Ventricular Defibrillation Threshold Research Articles

The effect of pinacidil on postshock activation and ventricular defibrillation threshold in canine hearts

To determine the postshock activation patterns with both successful and failed shocks in a canine model of ventricular fibrillation, and whether piniacidil, an early after-depolarization (EAD) inhibitor, altered the defibrillation threshold (DFT) and postshock activation patterns. In 6 beagles, a basket catheter with 64 unipolar electrodes was placed in the LV for global endocardial mapping, a monophasic action potential catheter was inserted into the LV apex, and a catheter with the negative electrode in the right ventricle and the positive electrode in the superior vena cava was inserted for defibrillation. The DFT, 90% action potential duration (APD(90)) and activation recovery interval (ARI) were evaluated before and after pinacidil administration (loading dosage 0.5 mg/kg and maintenance dosage 0.5 mg·kg(-1)·h(-1), iv). Electrical heterogeneities were defined with the dispersion of ARI. After successful and failed shocks with near-DFT strength, the earliest postshock activation patterns (focal or nonfocal endocardial activation), interval and location were detected. Pinacidil significantly decreased APD(90) (from 178±16 ms to 168±18 ms) and ARI from (152±10 ms to 143±10 ms) at pacing cycle length of 300 ms. The drug significantly increased VF activation rate (from 10.0±1.9 Hz to 10.8±2.0 Hz). The drug did not affect the dispersion of ARI, neither it changed DFT (baseline: 480±110 V; pinacidil: 425±55 V, P>0.05). The earliest postshock activation arose locally on the LV apical endocardium before and after the drug treatment. Pinacidil significantly prolonged the postshock cycle length of cycles 2 to 5 for the successful episodes but not for the failed episodes. Pinacidil increases the postshock cycle length suggesting that EAD may play a role in postshock activation, while it fails to alter DFT suggesting that EAD produced by shock does not determine a defibrillation success or failure.

Chronic Oral Amiodarone but not Dronedarone Therapy Increases Ventricular Defibrillation Threshold During Acute Myocardial Ischemia in a Closed-Chest Animal Model

Dronedarone, a recently approved antiarrhythmic drug, has been shown to have fewer side effects than amiodarone, particularly with regard to thyroid and neurologic events. Since the effects of either drug on ventricular defibrillation threshold during ischemia are unknown, the aim of this study was to compare the effects of dronedarone and amiodarone on defibrillation efficacy during ischemia in a closed-chest animal model. Dronedarone (30 mg·kg·d) and amiodarone (20 mg·kg·d) were administered orally for 3 weeks to 19 and 21 pigs, respectively. A control group (no treatment) comprised 19 pigs. A 2-lead endovascular defibrillation system was used. Each biphasic shock was delivered after 8 seconds of ventricular fibrillation. A step-up/step-down protocol was used to calculate mean defibrillation threshold before and 10 minutes after coronary artery occlusion using an angioplasty balloon in the left descending artery. At basal state, defibrillation threshold did not differ between the control (20.8 ± 4.8 J), amiodarone (21.2 ± 2 J), and dronedarone (19.5 ± 3 J) groups. After ischemia, the amiodarone group had a significantly higher defibrillation threshold than the control group (29.6 ± 3 J vs. 21.8 ± 5 J, respectively; P = 0.015), but the dronedarone (22.8 ± 4 J) and control groups had similar defibrillation threshold values. These data indicate that oral dronedarone treatment, unlike oral amiodarone, does not affect defibrillation threshold during ischemia in pigs.

The Effects of Acute Amiodarone on Short- and Long-duration Ventricular Defibrillation Threshold in Canines

