Risk Stratification in Heart Failure: The Role of Emerging Biomarkers
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1 Risk Stratification in Heart Failure: The Role of Emerging Biomarkers David G. Grenache, PhD Associate Professor of Pathology, University of Utah Medical Director, ARUP Laboratories Salt Lake City, UT
2 Heart Failure Complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood Heart unable to meet body s circulatory demands Dyspnea Fatigue Edema Most common causes in US include: Coronary heart disease Hypertension Diabetes
3 Heart Failure is a Burgeoning Health & Healthcare Problem About 20 million people in the world have heart failure (5.1 million in US) 825,000 new cases annually About half of people who develop heart failure die within 5 years of diagnosis Each year in the US, HF accounts for: >1 million hospitalizations >3 million physician office visits 57,000 deaths An estimated $32 billion in healthcare costs 20% of Medicare patients hospitalized with HF are re-hospitalized within 30 days of discharge (34% within 90 days) Go AS, et al. Circulation 2014;129: Jencks SF, et al. NEJM 2009;360:
4 Stages & Classifications of Heart Failure ACC/AHA Stage NYHA Classification A At high risk for HF but without structural heart disease or symptoms of HF None B Structural heart disease but without signs or symptoms of HF I I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF C Structural heart disease with prior or current symptoms of HF II III Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF D Refractory HF requiring specialized interventions IV IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest ACCF/AHA Practice Guideline. Circulation 2013;128:e
5 How Can Biomarkers Help Heart Failure Patients? Predict who is at risk for adverse events Identify those needing interventions to prevent hospital readmission
6 Mechanisms of Action of Heart Failure Biomarkers Myocardial Insult Myocyte Stretch BNP, NT-proBNP Mycardial Injury Troponins Oxidative Stress Myeloperoxidase, oxldl Maladaptive Remodeling Inflammation CRP, TNF-α, Fas, interleukins, osteoprotegerin, adiponectin Hypertrophy/fibrosis MMPs, collagen propeptides, soluble ST2, galectin-3 Apoptosis Neurohormonal Activation Renin Angiotensin System Renin, angiotensin II, aldosterone Sympathetic Nervous System Norepinephrine, chromogranin A Arginine Vasopressin System Arginine vasopressin Kim HN, et al. Curr Treat Options Cardiovasc Med 2010;12:
7 ST2 Member of the interleukin (IL)-receptor family Involved in inflammation and immune tolerance Two isoforms Membrane-bound ST2 ligand (ST2L) Soluble ST2 (sst2) Ligand is IL-33 Secreted by stretched cardiac fibroblasts/myocytes Prevents myocardial hypertrophy and fibrosis sst2 functions as decoy receptor Secreted by stretched cardiac fibroblasts/myocytes Inhibits IL-33 action Kakkar R, et al. Circ Res 2010;106:47-57
8 Elevated sst2 Predicts Short-term Mortality Dyspnea w/ HF N=593 Dyspnea w/o HF Januzzi JL, et al. J Amer Coll Cardiol 2007;50:
9 Elevated sst2 Predicts Long-term Mortality N=134 Shah RV, et al. Circ Heart Fail 2009;2:
10 Prognostic Value of sst2 is Additive to That of NTproBNP N=593 w/ & w/o HF N=208 w/ HF Red bars = sudden cardiac death White bars = survivors Januzzi JL, et al. J Amer Coll Cardiol 2007;50: Pascual-Figal DA, et al. J Amer Coll Cardiol 2009;54:
11 sst2 Identifies Heart Failure Patients Who May Benefit from Beta Blocker Therapy N=151 Gaggin HK, et al Circ Heart Fail;6:
12 Increases in sst2 are Associated with Increased Mortality N= % decrease 33% risk of death >15.5% decrease 7% risk of death Boisot S, et al. J Card Fail 2008;14:
13 Galectin-3 β-galactosidase-binding lectin Expressed and secreted by activated macrophages Induces proliferation of cardiac fibroblasts and deposition of type I collagen Result is scar formation, cardiac remodeling, and dilatation Stable Heart Failure Myocardial Injury Inflammation/Wound Healing Cardiac Remodeling Galectin-3-mediated Fibrosis Galectin-3-mediated Heart Failure
14 Elevated Galectin-3 Predicts Adverse Outcomes in Patients with Acute Heart Failure N=209 van Kimmenade RR, et al. J Am Coll Cardiol 2006;48:
15 Elevated Galectin-3 Predicts Adverse Outcomes in Patients with Chronic Heart Failure N=248 N=248 de Boer RA, et al. Ann Med 2011;43:60-68
16 Galectin-3 Predicts the Development of Heart Failure in Patients with Acute Coronary Syndrome N=100 Grandin EW, et al. Clin Chem 2012;58:
17 Increases in Galectin-3 are Associated with Increased Adverse Outcomes N=1329 N=324 van der Velde, et al. Circ Heart Fail 2013;6:
18 2013 Heart Failure Guidelines Recommend Biomarkers of Myocardial Fibrosis for Hospitalized and Acute Patients ACCF/AHA Practice Guideline. Circulation 2013;128:e
19 Summary sst2 and galectin-3 are new biomarkers of maladaptive remodeling in heart failure Elevated concentrations of sst2 and galectin-3 are associated with increased cardiac fibrosis and increased risk of death and rehospitalization sst2 and galectin-3 provide information that is independent and complementary to that of the natriuretic peptides The optimal use of sst2 and galectin-3 in managing heart failure patients is uncertain and is an ongoing area of investigation
20 2014 ARUP Laboratories
21 Definition of Heart Failure Type I. Heart Failure with Reduced Ejection Fraction (HFrEF) II. Heart Failure with Preserved Ejection Fraction (HFpEF) a. HFpEF, Borderline b. HFpEF, Improved Ejection Fraction 40% 50% 41% to 49% >40% ACCF/AHA Practice Guideline. Circulation 2013;128:e Description Also referred to as systolic HF. Efficacious therapies have been demonstrated only in these patients. Also referred to as diastolic HF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. Efficacious therapies have not been identified. These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF. It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF.
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