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Biomedical subjects

R Lazzara

Publications and source records attributed to R Lazzara.

At least 127 records · Page 7Linked to original sources
PubMed1989

Localization of left free-wall and posteroseptal accessory atrioventricular pathways by direct recording of accessory pathway activation.

With the advent of catheter ablation techniques, precise localization of accessory AV pathways (AP) assumes greater importance. In an effort to define the course of AP fibers, we attempted to record activation of 56 left free-wall and 23 posteroseptal APs in 62 patients undergoing electrophysiological study. The coronary sinus (CS) and great cardiac vein (GCV) were mapped using orthogonal catheter electrodes, which provide a recording dipole perpendicular to the AV groove. The tricuspid annulus (TA) was mapped using a 2 mm spaced octapolar electrode catheter. Potentials were considered to represent AP activation only if they could be dissociated from both atrial and ventricular activation by programmed stimulation. Orthogonal catheter electrodes in the CS and GCV were advanced beyond the site of earliest retrograde atrial activation and/or earliest antegrade ventricular activation in 45 of the 56 left free-wall APs, and AP potentials were recorded from 42 (93%). An oblique course was identified in 36 APs, with the ventricular insertion being recorded 4-30 mm (median 15 mm) distal or anterior to the atrial insertion. In three patients, antegrade and retrograde conduction proceeded over different (but close) parallel fibers. AP potentials were recorded from 19 of 23 posteroseptal pathways. Ten pathways (left posteroseptal) were recorded from the CS, beginning 5-11 mm (median 9 mm) distal to the os, with potentials extending 8-18 mm (median 11 mm) distally. Four pathways (mid-septal) were recorded along the TA, anterior to the CS ostium and posterior to the His bundle catheter. Five pathways (right posteroseptal) were recorded along the TA, directly opposite or immediately posterior to the CS ostium. One of the patients had both midseptal and left posteroseptal pathways and three patients had both right posteroseptal and left posteroseptal pathways. We conclude: 1) left free-wall APs transit the AV groove obliquely and may be comprised of multiple, closely spaced, parallel fibers; 2) the anatomical location of "posteroseptal" pathways is variable and the presence of fibers at multiple sites is common; and 3) direct recordings of AP activation facilitate tracking of the accessory pathway along its course from atrium to ventricle and help identify the presence of multiple fibers.

Action Potentials↗
PubMed1988

Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that beta-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, beta-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.

Anti-Arrhythmia Agents↗
PubMed1988

Demonstration of a different sensitivity to epinephrine in isolated and in vivo hearts.

Studies in isolated preparations dealing with myocardial effects of catecholamines usually employ epinephrine concentrations 10-1,000 times higher (10(-7)-10(-5) M) than those observed during maximal cardiac adrenoceptor activation in vivo (10(-9)-5 x 10(-8) M) to obtain measurable cardiac responses. The reason for this discrepancy is still unclear, but it may reflect a diminished sensitivity to catecholamines in vitro. The main purpose of this study was to evaluate if a different myocardial sensitivity to epinephrine in vivo and in vitro does exist and to investigate which epinephrine concentrations in vitro mimic the effect of cardiac adrenoceptor activation in vivo. We compared concentration-response curves to cumulative increasing concentrations of of epinephrine, measured by high pressure liquid chromatography, in chloralose anesthetized or pithed rats (in vivo) and in isolated Langendorff perfused rat hearts (in vitro). We found that the amplitude of response to epinephrine was significantly higher in vivo at all concentrations. For example, an increase of 50 beats/min was observed at an epinephrine concentration of 29 +/- 6 nM in chloralose anesthetized, 25 +/- 4 nM in pithed rats and 149 +/- 52 nM in isolated hearts (P less than 0.05 vs. in vivo). Data on contractility closely parallel those on heart rate. These data indicate that, when methodological differences are minimized, there is a marked reduction in the amplitude of the response to epinephrine in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Generation of arrhythmias in myocardial ischemia and infarction.

