Background/Objectives: The clinical implications of sarcopenia and visceral obesity in patients with cardiovascular disease (CVD) are poorly understood. We evaluated the impact of sarcopenia and visceral obesity on clinical outcomes among older adults with CVD. Methods: This retrospective cohort study included patients aged 65 years and older who had cardiovascular disease and had undergone body composition analysis using dual-energy X-ray absorptiometry (DXA) between November 2021 and October 2022 and been followed through February 2024. Sarcopenia was defined using the 2019 Asian Working Group for Sarcopenia criteria, and visceral obesity was defined using Korean sex-specific visceral adipose tissue area. The primary outcome was a composite of all-cause mortality and major cardiovascular events, including myocardial infarction, stroke, hospitalization for heart failure, and coronary revascularization. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology reporting guidelines. Results: A total of 317 patients were included, of whom 118 patients (37.2%) had sarcopenia, 184 (58.0%) had visceral obesity, and 55 (17.4%) had sarcopenic obesity. The prevalence of sarcopenia or visceral obesity was 93.8% in patients with obesity and 69.3% in those without obesity. Sarcopenic obesity showed a mixture of characteristics of two metabolic conditions in terms of demographics and body mass index. Sarcopenia was associated with an increased risk of primary outcomes (hazard ratio [HR], 1.93; 95% CI, 1.02–3.66), with the highest risk observed in patients with sarcopenic obesity (HR, 6.74; 95% CI, 1.81–25.16). Conclusions: Sarcopenia was associated with 1.9-fold increased risk of cardiovascular events among older adults with CVD, with a greater than 6-fold increased risk when combined with visceral obesity.

It is uncertain whether the coronary lesion with intermediate stenosis is more likely to cause cardiovascular events than a normal or minimal lesion. We conducted a single-center, prospective cohort study to identify long-term clinical outcomes of patients with untreated non-culprit intermediate lesion and evaluate its predictor of cardiovascular events by using virtual histology-intravascular ultrasound (VH-IVUS). Subjects with non-culprit intermediate lesion underwent VH-IVUS were prospectively registered after percutaneous coronary intervention at the culprit lesion. Intermediate lesion was defined as 30 to 70% stenosis in coronary angiography and primary outcome was an occurrence of major adverse cardiovascular events (MACE) defined as all-cause death, intermediate lesion revascularization (InLR), minimal lesion revascularization (MnLR, unplanned revascularization elsewhere in the target vessel or in other coronary arteries which looked normal or minimal stenosis), cerebrovascular events, or non-fatal myocardial infarction (MI). The mean follow-up period was 4.2 years. Total 25 MACE, approximately 7% incidence annually, were identified during a follow-up period in 86 patients with 89 intermediate lesions. InLR (n = 13) was a most common event followed by MnLR (n = 6), non-fatal MI (n = 4), all-cause death (n = 3), and cerebrovascular events (n = 1). Diameter stenosis (OR 1.07, 95% CI 1.01–1.12, p = 0.015), plaque burden (PB, OR 1.07, 95% CI 1.00–1.15, p = 0.040), fibrofatty area (FFA, OR 1.61, 95% CI 1.10–2.38, p = 0.016), PB ≥ 70% (OR 3.93, 95% CI 1.28–12.07, p = 0.018), and area stenosis ≥ 50% (OR 2.94, 95% CI 1.01–8.56, p = 0.042) showed significant relationships with an occurrence of MACE. In multivariable Cox-proportional hazard analysis, FFA in intermediate lesion was an only independent predictor of MACE (HR 1.36, 95% CI 1.05–1.77, p = 0.019). Untreated intermediate lesions had a significantly higher chance for requiring revascularization compared with a normal or minimal lesion. And also, a large FFA in intermediate lesion was a significant predictor of cardiovascular events and which finding was mainly driven by coronary-related events, in particularly intermediate lesion progression.

