Heart failure

Increased concentrations of cTnI and cTnT have been found in patients with congestive heart failure (CHF) (8-12). Heart failure is a dynamic process with progressive severity and is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The specific underlying mechanisms of myocyte necrosis likely vary between etiologies of heart failure and in some instances remain unclear. In the majority of patients with heart failure studied, increased concentrations of cardiac troponin have been detected predominantly in patients with advanced CHF (New York Heart Association III and IV classifications) and are distinguished with evidence of increased cardiac events over a 2-yr period (Fig. 1) (8). Increased cTnI and cTnT values in patients with advanced heart failure are also independently associated with a decline in left ventricular ejection fraction (LVEF) and higher mortality. In addition, the prognostic information from cardiac troponin appears to be additive to other clinical indicators associated with the risk of death in heart failure. For example, the combination of increased cTnI and increased B-type natriuretic peptide (BNP) identifies heart failure patients with a markedly (12-fold)

Table 1

Clinical Settings Frequently Associated With Increased Cardiac Troponin Concentrations in Absence of ACSs

• Trauma, cardiac contusion

• Cardioversion, electrical defibrillation

• Pulmonary embolism, edemaa

• Sepsis, septic shocka

• Myocarditis

• Exercise, vital exhaustion

• Noncardiac, vascular surgery

• Hypertension

• Hypotension

• Critically ill intensive care patients a

• Aneurysmal subarachnoid hemorrhage

• Drugs of abuse toxicity, including ethanol

• Chemotherapy

• Heart surgery, transplantation

• Polymyositis, dermatomyositis

• Cardiomyopathy

• Rhabdomyolysis, trauma (nonchest)

• Hematological malignancies

• Acute pericarditis

• Amyloid cardiomyopathy

• Idiopathic dilated cardiomyopathy

• Lung disease a Evidence ofrole of cardiac troponin for risk stratification for short- or long-term outcomes.

10 15 20

Follow-up (months)

Fig. 1. Kaplan-Meier curves for patients with CHF assessed by cTnT concentration. (Reproduced from ref. 8.)

Fig. 2. Peak cTnI, CK-MB, and ratio of CK-MB to total CK in patients without cardiac contusion ( ) and with cardiac contusion (•). Horizontal lines indicates upper reference cutoffs. (Reproduced from ref. 15.)

higher risk of death (9). Furthermore, available evidence suggests that ongoing myofibrillar degradation, resulting in increased cardiac troponin concentrations, parallels the severity ofthe disease. A potential future clinical role for troponin testing in guiding treatment strategies for patients with heart failure is discussed in Chapter 8.

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