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Biomedical subjects

M Geiger

Publications and source records attributed to M Geiger.

At least 73 records · Page 4Linked to original sources
PubMed1990

Syncope in hypertrophic cardiomyopathy: multivariate analysis of prognostic determinants.

Twenty-nine consecutive patients with symptomatic hypertrophic cardiomyopathy and a mean age of 44.8 +/- 12.2 years (range 21 to 63) underwent complex invasive and noninvasive testing to identify a risk profile for syncope. Clinical, morphologic, electrophysiologic and hemodynamic variables at rest and at a symptom-limited pacing rate were analyzed for a significant association with syncope. Exact stepwise logistic regression analysis identified three variables as significant independent predictors of syncope in hypertrophic cardiomyopathy: 1) age less than 30 years (beta = 4.803; p = 0.0007); 2) left ventricular end-diastolic volume index less than 60 ml/m2 (beta = 3.302; p = 0.006); and 3) nonsustained ventricular tachycardia on 72 h ambulatory electrocardiographic monitoring (beta = 2.5909; p = 0.03). The combined occurrence of all three variables had a sensitivity and specificity of 100% in identifying eight patients with syncopal events. Thus, the risk for syncope in hypertrophic cardiomyopathy is high in young patients with the combination of low left ventricular filling volume and episodes of nonsustained ventricular tachycardia. This finding might also explain the mechanism of syncope in hypertrophic cardiomyopathy as low input-low output failure induced by a sudden increase in heart rate in the presence of a low filling volume.

Adult↗
PubMed1990

Diameters of lymphatic capillaries in patients with different forms of primary lymphedema.

Fluorescence microlymphography was performed near the medial ankle in 12 healthy controls, 12 patients with congenital and 12 with sporadic lymphedema of the lower extremities. Diameters of lymphatic capillaries were determined on the videoscreen by playback of the tape recordings using a morphometric technique. In the patients with congenital disease (Nonne-Milroy) aplasia of microlymphatics was diagnosed in 8 instances, ectasia in 4. Patients with sporadic lymphedema and manifestation after puberty exhibited initial lymphatics of normal caliber. In controls mean capillary diameter was 56.3 +/- 9.0 microns, in congenital disease with ectasia 99.3 +/- 9.0 microns (difference significant at the p less than 0.005 level) and in the sporadic form 49.7 +/- 7.7 microns. Congenital lymphedema may be subdivided into a form with aplastic and ectatic microvessels which possibly show different responses to therapy.

Adolescent↗
PubMed1990

[Risk of syncope in hypertrophic cardiomyopathy: a multivariate analysis of prognostic variables].

Twenty-nine consecutive patients with symptomatic hypertrophic cardiomyopathy and a mean age of 44.8 +/- 12.2 years (range 21 to 63 years) underwent complex invasive and noninvasive testing in an attempt to identify a risk profile for syncope. Clinical, morphologic and electrophysiologic as well as functional parameters at rest and at symptom-limited pacing rate were analyzed for significant association with syncope. Exact stepwise logistic regression analysis identified three variables as significant independent predictors of syncope in hypertrophic cardiomyopathy: 1) age less than 30 years (beta = 4.803; p = 0.0007); 2) left ventricular end-diastolic volume index less than 60 ml/m2 (beta = 3.302; p = 0.006) and 3) non-sustained ventricular tachycardia on 72 h ambulatory ECG monitoring (beta = 2.5909; p = 0.03). The combined occurrence of all three variables had a 100% sensitivity and specificity to identify eight patients with syncopal events. Thus, the risk for syncope in hypertrophic cardiomyopathy is high in young patients with the combination of low left ventricular filling volume and episodes of non-sustained ventricular tachycardia. This finding might also explain the mechanism of syncope in hypertrophic cardiomyopathy as low-input-low-output failure induced by a sudden increase in heart rate in presence of a low filling volume.

Adult↗
PubMed1989

Complex formation between urokinase and plasma protein C inhibitor in vitro and in vivo.

