CT Radiomics Of Coronary Artery Calcification Distinguish Vulnerable Plaques In Acute Coronary Syndrome- A Propensity-matched Study With Asymptomatic Subjects With Same Calcified Plaque Burden

2021 ◽  
Author(s):  
Ming-Ting Wu
Keyword(s):  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Coronary Artery Calcification ◽  
Plaque Burden ◽  
Coronary Syndrome ◽  
Vulnerable Plaques ◽  
Calcified Plaque ◽  
Asymptomatic Subjects ◽  
Matched Study

scholarly journals Cavitation on top of collision breaks the cover of coronary plaques and triggers acute coronary syndrome

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
H A I Duong ◽  
T Nguyen ◽  
B I N H Cao ◽  
T R A N Le
Keyword(s):  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Static Pressure ◽  
Stable Coronary Artery Disease ◽  
Retrograde Flow ◽  
Recirculating Flow ◽  
Coronary Syndrome ◽  
Cavitation Phenomenon ◽  
Vulnerable Plaques ◽  
Antegrade Flow

Abstract Background Coronary injuries are hypothesized to be caused by the cavitation phenomenon (explosion of air bubbles) which is seen frequently in industrial pipes. Based on hydraulics principles applied to the coronary circulation. during distal negative suctioning in diastole, if the coronary static pressure decreases below the vapor pressure (VP), bubbles will form. They explode when the coronary static pressure recovers > the VP during systole. These explosions create jet waves weakening and rupturing the cover of the coronary plaques, triggering acute coronary syndrome (ACS). How could these events be observed, recorded and compared? Methods Coronary angiograms of patients with ACS and stable coronary artery disease (CAD) (control) were selected. The arteries were recorded at 15 frames per second and saved in the electronic health records and reviewed image by image. After the index artery was completely filled with contrast, the following images showed the blood in white moving in on a background of black contrast. The flow could be laminar, turbulent (mixing of blood in white and contrast in black), antegrade or RETROGRADE (black column traveling backward). At the same time, an artificial intelligence (AI) program was used to detect and identify the flow. Results There were 104 patients with ACS enrolled and 20 patients with stable CAD as control. First, in the ACS group, 84 lesions (80%) were in the end of the proximal segment of the left anterior descending artery (LAD) and mid-segment of the right coronary artery (RCA). 20 lesions (19%) were at the distal RCA. Second, during diastole, 95% of the flow were laminar. The flow became turbulent at the beginning of systole. The turbulence was caused by the COLLISION of the antegrade flow (end of diastole) and the retrograde flow (at the beginning of systole). These collisions were seen in 95% at the location of vulnerable plaques of patients with ACS. In the control patients, there were only 2 cases (10%) with collision. Third, in the 20 patients with lesions at the distal RCA, the lesions were seen to be located at the areas of recirculating flow, at the ostium of the posterior descending artery (PDA) or proximal to the origin of the PDA. The cause of turbulence was most likely due to cavitation on top of collision. The cavitation happened because of continuous steady forward flow (of the PDA) in the myocardium during systole, while at the proximal RCA the blood flew forward more slowly. (Fig.1) The DSICREPANCY of velocities at the proximal and distal RCA allowed the formation of an empty gap (bubble of air). When the flow reversed during systole, this retrograde flow slammed on the bubble which collapsed violently, injured, ruptured the cover of the plaque and started ACS. Conclusions Rupture of bubbles (cavitation) on top of collision was most likely the cause of injury to the cover of vulnerable plaques, triggering ACS. Understanding the mechanism will help to better manage ACS. FUNDunding Acknowledgement Type of funding sources: None. Cavity formation and collision Formation of cavitation at the PDA

Admission Heart Rate Is Associated With Coronary Artery Disease Severity and Complexity in Patients With Acute Coronary Syndrome

Angiology ◽  
2019 ◽  
Vol 70 (8) ◽  
pp. 774-781 ◽  
Author(s):  
Xiaoteng Ma ◽  
Zhijian Wang ◽  
Jianlong Wang ◽  
Fang Liu ◽  
Dai Zhang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Heart Rate ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Disease Severity ◽  
Plaque Burden ◽  
Syntax Score ◽  
Coronary Syndrome ◽  
Coronary Artery Disease Severity ◽  
Artery Disease

We evaluated the relationship between admission heart rate (HR) and coronary artery disease severity and complexity in patients with acute coronary syndrome (ACS). A total of 884 patients (mean age 59 [11] years, 24.7% female) who underwent coronary angiography for ACS and were treated with primary or selective percutaneous coronary intervention were included in this cross-sectional study. The measurement of admission HR was based on the first available resting electrocardiogram after admission. The SYNTAX score (SS) was calculated. Patients with an SS ≤ 22 (n = 538) were classified as the low SS group and those with an SS > 22 (n = 346) were classified as the intermediate-to-high SS group. Admission HR was greater in the intermediate-to-high SS group compared with the low SS group (75 [10] bpm vs 67 [8] bpm, P < .001). Admission HR was positively and significantly correlated with the SS ( r = 0.475, P < .001). After multivariate analysis, admission HR (per 1 standard deviation, ie, 10 bpm) remained an independent predictor of intermediate-to-high SS (odds ratio: 3.135, 95% confidence interval: 2.538-3.873, P < .001). Admission HR is independently and positively associated with the SS. Thus, elevated admission HR may be useful to identify patients with ACS with a high coronary atherosclerotic plaque burden.

