Mechanisms of Supraventricular Tachycardia

In summary, we have found a close association between the stress of A-V nodal conduction and the occurrence of atrial dispersion or aberration. We could not explain atrial dispersion on the basis of incomplete recovery of atrial activity, slowing of atrial conduction, or the occurrence of atrial fusion. We postulate that the phenomenon of dispersion of atrial activation is related to the functional dissociation within the A-V node seen during situations which stress A-V conduction. This phenomenon may represent a mechanism whereby a second area of turnaround other than the A-V node is involved in reentry atrial tachyarrhythmias. Indeed, such a mechanism could provide a physiological basis for the concept of the atrial bridge being involved in supraventricular tachycardias and reciprocal beating

Primary Pericardial Sarcoma: A Case Report and a Brief Review

There are very few cases of primary pericardial sarcomas reported in the English literature. Pericardial tumors, like other cardiac tumors, are most likely to be metastatic in nature and are an extension of primary tumors from the surrounding structures. Sarcomas are the most common primary pericardial tumors. Surgical eradication of the tumor is considered to be the treatment of choice. We are presenting a case of a primary pericardial, high-grade pleomorphic undifferentiated sarcoma that was diagnosed at our institution. We discuss the available diagnostic modalities and also shed light on alternative therapies when patients are not ideal surgical candidates

Slow Conduction through an Arc of Block: A Basis for Arrhythmia Formation Post-Myocardial Infarction

Introduction The electrophysiologic basis for characteristic rate-dependent, constant-late-coupled (390 + 54 milliseconds) premature ventricular beats (PVBs) present 4–5 days following coronary artery occlusion were examined in 108 anesthetized dogs. Methods and results Fractionated/double potentials were observed in injured zone bipolar and composite electrograms at prolonged sinus cycle lengths (1,296 ± 396 milliseconds). At shorter cycle lengths, conduction of the delayed potential decremented, separating from the initial electrogram by a progressively prolonged isoelectric interval. With sufficient delay of the second potential following an isoelectric interval, a PVB was initiated. Both metastable and stable constant-coupled PVBs were associated with Wenckebach-like patterns of delayed activation following an isoelectric interval. Signal-averaging from the infarct border confirmed the presence of an isoelectric interval preceding the PVBs (N = 15). Pacing from the site of double potential formation accurately reproduced the surface ECG morphology (N = 15) of spontaneous PVBs. Closely-spaced epicardial mapping demonstrated delayed activation across an isoelectric interval representing “an arc of conduction block.” Rate-dependent very slow antegrade conduction through a zone of apparent conduction block (N = 8) produced decremental activation delays until the delay was sufficient to excite epicardium distal to the original “arc of conduction block,” resulting in PVB formation. Conclusion The present experiments demonstrate double potential formation and rate-dependent constant-coupled late PVB formation in infarcted dog hearts. Electrode recordings demonstrate a prolonged isoelectric period preceding PVB formation consistent with very slow conduction (<70 mm/s) across a line of apparent conduction block and may represent a new mechanism of PVB formation following myocardial infarction

Diverse Spectrum of Presentation of Coronary Slow Flow Phenomenon: A Concise Review of the Literature

The coronary slow flow phenomenon (CSFP) is a disease entity characterized by slow progression of angiographic contrast in the coronary arteries in the absence of stenosis in the epicardial vessels. CSFP has a diverse presentation from mild chest discomfort to ST-segment elevation myocardial infarction. It can also have severe morbidity and mortality implications and can significantly hamper the quality of life of those affected. In this paper we present two patients with CSFP highlighting the diverse spectrum of presentation. A concise review of the literature is also provided emphasizing the epidemiology, pathogenesis, diagnostic parameters, treatment modalities, and clinical significance of this phenomenon

Sympathetic activation, ventricular repolarization and Ikrblockade: Implications for the antifibrillatory efficacy of potassium channel blocking agents

AbstractObjectives. The aim of the present study was to test, in vivo and in vitro, the influence of adrenergic activation on action potential prolongation induced by the potassium channel blocking agent d-sotalol.Background. d-Sotalol is not effective against myocardial ischemia-dependent ventricular fibrillation in the presence of elevated sympathetic activity. Most potassium channel blockers, such as d-sotalol, affect only one of the two components of Ik(Ikr) but not the other (Iks). Iksis activated by isoproterenol. An unopposed activation of Iksmight account for the loss of anti-fibrillatory effect by d-sotalol in conditions of high sympathetic activity.Methods. In nine anesthetized dogs we tested at constant heart rate (160 to 220 beats/min) the influences of left stellate ganglion stimulation on the monophasic action potential prolongation induced by d-sotalol. In two groups of isolated guinea pig ventricular myocytes we tested the effect of isoproterenol (10−9mol/liter) on the action potential duration at five pacing rates (from 0.5 to 2., Hz) in the absence (n = 6) and in the presence (n = 8) of d-sotalol.Results. In control conditions, both in vivo and in vitro, adrenergic stimulation did not significantly change action potential duration. d-Sotalol prolonged both monophasic action potential duration in dogs and action potential duration of guinea pig ventricular myocytes by 19% to 24%. Adrenergic activation, either left stellate ganglion stimulation in vivo or isoproterenol in vitro, reduced by 40% to 60% the prolongation of action potential duration produced by d-sotalol.Conclusions. Sympathetic activation counteracts the effects of potassium channel blockers on the duration of repolarization and may impair their primary antifibrillatory mechanism. An intriguing clinical implication is that potassium channel blockers may not offer effective protection from malignant ischemic arrhythmias that occur in a setting of elevated sympathetic activity

