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

Multidetector computed tomography for characterization of calcium deposits in reperfused myocardial infarction

2009 ◽  
Vol 50 (4) ◽  
pp. 396-405 ◽  
Author(s):  
M. Carlsson ◽  
P. C. Ursell ◽  
D. Saloner ◽  
M. Saeed
Keyword(s):  
Computed Tomography ◽  
Coronary Artery ◽  
Multidetector Computed Tomography ◽  
Left Ventricular ◽  
Remote Myocardium ◽  
Wall Thickening ◽  
Regional Wall ◽  
Infarction Size ◽  
Calcium Deposits ◽  
Systolic Wall Thickening

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.

Effect of superoxide dismutase and catalase on regional dysfunction after exercise-induced ischemia

1992 ◽  
Vol 263 (2) ◽  
pp. H392-H398 ◽  
Author(s):  
D. C. Homans ◽  
R. Asinger ◽  
T. Pavek ◽  
M. Crampton ◽  
P. Lindstrom ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Coronary Artery ◽  
Myocardial Stunning ◽  
Coronary Artery Stenosis ◽  
Left Ventricular ◽  
Artery Stenosis ◽  
Regional Myocardial Blood Flow ◽  
Wall Thickening ◽  
Regional Wall ◽  
Exercise Induced

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.

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 ◽  
...  
Keyword(s):  
Human Subjects ◽  
Left Ventricular ◽  
Dobutamine Infusion ◽  
Wall Thickening ◽  
Regional Wall ◽  
Normal Human

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 Isolated Left Ventricular Noncompaction in a Case of Sotos Syndrome: A Casual or Causal Link?

2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Patrizia Saccucci ◽  
Federica Papetti ◽  
Roberta Martinoli ◽  
Alessandro Dofcaci ◽  
Ursula Tuderti ◽  
...  
Keyword(s):  
Physical Examination ◽  
Causal Link ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Ventricular Wall ◽  
Sotos Syndrome ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Cardiac Evaluation ◽  
Chromosome 5Q35

A 16-year-old boy affected by Sotos syndrome was referred to our clinic for cardiac evaluation in order to play noncompetitive sport. Physical examination was negative for major cardiac abnormalities and rest electrocardiogram detected only minor repolarization anomalies. Transthoracic echocardiography showed left ventricular wall thickening and apical trabeculations with deep intertrabecular recesses, fulfilling criteria for isolated left ventricular noncompaction (ILVNC). Some sporadic forms of ILVNC are reported to be caused by a mutation on CSX gene, mapping on chromosome 5q35. To our knowledge, this is the first report of a patient affected simultaneously by Sotos syndrome and ILVNC.

Evidence for enhanced eNOS function in coronary microvessels during the second window of protection

2007 ◽  
Vol 292 (5) ◽  
pp. H2152-H2158 ◽  
Author(s):  
Song-Jung Kim ◽  
Xiaoping Zhang ◽  
Xiaobin Xu ◽  
Alice Chen ◽  
Joaquin B. Gonzalez ◽  
...  
Keyword(s):  
Ace Inhibitors ◽  
Calcium Ionophore ◽  
Left Ventricular ◽  
Wall Thickening ◽  
No Production ◽  
Ionophore A23187 ◽  
Nitrite Production ◽  
Hoe 140 ◽  
Enos Protein ◽  
Second Window Of Protection

Nitric oxide (NO) derived from endothelial NO synthase (NOS) (eNOS) has been identified as a trigger for the second window of protection (SWOP), but its role as a mediator during the SWOP is a matter of debate. Eighteen mongrel dogs were chronically instrumented to measure left ventricular function, coronary blood flow, and wall thickening. Myocardial preconditioning was induced by 10 min coronary artery occlusion. After 24 h of reperfusion (during the SWOP), the hearts were excised. Coronary microvessels were isolated and incubated in presence of 1) the endothelium-dependent agonists carbachol and bradykinin, 2) the calcium ionophore A23187, and 3) the angiotensin-converting enzyme (ACE) inhibitors enalaprilat and ramiprilat. Nitrite, a metabolite of NO, was measured. Under baseline conditions, nitrite production in microvessels from SWOP was 30% higher than that from normal (96 ± 4 vs. 74 ± 3 pmol/mg, P < 0.01, respectively). Nitrite production in response to carbachol, bradykinin, and A23187 was also enhanced in microvessels from SWOP ( P < 0.05). These enhanced responses were abolished by NG-nitro-l-arginine methyl ester (l-NAME) or the endothelial receptor-specific antagonists atropine and HOE-140. The level of eNOS protein in the SWOP myocardium was twofold higher than that in the non-SWOP myocardium. Nitrite production in response to the ACE inhibitors was greater in microvessels from SWOP. These effects were blocked by l-NAME, HOE-140, or dichloroisocoumarin (which inhibits kinin formation). We found that a brief ischemic episode induced delayed, enhanced NO production in coronary microvessels and an upregulation of eNOS protein. These findings suggest that eNOS is a mediator during the SWOP. The ability of ACE inhibitors to enhance NO release during the SWOP points to an additional clinical application for these drugs.

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