scholarly journals The Effect of Periplaque Fat on Coronary Plaque Vulnerability in Patients with Stable Coronary Artery Disease – a 128-multislice CT-based Study

2018 ◽  
Vol 3 (2) ◽  
pp. 69-76
Author(s):  
Nóra Raț ◽  
Diana Opincariu ◽  
Emese Márton ◽  
Ramona Zavate ◽  
Mirela Pintican ◽  
...  

Abstract Background: The role of periplaque fat (PPF), as a fragment of the total epicardial adipose tissue, measured in the vicinity of a target coronary lesion, more specifically within the close proximity of a vulnerable plaque, has yet to be evaluated. The study aimed to evaluate the interrelation between PPF and coronary plaque vulnerability in patients with stable coronary artery disease (CAD). Secondary objective: evaluation of the relationship between the total pericardial fat and markers for plaque vulnerability. Materials and methods: We prospectively enrolled 77 patients with stable CAD, who underwent 128-multislice computed tomography coronary angiography (CTCA), and who presented minimum one lesion with >50% stenosis. CTCA analysis included measurements of: total pericardial fat and PPF volumes, coronary plaque characteristics, markers for plaque vulnerability – positive remodeling (PR), low attenuation plaque (LAP), spotty calcifications (SC,) napkin ring sign (NRS). Study subjects were divided into two categories: Group 1 – 1 marker of plaque vulnerability (n = 36, 46.75%) and Group 2 – ≥1 marker of vulnerability (n = 41, 53.25%). Results: The mean age of the population was 61.77 ± 11.28 years, and 41 (53.24%) were males. The analysis of plaque characteristics showed that Group 2 presented significantly longer plaques (16.26 ± 4.605 mm vs. 19.09 ± 5.227 mm, p = 0.02), remodeling index (0.96 ± 0.20 vs. 1.18 ± 0.33, p = 0.0009), and vessel volume (p = 0.027), and more voluminous plaques (147.5 ± 71.74 mm3 vs. 207.7 ± 108.9 mm3, p = 0.006) compared to Group 1. Group 2 presented larger volumes of PPF (512.2 ± 289.9 mm3 vs. 710.9 ± 361.9 mm3, p = 0.01) and of thoracic fat volume (1,616 ± 614.8 mm3 vs. 2,000 ± 850.9 mm3, p = 0.02), compared to Group 1, but no differences were found regarding the total pericardial fat (p = 0.49). Patients with 3 or 4 vulnerability markers (VM) presented significantly larges PPF volumes compared to those with 1 or 2 VM, respectively (p = 0.008). There was a significant positive correlation between PPF volume and the non-calcified (r = 0.474, 95% CI 0.2797–0.6311, p <0.0001), lipid-rich (r = 0.316, 95% CI 0.099–0.504, p = 0.005), and fibro-fatty (r = 0.452, 95% CI 0.2541–0.6142, p <0.0001) volumes. The total pericardial fat was significantly correlated only with the volume of lipid-rich plaques (p = 0.02). Conclusions: Periplaque fat volume was associated with a higher degree of coronary plaque vulnerability. PPF was correlated with lipid-rich, fibro-fatty, and non-calcified plaque-related volumes, as markers for enhanced plaque vulnerability. PPF volume, assessed with native cardiac computed tomography, could become a novel marker for coronary plaque vulnerability.

2016 ◽  
Vol 1 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Roxana Hodaş ◽  
Sorin Pop ◽  
Diana Opincariu ◽  
Nora Rat ◽  
Laura Jani ◽  
...  

