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Incidence and patterns of cardiomyopathy in carbon monoxide-poisoned patients with myocardial injury.
Clinical Toxicology 2016 July
OBJECTIVES: Sustained myocardial injury is a significant predictor of mortality in carbon monoxide (CO) poisoning. There are few reports in the literature regarding the presence of CO-induced cardiomyopathy from early stages in the emergency department (ED). We prospectively investigated the early incidence of CO-induced cardiomyopathy and its patterns in patients with cardiomyopathy.
MATERIALS AND METHODS: During a 10-month period, transthoracic echocardiography (TTE) was performed in 43 consecutive patients with CO poisoning and myocardial injury, which was defined as elevated high-sensitive troponin I within 24 h after ED arrival. Measurements of left ventricular ejection fraction and wall motion abnormalities were performed to evaluate cardiac function. If a patient had CO-induced cardiomyopathy, we measured cardiac function at the time of patient admission, day 1, day 2, and once within seven days of hospitalization.
RESULTS: The incidence of cardiomyopathy was as high as 74.4% (32 of 43 patients) in CO-poisoned patients with myocardial injury based on initial ED results. Echocardiographic patterns included non-cardiomyopathy (25.6%), global dysfunction (51.2%), and Takotsubo-like cardiomyopathy (23.2%). Patients in the global dysfunction group had significantly more normalized cardiac dysfunction within 72 h than did those in the Takotsubo-like cardiomyopathy group (81.8% vs. 22.2%, p = 0.001).
DISCUSSION AND CONCLUSION: Patients with CO poisoning and myocardial injury experienced cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern. Investigation of cardiomyopathy needs to be considered in patients with CO poisoning and myocardial injury.
MATERIALS AND METHODS: During a 10-month period, transthoracic echocardiography (TTE) was performed in 43 consecutive patients with CO poisoning and myocardial injury, which was defined as elevated high-sensitive troponin I within 24 h after ED arrival. Measurements of left ventricular ejection fraction and wall motion abnormalities were performed to evaluate cardiac function. If a patient had CO-induced cardiomyopathy, we measured cardiac function at the time of patient admission, day 1, day 2, and once within seven days of hospitalization.
RESULTS: The incidence of cardiomyopathy was as high as 74.4% (32 of 43 patients) in CO-poisoned patients with myocardial injury based on initial ED results. Echocardiographic patterns included non-cardiomyopathy (25.6%), global dysfunction (51.2%), and Takotsubo-like cardiomyopathy (23.2%). Patients in the global dysfunction group had significantly more normalized cardiac dysfunction within 72 h than did those in the Takotsubo-like cardiomyopathy group (81.8% vs. 22.2%, p = 0.001).
DISCUSSION AND CONCLUSION: Patients with CO poisoning and myocardial injury experienced cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern. Investigation of cardiomyopathy needs to be considered in patients with CO poisoning and myocardial injury.
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