Some studies have shown that the defibrillation threshold (DFT) differs between short-duration ventricular fibrillation (SDVF, <1 minute) and long-duration ventricular fibrillation (LDVF > 1 minute). The goal of this study is to evaluate the effects of acute intravenous amiodarone on SDVF-DFT and LDVF-DFT and its possible mechanism as well. Twelve open-chest dogs were randomly divided into 2 groups (control group, normal saline, 10 mL·kg·h maintenance, n = 6; amiodarone group, loading dose 10 mg/kg over 10 minutes, maintenance dose 5 mg·kg·h, n = 6). VF was electrically induced and recorded with a 12 × 12 unipolar electrode plaque (2-mm spacing) sutured on the left ventricular epicardium and a plunge needle (6 unipolar electrode) inserted in the left ventricular apex. The DFTs of SDVF and LDVF were determined 20 seconds and 3 minutes after VF induction, respectively. Restitution was estimated from activation recovery intervals during pacing from the plaque and plunge needle electrodes. The activation rate was estimated by Fast Fourier Transform analysis of VF at same electrodes. The VF cycle length was defined as the reciprocal of the activation rate. The epicardial and transmural dispersion of the maximal slope of the restitution curve and VF cycle length of SDVF and LDVF were calculated, respectively. : In controls, LDVF-DFT was higher than SDVF-DFT (645 ± 61 vs. 520 ± 63 V, P < 0.01). Amiodarone did not significantly alter SDVF-DFTs (496 ± 49 vs. 552 ± 69 V, P > 0.05) but decreased LDVF-DFT by 31% (P < 0.01). Compared with control, amiodarone significantly reduced the maximum slope of the restitution curve (1.12 ± 0.35 vs. 0.81 ± 0.25, P = 0.03) and its epicardial dispersion (0.32 ± 0.07 vs. 0.24 ± 0.04,coefficient of variation, P = 0.017). Amiodarone significantly increased the SDVF-CL (92 ± 8 vs. 99 ± 10 milliseconds, P < 0.01) and epicardial dispersion 0.14 ± 0.06 vs. 0.18 ± 0.05, P < 0.01. Amiodarone did not change the LDVF-CL (228 ± 12 vs. 226 ± 10 milliseconds, P > 0.05) or epicardial dispersion (0.17 ± 0.03 vs. 0.15 ± 0.02, P > 0.05) compared with control. However, the drug significantly decreased the transmural dispersion of LDVF-CL (68 ± 28 vs. 39 ± 14 milliseconds, P < 0.01) without changing the transmural dispersion of SDVF-CL (29 ± 22 vs. 32 ± 30 milliseconds, P > 0.05). Acute amiodarone significantly decreased the LDVF-DFT. The decreased transmural dispersion of LDVF-CL by amiodarone might contribute to the decreased LDVF-DFT.

Effect of rosiglitazone on cardiac electrophysiology, infarct size and mitochondrial function in ischaemia and reperfusion of swine and rat heart

Rosiglitazone, a peroxisome proliferator-activated receptor γ agonist, has been used to treat type 2 diabetes. Despite debates regarding its cardioprotection, the effects of rosiglitazone on cardiac electrophysiology are still unclear. This study determined the effect of rosiglitazone on ventricular fibrillation (VF) incidence, VF threshold (VFT), defibrillation threshold (DFT) and mitochondrial function during ischaemia and reperfusion. Twenty-six pigs were used. In each pig, either rosiglitazone (1 mg kg(-1)) or normal saline solution was administered intravenously for 60 min. Then, the left anterior descending coronary artery was ligated for 60 min and released to promote reperfusion for 120 min. The cardiac electrophysiological parameters were determined at the beginning of the study and during the ischaemia and reperfusion periods. The heart was removed, and the area at risk and infarct size in each heart were determined. Cardiac mitochondria were isolated for determination of mitochondrial function. Rosiglitazone did not improve the DFT and VFT during the ischaemia-reperfusion period. In the rosiglitazone group, the VF incidence was increased (58 versus 10%) and the time to the first occurrence of VF was decreased (3 ± 2 versus 19 ± 1 min) in comparison to the vehicle group (P < 0.05). However, the infarct size related to the area at risk in the rosiglitazone group was significantly decreased (P < 0.05). In the cardiac mitochondria, rosiglitazone did not alter the level of production of reactive oxygen species and could not prevent mitochondrial membrane potential changes. Rosiglitazone increased the propensity for VF, and could neither increase defibrillation efficacy nor improve cardiac mitochondrial function.

