Spontaneous progression of severe congestive heart failure is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The cardiac troponin I (cTnI), one of the subunits of the troponin regulatory complex, binds to actin and inhibits interaction between actin and myosin. cTnI is uniquely expressed in the adult human myocardium, and an increase in its circulating levels is highly indicative of myocardial injury. In this study, we addressed the usefulness of cTnI as a sensitive and specific molecular marker for severity in patients with congestive heart failure.

cTnI, creatinin kinase-MB (CK-MB), and myoglobin were assessed in 59 patients with severe congestive heart failure diagnosed by the echo-cardiography and gated equilibrium blood pool heart scan. Also we assesed cTnI, creatinin kinase-MB (CK-MB), and myoglobin in 25 persons without cardiac disease in echocardiography.

1) The cTnI con-centration was 89.6±69.3 pg/mL in patients with congestive heart failure and its level was greater than that of the control group (22.4±17.1, p=0.001). 2) The cTnI level differed significantly according to left ventricular ejection fraction (EF), 117.3±73.8 pg/mL in patients with EF\<40% (28 patients), 66.3±44.5 pg/mL in patients with EF≥40% (31 patients), 22.4±17.1 pg/mL in the control group (25 persons) (p=0.001).

cTnI was useful as a specific and sensitive serum molecular marker in patients of congestive heart failure. And its level reflected the severity of congestive heart failure.