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

Young rabbits (1-2 months of age) inoculated with trypomastigote forms of the Colombia strain of Trypanosoma cruzi have been shown to develop cardiac pathological changes (together with parasitological and immunological alterations) which are very similar to those observed in the acute and chronic phases of Chagas' disease in man. The cardiac alterations in the acute phase are characterized grossly by slight cardiomegaly with dilatation of the right-sided chambers. Microscopically they are characterized by mild focal myocarditis. The chronic phase is characterized by moderate to marked cardiomegaly with hypertrophy and dilatation of both ventricular chambers. There is thinning of the apical region (apical aneurysm), particularly of the left ventricle. Focal myocarditis is seen microscopically with areas of myocytolytic necrosis, atrophic and hypertrophic myofibers, an inflammatory response predominantly composed of mononuclear cells and interstitial fibrosis. Cineventriculography in the left ventricle of rabbits during the chronic phase disclosed regional myocardial dysfunction, with typical apical systolic bulging. The pathogenesis of Chagasic cardiomyopathy is briefly discussed in the light of these findings. Our investigation has further shown that this animal model is particularly suitable for studies on on the mechanisms, pathology and treatment of Chagas' heart disease.
Int J Cardiol 1986 Mar
PMID:The evolution of experimental Trypanosoma cruzi cardiomyopathy in rabbits: further parasitological, morphological and functional studies. 351 79

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)
Adv Cardiol 1986
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.
J Am Coll Cardiol 1987 Jun
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

This investigation was undertaken to assess the prevalence of systolic dysfunction, left ventricular (LV) wall thinning and cavity enlargement in a large population of patients with hypertrophic cardiomyopathy (HC), and to determine the role of these conditions in the natural history of this disease. Of 217 consecutively studied patients with HC, most of whom were severely symptomatic, 197 (91%) had an LV ejection fraction of 50% or more and 20 (9%) had an ejection fraction of less than 50% as assessed with radionuclide angiography. Changes in LV wall thickness and cavity dimension were evaluated using serial M-mode and 2-dimensional echocardiography over an average follow-up of 3.6 years in 67 of the 217 patients (54 with ejection fraction of greater than or equal to 50% and 13 with ejection fraction less than 50%). A substantial decrease (at least 5 mm) in LV wall thickness was seen in 8 of the 13 patients (62%) with an ejection fraction greater than or equal to 50%, but in only 2 of the 54 patients (4%) with an ejection fraction greater than or equal to 50% (p less than 0.001). LV cavity dimension increased significantly over the period of follow-up in the 13 patients with depressed ejection fraction (from 44 +/- 5 to 49 +/- 7 mm, p less than 0.005); however, absolute cavity size remained normal (less than or equal to 52 mm or less) in 10 of these 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1987 Jul 01
PMID:Occurrence and significance of progressive left ventricular wall thinning and relative cavity dilatation in hypertrophic cardiomyopathy. 360 25

It is hypothesized that myocardium subjected to a 5 minute period of coronary occlusion and a 30 minute period of reperfusion has latent abnormalities that become overt when the reperfused myocardium is "challenged" by a subsequent coronary occlusion. This hypothesis is clinically relevant because reperfused myocardium is frequently subjected to recurrent ischemia, as in patients with unstable angina, vasospastic angina or recurrent thrombosis after initial coronary occlusion and thrombolysis. In 19 open chest dogs, the response of regional myocardial function to brief coronary occlusions was studied. Systolic wall thickening and diastolic thinning were measured using a specially developed miniature 5 MHz echocardiographic transducer fixed to the epicardium by suction. All 19 dogs underwent an initial "challenge" coronary occlusion (30 seconds). Thereafter, the control group (n = 8) underwent no intervention for 30 minutes, while the intervention group (n = 11) underwent 5 minutes of coronary occlusion followed by 30 minutes of reperfusion. All dogs were then subjected to a second "challenge" coronary occlusion (30 seconds). In the control group, responses to the second challenge occlusion were the same as to the first occlusion. In the intervention group, regional and global systolic function and myocardial perfusion after the 5 minute coronary occlusion intervention returned to baseline levels, but the response to the second challenge coronary occlusion was significantly different in the intervention group.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1987 Oct
PMID:Altered response of reperfused myocardium to repeated coronary occlusion in dogs. 365 54

