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

Left ventricular hypertrophy due to aortic stenosis, hypertension and other forms of heart disease is associated with abnormalities of diastolic function. It is uncertain whether these changes are an inherent consequence of the hypertrophic process or represent additional pathologic factors. To investigate this issue, echocardiographic indexes of left ventricular early diastolic function in highly trained athletes were compared with those in age-matched normal control subjects. Athletes were equally classified into two groups: 11 swimmers who had a pattern of myocardial hypertrophy with normal wall thickness to dimension ratio and 11 power lifters whose wall thickness to dimension ratio was increased. The peak rates of left ventricular dimension increase and wall thinning in swimmers and power lifters were greater than in control subjects despite significantly higher left ventricular wall thickness and left ventricular mass index in the athletes. This increase in diastolic function indexes was associated with greater ventricular size and systolic performance. Normalization of the peak rate of dimension increase for end-diastolic dimension and adjustment of the peak rate of wall thinning for the fractional systolic thickening resolved any differences between groups. Thus, after the effects of ventricular size and systolic function were taken into consideration, diastolic function was normal in these subjects with considerable physiologic hypertrophy. This is in contrast to the findings in patients with hypertrophy associated with left ventricular pressure or volume overload, and suggests that abnormalities of diastolic function seen in pathologic hypertrophy are due to factors other than cardiac hypertrophy itself.
J Am Coll Cardiol 1985 Sep
PMID:Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy. 316 24

Studies of normal hearts have revealed a variety of intrinsic connective tissue structures that surround and interconnect myocytes and ventricular mural layers. Among these structures, springlike coiled perimysial fibers, arrayed parallel to myocytes in the interstitial space, have been described in papillary muscle and ventricle. To evaluate the role of the coiled perimysial fibers under perturbed conditions, rat ventricles were filled with barium-gelatin under different pressures and fixed, and then the myocardium was impregnated with silver to visualize the connective tissue. Ventricles were filled at 30, 70 and 100 to 120 mm Hg. The coiled perimysial fibers were studied for their orientation, stretch, integrity and relation to sarcomere length. The coils were noted to embed within the fibrous anulus and to knot into an umbilical-like mass at the apex, thus anchoring them at both ends of the ventricle. They underwent focal straightening even at 30 mm Hg, with generalized straightening and disruption at the highest pressure; changes were most pronounced in the midventricle. Sarcomeres were maintained below 2.2 micron at 30 and 70 mm Hg of cavity pressure in regions of coiled perimysial fiber stretch; only with fiber disruption at 100 to 120 mm Hg were sarcomeres significantly lengthened. Other findings included connective tissue disruption between ventricular wall layers that allowed slippage of myocytes and mural thinning. These observations suggest that coiled perimysial fibers may act as a buffer to protect myocytes from damage under the effects of high cavity pressure.
J Am Coll Cardiol 1988 Dec
PMID:The effects of acutely increased ventricular cavity pressure on intrinsic myocardial connective tissue. 319 55

