Carbon monoxide poisoning (COP) may lead to ischemic changes in organs, and heart is one of the most susceptible targets to ischemic condition. The objective of this study is to evaluate the risk of myocardial infarction following COP. Using a nationwide database of insurance claims in Taiwan, we conducted a population-based cohort study to identify COP patients diagnosed between 1999 and 2012. At a ratio of 3:1, we identified non-COP patients who were matched by the index date and age and compared the risk of myocardial infarction between the two cohorts by time after the index dates of the COP patients, until 2013. We identified 22,258 COP patients and 66,774 non-COP patients. COP patients had an increased risk of myocardial infarction, with an incidence rate ratio of 1.45 (95% confidence interval 1.06–1.98) in comparison with the non-COP patients after adjusting for other independent predictors, including older age, male sex, and underlying comorbidity of hypertension, diabetes, and renal disease. Stratified analyses showed that the increased risk was more prominent in patients with a young age (< 34 years), female sex, and liver disease, and occurred only in the first month of follow-up. We concluded that COP increased the risk of myocardial infarction, but the increased risk was only observed in the first month after COP, which indicated that the impact of COP on the heart was mainly acute. Patients who were younger than 34 years, female, and with liver diseases were more prone to myocardial infarction after COP.
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C-C Huang and H-RG designed and conceived this study and wrote the manuscript. H-CH and Y-CC performed the statistical analysis and wrote the manuscript. H-JL, C-C Hsu, J-JW, and S-BS provided professional suggestions and wrote the manuscript. All the authors have read and approved the final manuscript.
This study was supported by Grants CMFHR10677 and CMFHR10734 from the Chi-Mei Medical Center.
Compliance with Ethical Standards
Conflict of interest
The authors declare no potential conflicts of interest.
This study involved human data and was conducted in strict accordance with the Declaration of Helsinki. The study protocol was approved by the Institutional Review Board (IRB) at the Chi-Mei Medical Center.
The two databases consisted of depersonalized information, and so the requirement of informed consent was waived by the IRB as the study did not affect the welfare of the participants.
Weaver, L. K. (2009). Clinical practice. Carbon monoxide poisoning. New England Journal of Medicine 360, 1217–1225.CrossRefGoogle Scholar
Hampson, N. B., & Weaver, L. K. (2007). Carbon monoxide poisoning: A new incidence for an old disease. Undersea & Hyperbaric Medicine, 34, 163–168.Google Scholar
Lee, F. Y., Chen, W. K., Lin, C. L., et al. (2015). Carbon monoxide poisoning and subsequent cardiovascular disease risk: A nationwide population-based cohort study. Medicine (Baltimore), 94, e624.CrossRefGoogle Scholar
Pan, Y. J., Liao, S. C., & Lee, M. B. (2010). Suicide by charcoal burning in Taiwan, 1995–2006. Journal of Affective Disorders, 120, 254–257.CrossRefGoogle Scholar
Lee, D. T., Chan, K. P., Lee, S., et al. (2002). Burning charcoal: A novel and contagious method of suicide in Asia. Archives of General Psychiatry, 59, 293–294.CrossRefGoogle Scholar
Ernst, A., & Zibrak, J. D. (1998). Carbon monoxide poisoning. New England Journal of Medicine, 339, 1603–1608.CrossRefGoogle Scholar
Zou, J. F., Guo, Q., Shao, H., et al. (2015). Lack of pupil reflex and loss of consciousness predict 30-day neurological sequelae in patients with carbon monoxide poisoning. PLoS ONE, 10, e0119126.CrossRefGoogle Scholar
Zou, J. F., Guo, Q., Shao, H., et al. (2014). A positive Babinski reflex predicts delayed neuropsychiatric sequelae in Chinese patients with carbon monoxide poisoning. BioMed Research International, 2014, 814736.Google Scholar
Kalay, N., Ozdogru, I., Cetinkaya, Y., et al. (2007). Cardiovascular effects of carbon monoxide poisoning. The American Journal of Cardiology, 99, 322–324.CrossRefGoogle Scholar
Satran, D., Henry, C. R., Adkinson, C., et al. (2005). Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. Journal of the American College of Cardiology, 45, 1513–1516.CrossRefGoogle Scholar
Hampson, N. B., Piantadosi, C. A., Thom, S. R., et al. (2012). Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. American Journal of Respiratory and Critical Care Medicine, 186, 1095–1101.CrossRefGoogle Scholar
Brown, S. D., & Piantadosi, C. A. (1989). Reversal of carbon monoxide–cytochrome c oxidase binding by hyperbaric oxygen in vivo. Advances in Experimental Medicine and Biology, 248, 747–754.CrossRefGoogle Scholar
Brown, S. D., & Piantadosi, C. A. (1990). In vivo binding of carbon monoxide to cytochrome c oxidase in rat brain. Journal of Applied Physiology, 68, 604–610.CrossRefGoogle Scholar
Brown, S. D., & Piantadosi, C. A. (1992). Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. Journal of Clinical Investigation, 89, 666–672.CrossRefGoogle Scholar
Piantadosi, C. A., Zhang, J., Levin, E. D., et al. (1997). Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat. Experimental Neurology, 147, 103–114.CrossRefGoogle Scholar
Thom, S. R. (1990). Antagonism of carbon monoxide–mediated brain lipid peroxidation by hyperbaric oxygen. Toxicology and Applied Pharmacology, 105, 340–344.CrossRefGoogle Scholar
