[Myocardial scintigraphy in patients with acute and chronic coronary insufficiency].
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Biomedical subjects
Publications and source records attributed to D Durrer.
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The effect of amiodarone in the Wolff-Parkinson-White syndrome was studied with programmed electrical stimulation of the heart in 15 patients. All 15 patients had circus movement tachycardias; 7 also had atrial fibrillation. Programmed electrical stimulation was performed before and after 14 days of oral administration of amiodarone. The effective refractory period of the accessory pathway lengthened in an atrioventricular direction in all patients and in a ventriculoatrial direction in eight patients. The effective refractory period of the atrium and ventricle lengthened in 14 and 12 patients, respectively. After administration of amiodarone, circus movement tachycardia could no longer be initiated in five patients. The zone of tachycardia narrowed in four patients, did not change in two and increased in seven. The effect of amiodarone on initiation of circus movement tachycardia could be related to differences in effect of the drug and in the mechanism of tachycardia in individual patients. In all patients in whom tachycardias could still be initiated after treatment with amiodarone the heart rate during tachycardia was slower than before treatment. This slowing was caused by a decrease in conduction velocity of the circulatory wave in different parts of the tachycardia circuit. The effect of amiodarone in prolonging the refractory period of the accessory pathway makes this drug especially useful in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation.
Five human fetal hearts of gestational ages ranging from 12 to 16 weeks were studied with both electrophysiological and anatomical techniques. The electrophysiological behavior of these hearts was comparable with results obtained with other animal species and adult human hearts. This indicates that the fetal heart is functionally mature from an early stage of development; however the tissues are not fully differentiated from an anatomical standpoint. Results of mapping experiments indicated that atrial activation occurred through broad wave fronts, and no electrophysiological evidence was found to support the concept of "specialized internodal conduction." In two hearts, the node and bundle were found to be anatomical contiguity with ventricular myocardium throughout their length, but the conducting tissues were already functionally insulated from the ventricles. The results have significance with regard to concepts of the "sudden death in infancy syndrome" and ventricular pre-excitation.
Pathological findings in the heart and particularly in the coronary arteries are reported from 70 patients dying from pump failure after acute myocardial infarction. Fifty of the patients had died in cardiogenic shock, the remainder from refractory congestive heart failure. Three-vessel disease (greater than or equal to 75% occlusion) was present in 68 per cent of the group with cardiogenic shock but in only 35 per cent of those with fatal congestive heart failure (P less than 0-02). In both groups there was an almost equal incidence (84% for cardiogenic shock and 80% for congestive heart failure) of severe disease (greater than or equal to 75% occlusion) over a long segment of the left anterior descending artery. However, there were differences between the two groups regarding the involvement of the other coronary arteries. Whereas patients with cardiogenic shock generally showed severe disease over a long segment in all coronary arteries, in 60 per cent of those with congestive heart failure there was only local severe narrowing of the right coronary artery with little or no narrowing of the peripheral part. Similarly, 60 per cent of those with congestive heart failure had less than 75 per cent narrowing in the left circumflex artery. These anatomical findings may be of relevance with regard to desirability of acute coronary bypass surgery in patients with pump failure after acute myocardial infarction.
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Cycle-length-dependent changes in AV nodal cell activation were studied in isolated preparations from rabbit hearts. Transmembrane action potentials were recorded from the node while it was propagating impulses initiated in the atrium with an accelerating train of stimuli. This train consisting of five successive stimuli separated by progressively shorter intervals was uniformly repeated at every 10th basic beat, each time reproducing a sequence of five different increasing AV nodal delays. The AN and NH cells were found to contribute only slightly to the cycle-length-dependent AV nodal delay which developed mainly in the small N zone, located centrally in the AV node. With the increasing delay, the action potentials from this N zone typically dissociated into two components synchronous with late AN and early NH activity, respectively. The amplitude of the first component decreased, wheareas that of the second increased progressively in N cells activated progressively later. No cells were activated at an intermediate time between the two components. This dissociation was not accompanied by changes in the activation pattern of the AV node. The different nodal cells classified according to their response to the accelerating train delineated functional zones corresponding to different anatomic structures. The possible mechanisms which would explain the cycle-length-dependent AV nodal delay are discussed.
