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Biomedical subjects

R Lazzara

Publications and source records attributed to R Lazzara.

At least 181 records · Page 10Linked to original sources
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 2. Patterns of initiation and termination of re-entry.

The electrophysiologic mechanisms for the initiation and termination of re-entrant ventricular arrhythmias (RVA) were critically analyzed in dogs 3-7 days following ligation of the anterior descending coronary artery, utilizing direct recordings of the re-entrant pathway (RP) from the epicardial surface of the infarction zone. Re-entry could occur during a regular cardiac rhythm if the heart rate is within the narrow critical range during which conduction in a potentially RP exhibits a Wenckebach-like (W) pattern with a beat-to-beat increment of conduction delay until the activation waveform is sufficiently delayed to re-excite normal myocardium. If a regular cardiac rhythm is associated with limited conduction delay in a potentially RP, premature beats within a critical range of coupling intervals could result in sufficient conduction delay to induce re-entry. Re-entrant ventricular arrhythmias may be unmasked on abrupt termination of a critical fast rate of cardiac pacing only if pacing was terminated during those beats of a W pattern associated with marked conduction delay in a RP. RVA could be ended by one or more properly timed premature beats that would pre-excite part of the RP. An electrophysiologic mechanism for R-on-T and its relationship to onset of ventricular fibrillation was shown, based on markedly delayed RP conduction of the beat prior to the one apparently coupled to the premature beat.

Animals↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 3. Manifest and concealed extrasystolic grouping.

Re-entrant beats with regular extrasystolic grouping were seen in 44- of dogs 3--7 days following ligation of the anterior descending coronary artery. Utilizing direct recording of the re-entrant pathway (RP) from the epicardial surface of the infarction zone, we found extrasystolic grouping to be based on the infarction tachycardia-dependent conduction disorders in a potentially RP. Trigeminy and quadrigeminy were related, respectively, to a 3:2 and 4:3 Wenckebach-like conduction cycle in a RP. However, quadrigeminy could also be due to an underlying bigeminal rhythm with concealment of alternate re-entrant beats, i.e., concealed bigeminy. A bigeminal rhythm was the result of a 2:1 conduction pattern in a re-entrant pathway with a sufficient degree of conduction delay during the conducted beat of the 2:1 cycle to result in re-entry. A trigeminal or quadrigeminal rhythm could change to a bigeminal rhythm on critical shortening of the cardiac cycle. Fixed and variable coupling were related, respectively, to stable and changing conduction pattern in a re-entrant pathway. On the other hand, extrasystolic grouping could be concealed due to either block in the re-entrant pathway or entrapment in a small area of the closely bordering normal zone.

Animals↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine.

The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected. The impairment of conduction induced by lidocaine in the RP was directly related to its ability to abolish re-entrant ventricular beats and tachycardia. Gradual slowing of conduction in the RP consistently developed before abolition: lengthening of coupling of extrasystolic beats in surface leads and gradual slowing of ventricular tachycardia rate occurred. The termination of re-entry was characteristically associated with complete block in the RP. A "selectivity hypothesis" for the antiarrhythmic action of lidocaine is proposed.

Animals↗
PubMed1977

Second-degree atrioventricular block in the His-Purkinje system following acute myocardial infarction. Clinical observations on its evolution.

The evolution of second-degree atrioventricular block in the His-Purkinje system was studied in four patients with acute myocardial infarction, utilizing continuous electrocardiographic monitoring and serial His bundle recordings. Three patients had anterior wall infarction; all developed acute right bundle-branch block and two also showed a left anterior hemiblock one to four hours prior to onset of second-degree atrioventricular block. The fourth patient had an old anteroseptal infarction and chronic right bundle-branch block and left anterior hemiblock; he developed second-degree atrioventricular block following an acute lateroposterior infarction. His bundle electrograms were obtained during the insertion of a temporary ventricular pacemaker within the first 24 hours of onset of chest pain. A second His bundle electrogram was obtained during removal of the temporary paceemaker 7 to 14 days after the first recording. In all cases the block was localized in the His-Purkinje system. In three patients the first His bundle recording showed second-degree atrioventricular block with minimal increment of delay in conduction (3 to 10 msec) prior to the blocked beat (equivalent of Mobitz type 2 block). The second His bundle electrogram showed the development of significant increment of delay in conduction (35 to 210 msec) prior to block (equivalent of Wenckebach conduction). The fourth patient illustrated the reverse order of the observations seen in the other three. Three patients showed resumption of 1:1 atrioventricular conduction; however, when one patient was challenged with rapid atrial pacing, he developed repetitive block in the His-Purkinje system.