Vernakalant Selectively Prolongs Atrial Refractoriness With No Effect on Ventricular Refractoriness or Defibrillation Threshold in Pigs

Vernakalant is a novel antiarrhythmic agent that has demonstrated clinical efficacy for the treatment of atrial fibrillation. Vernakalant blocks, to various degrees, cardiac sodium and potassium channels with a pattern that suggests atrial selectivity. We hypothesized, therefore, that vernakalant would affect atrial more than ventricular effective refractory period (ERP) and have little or no effect on ventricular defibrillation threshold (DFT). Atrial and ventricular ERP and ventricular DFT were determined before and after treatment with vernakalant or vehicle in 23 anesthetized male mixed-breed pigs. Vernakalant was infused at a rate designed to achieve stable plasma levels similar to those in human clinical trials. Atrial and ventricular ERP were determined by endocardial extrastimuli delivered to the right atria or right ventricle. Defibrillation was achieved using external biphasic shocks delivered through adhesive defibrillation patches placed on the thorax after 10 seconds of electrically induced ventricular fibrillation. The DFT was estimated using the Dixon "up-and-down" method. Vernakalant significantly increased atrial ERP compared with vehicle controls (34 ± 8 versus 9 ± 7 msec, respectively) without significantly affecting ventricular ERP or DFT. This is consistent with atrial selective actions and supports the conclusion that vernakalant does not alter the efficacy of electrical defibrillation.

Using Floating Atrial Electrodes to Combat the Rising Tide of Inappropriate Defibrillator Therapies

Despite various implantable defibrillator algorithms and strategies used to improve discrimination between potentially life-threatening ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation [VT/VF]) and more benign supraventricular tachycardias (SVTs), this remains a problem. In addition to significant discomfort and impairment of quality of life, there is some suggestion that shocks may increase mortality.1 Recording atrial intracardiac electrograms during arrhythmic episodes would be expected to improve our ability to discriminate tachycardias and thus reduce the number of inappropriate shocks. It may also lead to the diagnosis of otherwise unsuspected atrial arrhyhmias that may require specific therapy, such as anticoagulation therapy for patients with atrial flutter or atrial fibrillation (AF). Article see p 56 The evidence available so far, however, does not clearly demonstrate that atrial electrograms reduce inappropriate shocks.2–7 Although some studies performed in patients with a dual-chamber device have shown a reduction in inappropriate detection, inappropriate shocks also were avoided in the single-chamber detection arm by using anti tachycardia pacing.2 In addition, placement of an atrial lead is associated with a risk of lead dislodgement (≈4.5%) and increased procedural and fluoroscopy times compared to a single-chamber defibrillator. Thus, there currently is no strong evidence to support the addition of an atrial lead for the sole purpose of SVT discrimination and reducing implantable cardioverter-defibrillator (ICD) shocks.8 Using a single-pass VDD defibrillator lead holds the promise of offering atrial electrograms without the additional risks and procedural time related to implantation of a separate atrial lead. Similar lead designs with integrated atrial electrodes have been used in VDD pacemakers.9 In a study published by Sticherling et al in this issue of Circulation: Arrythmia and Electrophysiology , the ADRIA (Study to Verify Proper Detection of Supraventricular Tachyarrhythmia With Single-Lead Dual-Chamber Implantable Cardioverter-Defibrillators) study, the authors investigated the use …

Effect of Ranolazine on Ventricular Vulnerability and Defibrillation Threshold in the Intact Porcine Heart

Extensive in vitro studies and clinical evidence (MERLIN trial) indicate an antiarrhythmic potential of ranolazine, a novel antianginal agent. Programmed electrophysiologic testing was performed to quantify ranolazine's effects on ventricular vulnerability and defibrillation thresholds and to gain insights into mechanisms. Effects of ranolazine (9.2 +/- 2.1 microM, plasma level) on surface ECG, right ventricular effective refractory period (ERP), and repetitive extrasystole (RE), ventricular fibrillation (VF), and defibrillation (DFT) thresholds were determined in 29 normal closed-chest anesthetized pigs. The single extrastimulus method was employed for ERP and for RE and VF thresholds. DFT(50) was determined using an up-down testing protocol with an implantable cardioverter-defibrillator. Ranolazine increased rate-corrected QT interval from 490 +/- 30 to 527 +/- 24 ms (P < 0.05) but did not alter T(peak)-T(end) interval (59 +/- 8 to 62 +/- 11, P = 0.65). ERP increased by 40 +/- 6 ms (P < 0.001). Compared with baseline, ranolazine raised RE threshold from 20 +/- 6 to 34 +/- 9 mA (P < 0.001) and VF threshold from 38 +/- 4 to 48 +/- 10 mA (P < 0.05). DFT(50) was unchanged (baseline: 14 +/- 2 J; ranolazine: 14 +/- 2 J; P = 0.6), whereas diastolic pacing threshold increased from baseline pulse width of 0.07 +/- 0.03 to 0.17 +/- 0.07 ms (P < 0.01) with 1V pulse amplitude. Ranolazine, at therapeutic concentrations, produces a mild increase in QT interval and a marked increase in both RE and VF thresholds. Thus, ranolazine does not augment and may improve dispersion of ventricular repolarization, suggesting a potential antiarrhythmic action. Ranolazine is unlikely to affect the margin of safety of defibrillation, given no significant effect on DFT, but could result in a mild increase in pacing threshold.

