Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
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PMID:[Advanced sequelae of apical hypertrophic cardiomyopathy: report of two cases with wall motion abnormalities]. 322 16

Chronic, rapid ventricular pacing produces congestive heart failure in the dog. Using echocardiography, the features of developing heart failure were analysed and the capacity of this model for recovery was assessed once pacing had been discontinued. Fifteen dogs were studied; nine were paced at 250 beats/min (bpm) to severe heart failure (5.0 +/- 1.8 weeks) and six served as sham controls. In the paced animals at severe heart failure, two-dimensional echocardiography demonstrated a significant increase in diastolic cross-sectional cardiac area (from 11 +/- 3 to 16 +/- 2 cm2, p less than 0.05), associated with a marked fall n area ejection fraction (54 +/- 8 to 21 +/- 8%, p less than 0.05), and significant left ventricular wall thinning (from 6.0 +/- 0.7 to 4.7 +/- 0.9 mm, p less than 0.05). In addition, significant increases in heart rate (77 +/- 7 to 126 +/- 13 bpm, sinus rhythm; p less than 0.05), respiratory rate (41 +/- 13 to 80 +/- 20 cycles/min, p less than 0.05), and body weight (21 +/- 1 to 24 +/- 3 kg, p less than 0.05) were noted. Serum sodium fell (146 +/- 3 to 140 +/- 8 mmol/L, p less than 0.05), while blood urea nitrogen (6 +/- 2 to 10 +/- 2 mmol/L, p less than 0.05) and creatinine (86 +/- 12 to 101 +/- 15 mmol/d, p less than 0.05) increased. Recovery was characterized by rapid improvement such that all measured parameters normalized by 1 week, except for cross-sectional cardiac area which remained dilated up to 4 weeks (14 +/- 3 cm2, p less than 0.05 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery from heart failure: structural and functional analysis in a canine model. 322 85

The late radiation response of the heart is of concern because of many reports of heart disease following radiation therapy of thoracic tumors. This study was done because of the clinical relevance of the pathophysiology of cardiopulmonary irradiation and because the heart is a good model for late effects of vasculoconnective tissue due to its lack of acutely responding parenchymal cells. Thoracic irradiation of adult beagle dogs including the heart and one third of the lung volume produced an early response in the heart at 1 and 3 months which consisted of an increase in left ventricle and septal wall thickness, decreased left ventricle ejection fraction, increased heart rates, intraventricular conduction disturbances and a high probability for pericardial effusion at 3 months. Radiation doses were 36, 44, or 52 Gy given in 4 Gy fractions in 4 weeks. Premature atrial contractions, paroxysmal atrial tachycardia, sustained atrial tachycardia and atrial fibrillation occurred at all dose levels. Evidence suggests that both early and late responses were due, at least in part, to direct injury to the cardiac microvasculature. The later effects appeared to be enhanced by injury to the lung. The early response appeared to resolve in 6 to 9 months, after which there was thinning of the myocardium at higher doses and resolution of pericardial effusions. At 12 months, elevations in right atrial pressure, but not pulmonary wedge pressure, were suggestive of right-sided congestive heart failure. Pulmonary hypertension was also present at 12 months presumably due to partial lung irradiations, and may have exacerbated right-sided congestive heart failure. The radiation injury may continue to increase with time leading to serious deficits in cardiopulmonary function. The functional studies may aid in predicting late effects and evaluating residual injury.
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PMID:Canine cardiomyopathy after whole heart and partial lung irradiation. 338 19

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.
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PMID:[Evolution of dilated cardiomyopathy from hypertrophic obstructive cardiomyopathy: a case report]. 344 76

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.
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PMID:Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study. 367 96

Echocardiographic evaluation of 42 patients with sarcoidosis disclosed 13 patients (group A) with abnormalities compatible with sarcoid heart involvement such as thickening or thinning of the septum (eight patients), pericardial effusion (four patients), and increased end-diastolic dimension of the left ventricle with decreased systolic function (three patients). The remaining 29 patients (group B) were diagnosed as having normal echocardiograms. The clinical data revealed no statistically significant difference between the groups regarding age, sex, chest x-ray stage, activity, and previous heart disease. Group A patients had older clinical onset of the disease (52 vs 83 months; p less than 0.05) and higher incidence of ECG abnormalities than group B patients. There were no statistically significant differences between the groups regarding two-dimensional echocardiographic internal dimensions of both ventricular chambers. The radionuclear right ventricular ejection fraction was low in both groups and the left ventricular ejection fraction was depressed in group A patients (p less than 0.01). As observed in pathologic studies, the septum is a target structure which can be characterized echocardiographically. Screening suspected sarcoid heart disease involvement is important to characterize patients with a relatively high risk of clinical cardiac abnormalities such as complete atrioventricular block, ventricular arrhythmias, congestive heart failure, and sudden death.
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PMID:Echocardiographic evaluation of patients with systemic sarcoidosis. 401 69