In recent years an enhanced interest among researchers combined with the availability of new technologies has increased our knowledge of the mechanisms that generate arrhythmias in patients with ischemic heart disease. Convincing evidence has been obtained to support the occurrence of reentry in ischemic myocardium. This has been especially apparent in canine studies in the surviving layers overlying infarctions several days after coronary occlusion. In this planar model, the reentry circuit forms a figure-8 configuration around an arc of functional block due to refractoriness; the center of the arc is the site of unidirectional block and reentry. The reentry circuit is sustained by wavefronts of activation encircling segments in which the tissue on either side is alternately receptive and refractory, a variant of the leading circle model of reentry. The relatively prolonged refractoriness in ischemic tissue is due to time-dependent refractoriness, i.e., postrepolarization refractoriness, which is most prominent in more severely depolarized cells. Slow conduction is related in part to primary depression of the fast channels. There is a great variation in refractory periods in ischemic tissue because of variation in action potential duration and in the duration of time-dependent refractoriness. The depolarized resting potentials of cells in acute ischemia are due in part to extracellular accumulation of potassium and intracellular accumulation of calcium. In the latter stages of ischemia it is likely that abnormalities of ion distribution across the sarcolemma play a role. It has also been demonstrated that ischemic Purkinje fibers show abnormal automaticity, i.e., enhanced phase 4 depolarization at depolarized diastolic potentials, and afterdepolarizations with triggered firing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Electrogram patterns predicting successful catheter ablation of ventricular tachycardia.

Ventricular tachycardia in patients with remote myocardial infarction is thought to be due to reentry. To improve the efficacy of catheter ablation, we sought to identify electrograms identifying essential components of the reentrant circuit. In this study we compared the efficacy of shocks delivered at sites of early ventricular activation during tachycardia (presumably exit sites from the reentrant circuit) with that of shocks delivered at sites recording mid-diastolic potentials that were not continuous with the main ventricular potential recorded during the QRS complex, but that always remained associated with the tachycardia during initiation, termination, and resetting with extrastimuli (presumably activation of a segment of the slowly conducting region of the reentrant circuit). A total of 20 attempts was made to ablate 14 monomorphic ventricular tachycardias in 10 patients with remote myocardial infarction with use of one to five shocks of 50 to 370 J (200 J in 70%). All seven tachycardias in which isolated mid-diastolic potentials were targeted were successfully ablated, although one required a second attempt. Twelve attempts were made to ablate seven tachycardias by delivering shocks at sites of early activation during tachycardia when mid-diastolic potentials were not identified. Only three attempts (25%) were successful. Activation preceded the QRS complex by 60, 85, and 120 msec in the three successful attempts and by 20 to 110 msec (median 55 msec) in the nine unsuccessful attempts. For the total 20 attempts, there was no significant difference between successful and nonsuccessful ablation in the number of shocks or total energy delivered.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

New catheter technique for recording left free-wall accessory atrioventricular pathway activation. Identification of pathway fiber orientation.

The ability to record accessory atrioventricular (AV) pathway activation consistently may be uniquely beneficial in improving pathway localization, identifying anatomic relations, and providing insight into unusual conduction properties. For the purpose of recording left AV accessory pathway activation, an electrode catheter was specially designed for use in the coronary sinus. The orthogonal catheter has three sets of four electrodes spaced evenly around the circumference. Electrograms were recorded at low gain (less than 1 cm/mV) between adjacent electrodes on the same set (interelectrode distance, 1.5 mm, center to center). This provides a recording dipole perpendicular to the atrioventricular groove to enhance recording of accessory pathway activation while minimizing overlapping atrial or ventricular potentials. The orthogonal electrode catheter was used in the electrophysiological study of 48 consecutive patients with 59 left AV accessory pathways. The catheter could be advanced along the coronary sinus beyond the site of earliest retrograde atrial activation in 49 of the 59 accessory pathways. Activation potentials were recorded from 45 of the 49 (92%) accessory pathways accessible to the catheter (5 of 5 anterior, 8 of 8 anterolateral, 15 of 16 lateral, 5 of 5 posterolateral, 5 of 5 posterior, and 7 of 10 posteroseptal). Accessory pathway potentials were validated by dissociating them from both atrial and ventricular activation by programmed-stimulation techniques. During surgery, accessory pathway potentials were identified from orthogonal catheter electrodes in the coronary sinus in 14 of 16 accessory pathways (12 patients). Epicardial mapping confirmed the location of the accessory pathway, and direct pressure over the orthogonal catheter electrode that recorded the accessory pathway potential resulted in transient conduction block in nine of the 14 accessory pathways. Orthogonal electrode maps of the coronary sinus identified an oblique course in 39 of 45 recorded accessory pathways. Thirty-two of 38 left free-wall accessory pathways were oriented with atrial insertion 4-30 mm (median, 14 mm) proximal (posterior) to the ventricular insertion. In the remaining six free-wall accessory pathways, the lateral excursion could not be determined because either only the atrial end of the accessory pathway was recorded or activation of multiple pathway fibers prevented tracking of individual strands. The seven recorded posteroseptal pathways exhibited accessory pathway potentials throughout an 8-18-mm (median, 10 mm) length of the proximal coronary sinus, but fiber orientation was difficult to determine.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrioventricular Node↗
PubMed1988

