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Preexisting Cardiovascular Risk Factors and Coronary Artery Atherosclerosis in Patients with and without Cancer.

ABSTRACT: Cancer survivors suffer a higher risk of coronary artery atherosclerosis (CAA). Whether cancer patients had increased baseline CAA burden prior to cardiotoxic therapy remains unclear. We conducted a case-control study, and 286 consecutive patients were finally included. Among these patients, 181 had newly diagnosed cancer and 105 had nonmalignant diseases. Cancer was confirmed by biopsy. The severity of CAA was determined by coronary angiography and evaluated using the percentage of stenosis or Gensini scoring (GS). Patients with cancer versus cancer-free controls were older (OR = 1.052, 95% CI: 1.021-1.084, p < 0.001), more commonly male (OR = 0.048, 95% CI: 1.004-2.676, p=0.048), and more severely exposed to smoking (OR = 1.020, 95% CI: 1.007-1.033, p=0.003). Cancer patients were significantly more commonly complicated by ≥90% coronary stenosis than the gender- and age-matched cancer-free controls (9/93 versus 1/93, OR = 4.875, 95% CI: 1.024-23.213, p=0.047). After adjustment for age, gender, hypertension, diabetes, smoking history, blood glucose, and total cholesterol, cancer was significantly associated with high GS (adjusted OR = 2.208, 95% CI: 1.077-4.524, p=0.031). Our study demonstrated that cancer patients had increased CAA burden prior to cardiotoxic therapy. Further study is necessary to investigate the link between CAA and cancer.

SUBMITTER: Guo J

PROVIDER: S-EPMC8826118 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Preexisting Cardiovascular Risk Factors and Coronary Artery Atherosclerosis in Patients with and without Cancer.

Guo Junyi J Fang Peng P Shi Wei W Luo Pengcheng P Huo Shengqi S Yan Dan D Wang Moran M Peng Dewei D Men Lintong L Li Sheng S Lv Jiagao J Lin Li L

Cardiology research and practice 20220201

Cancer survivors suffer a higher risk of coronary artery atherosclerosis (CAA). Whether cancer patients had increased baseline CAA burden prior to cardiotoxic therapy remains unclear. We conducted a case-control study, and 286 consecutive patients were finally included. Among these patients, 181 had newly diagnosed cancer and 105 had nonmalignant diseases. Cancer was confirmed by biopsy. The severity of CAA was determined by coronary angiography and evaluated using the percentage of stenosis or ...[more]

PMID: 35154824

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Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.

Dataset Information

Preexisting Cardiovascular Risk Factors and Coronary Artery Atherosclerosis in Patients with and without Cancer.

Publications

Preexisting Cardiovascular Risk Factors and Coronary Artery Atherosclerosis in Patients with and without Cancer.

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