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Myocardial velocities measured during adenosine, dobutamine and supine bicycle exercise: a tissue Doppler study in healthy volunteers.

BACKGROUND: Dobutamine stress echocardiography (DSE) quantified by tissue Doppler (TVI) have improved the diagnostic capacity of the procedure. Quantification of other stress modalities, e.g. adenosine stress echo (ASE) and exercise stress echocardiography (ESE) are necessary for assessing any pathophysiological differences in different forms of stress. METHODS: Ten healthy individuals underwent ASE, DSE, and ESE during a span of 2-5 days. Left ventricular (LV) apical images at rest and peak stress (max) were postprocessed using TVI on a GE System FiVe equipment. ECG-derived QRS duration (QRSD, ms), heart rate (HR, bpm), TVI-estimated basal systolic velocities (S2V, cm s(-1)), ejection time (S2T, ms) and strain (S, %) were computed off-line and compared. Longitudinal displacement imaging, tissue tracking, was also made. RESULTS: Data for ASE, DSE and ESE during peak stress were (HR: 84 +/- 12***, 142 +/- 19, 137 +/- 27; P<0.001) (QRSD: 92 +/- 18**, 74 +/- 13, 79 +/- 9; P<0.05), (S2T: 307 +/- 34***, 175 +/- 53, 192 +/- 25; P<0.001) and (S%: 26.0 +/- 3.0, 21.2 +/- 7.3, 22.1 +/- 5.1; P = n.s.) respectively. Velocity response, registered in the LV septum at max, was lowest during ASE (7.4 +/- 1.4) highest during DSE (13.0 +/- 2.7; P<0.001 versus ASE) and somewhat intermediate during ESE (11.3 +/- 3.5; P<0.001 versus ASE). In contrast, strain and displacement did not differ. CONCLUSION: ASE evokes significantly less LV systolic response compared with both DSE and ESE. Increased velocity (P<0.05 versus rest) and strain (P>0.05) response at a much lower HR indicates that adenosine has minor effects on contraction presumably secondary to vasodilatation. Powerful chronotropic response to DSE and ESE is probably prerequisite for strong velocity response at the expense of strain and displacement. TVI-assisted stress echocardiography thereby shows different LV systolic response in healthy individuals, depending on stress modality.

Adenosine↗

Vertical gradients of lung density in supine subjects with fibrosing alveolitis or pulmonary emphysema.

Computed tomography was used to determine the vertical gradient of density in the peripheral lung tissue of 12 patients with histologically proved fibrosing alveolitis and 12 patients with chronic bronchitis and evidence of pulmonary emphysema on the computed tomograms. Measurements were made at total lung capacity and at residual volume and compared with similar measurements from 12 normal subjects reported in a previous study. At residual volume the mean peripheral tissue density in the emphysematous lungs was 0.081 kg/l compared with 0.426 kg/l in the fibrotic lungs and 0.323 kg/l in the normal lungs. The observed densities in the three groups were compared with those in a theoretical model predicting the vertical changes of lung density caused by gravitational effects that would be found in lungs with differing compliance. The emphysematous lungs showed a much greater increase of density with descent down the lung than that predicted for normal lungs, and the results were explicable by an increase in compliance. The fibrotic lungs showed considerably less change in density than expected, implying loss of compliance. It is suggested that local changes of compliance are important determinants of vertical density gradients in diseased lungs.

Adult↗

Redistribution of pulmonary blood flow during unilateral hypoxia in prone and supine dogs.

We used fluorescent-labeled microspheres in pentobarbital-anesthetized dogs to study the effects of unilateral alveolar hypoxia on the pulmonary blood flow distribution. The left lung was ventilated with inspired O2 fraction of 1.0, 0.09, or 0.03 in random order; the right lung was ventilated with inspired O2 fraction of 1.0. The lungs were removed, cleared of blood, dried at total lung capacity, then cubed to obtain approximately 1,500 small pieces of lung ( approximately 1.7 cm3). The coefficient of variation of flow increased (P < 0.001) in the hypoxic lung but was unchanged in the hyperoxic lung. Most (70-80%) variance in flow in the hyperoxic lung was attributable to structure, in contrast to only 30-40% of the variance in flow in the hypoxic lung (P < 0.001). When adjusted for the change in total flow to each lung, 90-95% of the variance in the hyperoxic lung was attributable to structure compared with 70-80% in the hypoxic lung (P < 0.001). The hilar-to-peripheral gradient, adjusted for change in total flow, decreased in the hypoxic lung (P = 0.005) but did not change in the hyperoxic lung. We conclude that hypoxic vasoconstriction alters the regional distribution of flow in the hypoxic, but not in the hyperoxic, lung.

Animals↗