scholarly journals Coronary plaque tissue characterization in patients with premature coronary artery disease

2020 ◽  
Vol 36 (6) ◽  
pp. 1003-1011
Author(s):  
Jianchang Xie ◽  
Jie Qi ◽  
Hengyi Mao ◽  
Ningfu Wang ◽  
Xianhua Ye ◽  
...  

Abstract Premature coronary artery disease (CAD) studies rarely involve coronary plaque characterization. We characterize coronary plaque tissue by radiofrequency intravascular ultrasound (IVUS) in patients with premature CAD. From July 2015 to December 2017, 220 patients from the Department of Cardiology, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine with first occurrence of angina or myocardial infarction within 3 months were enrolled. Patients with premature CAD (n = 47, males aged < 55 years, and females aged < 65 years) or later CAD (n = 155) were retrospectively compared for cardiovascular risk factors, laboratory examination findings, coronary angiography data, gray-scale IVUS, and iMap-IVUS. The mean age was 53.53 ± 7.24 vs. 70.48 ± 8.74 years (p < 0.001). The groups were similar for traditional coronary risk factors except homocysteine (18.60 ± 5.15 vs. 17.08 ± 4.27 µmol/L, p = 0.043). After matching for baseline characteristics, LDL cholesterol (LDL-C) was higher for premature CAD than later CAD (2.50 ± 0.96 vs. 2.17 ± 0.80 mmol/L, p = 0.019). Before the matching procedure, the premature CAD group had shorter target lesion length [18.50 (12.60–32.00) vs. 27.90 (18.70–37.40) mm, p = 0.002], less plaque volume [175.59 (96.60–240.50) vs. 214.73 (139.74–330.00) mm3, p = 0.013] than the later CAD group. After the matching procedure, the premature CAD group appeared to be less plaque burden (72.69 ± 9.99 vs. 74.85 ± 9.80%, p = 0.005), and positive remodeling (1.03 ± 0.12 vs. 0.94 ± 0.18, p = 0.034), and lower high risk feature incidence (p = 0.006) than the later CAD group. At the plaque’s minimum lumen, premature CAD had more fibrotic (p < 0.001), less necrotic (p = 0.001) and less calcified areas (p = 0.012). Coronary plaque tissue was more fibrotic with less necrotic and calcified components in premature than in later CAD, and the range and degree of atherosclerosis were significantly lower.

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Morten K Christiansen ◽  
Jesper M Jensen ◽  
Hans Erik Bøtker ◽  
Henrik K Jensen

Introduction: A family history of premature coronary artery disease (CAD) is a well-known risk factor for adverse coronary events with age of onset being inversely related to the degree of heritability. Hypothesis: We hypothesized that asymptomatic first degree relatives, of patients with premature CAD, suffer a high burden of subclinical coronary atherosclerosis. Methods: First degree relatives, aged 30-65 years, of patients with a documented coronary revascularization procedure before the age of 40 years, were invited to participate in the study. Participants were matched by age, sex and absence of a family history, with patients referred for coronary CT angiography (CTA) because of atypical angina or non-anginal chest pain. A pooled blinded analysis was performed. The main outcome measure was the number of plaque-affected coronary segments. Results: 88 relatives and 88 symptomatic controls underwent CTA. Treatment of hypertension and dyslipidemia tended to be more common among controls (p=0.06). 4 relatives reported vague symptoms of which none had angiographic signs of obstructive CAD (any luminal stenosis above 50%). The calculated SCORE risk among relatives was generally low (85% having a 10-year risk of ≤1%). Relatives had significantly (p=0.006) more affected segments than controls (0 segments: 29,6% vs. 48,9%, 1-2 segments: 27,3% vs. 31,8%, 3-5 segments: 23,9% vs. 11,4% and ≥6 segments: 19,3% vs. 8,0%). In a multivariable logistic regression analysis, the presence of any CAD (OR 3.16 (1.50;6.70)) as well as non-calcified plaques (OR 2.2 (1.14;4.26)), mixed plaques (OR 6.77 (2.7;16.98)) and calcified plaques (OR 2.34 (1.01;5.43)) were more frequent. Although increased, the presence of obstructive plaques, however, did not differ statistically significantly between relatives and controls (OR 2.58 (0.85;7.83)). Conclusions: Asymptomatic relatives of patients with premature CAD suffer a high coronary plaque burden even when compared with symptomatic patients with an a priori higher risk of CAD. Our results indicate a strong genetic component in the genesis of coronary atherosclerosis and, moreover, underline the limitations of current guidelines on prevention of CAD.


