21 research outputs found

    A new animal model of atrial flutter

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    A new, simple and reliable model of atrial flutter utilizing postpericardiotomy pericarditis was developed in the dog. Using a sterile technique, the pericardium was opened by way of a right thoracotomy, Teflon-coated, stainless steel wire electrodes were fixed to three selected sites on the atria and exteriorized, the atrial surfaces were generously dusted with talcum powder and a single layer of gauze was placed on the free left and right atrial walls. The dogs were allowed to recover. Subsequently, the inducibility of atrial flutter and selected electrophysiologic properties of the atria were determined by daily programmed atrial stimulation studies with the dogs in the conscious, nonsedated state.Atrial flutter could be induced in 23 of 25 dogs initially studied. It was sustained (that is, lasting ≥5 min) in 17 of the 23. Neither atrial excitability, Intraatrial conduction time nor atrial refractoriness determined by pacing and recording from the three fixed sites predicted the inducibility of atrial flutter. One hundred thirty-nine episodes of atrial flutter induced in these 23 dogs were analyzed. The mean sustained atrial flutter cycle length was 131 ± 20 ms (mean ± SD) (range 100 to 170); the atrial flutter cycle length was 150 ms or more in 23 episodes, between 120 and 150 ms in 64 episodes and 120 ms or less in 52 episodes.In five dogs, the stability of the atrial flutter cycle length during sustained atrial flutter was studied and shown to be remarkably stable in all five until interrupted by rapid atria) pacing 35 to 95 minutes after its induction. Seventeen dogs were submitted to reoperation for epicardial mapping purposes and atrial flutter could be induced in the open chest state in 12. In conclusion, this sterile pericarditis model of atrial flutter in the canine heart proved to be highly reliable, reproducible and easy to create

    Value of early postoperative epicardial programmed ventricular stimulation studies after surgery for ventricular tachyarrhythmias

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    The value of early postoperative epicardial programmed ventricular stimulation studies after electrophysiologically-directed surgery for ventricular tachyarrhythmia was assessed in 34 patients who underwent epicardial stimulation within 7 to 30 days (mean 9.8) of surgery and were followed up for at least 6 months. The antiarrhythmic operation performed was an endocardial ventriculotomy (full encircling or limited), an endocardial resection, a wall resection or a combination of these procedures. All these interventions were directed by intraoperative mapping during sinus rhythm. Temporary epicardial wire electrodes left at the time of surgery rather than endocardial catheter electrodes were used to perform the pacing. The stimulation protocol included the introduction of up to three ventricular extrastimuli and incremental burst ventricular pacing performed at twice diastolic threshold (9.2 ± 5.8 mA for the right ventricle and 6.0 ± 3.5 mA for the left ventricle). A study was considered positive when ventricular tachycardia, defined as 10 or more consecutive ventricular beats, was induced by any pacing modality.Nineteen patients (Group I) had a negative study: after stimulation of both ventricles in 15 patients and of the left ventricle only in 4. Fifteen patients (Group II) had a positive study: after stimulation of the right ventricle in nine patients and of the left ventricle in six. The two groups were comparable with respect to preoperative clinical status, surgical procedures performed and postoperative ejection fraction. No arrhythmic events were observed in Group I during a mean follow-up period of 19.5 months (range 4 to 37), whereas seven arrhythmic events (47% incidence) occurred (p = 0.0008) in Group II during a mean follow-up period of 17.7 months (range 5 to 39). These arrhythmic events were sudden death (five patients) and sustained ventricular tachycardia (two patients).It is concluded that temporary epicardially-placed electrodes can be used satisfactorily to perform programmed ventricular stimulation studies in the postoperative period, thereby avoiding the cardiac catheterizations otherwise necessary to perform these studies. In addition, the protocol used in this report of epicardial programmed ventricular stimulation early after surgery for ventricular tachyarrhythmia predicts a good outcome if the study is negative and identifies patients at a high risk for future arrhythmic events when positive

    A united statement of the global chiropractic research community against the pseudoscientific claim that chiropractic care boosts immunity.

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    BACKGROUND: In the midst of the coronavirus pandemic, the International Chiropractors Association (ICA) posted reports claiming that chiropractic care can impact the immune system. These claims clash with recommendations from the World Health Organization and World Federation of Chiropractic. We discuss the scientific validity of the claims made in these ICA reports. MAIN BODY: We reviewed the two reports posted by the ICA on their website on March 20 and March 28, 2020. We explored the method used to develop the claim that chiropractic adjustments impact the immune system and discuss the scientific merit of that claim. We provide a response to the ICA reports and explain why this claim lacks scientific credibility and is dangerous to the public. More than 150 researchers from 11 countries reviewed and endorsed our response. CONCLUSION: In their reports, the ICA provided no valid clinical scientific evidence that chiropractic care can impact the immune system. We call on regulatory authorities and professional leaders to take robust political and regulatory action against those claiming that chiropractic adjustments have a clinical impact on the immune system

    Spatially Divergent Cardiac Responses to Nicotinic Stimulation of Ganglionated Plexus Neurons in the Canine Heart

