Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a naturally occurring model of congestive cardiomyopathy-round heart disease of turkeys, Ca2+ transport of isolated cardiac sarcoplasmic reticulum was evaluated at 1, 10, 28, and 56 days of age. Ca2+ binding in round heart disease birds was reduced to between 55% and 75% of values measured in age-matched commercial control turkeys (P less than 0.05 to less than 0.01). Similarly, Ca2+ uptake in round heart disease birds was reduced to between 52% and 87% of values measured in age-matched commercial control turkeys (P less than 0.05 and less than 0.01). Ca2+-stimulated ATPase values were similar in 1-, 10-, and 28-day-old round heart disease and commercial control turkeys. However at 56 days of age, when all round heart disease birds showed moderate to marked left ventricular dilatation. Ca2+-stimulated ATPase was reduced to 75% of control values (P less than 0.05). Depression of Ca2+ binding and Ca2+ uptake preceded the appearance of cardiac dilatation and may contribute to the pathogenesis of round heart disease. Depression of Ca2+-stimulated ATPase, present only after cardiac dilatation developed, appears to be secondary to cardiac failure. Sarcoplasmic reticulum function in round heart disease birds immunosuppressed by cyclophosphamide treatment (40 mg . kg-1 . d-1 for the first 4 days of age) was evaluated at 10 days of age. This treatment increased Ca2+ binding by 73% (P less than 0.05), and Ca2+-uptake by 58% (P less than 0.01) over values measured in untreated round heart disease birds. Reversal of the altered Ca2+ transport in sarcoplasmic reticulum by early immunosuppression supports the hypothesis that the immune system plays an integral part in the development of the congestive cardiomyopathy of round heart disease.
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PMID:Early alterations in the function of sarcoplasmic reticulum in a naturally occurring model of congestive cardiomyopathy. 645 87

This study examined inducibility of ventricular tachyarrhythmias in turkeys with and without naturally occurring dilated cardiomyopathy. Using a transvenously positioned electrode catheter, 32 cardiomyopathy and 12 control unsedated turkeys aged 2 to 4 months were studied by right ventricular endocardial extrastimulus testing at basic pacing cycle lengths of 200 and 170 ms with both 1 and 2 extrastimuli and burst pacing at progressively shorter cycle lengths (200 to 100 ms). Following study, a dilatation index (determined as the ratio of left ventricular endocardial and epicardial diameter at level of the apex-base midpoint) was utilized to assess the functional severity of cardiomyopathy. All control turkeys had a dilatation index less than 0.3. In cardiomyopathic turkeys, dilatation index was normal (less than 0.3) in 3/32, showed mild to moderate dilatation in 25/32 (0.3 to 0.6), and severe dilatation in 4/32 (greater than 0.6). Results showed no difference in right ventricular effective or functional refractory periods between control and cardiomyopathic turkeys. Control turkeys had no inducible ventricular tachyarrhythmias, but 16/32 cardiomyopathic turkeys (p less than 0.005) had inducible ventricular tachyarrhythmias, consisting most frequently of two beats of rapid ventricular tachycardia supervened by ventricular fibrillation. In the cardiomyopathic turkeys, inducible tachyarrhythmias occurred in 1/3 with normal dilatation index, in 11/25 with mild to moderate dilatation, and in 4/4 with severe dilatation. Thus, inducibility of ventricular tachyarrhythmias in cardiomyopathic turkeys is closely associated with increasing ventricular dilatation, but does not correlate with altered right ventricular refractoriness. This model may be suitable for studying the relationship between ventricular tachyarrhythmias and cardiomyopathy.
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PMID:Inducible ventricular arrhythmias in a naturally occurring model of cardiomyopathy. 648 34

Findings in 20 patients with congestive, in 14 with hypertrophic and in one with restrictive cardiomyopathy are described. In congestive cardiomyopathy, there predominated left ventricular dilatation and diffuse hypokinesis with decreased ejection fraction. The main criteria are reported for differentiating it from advanced diffuse ischaemic heart disease. More detailed characterization is presented of the type of asymmetric septal hypertrophy and of the systolic anterior motion of the mitral apparatus and the possible causes of this finding are discussed. In a patient with restrictive cardiomyopathy there predominated a symmetric thickening of the left ventricle, with diffusely decreased kinetics and increased density of all structures.
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PMID:Possibilities of two-dimensional echocardiography in cardiomyopathies. 653 93