1993 ◽  
Vol 82 (2) ◽  
pp. 162-165 ◽  
Author(s):  
Y Beigel ◽  
J George ◽  
L Leibovici ◽  
A Mattityahu ◽  
S Sclarovsky ◽  
...  

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Youssef A Elnabawi ◽  
Amit K Dey ◽  
Agastya D Belur ◽  
Aditya Goyal ◽  
Jacob W Groenendyk ◽  
...  

Introduction: Serum uric acid (sUA), a known inflammosome-inducer, is associated with prospective risk of coronary artery disease in a dose-dependent fashion. Psoriasis (PSO), a chronic inflammatory disease associated with elevated burden of systemic inflammation and subclinical coronary artery disease, provides a reliable human model to study how sUA may relate to non-calcified coronary plaque burden (NCB) measured by computed coronary tomography angiography (CCTA). Hypothesis: We hypothesized that sUA would directly associate with NCB beyond traditional cardiovascular (CV) risk factors. Methods: 103 consecutive PSO patients and 47 healthy volunteers (HV) underwent CCTA (320 detector row, Toshiba) for coronary plaque burden quantification using QAngio (Medis). PSO severity was assessed by Psoriasis Area Severity Score (PASI) and divided into severe PSO (PASI>10) and mild-moderate PSO (PASI<10). All patients had fasting blood draws for the measurement of sUA at a certified clinical lab. Results: PSO patients were older than HV and had a higher CV risk by Framingham risk score (FRS) (Table 1). We observed a significant trend towards increase in sUA among severe PSO, mild-moderate PSO, and HV groups (mean 6.4, 5.9, 5.4 respectively, p=0.02 for trend). A positive association was observed between sUA and NCB, which was stronger in severe PSO after adjustment for traditional CV risk, alcohol, statins, and systemic/biologic PSO treatment (Severe PSO: β=0.27, p<0.001; Mild-moderate PSO: β=0.18, p=0.03), not significant in HV (β=0.18, p=0.12). Conclusions: sUA is independently associated with NCB in states of chronic inflammation such as PSO, and as such, may potentially serve as a biomarker for subclinical coronary atherosclerosis. However, larger prospective studies of CV outcomes in chronic inflammatory diseases are needed to confirm these results.


Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1036
Author(s):  
Karolina E. Kryczka ◽  
Mariusz Kruk ◽  
Marcin Demkow ◽  
Barbara Lubiszewska