Abstract Background: Epicardial fat has been recently identified as a major player in the development of the atherosclerotic process. Study aim: The aim of this study was to correlate the epicardial fat volume (EFV), determined by Multisclice CT, and the severity of the coronary lesions, expressed by the Coronary Calcium Score (CCS) and Syntax Score (SxS) in patients with established coronary artery disease (CAD). Material and methods: One-hundred-twenty-six patients underwent Multisclice 64 CT assessment of coronary lesions and epicardial fat quantification. Calculation of CCS was performed on all the three coronary vessels and was followed by determination of SxS according to guidelines. The patients were divided into 2 groups: Group 1 – patients with CCS >400 (n = 26), and Group 2 — patients with CaS <400 (n = 100). Results: The mean age of the study population was 65.32 years for Group 1 and 54 years for Group 2 (p <0.0001). However, patients >65 years of age had a high CCS in a more significant extent than younger patients (50% in Group 1 vs. 17% in Group 2, p = 0.0115). Female gender was recorded in 48% of cases in Group 2 and in 19% of cases in Group 1 (p = 0.008). Several factors were identified in a higher extent in the group with high CCS as compared with the group with low CCS, such as the presence of significant stenosis (>50%) of the left anterior descending artery (LAD) (46% vs. 9%, p <0.0001), the presence of multi-vessel coronary disease (50% vs. 5%, p <0.0001) and a high SxS, above 23 (23% vs. 4%, p = 0.006). The epicardial fat volume was 117.81 ± 40.4 ml (95% CI: 97.98–138.2 ml) in Group 2 and 89.77 ± 37.7 ml (95% CI: 80.4–101.5 ml) in Group 1 (p = 0.0033). Conclusions: Epicardial fat volume could represent a new imaging-derived biomarker, useful for classification of the severity of coronary artery disease, increased values of EFV being associated with other biomarkers of disease severity, such as calcium score.


Angiology ◽  
2021 ◽  
pp. 000331972199141
Author(s):  
Arafat Yildirim ◽  
Mehmet Kucukosmanoglu ◽  
Fethi Yavuz ◽  
Nermin Yildiz Koyunsever ◽  
Yusuf Cekici ◽  
...  

Many parameters included in the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) and CHA2DS2-VASc (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, stroke, vascular disease, age 65-74 years, sex category) scores also predict coronary artery disease (CAD). We modified the ATRIA score (ATRIA-HSV) by adding hyperlipidemia, smoking, and vascular disease and also male sex instead of female. We evaluated whether the CHA2DS2-VASc, CHA2DS2-VASc-HS, ATRIA, and ATRIA-HSV scores predict severe CAD. Consecutive patients with coronary angiography were prospectively included. A ≥50% stenosis in ≥1epicardial coronary artery (CA) was defined as severe CAD. Patient with normal CA (n = 210) were defined as group 1, with <50% CA stenosis (n = 178) as group 2, and with ≥50% stenosis (n = 297) as group 3. The mean ATRIA, ATRIA-HSV, CHA2DS2-VASc, and CHA2DS2VASc-HS scores increased from group 1 to group 3. A correlation was found between the Synergy between PCI with Taxus and Cardiac Surgery score and ATRIA ( r = 0.570), ATRIA-HSV ( r = 0.614), CHA2DS2-VASc ( r = 0.428), and CHA2DS2-VASc-HS ( r = 0.500) scores ( Ps < .005). Pairwise comparisons of receiver operating characteristics curves showed that ATRIA-HSV (>3 area under curve [AUC]: 0.874) and ATRIA (>3, AUC: 0.854) have a better performance than CHA2DS2-VASc (>1, AUC: 0.746) and CHA2DS2-VASc-HS (>2, AUC: 0.769). In conclusion, the ATRIA and ATRIA-HSV scores are simple and may be useful to predict severe CAD.


