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Biomedical subjects

W D Bussmann

Publications and source records attributed to W D Bussmann.

At least 127 records · Page 7Linked to original sources
PubMed1981

[Cardiac tamponade, a usually fatal complication of central venous catheterisation (author's transl)].

Cardiac tamponade is a complication of central venous catheterisation. It is not very rare and may, according to the literature, be fatal in 75%. The diagnosis is established by loss of blood pressure, extreme tachycardia, congestive heart failure, and markedly increased central venous pressure accompanied by a venous catheter in situ. Two out of four patients with cardiac tamponade survived this complication.

Adult↗
PubMed1981

[Transluminal dilatation of renal artery stenoses for treatment of renovascular hypertension (author's transl)].

Transluminal angioplasty according to Grüntzig was performed for 10 stenoses in 7 patients with renovascular hypertension. Nine out of 10 renal artery stenoses were passable and could be dilated. Definite angiographic improvement could be shown in each case. The degree of stenosis could be decreased from 86% to 38% on average. At the narrowest point the diameter was enlarged by a factor of 3.1. The pressure gradient at the stenosis fell on average from 147 to 26 mm Hg. The maximal arterial blood pressure which was on average 254/124 mm Hg before drug treatment, and 169/97 mm Hg after high dosage antihypertensive treatment, fell to 140/84 mm Hg immediately after dilatation. Before dilatation there was a definite increase in peripheral plasma renin activity in every case which fell from 41 to 12 ng AI/ml . h. In one out of 5 patients restenosis occurred after 3 months which could again be successfully dilated. In the two younger patients blood pressure 3 to 9 months later was normal even without antihypertensives. In the older patients normal blood pressure could be maintained with mild antihypertensive treatment.

Adult↗
PubMed1981

[The long Q-T syndrome without Q-T prolongation (author's transl)].

Case description of a 30 year-old woman with recurrent attacks of symptomatic ventricular tachyarrhythmias but without Q-T prolongation in the electrocardiogram. All conventional antiarrhythmic agents failed to suppress the arrhythmia and electrical defibrillation had to be carried out 99 times. Blockade of the left stellate ganglion with lidocaine followed by stellectomy led to successful control of the dangerous rhythm disturbance for a follow-up period of 1.5 years. As in patients with the classical long Q-T syndrome stellate ganglion blockade and stellectomy might be indicated in cases with the so called latent Q-T syndrome and life threatening ventricular arrhythmias resistant to antiarrhythmic agents.

Adult↗
PubMed1981

Reduction of CK and CK-MB indexes of infarct size by intravenous nitroglycerin.

The effect of i.v. nitroglycerin administration on indexes of infarct size was examined in 31 patients with acute myocardial infarction. Serial creatine kinase (CK) and CK-MB isoenzyme determinations were used to calculate infarct size. Twenty-nine patients served as controls. Two subgroups of the study group were formed to evaluate differences between early and late intervention. In the first group (n = 22), continuous infusion of nitroglycerin over 48 hours was initiated within 8 hours (mean 4.5 hours) after the onset of symptoms. Peak CK activity for the nitroglycerin-treated patients (n = 9) in this subgroup was 544 U/1 vs 871 U/1 for the controls (n = 13) (p less than 0.05). The rate of CK release was reduced from 79 to 33 U/1.hr (58%), as was total CK and CK-MB release (p less than 0.02). Calculated infarct size was 69 gEq in the controls and 48 gEq in patients receiving nitroglycerin (CK-MB: 69 vs 43 gEq, p less than 0.05). In the late intervention subgroup, nitroglycerin therapy was begun more than 8 hours (mean 12.8 hours) after the onset of symptoms. Here, too, use of the agent was associated with lower peak CK and CK-MB levels as well as a reduction in calculated infarct size (p less than 0.05). Hemodynamic measurements, recorded every 4 hours, showed that nitroglycerin also reduced left ventricular filling pressure significantly and cardiac output increased. Blood pressure fell slightly, and systemic vascular resistance declined. The results indicate that i.v. nitroglycerin reduces CK and CK-MB release and thus calculated infarct size in both early and late intervention.

Adult↗
PubMed1981

[Left ventricular function at rest and during leg raising in patients with cardiomyopathy (author's transl)].

