Regional left ventricular wall thickness early and late after coronary occlusion in the conscious dog

1981 ◽  
Vol 240 (2) ◽  
pp. H293-H299 ◽  
Author(s):  
S. Sasayama ◽  
K. P. Gallagher ◽  
W. S. Kemper ◽  
D. Franklin ◽  
J. Ross
Keyword(s):  
Wall Thickness ◽  
Recovery Of Function ◽  
Close Correlation ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Tissue Loss ◽  
Wall Thickening ◽  
Circumflex Artery ◽  
Regional Wall ◽  
Before And After

Regional wall thickness and endocardial segment lengths in normal and ischemic zones of the left ventricle were measured simultaneously with ultrasonic-dimension gauges before and after chronic circumflex artery occlusion in conscious dogs. After 3 wk, end-diastolic segment lengths (EDL) in normal zones increase 10% (P less than 0.01), shortening increased 22% (P less than 0.05), and end-diastolic wall thickness (EDWT) was reduced by 12.8% (P less than 0.01). In ischemic zones at 3 wk, EDL was reduced by 15.4% (P less than 0.01), and subendocardial shortening recovered slightly to 15% of control; EDWT increased 11% at 3 days postocclusion and thereafter remained near control values (change not significant), but systolic wall thickening improved substantially, reaching 38% of control at 3 wk. Thus, tissue loss and slight return of function occurred in the ischemic subendocardium, whereas overall wall function (as reflected by regional wall thickening) improved considerably over time. These findings suggest that recovery of function in the outer layers of the wall after myocardial infarction modifies the close correlation between regional subendocardial segment and wall thickening dynamics observed acutely.

Assessment of Myocardial Viability in Persistent Defects on Thallium-201 SPECT after Reinjection Using Gradient-Echo MRI

1996 ◽  
Vol 35 (05) ◽  
pp. 146-152 ◽  
Author(s):  
A. Kögler ◽  
H.-A. Schmitt ◽  
D. Emrich ◽  
H. Kreuzer ◽  
D. L. Munz ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Myocardial Viability ◽  
Cardiac Cycle ◽  
Single Photon ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Gradient Echo ◽  
Systolic Wall Thickening

SummaryThis prospective study assessed myocardial viability in 30 patients with coronary heart disease and persistent defects despite reinjection on TI-201 single-photon computed tomography (SPECT). In each patient, three observers graded TI-201 uptake in 7 left ventricular wall segments. Gradient-echo magnetic resonance imaging in the region of the persistent defect generated 12 to 16 short axis views representing a cardiac cycle. A total of 120 segments were analyzed. Mean end-diastolic wall thickness and systolic wall thickening (± SD) was 11.5 ± 2.7 mm and 5.8 ± 3.9 mm in 48 segments with normal TI-201 uptake, 10.1 ± 3.4 mm and 3.7 ± 3.1 mm in 31 with reversible lesions, 11.3 ± 2.8 mm and 3.3 ± 1.9 mm in 10 with mild persistent defects, 9.2 ± 2.9 mm and 3.2 ±2.2 mm in 15 with moderate persistent defects, 5.8 ± 1.7 mm and 1.3 ± 1.4 mm in 16 with severe persistent defects, respectively. Significant differences in mean end-diastolic wall thickness (p <0.0005) and systolic wall thickening (p <0.005) were found only between segments with severe persistent defects and all other groups, but not among the other groups. On follow-up in 11 patients after revascularization, 6 segments with mild-to-moderate persistent defects showed improvement in mean systolic wall thickening that was not seen in 6 other segments with severe persistent defects. These data indicate that most myocardial segments with mild and moderate persistent TI-201 defects after reinjection still contain viable tissue. Segments with severe persistent defects, however, represent predominantly nonviable myocardium without contractile function.

scholarly journals Accuracy of computer-generated synthetic M-mode for left ventricular regional wall thickening

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

Dissociation of adenosine from metabolic regulation of coronary flow in the lamb

1986 ◽  
Vol 251 (1) ◽  
pp. H40-H46 ◽  
Author(s):  
S. E. Downing ◽  
V. Chen
Keyword(s):  
Coronary Flow ◽  
Metabolic Regulation ◽  
Close Correlation ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Tetraethylammonium Chloride ◽  
Close Link ◽  
O2 Extraction ◽  
Before And After

The objective of these studies was to evaluate the contribution of an adenosine mechanism to metabolic regulation of coronary flow. Cardiac O2 metabolism (MVO2) was altered by changing cardiac output while aortic pressure and heart rate were held constant (paced). Ganglionic (tetraethylammonium chloride) and beta blockade (propranolol) were employed. Relationships of coronary flow to MVO2 were determined in control and alloxan diabetic animals. The latter have previously been shown to have reduced sensitivity to adenosine [Am. J. Physiol. 243 (Heart Circ. Physiol. 12): H252-H258, 1982]. In each group, responses were measured before and after adenosine receptor blockade with aminophylline (10 mg/kg). Responses to infused adenosine were also compared. A linear relationship between adenosine infusion rate and flow was found in all conditions. Aminophylline caused a 70% reduction in adenosine sensitivity in controls. In the diabetics, adenosine sensitivity was much reduced and was identical with blocked controls. A close correlation between left ventricular work and MVO2 was found in both groups. Coronary flow increased linearly with MVO2, and the slopes before and after aminophylline were identical. Myocardial O2 extraction remained unchanged. The same relationships were found in the diabetics, and responses did not differ from controls. Thus, in two conditions of sharply reduced sensitivity to exogeneous adenosine, coronary flow (and resistance) were as equally well matched to MVO2 as in controls. These data suggest that mechanisms other than, or in addition to, adenosine provide the close link between MVO2 and coronary flow with changing cardiac work loads.

