Hospitalization for acute coronary syndrome increases the long-term risk of pneumonia: a population-based cohort study

Joonghee Kim,Won-Woo Seo,Sangbum Choi,Yeon Joo Lee,Sang Jun Park

doi:10.1038/s41598-021-89038-1

Abstract

It is well established that the risk of acute coronary syndrome (ACS) increases after respiratory infection. However, the reverse association has not been evaluated. We tested the hypothesis that the long-term risk of pneumonia is increased after a new ACS event. A matched-cohort study was conducted using a nationally representative dataset. We identified patients with admission for ACS between 2004 and 2014, without a previous history of ACS or pneumonia. Incidence density sampling was used to match patients, on the basis of age and sex, to 3 controls who were also free from both ACS and pneumonia. We examined the incidence of pneumonia after ACS until the end of the cohort observation (Dec 31, 2014). The analysis cohort consisted of 5469 ACS cases and 16,392 controls (median age, 64 years; 68.3% men). The incidence rate ratios of the first and the total pneumonia episodes in the ACS group relative to the control group was 1.25 (95% confidence interval [CI], 1.11–1.41) and 1.23(95% CI 1.11–1.36), respectively. A significant ACS-related increase in the incidence of pneumonia was observed in the Cox-regression, shared frailty, and joint frailty model analyses, with hazard ratios of 1.25 (95% CI 1.09–1.42), 1.35 (95% CI 1.15–1.58), and 1.24 (95% CI 1.10–1.39), respectively. In this population-based cohort of patients who were initially free from both ACS and pneumonia, we found that hospitalization for ACS substantially increased the long term risk of pneumonia. This should be considered when formulating post-discharge care plans and preventive vaccination strategies in patients with ACS.

Highlights

It is well established that the risk of acute coronary syndrome (ACS) increases after respiratory infection
Systemic and coronary artery inflammation increases cardiovascular r isk[17,18,19]; infection promotes platelet a ctivation[20,21] and thrombosis[22]; changes in nitric oxide (NO) synthase and cyclooxygenase (COX) lead to endothelial dysfunction[23,24]; pneumonia leads to changes in myocardial contractility, oxygen demand, and d elivery[25,26,27]; and the microorganism can have a direct effect on cardiovascular r isk[28,29]
We assembled a population-based cohort of patients with ACS and age-sex matched controls without ACS to verify the impact of a new ACS event on the incidence of pneumonia for up to 10 years

Summary

Introduction

It is well established that the risk of acute coronary syndrome (ACS) increases after respiratory infection. A significant ACS-related increase in the incidence of pneumonia was observed in the Cox-regression, shared frailty, and joint frailty model analyses, with hazard ratios of 1.25 (95% CI 1.09–1.42), 1.35 (95% CI 1.15–1.58), and 1.24 (95% CI 1.10–1.39), respectively In this population-based cohort of patients who were initially free from both ACS and pneumonia, we found that hospitalization for ACS substantially increased the long term risk of pneumonia. Recently demonstrated that hospitalization for pneumonia was associated with an increased long-term risk of CAD, for up to 10 years after the respiratory infection[16]. We assembled a population-based cohort of patients with ACS and age-sex matched controls without ACS to verify the impact of a new ACS event on the incidence of pneumonia for up to 10 years

Methods

Results

Conclusion