The effects of ischemic preconditioning on epicardial T-Q and S-T segment mapping, local activation, and coronary blood flow were analyzed in nine barbiturate-anesthetized pigs during four coronary occlusion (5 min)-reperfusion (20 min) sequences. In seven sham pigs, one occlusion was performed after a control period of 75 min. The first reperfusion induced a marked coronary hyperemia [11 +/- 4 ml/min (baseline) to 33 +/- 16 ml/min, P < 0.005] and a rapid recovery (30 to 150 s) of epicardial activation delays, T-Q segment depression, and S-T segment elevation in the ischemia area. This recovery was transiently associated with enlargement of intersite T-Q potential variability (alpha: 2.5 +/- 0.6 to 3.4 +/- 0.7 mV, P < 0.05), T-Q segment overshoot to +1.4 +/- 0.9 mV, and S-T segment reelevation. A brief T-Q segment depression (-2.3 +/- 0.9 mV) occurred during early reperfusion in 60 of 91 electrodes overlying the normal myocardium. Compared with the first, the fourth occlusion induced lower S-T segment elevation (3.4 +/- 2.0 to 1.7 +/- 1.9 mV, P < 0.05), and the fourth reperfusion elicited a faster reversal of T-Q segment dispersion (53 +/- 21 to 43 +/- 16 s, P < 0.05), S-T segment elevation (149 +/- 101 to 81 +/- 45 s, P < 0.05), and coronary hyperemia (8 +/- 2 to 5 +/- 1 min, P < 0.05). This trend of changes was not observed during a fourth occlusion in sham pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Persisting zones of slow impulse conduction in developing chicken hearts.

We performed a correlative electrophysiological and immunohistochemical study of embryonic chicken hearts during the septational period (Hamburger and Hamilton stages 13-31 [2-7 days of incubation]). The analyses yield conclusive evidence for slow conduction, up to 7 days of development, in the outflow tract, in the atrioventricular canal, and in the sinoatrial junction. The conduction velocity remains approximately 1 cm/sec in the outflow tract and increases in the ventricle 20-fold to approximately 20 cm/sec between 2 and 7 days of development. Transmembrane potentials of myocytes in the outflow tract and atrioventricular canal slowly rise (less than 5 V/sec), whereas in the atrium and ventricle, the upstroke velocity is eightfold to 13-fold higher. In the outflow tract, repolarization is completed only after the start of the next cycle. Because of the persistence of slow conduction, the myocardium flanking the developing atria and ventricle is thought to represent segments of persisting "primary" myocardium, whereas the more rapidly conducting "working" myocardium of the ventricle and atria is thought to represent more advanced stages of myocardial differentiation. The persisting primary myocardium was characterized by a continued coexpression of both the atrial and ventricular isoforms of myosin heavy chain. The developing atria and ventricle could be demarcated morphologically from the primary myocardium because the free walls of these segments only express their respective isoforms of myosin heavy chain. The slowly conducting myocardial zones appear to be essential for the function of the embryonic heart because 1) they provide the septating heart with alternating segments of slow and relatively fast conduction necessary for consecutive contraction of the atrial and ventricular segments and 2) their sphincterlike prolonged peristaltic contraction pattern can substitute for the adult type of one-way valves that start to develop at the end of septation.

Animals↗

PubMed1992

Reperfusion arrhythmias in isolated perfused pig hearts. Inhomogeneities in extracellular potassium, ST and TQ potentials, and transmembrane action potentials.

