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V Regitz

Publications and source records attributed to V Regitz.

23 records · Page 2Linked to original sources
PubMed1985

[Histologically detectable myocarditis in patients with impaired left ventricular function].

In patients with impaired left ventricular function in whom dilated cardiomyopathy is initially suspected after performance of comprehensive diagnostic studies, histologic evidence of myocarditis or status-post myocarditis is being documented with increasing frequency since the systematic use of endomyocardial biopsy has been incorporated into the work-up. This investigation was undertaken to analyze the histologic, clinical, hemodynamic and immunologic findings in these patients to delineate possible relationships between histologically-documented myocarditis and dilated cardiomyopathy. Incidence of histologically-documented myocarditis. In our patient population, 41 of 150 patients with impaired left ventricular function, the etiology of which had been unknown, histologic evidence of myocarditis was documented. In seven of eight in whom active myocarditis was diagnosed at initial biopsy, after a mean follow-up period of two years the histologic findings were consistent with dilated cardiomyopathy. In similar groups of patients comparable incidences of myocarditis have been reported by Parrillo et al. in 19 of 100 (19%) and Fenoglio et al. in 34 of 135 patients (25%). A higher incidence has been reported by Zee-Cheng et al. in 22 of 35 patients (63%). Accordingly, pooled data indicate that the overall incidence of histologically-documented myocarditis was 30% in 528 patients initially suspected to have dilated cardiomyopathy. The variances in the incidence reported by the respective authors may be attributable to differences in the histologic definition of myocarditis, number of biopsies obtained, size of the patient population and the epidemiologically-related incidence of viral disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1985

[Dilated cardiomyopathy: characterization by clinical and hemodynamic findings].

Dilated cardiomyopathy, a disease of the heart muscle of unknown origin, is characterized by impaired systolic function and dilatation of the left and right ventricles. In the Federal Republic of Germany, there are an estimated 4000 to 5000 new cases reported yearly [40]. Pathologic-anatomic studies have demonstrated that, in addition to an extent of dilatation of all heart chambers dependent on the stage of the disease, up to 60% of those who die can be found to have intracardiac thrombi [37]. Specific histologic changes are absent [34]. Disturbances of the microcirculation, a defect of autonomic innervation and biochemical alterations have been postulated as possible causes [7, 33, 35]. Circulating and bound antibodies against myocardial antigens and pathologic cellular immunoreactions have been reported in association with both myocarditis and dilated cardiomyopathy; this, in turn, has led to the hypothetical assumption of a secondary immunopathogenesis after myocarditis [6, 9, 12, 18, 26, 33]. Clinical and hemodynamic findings encompass a wide spectrum. With a mildly impaired ejection fraction to values between 40 and 54%, in our patients there was an associated enlargment of the end-systolic and end-diastolic ventricular volumes to 60 and 115 ml/m2 (upper normal limits 35 and 95 ml/m2), respectively. Those with increasing degrees of left ventricular function impairment to ejection fractions less than 40%, had additionally pathologic elevation of the filling pressures. In patients with marked impairment of the ejection fraction to values of less than 25%, cardiac output was reduced and systemic and pulmonary vascular resistances elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMedDate not supplied

Identification of human myocard proteins separated by two-dimensional electrophoresis.

N-Terminal sequencing, internal sequencing and amino acid analysis were used to identify twelve proteins of the human myocard two-dimensional gel electrophoresis (2-DE) pattern. Amino acid analysis was shown to be a powerful tool in addition to sequencing. The identification of a disease-associated N-terminally blocked protein by internal sequencing was not successful. The twelve identified proteins are the basis of a human myocard 2-DE database.

Amino Acid Sequence↗
PubMedDate not supplied

Mitochondrial damage during myocardial ischemia.

The effects of 3 hours of ischemia and 1 hour of reperfusion on biochemical, physiological and ultrastructural parameters were studied in 12 dogs. In the ischemic subendocardium without reperfusion, mitochondrial losses of adenine (ATP + ADP + AMP) and pyridine (NAD + NADH) nucleotides far exceeded those observed in whole tissue. Adenine nucleotide translocator (ANT) was severely inhibited and seemed to be a sensitive indicator of a lesion of the inner mitochondrial membrane. Postischemic reperfusion led to a slight loss of adenine and pyridine nucleotides from the reversibly damaged subepicardium and to an enormous loss from the irreversibly damaged subendocardium. The washout of nucleotides from irreversibly damaged areas caused the negative para-Nitro Blue Tetrazolium ( pNBT ) staining of the infarcted tissue. Diagnosis of cell death with pNBT failed after the occlusion period without reflow because pyridine, although lost from the mitochondria, was still present in the tissue. In reversibly injured areas, mitochondrial function and ultrastructure were restored after reperfusion, although a significant nucleotide loss was found in the tissue. These studies suggest that mitochondrial ultrastructure and function may play a key role in cellular viability during recovery from ischemia.

Adenine Nucleotides↗