To verify the role of infarct expansion (IE) in ventricular septal rupture (VSR) after transmural acute myocardial infarction (TAMI), topographic parameters were measured using tomographic imaging with two-dimensional echocardiography (2-D echo) and computer-aided analysis in four groups of patients: 8 patients with VSR (Group 1); 24 patients with TAMI but no mechanical complications (Group 2); 11 normal athletes (Group 3); 5 adults with congenital ventricular septal defect (Group 4). Measurements made on end-diastolic outlines of mid-left ventricular (LV) short-axis images included: LV asynergy (akinesis and/or dyskinesis), expansion index (asynergy/nonasynergy-containing endocardial segment length), thinning ratio (asynergic/nonasynergic wall thickness), and new indexes of regional shape distortion (RSD) by quantifying the deviation of the actual asynergic segment from the ideal asynergic arc constructed using the nearly circular nonasynergic contour. In Group 1, clinical IE (hypotension, congestive heart failure, no signs of new infarction) preceded detection of the VSR and portable 2-D echo showed the VSR associated with LV asynergy, marked IE, and RSD. Although Groups 1 and 2 had similar LV asynergy (28.7 vs. 26.9% LV) and ejection fraction (38.9 vs. 41.8%), Group 1 had higher expansion index (1.50 vs. 1.17, p less than 0.05), lower thinning ratio (0.54 vs. 0.67, p less than 0.005), and higher RSD parameters (e.g., peak distortion, Pk or maximum radial distance from the ideal arc, 19.3 vs. 3.9 mm, p less than 0.01; area of distortion, Ad, 7.4 vs. 1.1 cm2, p less than 0.05) than Group 2. Groups 3 and 4 had normal regional and global function and no evidence of expansion, thinning, or RSD. Thus, IE with marked diastolic RSD on an early 2-D echo after TAMI might identify patients at risk for VSR.
Clin Cardiol 1987 Nov
PMID:Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study. 367 96

Seven hundred fifty-two cases of instantaneous sudden cardiac death were studied. Alcoholic cardiomyopathy was found in 127 cases (16.9%), predominantly in men under age 50 (73%). The heart was enlarged, with an average mass of 441 +/- 8 g. Light microscopy revealed uneven thinning and atrophy of the cardiomyocytes, with fatty infiltration and development of fatty tissue around the vessels of the left ventricle and interventricular septum, up to the subendocardial areas. In the majority of cardiomyocytes, electron microscopy showed atrophy of the myofibrils, pronounced dilation of the sarcoplasmic reticulum, lipids in the cytoplasm, mitochondriosis and an increased number of lysosomes and alterations of the mitochondria. Unchanged cardiomyocytes were characterized by hypertrophy and numerous ribosomes, and had developed a granular endoplasmic reticulum. Also observed were interstitial edema, an enlarged cardiomyocyte-capillary space, thinning of the capillary walls, flattening of the endothelium and a plethora and aggregation of erythrocytes. Decreases in mitochondrial enzyme activity were studied by enzyme histochemistry. Analogous pathologic changes may be individually present in other types of myocardial disease, but the complex of changes is specific for alcoholic cardiomyopathy. The frequency of alcoholic cardiomyopathy among victims of sudden death suggests that alcoholic cardiomyopathy is a risk factor for sudden cardiac death.
J Am Coll Cardiol 1986 Jul
PMID:Alcoholic cardiomyopathy and sudden cardiac death. 371 41

