Heterogeneity of left ventricular regional wall thickening following dobutamine infusion in normal human subjects

1995 ◽  
Vol 16 (11) ◽  
pp. 1726-1730 ◽  
Author(s):  
A. C. BORGES ◽  
A. PlNGITORE ◽  
A. CORDOVIL ◽  
R. SlCARI ◽  
G. BAUMANN ◽  
...  
1983 ◽  
Vol 51 (10) ◽  
pp. 1667-1673 ◽  
Author(s):  
Natesa G. Pandian ◽  
David J. Skorton ◽  
Steve M. Collins ◽  
Herman L. Falsetti ◽  
Edmund R. Burke ◽  
...  

1991 ◽  
Vol 261 (4) ◽  
pp. H1060-H1066
Author(s):  
K. Takeda ◽  
K. Tamano ◽  
A. Okamura ◽  
N. Kobayashi ◽  
T. Shimizu ◽  
...  

We have introduced a new contractility index (Ec), i.e., the slope of the left ventricular (LV) end-systolic force-length (Fes-Les) relation. To examine whether Ec was dependent on the LV wall myocardial length, 16 normal hearts of human subjects were evaluated to determine the LV end-systolic force-dimension (Fes-Des) and pressure-dimension (Pes-Des) relations (dimension denotes the distance between the LV septum and posterior wall). LV end-systolic pressures and dimensions were estimated simultaneously by intra-arterial cannulation and LV echocardiography. In seven subjects, the effect of a dobutamine infusion was also assessed. The Fes-Des relation was found to be nearly linear. Slopes and extrapolated dimension intercepts were obtained for the LV Fes-Des and Pes-Des relations [Ec, slope of LV Pes-Des relation (Es), and extrapolated dimension intercept of LV Fes-Des (Do), and of Pes-Des relation (D'o), respectively]. Es showed a hyperbolic relation to the baseline LV Des, whereas Ec was unrelated to it. The average variation for Ec (9.5%) was smaller than that for Es (22.5%). Dobutamine infusion increased Ec, Es, and D'o, whereas Do was not changed. Thus the assumption of linearity of the LV Fes-Les relation was found to be reasonable in normal human hearts. Do appears to provide a more accurate parameter than D'o for estimating the actual unstressed myocardial length, whereas Ec could possibly serve as an index of LV wall performance in the normal human heart that is independent of myocardial length and nearly constant between individuals.


1996 ◽  
Vol 27 (2) ◽  
pp. 7 ◽  
Author(s):  
Michael R. Bauer ◽  
Jeffrey S. Soble ◽  
Inhee Song ◽  
Alex Neumann ◽  
Philip R. Liebson ◽  
...  

1979 ◽  
Vol 44 (7) ◽  
pp. 1311-1317 ◽  
Author(s):  
James D. Marsh ◽  
Laurence H. Green ◽  
Joshua Wynne ◽  
Peter F. Cohn ◽  
William Grossman

2009 ◽  
Vol 50 (4) ◽  
pp. 396-405 ◽  
Author(s):  
M. Carlsson ◽  
P. C. Ursell ◽  
D. Saloner ◽  
M. Saeed

Background: Calcium overload is a major cause of reperfusion myocardial injury. Multidetector computed tomography (MDCT) has been previously used in visualizing coronary artery calcium, but not calcium deposits in reperfused infarction. Purpose: To assess the ability of MDCT to 1) noninvasively visualize and characterize calcium deposits in reperfused infarcts, and 2) monitor regional wall swelling, regional systolic wall thickening, and infarct resorption. Material and Methods: Reperfused myocardial infarcts were created in seven pigs by 2-hour occlusion of the left anterior descending coronary artery (LAD) after coronary catheterization. A 64-slice MDCT scanner was used for non-contrast images to depict calcium deposits. Furthermore, cine and delayed contrast-enhanced (DE) MDCT imaging were acquired to assess the chronological changes (2–4 hours, 1 week, and 8 weeks) in regional wall swelling, systolic wall thickening, and infarct size. Results: Non-contrast MDCT images depicted calcium deposits as “hot-spots.” Attenuation of calcium deposits was greater (89±6 Hounsfield units [HU]) than remote myocardium (36±3 HU; P<0.05). Calcium deposits were not evident at 2–4 hours and were substantially smaller at 8 weeks compared to 1 week. Correlations were found between the extent of calcium deposits, ejection fraction ( R=0.81), and infarction size ( R=0.70). Cine MCDT images demonstrated transient wall swelling (edema formation and resorption) at 2–4 hours and differences in regional systolic wall thickening among infarcted, peri-infarcted, and remote myocardium. Calcium-specific von Kossa stain confirmed the presence of calcium deposits in infarcted myocardium. Conclusion: 64-slice MDCT has the potential to demonstrate the progression and regression of calcium deposits, interstitial edema, and infarction. The presence of calcium deposits was transient and associated with reperfused recent infarction. The extent of calcium deposits was positively correlated with infarction size and negatively with global left-ventricular function.


1988 ◽  
Vol 11 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Robert O Bonow ◽  
Dino F Vitale ◽  
Stephen L Bacharach ◽  
Barry J Maron ◽  
Michael V Green

1992 ◽  
Vol 263 (2) ◽  
pp. H392-H398 ◽  
Author(s):  
D. C. Homans ◽  
R. Asinger ◽  
T. Pavek ◽  
M. Crampton ◽  
P. Lindstrom ◽  
...  

This study was designed to test the hypothesis that the oxygen free radical scavengers superoxide dismutase (SOD) and catalase may reduce myocardial “stunning” after exercise-induced ischemia. To test this hypothesis, 8 mongrel dogs performed treadmill exercise for 10 min in the presence of a flow-limiting coronary artery stenosis. Regional left ventricular function was measured with ultrasonic microcrystals implanted to measure regional wall thickening. Regional myocardial perfusion was measured with radioactive microspheres. The combination of SOD (5 mg/kg iv) and catalase (5 mg/kg iv) did not affect heart rate, blood pressure, coronary artery flow, or regional myocardial blood flow at rest, during exercise, or in the postexercise period. SOD and catalase had no effect on regional wall thickening at rest before exercise. During exercise in the absence of a coronary artery stenosis, thickening was slightly lower during SOD and catalase infusion (27 +/- 11.0 vs. 30.8 +/- 11.5%, SOD vs. control P = 0.05). During exercise in the presence of a coronary artery stenosis, there was no difference in thickening. Infusion of SOD and catalase affected neither the transient rebound function occurring early after exercise nor the prolonged period of stunning. These results indicate that the myocardial stunning that follows exercise-induced ischemia is unlikely to be mediated by oxygen free radicals.


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