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Biomedical subjects

W Bleifeld

Publications and source records attributed to W Bleifeld.

At least 199 records · Page 11Linked to original sources
PubMed1976

[Significance of the size of an acute infarct for left ventricular haemodynamics (author's transl)].

Acute infarct size was estimated from serial determinations of creatine-kinase (CK) activity. In 15 patients the infarct size was obtained post-mortem, using nitro-blue-tetrazolium stain. There was good correlation between the two measurements (r = 0.98). The relationship between the calculated infarct size and haemodynamic values was obtained in 50 patients (end-diastolic pulmonary arterial pressure [PAEDP], cardiac output, stroke volume, stroke volume/filling pressure of left ventricle [SVI/PAEDP]). On average there was a tendency towards impaired left ventricular haemodynamics with increasing infarct size. Among the survivors the infarct size (51 g) was significantly less (P less than 0.05) than that of those who had died (83 g). PAEDP at 24 mm Hg was significantly higher in those who died than in the survivors (17 mm Hg), cardiac index was 2.95 l/min-m2 in the survivors compared with 2.14 l/min-m2, while SVI/PAEDP was 2.4 ml/m2-mm Hg in the former and 0.9 ml/m2-mm Hg in the latter. However, in individual cases the infarct size sometimes did not correlate with haemodynamic values. Taking into account infarct size and haemodynamics, four classes could be distinguished: (a) infarct size less than 65 g with good haemodynamics (PAEDP less than 18 mm Hg, normal cardiac index); (b) infarct size greater than 65 g with PAEDP greater than 18 mm Hg and markedly reduced cardiac index). Only 10% of those a to c had previously had infarcts, compared with 60% of those in class d (infarct less than 65 g, PAEDP above 18 mm Hg). Small infarcts with markedly impaired haemodynamics thus indicate that there has been previous damage to remaining myocardium.

Acute Disease↗
PubMed1976

[Changes of left ventricular transverse diameter and of contractility after haemodialysis (author's transl)].

In 26 patients (8 women, 18 men; mean age 47 +/- 3 years) who participated in a regular dialysis programme twice weekly the left ventricular diameter, the mean velocity of fibre shortening, the ventricular wall thickness, and the muscle mass were determined echocardiographically. Left ventricular muscle mass (187 +/- 13 g), left ventricular posterobasal wall thickness (14,7 +/- 0,6 mm) and septal thickness (16,4 +/- 0,8 mm) were pathologically increased due to chronic pressure and volume overloading. After an average dialysis time of 12 hours the body weight was reduced by 2,6 +/- 0,4 kg (+ 1,0 to -7,8 kg). The left ventricular transverse diameter changed from 55,3 to 50,2 mm (P less than 0,001) which correlated with a decrease of the enddiastolic volume from 160 +/- 11 to 125 +/- 10 ml (P less than 0,01(. Despite increased cardiac frequency and unchanged diastolic and systolic pressure no significant increase of the mean velocity of fibre shortening (0,93 +/- 0,06 vector 1,13 +/- 0,09 circ/s) occurred. The results show that loss of fluid during haemodialysis led to a significant decrease of the enddiastolic transverse diameter and the enddiastolic left ventricular volume. However, dialysis does not lead to an increase of the mean velocity of fibre shortening as a parameter of improved contractility.

Adult↗
PubMed1976

[Idiopathic hypertrophic subaortic stenosis in aortic valve disease-diagnosis using echocardiography].

In three patients with valvular aortic disease in addition isiopathic hypertrophic subaortic stenosis (IHSS) was proven by echocardiography. From the clinical standpoint the dynamic subvalvular stenosis was not supposed in all cases. IHSS was echocardiographically characterized by asymmetrical septum hypertrophy and systolic anterior movement of the anterior mitral leaflet. Isolated aortic valve insufficiency was found in two patients, and combined stenosis and insufficiency in one patient. Mitral leaflet fluttering - indicative of aortic valve insufficiency - was observed in two patients. The identification of the dynamic subvalvular stenosis in patients with valvular aortic disease is important for the therapeutical approach. Echocardiography is very suitable for the diagnosis of this combined heart disease.

