Title of article :
G Protein-Coupled Receptor Kinase 2 in Patients With Acute Myocardial Infarction
Author/Authors :
Santulli، نويسنده , , Gaetano and Campanile، نويسنده , , Alfonso and Spinelli، نويسنده , , Letizia and Assante di Panzillo، نويسنده , , Emiliano and Ciccarelli، نويسنده , , Michele and Trimarco، نويسنده , , Bruno and Iaccarino، نويسنده , , Guido، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2011
Pages :
6
From page :
1125
To page :
1130
Abstract :
Lymphocyte G protein–coupled receptor kinase 2 (GRK2) levels are increased in patients with chronic heart failure, and in this condition, they correlate with cardiac function. The aim of this study was to assess the prognostic role of GRK2 during acute cardiac dysfunction in humans. A study was designed to investigate the role of GRK2 levels in patients with acute coronary syndromes. Lymphocyte GRK2 levels were examined at admission and after 24 and 48 hours in 42 patients with acute coronary syndromes, 32 with ST-segment elevation myocardial infarction and 10 with unstable angina as a control group. Echocardiographic parameters of systolic and diastolic function and left ventricular remodeling were evaluated at admission and after 2 years. GRK2 levels increased during ST-segment elevation myocardial infarction and were associated with worse systolic and diastolic function. This association held at 2-year follow-up, when GRK2 was correlated with the ejection fraction and end-systolic volume, indicating a prognostic value for GRK2 levels during acute ST-segment elevation myocardial infarction. In conclusion, lymphocyte GRK2 levels increase during acute myocardial infarction and are associated with worse cardiac function. Taken together, these data indicate that GRK2 could be predictive of ventricular remodeling after myocardial infarction and could facilitate the tailoring of appropriate therapy for high-risk patients.
Journal title :
American Journal of Cardiology
Serial Year :
2011
Journal title :
American Journal of Cardiology
Record number :
1900679
Link To Document :
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