The role of computed tomography angiography in assessing the correlation between properties of coronary atherosclerotic plaque and blood lipids

Abstract

BACKGROUND:

Coronary atherosclerotic heart disease (CAHD) is the leading cause of death in developed countries.

OBJECTIVE:

This study aimed to explore the correlation between the properties of coronary atherosclerotic plaque and blood lipids using computed tomography angiography (CTA).

METHODS:

A total of 83 patients with coronary heart disease were included in this study (males: 50; females: 33; average age: [59 $\pm$ 8] years old). They were classified into the stable angina group and unstable angina group. Atherosclerotic plaques were classified as fatty plaques (soft plaques), fibrous plaques, and calcified plaques based on the computed tomography (CT) values. SPSS 17.0 statistical software was used to analyze the correlation between the properties of angina and the CT values of atherosclerotic plaques, blood lipids, and plaque properties, and then compared between the stable and unstable angina groups.

RESULTS:

There were statistically significant differences in plaque properties between the stable and unstable angina groups ( $P<$ 0.001). During CTA examination, we found statistically significant differences in the CT density values of atherosclerotic plaques between the stable and unstable angina groups ( $P<$ 0.001). There were statistically significant differences between the properties of angina and the level of blood lipids ( $P<$ 0.05).

CONCLUSION:

Anginal properties negatively correlated with calcified plaques and positively correlated with non-calcified plaques. Calcified plaques negatively correlated with total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and positively correlated with high-density lipoprotein cholesterol (HDL-C). Non-calcified plaques negatively correlated with HDL-C and positively correlated with TC, LDL-C, and TG.

Keywords

Angina atherosclerotic plaques blood lipids coronary artery multi-slice spiral CT

1. Introduction

Coronary atherosclerotic heart disease (CAHD) is the leading cause of death in developed countries [1]. Genetics, unhealthy lifestyles and behaviors, and other factors are major contributors [2]. According to reports, CAHD is the second leading cause of death among people in China [3]. Vascular stenosis caused by plaque obstructs blood and oxygen supply to the heart, putting patients in life-threatening situations in severe cases [4]. Atypical metabolism of blood lipids and inflammatory factors can result in vascular endothelium lesions, which can progress to atherosclerosis [5]. Hardened plaque rupture can result in platelet aggregation and thrombosis, which can lead to coronary artery occlusion [6]. Acute coronary artery occlusion is closely related to the morphology, lipid levels, and progression of plaque [7]. Coronary angiography is often regarded as the gold standard for the diagnosis of coronary heart disease in clinical practice, with an accuracy rate of over 90% [8]. Computed tomography (CT) can be used to measure vascular stenosis caused by plaque in a reliable and accurate manner. The use of CT can reduce the need for invasive digital subtraction angiography (DSA) examinations and iatrogenic injury [9]. Thin fibrous cap atheroma (TCFA) is the primary vulnerable plaque type – it has a thin fibrous cap (thickness $<$ 65 $\mu$ m), a large necrotic core, punctate calcification, and positive remodeling [10]. Many studies have found that fibrous cap thinning is a high-risk factor for plaque rupture, which is characterized by a large and lipid-rich necrotic core, thin fibrous cap coverage ( $<$ 65 $\mu$ m), positive remodeling, neovascularization in the nourishing layer, intraplaque bleeding, and spot-like calcification [11, 12]. A ruptured plaque releases tissue factors, which result in a large number of microthrombi and, eventually, acute myocardial ischemia [13]. The imaging characteristics of fibrous cap atherosclerotic plaques differ from those of stable plaques, specifically, larger plaque volume and punctate calcification [14]. Advanced temporal and spatial resolution facilitates assessments of illness severity and formulations of appropriate clinical interventions [15]. Intravascular ultrasound (IVUS) is used to accurately measure vascular diameter and cross-sectional area to determine whether stenting or increased drug therapy is required based on stenosis degree and lesion type [16]. According to studies, IVUS is far superior to coronary angiography in detecting coronary artery lesions [17]. When it comes to determining the degree of coronary artery stenosis, intracoronary ultrasound has a higher detection rate than coronary angiography [18]. Despite its effectiveness in studying plaque compositions and fibrous caps, optical coherence tomography (OCT) is not used frequently due to its complex operation and high technical requirements [19].

