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Plasminogen Activator Inhibitor‐1 after Acute Myocardial Infarction in Obstructive Sleep Apnea Patients
Author(s) -
Svatikova Anna,
Singh Prachi,
Kuniyoshi Fatima,
Gami Apoor,
Somers Virend K.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.572.1
Subject(s) - medicine , obstructive sleep apnea , myocardial infarction , polysomnography , cardiology , hypoxemia , sleep study , morning , apnea , tissue plasminogen activator , sleep apnea , plasminogen activator , anesthesia
Background Acute cardiac and vascular events, including myocardial infarction (MI) exhibit a peak onset between 6 AM and 11 AM. Plasminogen activator inhibitor‐1 (PAI‐1) is a main inhibitor of tissue‐plasminogen activator and a key indicator of prothrombotic state. Elevated levels of PAI‐1 have been linked to increased cardiac and vascular risk. Obstructive sleep apnea (OSA) has also been associated with increased risk of MI. Hypoxemia, as well as OSA, increase PAI‐1. We tested the hypothesis that the early morning after awakening is associated with higher PAI‐1 activity in subjects with acute MI who also have OSA. Methods We studied 56 subjects after acute myocardial infarction (mean age 60±2 years; BMI 28±1 kg/m 2 ). All subjects underwent complete overnight sleep polysomnography within 2 weeks after MI to assess for presence and severity of OSA. PAI‐1 activity was measured in all 56 subjects, first before sleep (at 9 PM), and then immediately after awakening in the morning (at 6 AM). A third measurement of PAI‐1 was obtained in all subjects at 11 AM. Results For the group, PAI‐1 activity almost doubled from 12.5±1.6 U/mL at 9 PM to 22.5±2.5 U/mL after waking at 6 AM and decreased to 14.2±2.4 U/mL by 11 AM (P<0.0001). Fifty seven percent of patients were observed to have OSA, with apnea hypopnea index of >10 events/hour. Sleep apnea did not contribute to further elevation of morning PAI‐1 activity level in acute MI patients (9 PM, 6 AM and 11 AM PAI‐1 activity respectively: no OSA 11.6±2.5 U/mL, 24.1±3.8 U/mL and 15.2±3.5 U/mL; OSA 13.3±2.1 U/mL, 21.1±3.3 U/mL and 13.3±3.3 U/mL; P=0.8 for between group comparison). Conclusions Increased PAI‐1 activity in acute MI patients may be an important mechanism underlying the early morning peak in cardiovascular events. The presence of OSA however does not appear to further accentuate the already elevated PAI‐1 activity in acute MI patients. In patients after acute MI, the diurnal variation in PAI‐1, rather than apnea, may drive the impaired fibrinolysis. Support or Funding Information ‐‐R01 grant HL65176‐‐This study was also supported in part by a gift to the Mayo Foundation by the Philips Respironics Foundation. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .