الفهرس 
Acute myocardial infarctionOnly 14 pages are availabe for public view
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Abstract
Left ventricular dilatation may occur early after infarction, probably in part because of elevated filling pressure within the ventricle (Popovic AD, et al., 1994).
Early identification of patients at risk of left ventricular dilatation may have important therapeutic implications (Leonardo Bolognese, et al., 2002).
It has been shown that left ventricular volumes indices and ejection fraction are major important predictors of left ventricular dilatation and remodeling following acute myocardial infarction (White HD, et a.l, 1987).
Doppler echocardiography has provided a rapid, feasible, and simple noninvasive method of assessing left ventricular filling in various cardiac diseases in which diastolic abnormalities have been observed, including acute myocardial infarction (Giampaolo Cerisano, et al, 2001).
Doppler echocardiography has provided evidence that serial changes in diastolic filling pattern may parallel the evolutionary changes in left ventricular dimensions after acute myocardial infarction (Pier L, et al, 2004).
Shortening of the deceleration time (DT) of the early filling wave, indicative of a ”restrictive” filling pattern, has been found to predict an adverse outcome of post infarction patients ( Nijland F et al, 1997 and Giampaolo Cerisano, et al, 2001).
We aimed in this study to evaluate the role of Doppler-derived mitral deceleration time (DT) as an early predictor of left ventricular dilatation following acute myocardial infarction in correlation to left ventricular volume indices, ejection fraction and wall motion score index.
We have studied 34 patients with first acute anterior myocardial infarction, but we exclude results of 4 patients from the present study as they did not complete the follow up. All patients with acute myocardial infarction have been diagnosed by a history of typical chest pain, ST segment elevation in two contiguous leads and a transient increase in Createnin kinase level more than twice the upper limits of normal. 2-dimensional and Doppler echocardiographic examinations have been done to all patients on day 3 of admission, on day 7, one month, and 3 months after the index infarction. Mitral flow velocities, Left ventricular volume indexes, wall motion score index and ejection fraction were measured, any increase in end diastolic volume index >20% was considered left ventricular dilation (Bolognese L, et al., 2002). To avoid the effects of acute ischemia on LV filling patterns, we choose to measure baseline early mitral deceleration time (DT) on day 3 after the index infarction. Patients have been divided according to the early mitral deceleration time (DT) duration which have been assessed at day 3 into 2 groups, group I (nonrestrictive group with early mitral deceleration time (DT) >130 ms) and group II (restrictive group with early mitral deceleration time (DT) 130 ms).
We have found that left ventricular volume indices continue to increase during follow up time in group II indicating continuous LV remodeling. Our findings in the percentage of LV end diastolic volume index change during follow up at 3 moths was 29.92 ±5.57% in group II indicative for left ventricular dilatation. Volume changes are inversely correlated with early mitral deceleration time at day 3 after myocardial infarction. A significant inverse correlation was found between the 2 variables (r = -0.911, P = 0.000). Similarly there was a direct relation, but less than DT, between changes in LV end-diastolic volume index and peak CPK (r = 0.828, P = 0.0001) and WMSi on admission (r = 0.768, P = 0.0001). So it appears that early mitral deceleration time at day 3 after acute myocardial infarction is an early strong predictor for left ventricular remodeling.