The Impact of Acute Myocardial Ischemia on the Ventricular Defibrillation Threshold During Chronic Oral Azimilide Therapy

The effects of chronic oral azimilide therapy on the ventricular defibrillation threshold (DFT) during ischemia are unknown. The effects of azimilide on defibrillation efficacy under ischemic condition were investigated in a closed-chest animal model. Azimilide (20 mg/kg/d) was administered orally for 7 days to 10 pigs (20 to 25 kg). The control group (no treatment) comprised 15 pigs. A 2-lead defibrillation system was used. Each shock was delivered after 8 seconds of ventricular fibrillation. A step-up and step-down protocol was used to calculate mean DFT before and 10 minutes after coronary artery occlusion using an angioplasty balloon in the left descending artery. The basal DFT of the azimilide group did not differ from controls (20.8 +/- 4.8 versus 18.8 +/- 2.8; P = 0.33). After ischemia, the mean DFT of the azimilide-treated animals was similar to controls (21.8 +/- 5.2 versus 23.2 +/- 3.8 J; P = 0.54), despite significant lengthening of ventricular repolarisation (428.2 +/- 51.8 versus 494.1 +/- 46.6 msec; P = 0.005) and significant prolongation of the ventricular fibrillation cycle length (85.1 +/- 13 versus 104.7 +/- 24 msec; P < 0.04). Chronic oral azimilide treatment does not affect the DFT at baseline or during acute myocardial ischemia.

IKs Block by HMR 1556 Lowers Ventricular Defibrillation Threshold and Reverses the Repolarization Shortening by Isoproterenol Without Rate‐Dependence in Rabbits

The slow delayed rectifier K+ current (I(Ks)) contributes little to ventricular repolarization at rest. It is unclear whether I(Ks) plays a role during ventricular fibrillation (VF) or ventricular repolarization at rapid rates during beta-adrenergic stimulation. In an in vivo rabbit model, we evaluated the effects of HMR 1556 (1 mg Kg(-1) + 1 mg kg(-1) hr(-1) i.v.), a selective I(Ks) blocker, on monophasic action potential duration at 90% repolarization (MAPD90), ventricular effective refractory period (VERP), and defibrillation threshold (DFT). In perfused rabbit hearts, the effects of HMR 1556 (10 and 100 nM) in the presence of isoproterenol (5 nM) on MAPD90 and VERP were studied at cycle lengths (CLs) 200-500 msec. In vivo, HMR 1556 prolonged MAPD90 by 6 +/- 1 msec at CL 200 msec (P < 0.01, n = 6), lowered DFT from 558 +/- 46 V to 417 +/- 31 V (P < 0.01), and decreased the coefficient of variation in the VF inter-beat deflection intervals from 8.9 +/- 0.6% to 6.5 +/- 0.4% (P < 0.05) compared with control. In perfused rabbit hearts, isoproterenol shortened MAPD90 by 5 +/- 1 msec at CL 200 msec and 11 +/- 4 msec at CL 500 msec (P < 0.05, n = 7). This shortening was reversed by HMR 1556 (P < 0.05), and both effects were rate-independent. I(Ks) block increases VF temporal organization and lowers DFT, and I(Ks) that is activated following beta-adrenergic stimulation contributes to ventricular repolarization without rate dependence.