A continuing theme in our laboratory has been the use of echocardiographically-measured systolic myocardial wall thickening to demonstrate and evaluate the consequences of regional myocardial ischemia. This presentation focuses on two areas: the immediate mechanical consequences of induced myocardial ischemia in two experimental models: canine and human; the correlation between persistent regional myocardial dysfunction and morphologic infarction after sequences of coronary artery occlusion and reperfusion. Many experiments using animal models have demonstrated that acute myocardial ischemia produces almost immediate replacement of normal systolic myocardial wall thickening by systolic thinning. Less is known about the immediate mechanical response of human myocardium to acute ischemia. This was studied in 5 open-chest humans undergoing various cardiac operations. Wall thickening was continuously displayed by a 7 MHz M-mode echocardiographic transducer coupled to the epicardium by suction to maintain constant position. Coronary flow velocity was displayed by a pulsed Doppler device coupled to an epicardial coronary artery by suction. Ischemia was induced by the surgeon who manually occluded the coronary artery with a soft-tipped Kitner dissector or vascular forceps for 30 seconds. It was found that cessation of coronary flow was accompanied by reductions in normal systolic thickening but systolic thinning or expansion only rarely occurred. In contrast, when the identical techniques were used in 5 dogs, systolic thinning always occurred immediately after coronary arterial occlusion. This suggests that there are important species differences between canine and human myocardium in the immediate mechanical response to myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Can J Cardiol 1986 Jul
PMID:Transient myocardial ischemia: experimental echocardiographic demonstration and evaluation of myocardial contraction abnormalities. 375 77

To determine left ventricular (LV) structural and functional changes induced by ultraendurance exercise training, M-mode LV echograms and Doppler recordings of LV inflow velocity in 26 triathletes and 17 normal subjects were studied. All triathletes trained 20 to 40 hours/week in swimming, cycling and running for more than 2 years. Structurally, triathletes had normal LV systolic and diastolic cavity dimensions, but increased wall thickness (1.05 +/- 0.26 vs 0.80 +/- 0.27 cm in normal subjects, p less than 0.001), increased relative wall thickness, or h/R ratio (0.41 +/- 0.10 cm vs 0.33 +/- 0.11 cm in normal subjects, p less than 0.001), and increased LV mass (226 +/- 60 vs 143 +/- 54 g in normal subjects, p less than 0.001). LV mass correlated closely with mean exercise blood pressure during an 8-hour exercise test in 14 triathletes (r = 0.88). Systolic function at rest was similar in both groups, with no differences in fractional shortening or end-systolic stress. Diastolic LV function measured by digitized M-mode echo was similar in normal subjects and triathletes, with no differences in peak rates of cavity enlargement and wall thinning by echocardiogram. In contrast, the Doppler-derived ratio of early-to-late LV inflow velocities was slightly increased in triathletes (p less than 0.05). It is concluded that ultraendurance training produces a physiologic pattern of moderate pressure overload LV hypertrophy, in proportion to the hemodynamic load imposed during prolonged exercise. Unlike the abnormal hypertrophy of systemic hypertension, early diastolic function remains normal in the triathlete heart.
Am J Cardiol 1986 Oct 01
PMID:Left ventricular structure and function by echocardiography in ultraendurance athletes. 376 22

The ability of magnetic resonance imaging (MRI) to detect and localize healed myocardial infarction (MI) was assessed. Seventeen consecutive patients with healed MI assessed by biplane contrast ventriculography underwent MRI using oblique imaging planes. Seven normal subjects underwent MRI as controls. In each patient, ventriculography identified regional wall motion abnormalities. MRI, performed with a 0.15-Tesla resistive magnet and oblique imaging planes relating to the left ventricle, detected zones of regional wall thinning conforming to the wall motion abnormalities localized by ventriculography in 16 patients. In these patients, adjacent areas of intact myocardium were identified in areas shown by ventriculography to be normal. The left ventricular wall thickness at the site of MI was significantly less than adjacent noninfarcted myocardium (p less than 0.001) and normal hearts (p less than 10(-6)). The ratio of the thickness of the infarct to adjacent normal wall averaged 0.40 (range 0.22 to 0.62). MRI could differentiate healed MI from adjacent noninfarcted myocardium and normal hearts.
Am J Cardiol 1987 Jan 01
PMID:Assessment of left ventricular wall thickness in healed myocardial infarction by magnetic resonance imaging. 381 50


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