2019 ◽  
Vol 91 (9) ◽  
pp. 26-31
Author(s):  
N Y Grigorieva ◽  
T P Ilyushina ◽  
E M Yashina

Aim: to compare the antianginal and pulse slowing effects, the impact on the ectopic myocardial activity as well as the safety of the treatment with beta - adrenoblocker bisoprolol, calcium antagonist verapamil and the combination of bisoprolol with amlodipine in patients with stable angina (SA) and bronchial asthma (BA). Materials and methods. The study included 90 patients with SA II-III functional class (FC) having concomitant persistent asthma of moderate severity, controlled, without exacerbation. The patients were divided into three groups with 30 individuals in each one depending on the main antianginal drug prescribed. Group 1 patients received a cardio - selective beta - adrenergic blocker bisoprolol (Concor) at the dose of 5 mg/day, patients of group 2 were treated by a calcium antagonist verapamil at the dose of 240 mg/day, patients of group 3 received combined therapy with bisoprolol at the dose of 5 mg/day and amlodipine at the dose of 5 mg/day given as a fixed combination (Concor AM 5/5). All the patients were investigated by the methods of daily ECG monitoring and respiratory function study (RFS) in addition to physical examination at baseline and after 4 weeks of treatment. Results. After 4 weeks of treatment, patients of group 1 and group 3 did not complain of angina attacks and did not use nitroglycerin unlike patients of group 2. The achieved heart rate (HR) in group 1 patients was 68.6±8.5 beats/min, in group 2 - 74.3±5.6 beats/min, in group 3 - 67.3±4.8 beats/min. A significant decrease in the number of supraventricular and ventricular extrasystoles occurred in patients of group 1 and group 3 only. Thus, the pulse slowing, antianginal, antiischemic and antiarrhythmic effect of the calcium antagonist verapamil, even at the dose of 240 mg/day, is not always sufficient for the patients with SA II-III FC and concomitant BA, unlike therapy with the inclusion of beta - blocker bisoprolol. During the study there was no registered deterioration in the indices of bronchial patency according to the RFS data in the patients of all three groups. Conclusion. In patients with coronary artery disease and concomitant asthma, all three types of pulse slowing therapy do not have any negative effects on bronchial patency. Therapy with the inclusion of beta - blockers (bisoprolol or its combination with amlodipine), in contrast to verapamil, reliably reduces heart rate and the number of supraventricular and ventricular extrasystoles in addition to a good antianginal effect.


2020 ◽  
Vol 9 (6) ◽  
pp. 1899 ◽  
Author(s):  
Robert Schönbauer ◽  
Michael Lichtenauer ◽  
Vera Paar ◽  
Michael Emich ◽  
Monika Fritzer-Szekeres ◽  
...  

Background: Low levels of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were reported in patients with coronary artery disease, heart failure, chronic kidney disease and diabetes mellitus. Soluble cluster differentiation 163 (sCD163) serum levels are related to M2 macrophages, having anti-inflammatory attributes. As sport is well-known for its anti-inflammatory and cardioprotective effects we aimed to investigate the influence of eight months of physical activity on serum sCD163 and sTWEAK levels. Methods: In total, 109 subjects with at least one cardiovascular risk factor were asked to perform endurance training within the calculated training pulse for eight months. Overall, 98 finished the study. The performance gain was measured/quantified by bicycle stress tests at the beginning and end of the observation period. The cohort was divided into four groups, dependent on their baseline performance and performance gain. sCD163 and sTWEAK were measured at baseline and after two, six and eight months by ELISA. Results: Those participants who had a performance gain of ≤2.9% (mean gain 12%) within eight months showed a significant increase in sTWEAK (group 2: from 133 to 200 pg/mL, p = 0.002 and group 4: from 166 to 212 pg/mL, p = 0.031) and sCD163 levels (group 2: from 255 to 348 ng/mL, p = 0.035 and group 4: from 247 to 288 ng/mL, p = 0.025) in contrast to subjects without performance gain (sTWEAK: group 1: from 161 to 177 pg/mL, p = 0.953 and group 3: from 153 to 176 pg/mL, p = 0.744; sCD163: group 1: from 289 to 256 ng/mL, p = 0.374 and group 4: from 291 to 271 ng/mL, p = 0.913). Baseline sCD163 correlated with erythrocyte count, hematocrit, ASAT and lipoprotein a, the presence of hypertension and a BMI > 30 kg/m2. Conclusion: Regular physical activity leads to a significant increase in sCD163 and sTWEAK levels of up to 37% and 50%, respectively. It is well-known that physical activity prevents or retards the onset and genesis of chronic inflammatory disease. One possible way of how training evolves its beneficial effect might be by modifying the inflammation status using the sTWEAK–sCD163 axis. Brief Summary: Regular physical activity leads to a significant increase in sTWEAK and sCD163 levels. Both factors are diminished in patients with chronic (inflammation-based) diseases, such as coronary artery disease, heart failure, pulmonary artery hypertension, chronic kidney disease and diabetes mellitus. It seems that the amounts of soluble TWEAK and CD163 are essential for a healthy balance and modulation between pro- and anti-inflammatory processes, and regular physical training could use the sCD163–sTWEAK axis to unfold its beneficial effect.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Yamamoto ◽  
H Otake ◽  
T Shinke ◽  
T Yamashita ◽  
H Kawamori ◽  
...  

