Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 253 records · Page 14Linked to original sources

PubMed1994

[Lymphocyte subpopulations in bronchoalveolar lavage fluid in AIDS].

Lymphocyte subpopulations in peripheral blood and bronchoalveolar lavage fluid (BAL) were examined in 29 patients with AIDS (26 men, three women; median age 32 [16-55] years). Patients in group 1 (n = 12) had no lung disease, in group 2 (n = 11) had Pneumocystis carinii pneumonia, in group 3 (n = 6) had other lung disease. There were 13 men and two women (median age 48 [21-80]) in the control group (bronchoscoped for mild pulmonary symptoms: no abnormal findings in the BAL). Compared with the control group, patients with AIDS had a significant deficiency in helper cells, both in blood (7-23% vs 50%; P < 0.01) as well as in the BAL (7-24% vs 52%; P < 0.001). There was a correlation of the percentage helper cell proportion in peripheral blood and BAL (for both group 1 and 2, rs = 0.75; P < 0.05). The proportion of helper cells in peripheral blood and BAL in AIDS patients was significantly lower in those with than without lung disease (group 1: 23% blood, 24% BAL vs group 2: 9% blood, 7% BAL; group 3: 7% blood, 7% BAL; P < 0.02 blood, P < 0.004 BAL). The percentage proportion of suppressor cells was greater in both blood and BAL in AIDS patients (group 1: blood 47%, BAL 63%; group 2: blood 44%, BAL 76%; group 3: blood 52%, BAL 75%) than in the controls (blood 28%, BAL 33% [P < 0.01], but there was no correlation between peripheral blood and BAL. In addition, the absolute number of suppressor cells in the lavage (30 cells/microliters in group 1 and 3, 65 cells/microliters in group 2) was significantly higher than in the controls (8 cells/microliters).--In AIDS patients there occurs a lymphocytosis in the BAL, while in blood there is a lymphopenia. The concordant decrease in helper cells in blood and BAL is decisive for the severity of any pulmonary infections.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Color-coded Doppler imaging of the vena contracta as a basis for quantification of pure mitral regurgitation.

The narrowest central flow region of a jet is defined as the vena contracta. This term is applied also to the contracted zone of the Doppler color flow image of a jet at its passage through an incompetent mitral valve. The clinical applicability of measuring the size of the vena contracta by transthoracic color-coded Doppler echocardiography for estimating the severity of mitral regurgitation (MR) was evaluated. In 78 of 82 patients with angiographically proved MR, a coherent flow image across the valve was visualized. The maximal diameter in the apical long-axis view was considered as a representative value for the size of the vena contracta. In comparison with the maximal left atrial velocity pixel area, this parameter revealed higher correlations to the angiographic degree of MR and to the regurgitant volume (r = 0.94 vs 0.72, and 0.83 vs 0.71, respectively). The highest positive and negative predictive accuracies for differentiating mild-to-moderate from severe MR were determined for a diameter of 6.5 mm (88 and 96%, respectively). Because the vena contracta is directly related to the severity of MR, it is concluded that it is helpful to use this parameter instead of the maximal velocity pixel area for semiquantitative grading.

Adult↗

PubMed1994

Carotid artery stenosis and tachyarrhythmias: regional cerebral blood flow during high-rate ventricular pacing after one vessel occlusion in rats.

The aim of the present study was to investigate the effect of hypotensive tachycardias on cerebral blood flow (CBF) in the presence of significant carotid stenosis. The experiments were performed in 57 spontaneously breathing rats during arterial normoxia and normocapnia anesthetized with thiobarbital. CBF was determined with radiolabeled microspheres during control conditions (normofrequent sinus rhythm, normotension; group A; n = 15), during high-rate left ventricular pacing (660-840 ppm) at normotension (group B1; n = 13), borderline hypotension (group B2; n = 15) and severe hypotension (group B3; n = 7). In addition, CBF measurements were performed during borderline hypotension induced by hemorrhage (group C; n = 7). Global CBF was 1.09 +/- 0.29 ml g-1 min-1 in group A, 0.93 +/- 0.40 in group B1, 0.68 +/- 0.31 in group B2 (P < 0.05 vs. A), 0.42 +/- 0.16 in group B3 (P < 0.05 vs. A) and 0.83 +/- 0.2 in group C. The highest CBF values were found in the cerebellum (A; 1.43 +/- 0.5 ml g-1 min-1) and the lowest in the postocclusive tissue of the ipsilateral hemisphere (A; 0.74 +/- 0.2 ml g-1 min-1). In all groups a 15% mean CBF reduction in the right hemispherical cerebrum in comparison to the left hemisphere was observed (P < 0.01). In contrast, hemispherical CBF of the cerebellum did not differ. The CBF blood pressure relationship shifted to lower CBF values, the threshold of CBF regulation shifted to higher blood pressure values in the tissue regions distal to the occluded vessel during hypotensive tachycardias.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Time course of myocardial and cerebral blood flow during stable but hemodynamically compromising ventricular tachycardias. Laboratory investigations.

