Biomarker for Cardiomyopathy-B-Type Natriuretic Peptide

Abstract

Cardiomyopathy is cardiac condition in which the normal muscular function of the myocardium has been altered by a variety of etiologies. Atherosclerotic coronary artery disease is the most common cause of cardiomyopathy in North America and Europe. Idiopathic cardiomyopathy is the second most common cause, although this may partially include undiagnosed etiologies such as viral infection, drug toxicity, and genetic factors. Other causes include endocrine diseases, collagen vascular diseases, metabolic disorders (hemochromatosis, amyloidosis, glycogen storage disease), neuromuscular disorders, and granulomatous diseases (sarcoidosis). The cardiac malfunctions are variable, namely left ventricular (LV) systolic dysfunction, LV diastolic dysfunction, or both in accordance with etiologies and morphological findings (cardiac hypertrophy or dilatation). For example, hypertrophic cardiomyopathy initially has LV diastolic dysfunction, while amyloidosis that shows similar morphological change has LV systolic dysfunction. Ischemic or idiopathic cardiomyopathy with ventricular dilatation is represented by systolic dysfunction. Cardiac malfunctions are also altered on disease course. Initially, patients with cardiomyopathy may have asymptomatic LV systolic or diastolic dysfunction alone. However, adverse disease processes finally lead to both dysfunctions. Imbalance between cardiac malfunctions and compensatory mechanisms worsens an outcome of cardiomyopathy. When abnormal LV filling pressure and volume is unable to be compensated by hemodynamic alterations such as the increases in heart rate and peripheral vascular tone by the accelerated vasoconstrictors including norepinephrine (NE), endothelin-1 (ET-1), and the renin-angiotensin-aldosterone (RAA), this imbalance precipitates decompensated heart failure (HF). Early and simply identifying the decompensatory process is important therapeutic strategy in cardiomyopathy. Clinical utility of B-type natriuretic peptide (BNP) sensitively produced and secreted from heart in response to LV overload has been extended rapidly in patients with HF. At first, BNP emerged as a diagnostic marker for decompensated HF. Furthermore, BNP has been proved to predict a subsequent outcome in patients with HF. Recently, the efficiency of BNP-guided therapy in patients with HF has been demonstrated. In this chapter, we discuss about clinical utility of BNP assessments in patients with cardiomyopathy.