Aged↗
PubMed1977

The induction of ventricular arrhythmias in acute myocardial ischemia by atrial pacing with long-short cycle sequences.

Recent studies emphasize the importance of heart rate in the genesis of ventricular arrhythmias during myocardial ischemia. The role of alterations in rhythm has not previously been systematically investigated. In 20 dogs subjected to acute myocardial ischemia and crushing of the sinus node, standard electrocardiographic leads were recorded, as well as His bundle and epicardial electrograms from the normal and ischemic areas. Abrupt pauses in regular atrial pacing did not cause arrhythmias prior to the onset of ischemia; however, during ischemia, atrial pacing with intermittent abrupt pauses resulted in the induction of ventricular arrhythmias beginning after the second conducted beat following each pause (ventricular premature beats, 20/20; ventricular tachycardia, 19/20; and ventricular fibrillation, 8/20). Onset of the arrhythmia was associated with increased delay in activation of ischemic epicardium and fractionation of the electrogram potential of the second conducted impulse. Typical Gouaux-Ashman phenomenon was an incidental observation. Unlike the Gouaux-Ashman phenomenon, which is restricted to the His-Purkinje system, the phenomenon we observed orginated within ischemic myocardium. In vitro studies indicate that the underlying mechanism may be related to postrepolarization refractoriness induced by ischemia.

Animals↗
PubMed1977

Long-term clinical and hemodynamic studies after ventricular aneurysmectomy and aorta-coronary bypass.

Late clinical and hemodynamic evaluations in 18 patients with ventricular aneurysmectomy and aorta-coronary bypass are presented. Tne patients had significant obstructive lesions in two major vessels (55 per cent), and 6 had extensive three vessel disease (33 per cent). In 13 patients, 21 aorta-coronary saphenous bypass grafts were performed in addition to aneurysmectomy. The operative mortality rate was 11 per cent. One patient died suddenly 5 months after the operation (one year mortality rate 17 per cent). The 15 surviving patients have been followed up for 12 to 41 months (average 24 months). Clinical results were considered excellent in 2 patients who have been asymptomatic (Class I, N.Y.H.A.). Nine others were considered to have good clinical results (Class II). Five patients have continued to have congestive heart failure and angina on minimal effort (Class III or IV). Six of the 11 patients considered to have excellent or good results underwent postoperative hemodynamic studies 6 to 34 months after the operation. A significant increase in cardiac index was documented in all 6 patients. Paradoxic movement was not detected in any of the postoperative ventriculograms. Five of the seven venous grafts inserted were patent. Elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index, and a persistent dyskinetic area in the left ventricle were found in 2 patients considered to have poor clinical results. Clinical and hemodynamic evaluations have shown a significant improvement in most patients surviving ventricular aneurysmectomy. However, postoperative systemic embolism, myocardial infarction, progression of coronary artery disease, transient cerebral ischemic attacks, graft occlusion, arrhythmias, and mitral regurgitation in previously prolapsed mitral valve leaflets account for progressive disability and limited activity after a successful operation.

Adult↗
PubMed1976

Mitral valve prolapse. Recent concepts and observations.

The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.

Animals↗
PubMed1976

Selective versus non-selective His bundle pacing.

His bundle pacing was achieved in 10 anaesthetized open chest dogs by stimulation from bipolar electrode catheters positioned in the aortic root and right heart. Recordings were taken directly through plunge wires from the right atrium, high ventricular septum, and epicardial sites on the right and left ventricles. Six types of response were seen during A-V junctional stimulation: (1) low atrial pacing; (2) combined atrial and His bundle pacing; (3) His bundle pacing; (4) combined atrial, ventricular septal, and His bundle pacing; (5) combined septal and His bundle pacing; and (6) ventricular pacing. Pacing of the His bundle in combination with the atrium and/or ventricular septum is designated as non-selective, whereas stimulation of the His bundle alone is considered selective pacing. Non-selective His bundle pacing can be recognized from the surface leads by changes in onset and amplitude of the QRS with appreciable T-wave alterations. Although electrode position was an important determinant of the type of pacing achieved, a variety of patterns of stimulation resulted from variation in the modalities of the pacing stimulus, ie, polarity, intensity, and duration. Unless these factors are considered, selective His bundle pacing may not be achieved.

