<Originals>β-adrenergic stimulation can induce ST-segment elevation without evolution of left ventricular dilation or myocardial ischemia one month after myocardial infarction

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Background Recent studies have shown that β-adrenergic stimulation can induce ST-segment elevation similar to exercise, after myocardial infarction. However, how enhanced β-adrenergic activity attributes to ST-segment elevation is unknown. The purpose of the present study was to examine the mechanism of ST-segment elevation as measured by left ventricular function during β-adrenergic stimulation. Methods Subjects comprised 13 patients (12 men, 55±10 years) with first documented anterior myocardial infarction with single vessel disease of the left anterior descending artery elapsed one month after onset. The patients underwent coronary angiograms followed by digital subtraction left ventriculograms before and during isoproterenol infusion. Left ventricular volume, ejection fraction, and asynergic extent as measured by the centerline method were analyzed. Results Isoproterenol induced ST-segment elevation (ΔΣST V2,3,4 6.2±3.5 mm, p<0.01) along with decreased left ventricular volume index both at end-diastole (75.8±18.4 to 59.2±11.5 ml・m^<-2>, p<0.01) and at end-systole (42.6±16.5 to 28.7±12.0 ml・m^<-2>, p<0.01), and improved ejection fraction (45.1±8.8 to 53.4±12.7%, p<0.01) and asynergic extent (38.6±20.4 to 30.6±18.6%, p<0.01). The magnitude of the ST-segment elevations positively correlated to left ventricular volume and asynergic extent, and negatively to ejection fraction both before and during stress. Moreover, the magnitude of ST-elevations correlated to decreases in left ventricular volume during stress, indicating that the more left ventricular volumes were decreased the more pronounced ST-segment elevations were induced. Conclusions ST-segment elevation during β-adrenergic stimulation is accompanied by a significant decrease in left ventricular volume and an improvement in both regional and global function during stress even though left ventricular function is severely impaired. Such favorable responses do not connect the ST-elevation to deterioration of wall motion abnormalities or myocardial ischemia. Improved function of both normal and adjacent territories to the infarction suggests that an enhanced sensitivity to β-adrenergic stimulation in the noninfarcted territory may attribute to stress-induced ST-segment elevation after myocardial infarction.
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<Originals>β-adrenergic stimulation can induce ST-segment elevation without evolution of left ventricular dilation or myocardial ischemia one month after myocardial infarction

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