Multi-slice spiral computed tomography (MSCT) is advantageous because of its high temporal and spatial resolution, safety, non-invasiveness, and powerful image post-processing capabilities [20]. Coronary artery computed tomography angiography (CTA) reliably detects plaque status and degree of coronary artery stenosis [21], with a diagnostic accuracy of 100% for negative plaque [22]. Coronary artery CTA can be used to determine the occurrence and status of coronary artery disease (CAD) based on the evaluation of the stenosis degree and plaque properties of the coronary arteries; thus, it is commonly used in clinical diagnosis of CAD [23, 24]. MSCT can effectively distinguish the properties of plaque based on CT values. However, when identifying plaques with extensive calcification, these CT values cannot reliably differentiate between non-calcified components within calcified plaques and non-calcified components adjacent to the calcification. As a result, while emphasizing the benefits of MSCT in examinations, it is imperative to also consider changes in blood lipids.

The lipid infiltration theory or lipid hypothesis, which postulates a link between abnormalities in blood lipids and the onset and progression of atherosclerosis, is the most influential theory related to the diagnosis of the early stages of atherosclerosis (AS) [25]. Serum lipoprotein (a) (LP[a]) is a special plasma protein. A high level of LP (a) is closely related to the development of atherosclerosis [26]. Adiponectin (ANP) is a cytokine secreted by adipocytes and is a protective factor for coronary heart disease and myocardial infarction [27]. In another study, the coronary heart disease group and the non-coronary heart disease group exhibited various alterations in their lipid profiles [28]. Homocysteine (Hcy) has been shown to accelerate the progression of vascular inflammation and atherosclerosis by activating nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasomes in macrophages via reactive oxygen species (ROS)-dependent pathways resulting in endothelial dysfunction [29].

This study aimed to determine stable and unstable plaques based on CT values of plaques using spiral CT and observed how blood lipids correlate to stable and unstable plaques, and to investigate the correlation between plaque properties and blood lipids.

2. Data and methods

2.1 Case collection

A total of 83 patients with coronary heart disease (males 50, females 33; average age [59 $\pm$ 8] years old; BMI: 18.5 $\sim$ 22.9) treated at the Affiliated Hospital of Beihua University from 2020 to 2022 were included in this study. Diagnose stable angina and unstable angina according to Chest pain of recent onset (NICE clinical guideline 95). Among them, 36 cases diagnosed with stable angina were enrolled in to stable angina (SA) group (males 28, females 8; non-calcified plaques 35 pieces, calcified plaques 90 pieces), and 47 cases diagnosed with unstable angina were enrolled into unstable angina (UA) group (males 38, females 9; non-calcified plaques 135 pieces, calcified plaques 16 pieces). All patients reported symptoms of chest tightness or discomfort in the precordial region after exertion and had not recently received lipid-lowering treatments. None of the patients included in this study had myocardial infarction.

2.2 CTA examination method

We used computed tomography scanner (128-slice multi-slice spiral CT, Brilliance iCT, Siemens AG, Erlangen, Germany). Before scanning, a routine iodine allergy test and breath-holding training were performed and the heart rate of the participants was maintained below 70 beats per minute. Patients with heart rates above 70 beats per minute received oral 25–50 mg of metoprolol tartrate to maintain the rate below 70 beats per minute. Sublingual nitroglycerin 0.5 mg was administered to dilate the coronary arteries for better lesion display. Using a double-barreled high-pressure injector, 75–80 mL of contrast agent (Ultravist [iopromide] 370 mg/mL, Bayer Schering Pharma) was injected into the antecubital vein at a rate of 4.0 mL/s followed by injection of 50 mL of saline at the same rate. The ascending aorta root plane was selected for closure monitoring, with a threshold value of 100 HU. A scan was performed at the ascending aorta root plane for comparison before injection of the contrast agent. An image of the same plane was obtained every second after injection of the contrast agent. The coronary artery scan was delayed by 5 seconds after the CT closure value at the ascending aorta root reached 100 HU. The level below the tracheal prominence to the level of the heart base was selected for scanning. Scanning parameters: Tube voltage 120 kV, tube current 870 mAs, collimation 64 $\times$ 0.6 mm, pitch 0.2, and rotation speed 0.33 s/360^∘. Image analysis: Siemens MMWP system processes the reconstructed image; If the stenosis degree of the patient is more than 25%, the reconstruction index, plaque composition and volume are automatically calculated. CT values were used to determine whether the plaque was calcified. Using magnetic suspension rack drive technology, 360-degree scanning takes only 0.3 seconds, the spatial resolution reaches 30 line pairs/cm, the Z-axis resolution is 0.33 MM, and the thinnest layer can be scanned up to 0.6MM, which can provide a fast synchronous scanning of 128 layers and can scan a range of 200 cm at a time. Using the retrospective electrocardiogram (ECG) gating method, the phase with the clearest display of the coronary artery (65% to 75% R-R interval) was selected for transverse thin-layer reconstruction (layer thickness 0.75 mm and layer spacing 0.5 mm). The three-dimensional reconstruction methods included volume rendering technology, maximum intensity projection (MIP), and curved planar reconstruction.