Abstract Background Diabetes mellitus has been known as an important factor of coronary artery disease (CAD) progression despite of widespread with lipid-lowering therapy. Although we have reported that large glucose fluctuation is associated with the development of cardiovascular disease in both diabetes mellitus (DM) and non-DM patients, the underlying mechanisms remain unclear. Monocytes play a key role for atherosclerotic plaque formation. Monocytes in human peripheral blood are divided into three subsets: CD14++CD16− monocytes, CD14++CD16+ monocytes, and CD14+CD16++ monocytes. The CD14++CD16+ monocyte subset has recently received attention because it is reported to be associated with future cardiovascular events such as acute myocardial infarction. However, their impact on coronary plaque vulnerability in coronary artery disease (CAD) patients with or without DM remains unclear. Purpose The aim of this study was to investigate the impact of CD14++CD16+ monocyte levels on coronary plaque vulnerability and glucose fluctuation in stable CAD patients with well-regulated lipid levels. Methods This prospective observational study included 50 consecutive patients with CAD (DM [n=22], Non-DM [n=28]), receiving lipid-lowering therapy and undergoing coronary angiography and optical coherence tomography (OCT). Patients were divided into 3 tertiles according to the CD14++CD16+ monocyte percentages assessed by flow cytometry. Standard OCT parameters including lipid arc, lipid length, fibrous cap thickness (FCT) on lipid rich plaque, were assessed for 97 angiographically intermediate lesions (diameter stenosis: 30–70%). The presence of thin-cap fibroatheroma (TCFA), defined as a thin fibrous cap (<65μm) overlying a lipid-rich plaque (>90°), was also assessed. Daily glucose fluctuation assessed by using continuous glucose monitoring system was analyzed by measuring the mean amplitude of glycemic excursion (MAGE). Results CD14++CD16+ monocytes negatively correlated with FCT on lipid rich plaque (r=0.508, p<0.01) (Figure. 1). The presence of thin-cap fibroatheroma (TCFA) was increased stepwise according to the tertile of CD14++CD16+ monocytes (0 [tertile 1] vs. 5 [tertile 2] vs. 10 [tertile 3], p<0.01). CD14++CD16+ monocytes were a significant determinant of TCFA (OR 1.279, p=0.001). Although CD14++CD16+ monocytes were not significantly correlated with MAGE in DM patients (r=0.259, p=0.244), a significant relationship was found between CD14++CD16+ monocytes and MAGE in non-DM patients (r=0.477, p=0.018) (Figure 2). Conclusions CD14++CD16+ monocytes were associated with coronary plaque vulnerability in CAD patients with well-regulated lipid levels both in DM and non-DM patients. Cross-talk between glucose fluctuation and CD14++CD16+ monocytes may enhance plaque vulnerability, particularly in non-DM patients. CD14++CD16+ monocytes could be a possible therapeutic target for coronary plaque stabilization.


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