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    Ganglionated plexuses (GPs) are major constituents of the intrinsic cardiac nervous system, the final common integrator of regional cardiac control. We hypothesized that nicotinic stimulation of individual GPs exerts divergent regional influences, affecting atrial as well as ventricular functions. In 22 anesthetized canines, unipolar electrograms were recorded from 127 atrial and 127 ventricular epicardial loci during nicotine injection (100 mcg in 0.1 ml) into either the 1) right atrial (RA), 2) dorsal atrial, 3) left atrial, 4) inferior vena cava-inferior left atrial, 5) right ventricular, 6) ventral septal ventricular or 7) cranial medial ventricular (CMV) GP. In addition to sinus and AV nodal function, neural effects on atrial and ventricular repolarization were identified as changes in the area subtended by unipolar recordings under basal conditions and at maximum neurally-induced effects. Animals were studied with intact AV node or following ablation to achieve ventricular rate control. Atrial rate was affected in response to stimulation of all 7 GPs with an incidence of 50-95% of the animals among the different GPs. AV conduction was affected following stimulation of 6/7 GP with an incidence of 22-75% among GPs. Atrial and ventricular repolarization properties were affected by atrial as well as ventricular GP stimulation. Distinct regional patterns of repolarization changes were identified in response to stimulation of individual GPs. RAGP predominantly affected the RA and posterior right ventricular walls whereas CMVGP elicited biatrial and biventricular repolarization changes. Spatially divergent and overlapping cardiac regions are affected in response to nicotinic stimulation of neurons in individual GPs

    Myocardial electrical alteration in canine preparations with combined chronic rapid pacing and progressive coronary artery occlusion.

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    Our objective was to create an animal preparation displaying long-term electrical alterations after chronic regional energetic stress without myocardial scarring. An Ameroid (AM) constrictor was implanted around the left circumflex coronary artery (LCx) 2 wk before chronic rapid ventricular pacing (CRP) was initiated at 240 beats/min for 4 wk (CRP-AM). Comparisons were made with healthy canines and canines with either AM or CRP. Unipolar electrograms were recorded from 191 sites in the LCx territory in open-chest, anesthetized animals during sinus rhythm and while pacing at 120-150 beats/min, with bouts of transient rapid pacing (TRP; 240/min). In CRP-AM and AM, ST segment elevation was identified at central sites and ST depression at peripheral sites, both increasing with TRP. In CRP-AM and CRP, the maximum negative slope of unipolar activation complexes was significantly depressed and activation-recovery intervals prolonged. Areas of inexcitability as well as irregular isocontour patterns displaying localized activation-recovery intervals shortening and gradients >20 ms between neighboring sites were identified in one-third of CRP-AM at slow rate, with increasing incidence and magnitude in response to TRP. In CRP-AM, programmed stimulation-induced marked conduction delay and block as well as polymorphic ventricular tachycardias, which stabilized into monomorphic tachycardias with the use of lidocaine or procainamide. Whole cell Na(+) current and channel protein expression were reduced in CRP-AM and CRP. Despite complete constrictor closure, small areas of necrosis were detected in a minority of CRP-AM. Long-term electrical alterations and their exacerbation by TRP contribute to arrhythmia formation in collateral-dependent myocardium subjected to chronic tachycardic stress

    Spinal Cord Stimulation Suppresses Bradycardias and Atrial Tachyarrhythmias Induced by Mediastinal Nerve Stimulation in Dogs

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    Spinal cord stimulation (SCS) applied to the dorsal aspect of the cranial thoracic cord imparts cardioprotection under conditions of neuronally dependent cardiac stress. This study investigated whether neuronally induced atrial arrhythmias can be modulated by SCS. In 16 anesthetized dogs with intact stellate ganglia and in five with bilateral stellectomy, trains of five electrical stimuli were delivered during the atrial refractory period to right- or left-sided mediastinal nerves for up to 20 s before and after SCS (20 min). Recordings were obtained from 191 biatrial epicardial sites. Before SCS (11 animals), mediastinal nerve stimulation initiated bradycardia alone (12 nerve sites), bradycardia followed by tachyarrhythmia/fibrillation (50 sites), as well as tachyarrhythmia/fibrillation without a preceding bradycardia (21 sites). After SCS, the number of responsive sites inducing bradycardia was reduced by 25% (62 to 47 sites), and the cycle length prolongation in residual bradycardias was reduced. The number of responsive sites inducing tachyarrhythmia was reduced by 60% (71 to 29 sites). Once elicited, residual tachyarrhythmias arose from similar epicardial foci, displaying similar dynamics (cycle length) as in control states. In the absence of SCS, bradycardias and tachyarrhythmias induced by repeat nerve stimulation were reproducible (five additional animals). After bilateral stellectomy, SCS no longer influenced neuronal induction of bradycardia and atrial tachyarrhythmias. These data indicate that SCS obtunds the induction of atrial arrhythmias resulting from excessive activation of intrinsic cardiac neurons and that such protective effects depend on the integrity of nerves coursing via the subclavian ansae and stellate ganglia
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