Adult↗
PubMed1975

[Echocardiographic criteria of asymmetrical hypertrophy of the ventricular septum without outflow tract obstruction (author's transl)].

Asymmetrical septal hypertrophy (ASH) without outflow tract obstruction is a genetic variant of idiopathic hypertrophic subaortic stenosis (IHSS). Without difficulty and risk echocardiography can distinguish both diseases. Comparison in 33 patients with ASH but no outflow tract obstruction and in 29 with IHSS revealed following identical findings: (1) excessive hypertrophy of the ventricular septum when compared with the posterior wall of the left ventricle (asymmetrical septal hypertrophy); (2) decreased systolic motion of the septum; (3) slowed early diastolic closure of the anterior mitral leaflet; (4) relatively small end-diastolic and systolic diameter of the left ventricle. But the important distinction was that, while in IHSS there was a systolic forward movement of the anterior or both mitral leaflets, this not recorded in patients with ASH without outflow tract obstruction. The posterobasal portion of the left ventricle is thickened in patients with IHSS, due to the outflow tract obstruction.

Adolescent↗
PubMed1975

[Diagnostic criteria of idiopathic hypertrophic subaortic stenosis in the echocardiogram(author's transl)].

Idiopathic hypertrophic subaortic stenosis (IHSS) is morphologically characterized by ventricular septal hypertrophy. It is asymmetrical because there is no corresponding hypertrophy of the posterior wall of the ventricle. The proportion between septal thickness and posterior wall thickness is more than 1.2. In addition, the anterior mitral leaflet moves towards the ventricular septum during the ventricular systole. Finally, the aortic cusps may close prematurely, even during ventricular systole, if there is a marked outflow-tract obstruction. The thickness of the septum and posterior wall, as well as the movement of the mitral and the aortic valves, can be easily registered by the echocardiograph. IHSS is, therefore, more easily diagnosed by this non-invasive method than by any other method. The echocardiogram demonstrates (1) asymmetrical septal hypertrophy, (2) anterior movement of the anterior and frequently also the posterior mitral leaflet in midsystole, (3) partial or complete closure of the aortic valve in mid-systole, (4) relatively small end-diastolic and systolic diameters of the left ventricle, (5) delayed early-systolic closure movement of the anterior mitral leaflet in the sense of a functional mitral stenosis, (6) decreased systolic septal movement.

Adult↗
PubMed1975

[Influence of a streptokinase-induced fibrinolysis on the extent of the acute experimental myocardial infarction (author's transl)].

In 17 unaesthetized dogs several side branches of the left descending coronary artery were ligated. The ST-segment elevation in the epicardial ECG ascended to 22 mV after 5 min and to 19 mV after 20 min. Aortic pressure, left ventricular enddiastolic pressure, heart rate and hemostasiological parameters (thrombin-time, thrombin-coagulase-time, reptilase-time, plasma-fibrinogen, staphylococcal clumping test) did not change significantly. 20 min after the beginning of coronary occlusion, the vessels were reopened. When ST-segment elevation had disappeared, a controlled fibrinolytic therapy (Streptokinase 1.5 Mega I.E. in 30 min, later on 0.75 Mega I.E./h) was induced. When an effective fibrinolysis could be demonstrated by the hemostasiological parameters, the same vessels were occluded again. Now the hemodynamic parameters too did not change significantly, but the ST-segment elevation was significantly diminished for more than 50% compared with simple ligation. A control group, which only got the solvent of the streptokinase, showed the same ST-segment elevation. This effect, induced by streptokinase is ascribed to fibrinogen degradation products and a diminution in the amount of fibrinogen which cause an improvement of microcirculation.