Protein C inhibitor (PCI) and plasminogen activator inhibitor 3 (PAI-3; urinary urokinase inhibitor) are immunologically identical. The role of PCI for urokinase (uPA) inhibition in vivo was investigated. We therefore developed an enzyme-linked immunosorbent assay (ELISA) specific for uPA-PCI complexes: Rabbit anti-PCI IgG was immobilized on a microtiter plate and following incubation with uPA-PCI complex-containing samples, bound uPA-PCI complexes were quantified with a horseradish-peroxidase-linked monoclonal antibody (MoAb) to uPA. Using this assay, time, dose, and heparin-dependent complexes were detected when uPA was incubated with normal plasma or purified urinary PCI, whereas no complexes were measurable using PCI-immunodepleted plasma. Plasma samples (containing 20 mmol/L benzamidine to prevent complex formation ex vivo) from patients undergoing systemic urokinase therapy (1 x 10(6) IU/60 min intravenously [IV]) after myocardial infarction were also studied. uPA present in these plasma samples (up to 1,200 ng/mL) had only 43% to 70% of the specific activity of purified 2-chain uPA, suggesting that a major portion of uPA is complexed to inhibitors. In these plasma samples uPA-PCI complexes were present in a concentration corresponding to 21% to 25% of inactive uPA antigen. These data suggest that at high uPA concentrations, such as during uPA therapy, plasma PCI might contribute significantly to uPA inhibition in vivo.

Enzyme-Linked Immunosorbent Assay↗
PubMed1989

Functional assays for protein C activity and protein C inhibitor activity in plasma.

An assay system for protein C (PC) activity and PC-inhibitor in plasma was developed. The assay was based on: (1) binding of PC to wells of a microtiter plate coated with a murine monoclonal anti-PC antibody (C3) that did not interfere with the activity or activation of PC; (2) activation of immobilized PC with Protac C; (3) incubation with or without a source of activated PC inhibitor; and (4) measurement of amidolytic activity using the substrate S-2366. The activity assay was specific for PC and sensitive to less than 1 microliter of plasma or 4 ng PC. Inhibition of activated PC by plasma followed pseudo first order kinetics. Heparin caused a dose dependent increase in the inhibition rate with half maximal stimulation at approximately 3 U/ml and maximal stimulation at heparin concentrations greater than or equal to 10 U/ml. This assay is suitable not only for determination of functional plasma levels of PC and PC inhibitor activities but also for kinetic studies of inhibition of activated PC in complex systems, such as plasma. Studies showed that urokinase interfered with the inhibition of APC by plasma inhibitor(s).

Antibodies, Monoclonal↗
PubMed1989

Diprafenone for treatment of Wolff-Parkinson-White syndrome.

The effect of intravenous (1.5 to 2.0 mg/kg body weight) and oral (300 to 375 mg/d) diprafenone was studied in 15 patients with the Wolff-Parkinson-White syndrome and symptomatic supraventricular tachycardia. Intravenous application of diprafenone significantly increased atrioventricular nodal conduction time as well as the effective refractory periods of the right ventricle and the accessory pathway in both the antegrade and retrograde directions. Antegrade conduction block in the accessory pathway occurred in two patients after the dose was increased to 2.0 mg/kg body weight. Intravenous diprafenone suppressed the inducibility of supraventricular tachycardia in two patients, but the tachycardia cycle length was significantly increased in all other patients. Fourteen patients were treated with oral diprafenone, and 11 were asymptomatic during a 17-month follow-up, two of these after the dose had been increased to 375 mg/d. Oral therapy had to be withdrawn in two patients because of adverse gastrointestinal side effects and in one because of recurring bronchospasm.

Administration, Oral↗
PubMed1989

The influence of pH-adjusted 2-chloroprocaine on the quality and duration of subsequent epidural bupivacaine analgesia during labor: a randomized, double-blind study.

A randomized, double-blind study was performed to determine whether pH-adjustment of 2-chloroprocaine hastens the onset of epidural analgesia, and improves the quality and duration of subsequent epidural bupivacaine analgesia during labor. One milliliter of either 8.4% sodium bicarbonate or normal saline was added to a 30-ml vial of 2% 2-chloroprocaine. At 0, 5, and 7 min, each patient received 2, 5, and 3 ml of 2-chloroprocaine, respectively. At 22 min, any patient who did not yet have satisfactory analgesia received an additional 5 ml of 2-chloroprocaine. At 35, and, again, at 36 min, each patient received 5 ml of 0.25% bupivacaine. The median onset of 2-chloroprocaine analgesia was slightly more rapid in the bicarbonate group than in the saline-control group (12 versus 14 min, P less than .05). Two of 31 women in the bicarbonate group, versus 10 of 31 women in the saline-control group, required an additional 5 ml of 2-chloroprocaine at 22 min to achieve satisfactory analgesia (P = .01). There was no significant difference between groups in median duration of subsequent bupivacaine analgesia (60 min in each group) or mean (+/- SD) dosage of bupivacaine during the first stage of labor (64 +/- 43 versus 72 +/- 57 mg). Also, there was no significant difference between groups in pain scores over time.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia, Epidural↗
PubMed1989

Metoclopramide versus droperidol for prevention of nausea and vomiting during epidural anesthesia for cesarean section.