Effect of Amiodarone and Sotalol on Ventricular Defibrillation Threshold

Many patients with implanted cardioverter defibrillators (ICDs) receive adjunctive antiarrhythmic drug therapy, most commonly amiodarone or sotalol. The effects of these drugs on defibrillation energy requirements have not been previously assessed in a randomized controlled trial. The Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) trial was a randomized clinical trial evaluating the efficacy of amiodarone plus beta-blocker and sotalol versus beta-blocker alone for reduction of ICD shocks. Within OPTIC, a prospectively designed substudy evaluated the effects of the 3 treatment arms on defibrillation energy requirements. Defibrillation thresholds (DFTs) were measured (binary step-down protocol) at baseline and again after 8 to 12 weeks of therapy in 94 patients, of whom 29 were randomized to receive beta-blocker therapy (control group), 35 to amiodarone plus beta-blocker, and 30 to sotalol. In the control group, the mean DFT decreased from 8.77+/-5.15 J at baseline to 7.13+/-3.43 J (P=0.027); in the amiodarone group, DFT increased from 8.53+/-4.29 to 9.82+/-5.84 J (P=0.091). In the sotalol group, DFT decreased from 8.09+/-4.81 to 7.20+/-5.30 J (P=0.21). DFT changes in the beta-blocker and the amiodarone group were significantly different (P=0.006). In all patients, adequate safety margins for defibrillation were maintained. No clinical variable predicted baseline DFT or changes in DFT on therapy. Although amiodarone increased DFT, the effect size with modern ICD systems is very small. Therefore, DFT reassessment after the institution of antiarrhythmic drug therapy with amiodarone or sotalol is not routinely required.

P1-60: Ventricular defibrillation thresholds using a novel ventricular support device

P1-60: Ventricular defibrillation thresholds using a novel ventricular support device

592 Induction of atrial fibrillation during ventricular Defibrillation Threshold Testing shock on t vs. direct current

592 Induction of atrial fibrillation during ventricular Defibrillation Threshold Testing shock on t vs. direct current

592 Induction of atrial fibrillation during ventricular Defibrillation Threshold Testing shock on t vs. direct current

592 Induction of atrial fibrillation during ventricular Defibrillation Threshold Testing shock on t vs. direct current

Is the ventricular defibrillation threshold higher in patients with the Brugada syndrome?

Dysfunction of the sodium current channel is responsible for distinctive electrophysiologic changes in patients with the Brugada syndrome (BS). High energy requirements for ventricular defibrillation (DF) have been reported in isolated patients with BS, but it has never been systematically studied.

Effects of Transient Myocardial Ischemia on the Ventricular Defibrillation Threshold

Acute myocardial ischemia and the mode of ventricular fibrillation (VF) induction influence the ventricular defibrillation threshold (DFT). The purpose of this study was to determine the effects of transient regional left ventricular (LV) ischemia on the DFT. Ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and DFT were measured under nonischemic conditions (control) in 26 pigs weighing 25-35 kg. Myocardial ischemia was then induced by occlusion of the mid left anterior descending coronary artery, and measurements of ERP and VFT were repeated after 2 minutes of occlusion. The coronary artery ligation was released immediately after the onset of VF and DFT was measured. LV ERP was unchanged by ischemia (199 +/- 19 ms at control vs. 200 +/- 22 ms under ischemic conditions, P = 0.799), whereas VFT was significantly lower during coronary occlusion (10.7 +/- 5.4 mA vs. 37.7 +/- 13 mA, P = 0.000). Brief myocardial ischemia caused a significant increase in DFT (13.5 +/- 12.6 J after coronary occlusion vs. 6.8 +/- 6.8 J at control, P = 0.023). The duration of coronary occlusion was not correlated with the amounts of energy required to defibrillate (P = 0.526). This experimental study shows that transient myocardial ischemia markedly increases the DFT, suggesting that specific defibrillation algorithms should be designed for recipients of implantable defibrillators at risk of myocardial ischemia.

Myocardial ischaemic preconditioning in the pig has no effect on the ventricular fibrillation and defibrillation thresholds

