title: Decreased thickening of normal myocardium with transient increased wall thickness during stress echocardiography with atrial pacing.
abstract: Stress echocardiography is used increasingly in the evaluation of coronary artery disease. The echocardiographic evaluation of ischemia is based on stress-induced changes in wall motion and wall thickening of the ischemic segments. Studies have demonstrated that left ventricular volumetric changes may induce changes in wall thickness. The aim of the study was to evaluate whether significant changes in ventricular volume, wall thickness, and wall thickening occur during stress echocardiography with atrial pacing. Seven German Landrace female pigs were studied 4 weeks after the induction of a small myocardial infarction. Echocardiographic measurements were conducted in noninfarcted segments on the short-axis view at baseline and during atrial pacing at 120, 150, and 180 beats/min. End-diastolic circumferential area decreased from 12.3 +/- 2.0 cm2 at baseline to 8.9 +/- 1.9 cm2 at 180 beats/min of atrial pacing (p < 0.01). Mean wall thickness (interventricular septal plus posterior wall thickness divided by 2) increased markedly and progressively from 6.7 +/- 0.6 mm at baseline to 9.8 +/- 1.0 mm at 180 beats/min (p < 0.01). The increase in wall thickness correlated inversely with end-diastolic area (r = -0.57; p < 0.01). Percent systolic thickening decreased from 38.9 +/- 12.0 at baseline to 14.9 +/- 7.4 at 180 beats/min of atrial pacing (p < 0.01). The decrease in percent wall thickening correlated with the increase in wall thickness (r = -0.71; p < 0.01). In conclusion, this study shows that a marked increase in wall thickness (pseudohypertrophy) and decrease in percent systolic thickening are observed during rapid atrial pacing in normal myocardium and do not indicate stress-induced left ventricular dysfunction.
authors.affiliation: Neufeld Cardiac Research Institute, Sackler School of Medicine, Tel Aviv University, Tel Hashomer, Israel.
authors.forename: B
authors.initials: B
authors.lastname: Beker
authors.forename: Z
authors.initials: Z
authors.lastname: Vered
authors.forename: N V
authors.initials: NV
authors.lastname: Bloom
authors.forename: D
authors.initials: D
authors.lastname: Ohad
authors.forename: A
authors.initials: A
authors.lastname: Battler
authors.forename: E
authors.initials: E
authors.lastname: Di Segni
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D003971:Diastole; D004452:Echocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006346:Heart Septum / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D013552:Swine; D013599:Systole; D016277:Ventricular Function, Left / Q000502:physiology