Myocardial and cerebral blood flow were determined with radiolabeled microspheres in 20 Sprague-Dawley rats during sinus rhythm and during stable but hemodynamically compromising ventricular tachycardias. In addition, in 10 animals the measurements were performed at hypotension induced by exsanguination. In controls (n = 10), myocardial and cerebral blood flow were 5.14 +/- 0.6 and 1.03 +/- 0.3 ml/g per minute, respectively. The range of myocardial blood flow values was markedly enlarged after onset of tachycardia induced by epicardial pacing. The mean values of myocardial blood flow were 5.80 +/- 1.9 ml/g per minute (n.s.) after 1 min and 7.46 +/- 3.9 ml/g per minute (n.s.) after 5 min. Cerebral blood flow, however, significantly decreased after 1 min (0.57 +/- 0.1 ml/g per minute, P < 0.01) and after 5 min (0.71 +/- 0.3 ml/per minute, P < 0.05). In contrast, 1 min after exsanguination myocardial blood flow significantly decreased (4.03 +/- 1.5 ml/g per minute, P < 0.05) and recovered after 5 min (6.06 +/- 1.2 ml/g per minute, n.s.) Cerebral blood flow was below control levels 1 min (0.70 +/- 0.2 ml/g per minute, P < 0.05) after onset of hypotension due to exsanguination and returned to normal values with the next 4 min (0.90 +/- 1 ml/g per minute, n.s.). The results suggest that stable but hemodynamically compromising ventricular tachycardias markedly affect cerebral blood flow, whereas in most cases myocardial blood flow is maintained within normal ranges, or even increases. An augmented myocardial autoregulation can be concluded from the autoregulatory index. This maintainance of regulatory ability might be due to the increase of myocardial oxygen consumption at decreased coronary perfusion pressure during tachycardias. In contrast, during hypovolemic hypotension, myocardial as well as cerebral blood flow decreased. During stable but hemodynamically compromising ventricular tachycardias, cerebral blood flow initially drops drastically and recovers slowly over the next 5 min. This finding contrasts with the results of hypovolemic and drug-induced hypotension models.

Animals↗

PubMed1994

Interactions between drugs and devices: experimental and clinical studies.

It is important to understand the potential interactions between the implantable cardioverter defibrillator (ICD) and antiarrhythmic therapy in patients who receive pharmacologic therapy as an adjunct to ICD therapy. In our cohort of 101 patients, antiarrhythmic agents were prescribed in 67% of the patients during long-term therapy for the following reasons: to suppress ventricular tachycardia/ventricular fibrillation episodes (50%), to lower the rate of ventricular tachycardia (19%), to prevent supraventricular tachyarrhythmia (21%), and for other reasons (10%). The potential influence of antiarrhythmic drugs on the defibrillation threshold (DFT) is the most important issue. In animal studies lidocaine increased the DFT in a dose-dependent manner. Quinidine, procainamide, propafenone, and flecainide did not affect the DFT or, in some cases, led to a small increase. Sotalol even decreased the energy requirements for internal defibrillation. In a prospective investigation we were able to document a significant increase of DFT (from 14.1 + 3.0 to 20.9 + 5.4 J, p < 0.001) by the use of amiodarone (400 mg/day), whereas this effect was not found in patients who received mexiletine (720 mg/day). In conclusion, the DFT or the safety margin for defibrillation should be known before antiarrhythmic agents are administered to patients with an ICD. In case of a small safety margin, the DFT should be reassessed after antiarrhythmic drug therapy is begun.