In a randomized, double-blind study, we compared the efficacy of metoclopramide hydrochloride with that of low-dose droperidol for prevention of nausea and vomiting during and after elective cesarean section with epidural anesthesia. Immediately after the umbilical cord was clamped, each patient received fentanyl (50 micrograms) and the study drug intravenously over 30 to 60 seconds. In one study group, 40 women received metoclopramide (15 mg); in the other group, 41 women received droperidol (0.5 mg). Twelve women (30%) in the metoclopramide group, versus eight (20%) in the droperidol group, had intraoperative, postdelivery nausea (P = NS). One woman (3%) in the metoclopramide group, versus two women (5%) in the droperidol group, had intraoperative, postdelivery vomiting (P = NS). During the first four postoperative hours, five women (12%) in each group complained of nausea. Three women (7%) in each group had postoperative vomiting. We conclude that metoclopramide (15 mg) and droperidol (0.5 mg) were similarly effective.

Adult↗
PubMed1989

Ablation of a left-sided free-wall accessory pathway by percutaneous catheter application of radiofrequency current in a patient with the Wolff-Parkinson-White syndrome.

A case is presented of a 20-year-old woman with a history of three episodes of syncope within the last 4 years, which was caused by a rapid ventricular response to atrial fibrillation via a left-sided posterior accessory pathway. A variety of antiarrhythmic agents had failed to control the arrhythmia. Using a novel dual catheter approach, with one catheter in the coronary sinus and an adjacent catheter in the left ventricle close to the mitral annulus, accessory pathway conduction was successfully interrupted by two radio-frequency current applications between the tip electrodes of the two catheters. During follow-up, 12-lead electrocardiograms have been normal and the patient has been asymptomatic.

Adult↗
PubMed1989

Pleomorphic ventricular tachycardia: demonstration of conduction reversal within the reentry circuit.

A case is presented of a patient with incessant ventricular tachycardia of left bundle branch block morphology. Endocardial mapping revealed the site of earliest activation during tachycardia to be the proximal right ventricular septum. Pacing at this site elicited the clinical tachycardia, whereas pacing at the proximal left ventricular septum induced a right bundle branch block morphology identical to that of a previously recorded spontaneous ventricular tachycardia. Electrophysiological evidence is given that both types of tachycardia originate from a single reentry circuit located in the proximal ventricular septum in which the reentrant wavefront may travel either orthodromically (during spontaneous tachycardia and right ventricular pacing) or antidromically (during left ventricular pacing).

Animals↗
PubMed1988

[Catheter-induced modulation of the electric conductivity of the atrioventricular node by high-frequency current].

A radio-frequency current was delivered via a catheter to the atrioventricular (AV) node in 13 patients with supraventricular arrhythmias (maximal heart rate 215/min). In nine patients with atrial fibrillation, three with AV nodal re-entry tachycardia and one with AV re-entry tachycardia, AV node conduction time was prolonged from 95 +/- 43 ms to 168 +/- 72 ms. In three patients the radio-frequency current had no lasting effect, necessitating AV node ablation with a direct-current shock. During a mean observation period of five months, all ten patients in whom the radio-frequency current had been successfully applied remained free of symptoms without any anti-arrhythmia treatment. There were no complications during or after treatment.

Adult↗
PubMed1988

Plasminogen activation by tissue plasminogen activator in the presence of stimulating CNBr fragment FCB-2 of fibrinogen is a two-phase reaction. Kinetic analysis of the initial phase of slow plasmin formation.

Plasminogen activation by tissue-type plasminogen activator (t-PA) is stimulated by fibrin. In a purified system maximal fibrin-enhanced plasmin formation occurs with a delay after an initial phase of slow plasmin formation (lag phase). In the present study purified stimulating CNBr-fragment FCB-2 of fibrinogen was used, and kinetics of plasminogen activation by t-PA were analyzed with respect to the lag phase. At constant FCB-2 concentration the duration of the lag phase decreased with increasing concentrations of t-PA and plasminogen. During this period the rate of plasmin formation/min increased linearly with time with a slope dependent on the initial concentrations of FCB-2, plasminogen, and t-PA. Plasmin pretreatment of FCB-2 resulted in a dose- and time-dependent shortening of the lag phase, and at plasmin concentrations greater than or equal to 1 nM and preincubation times greater than or equal to 3 min maximal plasmin formation occurred without a lag phase. Kinetics during the phase of maximal and constant plasmin formation were not influenced by plasmin pretreatment of FCB-2. We therefore conclude that maximal t-PA-dependent plasmin formation in a system stimulated by purified FCB-2 requires plasmin modification of FCB-2.

Cyanogen Bromide↗