Background: The mechanism of in-stent restenosis (ISR) is multifactorial, which includes biological, mechanical and technical factors. This study hypothesized that increased inflammatory reaction, which is known to be an important atherosclerotic process, at a culprit lesion may lead to higher restenosis rates. Methods: The study population consisted of 241 patients who had undergone percutaneous coronary intervention with virtual histology-intravascular ultrasound (VH-IVUS) and a 9-month follow-up coronary angiography. Compared herein is the coronary plaque composition between patients with ISR and those without ISR. Results: Patients with ISR (n = 27) were likely to be older (66.2 ± 9.5 years vs. 58.7 ± 11.7 years, p = 0.002) and have higher levels of high-sensitivity C-reactive protein (hs-CRP, 1.60 ± 3.59 mg/dL vs. 0.31 ± 0.76 mg/dL, p < 0.001) than those without ISR (n = 214). VH-IVUS examination showed that percent necrotic core volume (14.3 ± 8.7% vs. 19.5 ± 9.1%, p = 0.005) was higher in those without ISR than those with ISR. Multivariate analysis revealed that hs-CRP (odds ratio [OR] 3.334, 95% con­fidence interval [CI] 1.158–9.596, p = 0.026) and age (OR 3.557, 95% CI 1.242–10.192, p = 0.018) were associated with ISR. Conclusions: This study suggests that ISR is not associated with baseline coronary plaque composition but is associated with old age and increased expression of the inflammatory marker of hs-CRP. (Cardiol J 2018; 25, 1: 7–13) Background: The mechanism of in-stent restenosis (ISR) is multifactorial, which includes biological, mechanical and technical factors. This study hypothesized that increased inflammatory reaction, which is known to be an important atherosclerotic process, at a culprit lesion may lead to higher restenosis rates. Methods: The study population consisted of 241 patients who had undergone percutaneous coronary intervention with virtual histology-intravascular ultrasound (VH-IVUS) and a 9-month follow-up coronary angiography. Compared herein is the coronary plaque composition between patients with ISR and those without ISR. Results: Patients with ISR (n = 27) were likely to be older (66.2 ± 9.5 years vs. 58.7 ± 11.7 years, p = 0.002) and have higher levels of high-sensitivity C-reactive protein (hs-CRP, 1.60 ± 3.59 mg/dL vs. 0.31 ± 0.76 mg/dL, p < 0.001) than those without ISR (n = 214). VH-IVUS examination showed that percent necrotic core volume (14.3 ± 8.7% vs. 19.5 ± 9.1%, p = 0.005) was higher in those without ISR than those with ISR. Multivariate analysis revealed that hs-CRP (odds ratio [OR] 3.334, 95% con­fidence interval [CI] 1.158–9.596, p = 0.026) and age (OR 3.557, 95% CI 1.242–10.192, p = 0.018) were associated with ISR. Conclusions: This study suggests that ISR is not associated with baseline coronary plaque composition but is associated with old age and increased expression of the inflammatory marker of hs-CRP. (Cardiol J 2018; 25, 1: 7–13)

Lee CS, et al. Korean Circ J. 2012 Nov;42(11):747-752. https://doi.org/10.4070/kcj.2012.42.11.747

It is unclear which plaque component is related with long-term clinical outcomes in patients with coronary artery occlusive disease (CAOD). We assessed the relationship between plaque compositions and long-term clinical outcomes in those patients. The study subjects consisted of 339 consecutive patients (mean 61.7±12.2 years old, 239 males) who underwent coronary angiogram and a virtual histology-intravascular ultrasound examination. Major adverse cardiac and cerebrovascular events (MACCE), including all-cause death, non-fatal myocardial infarction, cerebrovascular events, and target vessel revascularization were evaluated during a mean 28-month follow-up period. Patients with high fibrofatty volume (FFV, >8.90 mm3, n=169) had a higher incidence of MACCE (25.4% vs. 14.7%, p=0.015), male sex (75.7% vs. 65.3%, p=0.043), acute coronary syndrome (53.3% vs. 35.9%, p=0.002), multivessel disease (62.7% vs. 41.8%, p<0.001) and post-stent slow flow (10.7% vs. 2.4%, p=0.002) than those with low FFV (FFV≤8.90 mm3, n=170). Other plaque composition factors such as fibrous area/volume, dense calcified area/volume, and necrotic core area/volume did not show any impact on MACCE. Cardiogenic shock {hazard ratio (HR)=8.44; 95% confidence interval (CI)=3.00-23.79; p<0.001} and FFV (HR=1.85; 95% CI=1.12-3.07; p=0.016) were the independent predictors of MACCE by Cox regression analysis. Thin-cap fibroatheroma, necrotic core area, and necrotic core volume were not associated with MACCE. FFV of a culprit lesion was associated with unfavorable long-term clinical outcomes in patients with CAOD.