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Biomedical subjects

P Mathes

Publications and source records attributed to P Mathes.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Hypertrophic cardiomyopathies (author's transl)].

Because of their rapidly changing hemodynamic inconstancy depending on many, sometimes competing, processes, hypertrophic cardiomyopathies present a clinical picture extraordinary among the cardiac diseases, with severely altered diastolic compliance of the left ventricle and a functional stenosis in the obstructive forms. They are of increasing importance for the doctor in hospital or general practive, particularly because they are among the very few diseases in which the usual cardiac therapy with digitalis or else the administration of sympathomimetics is contraindicated.

Atrial Fibrillation↗
PubMed1976

[Haemodynamic effect of dobutamine in cardiac failure (author's transl)].

Dobutamine, a new catecholamine with a positive inotropic action, was given by infusion to 9 patients with cardiac failure in a dosage of 5 and 7.5 mug/kg-min over a period of 15 minutes. An improvement of left ventricular function was proven by an increase of cardiac output by 33%, a reduction of end-diastolic pressure from 21 to 14 mm Hg, an improvement of left ventricular ejection fraction from 29 to 39% and of the mean circumferential fibre contraction velocity from 0.4 to 0.8 circ/s. The systolic aortic pressure increased by a mean of 14% (5 mug/kg-min) and 23% (7.5 mug/kg-min). However, the resistance of the systemic circulation decreased from 1858 to 1439 and 1444 dyn-s-cm-5. Cardiac frequency remained unchanged with a dosage of 5 mug/kg-min and increased by a mere 7 beats/min with a dosage of 7.5 mug/kg-min. There was no increased tendency for arrhythmia. Dobutamine thus appears to act relatively selectively on myocardial beta-1 receptors. Results so far indicate therapeutic success in patients with severe cardiac failure, particularly in the low-output syndrome.

Adult↗
PubMed1976

[Regional contraction of the left ventricle in congestive cardiomyopathy].

Regional analysis of ventricular angiograms obtained at diagnostic cardiac investigation was undertaken in 22 patients with congestive cardiomyopathy and 16 healthy subjects. Applying the concept of radial motion, directed towards the centre of the left ventricle, akinetic zones of 20 to 50% of left ventricle circumference were found in more than half the cases of congestive myopathy. The greater the area of regional abnormal motion, the greater the reduction in haemodynamic variables and left ventricular function. The clinical status of nearly all patients with large akinetic areas deteriorated in the subsequent period of observation (6-48 months, averaging 26 months). But in patients without additional abnormal regional wall motion the clinical condition remained stable. A large akinetic area in congestive myopathy indicates severe reduction in left ventricular function and is an unfavourable prognostic sign.

Adult↗
PubMed1976

[Clinical features and course of congestive cardiomyopathy of unknown aetiology (author's transl)].

Clinical, haemodynamic and angiographic findings in 50 patients with congestive cardiomyopathy were related to subsequent clinical course (mean observation period of 40 months). Ejection fraction and changes in mean pulmonary "wedge" pressure on ergometric exercise proved to be the most reliable criteria for judging left-ventricular function. During the period of observation 11 patients had died, in 15 the clinical state had deteriorated by one or two functional classes, and in 24 there had been no change. Patients with progressing disease differed from those clinically unchanged by having a smaller cardiac index, increased end-diastolic left ventricular pressure, higher pulmonary arterial pressure and smaller ejection fraction. Prognosis was no worse with atrial fibrillation than with sinus rhythm. Four of 13 patients with left bundle branch block died during the observation period and in seven the clinical state had deteriorated by one or two functional classes. The tested variables apparently have a good prognostic value.

Adolescent↗
PubMed1976

[Heart muscle after heart infarct. Function of surviving heart muscle following acute myocardial infarct].

In the initial phase of the infarction, there is a decrease of ventricular function due to loss of contractile activity. In addition, a negative effect of the paradoxical movement of the infarcted area on the hemodynamics of the ventricle is noted. The stiffening of the infarcted area in the early stage has a favorable influence on ventricular function, leading to a change in the elastic properties of the ventricle. The loss of ventricular compliance persists after the infarction, and its severity depends on the extent of myocardial destruction. In the non-compliant ventricle, the end-diastolic pressure rises without a proportionate increase in volume. Consequently, the ventricular function curve shows a shift downward and to the right, making it difficult to distinguish between the loss of contractile function or compliance in the heart in situ. Evaluation of the contractile properties of the surviving cardiac muscle in situ is, however, hardly possible due to the changed geometry and the additonal elastic elements functioning in series with the surviving muscle. To exclude these factors, a study of the contractile properties of the surviving cardiac muscle in the isolated state was carried out following experimental myocardial infarction in cats. By ligating several coronary branches, infarctions in the area of the left ventricle were caused; to avoid the ischaemic border zone of the infarction, right ventricular papillary muscles were studied. Haemodynamic investigations showed an increase in right ventricular end-diastolic pressure which persisted 6 weeks after infarction. As early as 48 hours but, more significantly 1 week after infarction, there was a decrease of actively developed force in the surviving cardiac muscle due to a lower rate of force development. The resting length tension curve of the surviving cardiac muscle after infarction showed no alterations; and 6 weeks following infarction, almost normal contractility parameters were observed. As a result of the infarction, a decrease in contractility in the surviving cardiac muscle is observed during the early stage, which regresses after complete recuperation.

Acute Disease↗
PubMed1976

Experimental myocardial infarction in the cat. I. Reversible decline in contractility of noninfarcted muscle.

The contractile state of the noninfarcted myocardium was examined in adult cats after myocardial infarction produced by ligation of several branches of the left coronary artery. At 2 days, 7 days, and 6 weeks after infarction, and after determination of intracardiac pressures, papillary muscles were exicised from the noninfarcted segment of the right ventricle and attached to a myograph for analysis of contractile function. One week after infarction there was a decline in actively developed force at Lmax, caused by a decrease in the rate of force development. In addition, the response to procedures that augment myocardial contractility, such as paired stimulation and increasing the frequency of electrical stimulation, was significantly depressed. Two days after infarction, changes were less significant, although similar in direction. Six weeks after infarction, developed force at Lmax had returned to normal values. The response to procedures augmenting contractility also had returned to normal. There appears to be a distinct, reversible loss of contractility in the remaining viable myocardium in the early phase after experimental infarction.

Animals↗
PubMed1975

[Contractility of the surviving myocardium following experimental infarct].

The contractile function of the non-infarcted myocardium was examined in adult cats following myocardial infarction produced by ligation of several branches of the LAD and circumflex coronary artery. Two and seven days following infarction, after determination of intracardiac pressures, papillary muscles were excised from the non-infarcted portion of the right ventricle and transferred into a myograph for analysis of contractile function. One week following infarction, force-velocity relations of the surviving myocardium showed a shift downward and to the left in comparison to sham-operated controls. At the same time, there was a decline in actively developed force at Lmax to be deserved, which appeared to be caused by a decrease in the rate of force development. Two days following infarction, similar changes were to be observed, although to a lesser extent. There appears to be a distinct loss of contractility in the remaining viable myocardium following experimental infarction.

Animals↗