Animals↗

PubMed1994

Clinical efficacy of shock waveforms and lead configurations for defibrillation.

A randomized, prospective comparison of the defibrillation efficacy of various shock waveforms and nonthoracotomy lead configurations was performed in five distinct patient groups undergoing implantation of a cardioverter defibrillator. In the first group using a bidirectional lead configuration, there was no significant difference in the mean defibrillation threshold (DFT) between simultaneous and sequential monophasic shocks (17.8 +/- 5.8 joules versus 17.3 +/- 2.7 joules). In the second group using a bidirectional lead configuration, the mean DFT was 21.9 +/- 7.3 joules with monophasic shocks and 14.9 +/- 5.0 joules with biphasic shocks (p < 0.001). In the third group using a unidirectional lead configuration, the mean DFT was significantly higher (p < 0.001) with monophasic shocks (22.1 +/- 4.2 joules) compared with biphasic shocks (15.0 +/- 5.4 joules). In the fourth group, an intraindividual comparison with monophasic shock waveforms showed no significant differences in DFT using either a bidirectional (21.3 +/- 5.8 joules) or a unidirectional (21.7 +/- 2.6 joules) lead configuration. In the fifth group, a simplified unipolar transvenous defibrillation lead system ("active can") demonstrated significant lower DFTs (9.7 +/- 3.8 joules) compared with a standardized unidirectional lead configuration (18.0 +/- 6.8 joules). It is concluded that: (1) there seems to be no significant difference in the DFT between simultaneous and sequential monophasic shocks; (2) biphasic waveforms require significantly less energy for defibrillation than their corresponding monophasic waveforms; and (3) the unipolar single-electrode defibrillation system is easy to implant and provides DFTs at energies comparable with epicardial lead systems.

Adolescent↗

PubMed1994

Heart rate during exercise: what is the optimal goal of rate adaptive pacemaker therapy?

The objective of minute ventilation (MV)-controlled pacemaker algorithms is to simulate the physiologic relationship of the sensed signal and the sinus node response during exercise. In our study we determined the relationship between heart rate and MV in healthy middle-aged subjects by measuring breath-by-breath gas exchange throughout peak exercise. Regarding several clinical limitations of peak exercise testing, we additionally evaluated whether a 35 W low-intensity treadmill exercise (LITE) protocol can be used as a substitute for peak exercise testing to determine the physiologic heart rate to MV slope. The results demonstrated that the heart rate to MV relationship is not linear throughout peak exercise but is curvilinear with a smooth logarithmic-type profile. To simulate this relationship, MV-based rate adaptive pacemakers should generate a decreasing heart rate to MV slope during higher levels of work. The heart rate to MV slope determined during the early, dynamic phase of low-intensity exercise represents the same slope derived from peak exercise below the anaerobic threshold. The low-intensity treadmill exercise protocol, with minimal patient effort, can thus be used as a substitute for peak exercise to optimize rate adaptive slope programming of MV-controlled pacemakers.

Algorithms↗

PubMed1994

Complications of pacemaker-defibrillator devices: diagnosis and management.

Treatment of resuscitated patients with implantable cardioverter defibrillators has become increasingly more common as a method for the prevention of sudden cardiac death. Major complications such as perioperative death (incidence 2% to 8%), infection (2% to 11%); and lead-related problems (3% to 27%) have been described in previous trials. In our experience with 140 patients, problems were related to leads (n = 11), the device (n = 2), pacing (n = 1), sensing (n = 13), and defibrillation function (n = 5). Additional problems that occurred during the perioperative period included infection (n = 11), hematoma, and seroma (n = 2). Thrombus formation along endocardial leads was observed in 13 of 62 (21%) patients. Different arrhythmias (n = 10), such as sinus tachycardia, atrial fibrillation, and nonsustained, slow or incessant ventricular tachycardia with shock delivery, were also detected. Surgical management (predominantly for the major problems) was used in 31 (48%) patients, drug treatment in 25 (39%), and reprogramming of the device in 24 (38%) patients. All of these problems can result in an increase in mortality rates. This article provides an overview of the complications of cardioverter defibrillator treatment and is based on both published data and our series.

