Evaluation of platelets in heart failure: Is platelet activity related to etiology, functional class, or clinical outcomes? ☆ ☆☆ ★ ★★

Abstract Objectives We sought to determine whether platelet activity in patients with heart failure is related to an ischemic versus nonischemic etiologic condition, clinical disease severity, or adverse clinical outcomes. Background Platelet activity may affect outcome in patients with heart failure. A prospective evaluation of the relation of baseline platelet function to etiologic condition, New York Heart Association (NYHA) class, and clinical outcomes has not been previously reported. Methods Ninety-six consecutive outpatients with ambulatory heart failure with an ejection fraction 2 , 6-keto PGF 1α , platelet contractile force, adenosine diphosphate/collagen shear-induced closure time, whole blood aggregation and CD41, CD31, CD62p, and CD51/CD61 by flow cytometry were determined. Survival status and hospitalizations were determined in the heart failure patient cohort. Results The median age of patients was 65 years (22% female, 64% white). An ischemic etiologic condition was present in 61% of patients. The population had mild to moderate heart failure: NYHA class I (1%), II (41%), III (46%), and IV (12.5%) and severe ventricular dysfunction (median ejection fraction=0.20). There were 39 clinical events (7 deaths, 3 cardiac transplants, 29 other first hospitalizations) in 305 median days of observation. Platelet activity, indicated by whole blood aggregation with 5 μmol adenosine diphosphate ( P =.04) and Tx B 2 ( P =.01), was higher in patients with heart failure. Whole blood aggregation was greater than the 90th percentile in 22% of patients with heart failure versus 7% of control subjects. Platelet function did not differ for any of the markers between the ischemic and nonischemic groups and was not affected by antecedent aspirin. There was no relation of NYHA class or the occurrence of events to platelet activity. Conclusion Platelet activity is heightened in 22% of outpatients with stable heart failure symptoms and is not affected by antecedent aspirin therapy. The degree of platelet activation is similar in ischemic and nonischemic patients with heart failure and is not related to clinical disease severity. Current methods to assess platelet activation do not appear to predict outcome. (Am Heart J 2002;143:1068-75.)

[1]  J. McMurray,et al.  Even low‐dose aspirin inhibits arachidonic acid–induced vasodilation in heart failure , 2000, Clinical pharmacology and therapeutics.

[2]  P. Elwood,et al.  Whole blood impedance platelet aggregometry and ischemic heart disease. The Caerphilly Collaborative Heart Disease Study. , 1990, Arteriosclerosis.

[3]  Robert R. Edelman,et al.  Fat‐Suppressed Breath‐Hold Magnetic Resonance Coronary Angiography , 1993, Circulation.

[4]  U. Goldbourt,et al.  Aspirin and mortality in patients treated with angiotensin-converting enzyme inhibitors: a cohort study of 11,575 patients with coronary artery disease. , 1999, Journal of the American College of Cardiology.

[5]  W. Lawson,et al.  Does aspirin attenuate the beneficial effects of angiotensin-converting enzyme inhibition in heart failure? , 2000, Archives of internal medicine.

[6]  D. Glogar,et al.  Platelet Survival in Patients with Dilated Cardiomyopathy , 1991, Thrombosis and Haemostasis.

[7]  C. Kessler,et al.  PFA-100™ System: A New Method for Assessment of Platelet Dysfunction , 1998, Seminars in thrombosis and hemostasis.

[8]  J. Mehta,et al.  Platelet Function Studies in Heart Disease: VI. Enhanced Platelet Aggregate Formation Activity in Congestive Heart Failure Inhibition by Sodium Nitroprusside , 1979, Circulation.

[9]  J. Cohn,et al.  Plasma Norepinephrine, Plasma Renin Activity, and Congestive Heart Failure Relations to Survival and the Effects of Therapy in V‐HeFT II , 1993, Circulation.

[10]  S. Yusuf,et al.  Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. A substudy of the Studies of Left Ventricular Dysfunction (SOLVD). , 1990, Circulation.

[11]  W. DeGrado,et al.  Agonist-activated αvβ3 on Platelets and Lymphocytes Binds to the Matrix Protein Osteopontin* , 1997, The Journal of Biological Chemistry.

[12]  D. Jackson,et al.  Platelet/endothelial cell adhesion molecule-1 serves as a costimulatory agonist receptor that modulates integrin-dependent adhesion and aggregation of human platelets. , 1998, Blood.