UNLABELLED: Clinical setting, presence and degree of heart failure (HF) of 80 consecutive patients who developed atrial fibrillation (AF) following acute myocardial infarction were compared to that of 620 patients with acute myocardial infarction and sinus rhythm admitted during the same period. 33 of 163 (20%) with initially mild HF developed AF compared to 5 of 74 (7%) with initially severe HF, and 42 of 463 (9%) without HF (P less than 0.01). Patients with mild HF who developed AF had a higher incidence of deterioration of clinical condition (39 vs 14%, P less than 0.005) and a higher mortality rate (52 vs 22%, P less than 0.001) than patients with mild HF and sinus rhythm. The presence of AF influenced neither the development of HF and mortality rate in patients without HF nor the degree of HF and mortality in patients with initially severe HF. Pericarditis was present in 12 of 42 (28%) with AF occurring in the absence of HF, compared to 3 of 38 (8%) with AF and initially mild HF and to 56 of 620 (9%) with sinus rhythm (P less than 0.05). CONCLUSIONS: (1) in the absence of HF, AF may be the consequence of pericarditis; (2) in patients with mild HF, AF may be consequence of HF; (3) the contribution of AF to the subsequent clinical course is only of prognostic significance in patients with mild HF.
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In a prospective study of 300 consecutive patients who survived the first 24 h of acute myocardial infarction, pericarditis was present in 44 patients (14-7%). The only factors independently associated with pericarditis were transmural myocardial infarction, extent of myocardial damage, atrial fibrillation, and longer duration of fever. Pericarditis did not affect immediate prognosis or incidence of cardiac rupture. These findings and the high incidence of atrial fibrillation suggest that anticoagulant therapy should not be discontinued in patients with pericarditis complicating acute myocardial infarction.
Of 880 patients admitted consecutively to a coronary-care unit with acute myocardial infarction, 200 had had a previous infarction. The mortality-rate in the first twenty-eight days after infarction was higher in the group with recurrent infarction (26 per cent) than in the group with first infarctions (16.9 per cent). When the patients were matched for sex and age this difference in mortality-rate was only statistically significant in men aged less than seventy. In patients with previous infarctions the short-term prognosis was worse in those with two or more previous infarctions, in those in whom infarction had occurred less than three months before, and in those with a previous infarction in the anteroseptal wall.
Right ventricular hypertrophy (RVH) of mild, moderate, or severe degree was produced in six dogs following systolic overload of the right ventricle by surgical banding of the pulmonary trunk. Activation of the myocardium and specialized conducting tissue of the right ventricle was studied using intramural multi-electrodes or an exploring electrode, first with the heart in situ and then with the heart in a modified Langendorff perfusion circuit. Normal epicardial and intramural activation patterns were found in RVH, and the prolonged excitation time was found to be due to the increased muscle mass. No delay in activation was found in any part of the specialized conducting tissue of the right ventricle. Late activated Purkinje fibres were found in the outflow tract of the right ventricle in the dogs with hypertrophy and in a control series of normal dogs. The present electrocardiographic criteria for complete and incomplete right bundle branch block (RBBB) are based on widening of the QRS complex and the rSR pattern. This type of change can occur also in RVH. Because it has been shown here that no delay occurs in the specialized conducting system of the right ventricle in RVH secondary to systolic loading; the application of criteria to electrocardiograms that also fulfil the criteria for RVH may be misleading. It is suggested that in such cases the diagnosis of a conduction disturbance must also depend upon other methods, and that the terms "incomplete' and "complete' RBBB should be handled with care in this context.
Myocardial imaging using 201Tl was performed in 10 patients with supposedly normal myocardial perfusion and in 11 patients with acute myocardial infarction. In all patients with acute myocardial infarction the scintiscan showed an area with diminished radioactivity at the site corresponding the electrocardiographic localization of the infarction. 210Tl seems to be of diagnostic value for recognizing acute myocardial infarction in the very first hours after its onset and for visualizing infarction in patients in whom pre-existing electrocardiographic abnormalities prevent its diagnosis and/or localization.
