Cardiac troponin I levels in patients with left heart failure and cor pulmonale

Cardiac troponin levels are regarded as the most specific of currently avai lable biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflect ing small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnI) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patie nts with right heart failure (n = 17) resulting from chronic obstructive pu lmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnI levels were measured in 32 healthy subjects as c ontrol group. Protein markers of myocardial injury (cTnI and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 d ays. Elevated levels of serum cTnI were found in patients with nonischemic (0.83 +/-0.6 ng/mL, p < 0.01) and ischemic left heart failure (0.9 +/-0.5 ng/mL, p < 0.01) when compared to healthy subjects, whereas serum cTnI levels in patients with right heart failure due to chronic obstructive pulmonary dise ase were not significantly different from those of control subjects (0.22 < plus/minus>0.1 vs 0.16 +/-0.1 ng/mL, p > 0.05). In addition, creatine kinas e MB band and myoglobin levels were not significantly different between pat ient and healthy groups. The mean of cTnI levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but w ithout significant creatine kinase MB band and myoglobin elevations. But cT nI levels were not increased in patients with right heart failure due to ch ronic obstructive pulmonary disease. These data indicate that the cTnI leve ls are abnormal in left heart failure but not in cor pulmonale.