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Biomedical subjects

W Voelker

Publications and source records attributed to W Voelker.

104 records · Page 6Linked to original sources
PubMed1987

[Anterior wall infarct in an 18-year-old patient with Hodgkin's disease. Possible relation between mediastinal irradiation, accelerated arteriosclerosis and vincristine chemotherapy].

An 18-year-old male patient with Hodgkin's disease, having undergone radiotherapy to the mediastinum two-and-a-half years previously, developed symptoms of an acute myocardial infarction within three hours of a vincristine injection (the first course of vincristine chemotherapy had been finished eight days previously). Invasive investigation after three weeks revealed single-vessel occlusion of the anterior interventricular branch with an anterior-wall aneurysm. The most likely cause of the coronary heart disease in this patient is changes in the anterior interventricular branch resulting from the mediastinal radiotherapy. The infarct itself occurred in close temporal relationship to the vincristine injection, which in several case reports has been implicated in the triggering of coronary spasms.

Adolescent↗
PubMed1987

[Percutaneous transluminal coronary angioplasty and aortocoronary bypass surgery in unstable angina pectoris and coronary multivessel disease].

In 113 patients demonstrating the clinical syndrome of unstable angina, acute-stage coronary angiography revealed multivessel disease. Acute PTCA of the ischaemia-related coronary artery or bypass grafting was performed depending on angiographic criteria. Of the total of 68 patients in whom PTCA was performed, 45 had two-vessel disease (2 vd) and 23 three-vessel disease (3 vd). 12 of the 45 patients with bypass operation had a left main stem stenosis, whereas 33 had three-vessel disease. The primary success rate of PTCA was 81%, 89% in patients with 2 vd and 70% in patients with 3 vd. Acute post-PTCA bypass grafting was necessary in 2 patients having 2 vd and in 5 patients suffering from 3 vd. 5 of the 68 patients treated with PTCA developed a transmural myocardial infarct and one patient died after PTCA and emergency bypass surgery. 8 of the 45 operated patients had a perioperative or postoperative myocardial infarct and 5 patients died intraoperatively or postoperatively. The overall morbidity was 11.5%, and the mortality of hospitalised patients was 5.3% (6/113). Combination of PTCA with emergency bypass grafting offers a new and effective treatment with an acceptable risk even in multivessel disease patients and in those having unstable angina pectoris. The additional use of PTCA definitely improves therapeutic management in this high-risk population.

Angina Pectoris↗
PubMed1987

Changes in haemodynamics and left ventricular function during intravenous nifedipine infusion with and without additional propranolol in patients with coronary artery disease. A randomized, placebo controlled trial.

The haemodynamic effects of a combined intravenous treatment of nifedipine and propranolol in ten patients with coronary artery disease compared to a single treatment with nifedipine or placebo were investigated. Nifedipine infusion resulted in a reduction of left ventricular (LV) afterload and LV volumes with an increase in heart rate and EF and no change of the double product, coronary sinus flow, LV diastolic parameters and dp/dtmax. Addition of propranolol lowers myocardial oxygen demand by reducing heart rate and dp/dtmax together with a sustained afterload reduction with no change in LV volumes and EF. The vasodilatatory action of nifedipine pretreatment balanced the negative effects of acute beta-receptor blockade on LV function and allows the reduction of myocardial oxygen demand without a deterioration of LV function.

Angiography↗
PubMed1987

Influence of sampling site and flow area on cardiac output measurements by Doppler echocardiography.

In 40 patients cardiac output was simultaneously determined by pulsed Doppler echocardiography and thermodilution (range 4.0 to 10.2 liters/min). The sample volume was located in the center of the mitral anulus, at the tips of the mitral leaflets and in the center of the aortic anulus. Circular cross-sectional areas of the mitral anulus, aortic anulus and aortic bulbus were calculated from M-mode and two-dimensional echocardiographic diameters. The varying short axis of the elliptical mitral opening area was obtained from the diastolic leaflet separation in the M-mode, and the long axis was derived from the maximal mitral orifice area or mitral anulus diameter. Cardiac output was calculated by multiplying time-velocity integrals with the different areas and heart rate. Doppler flow measurements correlated significantly with the thermodilution method (r = 0.79 to 0.93). Flow measurements at the aortic anulus were most accurate (r = 0.93, SEE = 0.589 liter/min) if the annular area was derived from the M-mode tracing. Measurement of the anulus in the apical five chamber view yielded a significant underestimation and the area of the aortic bulbus provided an overestimation of cardiac output. Left ventricular inflow was underestimated at the mitral leaflet tips and overestimated at the mitral anulus. The accuracy of pulsed Doppler cardiac output measurements strongly depends on the assumed flow area and sampling site. Both should be determined at the same level in the inflow or outflow tract of the left ventricle. Measurement of cardiac output in the center of the aortic anulus provided the highest accuracy.

