Coronary artery disease and age: beyond atherosclerosis

Shah, Mit; Sikkel, Markus B.

doi:10.1113/jphysiol.2013.263400

Cited by 7 publications

(11 citation statements)

References 4 publications

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“…The iMap-IVUS data are listed in Table 3. Before the matching procedure, the target lesion length in the premature CAD group was shorter than that in the later CAD group [18.50 (12. 3 , p = 0.013], although these differences were not significant after the matching procedure. Furthermore, in the premature CAD group, the plaque burden was lower compared to the later CAD group (72.69 ± 9.99 vs. 74.85 ± 9.80%, p = 0.005) with less negative remodeling (1.03 ± 0.12 vs. 0.94 ± 0.18, p = 0.034).…”

Section: Plaque Characteristics From Imap-ivusmentioning

confidence: 91%

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Coronary plaque tissue characterization in patients with premature coronary artery disease

Xie

Mao

et al. 2020

Int J Cardiovasc Imaging

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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) mm 3 , 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.

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Section: Plaque Characteristics From Imap-ivusmentioning

confidence: 91%

“…CAD is a progressive disease that takes time to develop [2]. Therefore, age is a significant contributory factor for CAD [3]. When CAD occurs in younger than expected patients it is considered to be premature CAD.…”

Section: Introductionmentioning

confidence: 99%

Coronary plaque tissue characterization in patients with premature coronary artery disease

Xie

Mao

et al. 2020

Int J Cardiovasc Imaging

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“…Indeed, advancing age is one of the major non-modifiable risk factors for CAD. The prevalence of CAD increases progressively with age, and more than 50% of CAD-related deaths occur in individuals older than 75 (61, 64). The population aged 65 and older in the US is projected to double to 83.7 million by the year 2050 (20), causing a growing public health concern.…”

Section: Introductionmentioning

confidence: 99%

“…These heterogeneous patterns of Ca 2+ dysregulation are similar to the heterogeneity of metabolic dysfunction (65). There is a paucity of data regarding age-related alterations in Ca 2+ regulation in coronary smooth muscle (CSM), which would precede extracellular CAC, an event that has been extensively documented in aging (64). The pathophysiology of MetS- and aging-induced atherosclerotic disease may be different; however, MetS-induced and aging-induced atherosclerotic CAD and the associated alterations in CSM intracellular Ca 2+ signaling have yet to be compared directly.…”

Section: Introductionmentioning

confidence: 99%

Effect of metabolic syndrome and aging on Ca2+ dysfunction in coronary smooth muscle and coronary artery disease severity in Ossabaw miniature swine

Badin

Bruning

Sturek

2018

Experimental Gerontology

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“…Age is a critical contributing factor for the risk of CAD, age-related functional impairment including weak immune and inflammatory system, and other mechanisms involved in the regulation of the flow in the coronary arteries, exerted crucial effects during CAD development [ 8 ]. Thus, in order to exclude the effects of age-related dysfunction of CAD associated mechanisms, the association analysis of these four SNPs in lipids metabolism-related genes with the risk of CAD was performed only among the early-onset CAD subjects.…”

Section: Introductionmentioning

confidence: 99%

The association of APOC4 polymorphisms with premature coronary artery disease in a Chinese Han population

Cheng

et al. 2015

Lipids Health Dis

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BackgroundHypercholesterolemia arising from abnormal lipid metabolism is one of the critical risk factors for coronary artery disease (CAD), however the roles of genetic variants in lipid metabolism-related genes on premature CAD (≤60 years old) development still require further investigation. We herein genotyped four single nucleotide polymorphisms (SNPs) in lipid metabolism-related genes (rs1132899 and rs5167 in APOC4, rs1801693 and rs7765781 in LPA), aimed to shed light on the influence of these SNPs on individual susceptibility to early-onset CAD.MethodsGenotyping of the four SNPs (rs1132899, rs5167, rs1801693 and rs7765781) was performed in 224 premature CAD cases and 297 control subjects (≤60 years old) using polymerase chain reaction-ligation detection reaction (PCR–LDR) method. The association of these SNPs with premature CAD was performed with SPSS software.ResultsMultivariate logistic regression analysis showed that C allele (OR = 1.50, P = 0.027) and CC genotype (OR = 2.84, P = 0.022) of APOC4 rs1132899 were associated with increased premature CAD risk, while the other three SNPs had no significant effect. Further stratified analysis uncovered a more evident association with the risk of premature CAD among male subjects (C allele, OR = 1.65, and CC genotype, OR = 3.33).ConclusionsOur data provides the first evidence that APOC4 rs1132899 polymorphism was associated with an increased risk of premature CAD in Chinese subjects, and the association was more significant among male subjects.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-015-0065-7) contains supplementary material, which is available to authorized users.

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Coronary artery disease and age: beyond atherosclerosis

Cited by 7 publications

References 4 publications

Coronary plaque tissue characterization in patients with premature coronary artery disease

Coronary plaque tissue characterization in patients with premature coronary artery disease

Effect of metabolic syndrome and aging on Ca2+ dysfunction in coronary smooth muscle and coronary artery disease severity in Ossabaw miniature swine

The association of APOC4 polymorphisms with premature coronary artery disease in a Chinese Han population

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