The Unusual Presentation of Non-ST Elevation Myocardial Infarction Following Acute Carbon Monoxide Poisoning in an Elderly Female: A Case Report

Abstract

Carbon monoxide (CO) poisoning is a leading cause of poisoning-related deaths, particularly affecting organs with high oxygen demands such as the heart and brain. Cardiac complications, including non-ST elevation myocardial infarction (NSTEMI), can occur due to CO poisoning but are not frequently reported in the elderly. We present the case of an 82-year-old female with a medical history of diabetes, hypertension, dyslipidemia, and previous ischemic heart disease. She was brought to the emergency department after being found drowsy in a closed room with a burning charcoal heater. The initial assessment revealed a carboxyhemoglobin level of 33.5%, which decreased to 9.3% after high-flow oxygen therapy and hyperbaric oxygen therapy (HBOT). Laboratory tests indicated elevated troponin levels, and an ECG showed asymmetrical T-wave inversion and ST depression. Despite the improvement in carboxyhemoglobin, the patient experienced persistent chest pain and rising troponin levels. She was treated with dual antiplatelet therapy and low molecular weight heparin as per acute coronary syndrome protocol, leading to a gradual improvement and a subsequent discharge in a stable condition. This case highlights the potential for CO poisoning to induce NSTEMI in elderly patients. A prompt diagnosis and appropriate management, including the use of HBOT, were crucial for the patient’s recovery.

1. Introduction

Carbon monoxide (CO) poisoning is a major cause of death related to poisoning [1,2]. Worldwide, there are approximately 137 cases of CO poisoning per million people, with a death rate of 4.6 per million. The incidence of CO poisoning has remained stable over the last two decades, while mortality has declined significantly by 40%. Interestingly, the incidence is similar between genders, but the mortality rate is twice as high in men. The age groups most affected by CO poisoning are 0–14 years and 20–39 years, with mortality rates increasing significantly in those aged 80 years or older [3,4].

CO is a colorless and odorless gas, which makes it difficult to detect in usual circumstances [5]. When inhaled, CO binds to hemoglobin with a significantly greater affinity compared to oxygen, resulting in the formation of carboxyhemoglobin (COHb). This binding impairs the transportation and utilization of oxygen throughout the body, leading to tissue hypoxia and cellular injury [6]. In cases of acute CO poisoning, organs with higher oxygen demands are usually affected; this includes the heart and the brain [7]. Multiple cardiac manifestations have been reported in cases of CO poisoning, including acute myocardial infarction, arrhythmias, pulmonary edema, and cardiogenic shock [8].

This report presents the case of an 82-year-old female who developed a non-ST elevation myocardial infarction (NSTEMI) following accidental CO exposure. Her case underscores the critical need for early recognition and management of cardiac complications in CO poisoning, particularly in elderly patients with pre-existing cardiovascular conditions.

2. Case Presentation

An 82-year-old woman was escorted to the emergency department (ED) by emergency medical services after she was found drowsy at her home in a poorly ventilated room close to a burning charcoal heater. Her family reported that she usually uses a charcoal heater during the winter for several hours each day. Her medical history was significant for hypertension, diabetes, dyslipidemia, and ischemic heart disease, including a percutaneous coronary intervention one year ago, and ischemic cardiomyopathy with a reduced ejection fraction of 35%.

Upon reaching the emergency department, her vital signs showed a blood pressure of 152/10 mmHg, a heart rate of 102/minute, and a respiratory rate of 22/minute with 95% oxygen saturation on room air. She was conscious but disoriented. She was immediately connected to high-flow oxygen administered via a non-rebreather mask. Her initial blood gas revealed the following: a CO level of 33.5%, a pH of 7.4, a pCO₂ of 37.9 mmHg, and a lactate of 3 mmol/L. Her CO level dropped to 9.3% after 2 h from initial resuscitation. Other significant laboratory investigations included a rising troponin level, from an initial value of 203 ng/L on presentation to 592 ng/L in 3 h (Figure 1), and a serum creatinine level of 84 µmol/L. Her initial electrocardiogram (ECG) revealed T-wave inversion in leads III and aVF, with ST-depression in lead V4 (Figure 2). However, the subsequent ECG showed a diffuse inversion of T-waves in leads V3-V6, II, III, and aVF (Figure 3).

A non-contrast head CT showed no evidence of acute intracranial insults. Subsequently, the patient received a session of hyperbaric oxygen therapy (HBOT) resulting in a dramatic drop in her CO level to 1.9%. Over the next few hours, while being admitted to the high-dependency unit, her cognitive function returned to normal. However, she was complaining of persistent chest pain and shortness of breath. Her repeated troponin level continued to rise and was now 748 ng/L. The repeated ECG after the HBOT showed T-wave inversions (Figure 3). The cardiology team was consulted, and the patient was started on dual antiplatelet therapy and a therapeutic dose of low molecular weight heparin as per acute coronary syndrome (ACS) protocol.

