TY - JOUR
T1 - Restrictive left ventricular filling pattern and risk of new-onset atrial fibrillation after acute myocardial infarction
AU - Aronson, Doron
AU - Mutlak, Diab
AU - Bahouth, Fadel
AU - Bishara, Rema
AU - Hammerman, Haim
AU - Lessick, Jonathan
AU - Carasso, Shemy
AU - Dabbah, Saleem
AU - Reisner, Shimon
AU - Agmon, Yoram
PY - 2011/6/15
Y1 - 2011/6/15
N2 - Mechanisms for atrial arrhythmias that occur in the context of acute myocardial infarction (AMI) have not been well characterized. AMI often leads to alterations in left ventricular (LV) filling dynamics, which may result in advanced diastolic dysfunction. Diastolic dysfunction may produce increased left atrial (LA) pressure and initiate LA remodeling, promoting the progression to atrial fibrillation (AF). We studied 1,169 patients admitted with AMI. Advanced diastolic dysfunction was defined as a restrictive filling pattern (RFP), defined as ratio of early to late transmitral velocity of mitral inflow >1.5 or deceleration time <130 ms. The relation between RFP and the primary end point of new-onset AF occurring within 6 months was analyzed using multivariable Cox models. Of 1,169 patients (70% men, mean ± SD 64 ± 10 years of age), 110 (9.4%) developed new-onset AF (19.6% and 7.5% in patients with and without RFP, respectively, p <0.0001). RFP was associated with a hazard ratio of 2.72 for AF (95% confidence interval 1.83 to 4.05, p <0.0001). After multivariable adjustments for clinical variables, LV ejection fraction (EF) and LA size, RFP remained an independent predictor of AF (hazard ratio 2.17, 95% confidence interval 1.42 to 3.32, p <0.0001). Risk of AF was higher in patients with RFP for preserved (<45%, hazard ratio 2.14, 95% confidence interval 1.09 to 4.20, p = 0.03) or decreased (hazard ratio 2.80, 95% confidence interval 1.63 to 4.82, p <0.0001) LVEF. In contrast, decreased LVEF in the absence of RFP was similar to that of patients with preserved LVEF and without RFP. In conclusion, in patients with AMI, presence of advanced diastolic dysfunction was independently associated with new-onset AF, suggesting that increased filling pressures may contribute to the development of AF after AMI.
AB - Mechanisms for atrial arrhythmias that occur in the context of acute myocardial infarction (AMI) have not been well characterized. AMI often leads to alterations in left ventricular (LV) filling dynamics, which may result in advanced diastolic dysfunction. Diastolic dysfunction may produce increased left atrial (LA) pressure and initiate LA remodeling, promoting the progression to atrial fibrillation (AF). We studied 1,169 patients admitted with AMI. Advanced diastolic dysfunction was defined as a restrictive filling pattern (RFP), defined as ratio of early to late transmitral velocity of mitral inflow >1.5 or deceleration time <130 ms. The relation between RFP and the primary end point of new-onset AF occurring within 6 months was analyzed using multivariable Cox models. Of 1,169 patients (70% men, mean ± SD 64 ± 10 years of age), 110 (9.4%) developed new-onset AF (19.6% and 7.5% in patients with and without RFP, respectively, p <0.0001). RFP was associated with a hazard ratio of 2.72 for AF (95% confidence interval 1.83 to 4.05, p <0.0001). After multivariable adjustments for clinical variables, LV ejection fraction (EF) and LA size, RFP remained an independent predictor of AF (hazard ratio 2.17, 95% confidence interval 1.42 to 3.32, p <0.0001). Risk of AF was higher in patients with RFP for preserved (<45%, hazard ratio 2.14, 95% confidence interval 1.09 to 4.20, p = 0.03) or decreased (hazard ratio 2.80, 95% confidence interval 1.63 to 4.82, p <0.0001) LVEF. In contrast, decreased LVEF in the absence of RFP was similar to that of patients with preserved LVEF and without RFP. In conclusion, in patients with AMI, presence of advanced diastolic dysfunction was independently associated with new-onset AF, suggesting that increased filling pressures may contribute to the development of AF after AMI.
UR - http://www.scopus.com/inward/record.url?scp=79957941944&partnerID=8YFLogxK
U2 - 10.1016/j.amjcard.2011.02.334
DO - 10.1016/j.amjcard.2011.02.334
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C2 - 21497781
AN - SCOPUS:79957941944
SN - 0002-9149
VL - 107
SP - 1738
EP - 1743
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 12
ER -