Electrophysiological mechanisms for ventricular arrhythmias.

The proposed mechanisms for ventricular arrhythmias include reentry, reflection, enhanced and abnormal automaticity, afterpotential triggering, and repolarization re-excitation. The original model for re-entrant excitation, the ring model, has been augmented by newer models applicable to three-dimensional propagation in the cardiac syncytium, the "leading circle" and the "figure of eight." Heterogeneous refractory properties are important for slow conduction, unidirectional block, and formation of a barrier. Abnormal cellular properties such as depressed excitatory current and cell uncoupling contribute to slow conduction and block. Tachyarrhythmias can result from enhanced normal automaticity or abnormal automaticity in which the pacemaker currents differ. Excess calcium loading and depression of repolarizing currents have been identified as important factors in the induction of after depolarizations, which may play a role in ventricular arrhythmias related to cardiac glycosides, in certain stages of ischemia, and in the long QT syndromes.

Action Potentials↗
PubMed1988

An introduction to high-resolution ECG recordings of cardiac late potentials.

High-resolution electrocardiography utilizes computer processing to record low-levels signals not normally observed on standard electrocardiographs. Cardiac late potentials occur at the end of or after the QRS complex and require these methods to be quantified. A brief overview of the methods used to record late potentials is presented. These include lead placement, computer-implemented signal averaging, high-pass filtering, and feature extraction for characterizing the late potential. The major application of late- potential analysis has been in patients after myocardial infarction. Several of these studies are reviewed that demonstrate the usefulness of this new approach in identifying those patients at greatest risk for developing ventricular tachycardia. The most impressive studies have been those that compare late potentials with measures of ventricular performance and ventricular ectopy.

Action Potentials↗
PubMed1987

Atenolol for ventricular ectopy: a dose-response study.

The antiarrhythmic efficacy, safety, and tolerance of atenolol was evaluated in 32 patients with an average of at least 60 ventricular ectopic depolarizations/hr. Patients received, single-blind, the following treatments for 2 weeks each: placebo and atenolol, 50, 100, and 200 mg daily. A 24-hour ambulatory ECG recording was obtained each week. Reduction in ventricular ectopic frequency by at least 75% occurred in six of 32 patients receiving 50 mg daily, five of 30 patients receiving 100 mg daily, and three of 21 patients receiving 200 mg daily (P = not significant for any paired dose comparison). No patient who failed to respond to a lower dose responded to 200 mg daily. The frequency of ventricular tachycardia was reduced by at least 75% in eight of 17 patients receiving 50 mg daily, seven of 16 patients receiving 100 mg daily, and eight of 11 receiving 200 mg daily (P = not significant for any paired dose comparison). Atenolol was discontinued because of adverse effects in 12 patients. The results indicate that atenolol is more effective in suppressing ventricular tachycardia than in suppressing overall ventricular ectopy.

Adult↗
PubMed1986

Mechanism of prevention of sudden death by nadolol: differential actions on arrhythmia triggers and substrate after myocardial infarction in the dog.

