obesity, n (%)	76 (34.5%)	95 (44.2%)	0.040*
Cerebrovascular diseases, n (%)	8 (3.6%)	9 (4.2%)	0.767
Peripheral vascular diseases, n (%)	18 (8.2%)	21 (9.8%)	0.563
Family history of IHD, n (%)	54 (24.5%)	72 (33.5%)	0.040*
Lack of physical activity, n (%)	104 (47.3%)	117 (54.4%)	0.136
Anti-hypertensive medication use, n (%)	56 (25.5%)	59 (27.4%)	0.638
Cholesterol-lowering medication use, n (%)	153 (69.5%)	146 (67.9%)	0.712
Anti-platelets medication use, n (%)	183 (83.2%)	178 (82.8%)	0.914
Nitroglycerin use, n (%)	90 (40.9%)	85 (39.5%)	0.770
Framingham risk score (%)	7.86 ± 4.85	9.74 ± 5.87	0.001*
Pretest probability (%)	11.57 ± 10.1	11.74 ± 8.50	0.845
Chest pain:
Typical, n (%)	62 (28.2%)	69 (32.1%)	0.374
Atypical, n (%)	97 (44.1%)	77 (35.8%)	0.078
Non-cardiac, n (%)	61 (27.7%)	69 (32.1%)	0.320
Dyspnea, n (%)	53 (24.1%)	59 (27.4%)	0.424
ECG
Normal finding (%)	114 (51.8%)	112 (52.1%)	0.954
Non-specific changes (%)	106 (48.2%)	103 (47.9%)

IHD ischemic heart diseases, ECG electrocardiogram, *significant P value

As regards physical and laboratory assessment, the patients in group II had a noticeably greater body mass index (BMI) (27.82 ± 3.82 vs. 26.30 ± 3.84 kg/m2) and higher systolic blood pressure (134.6 ± 17.0 vs. 127.3 ± 13.9 mmHg) than the others in group I, with P = 0.001 for both. Nevertheless, other clinical and laboratory findings showed no statistical difference. Moreover, there was a significant increase in coronary artery calcium score in group II (463.1 ± 52.1 vs. 140.9 ± 85.4, P = 0.001) with no significant difference in the number of diseased vessels. According to the distribution and site of the non-obstructive plaques using MSCT-CA, group II had a significant increase in the incidence of diseased left anterior descending (LAD) vessels (47.9% vs. 38.2%), and the prevalence of lesion distribution at the proximal site of vessels was higher in group II than group I (41.9% vs. 32.7%), with no other noticeable significant variations as demonstrated in (Table 2).

Table 2.

Clinical, laboratory findings, and computerized tomography coronary angiography data of all patients in both groups

	Group I (n = 220) Calcium score < 400	Group II (n = 215) Calcium score > 400	P value
BMI, (kg/m2)	26.30 ± 3.84	27.82 ± 3.82	0.001*
Systolic BP, mmHg	127.3 ± 13.9	134.6 ± 17.0	0.001*
Diastolic BP, mmHg	81.73 ± 10.6	81.95 ± 13.1	0.843
Heart rate, (bpm)	84.39 ± 8.82	83.75 ± 8.09	0.433
LVEF, (%)	61.71 ± 4.05	62.41 ± 4.28	0.081
Fasting plasma glucose (mg/dl)	114.4 ± 20.6	113.4 ± 16.6	0.590
2-h post prandial plasma glucose (mg/dl) (mg/dl) (mmol/L)	167.0 ± 69.1	164.1 ± 67.1	0.657
HbA1c %	6.28 ± 0.71	6.19 ± 0.77	0.208
Hemoglobin, g/dl	12.53 ± 0.81	12.41 ± 0.72	0.105
Total cholesterol (mg/dl)	222.1 ± 33.9	224.9 ± 36.0	0.399
TG (mg/dl)	152.8 ± 26.4	156.1 ± 27.3	0.209
LDL (mg/dl)	126.4 ± 24.1	128.9 ± 17.8	0.226
HDL (mg/dl)	44.77 ± 6.85	45.58 ± 6.77	0.214
Serum creatinine (mg/dl)	1.08 ± 0.23	1.10 ± 0.24	0.292
e-GFR (mL/min/1.73 m2)	96.4 ± 12.5	95.0 ± 12.7	0.237
TSH (mlU/L)	3.70 ± 1.26	3.75 ± 1.04	0.655
CRP (mg/L)	4.38 ± 1.18	4.49 ± 1.01	0.292
Uric acid (mg/dl)	6.16 ± 0.59	6.23 ± 0.69	0.215
Serum troponin I (ng/ml)	0.032 ± 0.01	0.031 ± 0.01	0.715
CAC score (Agatston score)	140.9 ± 85.4	463.1 ± 52.1	0.001*
Number of diseased vessels, lesions < 50%
Single vessel, n (%)	79 (35.9%)	68 (31.6%)	0.345
Two vessels, n (%)	87 (39.5%)	80 (37.2%)	0.616
Multi-vessels, n (%)	54 (24.6%)	67 (31.2%)	0.124
Diseased vessels, lesions < 50%
Left main, n (%)	3 (1.4%)	2 (0.9%)	0.672
LAD, n (%)	84 (38.2%)	103 (47.9%)	0.041*
LCX, n (%)	63 (28.8%)	70 (32.6%)	0.392
RCA, n (%)	76 (34.5%)	88 (40.9%)	0.170
Site of the lesions,
Proximal segment, n (%)	72 (32.7%)	90 (41.9%)	0.049*
Mid segment, n (%)	99 (45.0%)	86 (40.0%)	0.292
Distal segment, n (%)	89 (40.5%)	79 (36.7%)	0.427

