Myocardial Infarction After Acute Carbon Monoxide Poisoning: Case Report

Ebisuno, Shoji; Yasuno, Masao; Yamada, Yoshio; Y, Nishino; Hori, Masatsugu; Inoue, Michitoshi; Kamada, Takenobu

doi:10.1177/000331978603700810

Cited by 28 publications

(8 citation statements)

References 12 publications

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“…Most of the recent literature focuses on ST elevation and T wave inversions in patients with CO poisoning. 7,8,9,10 Contrary to this, our patient did not exhibit any EKG changes at any point during his hospital course. It is reported that other cardiac groups may not show any ischemic changes on EKG.…”

Section: Discussioncontrasting

confidence: 88%

“…6 The trend of elevation in serum troponin levels in our patient was similar to the trend previously reported, which spans from 2-8 hours. 1,7,8 The rise in troponin levels correlates to the half life of CO in patients. It has been reported that CO has a half life of 300 minutes if the patient is breathing room air, though this is decreased to 90 minutes with use of a non-breather mask and 30 minutes if hyperbaric oxygen treatment is provided.…”

Section: Discussionmentioning

confidence: 99%

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Carbon Monoxide: A Rare Cause of Myocardial Ischemia

Mansoor¹,

Parkins²,

Wilson³

et al. 2019

Marshall Journal of Medicine

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Section: Discussioncontrasting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide: A Rare Cause of Myocardial Ischemia

Mansoor¹,

Parkins²,

Wilson³

et al. 2019

Marshall Journal of Medicine

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“…CO may make the endothelial cell relatively hypoxic, a powerful stimulus of prostacyclin (PGI 2 ) production, or less likely exert a direct toxic effect on the endothelial cells [23]. Furthermore, survivors of CO exposure may present a clinical pattern of ischemic heart disease [24,25,26] which can be recovered by hyperbaric oxygenation treatment [27,28].…”

Section: Introductionmentioning

confidence: 99%

Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

Fineschi

Agricola

Baroldi

et al. 2000

International Journal of Legal Medicine

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The aim of this study was to define the status of the myocardium in selected human cases of acute, fatal carbon monoxide intoxication and the myocardial changes in rats exposed to carbon monoxide in relation to the type of cardiac arrest and the effects of reoxygenation following pre-fatal CO intoxication. The human study consisted of 26 cases (17 accidental and 9 suicide) of acute, fatal CO intoxication, without evidence of obstructive coronary atherosclerosis or history of ischemic heart disease which were compared with 45 cases of fatal head trauma in subjects who died instantaneously (26 cases) or within 1-12 h (19 cases). Inhalation of a lethal dose of CO in rats was compared with sub-lethal doses plus reoxygenation with and without pre-treatment by a betablocker. In all human and experimental histological sections, changes were normalised per mm2 area. In the human cases the myocardium did not show any ischemic types of changes or other lesions. Only in "three accidental" cases a few, small foci of coagulative myocytolysis were detected. In the case of spontaneous death in 31 rats following CO intoxication, no pathological myocardial changes were seen. Of the 15 "reoxygenated" rats, 2 of the 7 spontaneous deaths presented coagulative myocytolysis with 15 +/- 6 foci and 381 +/- 255 necrotic myocells. All the eight rats sacrificed at 3 h had coagulative myocytolysis with 5 +/- 4 foci and 60 +/- 47 myocells. Of the 24 reoxygenated rats pre-treated with a betablocker, 5 died spontaneously after a short survival and 2 of these showed 11 +/- 9 foci and 21 +/- 20 myocells. The 19 rats sacrificed after 3 h all presented coagulative myocytolysis with figures of 75 +/- 43 and 356 +/- 301 with 0.5 mg/kg of propranolol hydrochloride and 55 +/- 45 and 253 +/- 216 with 2 mg/kg, respectively.

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“…Chest discomfort or pain can be resulted from myocardial ischemia or necrosis in the presence and in the absence of coronary artery disease. [10][11][12] Shortness of breath and low blood pressure can be symptoms of cardiac dysfunction. 13) In this patient, shortness of breath and tachycardia were noted at the time of admission and these symptoms suggesting the presence of cardiac dysfunction.…”

Section: D a Bmentioning

confidence: 99%

Transient Left Ventricular Systolic Dysfunction Associated with Carbon Monoxide Toxicity

Jang

Park

2010

J Cardiovasc Ultrasound

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I In nt tr ro od du uc ct ti io on nCarbon monoxide (CO) can cause functional and morphological alternations of the heart mainly due to myocardial hypoxemia and direct action of CO on the heart. 1)2) CO has about 250-fold higher affinity for hemoglobin as compared to oxygen and forms carboxyhemoglobin (CO-Hb). In the presence of CO-Hb, a leftward shift of the oxygenated hemoglobin dissociation curve observed and leads to impairment of tissue oxygen delivery and makes cellular hypoxia. 1)CO induced cardiotoxicity has many clinical manifestations including arrhythmias, pulmonary edema and heart failure, and myocardial infarction. Echocardiography is known as the most useful method in the detection the presence of cardiac toxicity and assessment of its severity. We report a case with transient severe left ventricular dysfunction after intentional exposure to CO. The patient was early detected with an echocardiographic exam and treated with conventional treatment including high concentration of oxygen. C Ca as se eA 28-year-old man was admitted to our emergency room for altered mentality due to intentional exposure to CO. On his arrival, blood pressure was 104/80 mmHg, the pulse 126 beat per minute, axillary temperature 37.7°£C and the respirations were 32 breaths per minute. On blood analysis, AST/ALT 37/29 IU/L, CK 412 U/L, CK-MB 6.9 ng/mL, troponin I 0.96 ng/mL, N-terminal pro B-type natriuretic peptide 451.5 pg/mL, and CO-Hb 27.7%. The patient was intubated and treated with high concentration of oxygen therapy. A radiograph of the chest showed pulmonary edema and mild cardiomegaly (Fig. 1A). An electrocardiogram revealed sinus tachycardia of heart rate 120 per minute. Transthoracic echocardiogram showed global hypokinesia of left ventricle with severe systolic dysfunction ( Fig. 2A and B). He was treated with diuretics, angiotensin converting enzyme inhibitor and urine alkalinization. Cardiac enzymes were elevated to CK 5,994 U/L, CK-MB 38.6 ng/mL, and troponin I 11.7 ng/mL on the third admission day. CK level was elevated to 15,951 U/L due to rhabdomyolysis and normalized with urine alkalinization. The follow-up chest radiograph showed normalized cardiac size and disappearance of pulmonary edema (Fig. 1B). The echocardiography Carbon monoxide (CO) is one of well known chemical asphyxiants which cause tissue hypoxia with prominent neurologic and cardiovascular injury. Cardiac dysfunction after CO poisoning can be presented as two clinical patterns. One is transient global left ventricular (LV) dysfunction and the other is LV dysfunction with regional wall motion abnormalities. In this case report, we present a case with transient LV systolic dysfunction caused by intentional exposure to CO. After conservative treatment including high concentration of oxygen, the patient recovered completely without any complication.

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Myocardial Infarction After Acute Carbon Monoxide Poisoning: Case Report

Cited by 28 publications

References 12 publications

Carbon Monoxide: A Rare Cause of Myocardial Ischemia

Carbon Monoxide: A Rare Cause of Myocardial Ischemia

Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

Transient Left Ventricular Systolic Dysfunction Associated with Carbon Monoxide Toxicity

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