Isovolumetric and auxotonic contractility parameters were analyzed at rest and following leg raising in 16 patients with predominantly congestive cardiomyopathy. Regional ventricular function was calculated using the hemiaxis method. In patients with mild cardiomyopathy, ventricular function improved following leg raising with an increase in the mean velocity of circumferential fiber shortening and a decrease in endsystolic volume. By contrast, patients with moderate and severe cardiomyopathy displayed deterioration of ventricular function with increased hypokinesia, particularly in the anterior and apical region. Endsystolic volume increased; mean velocity of circumferential fiber shortening, regional wall velocity, and ejection fraction decreased. These results suggest that in the early phase regional disturbances of ventricular function may regress in response to passive leg raising. In the severe forms of cardiomyopathy, the preexisting regional or generalized hypokinesia increased markedly following leg raising, reflecting limited or absent left ventricular contractility reserve.

Adult↗
PubMed1981

[Correlation between isovolumic and auxotonic indexes of left ventricular contractility at rest and during exercise (author's transl)].

The validity of isovolumic parameters of left ventricular contractility in assessing ventricular function at rest has been questioned repeatedly, and with some justification. By contrast, auxotonic parameters such as left ventricular ejection fraction provide a clinically useful index of functional impairment even under resting conditions. The correlation between isovolumic and auxotonic parameters during exercise remains unclear, however. To evaluate this relation, isovolumic m (max dP/dt, Vpm) and auxotonic (EF, Vcf) parameters of contractility were determined simultaneously at rest and after both leg raising and exercise using a manometer-equipped angiography catheter in 45 patients. Under resting conditions, there was no significant correlation between the parameters (Vpm: Vcf,r = 0,226). After leg raising (r = 0.543) and exercise (r = 0.801), the correlation became markedly closer. The presence of hypo- or akinetic regions did not affect the correlation. In patients with cardiomyopathy and uniform functional impairment, the correlation did not improve in comparison with the group of patients characterized by asynergy. The specificity of the various parameters was evaluated in patients with and without significant coronary-artery stenosis. The Vcf values during exercise yielded virtually optimal separation of the two groups, whereas isovolumic parameters were far less specific.

Blood Volume↗
PubMed1980

Controlled study of intravenous nitroglycerin treatment for two days in patients with recent myocardial infarction.

Hemodynamic measurements were obtained for 48 h in 46 patients with recent myocardial infarction. Patients were randomized to treatment with (n = 22) and without nitroglycerin (NTG) n = 24). In patients with diastolic pulmonary arterial pressure (PAEDP) less than 20 mmHg (group I), NTG decreased PAEDP from 15 to 11 mmHg (n = 13); in the untreated control group PAEDP remained unchanged (n = 15). Cardiac output decreased in the NTG group from 5.4 to 5.0 1/min and in the control group from 4.7 to 4.4 1/min. Mean arterial pressure decreased in both groups, in the NTG group from 106 to 97 mmHg and in the control group from 102 to 94 mmHg. In patients with left ventricular failure and PAEDP greater than 20 mmHg (group II) the decrease in left ventricular filling pressure was significantly greater (25 to 17 mmHg, n = 9) than in the control group (24 to 20 mmHg, n = 9). Cardiac output increased during NTG treatment from 4.2 to 5.1 1/min. In the control group, however, cardiac output decreased from 4.2 to 3.6 1/min. Mean arterial pressure decreased from 103 to 95 mmHg in the NTG group and from 114 to 96 mmHg in the control group. Heart rate did not change significantly. Thus, PAEDP decreased significantly in patients who received NTG treatment for 48 h compared to an untreated control group. Cardiac output increased in treated patients, especially those with left ventricular failure, but decreased in the control group. Mean arterial pressure decreased to the same degree in treated patients and in controls.

Aged↗
PubMed1980

Comparison of antiarrhythmic effects of oral prajmalium bitartrate and intravenous lidocaine in acute myocardial infarction.