2.3 Clinical data

Total cholesterol (TC), triglycerides (TG), low-density lipoprotein, high-density lipoprotein, apolipoprotein A, apolipoprotein B, and other biochemical tests were conducted. All these tests were conducted on venous blood collected from the patients on the second day after admission to the hospital, on an empty stomach.

2.4 Classification of coronary atherosclerotic plaques

CT values of the plaques were measured using the point pixel capabilities of the PACS (Picture Archiving and Communication System) workstation on thin slice reconstructed images of the transverse axis. Measurement and calculation of parameters of calcium-containing plaque in coronary arteries: The measurement and calculation of calcium-containing plaque in this study refer to Moselewski’s method. Calcifying lesions were defined as CT values $\geqslant$ 130 HU and $\geqslant$ 3 contiguous voxels. Measurement and segmentation of CT values: Each calcium-containing plaque was selected as the study object, and the average CT value was calculated automatically by software according to the histogram of the distribution of CT values of all calcified voxels in calcium-containing plaques. Each calcium-containing plaque was divided into four parts according to the range of CT values, and the proportion (%) of each part after segmentation was calculated, that is, the composition ratio of each segment. The plaques were classified into three types based on their CT values: Fatty plaques (soft plaques), fibrous plaques, and calcified plaques, with CT values less than 50 HU, 70 HU–100 HU, and greater than 130 HU, respectively [2]. CT values ranging from 50 HU–70 HU and 100 HU–130 HU were abandoned. During data analysis, plaques were categorized as non-calcified, calcified, or mixed plaques. Non-calcified plaques included fatty and fibrous plaques. As CTA only revealed a small thickness or roughness of the coronary artery wall in certain patients and CT values were difficult to measure, these plaques were classified as non-calcified plaques. Mixed plaques referred to atherosclerotic plaques with both non-calcified and calcified components.

2.5 Analysis of biochemical test indicators of blood lipids

Cases with coronary artery atherosclerotic plaques prompted by CTA were classified as the case group. We analyzed how the degree of coronary artery stenosis caused by atherosclerotic plaques in the case group (taking the maximum degree of stenosis of coronary arteries) correlated to the levels of total cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein.

2.6 Statistical software

SPSS 17.0 statistical software was used for all statistical analyses with a significance level of $\alpha=$ 0.05. Chi-squared test for a 2 $\times$ 2 contingency table or for a larger contingency table was used for rate or proportion test. If both these two indicators were normally distributed, the $t$ -test was used; Spearman’s rank correlation coefficient was used if one of these two indicators was not normally distributed.

3. Results

3.1 Comparison of the properties of lesion plaques and angina based on CTA examination

CTA demonstrated 1,162 segments of coronary arteries in these 83 patients. Mixed plaques with greater than 50% non-calcified plaque composition were classified as non-calcified plaques for the purpose of statistical analysis. In total, we found 170 non-calcified plaques, 106 calcified plaques, and 276 atherosclerotic plaques. There were 90 calcified plaques and 35 non-calcified plaques in patients with stable angina, and 16 calcified plaques and 135 non-calcified plaques in patients with unstable angina. The comparison of plaque properties between these two groups is shown in Table 1.

