PubMed Health⌕ Search

Biomedical subjects

L Bette

Publications and source records attributed to L Bette.

At least 37 records · Page 2Linked to original sources
PubMed1986

Noise reversion of a dual chamber pacemaker without noise.

Three patients are reported whose DDD pacemakers reverted to the asynchronous mode in the absence of skeletal muscle or electromagnetic (EMI) interference. In all three cases, the basic cardiac rhythm was atrial fibrillation with fast ventricular response due to intrinsic AV conduction. Noise reversion was triggered by the patients' own ventricular activity at cycle lengths shorter than the ventricular refractory period of the pulse generator. In one patient, asynchronous AV sequential pacing during atrial fibrillation was noted shortly after resuscitation from ventricular fibrillation; however, the initiation of the malignant ventricular arrhythmia by the pacemaker remains unproven. The mechanism of noise reversion by rapid cardiac activity and possible solutions to the problem by adequate pacemaker design are discussed.

Aged↗
PubMed1986

Persistent hemodynamic and clinical improvement after captopril in patients with pulmonary hypertension.

Ten patients with primary or secondary pulmonary hypertension who had normal left ventricular function (group I) and nine patients with pulmonary hypertension in response to impaired left ventricular function (group II) were given captopril. At peak effect (1.5 hours after administration) pulmonary vascular resistance fell from 935 to 717 dyn X s X cm-5 in group I and from 554 to 355 dyn X s X cm-5 in group II in association with a decrease in pulmonary arterial pressure by 8 and 12 mmHg, respectively (p less than 0.01). Systemic vascular resistance declined by 26 and 29 per cent, and cardiac index increased by 17 and 20 per cent, respectively (p less than 0.01). On re-catheterization four to 15 months later, seven chronically treated patients (five of group I; two of group II) showed additional reductions in pulmonary vascular resistance (25 per cent) and pulmonary arterial pressure (20 per cent), whereas systemic hemodynamics had almost reached pre-treatment values. All patients reported symptomatic improvement. The hemodynamic changes did not correlate with concomitant alterations in circulating renin or angiotensin II levels. These data suggest that captopril can produce sustained hemodynamic and clinical benefits in patients with pulmonary hypertension of various causes and may be useful for the chronic treatment of this disorder.

Adolescent↗
PubMed1985

[Atrial flutter and atrial fibrillation by DDD stimulation].

136 patients were followed after implantation a DDD pacemaker (PM) for a total of 1,919 patient-months (m = 14.1 months/patient). 22/136 patients had one or more episodes of atrial flutter or fibrillation (AF) postoperatively. In 121/136 patients (group A) AF had not been documented before, in 4 it was unknown at the time of implantation, but was verified retrospectively (group B). 11 patients (group C) had a positive history of previous AF. Post implantation 7.4% in group A and 81.8% in group C developed AF. In patients with sick sinus syndrome (SSS) the incidence was 10/37 (27%), in those with AV block (AV) 6/77 (7.8%) and in cases with both SSS and AV 6/22 (27.3%). The first AF episode occurred during the implantation itself (n = 2) or during the hospital course in 9/22 patients (A: 11%, B/C: 64% early attacks), and later on in 13 with a time delay of 1-24 months (m = 8.5, 8 patients) in group A and 2-15 months (m = 6.6, 4 patients) in groups B/C. 2 patients of group C had no AF episodes post implantation. In the individual patient the number of attacks ranged from 1 to 3 (10.4/100 patient-months) in group A and from 1 to 6 (20.1/100 patient-months) in groups B/C. During AF 16/22 patients had a ventricular rate of 110-185, m = 132 bpm. In 6 patients the tachycardia was mediated by the PM and in 10 by fast intrinsic AV conduction. 1 patient with SSS, 2 with SSS + AV (spontaneous ventricular rate less than 45 bpm) and 3 with AV needed ventricular backup-pacing during AF. In 7 patients a total of 15 attacks of atrial flutter could be terminated by atrial overdrive pacing, in 5 of these episodes by temporary high rate A00 stimulation via the implanted pacemaker lead system. Otherwise AF was converted to sinus rhythm by antiarrhythmic drugs. After termination AF often recurred, but only 3 patients developed chronic atrial fibrillation. In 2 patients a ventricular rate greater than 180 bpm during AF reverted the PM to asynchronous mode, a possible cause of ventricular fibrillation in one. No other complications due to the PM itself have been encountered. AF, therefore, common during DDD pacing, even in patients without any AF history before implant. Both the incidence and the recurrence of AF depend on the presence or absence of previous atrial arrhythmias.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

Sustained atrial flutter after cardiac surgery: successful termination by rapid atrial pacing.