Arrhythmias, Cardiac↗

PubMed1994

Predictors of outcome in patients with implantable transvenous cardioverter defibrillators.

The identification of patients who benefit most from implantable cardioverter defibrillator (ICD) therapy is of great interest. To find out if clinical variables, the signal-averaged electrocardiogram, and electrophysiologic study predict occurrence of appropriate ICD discharges and death, we followed-up on 76 patients after implantation of a transvenous ICD. During a mean follow-up period of 18.2 +/- 6.4 months, 29 patients (38.6%) experienced at least one appropriate episode. When these patients were compared with those who had either no therapy or inappropriate episodes, three variables were found to be significant in the identification of patients who experienced appropriate discharges: (1) The mean ejection fraction of patients who received appropriate discharges was 35.4% +/- 13.5% versus 45.1% +/- 15.3% in the other group (p < 0.05); (2) patients with appropriate therapy had sustained monomorphic ventricular tachycardia that was more likely to be inducible (75.9% vs 21.2%, p < 0.01); and (3) in patients with appropriate therapy ventricular fibrillation was less likely to be inducible (10.3% vs 25.5%, p < 0.05). The signal-averaged electrocardiograms were more often abnormal, but the differences were not significant. The total mortality rate in our patient group was 7.8%, with nonsudden cardiac death in four patients, noncardiac death in one patient, and sudden death in one patient. In our patient group a lower ejection fraction and inducible sustained monomorphic ventricular tachycardia were predictors of future ICD discharge after implantation. The survival rate after transvenous ICD implantation is excellent; a longer follow-up period is necessary to further define predictors of total mortality rate.

Cardiac Pacing, Artificial↗

PubMed1994

Patient acceptance of implantable cardioverter defibrillator devices: changing attitudes.

Clinical experience suggests that the implantable cardioverter defibrillator (ICD) can reduce sudden cardiac death and total mortality in patients with malignant ventricular arrhythmia who meet the selection criteria for implantation. In addition to surgical problems, patients are faced with psychological and social adjustments. Patient acceptance for such therapy is marked by perceived concerns regarding device discharge, life-style alterations, and complications. We included 57 patients with ICDs in a study of their acceptance of the device. Results of a specially designed questionnaire (state-trait personality inventory) showed that 47 of 57 patients felt that their symptoms improved with the ICD system, 32 were constantly aware of the device, and 24 patients acclimated to the ICD system within less than 2 months. With respect to the need for battery replacement, only 27 patients requested a repeat electrophysiologic evaluation, 20 patients stated fear of ICD discharges, 12 patients revealed physical discomfort from the device, and limited quality of life occurred in eight patients. Fifty-five of 57 patients answered that it was worth having an ICD device implanted, 30 (53%) patients returned to active life, and 56 (98%) would advise another patient to have an ICD implantation if necessary. In conclusion, in general, the acceptance of the ICD as a tool for management of life-threatening ventricular tachyarrhythmias is very high. Quality of life and patient acceptance are important criteria for successful ICD therapy in addition to the improved survival rate.

Attitude to Health↗

PubMed1994

Reduction of cerebral blood flow with induced tachycardia in rats and in patients with coronary artery disease and premature ventricular contractions.

A reduction of cerebral blood flow (CBF) was observed in experimental studies in rats immediately after the onset of parasystolic rhythm or with stable, but haemodynamically compromising, tachycardias. Based on these data and with a view to studying the effects of premature ventricular contractions (PVCs) on the cerebral circulation in humans, CBF was measured using the 133-Xenon inhalation method in 24 age matched human controls (group A1: age 58.5 +/- 6.2 years; group A2: 52.2 +/- 7.8 years) in nine coronary artery disease (CAD) patients without PVCs (B), in 11 CAD patients with frequent PVCs (> 300.h-1) (C) and in nine patients, after exclusion of CAD by angiography, also with frequent PVCs (> 300.h-1) (D). Holter monitoring was performed during the CBF measurement. CBF determined in the human control groups A1 and A2 was 79.9 +/- 9.9 ml.100 g.-1 min-1 and 81.5-13.0 ml. 100 g-1 min-1, respectively. CBF was 74.1 +/- 13.6 ml . 100 g.-1 min-1 (P = 0.267 vs A1) in group B, 65.8 +/- 11.8 ml.100 g-1 min-1 (P = 0.004 vs A1) in group C and 74.2 +/- 15.6 ml.100 g.-1 min-1 (P = 0.218 vs A2) in group D. The significant reduction of CBF in CAD patients with frequent PVCs suggests that arrhythmias have a significant impact on CBF. Non-CAD patients with frequent PVCs did not show significant CBF decreases in comparison with controls. One can hypothetize that an impairment of electrical postextrasystolic potentiation, due to premature ventricular depolarization, and hence myocardial dysfunction leads to CBF reduction in CAD patients. The CBF reduction with CAD could also reflect concomitant coronary and cerebral arteriosclerosis.

