BACKGROUND: There is evidence that chronic inflammation may promote atherosclerotic disease. The purpose of this study was to test the hypothesis that pelvic inflammatory disease (PID) is a risk marker for myocardial infarction (MI). METHOD: Using the Taiwan Longitudinal Health Insurance Database 2005 (LHID2005), this cohort study comprised patients with a recorded diagnosis of PID (N=68,668) between January 1, 2004 and December 31, 2005, with age-matched controls (1:2) (N=136,906). Each patient was followed-up using entry data until the end of 2006. Cox proportional hazard regressions were used to evaluate the up to 3-year MI-free survival rates, after adjusting for known confounding factors. RESULTS: We found that patients with PID were more likely to have MI than the control population after adjusting for potential confounders [adjusted hazard ratio (HR), 1.86, 95% confidence interval (CI), 1.23-2.81]. When stratified by patient's age, the adjusted HR for MI was 2.09 (95% CI, 1.24-3.52) for patients with PID aged over 55 years. However, the adjusted HR for MI occurring was not significant for patients with PID aged ≤ 55 years. CONCLUSIONS: PID is a risk marker for MI that is independent of traditional MI risk factors. Further research in this important area of public health is warranted.
BACKGROUND: There is evidence that chronic inflammation may promote atherosclerotic disease. The purpose of this study was to test the hypothesis that pelvic inflammatory disease (PID) is a risk marker for myocardial infarction (MI). METHOD: Using the Taiwan Longitudinal Health Insurance Database 2005 (LHID2005), this cohort study comprised patients with a recorded diagnosis of PID (N=68,668) between January 1, 2004 and December 31, 2005, with age-matched controls (1:2) (N=136,906). Each patient was followed-up using entry data until the end of 2006. Cox proportional hazard regressions were used to evaluate the up to 3-year MI-free survival rates, after adjusting for known confounding factors. RESULTS: We found that patients with PID were more likely to have MI than the control population after adjusting for potential confounders [adjusted hazard ratio (HR), 1.86, 95% confidence interval (CI), 1.23-2.81]. When stratified by patient's age, the adjusted HR for MI was 2.09 (95% CI, 1.24-3.52) for patients with PID aged over 55 years. However, the adjusted HR for MI occurring was not significant for patients with PID aged ≤ 55 years. CONCLUSIONS: PID is a risk marker for MI that is independent of traditional MI risk factors. Further research in this important area of public health is warranted.