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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether modulation of systolic ventricular interaction influences right ventricular performance during right heart ischemia, the effects of septal ischemia and inotropic stimulation were studied in 15 dogs in an open chest preparation. Right coronary branch occlusions led to right ventricular dilation and free wall dyskinesia, reversed septal curvature and reduced left ventricular diastolic volume. In systole, the septum thickened but bulged paradoxically into the right ventricle generating an active but depressed right ventricular systolic pressure (28.9 +/- 5.5 to 22.1 +/- 4.5 mm Hg), with associated decreases in right ventricular stroke work (5.66 +/- 0.94 to 1.92 +/- 0.53 g.m/m2) and left ventricular systolic pressure (123 +/- 11 to 80 +/- 10 mm Hg). Septal ischemia induced systolic septal thinning, left ventricular dilation and decreased left ventricular systolic pressure (80 +/- 10 to 55 +/- 10 mm Hg) and stroke work. Although the extent of paradoxic septal displacement increased, there were further decrements in right ventricular systolic pressure (22.1 +/- 4.5 to 18.7 +/- 4.3 mm Hg) and stroke work (1.92 +/- 0.53 to 0.7 +/- 0.2 g.m/m2). Dopamine infusion augmented left ventricular free wall contraction and increased left ventricular systolic pressure (55 +/- 10 to 172 +/- 17 mm Hg) and stroke work. Although systolic septal thinning persisted, the extent of paradoxic septal displacement increased strikingly and, despite continued right ventricular free wall dyskinesia, right ventricular systolic pressure increased (18.7 +/- 4.3 to 39.6 +/- 6.2 mm Hg) as did right ventricular stroke work (0.7 +/- 0.2 to 7 +/- 1.6 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of left ventricular function and systolic ventricular interaction to right ventricular performance during acute right heart ischemia. 153 32

To determine whether the extent of left ventricular dysfunction and the degree of shape distortion can predict outcome in survivors of moderate-sized anterior Q wave myocardial infarction who are undergoing exercise training, these variables were measured by two-dimensional echocardiography before and after 12 weeks of a low level exercise training program starting 15 weeks after infarction in 13 patients (7 in group 1 and 6 in group 2) and 12 weeks apart in 24 matched control patients without training. By the end of training, the functional class score had increased in group 2 (from 2.25 to 2.67, p less than 0.005) but had not changed in group 1. Further discrimination of groups 1 and 2 was provided by an initial asynergy (akinesia or dyskinesia, or both) less than 18% or greater than or equal to 18%. Compared with group 1, group 2 had greater initial asynergy (32 versus 6%, p less than 0.001), expansion index (asynergic/normal endocardial segment length: 1.8 versus 1.6, p less than 0.025) and peak shape distortion index (12.2 versus 1.0 mm, p less than 0.005) but lower ejection fraction (43 versus 59%, p less than 0.05) and thinning ratio (asynergic/normal wall thickness: 0.61 versus 0.74, p less than 0.05). These variables did not change with training in group 1. However, in group 2, training caused significant increase in asynergy (from 32 to 40%, p less than 0.05), expansion index (from 1.8 to 2.0, p less than 0.01) and peak shape distortion (from 12.2 to 20.9 mm, p less than 0.05) associated with a decrease in thinning ratio (from 0.61 to 0.51, p less than 0.001) and ejection fraction (from 43 to 30%, p less than 0.005). Initial values for these variables were similar for corresponding control groups but did not change over the 12 weeks. Thus, patients with greater than or equal to 18% left ventricular asynergy on the initial echocardiogram showed more shape distortion, expansion and thinning before exercise training and developed further functional and topographic deterioration with training.
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PMID:Exercise training after anterior Q wave myocardial infarction: importance of regional left ventricular function and topography. 276 17

