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Biomedical subjects

U Baandrup

Publications and source records attributed to U Baandrup.

At least 73 records · Page 4Linked to original sources
PubMed1986

The myocardium in epileptics.

The main purpose of this investigation was to examine by quantitative methods if pathological fibrosis could be found in the myocardium of epileptics. The investigation was retrospective and included 23 epileptics and 30 controls who were age- and sex-matched with the epileptics. No difference was found between epileptics and the control group as far as cellular infiltration, single myocyte necrosis, basophilic cell degeneration, and fresh bleeding were concerned. Fibrosis of the myocardium was measured quantitatively by point counting. The fibrosis was approximately 6% of the muscle mass in both groups. In conclusion, no structural difference in the myocardial composition was found between epileptics and the control group.

Adult↗
PubMed1986

Aggressive long-term antihypertensive therapy with pinacidil does not cause regression of cardiovascular hypertrophy in the spontaneously hypertensive rat.

After dosage titration from the age of 1 month to the age of 3 months, spontaneously hypertensive rats (SHR) were treated with pinacidil 10 mg/kg daily until the age of 6 or 12 months. Morphometric data were obtained from the treated SHR as well as from untreated age-matched SHR and normotensive Wistar-Kyoto rats (WKY) at these two developmental stages. Heart:body weight ratios and media:lumen ratios for resistance vessels were determined. Vessels obtained from the mesenteric region were investigated on a myograph. Vessels from heart, kidney and lung were investigated by morphometric analysis of histological sections, only specimens from 12-month-old rats were used. In SHR no effects of either ageing or treatment were detectable, although their blood pressure had been effectively held at normotensive levels throughout the life of the treated animals from the age of 3 months. With the exception of the media index of the pulmonary vessels, which was not statistically different from treated or control SHR, the WKY morphological parameters were significantly lower. In conclusion, pinacidil normalized blood pressure without complications, but this did not affect SHR cardiovascular structure. It is suggested that development of this strain-specific enlargement can only be modified if blood pressure is kept at hypotensive levels, or if the effect of a hitherto unidentified causative factor is antagonized by more-specific pharmacological treatment.

Animals↗
PubMed1986

Endomyocardial biopsy in children with cardiac hypertrophy.

Transvascular right ventricular endomyocardial biopsy was carried out on three boys with severe hypertrophic hearts. There were no complications, but technically the use of the thin-walled, long introducer-sheath (available for the child-size bioptome) was rather troublesome because of its tendency to kink. Light-microscopy was helpful in diagnosing hypertrophic cardiomyopathy and possible endocardial fibroelastosis in two cases and in excluding eosinophilic myocarditis in the third case. Concealed storage disease (amyloidosis) was excluded and therefore the use of experimental cytotoxic therapy--with potential adverse effects--was avoided. A more stable sheath material ought to be developed to prevent untoward incidents during biopsy procedures in children.

Adolescent↗
PubMed1986

Chronic anthracycline cardiotoxicity: haemodynamic and histopathological manifestations suggesting a restrictive endomyocardial disease.

Of 38 patients referred with suspected cardiotoxicity after administration of antineoplastic drugs, 11 patients with signs of manifest or latent anthracycline cardiotoxicity were selected for heart catheterisation with endomyocardial biopsy. Ultrastructural abnormalities of the myocytes with myofibrillar loss and cytoplasmic vacuolation were present in most patients and these findings were more pronounced in biopsy specimens from the left ventricle. Surprisingly, light microscopy showed considerable fibrous thickening of the endocardium in 10 of 11 patients, primarily in the left ventricle. These morphological findings together with the echocardiographic and the haemodynamic data suggest that chronic anthracycline cardiotoxicity is a restrictive endomyocardial disease. The biochemical mechanisms responsible for endocardial fibrosis are unknown, but drug induced damage to the endocardium, possibly mediated via hormonal or humoral agents, may feature in the initial phase of the toxic process. The present observations contribute toward the understanding of the pathophysiology of human anthracycline cardiotoxicity.

Adult↗
PubMed1986

Clinical and non-invasive assessment of anthracycline cardiotoxicity: perspectives on myocardial protection.

