Transesophageal Atrial Pacing during Echocardiography Exams

Influence of pacing-induced myocardial ischemia on left atrial regurgitant jet: a transesophageal echocardiographic study.

Kamp O, de Cock CC, van Eenige MJ, Visser CA. Free University Hospital, Amsterdam. J Am Coll Cardiol 1994; 23(7):1584-91. OBJECTIVES. We investigated the influence of pacing-induced myocardial ischemia on systolic regurgitant jet in the left atrium, using simultaneous transesophageal echocardiography and transesophageal atrial pacing. BACKGROUND. In vitro studies have shown that ischemia-induced mitral regurgitation may occur as a result of mitral leaflet malcoaptation or (global) left ventricular dysfunction. However, no transesophageal echocardiographic study has thus far been performed to demonstrate the mechanism and extent of mitral regurgitation during myocardial ischemia in patients. METHODS. In 24 patients (mean [+/-SD] age 57 +/- 10 years) with (15 patients) and without (9 control subjects) coronary artery disease, heart rate, blood pressure and systolic regurgitant jet were assessed before and immediately after pacing. Pacing was increased stepwise up to 160 beats/min to provoke wall motion abnormalities while the left ventricular short axis was monitored at the midpapillary muscle level. Other variables obtained before and at peak pacing included left ventricular end-diastolic and end-systolic areas and left ventricular end-diastolic and end-systolic endocardial segmental lengths. RESULTS. Heart rate and blood pressure before and after pacing were not significantly different in control subjects or in patients. At baseline, a jet was present in all but three control subjects. New or increased anterior or posterior wall motion abnormalities were observed during pacing in seven and eight patients, respectively. End-systolic left ventricular areas and segment lengths were significantly reduced in control subjects compared with patients with coronary artery disease at peak pacing (p < 0.05). The increase in systolic regurgitant jet was significantly greater in patients (2.0 +/- 1.1 to 3.1 +/- 1.8 cm2 vs. 0.7 +/- 0.7 to 0.9 +/- 0.9 cm2 [after pacing], p < 0.01). This effect was greater in patients with posterior than with anterior wall motion abnormalities (3.5 +/- 1.6 vs. 2.1 +/- 1.2 cm2 [after pacing], p < 0.05). CONCLUSIONS. Quantitative changes in geometry and function of the left ventricle caused by pacing-induced myocardial ischemia augments systolic regurgitant jet size. An increase in the jet during atrial pacing is associated with new or increased wall motion abnormalities, especially of the posterior wall. Pacing-induced anterior wall motion abnormalities appear not to be related directly to an increase in the jet.

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