Our understanding of the correlation between postdischarge cancer and mortality in patients with coronary artery disease (CAD) remains incomplete. The aim of this study was to investigate the relationships between postdischarge cancers and all-cause mortality and cardiovascular mortality in CAD patients.

In this retrospective cohort study, 25% of CAD patients without prior cancer history who underwent coronary artery angiography between January 1, 2011 and December 31, 2015, were randomly enrolled using SPSS 26.0. Patients were monitored for the incidence of postdischarge cancer, which was defined as cancer diagnosed after the index hospitalization, survival status and cause of death. Cox regression analysis was used to explore the association between postdischarge cancer and all-cause mortality and cardiovascular mortality in CAD patients.

A total of 4085 patients were included in the final analysis. During a median follow-up period of 8 years, 174 patients (4.3%) developed postdischarge cancer, and 343 patients (8.4%) died. A total of 173 patients died from cardiovascular diseases. Postdischarge cancer was associated with increased all-cause mortality risk (HR = 2.653, 95% CI: 1.727–4.076, P < 0.001) and cardiovascular mortality risk (HR = 2.756, 95% CI: 1.470–5.167, P = 0.002). Postdischarge lung cancer (HR = 5.497, 95% CI: 2.922–10.343, P < 0.001) and gastrointestinal cancer (HR = 1.984, 95% CI: 1.049–3.750, P = 0.035) were associated with all-cause mortality in CAD patients. Postdischarge lung cancer was significantly associated with cardiovascular death in CAD patients (HR = 4.979, 95% CI: 2.114–11.728, P < 0.001), and cardiovascular death was not significantly correlated with gastrointestinal cancer or other types of cancer.

Postdischarge cancer was associated with all-cause mortality and cardiovascular mortality in CAD patients. Compared with other cancers, postdischarge lung cancer had a more significant effect on all-cause mortality and cardiovascular mortality in CAD patients.

Clinical studies have shown that atherosclerotic cardiovascular disease and cancer often co‐exist in the same individual. The present study aimed to investigate the role of high‐fat‐diet (HFD)‐induced obesity in the coexistence of the two diseases and the underlying mechanism in apolipoprotein E‐knockout (ApoE^−/−) mice.

Male ApoE^−/− mice were fed with a HFD or a normal diet (ND) for 15 weeks. On the first day of Week 13, the mice were inoculated subcutaneously in the right axilla with Lewis lung cancer cells. At Weeks 12 and 15, serum lectin‐like oxidized low‐density lipoprotein receptor‐1 (LOX‐1) and vascular endothelial growth factor levels were measured by enzyme‐linked immunosorbent assay, and blood monocytes and macrophages were measured by fluorescence‐activated cell sorting. At Week 15, the volume and weight of the local subcutaneous lung cancer and metastatic lung cancer and the amount of aortic atherosclerosis were measured.

At Week 15, compared with mice in the ND group, those in the HFD group had a larger volume of local subcutaneous cancer (p = 0.0004), heavier tumors (p = 0.0235), more metastatic cancer in the lungs (p < 0.0001), a larger area of lung involved in metastatic cancer (p = 0.0031), and larger areas of atherosclerosis in the aorta (p < 0.0001). At Week 12, serum LOX‐1, serum vascular endothelial growth factor, and proportions of blood monocytes and macrophages were significantly higher in the HFD group than those in the ND group (p = 0.0002, p = 0.0029, p = 0.0480, and p = 0.0106, respectively); this trend persisted until Week 15 (p = 0.0014, p = 0.0012, p = 0.0001, and p = 0.0204).

In this study, HFD‐induced obesity could simultaneously promote progression of lung cancer and atherosclerosis in the same mouse. HFD‐induced upregulation of LOX‐1 may play an important role in the simultaneous progression of these two conditions via the inflammatory response and VEGF.

Coronary artery disease (CAD) is associated with cancer. The role of inflammation in the association of CAD with cancer remains unclear. The study investigated whether inflammation could impact the relationship between CAD and lung cancer.

The study involved 96 newly diagnosed lung cancer patients without receiving anti-cancer therapy and 288 matched non-cancer patients. All the patients underwent coronary angiography and were free from previous percutaneous coronary intervention or coronary artery bypass grafting. SYNTAX score (SXscore) were used to assess severity of CAD. High SXscore (SXhigh) grade was defined as SXscore > 16 (highest quartile). Neutrophil-to-lymphocyte ratio (NLR) served as an inflammatory biomarker. NLR-high grade referred to NLR > 2.221 (median).

Among 384 study patients, 380 patients (98.96%) had NLR value (median: 2.221, interquartile range: 1.637–3.040). Compared to non-cancer patients, lung cancer patients had higher rate of SXhigh among total study patients (P = 0.014) and among patients with NLR-high (P = 0.006), but had not significantly higher rate of SXhigh among patients with NLR-low (P = 0.839). Multivariate logistic regression analysis showed that SXhigh was associated with lung cancer [odds ratio (OR) = 1.834, 95% CI: 1.063–3.162, P = 0.029]. Subgroup analysis showed that SXhigh was associated with lung cancer among patients with NLR-high (OR = 2.801, 95% CI: 1.355–5.794, P = 0.005), however, the association between SXhigh and lung cancer was not significant among patients with NLR-low (OR = 0.897, 95% CI: 0.346–2.232, P = 0.823).

Inflammation could lead different association between anatomical severity of CAD and lung cancer. Severity of CAD was significantly associated with increased risk of lung cancer among patients with high inflammation rather than among patients with low inflammation.