In view of the paucity of reports describing symptoms of increased degree, and deterioration of left ventricular systolic function in patients with apical hypertrophic cardiomyopathy (apical HCM), two cases with congestive heart failure and progressive thinning of previously hypertrophied apical portions of the left ventricle are reported. These were among 13 patients observed from eight to 10 years. Case 1: A 56-year-old man was diagnosed as having apical HCM at the age of 49 years. Severe left ventricular hypertrophy and prominent ST-T changes were observed on ECG during his first admission. His left ventricular end-diastolic pressure (LVEDP) was 24 mmHg and a left ventriculo-gram revealed a decrease in the left ventricular cavity in the apex and marked hypertrophy of the apical wall. Moderate interstitial fibrosis without hypertrophy or disarray of myocytes was observed in a left ventricular endomyocardial biopsy specimen. In two episodes of cardiac arrest he was successfully resuscitated at the age of 50 years. At the age of 55 years, two-dimensional echocardiography revealed thinning and abnormal motion in the apical wall, and a defect in 201T1 accumulation was observed in the same region by perfusion scintigraphy. This patient was readmitted with a diagnosis of cerebral embolism at the age of 56 years. Cardiac catheterization revealed normal LVEDP (8 mmHg), and a left ventriculogram revealed an aneurysm in the left ventricular apex with normal major epicardial coronary arteries. He has been under treatment with antiarrhythmic medications, calcium antagonists and anticoagulants, and has become relatively asymptomatic. Case 2: A 69-year-old-man was diagnosed as having apical HCM after a complete evaluation, including cardiac catheterization, at the age of 59 years. His LVEDP was elevated (17 mmHg), and a left ventricular angiogram revealed marked hypertrophy localized to the apex. Ejection fraction was 64%. A left ventricular endomyocardial biopsy revealed interstitial fibrosis without hypertrophy of myocytes. Thereafter, he has been followed as a New York Heart Association functional class III to IV with occasional elevation of cardiac enzymes but without chest pain or acute changes in his ECGs. However, atrial fibrillation with complete right bundle branch block developed at the age of 60 years. Apical wall thinning and dyskinesis were diagnosed by 2D echocardiography and a defect in the 201T1 accumulation was observed at about 65 years of age. He was readmitted in severe cardiac failure at the age of 69 years, and he was diagnosed as having cardiac asthma with pulmonary capillary wedge pressure of 35 mmHg.(ABSTRACT TRUNCATED AT 400 WORDS)
J Cardiol 1988 Mar
PMID:[Advanced sequelae of apical hypertrophic cardiomyopathy: report of two cases with wall motion abnormalities]. 322 16

The authors describe the case of a girl who developed Friedreich's ataxia at, approximately, the age of 7, with evidence of cardiac involvement being detected by electrocardiography and echocardiography at a later date. Cardiac function was moderately impaired and remained unchanged for a number of years, during which a picture of hypertrophic left ventricle seemed to be firmly established. Later still, however, the cardiac situation shifted gradually toward a hypokinetic form of the disease, with a progressive thinning of the interventricular septum and posterior wall of the left ventricle, associated enlargement of the ventricular chambers and increasingly severe hypokinesia leading to repeated episodes of heart failure.
G Ital Cardiol 1988 Jul
PMID:Progression of hypertrophic into a dilated left ventricle in Friedreich's ataxia. 323 61

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.
J Cardiol Suppl 1988
PMID:[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction]. 325 3

Proton NMR imaging of myocardial ischemia without infarction requires the use of paramagnetic contrast agents. Even during the first few hours of infarction, imaging without contrast enhancement reveals only slight natural image contrast. Myocardial infarction, however, is much more readily detected during the first few days and weeks post coronary occlusion; this is due to a marked elevation in T2 during this time period. Chronic infarction, several months after the acute event, does not demonstrate altered signal intensity, but can be detected by visualizing myocardial wall thinning and aneurysm formation. Information regarding high energy phosphate metabolism can be acquired in vivo in ischemic animal preparations; preliminary data has demonstrated that it is possible to acquire similar information noninvasively in man. Development of this technique will eventually permit the study of pharmacological and mechanical interventions aimed at preserving myocardium in the ischemic heart. Exogenous labelling of myocardial tissue with carbon-13 permits the study of the effects of substrates on cellular metabolism. Ultimately, the technique of chemical shift imaging will provide a method of spatially resolving valuable metabolic information in the form of an NMR image. Eventually, with the gradual development of NMR technology, imaging and spectroscopy will become truly important clinical tools in the investigation of ischemic heart disease in man.
Can J Cardiol 1988 Apr
PMID:Evaluation of myocardial ischemia and infarction by nuclear magnetic resonance techniques. 328 14

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.
J Am Coll Cardiol 1988 Aug
PMID:Exercise training after anterior Q wave myocardial infarction: importance of regional left ventricular function and topography. 276 17