Table 1
Comparison of plaque properties between the two groups

Groups	$n$	Non-calcified plaque	Calcified plaque	Total
Stable angina group	36	35	90	125
Unstable angina group	47	135	16	151

Note: Plaque properties were significantly different between the stable angina and unstable angina groups ( $X^{2}=$ 192.11, $P<$ 0.001).

Table 2

Comparison of local CT density values of lesions examined by CTA between the two groups

Groups	$n$	CT density value (HU)
Stable angina group	36	180 $\pm$ 54
Unstable angina group	47	33 $\pm$ 19

Note: CT, computed tomography (CT); CTA, computed tomography angiography. Local CT density values of lesions were significantly different between the stable angina and unstable angina groups ( $t^{\prime}=$ 15.61, $P<$ 0.001).

Figure 1.

The stable and unstable plaques using computed tomography angiography. A: The stable plaques; B: The unstable plaques.

3.2 Comparison of CT density values of lesions using CTA between the stable angina group and the unstable angina group

The stable and unstable plaques using CTA were shown in Fig. 1. The CT density values of lesions in the two groups were measured separately during CTA examinations (Table 2).

Analysis results: There was a significant difference in CT density values of lesions based on CTA examination between the two groups.

3.3 Correlation between angina properties and blood lipid levels

Lipid-lowering drugs were not administered systematically before hospitalization in both groups (Tables 3 and 4).

Table 3
Comparison of angina properties with blood lipid levels

	$n$	TC	LDL-C	HDL-C	TG
Stable angina group	36	4.22 $\pm$ 0.64	1.76 $\pm$ 0.20	2.49 $\pm$ 0.11	1.27 $\pm$ 0.20
Unstable angina group	47	5.85 $\pm$ 0.71	2.73 $\pm$ 0.43	3.75 $\pm$ 0.35	0.82 $\pm$ 0.13
T value		$-$ 10.77	$-$ 13.65	$-$ 23.37	12.06
$P$ value		0.001	0.001	0.001	0.001

Note: $P<$ 0.05 when compared to the stable angina group.

Table 4

Correlation between angina and plaque properties

		Angina
Calcified plaque	Pearson Correlation $r$	$-$ 0.391
	Sig. (2-tailed) $P$	0.005
Non-calcified plaque	Pearson Correlation $r$	0.369
	Sig. (2-tailed) $P$	0.002

Note: Angina is negatively correlated with calcified plaque and positively correlated with non-calcified plaque.

3.4 Plaque properties were related to various indicators of blood lipids

Table 5 displays the relationship between plaque properties and various indicators of blood lipids. Calcified plaques were negatively correlated with TC, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and positively correlated with high-density lipoprotein cholesterol (HDL-C). Non-calcified plaques were negatively correlated with HDL-C and positively correlated with TC, LDL-C, and TG.

Table 5
Correlation between plaque properties and blood lipid parameters

		TC	TG	LDL-C	HDL-C
Calcified plaque	Pearson Correlation $r$	$-$ 0.786	$-$ 0.382	$-$ 0.368	0.210
	Sig. (2-tailed) $P$	0.000	0.006	0.009	0.144
Non-calcified plaque	Pearson Correlation $r$	0.762	0.377	0.532	$-$ 0.311
	Sig. (2-tailed) $P$	0.000	0.002	0.000	0.010

Note: TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol.

4. Discussion

4.1 CTA in the assessment of the properties of angina plaque

The degree of coronary artery stenosis and the properties of coronary atherosclerotic plaque are the primary indicators in imaging techniques used in clinical settings to diagnose CAHD. The severity of CAHD can be predicted using these standards as indicators. Even though coronary artery CTA cannot be used to measure fibrous cap thickness or detect whether a plaque is prone to rupture, CT values can be used to ascertain plaque composition through coronary artery CTA measurements. Due to its ability to determine plaque properties, CTA technology can be used to determine coronary artery stenosis and plaque composition by observing coronary artery lesions of patients with coronary artery disease from multiple angles and spatial perspectives [30].

