Key result
Dobutamine is linked to ~32% lower inferior wall systolic thickening, mimicking ischemic hypokinesis.
Why the study?
Inotropic stimulation with dobutamine can induce heterogeneous left ventricular regional wall thickening, potentially mimicking ischaemic regional hypokinesis during stress echocardiography.
Observational (n=11)
Absolute Event Rate: 50% vs 73%
p-value: p=<0.01
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BACKGROUND: Pathophysiological data and pragmatic clinical experience with stress echocardiography suggest that inotropic stimulation with simultaneous changes in heart rate and loading conditions can affect the function of various myocardial regions asymmetrically, inducing heterogeneity in wall motion and thickening, possibly mimicking 'ischaemic' regional hypokinesis or lack of hyperkinesis during stress. OBJECTIVES: To describe, in a quantitative fashion, the physiological contractile response of different left ventricular regions following dobutamine infusion. METHODS: Two hundred and twenty-three in-hospital patients undergoing dobutamine stress echocardiography and coronary angiography were initially considered. Of these 223 patients, 18 had angiographically normal coronary arteries, normal resting function, negative ergonovine and exercise stress tests, and negative dobutamine stress echocardiograms; of the 18, only in 11 patients (six females, age = 56 +/- 10 years) was it possible to obtain quantitative measurements of the middle segments of the inferior, anterior, lateral, and septal walls. Two-dimensional echocardiographic measurements of wall thickness were obtained at the end-diastolic (onset of Q wave) and end-systolic phases, both at baseline (rest) and at the peak of the dobutamine infusion (40 micrograms.min-1.kg-1 plus atropine). RESULTS: Dobutamine increased heart rate (rest = 69 +/- 9 vs dobutamine = 138 +/- 13 beats.min-1; P < 0.01), whereas systolic blood pressure did not change significantly (rest = 136 +/- 15 vs dobutamine = 150 +/- 25 mmHg, P = ns). During stress, % systolic thickening decreased in the inferior wall (rest = 73 +/- 24 vs dobutamine +/- 50 +/- 9%; P < 0.01), whereas it tended to increase to a variable extent in the other regions, i.e. septal (rest = 46 +/- 17 vs dobutamine = 68 +/- 13%, P < 0.01), anterior (rest 62 +/- 19 vs dobutamine = 69 +/- 11%, P = ns), and lateral wall (rest = 48 +/- 16 vs dobutamine = 61 +/- 18%, P = ns). The decrease in % systolic thickening of the inferior wall was inversely correlated with the increase in end-diastolic wall thickness (r = -0.75; P < 0.01), but neither with heart rate (r = 0.15; P = ns) nor with systolic blood pressure changes (r = 0.05; P = ns). CONCLUSIONS: Heterogeneity of left ventricular wall thickening can be induced or magnified by dobutamine infusion even in subjects without coronary artery disease, with the inferior wall showing a lack of hyperkinesis, up to relative hypokinesis, in comparison with other myocardial regions. Caution in aggressive dobutamine stress echocardiography reading, especially in the inferior wall, might be warranted.
Borges et al. (1995) conducted an observational in Normal coronary arteries (n=11). Dobutamine infusion vs. Baseline (rest) was evaluated on Percentage of systolic thickening in the inferior wall (p=<0.01). Dobutamine infusion decreased % systolic thickening in the inferior wall from 73% at rest to 50% (P<0.01) in subjects without coronary artery disease, mimicking ischaemic hypokinesis.
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