Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

Abstract

Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

Cardiovascular biomarkers: exploring troponin and BNP applications in conditions related to carbon monoxide exposure

“…Proposed processes include CO-induced hypoxia producing cardiomyocyte necrosis [ 34 , 35 ], oxidative stress activating proteases [ 36 , 37 ], and apoptosis inducing membrane blebs with cTn release [ 38 – 40 ]. The degree of exposure, length of time, underlying heart condition, and measurement time all affect troponin elevation patterns [ 17 , 21 , 41 ]. Research indicates that peak troponin levels occur 24 h after CO exposure, which helps with both short- and long-term outcome prediction [ 42 ].…”

“…In cases of CO poisoning, novel troponin I assays such as those employed by Patel et al [ 21 ] (Table 1 ) link elevated troponin I to increased mortality, intensive care admission, and intubation. A different research by Koga et al [ 17 ] (Table 1 ) relates troponin I levels and corrected QT dispersion to successive disability following CO poisoning.…”

“…Known as a “silent killer,” carbon monoxide (CO) binds to hemoglobin (Hb) to decrease its ability to transport oxygen, which results in CO poisoning (COP) [ 16 ]. This odorless, colorless, very poisonous gas can cause tissue damage and severe hypoxia [ 17 ]. CO poisoning’s severe clinical symptoms and high morbidity and death rate make it a major worldwide health problem [ 18 ].…”

“…With 40% of those examined showing increased cardiac biomarkers, myocardial damage is prevalent in CO poisoning cases. This can lead to ischemia, arrhythmias, heart failure, cognitive decline, seizures, and coma [ 17 , 18 , 21 ].…”

“…Based on a study conducted in Lanzhou, China, the relative risks of daily ER visits were found to be 1.041 for total cardiovascular disease (CVD), 1.065 for ischemic heart disease (IHD), 1.083 for heart rhythm disturbances (HRD), 1.062 for heart failure (HF), and 1.057 for cerebrovascular diseases (CD) for every 1 mg/m3 increase in CO concentration [ 22 ]. Several investigations have examined the function of BNP and troponin in the diagnosis and prognosis of CO poisoning [ 17 , 21 , 23 ]. Greater levels of these biomarkers have been linked to poorer clinical outcomes, a greater risk of cardiac problems, and a worsening of CO poisoning [ 24 , 25 ].…”