Author + information
- Antonio Dueñas-Laita, MD, PhD, FACCP⁎ (, )
- Guillemo Burillo Puzte, MD,
- Santiago Nogué Xarau, MD, PhD and
- Marta Ruiz Mambrilla, MD, PhD
- ↵⁎Unidad Regional de Toxicologı́a Clı́nica, Hospital Universitario Rı́o Hortega, Rondilla de Santa Teresa 9, 47010 Valladolid, Spain
We read with interest the report by Satran et al. (1) on the cardiovascular manifestations of carbon monoxide (CO) poisoning. In the Hospital Rı́o Hortega of Valladolid (Spain), we followed CO poisonings prospectively for two years (2). The protocol included, among other parameters, carboxyhemoglobin (COHb) levels, electrocardiogram (ECG), creatine kinase (CK) and CK-MB. During the study period studied, 154 patients were included, of whom 20% (n = 31) presented sinusal tachycardia, 5% (n = 8) arrhythmias (mainly auricular fibrillation), and 4% (n = 6) ischemic changes, including one patient in whom cardiac catheterization was carried out without findings of coronary artery disease. Eight (7.2%) adult patients and 25.6% (n = 10) of patients under 10 years of age had elevated CK levels. Similarly, CK-MB levels were elevated in 1.8% (n = 2) of adults and in 12.7% (n = 5) of children (p < 0.01) (2). In our series, the percentage of patients with cardiovascular manifestations is inferior to that described by Satran et al. (1). We suggest that this is because our study population included all CO poisonings, of which 40% were mild (COHb <25%), whereas Satran et al. (1) included only moderate or severe poisonings. The fact that elevated CK and CK-MB levels occur more frequently in children than in adults suggests a greater toxicity or affinity of CO for the pediatric musculature, although this hypothesis remains to be verified.
Satran et al. (1) report that, in an unspecified number of patients, the etiology of the CO poisoning was fire exposure, and that eight patients died owing to burn injuries (1), but they make no reference to plasma lactate concentrations. Lactate is the principal marker of cyanide (CN) in the blood of patients who inhale fire smoke, and levels greater than 10 mmol/l suggest that, in these patients, CN plays a more important role than does CO (3,4). We suggest that a percentage of the myocardial ischemias described by Satran et al. (1) may be due to fire smoke inhalation syndrome and not solely to CO poisoning. Smoke from fires contains a mixture of gases, but of these it is CO and CN that provoke tissue hypoxia and may lead to death (5). Although the protagonism of CO in the multifactorial hypoxia of fire smoke inhalation syndrome is well known, the role of CN is less so (4). We suggest that CN may have had a synergetic effect with CO in the cellular hypoxia and myocardial ischemia seen in the cases reported by Satran et al. (1). We consider that in patients affected by the inhalation of fire smoke, plasma lactate concentrations are as important as COHb levels, especially where there is myocardial injury.
This LE is paired - LR JACC080405-2902
- American College of Cardiology Foundation