The purpose of this study was to determine whether two-dimensional echocardiography (2DE) can differentiate ischemic myocardial disease (IMD) from dilated cardiomyopathy (DCM). The subjects consisted of six cases of IMD which showed left ventricular dilatation (LVDd greater than or equal to 60 mm) and diffuse abnormality of wall motion, but did not show obvious localized myocardial infarction or left ventricular aneurysm on 2DE, and 16 cases of DCM. Two cases of IMD had previous myocardial infarction, and five cases of DCM had cardiomegaly following myocarditis. A short-axis image of the left ventricle was recorded at the chordal and the papillary muscle levels. Each image was divided into 4 segments, which were comprised of the septum, anterior wall, lateral (posterolateral) wall, and posterior (posteromedial) wall. Regional wall motion abnormality with reference to systolic thickening was analyzed qualitatively in each segment. The results were as follows: In ECG findings in IMD group, only one case showed abnormal Q waves and five cases showed left ventricular hypertrophy (LVH) similar to intraventricular conduction defect. On the other hand, in DCM group seven cases showed abnormal Q waves and five cases showed LVH. Two cases of IMD had two-vessel disease and four three-vessel disease, respectively. Left ventricular ejection fraction by cine-angiography ranged from 0.10 to 0.39 (mean 0.24) in IMD group and from 0.22 to 0.42 (mean 0.36) in DCM group. Mean LVDd showed no significant difference between these two groups. Five cases of DCM showed marked left ventricular dilatation (LVDd greater than or equal to 75 mm), but there were no such cases in IMD group. B-B' step was recognized in only one case of IMD, though it was present in eight cases in DCM. In regional wall motion, incidence of asynergy such as akinesis or dyskinesis was higher in IMD group than in DCM group. Left ventricular asynergy was more serious in the posteromedial wall than the posterolateral wall at the same image in five cases of IMD. However, in 12 cases of DCM, the degree of asynergy was equal at the both walls. In conclusion, it is recommended to examine echocardiographically the extent of severe asynergy in the posteromedial and posterolateral walls in order to differentiate IMD from DCM.
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PMID:[Echocardiography of ischemic heart disease simulating dilated cardiomyopathy, with special reference to abnormal wall movement on the short-axis]. 664 20

To investigate the genesis of the third ( IIIs ) and fourth heart sounds (IVs), apical phonocardiograms were recorded simultaneously with pulsed Doppler signals of the mitral flow and interventricular septal (IVS) and left ventricular posterior wall (PW) echoes by M-mode echocardiography in 26 cases with the IIIs and 11 cases with the IVs. The following results were obtained: Cases with the IIIs were classified into the following three groups according to the time relationship between the IIIs and a rapid filling wave (D wave) of the mitral flow velocity pattern. IIIs -peak group: The IIIs occurred coincidently with the peak of the D wave in five healthy adolescents and in 12 cases with absolute left ventricular volume overload including mitral regurgitation (MR: eight cases), postoperative atrial septal defect (ASD: three cases) and ventricular septal defect (one case). IIIs -delay group: The IIIs occurred about 38 msec after the peak of the D wave in eight cases with relative left ventricular volume overload including congestive cardiomyopathy (CCM: three cases) and ischemic heart disease (IHD: five cases). IIIs -early phase group: The IIIs occurred about 35 msec before the peak of the D wave in a case with acute MR due to chordal rupture. In the IIIs -peak group, the IIIs coincided in time with the points of inflection (check points) of both the IVS and PW during rapid filling phase in three cases with MR of mild to moderate degree and one case of postoperative ASD. In the IIIs -delay group, the IIIs occurred simultaneously with either the check point of the IVS or PW in two cases with CCM and one case with IHD, and it occurred before the check points of both the IVS and PW in two cases with severe MR of IIIs -peak group and in a case with acute MR due to chordal rupture of IIIs -early phase group. Cases with the IVs were classified into following 2 groups according to the time relationship between the IVs and the atrial contraction wave (A wave) of the mitral flow velocity pattern. IVs-peak group: The IVs occurred coincidentally with the peak of the A wave in six cases with left ventricular hypertrophy including hypertrophic cardiomyopathy (five cases) and hypertension (one case). IVs-delay group: The IVs occurred about 33 msec after the peak of the A wave in five cases with left ventricular dilatation or dysfunction including old myocardial infarction (two cases), CCM (one case), postoperative ASD (one case) and aortic regurgitation (one case). There were two types of IVs in time relationship between the IVs and the check points of the left ventricular wall during atrial contraction phase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the mechanisms of the third and fourth heart sounds: with special reference to the phase analysis of mitral flow velocity pattern]. 667 90

When fed furazolidone, 700 ppm, with their mash, most turkey poults develop dilated cardiomyopathy characterized by gross left ventricular dilatation with thinning of both the left ventricular free wall and ventricular septum. Birds fed propranolol, but not digoxin, did not develop this cardiomyopathy. It is not known what pharmacologic property of propranolol conferred protection or if mammals would receive similar protection.
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PMID:Protection of turkeys against furazolidone-induced cardiomyopathy. 668 89