Thom, S. R., Bhopale, V. M., Fisher, D., et al. (2004). Delayed neuropathology after carbon monoxide poisoning is immune-mediated. Proceedings of the National Academy of Sciences of the USA, 101, 13660–13665.CrossRefGoogle Scholar
Thom, S. R., Bhopale, V. M., & Fisher, D. (2006). Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity. Toxicology and Applied Pharmacology, 213, 152–159.CrossRefGoogle Scholar
Thom, S. R., Bhopale, V. M., Han, S. T., et al. (2006). Intravascular neutrophil activation due to carbon monoxide poisoning. American Journal of Respiratory and Critical Care Medicine, 74, 1239–1248.CrossRefGoogle Scholar
Thom, S. R. (2008). Carbon monoxide pathophysiology and treatment. In T. S. Neuman & S. R. Thom (Eds.), Physiology and medicine of hyperbaric oxygen therapy (pp. 321–347). Philadelphia: Saunders Elsevier.CrossRefGoogle Scholar
Thom, S. R., Bhopale, V. M., Milovanova, T. M., et al. (2010). Plasma biomarkers in carbon monoxide poisoning. Clinical Toxicology (Philadelphia), 48, 47–56.CrossRefGoogle Scholar
National Health Insurance Administration, Ministry of Health and Welfare, Taiwan, R.O.C. (2014). National Health Insurance Annual Report 2014–2015.Google Scholar
Henry, C. R., Satran, D., Lindgren, B., et al. (2006). Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA, 295, 398–402.CrossRefGoogle Scholar
Tritapepe, L., Macchiarelli, G., Rocco, M., et al. (1998). Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning. Critical Care Medicine, 26, 797–801.CrossRefGoogle Scholar
Dziewierz, A., Ciszowski, K., Gawlikowski, T., et al. (2013). Primary angioplasty in patient with ST-segment elevation myocardial infarction in the setting of intentional carbon monoxide poisoning. The Journal of Emergency Medicine, 45, 831–834.CrossRefGoogle Scholar
Sward, D. G., Sethuraman, K. N., Wong, J. S., et al. (2016). Carbon monoxide and ST-elevation myocardial infarction: case reports. Undersea & Hyperbaric Medicine, 43, 63–69.Google Scholar
Unlu, M., Ozturk, C., Demirkol, S., et al. (2016). Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning. Human & Experimental Toxicology, 35, 101–105.CrossRefGoogle Scholar
Mustafic, H., Jabre, P., Caussin, C., et al. (2012). Main air pollutants and myocardial infarction: A systematic review and meta-analysis. JAMA, 307, 713–721.CrossRefGoogle Scholar
Huang, C. C., Chung, M. H., Weng, S. F., et al. (2014). Long-term prognosis of patients with carbon monoxide poisoning: A nationwide cohort study. PLoS ONE, 9, e105503.CrossRefGoogle Scholar
Jónsdóttir, L. S., Sigfússon, N., Gudnason, V., et al. (2002). Do lipids, blood pressure, diabetes, and smoking confer equal risk of myocardial infarction in women as in men? The Reykjavik Study. Journal of Cardiovascular Risk, 9, 67–76.CrossRefGoogle Scholar
Anand, S. S., Islam, S., Rosengren, A., et al. (2008). Risk factors for myocardial infarction in women and men: Insights from the INTERHEART study. European Heart Journal, 29, 932–940.CrossRefGoogle Scholar
Prescott, E., Hippe, M., Schnohr, P., et al. (1998). Smoking and risk of myocardial infarction in women and men: Longitudinal population study. BMJ, 316, 1043–1047.CrossRefGoogle Scholar
Sarnak, M. J., Levey, A. S., Schoolwerth, A. C., et al. (2003). Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on kidney in cardiovascular disease, high blood pressure research, clinical cardiology, and epidemiology and prevention. Circulation, 108, 2154–2169.CrossRefGoogle Scholar
Allred, E. N., Bleecker, E. R., Chaitman, B. R., et al. (1989). Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. New England Journal of Medicine, 321, 1426–1432.CrossRefGoogle Scholar
Kleinman, M. T., Davidson, D. M., Vandagriff, R. B., et al. (1989). Effects of short-term exposure to carbon monoxide in subjects with coronary artery disease. Archives of Environmental Health, 44, 361–369.CrossRefGoogle Scholar
von Klot, S., Peters, A., Aalto, P., et al. (2005). Ambient air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infarction survivors in five European cities. Circulation, 112, 3073–3079.CrossRefGoogle Scholar
Bell, M. L., Peng, R. D., Dominici, F., et al. (2009). Emergency hospital admissions for cardiovascular diseases and ambient levels of carbon monoxide: Results for 126 United States urban counties, 1999–2005. Circulation, 120, 949–955.CrossRefGoogle Scholar
Nawrot, T. S., Perez, L., Künzli, N., Munters, E., & Nemery, B. (2011). Public health importance of triggers of myocardial infarction: A comparative risk assessment. Lancet, 377, 732–740.CrossRefGoogle Scholar
Yücel, M., Avsarogullari, L., Durukan, P., et al. (2016). BNP shows myocardial injury earlier than Troponin-I in experimental carbon monoxide poisoning. European Review for Medical and Pharmacological Sciences, 20, 1149–1154.Google Scholar
Szponar, J., Kołodziej, M., Majewska, M., et al. (2012). Myocardial injury in the course of carbon monoxide poisoning. Przegl Lek, 69, 528–534.Google Scholar
Lippi, G., Rastelli, G., Meschi, T., et al. (2012). Pathophysiology, clinics, diagnosis and treatment of heart involvement in carbon monoxide poisoning. Clinical Biochemistry, 45, 1278–1285.CrossRefGoogle Scholar
Cheng, C. L., Lee, C. H., Chen, P. S., et al. (2014). Validation of acute myocardial infarction cases in the national health insurance research database in taiwan. Journal of Epidemiology, 24, 500–507.CrossRefGoogle Scholar