Cardiomyopathie idiopathische und erworbene

Doerr, Wilhelm; Roßner, J. A.; Dittgen, R.; Rieger, Peter; Derks, Harald; Berg, Günter

doi:10.1007/978-3-662-06213-5_1

Cited by 5 publications

(3 citation statements)

References 16 publications

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“…1975a and b;Schaper etal. 1978;Themann et al 1980) and have also been found in idiopathic cardiomyopathies (Bulloch and Pearce 1977;Doerr et al 1979;Knieriem 1978;Kuhn et al 1978 and1980;Kunkel et al 1978 and1980). The tissue examined in the present study shows that autolytic phenomena do not affect the structure of the cell contractile apparatus importantly, at least during the first 3 h post mortem.…”

Section: Discussionsupporting

confidence: 70%

Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium

Chuaqui¹,

Garrido

1982

Virchows Arch. A Path. Anat. and Histol.

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Destructive myofibrillar lesions, particularly degenerative fibrillolysis in hypertrophied hearts, were studied with the electron microscope in left ventricular myocardium samples obtained from autopsies with post mortem periods not exceeding 195 min. The contractile protein composition of these samples was determined electrophoretically. 18 cases were studied, grouped as follows: Group I, composed of 5 cases showing normal hearts which were employed in the determination of normal electrophoretic values. Group II: 10 cases with hypertrophic hearts, 1 of them showing contraction bands and decreased myosin, 6 others with fibrillolytic lesions of which 3 presented a decrease in myosin and 3 possessed normal myosin values. None of the cases showed a decrease in actin values. Group III was composed of 3 cases of hearts with normal weights that showed ultrastructural alterations of the myofibrils: 1 with myofibrillar disarray and normal electrophoretic values, 1 with incomplete contraction bands and normal protein values and 1 with focal myofibrillar disgregation and myosin decrease. It is concluded that in some cases of degenerative fibrillolytic lessions a decrease of myosin occurs. The method employed does not rule out that apparently normal actin and myosin values might be due to the presence of contractile proteins in a denatured state that does not affect their electrophoretic mobility.

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Section: Discussionsupporting

confidence: 70%

Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium

Chuaqui¹,

Garrido

1982

Virchows Arch. A Path. Anat. and Histol.

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“…Possibly those areas in a state of repair represented by a higher fatty acid uptake are zones with increased β‐oxidation at the level of the mitochondria. This is supported by electron microscopy, where in patients with dilated and hypertrophic cardiomyopathy the number of mitochondriae are elevated [39,40]. Contradictorally, Thies et al [41], using the same theoretical and mathematical theorem in eight young patients with DCM (age 0.2–18 years), were unable to demonstrate a significant higher fatty acid uptake, possibly due to the fact that the investigation was carried out in a predominantly pediatric population.…”

Section: Discussionmentioning

confidence: 96%

[¹²³I]‐phenylpentadecanoic acid uptake in patients with dilated cardiomyopathy

Miche¹,

Radzewitz²,

Notohamiprodjo

et al. 2002

European J of Heart Fail

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Background: The rate constant for global fatty acid influx (k ) was studied in 12 male patients with dilated cardiomyopathy 1 (DCM). Method: 10 normal subjects served as controls. 201-Thallium ( TI) and w Ix-phenyl-pentadecanoic acid (IPPA) were 201 123 administered during bicycle exercise under fasting conditions. Results: All patients showed non-homogeneous tracer uptake defects for TI and IPPA. k was significantly higher in DCM patients than controls. k showed significant inverse correlation between 201 1 1 cardiac index, left-ventricular ejection fraction, left-ventricular enddiastolic pressure and echocardiographic left-ventricular ejection fraction. Conclusion: We presume that an increased regional rate constant of IPPA influx into the myocardial tissue in patients with DCM reflects a compensatory mechanism of altered myocardium.

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“…Bei bekannter Ursache (hier: Adriamycin) ist unser Fall in Konsequenz eine sekundäre Kardiomyopathie. Da funktionell die Störung in einem systolischen Pumpfehler liegt, ist das Epitheton kongestiv berechtigt (8).…”

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Sekundäre kongestive Kardiomyopathie nach Adriamycin^*

Kaduk¹,

Seiler²

1977

Dtsch med Wochenschr

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Doxorubicin at a dose of 470 mg/m2 body surface, was administered to a 15-year-old boy with metastasising osteosarcoma. The cumulative dose caused severe "secondary congestive cardiomyopathy", which ended fatally, although the cumulative dose was below the recommended limit of 550 mg/m2. No other treatment for the tumour had been given. Postmortem examination revealed obliterative lesions in the intramural coronary vessels and electron-microscopy showed all the features of a cardiomyopathy at cellular level.

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Cardiomyopathie idiopathische und erworbene

Cited by 5 publications

References 16 publications

Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium

Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium

[¹²³I]‐phenylpentadecanoic acid uptake in patients with dilated cardiomyopathy

Sekundäre kongestive Kardiomyopathie nach Adriamycin^*

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Cardiomyopathie idiopathische und erworbene

Cited by 5 publications

References 16 publications

Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium

Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium

[123I]‐phenylpentadecanoic acid uptake in patients with dilated cardiomyopathy

Sekundäre kongestive Kardiomyopathie nach Adriamycin*

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Resources

About

[¹²³I]‐phenylpentadecanoic acid uptake in patients with dilated cardiomyopathy

Sekundäre kongestive Kardiomyopathie nach Adriamycin^*