A series of 38 patients with solid tumours (N=29) and haematological malignancies (N=9) and with suspicion of cardiotoxicity (CTX) due to antineoplastic drugs was studied. The series comprised 22 females and 16 males (mean age 52 years). The patients were examined clinically by ECG, chest X-ray and echocardiography. Seventeen patients were classified as having moderate or severe chronic CTX; 16 patients developed either arrhythmias shortly after the administration of chemotherapy (acute CTX) or arrhythmias and/or signs of myocardial dysfunction (without overt congestive heart failure) at a later date, after chemotherapy had been suspended (latent CTX). In 5 cases the suspicion of CTX could not be confirmed. Weak and non-specific symptoms such as unexplained tachycardia or coughing at night should alert the clinician and result in ECG control and further non-invasive cardiological investigations (including radionuclide angiocardiography) before additional anthracycline is administered. Chest X-ray is a very insensitive method with respect to early diagnosis of chronic CTX; in cases of doubt heart catheterization with endomyocardial biopsy should be carried out to obtain a reliable estimate of the extent of morphological damage. As anthracycline CTX may present without prominent clinical symptoms or as latent disease, one should be aware of potential precipitating factors such as volume load (during i.v. chemotherapy), surgical trauma and general anaesthesia and alcohol abuse. Further effects to lessen CTX should be made, using supposed cardio-protective substances in randomized clinical trials. Promising research on coenzyme Q10 and carnitine may usher in a new era in the prevention of anthracycline cardiotoxicity.

Adolescent↗
PubMed1985

Myocardial changes in rats with lithium-induced uraemia.

The possible effects of lithium on myocardial morphology were studied at the light-microscopic level in three different rat models: (i) rats with chronic renal failure due to lithium administration for 8-16 weeks after birth, (ii) normal, adult rats treated with lithium for 16 weeks, and (iii) new-born rats exposed to lithium in their prenatal life. Morphological changes were found in 57% of the male rats with lithium-induced uraemia after lithium administration for 16 weeks postnatally. The changes comprised myocytic degeneration and necrosis associated with infiltration of lymphocytes, histiocytes and plasma cells. This morphological picture is different from the myocardial changes associated with chronic renal failure. Male rats with chronic uraemia after withdrawal of lithium 8 weeks postnatally showed no myocardial changes after 16 weeks. Also, male rats with normal renal function had no myocardial changes after 16 weeks on lithium, but these rats had a significantly lower plasma level of lithium than the lithium-uraemic rats (0.8 vs. 1.4 mmol/l). It is suggested that myocarditis was a consequence of persistent high plasma levels of lithium maintained in the lithium-uraemic rats and that cardiotoxic effects of lithium may be potentiated by concomitant renal failure.

Animals↗
PubMed1985

Familial right ventricular dilated cardiomyopathy.

Cardiomyopathy of unknown cause occurred in three of six siblings. The course of the illness was marked by life threatening supraventricular and ventricular arrhythmias, sinoatrial block, atrioventricular block, and embolism (in one patient). The disease was characterised by right ventricular dilatation. Two of the three patients died aged 32 and 48. No new cases of the disease were found when a further 33 family members from three generations were investigated.

Adult↗
PubMed1985

Evidence for hyperplasia in mesenteric resistance vessels of spontaneously hypertensive rats using a three-dimensional disector.

Cellular dimensions in mesenteric resistance vessels from 10 spontaneously hypertensive rats and 10 Wistar-Kyoto rats have been determined using a random volume with an unbiased counting rule as the counting unit (the disector). With this method, vessels first were mounted on a myograph. Media thickness (spontaneously hypertensive rats, 11.3 micron; Wistar-Kyoto rats, 8.6 micron; P less than 0.01), lumen diameter (spontaneously hypertensive rats, 178 micron; Wistar-Kyoto rats, 194 micron; P greater than 0.1), and maximum active wall tension response (spontaneously hypertensive rats, 3.2 N/m; Wistar-Kyoto rats, 2.5 N/m; P less than 0.05) were determined. After fixation, serial sections normal to the long axis of the smooth muscle cells were made. In each vessel, the disector was a defined volume of the vessel wall (volume ca. 25 X 10(3) micron3) which was contained in about eight of these sections. The number of nuclei within the disector was counted using an unbiased, three-dimensional counting rule. On the basis that cells were mononuclear (an assumption that was tested), the ratio of this number divided by disector volume equaled the numerical cellular density. Measurement of the fraction of media taken up by smooth muscle cells then gave mean cell volume (spontaneously hypertensive rats, 563 micron3; Wistar-Kyoto rats, 615 micron3; P greater than 0.1). From the myograph measurements, the number of cells per unit length (spontaneously hypertensive rats, 10.4/micron; Wistar-Kyoto rats, 7.4/micron; P less than 0.05) and maximum force production per cell (spontaneously hypertensive rats, 5.1 microN; Wistar-Kyoto rats, 5.7 microN; P greater than 0.1) could then be calculated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Long-term coenzyme Q10 therapy: a major advance in the management of resistant myocardial failure.