scholarly journals VULNERABLE ATHEROSCLEROTIC PLAQUES OF CORONARY ARTERIES IN PATIENTS WITH STABLE CORONARY ARTERY DISEASE

2018 ◽  
Vol 7 (3) ◽  
pp. 65-71 ◽  
Author(s):  
N. A. Kochergin ◽  
A. M. Kochergina ◽  
V. I. Ganjukov ◽  
O. L. Barbarash
Keyword(s):  
Coronary Artery Disease ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Stable Coronary Artery Disease ◽  
Lumen Area ◽  
Coronary Syndrome ◽  
Vulnerable Plaques ◽  
Luminal Stenosis ◽  
Artery Disease

Background. Acute coronary syndrome remains the leading cause of death worldwide. The rupture of vulnerable atherosclerotic plaque in the coronary artery is a common pathogenetic mechanism contributing to the onset of acute coronary syndrome. Therefore, one of the main goals of the practical cardiology is to ensure the development of sensitive early diagnostic methods and set preventive and treatment strategies for acute coronary event. Aim To evaluate the incidence of vulnerable plaques in the non-target coronary arteries in patients with stable coronary artery disease.Methods. 58 patients with stable coronary artery disease were included in a prospective observational cohort study. After the target vessel had been stented, virtual histology intravascular ultrasound (VH-IVUS) of the proximal and middle segments (6–8 cm) of one non-target artery (i.e. without any significant stenotic lesions on coronary angiography) was performed.Results. The mean age of patients was 60.4±6.6 years. In addition to the targeted hemodynamically significant lesions subjected to stenting, 56 patients had 58 lesions (96.5%) in the non-target coronary arteries. Of them, 5 lesions (8.6%) were with >70% luminal stenosis (including >70% luminal stenosis + lumen area <4 mm2 in 4 cases), 10 lesions (17.2%) – with minimum lumine area <4 mm2 and without any other signs of vulnerable plaque, 12 lesions (20.7%) – with a large necrotic core and a thin cap (including thin-cap fibroatheroma + >70% luminal stenosis in 2 patients; thin-cap fibroatheroma + lumen area <4 mm2 – 2 cases, thin-cap fibroatheroma + >70% luminal stenosis + lumen area <4 mm2 – 2 cases).Conclusion. In vivo evaluation of the plaques in the non-target vessels ensures the detection of vulnerable plaques in stable patients. The long-term follow-up of the study group allows assessing the risk of developing adverse cardiovascular events in those patients who have vulnerable coronary plaques.

Abstract 4223: Low Adiponectin Levels Are an Independent Predictor of Mixed and Non-Calcified Coronary Atherosclerotic Plaques

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Uli C Broedl ◽  
Corinna Lebherz ◽  
Michael Lehrke ◽  
Renee Stark ◽  
Helmholtz Zentrum ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Coronary Plaque ◽  
Plaque Burden ◽  
Atherosclerotic Plaques ◽  
Atypical Chest Pain ◽  
Coronary Syndrome ◽  
Coronary Atherosclerotic Plaque ◽  
Artery Disease

We sought to examine the relationship of adiponectin with coronary atherosclerotic plaque morphology in patients with stable typical or atypical chest pain. There is increasing recognition that lesion composition rather than size determines the acute complications of atherosclerotic disease. Low serum adiponectin levels are associated with coronary artery disease and future incidence of acute coronary syndrome. The impact of adiponectin on lesion composition still remains to be determined. Serum adiponectin levels were determined in 303 patients with stable typical or atypical chest pain, who underwent dual-source multi-slice CT-angiography to exclude coronary artery stenosis. Atherosclerotic plaques were classified as calcified, mixed or non-calcified plaques. In bivariate analysis adiponectin levels were inversely correlated with total coronary plaque burden (r=−0.22, p<0.0001), mixed (r=−0.20, p=0.0007) and non-calcified plaques (r=−0.18, p=0.003). No correlation was seen with calcified plaques (r=−0.05, p=0.39). In a fully adjusted multivariate model containing age, sex, body mass index, hypertension, diabetes mellitus, smoking, family history of coronary artery disease, LDL-cholesterol, HDL-cholesterol, triglycerides, hsCRP levels, medication and pericardial adipose tissue volume, adiponectin levels remained predictive of total plaque burden (estimate: −0.035, 95% CI: −0.051 to −0.019, p<0.0001), mixed (estimate: −0.083, 95% CI: −0.127 to −0.039, p=0.0002) and non-calcified plaques (estimate: −0.076, 95% CI: −0.114 to −0.038, p=0.0001). Since the majority of coronary plaques were calcified plaques, adiponectin levels account for only 3% of the variability in total plaque number. In contrast, adiponectin accounts for approximately 20% of the variability in mixed and non-calcified plaque burden. Adiponectin levels predict mixed and non-calcified coronary atherosclerotic plaque burden. Low adiponectin levels may contribute to coronary plaque vulnerability and may thus play a role in the pathophysiology of acute coronary syndrome.

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