Direct radioimmunoassay with capillary chromatography tubes.
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Biomedical subjects
Publications and source records attributed to A Pick.
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We reviewed electrocardiograms of 23 patients with intermittent left bundle-branch block. A characteristic electrocardiographic pattern consisting of right and mid-precordial deep symmetrical T-wave inversions was detected during normal conduction in 19 of the 23. Of the seven patients who had cardiac catheterization, only two had findings suggestive or organic heart disease and only one had significant obstructive coronary disease. Thus we conclude that patients with intermittent left bundle-branch block frequently have T-wave inversions in right and mid-precordial leads during normal conduction that do not necessarily reflect coronary disease. These T-wave changes are similar to those after termination of chronic right ventricular pacing (left bundle-branch pattern), suggesting that both patterns of abnormal ventricular activation can produce abnormal repolarization when activation returns to normal.
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Electrophysiological and histological observations were made on the heart of the African lungfish. Impulse origin and propagation were studied using simultaneously recorded epicardial and pericardial electrograms. The primary pacemaker site in the lungfish was found to be at the sinus venosus at its junction with the left cardinal vein. Under a variety of circumstances, pacemaker function shifted to other sites. In response to stress, probably under vagal influence, the regular and rapid sinus venosus rate was generally superseded by an irregular and slower atrial pacemaker. Heart rate and sinoatrial and atrioventricular conduction times varied with changes in temperature [Q10=3.77, 2.55, and 5.46, respectively]. Although alterations in impulse formation and conduction did occur, the site of impulse formation and the patterns of conduction between heart chambers were usually fixed, implying the existence of an organized conduction system. Nonetheless, extensive histological study failed to disclose either organized nodal structures or specialized conduction pathways.
Eleven patients with tachycardia-dependent, bradycardia-dependent, or "pseudobradycardia-dependent" bundle branch block (BBB) alternans were studied. This classification is based on the following criteria: 1) When alternans is initiated by a sudden acceleration in ventricular rate, or it appears with aberration of the second beat after a pause, the alternans is tachycardia-dependent and results from a 2:1 bidirectional block in the affected bundle branch. 2) When alternans begins with the aberrant complex terminating a pause it is bradycardia-dependent; such an alternans results from alternating bundle branch cycle lengths and refractoriness, possibly produced by alternating transseptal retrograde penetration of the affected bundle branch. 3) In cases referred to as "pseudobradycardia-dependent BBB" alternans, a change from alternans to persiscardia-dependent BBB" alternans, a change from alternans to persistent BBB occurs as the cycle lengthens; however, the disappearance of BBB with further increase of the cycle length proves the tachycardia-dependence of the conduction defect.
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Various mechanisms that cause deviations from the classical manifestations of a parasystolic rhythm are reviewed and illustrated by selected clinical electrocardiograms. They consist of: (1) Transient or continued fixed coupling of the ectopic beats, due to (a) synchronization of basic and parasystolic rhythms; (b) reversed coupling of the basic to the ectopic rhythm (unidirectional protection); (c) the operation of supernormal phase of excitability; and (d) intermittent parasystole, due to gap in the protection of the parasystolic center. (2) Irregularities in response to a regular parasystolic discharge may be caused by a second degree exit block, usually of Mobitz type II, rarely of type I. An electrophysiologic basis for the emergence and maintenance of parasystolic rhythms appears to be abnormal states of spontaneous diastolic (phase 4) depolarization in otherwise latent subsidiary cardiac pacemakers.
Multiple areas of concealed intraventricular conduction are deduced on the basis of aftereffects observed in His bundle recordings. Electrocardiograms and His bundle recordings are presented from two patients with unstable bilateral bundle branch block, the instability of which depended on the interval at which ventricular depolarization was initiated by sinus or paced impulses. This circumstance allows postulation of 1) concealed transseptal retrograde penetration of the left bundle branch system; 2) concealed transseptal retrograde penetration of the right bundle branch system; 3) alternate beat Wenckebach phenomenon with two areas of block in the bundle branch system with concealed penetration of the proximal area; 4) concealed re-entry in the right bundle branch system during an H-V Wenckebach cycle with resetting of the sequence of 2:1 H-V block and return of the re-entry wave to the A-V node causing subsequent A-H block; 5) proximal 2:1 block and distal Wenckebach block producing only two consecutively blocked beats; and 6) infrahisian Wenckebach block with changes both in A-V conduction and QRS contour.