Animals↗
PubMed1975

[Hemodynamic compensatory mechanisms of impaired left ventricular contraction in coronary artery disease (author's transl)].

The effect of chronic coronary insufficiency on the hemodynamics, the geometry and muscle mass of the left ventricle were studied in 30 patients and compared to 13 controls. In these patients the cardiac output was normal in spite of impaired contractility and left ventricular wall movement. The impaired cardiac performance was compensated by 1. hypertrophy and 2. dialatation of the left ventricle. In one-vessel disease of the the coronary arteries left ventricular muscle mass was modestly, but not significant increased. Hypertrophy decreased from +20% in one vessel disease to +10% in three vessel disease. In contrast, left ventricular dilatation increased from +23% in one vessel disease to 43% in two vessel disease and to 70% in patients with sclerotic lesions in three vessels. Left ventricular dilatation seems to be the main hemodynamic compensatory mechnism resulting in a relative increase of the pump function of the heart compared to non dilated hearts. However, dilatation leads in the end-phase to left ventricular failure. By increased wall tension in the presence of impaired coronary blood flow dilatation bears the risk of deterioration of left ventricular function.

Adult↗
PubMed1975

Creatine kinase release in acute myocardial infarction: correlation with clinical, electrocardiographic, and pathological findings.

Creatine kinase (CK) release curves were analysed in 40 patients with acute myocardial infarction. Three groups could be identified. Group A (duration of CK release less than 30 hours) comprised 15 patients whose CK release was completed within 22.8 hours. In these patients chest pain was noted on the first hospital day and necropsy in three showed a homogeneous myocardial infarction. Group B (duration of CK release greater then 30 hours) comprised 16 patients who had a significantly longer CK release time of 42.2 hours (P less than or equal to 0.05). Their chest pain persisted for two to three days and pathological examination in five patients showed a heterogeneous composition of the infarcted myocardium. Group C comprised nine patients who had a second rise of serum CK. This was always associated with chest pain. It reflected an extension of the infarct which accounted on average for 24 per cent of the size of the final infarct. We concluded that a CK release of short duration indicated infarction without extension, CK release of longer duration indicated a gradual extension of infarction, and a repeated CK release resulted from a sudden extension of an infarct. According to these criteria an extension of the infarct occurred in 62 per cent of our patients.

Aged↗
PubMed1975

Assessment of left ventricular function and hemodynamic reserve by volume loading in acute myocardial infarction.

Volume manipulations in 27 patients (volume loading n = 22; phlebotomy n = 5) with acute myocardial infarction (AMI) and 7 normal subjects has been performed in order to evaluate left ventricular performance in terms of cardiac index (CI) and pulmonary artery enddiastolic pressure (EDPAP). An EDPAP in the range of 18-22 mm Hg was in general associated with maximal cardiac output. In patients with AMI maximal cardiac performance was significantly lower compared to normal subjects (p less than 0.01). Volume loading that increased the EDPAP beyond the level of 18-22 mm Hg usually deteriorated cardiac performance in AMI. A phlebotomy in 5 subjects with severe pulmonary congestion decreased EDPAP significantly from 32 to 24 mm Hg (p less than 0.1) without a change of cardiac index (2.2 - 2.5 1/min/m2;NS). In 11 patients left ventricular performance was assessed during the acute and convalescent period. 4-6 weeks after AMI resting EDPAP decreased from initially 16 to 11 mm Hg (p less than 0.02), whereas cardiac index did not change significantly (3.1-3.3. 1/min/m2;NS) and even did not rise markedly after volume loading (3.3-3.4 1/min/m2;NS). By plotting the relative change of cardiac index after volume loading against the individual infarct size (n = 16), left ventricular hemodynamic reserve was assessed and revealed a significant depression compared to normal subjects (n = 7). A rough reverse relationship (r = -0.69) between left ventricular hemodynamic reserve and infarct size was observed.

Adult↗