Transesophageal Atrial Pacing during Echocardiography Exams

Altered left ventricular diastolic function post-atrial pacing in coronary artery disease and left ventricular hypertrophy: further insights by pulmonary venous flow analysis.

Hoffmann R, Lambertz H, Thoennissen G, Flachskampf FA, Hanrath P. Medical Clinic I, Klinikum RWTH Aachen, Germany. Eur Heart J 1994 Aug;15(8):1096-105. Left ventricular filling dynamics during acute pacing-induced myocardial ischaemia were assessed using transoesophageal atrial pacing and simultaneous Doppler measurements of pulmonary venous and mitral flow. All patients (10 with CAD and 12 with left ventricular hypertrophy due to hypertrophic cardiomyopathy; HCM) were in sinus rhythm and patients with mitral insufficiency were excluded. Data were compared with those of a control group (n = 10). Measurements were obtained at baseline (heart rate 84 +/- 14 beats.min-1) and immediately after atrial pacing via the same transoesophageal echocardiography (TEE) probe after stepwise increase of the pacing rate to 133 +/- 12 beats.min-1. Heart rate immediately after pacing was 83 +/- 13 beats.min-1. Time velocity integrals (TVI) were calculated at baseline and after pacing for the following flows: early (E) and late (A) mitral flows, as well as antegrade systolic (S), diastolic (D) and retrograde diastolic (R) pulmonary venous flows. In the control group none of the flow parameters changed significantly after pacing compared with baseline data. In contrast, in CAD patients, the TVI of the E wave, the TVI E/A ratio as well as the pulmonary venous flow changed significantly after pacing (7.3 to 5.5 cm, P < 0.05, 1.7 to 1.1, P < 0.01 and 1.0 to 2.1 cm, P < 0.001, respectively). HCM patients also showed significant changes: TVI E/A ratio post-pacing decreased from 1.9 to 1.4 (P < 0.05), and the pulmonary venous reverse flow integral increased from 1.3 to 2.8 cm (P < 0.0001). Analysis of variance showed the TVI E/A ratio to be significantly dependent on pacing (P = 0.012). The pulmonary venous retrograde flow was found to be influenced by the presence of disease (P = 0.033 before and P = 0.0001 after pacing) and in all cases by pacing (before vs after pacing P = 0.0001). Pacing resulted in significantly different changes in the TVI E/A ratio and the TVI of the retrograde pulmonary venous flow for CAD and HCM patients compared with those of control subjects. In patients with CAD and HCM, rapid atrial pacing results in a decreased early to late ventricular filling ratio because of impaired relaxation, despite presumably increased filling pressure. Retrograde pulmonary venous flow increased because of increased filling pressure and operating left ventricular stiffness.

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