We recorded direct current electrograms and local [K+]o at multiple sites and transmembrane potentials at selected sites during reperfusion after 5 minutes and 10 minutes of regional ischemia in isolated perfused pig hearts. After 10 minutes of ischemia, the incidence of ventricular fibrillation (VF) was 38%. At 80-90 seconds after reperfusion, [K+]o was 0.8 mM less than in normal tissue in half of the reperfused tissue, especially in the border zone. This was associated with TQ elevation of +4.5 mV and large peaked T waves. The latter was caused by an abrupt decrease of action potential duration in reperfused tissue, leading to a difference of up to 165 msec with normal tissue. Reperfusion VF started with a closely coupled ventricular premature beat. Activation block between reperfused and normal tissue permitted reentrant activation, leading to VF. Pretreatment with ryanodine (10(-6) M) and reperfusion with elevated [K+] (both of which prevent delayed afterdepolarizations) did not prevent closely coupled ventricular premature beats or VF. Five minutes of ischemia never caused VF. K+ depletion and TQ elevation in the reperfused zone was less frequent and smaller (-0.4 mM and 1.8 mV, respectively). Peaked T waves did not occur, and shortening of the action potential duration was less. We conclude that extracellular K+ depletion and marked action potential duration shortening in the reperfused tissue play a role in the genesis of reperfusion VF, which is caused by reentry. The closely coupled ventricular premature beat that initiates reentry is not caused by delayed afterdepolarizations but most likely by intramural reentry.

Action Potentials↗

PubMed1992

Body surface mapping of ectopic left ventricular activation. QRS spectrum in patients with prior myocardial infarction.

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.

Adult↗

PubMed1992

Possible mechanisms of arrhythmias in valvular heart disease.

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Arrhythmias, Cardiac↗

PubMed1992

Experimental models of ventricular tachycardia and fibrillation caused by ischemia and infarction.

Experimental animal models of ventricular arrhythmias have been developed to elucidate mechanisms of arrhythmogenesis in humans. Studies of animal models have enabled the vulnerable period of the ventricles to be discovered and characterized and should eventually lead to improved techniques of defibrillation. Animal models of ischemic heart disease and myocardial infarction have also helped investigators elucidate the mechanisms of arrhythmias occurring at each stage of infarct development and healing. Data obtained from the experimental studies have been shown to apply to the clinical situation.

Animals↗

PubMed1991

What a clinician needs to know about the mechanisms of action of antiarrhythmic drugs.

Vaughan Williams' classifications of antiarrhythmic drugs are briefly discussed, including the fact that these drugs are classified based upon their effects on normal cardiac cells; that more and more subclassifications need to be introduced; that many drugs have actions belonging to different classes. A plea is made not to consider just one effect of an antiarrhythmic drug--that is, its effect on conduction velocity only or on refractory period only, but to evaluate its effect on wavelength, the product of refractory period and conduction velocity. Experimental studies on atrial arrhythmias induced by electrical stimulation in chronically instrumented dogs have shown a very good correlation between wavelength and type of arrhythmia induced. The predictive value of wavelength was much greater than that of refractory period alone or conduction velocity alone. It is emphasized that drugs that shorten wavelength especially at rapid rates may exhibit dangerous proarrhythmic effects.

Animals↗

PubMed1991

Macroreentry in the infarcted human heart: the mechanism of ventricular tachycardias with a "focal" activation pattern.

Endocardial mapping of electrical activity was carried out in 150 patients to guide antiarrhythmic surgery for drug-resistant ventricular tachycardia in the chronic phase of myocardial infarction. In 20 of these patients, the activation pattern of 27 distinct tachycardias was focal and diastolic potentials were recorded at three or more sites. In 26 tachycardias, the sequence of diastolic potentials progressed from the area of latest activation of one cycle toward the "origin" of the next cycle. In two patients, the heart was stimulated during tachycardia, resulting in entrainment of the tachycardia in both. Late potentials were recorded during entrainment at sites where diastolic potentials occurred during tachycardia. In 11 of the 20 patients, endocardial mapping was performed during sinus rhythm. In four of these, late potentials were observed during sinus rhythm at sites where diastolic potentials were recorded during tachycardia. In two patients without late potentials during sinus rhythm, late potentials were observed during stimulation and induced ectopic beats. The results support the concept that the mechanism of several of these tachycardias is based on reentry in a macrocircuit comprising a tract of surviving tissue traversing the infarct and the remaining healthy tissue. They also indicate that the absence of late potentials during sinus rhythm does not guarantee the absence of arrhythmogenic pathways.