Animals↗
PubMed1976

Intermittent bundle-branch block in patients with accessory atrio-His or atrio-AV nodal pathways. Variants of the Lown-Ganong-Levine syndrome.

Intracardiac electrophysiological studies were performed in two patients with a documented history of repetitive supraventricular tachyarrhythmias. Case 1, with short PR interval and narrow QRS complexes had a short AH interval and intermittent right bundle-branch block. Thus the short PR wide QRS syndrome is not always a result of the Wolff-Parkinson-White syndrome but can also be seen in the Lown-Ganong-Levine syndrome coexisting with bundle-branch block. Case 2, with normal PR and AH at the lower limits of normal, showed the dual pathway response to atrial pacing that can occur in patients with Lown-Ganong-Levine syndrome. He also had tachycardia-dependent right bundle-branch block and left posterior hemiblock. Therefore, neither the short PR interval nor the narrow QRS complexes characterized these forms of pre-excitation. The constant features were, from the clinical viewpoint, the occurrence of repetitive supraventricular tachyarrhythmias, and electrophysiologically the abnormal response to atrial stimulation.

Arrhythmias, Cardiac↗
PubMed1976

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Arrhythmias, Cardiac↗
PubMed1976

Re-entry due to manifest and concealed. His bundle ectopic systoles. Report of a case.

Concealed (C) His bundle ectopic systoles (H') have been shown in man to give rise to first and second degree atrioventricular (A-V) block and to simulate nonconducted atrial premature beats (P'). This report outlines a hitherto undescribed electrophysiologic consequence of H' in a 69-year-old man with arteriosclerotic heart disease and a Wenckebach type second degree A-V block in the His-Purkinje system. During a His bundle study, H' were shown to conduct either to the atria and ventricles with varying relationships to P' and QRS, or to conduct only to the atria, simulating nonconducted P' or atrial fusion beats. Both types of H' could initiate a re-entrant arrhythmia during retrograde conduction. Of particular interest are late coupled H' that failed to conduct to the ventricles and also failed to activate the atria because of prior capture by the sinus impulse (CH'). These CH' could also initiate re-entry by conducting retrogradely to engage the subatrial re-entry circuit. Evidence is presented to suggest re-entry occurs by way of a retrograde concealed accessory pathway and antegrade conduction in the atrioventricular node.

Aged↗
PubMed1976

The His-Purkinje electrocardiogram in man: an initial assessment of its uses and limitations.

A methodology is described for noninvasive recording of the electrical activity generated by the His-Purkinje system of man utilizing filtering, high amplification, and signal averaging. A waveform ranging between 1 and 10mu V was observed during the P-R segment. In many individuals, there was temporal overlap between the terminal P wave and the initial portion of the His-Purkinje waveform. In ten patients with long P-R intervals there was a strong correlation (r greater than 0.95) between the H-V time measured by electrode catheter and the duration of the His-Purkinje waveform. In two patients with atrial fibrillation the resultant His-Purkinje waveform was similar in morphology and duration to those observed in the ten patients. In each group H-V time was determined noninvasively and a waveform associated with electrical activation of the major portions of the His-Purkinje system was obtained.

Action Potentials↗
PubMed1976

Regional refractoriness within the ventricular conduction system. An evaluation of the "gate" hypothesis.

We studied the refractoriness of Purkinje fibers with the intent of localizing critical sites of block of premature impulses. To preserve the ventricular conducting system (VCS) nearly intact in vitro, we used a modification of the Elizari preparation. This was superfused with a physiologic salt solution. Action potential durations increased progressively from the His bundle to the distal Purkinje fibers along three pathways: (1) the main right bundle branch and moderator band; (2) the anterior border fibers of the left bundle and anterior false tendons; (3) the posterior border fibers of the left bundle and posterior false tendons. The action potential durations near the terminations of the false tendons were the longest ones found. The interior fibers of the left bundle branch had action potentials of shorter duration and greater variability than those of simultaneously activated fibers in the right bundle branch or the border fibers of the left bundle branch. Similarly, on the right side, the septal branches of the right bundle had action potentials of shorter duration than those of the moderator band. We also found that the fibers with short action potential durations provided the quickest pathways to septal myocardium. When extrastimuli were applied to the His bundle, block in a bundle branch always occurred in the proximal 1 or 2 cm of the main bundle branch. Experiments performed in vivo in which extrastimuli were delivered to the atrium or His bundle and recordings made from the terminations of false tendons and the distal ends of the main right bundle branch confirmed the finding that the critical sites of block were located in the proximal main bundle branches.