BMI body mass index, BP blood pressure, LVEF left ventricle ejection fraction, HbA1c glycated hemoglobin, TG triglycerides, LDL low density lipoprotein, HDL high density lipoprotein, e-GFR estimated glomerular filtration rate, TSH thyroid stimulating hormones, CRP C-reactive protein, CAC coronary artery calcium, LM left main, LAD left anterior descending, LCX left circumflex, RCA right coronary artery, *significant P value

After 2 years of follow-up for all enrolled patients, the incidence of MACE increased in group II, with a significant increase in the incidence of unstable angina (14.9% vs. 8.6%, P = 0.043), MI (10.7% vs. 5.5%, P = 0.044), the need for revascularization in the form of PCI (15.3% vs. 9.1%, P = 0.046), and heart failure (7.4% vs. 3.2%, P = 0.047), as clarified in (Table 3), and (Figs. 1 & 2).

Table 3.

Major cardiovascular events of both groups after two years of follow-up

	Group I (n = 220) Calcium score < 400	Group II (n = 215) Calcium score > 400	P value
Mortality, n (%)	2 (0.9%)	4 (1.9%)	0.395
Unstable angina, n (%)	19 (8.6%)	32 (14.9%)	0.043*
Myocardial infarction, n (%)	12 (5.5%)	23 (10.7%)	0.044*
Revascularization procedure
PCI, n (%)	20 (9.1%)	33 (15.3%)	0.046*
CABG, n (%)	6 (2.7%)	10 (4.7%)	0.286
Arrhythmia, n (%)	9 (4.1%)	11 (5.1%)	0.610
Heart failure, n (%)	7 (3.2%)	16 (7.4%)	0.047*
Cardiac arrest, n (%)	6 (2.7%)	9 (4.2%)	0.404

PCI percutaneous coronary intervention, CABG coronary artery bypass grafting, *significant P value

Fig. 1.

Major cardiovascular events of both groups after two years of follow-up

Fig. 2.

65 years old male with CAC score 491.3 (LAD 205.6, CX 76.9, RCA 136.5). Images from 3 mm slice thickness reconstruction show (a) calcified plaque at proximal LAD encoded in yellow, (b) calcified plaque at proximal CX encoded in blue, (c) calcified plaque at mid RCA encoded in red. The patient underwent PCI after 385 days

Furthermore, multivariate regression analysis was performed to investigate the independent predictors affecting clinical outcomes, and the following results were obtained: age ≥ 55 years (OR = 1.182; 95% CI, 1.116–1.251; P = 0.001), Framingham risk score > 10 (OR = 5.891; 95% CI, 2.667–13.012; P = 0.001), CAC score (Agatston score) ≥ 400 (OR = 1.007; 95% CI, 1.005–1.009; P = 0.001), BMI ≥ 30 kg/m2 (OR = 2.858; 95% CI, 1,378–5.926; P = 0.005), and the site of the lesion in the proximal segment (OR = 3.032; 95% CI, 1.510–6.090; P = 0.002), as illustrated in (Table 4).