Coronary artery disease (CAD) is the leading cause of morbidity and mortality in women worldwide. Its social impact in the case of premature CAD is particularly devastating. Many differences in the presentation of the disease in women as compared to men, including atypical symptoms, microvascular involvement, and differences in pathology of plaque formation or progression, make CAD diagnosis in women a challenge. The contribution of different risk factors, such as smoking, diabetes, hyperlipidemia, or obesity, may vary between women and men. Certain pathological pathways may have different sex-related magnitudes on CAD formation and progression. In spite of the already known differences, we lack sufficiently powered studies, both clinical and experimental, that assess the multipathogenic differences in CAD formation and progression related to sex in different age periods. A growing quantity of data that are presented in this article suggest that thrombosis with fibrinogen is of more concern in the case of premature CAD in women than are other coagulation factors, such as factors VII and VIII, tissue-type plasminogen activator, and plasminogen inhibitor-1. The rise in fibrinogen levels in inflammation is mainly affected by interleukin-6 (IL-6). The renin–angiotensin (RA) system affects the inflammatory process by increasing the IL-6 level. Unlike in men, in young women, the hypertensive arm of the RA system is naturally downregulated by estrogens. At the same time, estrogens promote the fibrinolytic path of the RA system. In young women, the promoted fibrinolytic process upregulates IL-6 release from leukocytes via fibrin degradation products. Moreover, fibrinogen, whose higher levels are observed in women, increases IL-6 synthesis and exacerbates inflammation, contributing to CAD. Therefore, the synergistic interplay between thrombosis, inflammation, and the RA system appears to have a more significant influence on the underlying CAD atherosclerotic plaque formation in young women than in men. This issue is further discussed in this review. Fibrinogen is the biomolecule that is central to these three pathways. In this review, fibrinogen is shown as the biomolecule that possesses a different impact on CAD formation, progression, and destabilization in women to that observed in men, being more pathogenic in women at the early stages of the disease than in men. Fibrinogen is a three-chain glycoprotein involved in thrombosis. Although the role of thrombosis is of great magnitude in acute coronary events, fibrinogen also induces atherosclerosis formation by accumulating in the arterial wall and enabling low-density lipoprotein cholesterol aggregation. Its level rises during inflammation and is associated with most cardiovascular risk factors, particularly smoking and diabetes. It was noted that fibrinogen levels were higher in women than in men as well as in the case of premature CAD in women. The causes of this phenomenon are not well understood. The higher fibrinogen levels were found to be associated with a greater extent of coronary atherosclerosis in women with CAD but not in men. Moreover, the lysability of a fibrin clot, which is dependent on fibrinogen properties, was reduced in women with subclinical CAD compared to men at the same stage of the disease, as well as in comparison to women without coronary artery atherosclerosis. These findings suggest that the magnitude of the pathological pathways contributing to premature CAD differs in women and men, and they are discussed in this review. While many gaps in both experimental and clinical studies on sex-related differences in premature CAD exist, further studies on pathological pathways are needed.


1994 ◽  
Vol 109 (1-2) ◽  
pp. 23
Author(s):  
I. Keber ◽  
N. Ursˇicˇ ◽  
M. Stegnar ◽  
D. Keber ◽  
C. Krzˇisˇnik

Author(s):  
Laxmi H. Shetty ◽  
Rahul S. Patil ◽  
Jayashree Kharge ◽  
J. R. Vijay Kumar ◽  
Santu Ghosh ◽  
...  

Introduction Coronary artery disease (CAD) follows a different pattern in women and men, more so in the young (< 40 years). The gender differences in the risk factors, clinical presentation and diagnosis need to be understood, so that appropriate and timely treatment can be given. Objective The study contemplates to analyze the gender differences in the presence of major coronary risk factors, clinical presentation, diagnosis and immediate outcomes in patients who present with premature CAD (PCAD). Patients and Methods We evaluated 1,062 consecutive registry patients who presented with diagnosis of PCAD between 2018 to 2019 at our institution after satisfying the inclusion criteria. Results The study analyses 82 females and 980 males. The mean age of females was 35.4 ± 4.68 years and males was 34.2 ± 4.25 years. Males smoked more often (55.1%, p < 0.001). Females more often had abnormal BMI (84.1%, p < 0.001), increased waist-hip ratios (97.6%, p < 0.001), diabetes (35.4%, p < 0.001), dyslipidemia (17.1% vs. 11%) and hypertension (15.9% vs. 11.5%). STEMI was the most common presentation among males (80.4% vs. 71.9%). Majority of females (74.6%) presented 6 hours after index pain. NSTEMI was more common among females (20.7% vs. 16%). Single-vessel involvement was common in both sexes (84.1% in males and 85.2% in females). Obstructive CAD was less common in both groups. Conclusions Conventional risk factors play a major role for CAD in Indians. Smoking was common in males and metabolic syndrome in females. Also, females had a higher threshold for seeking treatment and referral. Measures have to be taken for early diagnosis and referral of females. Recanalized and thrombotic coronaries were common, indicating predominant thrombus burden in the young


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Benjamin Dao ◽  
Bishoy Elbebabawy ◽  
Ibrahim Sayid ◽  
Jagdesh Kandala ◽  
Harish Raj Seetha Rammohan ◽  
...  