A follow-up echocardiogram revealed left ventricular systolic dysfunction with an ejection fraction estimated at 35–40%, consistent with her previous echocardiographic findings. During her hospital stay, her neurological symptoms and chest pain gradually improved. Her troponin levels began trending down after the initiation of the ACS protocol, and she was later discharged in a stable condition. At her outpatient follow-up, her overall condition remained stable, with no new concerning signs or symptoms. She was referred to her primary cardiologist for further follow-up.

3. Discussion

This report highlights an unusual presentation of an elderly female with accidental exposure to CO leading to coronary ischemia prompting immediate antithrombotic therapy. Previous studies have investigated the relationship between carbon monoxide exposure and acute myocardial infarction (AMI). In a report published by Mujib et al., around 6% of patients with CO poisoning experienced AMI, with an in-hospital mortality of 9% [9].

The most likely hypothesis indicates that carboxyhemoglobin, formed when CO binds to hemoglobin, reduces oxygen transportation, resulting in hypoxia of the myocardial tissue. Other proposed mechanisms include coronary vasospasm leading to an increased permeability of the coronary vessels consequently enhancing platelet aggregation and thrombus formation. Another suggested mechanism is thrombus formation driven by CO binding to fibrinogen, resulting in increased platelet aggregation. CO also inhibits mitochondrial cytochrome c oxidase, reducing glutathione levels and causing hypoxia, lactic acidosis, and eventual cell apoptosis [10,11]. Unintentional CO poisoning often occurs during the winter season in temperate- or cold-climate regions, often due to faulty furnaces [10].

CO has a half-life of 300 min when patients breathe room air. The elimination half-life decreases to approximately 90 min with a non-rebreather mask and further shortens to 30 min with hyperbaric oxygen therapy. Given the time required for serum troponin levels to rise after myocardial injury and the known half-life of CO, it is hypothesized that troponin elevations typically occur within 2 to 8 h post-exposure. Interestingly, recent studies have emphasized ST-segment elevation and T-wave inversions in patients with CO poisoning; however, not all patients exhibit these electrocardiographic changes. Non-ischemic ECGs do not automatically exclude ongoing ischemia [10].

The primary treatment for CO poisoning involves the administration of 100% supplemental oxygen through a non-rebreather mask. Myocardial injury frequently occurs in cases of moderate to severe CO poisoning. It is, therefore, recommended to perform a baseline ECG and monitor serial cardiac biomarkers in all patients. Patients with ST-elevation on an ECG should undergo urgent coronary angiography, as CO poisoning can worsen underlying coronary arteriosclerosis. For patients admitted with NSTEMI, it is recommended to perform an echocardiogram and a nuclear stress test [1,10].

Patients with persistent left ventricular dysfunction, underlying coronary artery disease (CAD), or CAD risk factors may benefit from further evaluation, including angiography and revascularization. However, additional research is required to gain insight into the long-term clinical implications of myocardial injury and the effectiveness of hyperbaric oxygen therapy as an adjunctive treatment for cardiac injury induced by CO exposure [1,10].

A recent set of practical guidelines has been issued for the evaluation and management of cardiac injury induced by CO poisoning. Dong-Hyuk Cho et al. utilize the collective experience of managing over two thousand incidents of acute CO poisoning, supplemented by the peer-reviewed literature. They propose that the initial evaluation should include an echocardiography to assess features of Takotsubo cardiomyopathy or regional wall motion abnormalities (RWMA) that align with coronary artery territories. This approach helps guide the decision for coronary screening. If significant abnormalities are not detected, the recommendations suggest outpatient follow-up with an echocardiography or, if indicated, cardiac magnetic resonance imaging [11].

In our patient, despite receiving hyperbaric oxygen therapy, troponin levels continued to rise and anginal symptoms persisted. This necessitated a shared decision to treat her in line with ACS protocol, including heparin, dual antiplatelets, and statin therapy. This decision took into account her history of ischemic heart disease, recent coronary stenting, age, and the overall clinical picture. However, due to the absence of RWMA on the echocardiography and the overall improvement in her clinical status, the decision was made to defer the coronary angiography. Instead, the patient was referred to her primary cardiologist for further assessment and follow-up. As a result, we cannot conclusively determine the primary mechanism of myocardial injury in this case, which represents a limitation of this case report.

4. Conclusions

This case underscores the critical importance of the early recognition and comprehensive management of cardiac complications in carbon monoxide poisoning, particularly in elderly patients with pre-existing cardiovascular conditions. Despite the administration of hyperbaric oxygen therapy, our patient’s persistent cardiac symptoms and rising troponin levels necessitated treatment according to ACS protocols. This approach proved effective in stabilizing her condition. Further research is warranted to explore specific treatment strategies and improve outcomes for CO poisoning, particularly in high-risk populations.