STRESS-INDUCED LEFT-VENTRICULAR OUTFLOW TRACT OBSTRUCTION - A POTENTIAL CAUSE OF DYSPNEA IN THE ELDERLY

Objectives. We sought to identify the pattern of disturbed left ventri cular physiology associated with symptom development in elderly patien ts with effort-induced breathlessness. Background. Limitation of exerc ise tolerance by dyspnea is common in the elderly and has been ascribe d to diastolic dysfunction when left ventricular cavity size and systo lic function appear normal. Methods. Dobutamine stress echocardiograph y was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, an d the values were compared with those in 15 control subjects. Results. Before stress, left ventricular end diastolic and end-systolic dimens ions were reduced, fractional shortening was in creased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did no t differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was si gnificantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolume tric relaxation time was prolonged, and peak left ventricular minor ax is lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjec ts, but blood pressure did not change. Transmitral A wave velocity inc reased, but the E/A ratio did not change. Left ventricular outflow tra ct velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 mis, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0. 001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 bea ts/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0 .5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fe ll from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterio r motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function d id not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. Conc lusions. Although our patients fulfilled the criteria for ''diastolic heart failure,'' diastolic dysfunction was not aggravated by pharmacol ogic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and s ystolic anterior motion of the mitral valve. Their appearance correlat ed closely with the development of symptoms, suggesting a potential ca usative link. (C) 1997 by the American College of Cardiology.