Abnormalities of hemorheological, endothelial, and platelet function in patients with chronic heart failure in sinus rhythm: effects of angiotensin-converting enzyme inhibitor and beta-blocker therapy.
BACKGROUND
To investigate the hypothesis that abnormalities of hemorheological (fibrinogen, plasma viscosity), endothelial (von Willebrand factor [vWF]), and platelet (soluble P-selectin) function would exist in patients with chronic heart failure (CHF) who are in sinus rhythm, we conducted a cross-sectional study of 120 patients with stable CHF (median ejection fraction 30%). We also hypothesized that ACE inhibitors and beta-blockers would beneficially affect the measured indices.


RESULTS
In the cross-sectional analysis, plasma viscosity (P=0.001), fibrinogen (P=0.02), vWF (P<0.0001), and soluble P-selectin (P<0.001) levels were elevated in patients with CHF compared with healthy controls. Women demonstrated greater abnormalities of hemorheological indices and vWF than males (all P<0.05). Plasma viscosity (P=0.009) and fibrinogen (P=0.0014) levels were higher in patients with more severe symptoms (New York Heart Association [NYHA] class III-IV), but there was no relationship with left ventricular ejection fraction. When ACE inhibitors were introduced, there was a reduction in fibrinogen (repeated-measures ANOVA, P=0.016) and vWF (P=0.006) levels compared with baseline. There were no significant changes in hemorheological, endothelial, or platelet markers after the introduction of beta-blocker therapy, apart from a rise in mean platelet count (P<0.001).


CONCLUSIONS
Abnormal levels of soluble P-selectin, vWF, and hemorheological indices may contribute to a hypercoagulable state in CHF, especially in female patients and in those with more severe NYHA class. Treatment with ACE inhibitors improved the prothrombotic state in CHF, whereas the addition of beta-blockers did not. These positive effects of ACE inhibitors may offer an explanation for the observed reduction in ischemic events in clinical trials.
Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
C R
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Gibbs
A D
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Blann
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Watson
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Lip
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001146:Arrhythmia, Sinus; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D002908:Chronic Disease; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006331:Heart Diseases / Q000097:blood / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D006400:Hematocrit; D006801:Humans; D017706:Lisinopril / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000378:metabolism*; D010976:Platelet Count; D012044:Regression Analysis; D012212:Rheology; D012727:Sex Characteristics; D012995:Solubility; D018709:Statistics, Nonparametric; D014783:Viscosity; D014841:von Willebrand Factor / Q000378:metabolism*
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D019007:P-Selectin; D014841:von Willebrand Factor; D005340:Fibrinogen; D017706:Lisinopril