Sodium-Calcium Exchange Initiated by the Ca2+Transient An Arrhythmia Trigger Within Pulmonary Veins

ObjectivesThe hypothesis that an increased or prolonged Ca2+transient during an abbreviated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by enhanced forward sodium-calcium (Na-Ca) exchange was examined.BackgroundBecause pulmonary veins have the shortest action potential of any cardiac tissue, we examined this hypothesis in canine pulmonary vein sleeves during interventions further shortening the action potential and increasing the calcium transient.MethodsExtracellular bipolar electrode, intracellular microelectrode, and isometric force (a surrogate marker for the Ca2+transient) recordings were obtained from superfused canine pulmonary veins.ResultsAn elevation and prolongation of the terminal phase of repolarization (EADs) were observed during interventions increasing contractile force; isoproterenol or norepinephrine (3.2 × 10−11to 3.2 × 10−7M), hypothermia, and pacing (post-extrasystolic potentiation, post-pacing pause). The EAD formation was prevented by ryanodine (10 μM) or reversed by transiently increasing [Ca2+]ofrom 1.35 to 5 mM (inhibition of forward Na-Ca exchange). Pacing-induced EADs were enhanced by re-introduction of normal Tyrode solution (Na+= 130 mM) after substitution of 30 mM NaCl with 30 mM LiCl (stimulation of forward Na-Ca exchange). With norepinephrine or isoproterenol (3.2 × 10−8M) + acetylcholine (10−7M) (to enhance the Ca2+transient and further shorten the abbreviated action potential, respectively), tachycardia-pause initiated arrhythmia (1,132 ± 153 beats/min) lasting >1 s was observed. Rapid firing was prevented by either suppression of the Ca2+transient (ryanodine) or transiently increasing [Ca2+]o.ConclusionsThe data show EAD formation in superfused canine pulmonary veins, enhanced by an increased Ca2+transient and increased Na-Ca exchange current. With subsequent shortening of the action potential with acetylcholine, tachycardia-pause triggers rapid firing within the PV sleeve

Prevention and Reversal of Atrial Fibrillation Inducibility and Autonomic Remodeling by Low-Level Vagosympathetic Nerve Stimulation

ObjectivesWe hypothesized that autonomic atrial remodeling can be reversed by low-level (LL) vagosympathetic nerve stimulation (VNS).BackgroundPreviously, we showed that VNS can be antiarrhythmogenic.MethodsThirty-three dogs were subjected to electrical stimulation (20 Hz) applied to both vagosympathetic trunks at voltages 10% to 50% below the threshold that slowed sinus rate or AV conduction. Group 1 (n = 7): Programmed stimulation (PS) was performed at baseline and during 6-h rapid atrial pacing (RAP). PS allowed determination of effective refractory period (ERP) and AF inducibility measured by window of vulnerability (WOV). LL-VNS was continuously applied from the 4th to 6th hours. Group 2 (n = 4): After baseline ERP and WOV determinations, 6-h concomitant RAP+LL-VNS was applied. Sustained AF was induced by injecting acetylcholine (ACh) 10 mM into the anterior right ganglionated plexus (Group 3, n = 10) or applying ACh 10 mM to right atrial appendage (Group 4, n = 9).ResultsGroup 1: The ERP progressively shortened and the ΣWOV (sum of WOV from all tested sites) progressively increased (p < 0.05) during 3-h RAP then returned toward baseline during 3-h RAP+LL-VNS (p < 0.05). Group 2: 6-h concomitant RAP+LL-VNS did not induce any significant change in ERP and ΣWOV. Group 3 and Group 4: AF duration (AF-D) and cycle length (AF-CL) were markedly altered by 3-h LL-VNS (Group 3: baseline: AF-D = 389 ± 90 s, AF-CL = 45.1 ± 7.8 ms; LL-VNS: AF-D = 50 ± 15 s, AF-CL = 82.0 ± 13.7 ms [both p < 0.001]; Group 4: baseline: AF-D = 505 ± 162 s, AF-CL = 48.8 ± 6.6 ms; LL-VNS: AF-D = 71 ± 21 s, AF-CL = 101.3 ± 20.9 ms [both p < 0.001]).ConclusionsLL-VNS can prevent and reverse atrial remodeling induced by RAP as well as suppress AF induced by strong cholinergic stimulation. Inhibition of the intrinsic cardiac autonomic nervous system by LL-VNS may be responsible for these salutary results