The classic pattern of the typical WP's consists of (1) progressive lengthening of the P-R intervals with the largest increment occuring in the second conducted beat, (2) progressive decrease in P-R increment which accounts for the progressive shortening of successive R-R intervals, and (3) the pause produced by the nonconducted P-wave is less than two P-P intervals. In 45 patients with atrial pacing-induced Wendkebach periods of A-V conduction, the structure of these was studied with His bundle recordings. Of the 128 periods analyzed exceeding 3:2 A-V conduction ratios, 66 per cent were atypical. In 24 patients with spontaneous WP's of A-V conduction, the electrocardiographic records were studied. Of the 98 periods analyzed exceeding 3:2 A-V conduction ratios, 86 per cent were atypical. WP's with A-V conduction ratios greater than 6:5 were all atypical. Five categories of atypical WP's are described.
In eight patients we have demonstrated manifold types of impairment of impulse conduction produced by hyperkalemia. These abnormalities of impulse conduction occurred either simultaneously or in sequence, and were located in the atria, in the A-V junction, in the fascicular distribution of the ventricular conduction system, or in the free ventricular walls. In association with the abnormalities of conduction, abnormal impulse formation was also frequently observed as manifested by acceleration of normal pacemakers or the emergence of ectopic pacemakers. In one patient hyperkalemia produced alteration in sinus and A-V junctional impulse formation which overshadowed conduction disorders. In all of the eight cases the hyperkalemia was considered to be noniatrogenic. Hyperkalemia appears to potentiate subclinical conduction abnormalities, especially in the His-Purkinje system. However, the presence of pre-existent intraventricular conduction defects such as a bifascicular block does not exclude the possibility that the site of an A-V conduction delay during hyperkalemia can be in the A-V node, as demonstrated by His bundle recording in one instance after development of second-degree (type I) A-V block.
This report concerns pathologic findings in a 54 year old woman with intermittent preexcitation who died of carcinoma of the breast. Electrocardiograms revealed predominantly normal sinus rhythm with a normal P-R interval and narrow QRS complex. Episodes of sinus rhythm, short P-R interval and QRS widening (with delta wave) were also recorded. During preexcitation QS complexes were noted in leads II, III, aVF, V1 and V4 to V6. Delta waves were negative in leads II, III, aVF and V1 isoelectric in leads V4 to V6 and positive only in leads I, aVL, V2 and V3. This case thus defies classification into any known variety of preexcitation. Complete serial sections, cut through the entire conduction system and both atrioventricular (A-V) rims, totaled 18,600 sections. These revealed no bundle of Kent. Instead, Mahaim fibers histologically identified as His bundle tissue gave off from the A-V bundle to both the right and the left sides of the septum associated with the normal fibers of James. This case reveals that (1) fibers of James can bypass the A-V node, (2) fibers of Mahaim can conduct, and (3) there are types of preexcitation in addition to types A and B.
Our study has defined normal electrocardiographic standards for Macaca arctoides. It appears that certain species differences exist in the electrocardiogram (ECG) in monkeys and that different criteria for normality may be necessary. Thus, in apparently normal Macaca arctoides a high frequency of Q waves and ST segment elevations of the J point type are present compared to Macaca mulatta. It is suggested that normal ECG criteria be established for each species of monkeys to allow accurate interpretation.
Concealed intraventricular conduction is defined and the following classification of the manifestations of concealed conduction into the bundle branch system is proposed. 1. Trans-septal retrograde concealed intraventricular conduction responsible for (a) perpetuation of functional bundle branch block initiated by a premature supraventriculra impluse; (b) alternation of aberrant ventricular conduction in supraventricular bigeminy; (c) normalization of intraventricular conduction with acceleration or rate in bradycardia-dependent bundle branch block, and (d) prevention of the manifestation of Wenchbach periods of conduction in a bundle branch or fascicle. 2. Antegrade concealed intraventricular conduction responsible for (a) prevention of expected aberrant ventricular conduction when a short cycle follows a long one, and (b) exceptions to the "rule of bigeminy". 3. Retrograde concealed intraventricular conduction of a ventricular escape in association with unidirectional bundle branch or fasciular block responsible for (a) resumption of AV conduction in "paroxysmal AV block" with bundle branch block, and (b) facilitation (due to supernormality) of conduction in type II AV block due to bilateral bundle branch block. 4. Concealed intraventricular conduction of a premature ventricular impulse responsible for (a) initiation or termination of a re-entrant ventricular tachycardia; (b) resetting of an idioventricular pacemaker, and (c) pseudo-intraventricular or pseudo-AV block.
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