Adolescent↗
PubMed1987

[Clinical value of Doppler echocardiography in the determination of shunt size in atrial septal defect of adult patients].

The purpose of this study was to assess the clinical utility of pulsed Doppler echocardiography in the determination of shunt flow magnitude in adults with an atrial septal defect. Therefore, in 24 unselected, consecutive adult patients with an ostium-secundum type atrial septal defect, and in 16 patients without heart disease, Doppler echocardiography was performed to measure blood flow in the right and left ventricular outflow tract. In eight patients with an atrial septal defect, pulmonary flow measurement was impossible because of pulmonary insufficiency or poor visualization of the pulmonary annulus. The ratio between the pulmonary (Qp) and systemic blood flow (Qs) was between 0.83 and 1.13 in the control group and between 1.31 and 4.46 in patients with an atrial septal defect. In the control group the correlation between Qs and Qp was r = 0.96 (SEE = 0.417 l/min, y = 1.05x - 0.21). The correlation between Qp/Qs, determined by oximetry and pulsed Doppler echocardiography in patients with an atrial septal defect, was significant (r = 0.82, SEE = 0.54). Systematic differences between invasive and non-invasive shunt calculations did not occur. Thus, pulsed Doppler echocardiography is clinically useful in the determination of shunt flow magnitude in about two thirds of adult patients with an atrial septal defect and provides precise information for the decision for conservative or operative treatment.

Adult↗
PubMed1987

[Effect of rapid atrial pacing on left ventricular ejection fraction in patients without organic heart disease].

Pacing-induced decrease of left ventricular ejection fraction (LVEF) in patients with coronary artery disease has been proposed as a sign of myocardial ischemia, whereas a slight increase or no change is speculated to be the normal response to rapid atrial pacing. The studies of the pacing-induced effects in normals, however, are of limited value, because of either inhomogeneous patient population or different, mainly non-invasive, methods for determination of LVEF. It was therefore the aim of the present study to assess the pacing-induced changes of left ventricular ejection fraction in a homogeneous group of patients. In 10 patients (mean age: 48 +/- 2 years) with normal coronary arteriograms and normal LV-function at rest, rapid atrial pacing was performed stepwise to a maximal pacing rate of 150 beats per minute. In all patients left ventricular end-diastolic pressure LVEDP and time constant of relaxation period tau decreased, while the parameter of contractility Max Dp/dt increased due to increase in heart rate. Furthermore, there was no limited coronary reserve or myocardial lactate production during atrial stimulation as a sign of pacing-induced ischemia. In all patients biplane ventriculography was performed at rest and during maximal stimulation. While end-diastolic volume index EDVI decreased in every patient (71 +/- 5----42 +/- 4 ml/m2, p less than 0.005) and systolic volume index did not change (17 +/- 2----14 +/- 2 ml/m2, N.S.), there was a significant decrease of ejection fraction from 75 +/- 2 to 66 +/- 3% (p less than 0.005). Basal heart rate, age, sex or basal ejection fraction did not influence the response of ejection fraction to rapid atrial pacing. Even after drug-induce afterload reduction there was a significant pacing induced decrease of ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Comparison of Doppler echocardiographic methods of determining cardiac minute volume].