For termination of sustained atrial flutter, 28 rapid atrial stimulations were performed in 26 patients undergoing cardiac surgery, including coronary bypass surgery, and valvular heart surgery as well as surgery for primum and secundum atrial septal defect and anomalous connection of the pulmonary veins. In 18 patients rapid atrial pacing was successful in directly converting a flutter to a sinus rhythm, in 5 patients after a short period of transient atrial fibrillation. Atrial flutter could be changed to atrial fibrillation in a further 3 patients who remained in permanent atrial fibrillation and subsequently underwent DC cardioversion. Our results demonstrate that rapid atrial pacing is very effective in the treatment of sustained atrial flutter in patients following cardiac surgery and may be used alternatively to DC countershock.

Adolescent↗
PubMed1984

[Mechanism of action of oxyfedrine as a partial beta receptor agonist].

To investigate a possible dual action of oxyfedrine on beta-adrenergic receptors, hemodynamics and systolic time intervals were studied in 12 healthy volunteers during intravenous infusion of isoprenaline. The dose was titrated to a mean target heart rate of 113 bpm corresponding to an average dose of 6.16 micrograms/min. After return to baseline hemodynamics, oxyfedrine was administered as an intravenous bolus of 8 mg and the protocol was repeated. Compared to baseline, the percentage changes induced by isoprenaline at doses of 2.73 and 6.16 micrograms/min before and after (in parentheses) oxyfedrine were: heart rate: +33/+83% (+19/+62%); cardiac output: +90/153% (+30/+71%); systolic blood pressure: +16/+20% (+6/+7%); stroke volume: +42/+38% (+10/+6%); peripheral vascular resistance: -50/-63% (-31/-50%); cardiac work: +86/+148% (+19/+54%); pre-ejection period: -40/-56% (-27/-45%); isovolumic contraction time: -56/-79% (-29/-63%); systolic ejection rate: +67/+103% (+27/+52%); tension time index: +32/+50% (+7/+20%). Thus, the dose-dependent hemodynamic effects of isoprenaline were significantly attenuated by oxyfedrine pre-treatment with a shift of the dose-response curve to the right; this was attributed to a beta-antagonistic property of oxyfedrine. The results indicate that, in view of its well-known beta-stimulating effects, oxyfedrine exerts a dual action on adrenergic beta-receptors consistent with partial agonistic activity. Thereby, the different profiles of hemodynamic and metabolic actions of oxyfedrine compared to those of pure beta-agonistic agents can be explained as well as its beneficial therapeutic effects in patients with coronary heart disease.

Adolescent↗
PubMed1984

Echocardiographic evaluation of left ventricular dimensions and function in chronic hemodialysis patients with cardiomegaly.

Results obtained by echocardiography in chronic hemodialysis patients with cardiomegaly show that there is a cardiomyopathy of congestive type at least in a small number of hemodialysis patients. A reduced contractility of the left ventricular myocardium with increased dimensions of the left ventricle in a uremic metabolic situation suggests that these cardiomyopathies are of uremic origin. Possible causes of "uremic cardiomyopathy" are discussed with reference to the literature.

Adult↗
PubMed1983

[Acute and long-term effects of gallopamil (D 600) in stable angina pectoris--a randomized double-blind study].

The effects of the calcium-channel-blocking agent Gallopamil (D 600) were assessed in 20 patients with stable exertional angina pectoris in a randomized placebo-controlled double-blind protocol using serial exercise tests. Both after a single oral dose and during long-term treatment over 3 weeks, Gallopamil caused a dose-dependent increase in exercise duration and a reduction in ischemic ST segment depression that became clinically relevant using single doses of 50 mg. Since the rate-pressure product was not significantly affected by Gallopamil, its anti-anginal action cannot adequately be explained by a reduction in myocardial oxygen consumption as a result of this mechanism. The only side effects observed were asymptomatic second-degree sinoatrial block in one and first-degree atrioventricular block in another patient, each on 150 mg gallopamil daily. It thus seems justifiable to study the effectiveness of higher doses.

Adult↗
PubMed1983

[Incidence and significance of angina pectoris in aortic valve disease].

To determine the incidence and significance of angina pectoris in aortic valve disease, clinical, haemodynamic, and angiographic data concerning 111 consecutive patients aged 27-68 years (mean 52) were retrospectively analysed. 14.4% (group A) had significant, 85.6% (group B) had no coronary heart disease. There was a significant difference between the groups regarding the incidence of typical angina pectoris (62.5% vs 31.6%, p less than 0.01) and freedom from chest pain (12.5% vs 32.6%, p less than 0.05). No difference, however, could be found concerning the incidence of atypical chest pain (25% vs 35.8%). Of 12 patients aged over 50 years with coronary artery disease, no patient was free of angina pectoris. 83% had typical, 17% had atypical angina pectoris. Of 4 patients below 45 years with coronary artery disease, however, none had typical angina pectoris, 2 patients had atypical angina, and 2 patients had none. These results demonstrate that typical angina pectoris in patients with aortic valve disease is not a specific indicator of concomitant significant coronary artery disease. On the other hand, absence of chest pain does not predict absence of coronary artery disease, especially in younger patients. We therefore suggest that coronary angiography be carried out in all adult patients in whom aortic valve surgery is being considered.