The prognosis of patients with acute myocardial infarction is related to the infarction size. We evaluated the ability of a clinical technique, two-dimensional echocardiography, to assess infarct size based on the extent of regional contraction abnormalities. Conscious closed-chest dogs with preplaced coronary snares underwent permanent coronary occlusion. The animals were studied by two-dimensional echo 20 min and 2 days after occlusion. The extent of myocardial contraction abnormalities (systolic wall thinning instead of normal systolic thickening) was correlated with the infarct size determined pathologically. Some dogs had pressure-induced left ventricular hypertrophy. Extent of regional contraction abnormalities demonstrated by two-dimensional echo correlated well with infarct size both early (20 min) (r = 0.92) and late (2 days) (r = 0.94) after permanent coronary occlusion. Dyskinesis extent modestly overestimated the infarct size. The relationship between dyskinesis and infarct size were similar in both normal and left ventricular hypertrophied hearts. We then undertook a study to assess the effects of coronary reperfusion on dyskinesis-infarct size relationships. Conscious, closed-chest dogs underwent 1-2 h of coronary occlusion followed by 2-10 days of coronary reperfusion. Significant regional dyskinesis was present after 1-2 h of occlusion and decreased by 50-60% of the occlusion value after 2 days of reperfusion without further change in extent of dyskinesis between 2 and 10 days of reperfusion. Of importance, however, was that there was no significant correlation between infarct size and extent of regional dyskinesis by two-dimensional echo after reperfusion, either after 2 days (r = 0.09) or 10 days (r = 0.29) of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late effects of coronary reperfusion on regional left ventricular function. Can infarct size be estimated noninvasively? 353 3

Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last drug-induced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
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PMID:Effect of repeated episodes of drug-induced ventricular dyskinesia on subsequent regional function in the dog: comparison with myocardial stunning produced by repeated coronary occlusions. 358 22

The relative time courses of early changes in myocardial metabolism and function during anoxia, global ischemia, and regional ischemia were compared in isolated rat hearts. Transmural anoxic wave front was determined with NADH fluorescence photography, and oxygen saturation of myoglobin and dynamic systolic wall thickening were measured with spectrophotometry of light transmitted through the left ventricular free wall. In all three treatments, anoxic wave front first appeared in the subendocardium and reached the epicardial half of the myocardium in 10 s, when oxygen saturation of myoglobin decreased by 50% and tissue ATP and creatine phosphate remained at aerobic levels. During this period, systolic wall thickening decreased gradually in anoxia and global ischemia, whereas a marked decrease in systolic wall thickening and appearance of dyskinesia (wall thinning) occurred in regional ischemia. Thus the early extension of anoxic wave front and metabolic changes are similar with all three treatments, and dyskinesia, observed only in case of regional ischemia, occurs when the inner half is ischemic or anoxic.
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PMID:Transmural anoxic wave front and regional dysfunction during early ischemia. 361 98

The purpose of this study was to investigate the relation between abnormalities of left ventricular (LV) wall thickening during systole in ischemic regions and the interaction of LV pressure and regional intramyocardial pressure. Wall thickness was measured in 10 open-chest dogs with ultrasonic dimension gauges. LV pressure, aortic pressure, and intramyocardial pressure in the subendocardium were measured with catheter-tip micromanometers. Regional ischemia was produced by occlusion of the left anterior descending coronary artery. During the control period, peak subendocardial pressure exceeded LV pressure by 44 +/- 6 mm Hg. With hypokinesia, defined as a 50% to 89% reduction of systolic wall thickening, peak subendocardial pressure exceeded peak LV pressure but to a lesser extent (15 +/- 1 mm Hg). During akinesia, defined as a 90% to 100% reduction of systolic wall thickening, there was less than 1 mm Hg difference between peak subendocardial pressure and peak LV pressure. During dyskinesia, defined as systolic thinning of the ischemic wall, peak LV pressure exceeded peak subendocardial pressure by 29 +/- 6 mm Hg. These observations indicate that regional changes of LV wall thickness characterized by hypokinesia, akinesia, and dyskinesia are associated with pressure gradients between the LV cavity and the LV wall that are compatible with the abnormalities of wall motion.
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PMID:Relation of intramyocardial and intracavitary pressure to regional myocardial asynergy in the canine left ventricle. 621 65