Aged↗

PubMed1994

Loss of late potentials after radiofrequency catheter ablation of recurrent ventricular tachycardia in a patient with right bundle branch block.

The case of a patient with a history of myocardial infarction and recurrent ventricular tachycardia undergoing attempted radiofrequency catheter ablation with loss of late potentials is described. Prior to energy delivery fractionated, late activation could be found using the signal-averaged ECG despite the presence of a right bundle branch block. After successful catheter ablation, the clinical ventricular tachycardia was no longer inducible and the signal-averaged ECG, recorded the next day, showed marked changes indicating loss of late potentials. Our report emphasizes the possibility of late potential recordings despite the presence of bundle branch block.

Aged↗

PubMed1994

Myocardial and cerebral hemodynamics during tachyarrhythmia-induced hypotension in the rat.

BACKGROUND: The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension. METHODS AND RESULTS: MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias. CONCLUSIONS: The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.

Animals↗

PubMed1994

[Cerebral circulation in patients with dilated cardiomyopathy and aortic valve diseases].

The present study was performed in order to investigate the effect of dilated cardiomyopathy and severe aortic valve disease on cerebral blood flow. Cerebral perfusion was determined in 39 healthy volunteers representing two control groups of different age (77.7 +/- 8.7; 79.7 +/- 8.1 ml/100 g/min), in 7 patients with dilated cardiomyopathy (64.0 +/- 4.7 ml/100 g/min), in 11 patients with severe aortic stenosis (71.1 +/- 14.8 ml/100 g/min), and in 6 patients with severe aortic regurgitation (54.6 +/- 5.8 ml/100 g/min). Regional cerebral blood flow was measured with the 133Xenon inhalation method. Cerebral blood flow in severe aortic regurgitation patients (p = 0.006) was markedly and significantly reduced versus controls, whereas in dilated cardiomyopathy patients (p = 0.197) and in patients with severe aortic stenosis (p = 0.111) cerebral blood flow was not significantly reduced. A chronic adaptation of cerebral blood flow to the profound reduction of cardiac output is assumed in dilated cardiomyopathy patients. The collapsing pulse and the maximal reduction of mean arterial blood pressure in severe aortic regurgitation patients cause the reduction of autoregulatory capacity of cerebral blood flow with subsequent decrease of brain perfusion. Measurement of cerebral blood flow appears to be suitable for evaluation of perfusion deficits due to cardiac abnormalities. It provides an additional parameter for estimating the indication of valve replacement in patients with aortic valve disease.

Adult↗

PubMed1994

[Methods, topography and mechanisms of radiofrequency ablation of AV-nodal reentry tachycardia].