As shown by previous research, CTA sensitivity and specificity in diagnosing CAHD can reach 92% and 93%, respectively [31]. Furthermore, there are extensive studies that have demonstrated that spiral CT is relatively highly consistent with IVUS in determining plaque properties [32]. According to the findings of our study, the local average CT values of coronary artery plaques differed significantly between stable angina patients and unstable angina patients ( $P<$ 0.01). The study by Inoue et al. also confirmed that CTA has a certain degree of accuracy in determining the properties of coronary plaque [33]. CTA can therefore be used for preliminary screening of patients with high-risk of coronary heart disease. However, Pohle et al. Reported that the differentiation of “vulnerable” and “stable” plaques based on their CT attenuation is doubtful [34]. CT images are often affected by blooming artifacts and tend to overestimate the appearance of calcific stenosis. Post-processing calcium subtraction method could minimize stenosis-overestimation by blooming artifact [35]. In addition, optical coherence tomography (OCT) can provide a clear and detailed view of diseased plaques to assess the patient’s condition [36].

4.2 Correlation between properties of plaque and levels of blood lipids

Coronary artery plaque formation is a long-term process and includes multiple risk factors. There are many theories regarding its pathogenesis, however, the theory of injury response is currently accepted by most scholars. This theory can generally be divided into the following three processes: (1) Arterial intimal injury. Coronary heart disease risk factors can damage the coronary artery intima, leading to easier adherence of blood lipids to the vascular wall. (2) Fat deposition. Blood lipids deposit on the damaged arterial intima, which can further stimulate the worsening of coronary artery intimal injury, leading to increased lipid deposition. (3) Fibrosis. Lipid deposition can stimulate the proliferation of smooth muscle cells and fibroblasts in the coronary artery wall, which eventually develop into fibrous plaques. Therefore, abnormal blood lipids play an important role in the formation of coronary atherosclerosis. According to extensive clinical research conducted in recent years, coronary plaque rupture and thrombosis formation are the leading causes of acute cardiovascular adverse events, with calcified plaques being the potential cause of negative remodeling of local vessel lumens [37]. Consequently, exploring blood biochemical markers that reflect plaque vulnerability has become a current research focus. Based on the findings in this study, calcified plaques are negatively correlated with TC, LDL-C, and TG, and positively correlated with HDL-C, while non-calcified plaques are negatively correlated with HDL-C and positively correlated with TC, LDL-C, and TG. As a result, regular blood lipid level checks are simple, feasible, and effective measures for the prevention and early intervention of coronary atherosclerosis. Lipid-lowering therapy is crucial for the prevention and treatment of cardiovascular diseases, and early detection and intervention of blood lipid levels can delay and reverse the development of atherosclerosis.

4.3 Correlation between blood lipid levels and properties of angina

The pathological basis of coronary heart disease is an imbalance between lipid inflow and outflow, which causes coronary atherosclerosis and the formation of atherosclerotic plaques. According to recent clinical studies, plaque stability is more important than plaque size in predicting the development of acute coronary syndrome [38, 39]. The most important factor in the development of acute coronary syndrome is the rupture of the atherosclerotic plaque, with abnormal blood lipid metabolism also playing a significant role. The stability of the plaque depends on the level of blood lipids. Studies indicate that coronary plaques whose lipid content accounts for more than 40% of the total plaque are more prone to rupture [40]. These types of plaques typically possess a necrotic lipid core, also known as a lipid pool, which contains foam cells and other atherogenic lipids. In the event that such a plaque ruptures, its foam cells are released into the bloodstream causing platelet aggregation and activation of the coagulation system, which results in the formation of a blood clot. As high LDL-C levels increase the amount of lipid that enters the plaque and LDL-C has a chemotactic effect on monocytes, phagocytic cells then consume huge amounts of lipid to form foam cells. This can cause endothelial damage and allow inflammatory mediators to infiltrate, resulting in an inflammatory response. HDL-C, on the other hand, can transport excessive lipids from the coronary artery wall to the liver for decomposition and metabolism, thus delaying or reversing the progression of coronary plaques. Therefore, HDL-C is negatively correlated with the occurrence of cardiovascular adverse events. The findings of this study revealed that lipid levels differed significantly between patients with unstable angina and stable angina, and that angina properties were positively correlated with calcified plaques and negatively correlated with non-calcified plaques. Therefore, to improve lipid metabolism and stabilize plaques in patients with unstable angina, early use of lipid-lowering therapy is recommended.