Two cases with conduction disturbances in the His bundle are described. In each it was not possible to obtain both components, H and H', of the "split" His bundle potential at one time from a single bipolar electrode catheter with an interelectrode distance of 10 mm. Initial failure to record the proximal His component (H) let to the incorrect diagnosis of block located within the atrioventricular (A-V) node, of third degree, in patient A, and of first to second degree in patient B. However, careful withdrawal of the catheter resulted in the appearance of proximal components (H), accompanied by disappearance of the distal components (H') of the His bundle potential. Apparently the lesion in the His bundle and the recording electrodes were spatially related in such a way that the bipolar electrode could not override the lesion. In view of these findings it is advocated that in patients the A-V conduction disturbances the His bundle catheter should be withdrawn carefully, if the initial recording reveals His bundle potentials bearing a time relation to the ventricular complexes, or advanced carefully, if these His potentials are related to the atrial activations, in order to demonstrate the (co)existence of a lesion in the His bundle. Search for a proximal His potential by withdrawal of the catheter should be done, if possible, while the atrium is paced at a rate in excess of the spontaneous sinus rate since the H potential may be obscured by the atrial complex if the A-V nodal transmission time is short at the spontaneous rate, as was the case with patient A. In patient B the not yet described phenomenon of bradycardia-dependent block within the His bundle was observed.
To study the pathway of tachycardia in patients with the Wolff-Parkinson-White (WPW) syndrome and reciprocal tachycardias, results from intracavitary recordings and atrial and ventricular stimulation were reviewed in 71 patients with the WPW syndrome and 54 patients without pre-excitation. In all patients a reproducible tachycardia could be initated and terminated by appropriately timed electrical stimuli. The following findings were accepted as suggesting the participation of an accessory pathway in the tachycardia circuit: 1) no increase in ventriculo-atrial conduction (V-A C) time following ventricular stimuli given with increasing prematurity; 2) activation of right or left atrium (depending upon the location of the atrial end of the accessory pathway) prior to activation of atrium in the His bundle lead; 3) slowing of tachycardia following bundle branch block to the ventricle in which the accessory pathway inserts; 4) V-A C time of early stimuli on the ventricle during the tachycardia equal to or less than the V-A c time following QRS complexes during tachycardia; 5) inability to initiate tachycardia or slowing of tachycardia following the administration of drugs affecting the accessory pathway. Accepted as suggestive for atrioventricular (A-V) nodal re-entry were the following factors: 1) activation of atrium following initiation of tachycardia by a single atrial premature beat after activation of the bundle of His but before or simultaneous with ventricular activation in first and subsequent beats of tachycardia; 2) initiation of tachycardia following a gradual increase in V-A C time with the appearance of a His bundle electrogram in between the premature beat and retrograde atrial activation; 3) gradual increase in V-A C time with the appearance of a His bundle electrogram following ventricular premature beats given with increasing prematurity; 4) two-to-one block distal to the A-V node or His bundle with persistance of tachycardia. If only positive findings were accepted, 51 patients of the WPW group used their accessory pathway during tachycardia. In eight patients re-entry was confined to the A-V node. In the remaining 12 patients the mechanism was not clear. Of the patients not showing pre-excitation in A-V direction, 47 patients seemed to have their re-entry circuit in the A-V node, five patients used an accessory pathway in V-A direction, and in two patients the pathway of tachycardia could not be identified.
UNLABELLED: In order to evaluate the events preceding primary ventricular fibrillation (PVF), continuous tape recording was performed in 262 patients consecutively admitted to the hospital within six hours of infarction in whom antiarrhythmic therapy was withheld. Warning arrhythmias (defined as ventricular ectopic beats occurring with a frequency of more than five beats per minute, in runs, falling in the vulnerable phase of the cardiac cycle or being multiformed) were registered in an equal percentage in patients who did or did not develop PVF. Immediately prior to PVF seven patients showed sinus tachycardia, 10 a sinus rate ranging from 60 to 100 beats per minute and two bradycardia due to complete atrioventricular block. The ventricular ectopic beat initiating PVF had a late coupling interval (QR'/QT larger than or equal to 0.85) in 11 patients and a left bundle branch block configuration as frequent as a right bundle branch block. CONCLUSIONS: 1) Warning arrhythmias are not considered good criteria for institution of antiarrhythmic therapy in order to prevent PVF. 2) In patients with sinus rhythm there may be an association between heart rate and onset of PVF. 3) The malignancy of a ventricular ectopic beat is not determined by its coupling interval or its configuration.