In 40 patients without valvular disease, cardiac output was determined by pulsed Doppler echocardiography and thermodilution simultaneously. The sample volume was located in the center of the mitral valve ring, at the tips of the mitral leaflets and in the left ventricular outflow tract, directly proximal to the aortic valve leaflets. Circular cross-sectional areas of the mitral valve ring, aortic ring and bulbus of the aorta were calculated from the M-mode and two dimensional echocardiographic diameters. The mitral orifice was assumed to be an ellipse with varying short axes, determined as the mean diastolic leaflet separation in the M-mode and a constant long axis, derived from the maximal mitral orifice area or mitral ring diameter. Cardiac output was calculated by multiplying time-velocity integrals with different areas and heart rate. Cardiac output, measured by the thermodilution technique, ranged from 4.0 l/min to 10.2 l/min. Cardiac output determined by the different Doppler methods correlated significantly with the thermodilution measurements. Cardiac output measurements in the left ventricular outflow tract provided the best correlation coefficient (0.93) and a standard error of the estimate of 0.589 l/min, when the circular flow area was derived from the M-mode echo of the aortic ring.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Tricuspid valve insufficiency in patients with rheumatic mitral valve disease: angiographic diameter of the tricuspid ring and function of the right ventricle].

Dilatation of the right ventricle and a consecutive enlargement of the tricuspid valve ring are thought to be the main causes of functional tricuspid regurgitation in patients with rheumatic mitral valve disease. To study the effect of right ventricular dilatation as well as the dimension of the tricuspid valve ring, right ventricular volume indices, ejection fraction, regional shortening, pulmonary artery pressure, and the diameter and systolic shortening of the tricuspid valve were determined in 67 patients with rheumatic mitral valve disease (NYHA class II and III) from biplane ventriculographies. Patients with right ventricular enlargement (greater than 90 ml/m2) were divided into groups with (group IIA) and without (group IIB) tricuspid regurgitation and compared with patients with normal right ventricular size and function without tricuspid regurgitation (group I). There was no difference in the end-diastolic volume index, in the afterload or in the diameter of the tricuspid ring. Right ventricular ejection fraction was decreased in group IIA (51 +/- 9% vs. 59 +/- 10% (IIB) and 61 +/- 6% (control); (p less than 0.05). Regional function was also decreased in group IIA. 73% of the patients with tricuspid regurgitation had right ventricular enlargement, but only 44% of the patients with right ventricular enlargement had tricuspid regurgitation. Thus right ventricular dilatation promotes the development of a tricuspid insufficiency, but is not the only cause. Additional factors like decreased local wall motion, alterations of the valve or the valve apparatus may also account for functional tricuspid regurgitation.

Angiography↗
PubMed1985

[Clinical value of 2-dimensional echocardiography for quantifying mitral stenosis--possibilities and limits of the method].

In 70 consecutive patients with the clinical diagnosis of mitral valve disease quantification of the mitral valve area was performed by 2-D echocardiography. In only 39 of these 70 patients (58%) could the mitral valve be satisfactorily positioned in the short-axis view for correct quantification of the valve area. In 31 patients a sufficient echo could not be assessed because of anatomical disorders, calcification of the valve or postoperative deformities of the valve apparatus after commissurotomy. In 30 of the 39 patients, in whom 2-D echocardiography allowed to determine the valve area, the results of the echocardiographic study corresponded with the valve area determined by angiography using the modified Gorlin formula. A sufficient correlation between both methods, however, was found only in patients with combined mitral valve disease (r = 0.81); no correlation could be found in the group of patients with pure mitral stenosis. From these results we conclude that in the individual patient 2-D echocardiography is not sufficient for exact quantification of mitral stenosis. Definite preoperative diagnosis necessitates additional investigations.

Adult↗
PubMed1984

[Dynamics of critical stenosis in patients with unstable angina pectoris].