Table 4.

Multivariate regression analysis showing the independent predictors affecting major cardiovascular events

	Multivariate analysis		P. value
	OR	(95% CI)
Age ≥ 55 years	1.182	1.116– 1.251	0.001*
Hypertension	1.219	0.634– 2.342	0.553
Framingham risk score > 10	5.891	2.667– 13.012	0.001*
Family history of IHD	1.229	0.605– 2.495	0.569
CAC score (Agatston score) > 400	1.007	1.005– 1.009	0.001*
Body mass index ≥ 30 kg/m2	2.858	1.378– 5.926	0.005*
Diseased vessels, LAD	1.027	0.556– 1.899	0.932
Site of the lesions, proximal segment	3.032	1.510– 6.090	0.002*

IHD ischemic heart diseases, CAC coronary artery calcium, LAD left anterior descending, *significant P value

Discussion

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 [15, 16]. 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 [17]. The novel concept of vascular age was introduced to correspond to the patient’s biological age, which is more precise in a 10-year CV risk evaluation than the chronological age. Compared to conventional techniques such as carotid intimal thickness, CACS provided a novel tool that was more accurate in determining coronary arterial age. The idea of CACS depends on the direct imagining of vascular steady erosion during vascular atherosclerosis, which clarifies individual variance according to the multifactorial risk beyond the chronological age alone. Particularly in young individuals for whom ASVD estimation is still unreliable, CAC has a remarkable prognostic value for early vascular aging [18].

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 [19] and reinforced by the results of McClelland et al. [20], 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 a high prevalence of males relative to females [17, 20, 21]. 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. [22], Turner et al. [23], and Liaquat et al. [24] 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. [25] study was in parallel with our findings, as they 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. [26] 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. [27] 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 a 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. [28] 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. [29], 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. [30] 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. [31] 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. [32] proved that increased CACS was directly proportionate to an increase in coronary heart disease and cardiovascular events. Furthermore, Javaid et al. [33] 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 the Limpijankit et al. [34] study on 8687 patients with chronic stable angina. Similarly, Jensen et al. [25] established the relationship between BMI, CACS, and cardiac outcomes by studying 36,509 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. [35] 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 [36].

In parallel with the current results, which confirmed that CACS ≥ 400 was a strong independent predictor influencing CVD outcomes, Peng et al. [37] 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. [38] 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 [39]. Tummala et al. [40] 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. [41], who found that proximal plaques progressed more rapidly with a higher volume than distal plaques, making them more liable to impending plaque rupture and cardiac events.

Conclusions

This study established a compelling correlation between the existence of coronary artery calcium and future cardiovascular events. CAC distinguishes coronary artery atherosclerosis as a disease affliction, reflects its advance, and predicts cardiovascular events. As a result, the current evidence supports computed tomography-coronary angiography calcium score screenings and their role in early risk stratification of cardiovascular diseases and long-term prognosis.

Abbreviations

CVD

Cardiovascular diseases

CAC

Coronary artery calcium

CACS

Coronary artery calcium scoring

CAD

Coronary artery disease

MSCT-CA

Multi-slice computed tomography-coronary angiography

MACE

Major adverse cardiovascular events

MI

Myocardial infarction

PCI

Percutaneous coronary intervention.

CABG

Coronary artery bypass grafting

IHD

Ischemic heart diseases

ECG

Electrocardiogram

PTP

Pre-test probability

HR

Heart rate

BMI

Body mass index

LAD

Left anterior descending

Authors’ contributions

“ B E” writing methods, revision of patient data and results and draft the manuscript.” M H” and “M K” collecting data from the patients, follow up , revision of the manuscript and analyzing the results and preparing figures.“R E” performing CT coronary angiography for the patients and revision of the results All authors reviewed and approved the final manuscript.

Funding

this study was not funded.

Availability of data and materials

No datasets were generated or analysed during the current study.

Declarations

Ethical approval and consent to participate

This study was approved by the Ethics Committee in the Faculty of Medicine, Tanta University, reference number 35835/9/22, and with the Helsinki Declaration of 1964 and later revision.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.