Bacterial vegetations involving the aortic valves of six patients were studied by scanning and transmission electron microscopy. The microorganisms isolated were Staphylococcus aureus--2, coagulase-negative staphylococcus--1, Streptococcus fecalis--2 and Streptococcus MG--1. The surface of the vegetations was usually amorphous. However, in areas where the surface of the vegetation was broken, myriads of microorganisms were seen. Transmission electron microscopy revealed bacteria embedded in an electron dense matrix in all vegetations despite the fact that they were negative on culture. Cell wall rupture was common. Thinning, and in some instances thickening, of the cell wall was also observed. The Streptococcus MG cells showed abnormal division with daughter cells being unable to separate. It is likely that the altered morphology of these bacterial cells is due to antibiotic treatment, however studies of an animal model of endocarditis are needed to dissect out the various possible contributions to these changes: host defenses; bacterial malnutrition in the depths of the vegetation; and antibiotic effect.
Can J Cardiol 1987 Sep
PMID:Ultrastructure of cardiac bacterial vegetations on native valves with emphasis on alterations in bacterial morphology following antibiotic treatment. 342 27

A 20-year-old woman whose echocardiograms showed a rare evolution from hypertrophic to dilated cardiomyopathy during a nine year observation period is described. This patient was initially diagnosed as having hypertrophic obstructive cardiomyopathy (HOCM) at the age of 12 years. Her echocardiogram showed marked thickening of the interventricular septum (IVS) and left ventricular posterior wall (LVPW), asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM). Chest radiography revealed a prominent left ventricular border and a cardiothoracic ratio of 0.52. At 18 years of age she experienced onset of palpitation during the 16th week of pregnancy. Her echocardiogram recorded in June 1980 revealed a thickened IVS and LVPW with resolution of the SAM and of the narrow cavity. At 20 years of age she became pregnant again and was admitted to our hospital for the third time at 24 weeks gestation. On admission her blood pressure was 122/60 and her pulse was 56, and moist rales were audible over both lung fields. Peripheral edema was noted. Chest radiography revealed moderate cardiomegaly, a cardiothoracic ratio of 0.66, and congestion of the pulmonary vasculature. An echocardiogram showed thinning of the IVS and LVPW with hypokinesis and dilatation of the cavity compatible with dilated cardiomyopathy (DCM). She delivered a boy on July 15th 1982 at 32 weeks gestation following which she developed marked congestive heart failure. She expired one month later. A chest radiograph made one day before death revealed marked cardiomegaly, a cardiothoracic ratio of 0.76, prominent pulmonary vasculature and a pleural effusion. Autopsy was refused; therefore the terminal DCM-like features were not clarified pathologically. However, the slow progression from HOCM to HCM during eight years and then rapid progression from HCM to DCM during four months was most impressive.
J Cardiol 1987 Jun
PMID:[Evolution of dilated cardiomyopathy from hypertrophic obstructive cardiomyopathy: a case report]. 344 76

Positron emission computed tomography (PET) is regarded an excellent technique for quantitative measurements. However, its accuracy is related to the spatial resolution of the system. The relation between myocardial wall thicknesses as measured by X-ray CT or MRI and the radioactivity as measured using PET was studied in 37 patients. 1. In patients with transmural infarction, the infarcted myocardium was imaged as a region of low radioactivity. However, the myocardium usually exhibited wall thinning, so that partial volume effects must be taken into account in evaluating the radioactivity. 2. In the infarcted regions, the regions of the low radioactivity tended to be larger than those of wall thinning. 3. There were cases with the regional low radioactivity without wall thinning in myocardial infarction and in hypertrophic cardiomyopathy. Because patients with myocardial infarction frequently had regional wall thinning, it seems necessary to correct partial volume effects for the infarcted regions which differ from the normal. It was concluded that, to estimate regional myocardial blood flow or metabolism using PET, it is necessary to supplement another morphological diagnostic method to evaluate myocardial wall thickness.
J Cardiol 1987 Dec
PMID:[Problems related to tracer concentration and wall thickness: pitfalls in positron CT diagnosis]. 350 33


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