In 28 patients with unstable angina pectoris biplane coronary angiography was performed in the acute stage. Arteriography of the ischemia-related vessel was subsequently repeated in 14 patients after intracoronary infusion of 0.2 mg nifedipine and ten minutes later after 10 mg sublingual nifedipine (group I) and in 14 patients after intracoronary infusion of 0.4 mg 3-N-morpholinosyndnonimine (SIN-1) (group II). 17 patients were on intravenous nitroglycerin and 11 patients on high-dose oral isosorbide dinitrate therapy at the time of angiography. Pre- and postintervention, the degree of coronary stenosis of the ischemia-related vessel was determined by three morphometric methods: rmin, minimal diameter of the stenosis, Amin, planimetered area under the stenosis and minimal diameter ratio (min diam ratio), ratio of the minimal diameter of the stenosis and the pre- and poststenotic diameter. An increase in lumen was considered to be significant when two of the three parameters increased by more than 5%. Nifedipine application resulted in an increase in lumen in 13 patients of group I. After i.c. nifedipine the lumen increased by 16% and after s.l. nifedipine by an additional 9%. Combined i.c. and s.l. nifedipine increased the lumen of the critical stenosis by 24 +/- 6.8%. In 10 patients of group II, SIN-1 application was successful and resulted in a luminal increase of 28 +/- 2.6%. In more than 80% of our patients with unstable angina pectoris application of nifedipine and SIN-1 resulted in an increase of the lumen. Thus, coronary vasoconstriction seems to be the predominant mechanism next to organic stenosis in unstable angina.

Angina Pectoris↗
PubMed1984

[Spontaneous regression of residential stenosis of the infarct vessel following successful percutaneous transluminal coronary recanalization].

In 64 out of 90 patients with thrombolysis by intracoronary streptokinase (PTCR) in the acute stage of myocardial infarction coronary angiography was performed in the chronic stage after 28 +/- 20 days. 52 of 56 successfully treated patients had a patent infarct vessel in the chronic stage. 36 of these patients showed a spontaneous regression from the subacute to the chronic stage. In 49 of the 56 patients (age: 53.4 +/- 10.4 years) a residual stenosis of more than 75% after PTCR was found; in the chronic stage only 31 patients had a stenosis of more than 75%. Of 10 patients with a spontaneous regression of 25% or more (age: 48.0 +/- 14.9 years) 8 had a one-vessel disease. The infarct vessel was in 6 patients the left anterior descending, in 4 patients the right coronary artery and in no case the left circumflex branch. The results suggest that the indication for invasive interventions, such as acute coronary angioplasty or bypass surgery, does not only depend on the degree of the residual stenosis directly after reperfusion. If possible, the decision for further invasive treatment should depend on the clinical follow-up.

Adult↗
PubMed1982

Haemodynamic effects of prenalterol in patients with severe congestive heart failure--NYHA III-IV.

In 12 patients with severe congestive heart failure due to ischaemic heart disease (n = 6) and due to congestive cardiomyopathy (n = 6) the haemodynamic effects of a new beta 1-agonist, prenalterol, were studied. Left ventricular (LV) function was studied before and 20 min after infusion of 12 mg prenalterol. Heart rate was kept constant by atrial pacing at a rate of 100 min-1 unless intrinsic heart rate exceeded it. As a sign of positive inotropic support, prenalterol enhanced peak rate of LV pressure development (dP/dt) from 1160 +/- 100 mm Hg/s to 1590 +/- 190 mm Hg/s (p less than 0.005). In the mean LV end-diastolic and end-systolic volume determined by cineventriculography and two-dimensional echocardiography decreased. LV stroke work index measured with both methods increased with 4 ml/m and 5 ml/m, respectively (p less than 0.02). LV ejection fraction was improved by 6% and 8% (p less than 0.005). Increase of peak fall of left ventricular pressure (dP/dt) (1050 +/- 60 mm Hg/s to 1270 +/- 100 mm Hg/s, p less than 0.005) and shortening of time constant (T) of pressure fall from 64.5 +/- 5.0 ms to 44.5 +/- 6.0 ms (p less than 0.005) demonstrated the improved LV relaxation. Analysis of LV volume and myocardial compliance revealed decrease of left ventricular stiffness. Thus, LV filling pressure was reduced from 22.1 +/- 4 mm Hg to 14 +/- 3.5 mm Hg (p less than 0.001). Pressure volume analysis showed a significant increase of LV power and work, as well as a slight decrease of wall stress. Our study could demonstrate, even in patients with severe heart failure, a sustained positive inotropic effect of prenalterol leading to an improved left ventricular contractility, relaxation and compliance. LV power and work was enhanced. The increase of oxygen demand seemed to be counterbalanced by an improved perfusion of particularly subendocardial layers indicated by an increased transmyocardial pressure gradient.

Adrenergic beta-Agonists↗