Effect of activation sequence on MVO2 before and after coronary ligation

1978 ◽  
Vol 234 (3) ◽  
pp. H260-H265
Author(s):  
A. C. Kralios ◽  
T. J. Tsagaris
Keyword(s):  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Systemic Arterial Pressure ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Work Index ◽  
Before And After ◽  
Ventricular Activation ◽  
Ectopic Activation ◽  
Activation Sequence

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.

Nonuniform transmural recovery of contractile function in stunned myocardium

1989 ◽  
Vol 257 (2) ◽  
pp. H375-H385 ◽  
Author(s):  
R. Bolli ◽  
B. S. Patel ◽  
C. J. Hartley ◽  
J. I. Thornby ◽  
M. O. Jeroudi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Recovery Of Function ◽  
Left Ventricular ◽  
Stunned Myocardium ◽  
Wall Thickening ◽  
Base Line ◽  
Doppler Probe ◽  
Group 2 ◽  
Systolic Wall Thickening ◽  
Group 1

With the use of an epicardial Doppler probe, systolic wall thickening was selectively measured in the inner, mid, and outer layers of the left ventricular (LV) wall in 16 conscious dogs undergoing a 15-min left anterior descending artery (LAD) occlusion followed by 7 days of reperfusion (REP). Under control conditions, percent thickening fraction (ThF) was significantly greater (P less than 0.01) in the inner layer [36.0 +/- 2.3% (mean +/- SE)] than in the mid (28.6 +/- 2.1%) or outer (21.3 +/- 2.2%) layers. During LAD occlusion, 11 dogs exhibited transmural dyskinesis (group 1), whereas 5 had transmural hypokinesis (group 2). In group 1, all layers exhibited comparable degrees of paradoxical systolic thinning during LAD occlusion. After REP, however, recovery was delayed in the inner compared with the mid and outer layers. At 2 h, ThF averaged 34.2 +/- 11.9% of base line in the endocardium vs. 61.7 +/- 16.2% in the midmyocardium and 51.0 +/- 12.3% in the epicardium (F = 4.29, P less than 0.002); similar differences were noted at 3 and 4 h. In the mid and outer layers, ThF returned to base-line values by 24 h, whereas in the inner layer it was still significantly depressed (P less than 0.05) at 24 h (77.3 +/- 5.1% of base line) and recovered by 48 h. The inner-to-outer ThF ratio was decreased (P less than 0.01) for 24 h after REP, indicating maldistribution of thickening in the "stunned" myocardium. In group 2, all layers exhibited hypokinesis during LAD occlusion. Again, recovery of function after REP was delayed in the endocardium compared with the other layers. This study demonstrates that after both severe ischemia resulting in dyskinesis and mild ischemia resulting in hypokinesis, REP is associated with slower recovery of function in the inner than in the outer layers. Thus myocardial "stunning" is a nonuniform phenomenon with maximal severity in the subendocardium.

Pre-Clinical Evaluation of a Novel, Pneumatic, Ventricular Assist Device (Medos® HIA-VAD®) under Pathophysiological Conditions

1997 ◽  
Vol 20 (7) ◽  
pp. 389-396 ◽  
Author(s):  
F.R. Waldenberger ◽  
B. Meyns ◽  
H. Reul ◽  
R. Eilers ◽  
W. Flameng
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Assisted Circulation ◽  
Wall Thickening ◽  
Base Line ◽  
Assist Device ◽  
Circumflex Artery ◽  
Group I ◽  
Group Ii

To evaluate a new cardiac assist system, the Medos® HIA-VAD®, we studied the effects of mechanical unloading on regional and global myocardial dysfunction. As a model for the regional temporary contractile dysfunction we chose an anesthetized, open chest preparation in sheep. We occluded the diagonal coronary artery for 15 minutes and reperfused for 90 minutes. Hemodynamic parameters and wall thickening were monitored. Unloading with the 60-ml Medos® HIA-VAD® was performed either during ischemia (group II) or during reperfusion (group III). The recovery of non-uniformity indicated by post-ejection wall thickening was significantly faster (p<0.05) in both groups if compared to the non-assisted group (group I) (all groups n=4). Recovery of systolic wall thickening in the postischemic region in group I was only 76±12%, while it was 103±11% and 92±11% in groups II and III, respectively (p<0.05). In a canine model of global left ventricular failure, we occluded the left anterior descending coronary artery for 20 min, and after 5 minutes of reperfusion, the circumflex artery for 45 min (group I, n=5). After 5 min of CX occlusion in group II we performed assisted circulation for 90 min with the 10-ml (n=5) and the 25-ml (n=5) Medos® HIA-VAD®. In group I, no dog survided, in group II, all survided 4 hours of reperfusion (n=10). Lactate at the end of the experiment was 1.1±0.9 mmol/L (10-ml) and 1.1±0.2 mmol/L (25-ml) (p>0.05 vs. base line). We conclude that the Medos® HIA-VAD® is a reliable assist device that enhances myocardial recovery and allows sufficient peripheral circulation in the case of cardiogenic shock.

