Biomedical subjects

J Ort

Publications and source records attributed to J Ort.

At least 19 recordsLinked to original sources

PubMed2000

[Humoral profile of patients with severe aortic stenosis].

BACKGROUND: While the effect of neurohormones is often studied in congestive heart failure, their role in aortic stenosis needs to be elucidated. METHODS: 54 consecutive patients with symptomatic aortic stenosis without overt heart failure were studied at the age of 64.4 +/- 9.3 yrs with echocardiography, x-ray and catheterization. Levels of circulating atrial natriuretic factor endothelin-1, catecholamines, plasma renin activity, immunoreactive insulin and C-peptide were assessed, related to hemodynamic data and compared to those in 23 healthy controls, aged 59.2 +/- 12.8 yrs. RESULTS: Patients had significantly higher plasma levels of endothelin-1 (z-value 0.64 +/- 1.19, p = 0.019), atrial natriuretic factor (z-value 2.46 +/- 2.46, p < 0.001) and dopamine (z-value 0.91 +/- 2.33, p = 0.02). Levels of endothelin-1 and ANF positively correlated with mean (r = 0.631, p < 0.001) and wedged pulmonary artery pressures and with left atrial diameter index (r = 0.602, p < 0.001). Endothelin-1 levels correlated negatively with aortic valve area (r = -0.306, p = 0.041). No correlation was found between neurohumoral plasma concentrations and left ventricular mass index. CONCLUSIONS: In patients with symptomatic aortic stenosis without overt heart failure, elevated plasmatic levels of endothelin-1, atrial natriuretic factor and dopamine were documented. The increase of ET-1 levels is related to pulmonary hypertension and severity of the disease. Left ventricular hypertrophy is not related to neurohormonal levels. Neither circulating system renin-angiotensin nor noradrenaline are activated in these patients.

Adult↗

PubMed1994

[Amyloid light-chain amyloidosis with primary involvement of the cardiorespiratory system--2 case reports].

The authors describe the cases of two women suffering from AL amyloidosis with affection of the heart muscle in particular. In one of the patients there were also massive amyloid deposits in the lungs which is an exceptional finding. The observations confirm the adverse prognosis of amyloidosis, the rapid progression of the disease after the onset of symptoms of cardiac failure. The first cardial manifestation in both patients were palpitations. The first patient, but not the second one, had a myeloma confirmed on necropsy.

Amyloid↗

PubMed1993

[Clinical picture of various types of inferior myocardial infarcts. Clinico-electrocardiographic study].

In the submitted study the authors evaluate the relationship of the clinical course in patients with inferior myocardial infarction (AIM) in relation to the electrocardiographic (ECG) finding in standard and dextro-lateral leads. In a group of 96 patients (mean age 65 +/- 10 years, 66 men and 30 women) according to the ECG 38 had an isolated inferior AIM (group 1), 28 had signs of extension of the inferior AIM to the posterior wall of the left ventricle (group 2) and 30 patients in group 3 had an extension of the inferior AIM to the right ventricle, i.e. an infarction of the right ventricle. All three groups differed significantly as regards the extent of the AIM according to creatine kinase values (7.1 +/- 4.4 and 18.2 +/- 7.2 resp. and 24.8 +/- 11.6 resp.), as regards mortality (0 and 14% and 37% resp.). In group 2, contrary to the other groups, the significantly most frequent complication was pulmonary oedema (36%) and ventricular tachycardia (30%) and in group 3 the significantly most frequent complication was cardiogenic shock (30%) and advanced atrioventricular block (50%). The cause of death in these patients with infarctions of the right ventricle was cardiogenic shock (n = 6), cardiac rupture (n = 3) and electromechanical dissociation (n = 2). A total of 29 (30%) patients with inferior AIM were treated by temporary pacing: in group 1 21%, in group 2 14% and in group 3 57%. The prognosis of these patients was favourable in groups 1 and 2 (1 of 12 patients died) while in group 3 with infarctions of the right ventricle 9 of 17 patients died (p < or = 0.001). The authors found moreover that patients with precordial depression of the ST segment and inferior AIM have, as compared with patients without this depression, significantly higher creatine kinase values (12.5 +/- 5.5 vs. 5.2 +/- 1.3 mu kat; p < or = 0.001) and a higher general incidence of complications. Patients with inferior AIM are thus a non-homogeneous group from which we can differentiate, based on standard ECG examination and by recording right-sided thoracic leads, patients with an increased risk and start specific treatment in time.

Aged↗

PubMed1991

Investigation of human and rat inactive renin in plasma and kidney.

Under an initial interval of immobilization stress in rats, reciprocal changes of plasma active and inactive renin were observed, suggesting activation of circulating inactive renin. Molecular weight (MW) studies revealed that this activation might proceed via a MW shift from inactive renin with MW of 50,000 to active renin of MW 43,000. In a later interval of stress, under stimulated renin secretion, a lower MW form (38,000) of active renin was released into the circulation. This MW is close to that of active renin (39,000) found in rat kidney renin granules. In renin granules, equilibrated in fractions of 1.6 and 1.7 mol/L sucrose in discontinuous density gradient, trypsin-activatable renin activity formed 36 and 16% of total activity, respectively. In humans, under acute bicycle exercise, a lower MW form (39,000) of active renin was released into the circulation, while the content of inactive renin with MW in the range of 51,000-58,000 and at 47,000 did not substantially change. There was a slight decrease in circulating inactive renin passing through the kidney. The data suggest that, at least in rats, in vivo pathways for activation of inactive renin might exist, other than that proceeding before secretion from renin granules. Under the conditions of increased renin secretion, a lower MW form of active renin is mainly released into the circulation in both rats and humans.

Adrenal Medulla↗

PubMed1990