Cardiac Catheterization↗

PubMed1991

Ventricular tachycardia after in vivo DC shock ablation in dogs. Electrophysiologic and histologic correlation.

BACKGROUND: DC shock catheter ablation for the treatment of ventricular tachycardia (VT) may induce VT episodes that disappear within days. METHODS AND RESULTS: A 30-J cathodal shock was delivered to the endocardial left ventricular wall in 15 closed-chest dogs. All dogs had VT during the first day after ablation. Eleven of these dogs were studied on the first day. Extensive epicardial and endocardial activation mapping in vivo, in Langendorff-perfused hearts, and in tissue blocks in a tissue bath localized the site of origin of VT to subendocardial Purkinje fibers in a border zone surrounding the central necrotic ablation lesion. Intracellular recording showed that this zone consisted of a subendocardial superficial layer (SSL) of cells with abnormal characteristics, a resting membrane potential (RMP) of -58 +/- 11 mV (mean +/- SD), and an action potential amplitude (APA) of 61 +/- 20 mV. In addition, the steepness of phase 0 of the action potential was markedly reduced. In three dogs abnormal automaticity was found in a very small area. Immediately below the SSL, cells were normal with an RMP of -78 +/- 5 mV and an APA of 107 +/- 8 mV. Histology confirmed a thin SSL with edematous and necrotic cells, hemorrhage, and infiltration. The other four dogs were studied at 1 week after ablation when VT was absent. Microelectrode impalement in the SSL was either impossible or showed nearly normal action potential characteristics. Histological examination showed a markedly thickened fibrotic subendocardial layer at places where impalement was impossible. Normal subendocardium was found in other areas of the border zone. CONCLUSIONS: Our results indicate that VT after DC shock ablation originates from cells with abnormal automaticity in the superficial subendocardial border zone around the central ablation lesion. Within 1 week edematous and necrotic cells in this border zone are replaced by a fibrotic layer, and this transition is associated with the disappearance of VT.

Animals↗

PubMed1991

Dispersion of refractoriness in canine ventricular myocardium. Effects of sympathetic stimulation.

In 18 dogs on total cardiopulmonary bypass, the average interval between local activations during artificially induced ventricular fibrillation (VF interval) was measured from extracellular electrograms, simultaneously recorded from up to 32 ventricular sites. VF intervals were used as an index of local refractoriness, based on the assumption that during ventricular fibrillation, cells are reexcited as soon as they have recovered their excitability. In support of this, microelectrode recordings in two hearts during ventricular fibrillation did not show a diastolic interval between successive action potentials. Refractory periods determined at a basic cycle length of 300 msec with the extrastimulus method correlated well with VF intervals measured at the same sites. Thus, this technique allows assessment of spatial dispersion of refractoriness during brief interventions such as sympathetic stimulation. The responses to left, right, and combined stellate ganglion stimulation varied substantially among individual hearts. This was observed both in dogs with an intact (n = 12) and decentralized (n = 6) autonomic nervous system. Individual ventricular sites could show effects of both left and right stellate ganglion stimulation (42% of tested sites) or show effects of left-sided stimulation only (31%) or right-sided stimulation only (14%). In 13% of sites, no effects of stellate stimulation were observed. Apart from these regional effects, the responses could be qualitatively different; that is, within the same heart, the VF interval prolonged at one site but shortened at another in response to the same intervention, although shortening was the general effect and prolongation the exception. Whenever sites responded to stellate ganglion stimulation with a shortening of VF interval, this shortening was approximately 10% for left, right, or combined stimulation, whether the autonomic nervous system was intact or decentralized. In six of 12 hearts in the intact group, there was a distinct regional effect of left stellate ganglion stimulation; in the other six hearts, the effects were distributed homogeneously over the ventricles. In three hearts, the effect of left stellate ganglion stimulation was strongest in the posterior wall, and in the other three hearts, in the anterior wall. The effects of right stellate ganglion stimulation were restricted to the anterior or lateral part of the left ventricle. Dispersion of VF intervals increased after left and combined stellate ganglion stimulation in the intact group and after right stellate ganglion stimulation in the decentralized group, but not significantly in every heart. This points to a marked individual variation with regard to the effects of sympathetic stimulation on electrophysiological properties of the heart.