In 35 patients with acute myocardial infarction premature ventricular complexes were quantified from stored continuous electrocardiographic tape recordings using a semiautomated arrhythmia detection system. Seventeen patients, separated at random, received no antiarrhythmic drug and formed the control group. In nine patients prajmalium bitartrate was given orally at a dose of 60 mg. (20 mg. every 4 hours). Nine patients had permanent infusions of 2.1 mg./minute lidocaine (corresponding to a daily dose of 3 g.). In both treated groups premature ventricular complexes decreased significantly as compared to the spontaneous frequency in the control group. Six hours after the onset of therapy premature ventricular complexes were reduced to 37% of the initial value in the prajmalium bitartrate group and to 51% in the lidocaine group, whereas in the control group frequency increased (169%). The peak effect was reached after ten hours when premature ventricular complexes were reduced to 5% under prajmalium bitartrate and to 20% under lidocaine administration. Runs of premature ventricular complexes were nearly completely suppressed after administration of prajmalium bitartrate. Under lidocaine administration runs were moderately and not significantly reduced. Eight hours after the onset of therapy, runs were reduced to 8% of the initial value under prajmalium bitartrate and to only 79% under lidocaine. The effect of prajmalium bitartrate on runs of premature ventricular complexes was significantly more pronounced than the effect of lidocaine. The present study documents that orally administered prajmalium bitartrate is an alternative to intravenous administration of lidocaine in the treatment of ventricular arrhythmias after acute myocardial infarction.

Administration, Oral↗
PubMed1980

[Reduction of CK and CK-MB enzyme levels as indicators of infarct size by intravenous nitroglycerin (author's transl)].

Intravenous nitroglycerin has beneficial effects on hemodynamics and on myocardial ischemia. The aim of the present study was to investigate whether it also reduces final infarct size. In 60 patients with myocardial infarction serial blood samples were tested for creatine kinase (CK) and its isoenzyme CK-MB activity for infarct size calculations. Hemodynamic parameters were measured every 4 hours. Patients were randomized to a control (n = 29) and a nitroglycerin group (n = 31). In the early intervention group continuous perfusion of nitroglycerin for 48 hours was started < 8 hours (mean 4.5 hours) after onset of symptoms, and in the late intervention group > 8 hours (mean 12.8 hours) after onset of symptoms. In early intervention (n = 22) peak CK activity was 871 U/l in control patients and 544 U/l (p < 0.05) in the nitroglycerin group. The rate of CK release was reduced from 79 to 33 U/l x h, i.e. by a total of 58%, as was total CK and CK-MB release (p < 0.02). Calculated CK infarct size was 69 g equiv. in controls and 48 g equiv. in the nitroglycerin group. (CK-MB: 68 versus 43 g equiv., p < 0.05). In late intervention (n = 28) the differences were less pronounced. Nitroglycerin reduced left ventricular filling pressure significantly and increased cardiac output. Blood pressure changed insignificantly and peripheral vascular resistance decreased. In conclusion, nitroglycerin reduces CK and CK-MB release and hence calculated infarct size, particularly when treatment is begun within the first 8 hours after onset of symptoms.

Aged↗
PubMed1980

[The influence of ergonovine on coronary artery diameter and hemodynamics in patients with angina pectoris at rest (author's transl)].

The influence of methyl ergonovine on coronary artery diameter and regional ventricular function was studied in three groups of patients with and without suspected coronary artery spasm. Ten patients with angina at rest in whom spasm was suspected were compared to seven coronary heart disease patients with stable effort angina. Six patients without coronary heart disease served as controls. Ergonovine, an agent known to cause coronary vasoconstriction, was administered in order to identify the possible role of spasm in the various subgroups. The standardized study procedure comprised coronary and left ventricular angiography before and after 0.1 to 0.4 mg ergonovine i.v. as well as after 1.6 mg nitroglycerin sublingually. Following ergonovine provocation, narrowing of the anterior descending branch averaged 22 per cent in the patient group with suspected spasm, 3 per cent in patients with coronary heart disease, and 6 per cent in the control group. The spasm group also displayed regional ventricular hypokinesis and an increase in endsystolic volume. LVEDP increased from 15 +/- 6 to 28 +/- 7 mm Hg (p < 0.0005) mean circumferential fiber shortening (mean Vcf) decreased from 1.6 +/- 0.4 to 1.1 +/- 0.4 circ/s (p < 0.0025), and the velocity of shortening in the anterior apical hemiaxis (Vm3) declined from 1.9 +/- 0.2 to 0.8 +/- 0.4/s (p < 0.0005). These changes were much less evident in the coronary heart disease group. No significant hemodynamic changes were observed in the control group. Patients with angina at rest are much more susceptible to ergonovine-induced coronary artery narrowing than patients with stable exertional angina.

Adult↗