Newly hatched male White Pekin ducklings (n = 119) were allotted to 7 groups of 17 each and fed furazolidone (FZ) at dose levels of 0, 100, 250, 500, 750, 1,000, and 1,250 mg/kg of feed for 4 weeks. The frequency and severity of clinical signs of FZ toxicosis, including growth retardation, ascites, and mortality, were dose related. At necropsy, the affected ducklings had ascites, hydropericardium, and biventricular dilatation. The frequencies of cardiomyopathy, ascites, and mortality, respectively, for the several dose levels of drug were as follows: 0, 100, and 250 mg of FZ/kg of feed--0%, 0%, 0%; for the 500 mg/kg level--35%, 12%, 0%; for the 750 mg/kg level--100%, 53%, 18%; for the 1,000 mg/level--79%, 57%, 57%; and for the 1,250 mg/kg level--33%, 20%, 73%. Ducklings with FZ-induced congestive cardiomyopathy had decreased left ventricular free wall and ventricular septal thickness, increased left ventricular chamber diameter, increased left ventricular dilatation score, decreased absolute heart weight, and increased relative heart weight. Cardiac histopathologic changes were minimal; some ducklings had myocytolysis. Liver and lungs were congested. Furazolidone-induced cardiomyopathy in ducklings offers a model for studies of congestive cardiomyopathy in a species that is free from the hereditary cardiomyopathy ("round heart disease") seen in turkeys.
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PMID:Congestive cardiomyopathy induced in ducklings fed graded amounts of furazolidone. 682 29

Newly hatched male White Pekin ducklings (n = 92) were allotted to 2 groups of 46 each and fed 750 mg of furazolidone (FZ)/kg of feed either for 8 weeks (group 1) or for 4 weeks followed by 4 weeks of no FZ intake (group 2). Regression of FZ-induced toxicosis was observed in ducklings of group 2 after cessation of FZ consumption, as evidenced by decreased mortality, progressive decrease in ascites, and increases in body weight gains. Necropsy of 8-week survivors revealed decreased frequency and severity of ascites in ducklings of group 2. The severity of FZ-induced cardiac alterations also was diminished, with a decrease in left ventricular dilatation score and an increase in absolute heart weights in 8-week survivors in group 2. Further evidence of regression of FZ-induced congestive cardiomyopathy after cessation of FZ ingestion was gained from development of intermediate cardiac damage severity scores and frequency and severity of ascites at necropsy in ducklings (previously studied) examined after 4 weeks of FZ feeding, compared with those found in group 1 (FZ 8 weeks) or in group 2 (FZ 4 weeks, no FZ 4 weeks) of the present study. Furazolidone-induced cardiac disease in ducklings offers an attractive model for studies of the pathogenesis of congestive cardiomyopathy and cardiac failure.
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PMID:Furazolidone-induced congestive cardiomyopathy in ducklings: regression of cardiac lesions after cessation of furazolidone ingestion. 687 4

To assess the mechanism of mitral regurgitation in ventricular dilatation, 24 patients with dilated cardiomyopathy (13 with and 11 without mitral regurgitation) and 10 normal individuals were studied by two-dimensional echocardiography. Left ventricular dimensions and mitral ring diameters in systole and diastole were measured in the long-axis section, and systolic interpapillary muscle distance in the short-axis section. The results showed: Mitral ring diameter is increased in most patients with dilated cardiomyopathy. Neither increased ring diameter, reduced ring contraction, nor decreased interpapillary muscle distance determine the presence of mitral regurgitation. The only difference between those patients with and without mitral regurgitation was the degree of left ventricular dilatation (p less than 0.05).
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PMID:The mechanism of mitral regurgitation in dilated left ventricle. 688 27

In order to evaluate left ventricular function of dilated cardiomyopathy, 24 patients and ten healthy subjects were studied by exercise echocardiography. The patients with dilated cardiomyopathy were classified into 3 groups according to the presence or absence of mitral regurgitation and the severity of left ventricular dilatation: Group I was consisted of five cases with mitral regurgitation. Group II was consisted of seven cases without mitral regurgitation who had marked left ventricular dilatation, where the left ventricular end-diastolic dimension index (DdI) was greater than 46 mm/m2 and left ventricular end-systolic dimension index (DsI) was greater than 40 mm/m2. Group III was consisted of 12 cases without mitral regurgitation who had moderate left ventricular dilatation, where the DdI was less than 46 mm/m2 or DsI was less than 40 mm/m2. The ergometer exercise tests were performed for 3 min at 25 watts in a supine position. There was no significant differences of exercise-induced increases in heart rate, elevations of systolic blood pressure and increases of rate pressure product, respectively, between healthy subjects and each group of dilated cardiomyopathy. In healthy subjects, both DdI and DsI were unchanged on exercise. In Group I, DdI was unchanged but DsI decreased (p less than 0.02), thus percent fractional shortening of the left ventricle (delta D) was increased (p less than 0.05). In Group II, both DdI and DsI were unchanged. In Group III, DdI was increased (p less than 0.05) while DsI was unchanged, thus delta D was increased (p less than 0.02). These results suggested that the left ventricle is able to respond to exercise by its further dilatation (increase of preload) in mild to moderate dilated cardiomyopathy (Group III). On the other hand, in cases with marked left ventricular dilatation (Group II), the further dilatation is not induced. The same was true in dilated cardiomyopathy with mitral regurgitation (Group I), where the left ventricle had almost the same size as in Group II, although changes in DsI and delta D were not evaluated precisely because of the associated regurgitation.
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PMID:[Evaluation of left ventricular function in patients with dilated cardiomyopathy by exercise echocardiography]. 718 76


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