CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Daniel Satran, MD,
Christopher R. Henry, BS and
Timothy D. Henry, MD*
* Minneapolis Heart Institute Foundation, 920 East 28 Street, Suite 40, Minneapolis, Minneapolis 55407 (Email: henry003{at}umn.edu).
We read with interest the letter of Dr. Dueñas-Laita and colleagues regarding our study, "Cardiovascular Manifestations of Moderate to Severe Carbon Monoxide Poisoning." The Italian investigators found 7.2% (8 of 110) of adults and 25.6% (10 of 39) of children had elevated creatine kinase (CK) levels, whereas 1.8% (2 of 110) of adults and 12.7% (5 of 39) of children had elevated CK-MB levels in a series of patients with acute carbon monoxide (CO) poisoning (1). We found 37% of patients had myocardial injury based on elevated cardiac enzymes and electrocardiogram (ECG) (2). We agree with the investigators that the major difference between our study and their own can be attributed to the severity of CO poisoning. Our study focused on more critically ill patients: 187 (81%) experienced loss of consciousness, 106 (46%) had an abnormal Glasgow Coma Scale (<14), 116 (50%) were intubated, and 14 (6%) required blood pressure support. Another important difference between the two studies is the use of troponin, which is a more specific and sensitive indicator of myocardial injury and would be expected to increase the percentage of patients found to have myocardial injury. Myocardial injury determined by troponin has been shown to be an important indicator of both short- and long-term mortality (3–5). In fact, we recently reported preliminary data the long-term outcomes of our cohort and found patients with myocardial injury had 31.9% mortality compared to 16.3% in patients without myocardial injury at a median follow-up of 6.6 years (6).
Dr. Dueñas-Laita and colleagues suggest that cyanide poisoning from fire exposure contributed to a higher percentage of patients with myocardial injury in our study. We believe this is unlikely. In our series of 230 patients, 42 had CO poisoning from fire exposure and 12 (28%) had myocardial injury. By comparison, 188 patients had CO poisoning from other etiologies (faulty furnace, automobile exhaust, and so on) and 73 (39%) sustained myocardial injury. One patient exposed to fire did have confirmed cyanide poisoning, although our data are otherwise limited in this area. We agree with the researchers that testing serum lactate is reasonable in any patient with CO exposure from fire.
Finally, the data from Dueñas-Laita and colleagues indicate myocardial injury from even mild CO poisoning is frequent and adds to the literature regarding the myocardial effects of CO poisoning.
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1. Dueñas-Laita A, Ruiz-Mambrilla M, Gandia F, et al. Epidemiology of acute carbon monoxide poisoning in a Spanish region J Toxiol Clin Toxicol 2001;39:53-57.[CrossRef][Web of Science][Medline]2. Satran D, Henry CR, Adkinson C, Nicholson CI, Bracha Y, Henry TD. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning J Am Coll Cardiol 2005;45:1513-1516.[Abstract/Free Full Text] 3. Antman EM, Tanasijevic MJ, Thompson B, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes N Engl J Med 1996;335:1342-1349.[Abstract/Free Full Text] 4. Giannitsis E, Muller-Bardorff M, Kurowski V, et al. Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism Circulation 2000;102:211-217.[Abstract/Free Full Text] 5. Dierkes J, Domrose U, Westphal S, et al. Cardiac troponin T predicts mortality in patients with end-stage renal disease Circulation 2000;102:1964-1969.[Abstract/Free Full Text] 6. Henry CR, Satran D, Adkinson CD, Chaney CI, Henry TD. Myocardial injury associated with carbon monoxide poisoning predicts long-term mortality (abstr) Eur Heart J 2004;25:538.
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