Introduction: The effects of myocardial ischaemia preconditioning in pigs on the vulnerability to ventricular fibrillation during subsequent ischaemic events are controversial. This study examined the time course of changes in ventricular fibrillation (VFT) and defibrillation (DFT) thresholds during transient myocardial ischaemia after a 45 min preconditioning period. Methods and results: In five open-chest pigs, VFT was measured after 3 min of regional myocardial ischaemia, at time 0, 2, 15, 30, 60 and 90 min (Control group). In seven other pigs (Test group), VFT was measured before (time 0) and 2, 15, 30, 60 and 90 min after ischaemic preconditioning by three consecutive 5 min periods of regional coronary occlusion, followed by 10 min of reperfusion. DFT was measured by increasing the stored energy systematically until successful defibrillation. Ischaemic preconditioning caused no significant change in the effective refractory period (ERP), VFT or DFT over the 90 min of the experiments. In the Control group, ERP remained stable for 30 min, though was significantly lower at 90 min (178 ± 28 ms) than at baseline (204 ± 32 ms, P = 0.007). VFT and DFT remained unchanged throughout the experiments, and no difference was observed in ERP, VFT and DFT between the two groups at any time during the experiment. Conclusion: No changes were observed in the refractory duration, ventricular vulnerability or defibrillation energy requirements up to 90 min after ventricular ischaemic preconditioning in the pig.

Effect of rapid biphasic shock subpulse switching on ventricular defibrillation thresholds.

The aim of this study was to demonstrate that significant reductions in defibrillation threshold (DFT) can be achieved by rapidly switching defibrillation pulses within an overall biphasic envelope between multiple endovascular electrode sets. Defibrillation electrodes were implanted in four locations in nine anesthetized swine (41.7 +/- 8.7 kg). Electrodes were implanted into the right ventricular apex (RV), the superior vena cava (SVC), over the left pectoral region as a "hot can" (Can), and within the middle cardiac vein on the posterior left ventricular (LV) surface. The 50% DFT (level for which 50% of delivered shocks successfully defibrillated) for control shocks (7-ms first phase, 0.5-ms interpulse period, 4-ms second phase, RV- --> SVC+ + Can+) were determined to have energy of 20.5 +/- 5.5 J (mean +/- SD). Mean 50% DFTs were also determined for waveforms that split each phase of the same overall biphasic waveform between various electrode sets. Each phase was divided into 2, 3, 4, or 6 subpulses, the defibrillation shock was sequentially delivered to multiple electrode sets, and DFTs were determined (11.9 +/- 4.8 J, 11.7 +/- 2.9 J, 17.9 +/- 8.7 J, 16.7 +/- 6.1 J, respectively). DFT energy was statistically lower than the control (Wilcoxon sign rank test; P < 0.05) when each phase was divided into 2 or 3 subpulses. Rapid shock switching within an overall biphasic waveform between electrode sets including an electrode in the middle cardiac vein potentially can lower DFT energy by 40% or more.

The circadian variation of atrial defibrillation thresholds.

A circadian variation exists for ventricular defibrillation thresholds (DFTs) with a morning peak and a corresponding decrease in therapy success rates from implantable cardioverter defibrillators. Such a variation in atrial DFTs may have implications for the timing of internal cardioversion of atrial arrhythmias. The aim of this study was therefore to determine the circadian variation of atrial DFTs in patents with recurrent atrial fibrillation (AF). Data were collected as part of the worldwide Jewel AF-only study. Patients had recurrent persistent AF and no history of ventricular arrhythmias. The atrial DFT was assessed at device implantation using a step-up protocol and was recorded for 100 patients (age 63.0 +/- 11.7, 74% male, ejection fraction 49.6 +/- 17.8%, left atrial diameter 46 +/- 9 mm). The mean atrial DFT was 6.3 +/- 4.3 J. For the most commonly tested lead configuration (right atrium to coronary sinus in 56 patients), the atrial DFT for patients implanted in the morning (3.3 +/- 1.5 J) was significantly lower than for both the DFT measured in the afternoon (5.8 +/- 3.4 J, p < 0.01) and the DFT measured in the evening (7.4 +/- 5.9 J, p < 0.01). There may be a significant variation in measured atrial DFT for the right atrium to coronary sinus configuration, with a nadir in the morning. This is the converse to measurements of ventricular DFTs suggesting different regulatory electrophysiological mechanisms. Further investigation of this possible variation is warranted.

P2759 Impact of myocardial ischaemia on ventricular defibrillation threshold during chronic oral treatment with azimilide

P2759 Impact of myocardial ischaemia on ventricular defibrillation threshold during chronic oral treatment with azimilide

Myocardial ischemic preconditioning has no effect on the ventricular fibrillation and defibrillation threshold: Experiment study

Myocardial ischemic preconditioning has no effect on the ventricular fibrillation and defibrillation threshold: Experiment study