Action Potentials↗
PubMed1976

Hierarchy of ventricular pacemakers.

To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in virto, in normal hearts and in hearts 24 hours after myocardial infarction. Excape pacemaker foci were localized in vivo during vagally induced atrial arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographic limb leads. The VSCS was isolated using a modified Elizari preparation or preparations of each bundle branch. Peacemakers were located by extra- and intracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43+/-11 (mean+/-SD) beats/min. After beta-adrenergic blockade, the mean rate fell to 31+/-10 beats/min, but there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146+/-20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43+/-10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infarct zone. The mean firing rates were not influenced by beta-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, but after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence.

Animals↗
PubMed1975

Extracardiac recordings of His-Purkinje activity during conduction disorders and junctional rhythms.

Previous investigations have demonstrated a surface recording technique using signal averaging to detect electrical activity during the "isoelectric" P-R segment. Various physiological and pharmacological interventions suggest that the source of these potentials isthe His-Purkinje system (HPS). In order to assess the sensitivity of averaged recordings to changes in HPS activation, i.e., conduction defects in the HPS recordings were made directly from the heart surface using a bipolar, anterior-posterior epicardial lead in 15 dogs which underwent thoractomy. The signal was amplified, filtered and averaged using a digital computer for purposes of signal enhancement. The epicardial averaged lead (EAL) contained activity coincident with HPS depolarization and similar to those recorded by leads on the body surface of intact dogs from previous studies. The standard ECG and His bundle electrogram from an electrode catheter served as references in localizing and assessing several conduction disorders experimentally produced by traumatic and ischemic injury. Among the disorders produced were: 1) atrioventricular (A-V) nodal block which resulted in loss of recorded activity in the EAL following the P wave. 2) First and second degree intra-His bundle block produced by anterior septal artery ligation showed split His potentials in the HBE (1 degree) and 2:1 conduction with block in the His bundle (2 degrees). In the blocked beats the EAL showed a reproducible portion of the activity coincident with proximal His bundle activity of the split His potentials in both cases. 3) In four cases of proximal right bundle branch block produced by anterior septal artery ligation the relatively proximal portions of HPS activity in the EAL showed marked diminution. 4) Two cases of distal His bundle or bilateral bundle branch delay were seen as prolonged H-V time and a normal QRS pattern. The early and late portions of the HPS activity in the EAL were not markedly changed while the middle portion was prolonged and fractionated. 5) Junctional rhythms produced by crushing the SA node resulted in no atrial activity occurring prior to HPS depolarization in the EAL. However, the QRS was preceded by HPS activity whose onset was coincident with the H recorded in the His bundle electrogram. The EAL showed consistent and reproducible morphology and timing of HPS activity at different heart rates during normal conduction and consistent alterations of the HPS activity during abnormal conduction.

Animals↗
PubMed1975

Electroide cather recording during malignant ventricular arrythmia following experimental acute myocardial ischemia. Evidence for re-entry due to conduction delay and block in ischemic myocardium.

In 20 anesthetized opened-chest dogs, plunge wire and electrode catheter recordings of the this bundle electrogram which also showed septal activation, were monitored before and after ligation of the anterior septal artery. The average time to onset of ventricular tachycardia after ligation was 5-1/2 min. The evolution of the arrhythmia was temporally related to progressive fragmentation and delay of the septal potential, resulting in a marked increase in total ventricular activation time (up to 335 msec). In six experiments the fragmented, delayed septal depolarization was inscribed well beyond the T wave of the surface QRS prior to the onset of arrhythmias. Various conduction disorders involving the ischemic septal myocardium were observed which closely correlated to the patterns of conduction disorder in the ischemic proximal His-Purkinje system. First degree block, 2 degree block of the Mobitz II and Wenckebach types, higher degree block and paroxysmal complete block occurred. The onset of the arrhythmia was characteristically associated with a Wenckebach pattern of conduction delay of a part of the septal deflection. Conduction disorders of the ischemic myocardium were tachycardia-dependent. Bradycardia resulted in recovery of form, duration, and timing of the septal potential with the coincident disappearance of ventricular arrhythmias. The study shows that the basic prerequisites for re-entry do exist during the early period following occlusion of a major coronary artery and can explain the malignant phase of ventricular arrhythmias. Similar disorders in man may be detected by intracardiac electrode catheter recordings.

Acute Disease↗