4.4 Comparison between the properties of angina and the properties of plaque

Coronary artery calcification is often used as a risk marker to predict cardiovascular risk. There was a linear relationship between the degree of coronary artery calcification and plaque progression [41]. Different amounts, sizes, shapes, and positions of calcification may play different roles in plaque stability [42]. Many experts have reached a consensus on the pathological characteristics of calcified and noncalcified plaques after extensive clinical research. Non-calcified plaques, also known as vulnerable plaques, are prone to rupture, leading to thrombosis and acute cardiovascular adverse events. Numerous studies have demonstrated that CTA is reliable due to its high diagnostic accuracy for coronary stenosis and plaque characteristics [43, 44]. Calcified plaques, on the other hand, have a thick fibrous cap, a small or absent lipid necrotic center, more matrix and smooth muscle cells, and fewer inflammatory cells than non-calcified plaques. Calcified plaques have less influence on the occurrence and progression of coronary heart disease because they are stronger and less likely to rupture. According to the findings of our study, patients with unstable angina have significantly more non-calcified plaques in their coronary arteries and a significantly greater risk of thrombosis than patients with stable angina. These findings suggest that thrombosis caused by the rupture of non-calcified plaques is a significant pathological cause of acute cardiovascular events. Therefore, early intervention for non-calcified plaques has profound implications for the long-term prognosis of patients with coronary heart disease.

There were some limitations in the present study. This was a retrospective study, not blinded and no follow up is performed. Future studies will follow up the patients to explore the changes of coronary plaque after controlling blood lipids.

5. Conclusion

CTA is useful in assessing the properties of coronary atherosclerotic plaque in patients with stable and unstable angina. There is a significant correlation between the properties of plaque and the properties of angina, with non-calcified plaques being more prevalent in unstable angina populations than stable angina populations. Calcified plaques are negatively correlated with TC, LDL-C, and TG and positively correlated with HDL-C, whereas non-calcified plaques are negatively correlated with HDL-C and positively correlated with TC, LDL-C, and TG. TC, LDL-C, and TG can make plaques less stable, whereas HDL-C can make plaques more stable.

Funding

This study was supported by the TCM Science and Technology Project of Jilin Province (No. 2019126).

Ethics statement

This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of the Affiliated Hospital of Beihua University Written informed consent was obtained from all participants.

Footnotes

Conflict of interest

The authors declare that there is no conflict of interest.

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Achenbach

Cadet

, et al. Pericoronary adipose tissue computed tomography attenuation and high-risk plaque characteristics in acute coronary syndrome compared with stable coronary artery disease. JAMA Cardiol. 2018; 3(9): 858-863.

The role of computed tomography angiography in assessing the correlation between properties of coronary atherosclerotic plaque and blood lipids

Abstract

BACKGROUND:

OBJECTIVE:

METHODS:

RESULTS:

CONCLUSION:

Keywords

1. Introduction

2. Data and methods

2.1 Case collection

2.2 CTA examination method

2.3 Clinical data

2.4 Classification of coronary atherosclerotic plaques

2.5 Analysis of biochemical test indicators of blood lipids

2.6 Statistical software

3. Results

3.1 Comparison of the properties of lesion plaques and angina based on CTA examination

Table 1 Comparison of plaque properties between the two groups

3.3 Correlation between angina properties and blood lipid levels

Table 3 Comparison of angina properties with blood lipid levels

Table 5 Correlation between plaque properties and blood lipid parameters

4.1 CTA in the assessment of the properties of angina plaque

4.2 Correlation between properties of plaque and levels of blood lipids

4.3 Correlation between blood lipid levels and properties of angina

4.4 Comparison between the properties of angina and the properties of plaque

5. Conclusion

Funding

Ethics statement

Footnotes

Conflict of interest

References

Table 1
Comparison of plaque properties between the two groups

Table 3
Comparison of angina properties with blood lipid levels

Table 5
Correlation between plaque properties and blood lipid parameters