Introduction: Our group has shown the Wnt-pathway to be a key regulator of SMC function and to be expressed in human coronary atheroma. Dickkopf-related protein 1 (DKK-1) is a member of the Wingless (Wnt) signaling pathway molecules and has recently been shown to improve GRACIE-risk factor score prediction of coronary events in chest pain patients and to predict restenosis post coronary stenting. We tested its association with coronary plaque burden and cardiovascular risk factors in comparison with CRP-1; Hypothesis: DKK-1 may be associated with coronary artery plaque burden and cardiovascular risk factors and play a role in coronary artery disease through modulation of SMC. Methods: 218 patients with angiographic evidence of CAD (mildly obstructive CAD, n=35; obstructive stable CAD, n=154; unstable CAD, n=29) were enrolled in this study at the time of cardiac catherization. DKK-1 and CRP-1 were measured by ELISA. Data are shown as Mean p SEM. Values of DKK-1 and CRP1 were skewed, so non-parametric tests were used to determine the associations between DKK-1 and CRP-1 with Syntax Score, age, BMI, LDL, HDL, and HgbA1c. . Spearman’s Rank Order Correlation, Wilcoxon Rank Sum Test, and analysis of variance (ANOVA) were used to assess associations. Results: Data are shown as Mean p SEM.Variables were as follows: DKK-1 736 pg/ml p 129, CRP-1 0.108 mg/ml p 0.01, age 66 years p 1, BMI 32 p 0.5, LDL 97 p 3, HDL 46 p 2, HgbA1C 6.5 p 0.2, Syntax score 11 p 0.7. With DKK-1 the only statistically significant correlation observed was between DKK-1 and HgbA1c (r=0.18, P<0.05). There was no association between DKK-1 and CRP-1, Syntax Score, Age, BMI, LDL, and HDL. With CRP-1, however, we observed significant positive correlations with Syntax Score (r=0.2, P<0.05), BMI (r=0.18, P<0.05), LDL (r=0.18, P<0.05) and significant negative correlation with age (r= -0.19, P<0.05) and with HDL (r=-0.18, P<0.05). There was no association between CRP-1 and HDL as well as HgbA1c. Conclusions: In patients with angiographically established CAD DKK-1 in contrast to CRP-1 is not a predictor of coronary plaque burden and has as only significant association a positive correlation with HgbA1c. Our data suggest that the reported role of DKK-1 in coronary event risk and in restenosis might be related to Diabetes mediated effects.


2012 ◽  
Vol 55 (4) ◽  
pp. 172-179 ◽  
Author(s):  
Beata Sarecka-Hujar ◽  
Iwona Zak ◽  
Jolanta Krauze

Background: The presence of several risk factors (genetic and non-genetic) has greater impact on the risk of premature coronary artery disease (CAD) than single risk factor. Objective: The aim of the study was to establish possible relations between genotypes and alleles of 677C>T polymorphism ofMTHFRgene and some traditional risk factors e.g. elevated levels of lipid parameters and smoking in development of premature CAD. Methods: The groups comprised 152 patients with angiographically documented premature CAD (aged 42.9 ± 5.5) and 121 age-matched blood donors (aged 42.3 ± 6.5) were studied. TheMTHFR677C>T polymorphism was genotyped with Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method. Results: Patients with TT genotype who simultaneously smoked had increased risk of premature CAD compared to non-smoking cases with CC genotype (OR = 24.62). We also found that individuals with TT genotype and elevated LDL-cholesterol (LDL-chol.) level had significantly higher risk of CAD (OR = 9.92) than individuals with normal LDL-chol. level and CC genotype. Conclusions: The present study shows that simultaneous presence ofMTHFRTT genotype and smoking or elevated levels of LDL-chol. influences the risk of premature CAD. This findings give interesting contribution to gene-environment interaction problem that may have clinical implications in the future.


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