Three different methods of radiofrequency catheter ablation of AV nodal reentrant tachycardia were investigated in 128 patients. Results, relapses, and complications using anterior approach (n = 15), moved catheter (n = 20), and posterior-inferior approach (n = 93) were compared. Eight mechanisms of ablation of AV nodal reentrant tachycardia were distinguished: 1) Ablation of fast pathway (n = 8), 2) of slow pathway (n = 22), 3) modification of fast (n = 12), 4) slow (n = 54), or 5) both pathways (n = 13), 6) Ablation of fast and modulation of slow pathways (n = 4), 7) ablation of slow and modulation of fast pathways (n = 12), and 8) ablation of both pathways (n = 3). The criteria of diagnosis of these mechanisms and a mapping grid of Koch's triangle were proposed. The fast pathway is located in the anterior septum in a region with identical amplitudes of atrial and ventricular deflections and the slow pathway could be found posteriorly in a more ventricular location. The anatomical location of the slow pathway differed more widely than the location of the fast pathway. The best method with lowest risk could be recommended as the ablation of the slow pathway. This method implicated the lowest incidence of complications. We observed relapses in 12 patients during control studies 30 min, 3-5 days, and 3-6 months after first ablation procedure. These arrhythmias could be ablated in a second attempt in eight and in a third procedure in four patients. With increasing experience the radiofrequency catheter ablation of AV nodal reentrant tachycardia will be the method of first choice in patients with recurrent tachycardia.

Adult↗

PubMed1994

[Intermittent focal cerebral ischemia in hypotension due to pacemaker syndrome].

A pacemaker syndrome manifested as transient sensoric aphasia in a 68-year-old woman with a VVI-pace-maker implanted after SA-block. The attack occurred during long-term blood pressure recording and Holter monitoring. Borderline hypotension was documented during ventricular pacing which induced a retrograde excitation of the atrium. Clinical investigations excluded any intracranial abnormality, any source of embolism or stenosis of extra- and intracranial cerebral arteries. Cerebral blood flow measurements revealed a significant increase during pacing at elevated heart rate. Therefore, a device for AV-sequential pacing was implanted and basic pacing rate was elevated. The present case report indicates that focal and not only global cerebral ischemia can be produced by an impairment of systemic hemodynamics due to hypotension and a pacemaker syndrome. Improvement of cerebral blood flow during pacing is an unexpected finding contrasting with the concept of autoregulation. In addition, pacemaker implantation should be discussed in patients with transient cerebral perfusion deficits if an improvement of cerebral blood flow is documented along with rising heart rate.

Aged↗

PubMed1994

[Atrial fibrillation and atrial flutter: pathophysiology and pathogenesis].

Chronic atrial fibrillation is a very common arrhythmia affecting 2 to 4% of the population older than 60 years of age. Atrial fibrillation may cause disabling symptoms and serious adverse effects, such as impairment of cardiac function or thromboembolic events. It is also associated with an increased risk of death. In the past, the most common underlying heart disease related to chronic atrial fibrillation was rheumatic heart disease. Today, this disease occurs relatively rarely. Nevertheless, the incidence of atrial fibrillation is likely to increase in the future due to the aging of the population, since its prevalence increases with age. In most patients with chronic atrial fibrillation, the arrhythmia can be attributed to organic heart disease or metabolic disorders. In western countries ischemic and hypertensive heart disease (including sick sinus syndrome) and alcohol (holiday heart syndrome) are numerically more important than the classical causes of atrial fibrillation--rheumatic heart disease and thyrotoxicosis--which are declining in incidence. Overall, atrial fibrillation is associated with an increased mortality. In about 15% of patients with chronic atrial fibrillation, no underlying cardiac or metabolic abnormality can be found, also the arrhythmia can itself give right to atrial dilatation. Atrial fibrillation consists most probably of several coexisting reentrant wave fronts of activation within the atria. Atrial activation and atrial fibrillation is as follows: multiple wavelets sweep round the atria in irregular, shifting patterns; completed reentrant circuits are the exception. Atrial flutter in its common form is characterized by evidence of atrial activity at a rate of 250-350 bpm, and usually almost exactly 300 bpm.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1994

[Non-pharmacologic therapy of atrial fibrillation].

Since patients with recurrent atrial fibrillation are prone to recurrences, even under treatment with antiarrhythmic agents, alternative treatment modalities are being sought. Today, the non-pharmacological treatment modalities such as modification or ablation of the AV node or the operative procedures ("maze" or "corridor" operation) do not cure these patients. The non-pharmacological therapies are indicated if severe symptoms are due to high ventricular rate with hemodynamic compromise. In such cases, His bundle ablation followed by rate adaptive pacing can achieve control of symptoms in the majority of patients. In the future, more refined techniques for ablation or the introduction of automatic atrial cardioverters will extend therapeutic options.

Anti-Arrhythmia Agents↗