Differential effects of postconditioning on myocardial stunning and infarction: a study in conscious dogs and anesthetized rabbits

2006 ◽  
Vol 291 (3) ◽  
pp. H1345-H1350 ◽  
Author(s):  
Nicolas Couvreur ◽  
Laurence Lucats ◽  
Renaud Tissier ◽  
Alain Bize ◽  
Alain Berdeaux ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Myocardial Stunning ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Segment Length ◽  
Wall Thickening ◽  
Area At Risk

Postconditioning, i.e., brief intermittent episodes of myocardial ischemia-reperfusion performed at the onset of reperfusion, reduces infarct size after prolonged ischemia. Our goal was to determine whether postconditioning is protective against myocardial stunning. Accordingly, conscious chronically instrumented dogs (sonomicrometry, coronary balloon occluder) were subjected to a control sequence (10 min coronary artery occlusion, CAO, followed by coronary artery reperfusion, CAR) and a week apart to postconditioning with four cycles of brief CAR and CAO performed at completion of the 10 min CAO. Three postconditioning protocols were investigated, i.e., 15 s CAR/15 s CAO ( n = 5), 30 s CAR/30 s CAO ( n = 7), and 1 min CAR/1 min CAO ( n = 6). Left ventricular wall thickening was abolished during CAO and similarly reduced during subsequent stunning in control and postconditioning sequences (e.g., at 1 h CAR, 33 ± 4 vs. 34 ± 4%, 30 ± 4 vs. 30 ± 4%, and 33 ± 4 vs. 32 ± 4% for 15 s postconditioning, 30 s postconditioning, and 1 min postconditioning vs. corresponding control, respectively). We confirmed this result in anesthetized rabbits by demonstrating that shortening of left ventricular segment length was similarly depressed after 10 min CAO in control and postconditioning sequences (4 cycles of 30 s CAR/30 s CAO). In additional rabbits, the same postconditioning protocol significantly reduced infarct size after 30 min CAO and 3 h CAR (39 ± 7%, n = 6 vs. 56 ± 4%, n = 7 of the area at risk in postconditioning vs. control, respectively). Thus, contrasting to its beneficial effects on myocardial infarction, postconditioning does not protect against myocardial stunning in dogs and rabbits. Conversely, additional episodes of ischemia-reperfusion with postconditioning do not worsen myocardial stunning.

Changes in regional myocardial function and external work in exercising dogs with ischemia

1993 ◽  
Vol 264 (1) ◽  
pp. H110-H116 ◽  
Author(s):  
S. Miyazaki ◽  
Y. Goto ◽  
B. D. Guth ◽  
T. Miura ◽  
C. Indolfi ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Left Ventricular ◽  
Time Difference ◽  
Wall Thickening ◽  
Stress Strain ◽  
External Work ◽  
Loop Area ◽  
Systolic Thickening ◽  
Exercise Induced ◽  
Systolic Wall Thickening

Changes in regional myocardial work of the nonischemic wall and left ventricular (LV) asynchrony of the nonischemic wall during exercise-induced ischemia were examined in seven conscious dogs instrumented with a micromanometer for LV pressure measurement and sonomicrometers for control and ischemic wall thickness and LV external short and long axes. Ischemia was produced during steady-state exercise by a pneumatic constrictor on the left circumflex coronary artery. Time difference between peak thickening of control (anterior) and ischemic (posterior) walls was measured as an index of LV asynchrony. LV pressure-wall thickness loop area of both the control wall (LVP-CW loop) and ischemic wall was calculated as an index of regional myocardial external work. With ischemia during exercise, peak LV pressure decreased by 11%, and time difference of peak thickening in the two walls increased, accompanied by marked deformation of the LVP-CW loop during early relaxation, which was related to protodiastolic thickening of the ischemic wall. Thus, despite a significant increase in percent systolic thickening during exercise, loop area of control wall was not enhanced. These changes of the LVP-CW loop were confirmed by calculation of stress-strain loop areas as an additional index of regional myocardial external work but having true dimensions of work. Stress-strain loop area in the control wall during ischemic exercise showed a similar value to that during control exercise, thereby confirming lack of compensatory increase. Thus, during exercise-induced ischemia, regional myocardial external work in the normal region does not increase despite an increase in systolic wall thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

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