Variability of the Plasma Lipidome and Subclinical Coronary Atherosclerosis

Objective: While the risk of acute coronary events has been associated with biological variability of circulating cholesterol, the association with variability of other atherogenic lipids remains less understood. We evaluated the longitudinal variability of 284 lipids and investigated their association with asymptomatic coronary atherosclerosis. Approach and Results: Circulating lipids were extracted from fasting blood samples of 83 community-sampled symptom-free participants (age 41–75 years), collected longitudinally over 6 months. Three types of coronary plaque volume (calcified, lipid-rich, and fibrotic) were quantified using computed tomography coronary angiogram. We first deconvoluted between-subject (CV g ) and within-subject (CV w ) lipid variabilities. We then tested whether the mean lipid abundance was different across groups categorized by Framingham risk score and plaques phenotypes (lipid-rich, fibrotic, and calcified). Last, we investigated whether visit-to-visit variability of each lipid was associated with plaque burden. Most lipids (72.5%) exhibited higher CV g than CV w . Among the lipids (N=145) with 1.2-fold higher CV g than CV w , 26 species including glycerides and ceramides were significantly associated with Framingham risk score and the 3 plaque phenotypes (false discovery rate <0.05). In an exploratory analysis of person-specific visit-to-visit variability without multiple-comparisons testing, high variability of 3 lysophospholipids (lysophosphatidylcholines 16:0, 18:0, and O-18:1) were associated with lipid-rich and fibrotic (noncalcified) plaque volume while high variability of diacylglycerol 18:1_20:0, triacylglycerols 52:2, 52:3, and 52:4, ceramide d18:0/20:0, dihexosylceramide d18:1/16:0, and sphingomyelin 36:3 were associated with calcified plaque volume. Conclusions: High person-specific longitudinal variation of specific nonsterol lipids are associated with the burden of subclinical coronary atherosclerosis. Larger studies are needed to confirm these exploratory findings.

Coronary Artery Calcification and Plaque Characteristics in People Living With HIV: A Systematic Review and Meta‐Analysis

Background Studies have reported that people living with HIV have higher burden of subclinical cardiovascular disease, but the data are not adequately synthesized. We performed meta‐analyses of studies of coronary artery calcium and coronary plaque in people living with HIV. Methods and Results We performed systematic search in electronic databases, and data were abstracted in standardized forms. Study‐specific estimates were pooled using meta‐analysis. 43 reports representing 27 unique studies and involving 10 867 participants (6699 HIV positive, 4168 HIV negative, mean age 52 years, 86% men, 32% Black) were included. The HIV‐positive participants were younger (mean age 49 versus 57 years) and had lower Framingham Risk Score (mean score 6 versus 18) compared with the HIV‐negative participants. The pooled estimate of percentage with coronary artery calcium >0 was 45% (95% CI, 43%–47%) for HIV‐positive participants, and 52% (50%–53%) for HIV‐negative participants. This difference was no longer significant after adjusting for difference in Framingham Risk Score between the 2 groups. The odds ratio of coronary artery calcium progression for HIV‐positive versus ‐negative participants was 1.64 (95% CI, 0.91–2.37). The pooled estimate for prevalence of noncalcified plaque was 49% (95% CI, 47%–52%) versus 20% (95% CI, 17%–23%) for HIV‐positive versus HIV‐negative participants, respectively. Odds ratio for noncalcified plaque for HIV‐positive versus ‐negative participants was 1.23 (95% CI, 1.08–1.38). There was significant heterogeneity that was only partially explained by available study‐level characteristics. Conclusions People living with HIV have higher prevalence of noncalcified coronary plaques and similar prevalence of coronary artery calcium, compared with HIV‐negative individuals. Future studies on coronary artery calcium and plaque progression can further elucidate subclinical atherosclerosis in people living with HIV.