[13]  J. Sixma,et al.  Biochemical Characterization of PECAM-1 (CD31 Antigen) on Human Platelets , 1991, Thrombosis and Haemostasis.

[14]  E. Mammen,et al.  Preliminary Data from a Field Trial of the PFA-100™ System , 1995, Seminars in Thrombosis & Hemostasis.

[15]  T. Levine,et al.  Platelet function, thrombin and fibrinolytic activity in patients with heart failure. , 1993, European heart journal.

[16]  C. O'connor,et al.  Usefulness of soluble and surface-bound P-selectin in detecting heightened platelet activity in patients with congestive heart failure. , 1999, The American journal of cardiology.

[17]  Carr Me Measurement of platelet force: the Hemodyne hemostasis analyzer. , 1995 .

[18]  W. Herzog,et al.  Could coenzyme Q10 affect hemostasis by inhibiting platelet vitronectin (CD51/CD61) receptor? , 1997, Molecular aspects of medicine.

[19]  W. Rand,et al.  Antiplatelet agents and survival: a cohort analysis from the Studies of Left Ventricular Dysfunction (SOLVD) trial. , 1998, Journal of the American College of Cardiology.

[20]  E. Topol,et al.  Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction. , 1998, American heart journal.

[21]  E. Topol,et al.  Effects of reteplase and alteplase on platelet aggregation and major receptor expression during the first 24 hours of acute myocardial infarction treatment. GUSTO-III Investigators. Global Use of Strategies to Open Occluded Coronary Arteries. , 1998, Journal of the American College of Cardiology.

[22]  J. Cohn,et al.  Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. , 1984, The New England journal of medicine.

[23]  J. Cohn,et al.  Incidence of Thromboembolic Events in Congestive Heart Failure , 1993, Circulation.

[24]  D. S. Neblock,et al.  Analysis of GPIIb/IIIa receptor number by quantification of 7E3 binding to human platelets. , 1996, Blood.

[25]  C. O'connor,et al.  Role of soluble and platelet-bound P-selectin in discriminating cardiac from noncardiac chest pain at presentation in the emergency department. , 2000, American heart journal.

[26]  Salim Yusuf,et al.  Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients , 2000, The Lancet.

[27]  B. Coller The role of platelets in arterial thrombosis and the rationale for blockade of platelet GPIIb/IIIa receptors as antithrombotic therapy. , 1995, European heart journal.

[28]  J. Kjekshus,et al.  Interaction between enalapril and aspirin on mortality after acute myocardial infarction: subgroup analysis of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II) , 1997, The American journal of cardiology.

[29]  D. Lowry,et al.  Plasma thromboxane and prostacyclin are linear related and increased in patients presenting with acute myocardial infarction. , 1999, Prostaglandins, leukotrienes, and essential fatty acids.

[30]  B. Gersh,et al.  Effect of antithrombotic therapy on risk of sudden coronary death in patients with congestive heart failure. , 1997, The American journal of cardiology.

[31]  K. Song,et al.  Interaction of ACE Inhibitors and Aspirin in Patients with Congestive Heart Failure , 1999, The Annals of pharmacotherapy.

[32]  J. Cleland,et al.  The LIDO, HOPE, MOXCON and WASH studies , 1999 .

[33]  P. Gurbel,et al.  Effect of thrombolytic therapy on platelet expression and plasma concentration of PECAM-1 (CD31) in patients with acute myocardial infarction. , 1999, Arteriosclerosis, thrombosis, and vascular biology.

[34]  B. Massie,et al.  The interaction of ACE inhibitors and aspirin in heart failure: torn between two lovers. , 1999, American heart journal.

[35]  G. Pontone,et al.  Aspirin worsens exercise performance and pulmonary gas exchange in patients with heart failure who are taking angiotensin-converting enzyme inhibitors. , 1999, American heart journal.

[36]  V. D’Agati Does aspirin cause acute or chronic renal failure in experimental animals and in humans? , 1996, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[37]  K. Swedberg,et al.  Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. CONSENSUS Trial Study Group. , 1990, Circulation.

[38]  J. Cleland,et al.  Relationship between hemostatic abnormalities and neuroendocrine activity in heart failure. , 1994, American heart journal.