Electrocardiographic monitoring and provocative ventricular pacing were used to evaluate control and nadolol treatment groups 6 to 24 hours after left anterior descending coronary artery ligation in the dog. During the 6 to 24 hour period, the control group (n = 20) developed ventricular triplets at rates exceeding 270/min. Seven dogs spontaneously developed sustained monomorphic ventricular tachycardia (421 +/- 12 beats/min) at 13 +/- 2 hours. Sustained monomorphic ventricular tachycardia was present for 38 +/- 8 seconds before ventricular fibrillation developed. One dog developed recurrent monomorphic ventricular tachycardia, with six episodes lasting from 8 to 72 seconds (375 to 425 beats/min). At 24 hours, ventricular pacing produced sustained monomorphic ventricular tachycardia (378 +/- 12 beats/min) in 9 of 13 surviving animals. Nadolol administration 6 hours after coronary artery ligation (n = 19) lowered both the rate (241 +/- 8 versus 328 +/- 8 beats/min; p = 0.001) and the incidence (8 +/- 6 versus 198 +/- 61 per hour; p = 0.004) of rapid ventricular triplets and prevented sudden arrhythmic death (0%; p = 0.005). Nadolol failed to prevent sustained monomorphic ventricular tachycardia (88%; 365 +/- 12 beats/min) produced by ventricular pacing. The data suggest that nadolol prevents spontaneous sustained monomorphic ventricular tachycardia by selectively suppressing the arrhythmia trigger (rapid ventricular triplets) without altering the underlying arrhythmia substrate.

Animals↗
PubMed1986

New method for measuring myocardial blood flow by high resolution scintigraphy in the excised dog heart.

The standard method for measuring myocardial blood flow (MBF) with radioactive microspheres requires processing of selected tissue samples usually from the excised heart, and consequent loss of exact relation to myocardial morphology. A computer-based image processing method was developed by using [99mTc]microspheres (mean particle size 20 microns) for quantitative analysis of MBF in 25 dogs. A computer-controlled gamma camera was used to obtain the images of radioactive microsphere distribution in transaxial slices of the ex vivo heart. Any portion of these slice images could be quantitated by using a computer program based on modification of the formula for determining MBF by the standard microsphere method. Regional myocardial perfusion calculated by this technique correlated well with values obtained with reference microspheres (r = 0.96) over a broad range of MBF. The results show that our new method, accurately and with high resolution, delineated zones of differing MBF and confirmed the increase of MBF in surviving myocardium with healing.

Animals↗
PubMed1985

Ventricular arrhythmias following one-stage and two-stage coronary reperfusion: evidence for both reentry and enhanced automaticity.

We studied the effects of reperfusion in 60 dogs following a 30-45 minute period of left anterior descending coronary artery occlusion using electrocardiograms and composite electrogram recordings. One-stage reperfusion in 14 of 15 dogs produced ventricular arrhythmias which degenerated into ventricular fibrillation within 60 seconds. The onset of ventricular arrhythmias was associated with continuous electrical activity in epicardial and intramural electrograms recorded from the reperfused zone. Vagal slowing during reperfusion (64 +/- 8/min) did not prevent ventricular fibrillation (eight of eight dogs) and escape beats were often followed by one or more coupled ectopic beats associated with continuous electrical activity. Rapid atrial pacing (270/min) also did not prevent the appearance of ventricular arrhythmia with associated continuous electrical activity and ventricular fibrillation (six of six dogs) nor did 4 mg/kg lidocaine (15 of 16 dogs). In another group of 15 dogs reperfusion was performed in two stages resulting in no ventricular fibrillation but in 8 of 15 dogs ventricular arrhythmias were observed beginning within two minutes after reperfusion and lasting 20-30 minutes. These ventricular arrhythmias were not associated with continuous electrical activity in any of the recorded leads. Atrial pacing suppressed ventricular arrhythmias and idioventricular rate averaged 157 +/- 10/min versus 55 +/- 10/min pre-reperfusion control. The earliest site of activation indicated automatic foci arising in the subendocardium of the reperfused zone. Lidocaine (2-4 mg/kg) rapidly (less than 90 sec) restored normal sinus rhythm and suppressed automaticity (72 +/- 11/min) as did left anterior descending artery reocclusion (52 +/- 6/min). We conclude that both reentry and enhanced automaticity play a role in ventricular arrhythmias due to reperfusion. Lidocaine (2-4 mg/kg) suppresses automatic but not reentrant ventricular arrhythmias in this experimental setting.

Animals↗