Action Potentials↗

PubMed1991

Injury current and gradients of diastolic stimulation threshold, TQ potential, and extracellular potassium concentration during acute regional ischemia in the isolated perfused pig heart.

During acute regional myocardial ischemia, a "current of injury" flows between the ischemic and the normal tissue. Its direction and magnitude change during the cardiac cycle. During diastole, the injury current flows intracellularly from the ischemic cells toward the normal cells and tends to depolarize the latter. The gain insight into the possible role of the injury current in arrhythmogenesis, we simultaneously determined diastolic stimulation threshold, [K+]o and TQ potential at multiple sites closely spaced across the cyanotic border in Langendorff-perfused pig hearts during the first 10 minutes after occlusion of the left anterior descending coronary artery. The position of the electrodes relative to the border was validated by their response to 1) regional ischemia and 2) selective perfusion with a high-K+ perfusate of the left anterior descending coronary artery. A temporary decrease of diastolic stimulation threshold preceded a rapid increase in the central ischemic zone; a lasting reduction (by +/- 20%) without a concomitant increase of [K+]o was observed at seven sites (of 39 sites tested), five of which were less than 2 mm outside the electrophysiological border. Moreover, up to 4 mm inside the electrophysiological border, a similar lasting decrease of diastolic stimulation threshold was accompanied by a moderate increase of [K+]o. We conclude that 1) the injury current causes increased excitability in normal tissue close to the "ischemic" border and 2) increased excitability related to a moderately increased [K+]o may persist up to 10 minutes of ischemia at the ischemic side of the border. Both factors may facilitate the induction of life-threatening arrhythmias in acute myocardial ischemia.

Action Potentials↗

PubMed1991

Morphology of electrophysiologically identified junctions between Purkinje fibers and ventricular muscle in rabbit and pig hearts.

Purkinje fiber-ventricular muscle (PV) junctions were identified by extracellular recording in isolated, superfused preparations from rabbit and pig hearts. Microelectrode recordings from different cell types at the PV junctions were obtained, and the cells recorded from were retrieved microscopically. To this end 26 tissue blocks were serially sectioned at 4 microns. Microscopic identification of the very cell recorded from was obtained in five of seven Purkinje, five of 16 transitional, and two of two ventricular muscle cell recordings. In addition, some tissue blocks from both junctional and nonjunctional sites identified only by extracellular recording were examined in serial sections. Transitional cells in the rabbit heart are thin, broad bandlike cells (30-35 by 3-5 microns) arranged in one or two sheets in the subendocardium between the Purkinje layer and ventricular mass. Transitional cells are coupled via short, thin strands to both Purkinje and ventricular muscle cells. A second type of PV coupling was observed frequently in the pig, but in only one of 21 cases in the rabbit. Here, a short, linear segment of small transitional cells connected large-diameter Purkinje cells to ventricular muscle cells. Distances found between Purkinje-transitional cell coupling sites and transitional cell-ventricular muscle coupling sites varied from 100 to 1,000 microns in the rabbit heart and from 50 to several hundred micrometers in the pig heart. Action potentials from transitional cells typically showed multiple components in their upstroke. Both our morphological and electrophysiological findings are compatible with the existence of a relatively high-resistance barrier between Purkinje and transitional cells and between transitional and ventricular muscle cells.

Action Potentials↗

PubMed1990

[Can sudden cardiac death be prevented by anti-arrhythmia agents?].

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Anti-Arrhythmia Agents↗