Heart failure, a major and growing public health problem, appearsto result not only from cardiac overload or injury but alsofrom a complex interplay among genetic, neurohormonal, inflammatory,and biochemical changes acting on cardiac myocytes, the cardiacinterstitium, or both. An increasing number of enzymes, hormones,biologic substances, and other markers of cardiac stress andmalfunction, as well as myocyte injury — collectivelyreferred to as biomarkers — appear to have growing clinicalimportance. Although biomarkers include genetic variants, clinicalimages, physiological tests, and tissue-specimen biopsies, thisreview focuses on biomarkers derived from the blood or urineother than . . . [Full Text of this Article]
Inflammation
Oxidative Stress
Extracellular-Matrix Remodeling
Neurohormones
Myocyte Injury
Myocyte Stress
Natriuretic Peptides
Adrenomedullin
ST2
New Biomarkers
Future Directions
Source Information
From the Thrombolysis in Myocardial Infarction (TIMI) Study Group, Cardiovascular Division, Brigham and Women's Hospital, and the Department of Medicine, Harvard Medical School — both in Boston.
Address reprint requests to Dr. Braunwald at the TIMI Study Group, 350 Longwood Ave., Boston, MA 02115, or at ebraunwald@partners.org.
This article has been cited by other articles:
Devarajan, P.
(2008). Neutrophil gelatinase-associated lipocalin--an emerging troponin for kidney injury. Nephrol Dial Transplant
23: 3737-3743
[Full Text]
Tang, W.H. W., Francis, G. S.
(2008). The Year in Heart Failure. J Am Coll Cardiol
52: 1671-1678
[Full Text]
Ronco, C., Haapio, M., House, A. A., Anavekar, N., Bellomo, R.
(2008). Cardiorenal Syndrome. J Am Coll Cardiol
52: 1527-1539
[Abstract][Full Text]