Adult↗
PubMed1982

[Effects of oxyfedrine on sinus nodal function and AV-conduction (author's transl)].

In 20 patients the electrophysiologic effects of oxyfedrine at doses of 0.3 mg/kg/hr and 0.6 mg/kg/hr were studied. At the low dose, oxyfedrine caused a significant shortening of the absolute and rate-corrected sinus node recovery time by 16 and 27 percent, respectively. Sinus cycle length decreased slightly by 9 percent. Estimated sinoatrial conduction time tended to shorten, but not significantly so. AV-nodal conduction was slightly accelerated at sinus rhythm as well as during atrial stimulation; correspondingly paced cycle length at which Wenckebach AH-conduction occurred decreased. HV-interval remained unchanged. Increasing the dose of oxyfedrine had no additional effect on electrophysiologic parameters compared to the first dose used. The results demonstrate a moderate stimulatory action of oxyfedrine on sinus nodal automaticity and a slight acceleration of AV-nodal conduction. Whether the drug might be useful in the clinical setting for medical management of sinus nodal dysfunction or AV-conduction disturbances, remains to be elucidated on long-term studies; more pronounced effects of oxyfedrine than found in this investigation, however, are expected to be limited by its autoinhibitory action at higher dose levels.

Adult↗
PubMed1979

Complications with retained transvenous pacemaker electrodes.

Out of a series of 1,734 pacemaker patients, the clinical course of 46 patients was reviewed in whom a functionless endocardial electrode was retained. Non-infected electrodes (25 patients) were generally well tolerated without complications, except in one patient who experienced fatal catheter embolism into the pulmonary artery. In cases of infected electrodes (21 patients) a mortality rate of 25% was encountered due to septic complications. Catheter migration was fatal in two out of three patients. It is concluded that entrapped electrode catheters should be removed by thoracotomy if persisting infection is present or if catheter migration has occurred.

Adult↗
PubMed1979

Hemodynamic effects of pentazocine in acute myocardial infarction.

In 12 patients with acute myocardial infarction the hemodynamic effects of a single intravenous injection of 30 mg of pentazocine were investigated. The administration of pentazocine resulted in no significant hemodynamic changes. In particular, there was no increase in peripheral vascular resistance and no evidence of decreased left ventricular function or respiratory depression. In the occasional patients who demonstrated an elevation of pulmonary arterial pressure, it was probably due to a direct effect of the drug on the pulmonary vasculature.

Aged↗
PubMed1978

[The effects of oxyfedrine on the hemodynamics of patients with acute myocardial infarction].

In 16 patients with acute transmural myocardial infarction the effect of 8 mg of intravenous oxyfedrine followed by an infusion of 0.3 mg/kg body weight per hour on haemodynamics of the pulmonary and systemic circulation and dynamic cardiac indices was investigated. Cardiac rate, systemic arterial blood pressure, minute volume, cardiac output, and tension-time index remained unchanged on the whole. On the other hand oxyfedrine produced a persistant significant decrease of the mean and diastolic pulmonary artery pressure, pulmonary capillary pressure, and of the contraction and pressure-increase time. These effects were also demonstrable in patients previously treated with digitalis. No cardiac arrhythmias were observed. The positive inotropic effect of oxyfedrine is suggested as reason for these changes.

Aged↗
PubMed1978

[Effects of oxyfedrine on haemodynamics in patients with acute myocardial infarction (author's transl)].

In 16 patients with acute transmural myocardial infarction the effect of 8 mg of intravenous oxyfedrine followed by an infusion of 0.3 mg/kg body weight per hour on haemodynamics of the pulmonary and systemic circulation and dynamic cardiac indices was investigated. Cardiac rate, systemic arterial blood pressure, minute volume, cardiac output, and tension-time index remained unchanged on the whole. On the other hand oxyfedrine produced a persistant significant decrease of the mean and diastolic pulmonary artery pressure, pulmonary capillary pressure, and of the contraction and pressure-increase time. These effects were also demonstrable in patients previously treated with digitalis. No cardiac arrhythmias were observed. The positive inotropic effect of oxyfedrine is suggested as reason for these changes.

Aged↗