Coenzyme Q10 (CoQ10) treatment, orally administered as 100 mg daily dose, was initiated in a series of patients with advanced heart failure in an open, controlled design. They were all showing an insufficient response to classical therapy with diuretics and digitalis. Twelve patients with various causes of heart failure, classified clinically by echocardiography (ECHO), (12/12), and heart catheterization with endomyocardial biopsy, (10/12), were followed prospectively for a mean period of seven months. Serial assessments: Clinical examination (with questionnaire), ECG, chest X-ray, ECHO, systolic time intervals (STI) and blood levels of CoQ10 were performed. With a mean latency period of 30 days, eight out of 12 patients (67%) showed definite clinical improvement. Subjectively, the patients felt less tired, their general activity tolerance increased and dyspnoea at rest disappeared. There were obvious signs of decreased right-sided stasis (hepatic congestion). The heart rate fell significantly, and the heart volume (chest X-ray) decreased in the eight responders (although n.s.). A significant reduction in the left atrial size (ECHO) was registered, suggesting a reduced preload of the left ventricle, Furthermore, a significant decline in the PEP/LVET ratio (STI) was indicative of an improved myocardial performance. Preliminary CoQ10 withdrawal results showed severe clinical relapse with subsequent improvement on CoQ10 reinstatement, supporting the interpretation that treatment of these patients corrected a myocardial deficiency of CoQ10 and increased contractility. Hence CoQ10 appears to be an effective therapeutic agent in advanced cases of heart failure. This is an attractive circumvention of the traditional principles of therapy: supporting the myocardium directly by ameliorating a supposed underlying mitochondrial dysfunction (exhausted bioenergetics).

Adolescent↗
PubMed1984

Fatal mumps myocarditis.

A case of fatal mumps myocarditis in a 38-year-old male is reported. The disease started with orchitis, and severe cardiac symptoms developed within 1 1/2 month. The patient died 5 months later from congestive heart failure. The possible interrelation between late stages of viral myocarditis and dilated (congestive) cardiomyopathy is emphasized.

Adult↗
PubMed1984

Hypertrophic cardiomyopathy in combination with juvenile amaurotic idiocy. Chance or fundamentally related findings?

Hypertrophic cardiomyopathy and juvenile amaurotic idiocy (one of the ceroid lipofuscinoses ) were diagnosed in a 29 year old man. This combined finding may be one of pure coincidence, but hypertrophic cardiomyopathy like changes of the myocardium are known to occur in Friedreich's ataxia and lentiginosis . The occurrence may, therefore, indicate some fundamental interrelation.

Adult↗
PubMed1984

Cardiomyopathy in western Denmark.

A retrospective study was carried out to assess the incidence of cardiomyopathy in western Denmark (Jutland and Funen) (population 2 798 000) during a two year period (1980-81). The WHO/ISCF classification was strictly followed, and rigid criteria for exclusion and inclusion of patients were adopted. Thus cases in which specific heart muscle disorders (myocarditis, alcoholic heart disease, hypertension etc) were merely suspected were excluded. Forty one patients had dilated cardiomyopathy (overall incidence 7.3/10(6) population/year) and 20 hypertrophic cardiomyopathy (overall incidence 3.6/10(6) population/year). In men aged 40-59 years the occurrence of dilated cardiomyopathy was 23.4/10(6) population/year. Only one case of Löffler's endomyocardial disease was diagnosed during the study period. Since the investigation was retrospective and was a study of diseased persons and not a population, and since a specific set of criteria for exclusion and inclusion was rigidly applied, the results represent the minimum frequency of these diseases.

Adolescent↗
PubMed1983

Spontaneous dissecting aneurysm of the renal arteries. A case and a review of the literature.

A case of dissecting aneurysm of the renal arteries is presented. The patient suffered from an intractable subarachnoid bleeding and the kidneys had been selected for transplantation. One kidney was never transplanted, the other was transplanted and rejected after few days. Dissecting aneurysms were present in the main artery and its major ramifications in both kidneys. Many investigators have claimed that dissecting aneurysm and fibromuscular dysplasia of the renal artery are different stages of but one disease. A review of the accumulated literature on dissecting aneurysm of the renal artery reveals, however, that this disorder shows a preponderance of middle-aged men, whereas fibromuscular dysplasia of the renal artery affects adolescent girls. It is concluded that the two disorders of the renal artery most likely represent different vascular diseases.

Aortic Dissection↗