We investigated plasma fibrin clot properties in high-risk hypertensive patients with obstructive sleep apnoea (OSA) and assessed the impact of continuous positive airway pressure (CPAP) treatment on clot phenotype.
We studied 50 hypertensive patients with clinically significant OSA (age 50.0 ± 8.8 years, 39 M, 11 F). In total, 38 hypertensive patients without OSA balanced for age, sex, blood pressure, cardiovascular risk factors, and metabolic status served as controls. Plasma fibrin clot properties, including clot permeability coefficient, clot lysis time (CLT), and turbidimetric parameters of clot formation were determined. Patients underwent transthoracic echocardiography, carotid ultrasonography, evaluation of endothelial function and calcium score index of coronary arteries, and Doppler imaging of renal arteries.
Compared with controls, OSA patients were characterized by more compact fibrin structure (lower median clot permeability coefficient, 6.00 vs. 7.25 10−9 cm2; P < 0.001), impaired fibrinolysis (longer median CLT, 108.00 vs. 92.50 min; P < 0.001), and by faster clot formation (shorter median lag phase, 40.50 vs. 42.50 s; P = 0.041), and higher median maximum clot absorbency indicating denser fibrin networks (0.87 vs. 0.81; P = 0.028). Clot permeability coefficient and CLT correlated with apnoea–hypopnoea index (r = −0.46; P < 0.001 and r = 0.44; P < 0.001, respectively) as well with mean (r = 0.31; P = 0.003; r = −0.36; P = 0.001, respectively) and minimal oxygen saturation (r = 0.46; P < 0.001; r = −0.49; P < 0.001, respectively). After 3 months of CPAP treatment we observed an increase in clot permeability coefficient (5.95 vs. 7.60 10−9 cm2; P = 0,001), shortened CLT (107.00 vs. 87.00; P = 0.006), a longer lag phase of fibrin formation (40.00 vs. 43.50 s; P = 0.013), and a trend toward lower maximum clot absorbency (0.86 vs. 0.81; P = 0.058).
In hypertensive patients at high cardiovascular risk, OSA was associated with unfavourable prothrombotic fibrin clot characteristics, including hypofibrinolysis, which significantly improve as early as after 3 months of CPAP treatment.
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aDepartment of Hypertension, Institute of Cardiology, Warsaw
bInstitute of Cardiology, Jagiellonian University Medical College
cInnovative Laboratory Diagnostic Centre, John Paul II Hospital, Kraków
dII Department of Radiology, Medical University of Warsaw
e2nd Department of Respiratory Medicine, Institute of Tuberculosis and Lung Disease
fDepartment of Coronary and Structural Heart Diseases, Institute of Cardiology
gDepartment of Congenital Heart Diseases, Institute of Cardiology, Warsaw
hCracow Centre for Medical Research and Technologies, John Paul II Hospital, Kraków, Poland
Correspondence to Aleksander Prejbisz, PhD, MD, Department of Hypertension, Institute of Cardiology, Alpejska 42, 04-628 Warsaw, Poland. Tel: +48 22 3434339; fax: +48 22 343 45 17; e-mail: email@example.com
Abbreviations: ABPM, ambulatory blood pressure monitoring; AHI, apnoea-hypopnoea index; CIMT, carotid intima–media thickness; CLT, clot lysis time; CPAP, continuous positive airway pressure; hsCRP, high-sensitive C-reactive protein; LVM, left ventricle mass; LVMI, left ventricle mass index; MI, myocardial infarction; OBPM, office BP measurements; OSA, obstructive sleep apnoea; PAI-1, plasminogen activator inhibitor-1; PSG, polysomnography; TAFIa, activated thrombin-activatable fibrinolysis inhibitor; t-PA, tissue-type plasminogen activator
Received 1 July, 2016
Revised 19 December, 2016
Accepted 30 December, 2016
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