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

In 15 open-chest, anesthetized dogs, regional systolic wall thickening (% delta WT) was measured with sonomicrometry and regional blood flow was determined with tracer microspheres (7-10 micron) before and after various degrees of coronary artery narrowing were created with a hydraulic occluder. The stenoses were categorized into four groups by the effect on % delta WT, and the corresponding myocardial blood flow (MBF) was determined in four layers across the ventricular wall (layer 1: subendocardium; layer 4: subepicardium). In group 1, % delta WT decreased 44 +/- 10% and only layer 1 MBF was significantly reduced (-28%); in group 2, % delta WT decreased 77 +/- 8% and MBF was reduced in both layers 1 and 2 (-52% and -36%, respectively); in group 3, % delta WT decreased 104 +/- 3% and MBF was reduced in the three inner layers (layer 1: -65%; layer 2: -58%; layer 3: -34%); in group 4, % delta WT decreased 145 +/- 9% (systolic wall thinning) and transmural reduction of MBF was found (layer 1: -74%; layer 2: -68%; layer 3: -55%; layer 4: -29%). We conclude that (1) up to 75% reduction in systolic wall thickening may occur when perfusion to only the inner one-half of the myocardium is decreased; (2) akinetic wall motion may be observed when perfusion remains normal in the subepicardial one-fourth of the wall; and (3) dyskinesia (wall thinning) occurs when blood flow is reduced transmurally.
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PMID:Significance of regional wall thickening abnormalities relative to transmural myocardial perfusion in anesthetized dogs. 743 62

Lethal arrhythmias, including ventricular tachycardia and ventricular fibrillation, may occur in the absence of apparent morphological abnormalities. However, a recent study using magnetic resonance imaging (MRI) has suggested that localized, minor structural abnormalities of the right ventricle are responsible for right ventricular outflow tract ventricular tachycardia in a number of patients. We demonstrated regional wall thinning and systolic dyskinesia of the right ventricle by MRI in two patients with idiopathic ventricular fibrillation in whom other cardiac imaging modalities failed to show abnormalities. This finding implies that minor structural abnormalities do exist in patients with so-called idiopathic ventricular fibrillation.
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PMID:Localized right ventricular structural abnormalities in patients with idiopathic ventricular fibrillation: magnetic resonance imaging study. 883 58

Congenitally corrected transposition of the great arteries (CCTGA) is a rare and complex congenital anomaly characterized by atrial-ventricular (AV) discordance and ventricular-arterial discordance. Ventricular noncompaction (VNC) is a rare unclassified cardiomyopathy due to the arrest in intrauterine endomyocardial morphogenesis and it is characterized by numerous prominent trabeculations and intratrabecular recesses. We reported the case of a 47-year old female patient. When she was 35-year old an "isolated" CCTGA was diagnosed because of a heart murmur. Since then she attended periodically echocardiograms. She showed us 2 of them where right ventricle apical trabeculation was reported, without any others details. We performed a periodic evaluation in a patient still active, with a 6-month history of mild dyspnea occurring during exertion, no episodes of chest discomfort or palpitation. The ECG showed ectopic atrial rhythm, 83 bpm, normal QRS duration, QS complex in V1-V2 leads. The echocardiogram demonstrated: CCTGA, moderate enlargement and dysfunction of the right systemic ventricle, moderate to severe systemic AV valve regurgitation, severe thinning and dyskinesia of the basal segment of the septum, apical and mid-segments prominent and numerous trabeculations with deep intertrabecular recesses, better showed by color Doppler, in continuity with the ventricular cavity. This case presents some distinctive features: (1) the association between two rare congenital anomalies; (2) Striking right VNC, involving the apex and mid-segments, rarely described in literature; right VNC has been proposed according to the presence of 3 over 4 criteria proposed by Jenni et al. (Heart 86:666-671, 2001); (3) Severe thinning and dyskinesia of the basal segment of the septum, probably related to coronary artery abnormalities frequently described in CCTGA patients.
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PMID:Unusual association between "congenitally corrected transposition of the great arteries" and "noncompaction" of the right systemic ventricle. 1968 Jul 80


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