Epicardial Adipose Tissue Volume Is Associated with High Risk Plaque Profiles in Suspect CAD Patients

Objective. To explore the association between EAT volume and plaque precise composition and high risk plaque detected by coronary computed tomography angiography (CCTA). Methods. 101 patients with suspected coronary artery disease (CAD) underwent CCTA examination from March to July 2019 were enrolled, including 70 cases acute coronary syndrome (ACS) and 31 cases stable angina pectoris (SAP). Based on CCTA image, atherosclerotic plaque precise compositions were analyzed using dedicated quantitative software. High risk plaque was defined as plaque with more than 2 high risk features (spotty calcium, positive remolding, low attenuation plaque, napkin-ring sign) on CCTA image. The association between EAT volume and plaque composition was assessed as well as the different of correlation between ACS and SAP was analyzed. Multivariable logistic regression analysis was used to explore whether EAT volume was independent risk factors of high risk plaque (HRP). Results. EAT volume in the ACS group was significantly higher than that of the SAP group ( 143.7 ± 49.8 cm3 vs. 123.3 ± 39.2 cm3, P = 0.046 ). EAT volume demonstrated a significant positive correlation with total plaque burden ( r = 0.298 , P = 0.003 ), noncalcified plaque burden ( r = 0.245 , P = 0.013 ), lipid plaque burden ( r = 0.250 , P = 0.012 ), and homocysteine ( r = 0.413 , P ≤ 0.001 ). In ACS, EAT volume was positively correlated with total plaque burden ( r = 0.309 , P = 0.009 ), noncalcified plaque burden ( r = 0.242 , P = 0.044 ), and lipid plaque burden ( r = 0.240 , P = 0.045 ); however, no correlation was observed in SAP. Patients with HRP have larger EAT volume than those without HRP ( 169 ± 6.2 cm3 vs. 130.6 ± 5.3 cm3, P = 0.002 ). After adjustment by traditional risk factors and coronary artery calcium score (CACS), EAT volume was an independent risk predictor of presence of HRP (OR: 1.018 (95% CI: 1.006-1.030), P = 0.004 ). Conclusions. With the increasing EAT volume, more dangerous plaque composition burdens increase significantly. EAT volume is a risk predictor of HRP independent of convention cardiovascular risk factors and CACS, which supports the potential impact of EAT on progression of coronary atherosclerotic plaque.

Incidence and Mechanisms of Coronary Perforations during Rotational Atherectomy in Modern Practice

Objective. Heavy calcifications remain formidable challenges to PCI, even for well-experienced operators. However, rotational atherectomy (RA)-induced coronary perforations (CPs) still could not be obviated. This study was to explore incidence and mechanisms of RA-induced CP in real-world practice. Knowing why CPs occur in RA should help operators avert such mishaps. Method. Patients who received coronary RA from April 2010 to December 2019 with keywords related to perforations were retrieved from database. The procedure details, angiography, and clinical information were reviewed in detail. Results. A total of 479 RAs were performed with 11 perforations in 10 procedures among 9 patients documented. The incidence of RA-induced CP was 2.1%. The RA vessels were distributed in different territories, including first diagonal branch. Most CPs could be treated conservatively, but prolonged profound shock predisposed to poor outcome. CPs caused by rotawire tip occurred in 18.2% of cases, inappropriately sized burrs in 18.2% of cases, and rotawire damage with subsequent transection and perforation in another 18.2% of cases. A total of 5 (45.5%) perforations were caused by unintended and unnoticed bias cutting into noncalcified plaques (4, 36.4%) or through calcified vessel wall (1, 9.1%). The mechanisms for certain CPs were unique and illustrated in diagrams. Conclusion. CPs due to RA occur in certain percentage of patients. The mechanisms for CPs are diverse. Wire damage with subsequent transection could occur due to inappropriately repetitive burr stress on the wire body. A significant portion was due to unintended and unnoticed bias cutting into noncalcified plaque or through calcified vessel wall.