Clinical and morphologic findings are described in two patients with congenital hypoplasia of portions of both right and left ventricular free walls in the absence of associated coronary or valvular heart disease. One, a 61 year old man who had never had clinical evidence of cardiac dysfunction, died suddenly and unexpectedly. The second, a 55 year old woman, died of progressive, eventually intractable congestive heart failure of 29 months' duration. Although at least 22 necropsy patients have previously been reported to have "parchment-like" thinning of portions of the right ventricular free wall, only one patient has previously been described with such thinning of portions of both right and left ventricular free walls. The spectrum of right or right and left ventricular wall congenital hypoplasia is a broad one, with nearly half of described patients dying of congestive heart failure in the 1st year of life and the other half reaching adulthood with or without manifestations of cardiac dysfunction.
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PMID:Congenital hypoplasia of portions of both right and left ventricular myocardial walls. Clinical and necropsy observations in two patients with parchment heart syndrome. 743 1

In the past, hypertensive heart disease was the principal cause of congestive heart failure, but currently ischemic heart disease is the major etiologic factor. In the last 20 years, the role of myocardial infarction (MI) and the subsequent alteration in ventricular architecture of the infarcted and noninfarcted myocardium have become increasingly associated with a phenomenon known as ventricular remodelling. This process consists of left ventricular wall thinning in the infarction area, ventricular chamber dilatation, and compensatory hypertrophy of the noninfarcted portion of the myocardium. This article describes the pathophysiologic transformation that begins with MI and ventricular remodeling and ends in congestive heart failure.
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PMID:The pathophysiologic process of ventricular remodeling: from infarct to failure. 771 50

A double-blind placebo-controlled study to determine the acute hemodynamic and cardiac mechanical effects of the quinolinone derivative OPC-18790 was performed in 12 patients with New York Heart Association class III or IV congestive heart failure. Simultaneous echocardiographic, Doppler, and invasive hemodynamic studies were performed before and after a 6-hour intravenous infusion of drug at 2.5, 5.0, or 10.0 micrograms/kg/min or of placebo. OPC-18790 (mean dose 5.9 +/- 3.5 mg) caused significant increases in left ventricular (LV) ejection fraction (15% +/- 4% vs 23% +/- 5%; p < 0.05) and cardiac index (1.7 +/- 0.4 vs 2.5 +/- 0.6 L/min/m2; p < 0.05) and a rightward and upward shift in the stress-shortening relation. LV end-diastolic volume and heart rate were unchanged. LV filling and posterior LV wall thinning rates from digitized M-mode echocardiographic studies (0.49 +/- 0.16 vs 0.75 +/- 0.21 cm/sec and 2.0 +/- 0.9 vs 3.0 +/- 1.4 cm/sec, respectively; both p < 0.05), transmitral deceleration time (67 +/- 24 vs 81 +/- 19 msec, p < 0.05), and atrial filling fraction (31.0% +/- 11.2% vs 38.9% +/- 13.9%, p < 0.05) increased with OPC-18790 infusion. Despite a significant decrease in pulmonary capillary wedge pressure (28 +/- 9 vs 18 +/- 10 mm Hg) there was no change in the velocity-time integral of early diastolic filling (53 +/- 12 vs 59 +/- 22 cm), suggesting improved LV relaxation. Hemodynamics and parameters of LV function were unchanged in the 3 patients receiving placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a novel inotropic agent (OPC-18790) on systolic and diastolic function in patients with severe heart failure. 798 96

We assessed the therapeutic efficacy of a low-dose combination of metoprolol and captopril given orally to C3H/Hej mice that developed dilated and hypertrophied hearts after being inoculated with the encephalomyocarditis virus. Mice were randomly assigned to one of six 8-week oral regimens: 1 mg/kg/day of metoprolol (group 1); 10 mg/kg/day of metoprolol (group 2); 1.2 mg/kg/day of captopril (group 3); 12 mg/kg/day of captopril (group 4); 1 mg/kg/day of metoprolol plus 1.2 mg/kg/day of captopril (group 5); or distilled water (control group). Group 4 exhibited a significantly lower survival rate and body weight than the control group (p < 0.01). Survival rates and body weights were similar in groups 1, 2, 3, 5, and the control group. Low-dose metoprolol plus captopril is superior to low-dose metoprolol, high-dose metoprolol, and low-dose captopril with regard to heart weight and the heart weight/body weight ratio. The left and right ventricular cavity dimensions as well as myocardial necrosis, calcification, and fibrosis were less severe in groups 4 and 5 than in the control group. The left ventricular free wall showed significantly more thinning in group 4 than in the control group (p < 0.01). Our results show that the administration of low-doses of metoprolol and captopril given in combination was effective in this animal model of congestive heart failure and was associated with a reduction in biventricular cavity dimensions and myocardial necrosis.
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PMID:Low-dose combination therapy with metoprolol and captopril for congestive heart failure in mice. 811 Jun 23


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