Reperfusion Ventricular Fibrillation Research Articles

Evaluation of the effect of small single intravenous dose of amiodarone on the prevention of arrhythmias in patients who underwent coronary artery bypass graft surgery: A randomized controlled trial

AbstractBackgroundAtrial fibrillation (AF) is the most frequent arrhythmia after cardiac surgery causing a range of clinical symptoms and treatments that develop in around one‐third of coronary artery bypass surgery patients. We aimed to evaluate the effect of Amiodarone in preventing arrhythmia in patients undergoing coronary artery bypass surgery.MethodIn this double‐blind randomized clinical trial, 60 patients candidate for coronary artery bypass surgery above the age of 18 were included and randomly divided into two groups of intervention, receiving an infusion of Amiodarone (3 mg/kg) 10 min (in 100 cc Normal saline) before declamping of the aorta, and a control group, receiving 100 cc of saline 10 min before declamping of the aorta. The patient's demographic, clinical features, and hospital and clinical course were recorded.ResultsAfter undergoing operation, 22 (36.67%) of patients were developed arrhythmia. The Amiodarone group demonstrated significantly lower reperfusion ventricular fibrillation (RVF) rates (26.7% vs. 70%; p = .001) and AF occurrence (13.3% vs. 60%; p < .001) during the initial 24 h after surgery compared to the placebo group. There was no significant difference between the two groups regarding the need for D/C shock after removing the aortic clamp. (p = .117) Furthermore, the intensive care unit stay among the amiodaron group was significantly lower than the control group (2.43 vs. 3.07 days; p = .013).ConclusionThe predictive properties in the administration of single intravenous low‐dose Amiodarone 10 min before the declamping of the aorta can significantly lower the rates of RVF and AF after coronary artery bypass grafting, while also decreasing hospitalization duration.

Comparison of amiodarone and esmolol for prevention of reperfusion ventricular fibrillation in individuals undergoing heart valve or aortic surgery: a study protocol for a randomized controlled clinical trial

BackgroundAmiodarone and esmolol can help to prevent and treat post-cardiac surgery reperfusion ventricular fibrillation. However, the relative efficacies of these two drugs remain unknown. The aim of the current trial is to compare the performances of amiodarone and esmolol for preventing reperfusion ventricular fibrillation following open heart surgery.Methods/designThis is a single-center, prospective, double-blind, controlled clinical trial. A total of 260 patients undergoing heart valve or aortic surgery will be assigned randomly to treatment with prophylactic esmolol (intervention group) or amiodarone (control group). The main outcome is the incidence of reperfusion ventricular fibrillation following aortic opening during extracorporeal circulation. The secondary outcomes are the rate of automatic cardiac resuscitation, energy and frequency of electrical defibrillation, number of electrical defibrillations, and pacemaker use in the two groups of patients. Information on the patients’ general condition and the durations of anesthesia, extracorporeal circulation, aortic occlusion, and operation time will be recorded. We will also compare the heart rate, mean arterial pressure, and central venous pressure between the two groups of patients at induction of anesthesia (T1), start of surgery (T2), start of extracorporeal circulation (T3), aortic block (T4), aortic opening (T5), after opening for 10 (T6), 20 (T7), and 30 min (T8), at cessation of extracorporeal circulation (T9), and at the end of surgery (T10) and compare blood gas analysis results at T1, T5, T9, and T10.DiscussionThis study will determine if prophylactic esmolol is more effective than amiodarone for reducing the incidence of reperfusion ventricular fibrillation in patients undergoing heart valve or aortic surgery.Trial registrationChina Clinical Trials Registry ChiCTR1900026429. Registered on 2019.10.9.

The Effect of Prophylactic Intravenous Amiodarone Administration on Reperfusion Ventricular Fibrillation in Patients With Left Ventricular Hypertrophy Undergoing Cardiopulmonary Bypass Surgery: Protocol for a Randomized Double-Blind Clinical Trial

Ventricular fibrillation (VF) is a common arrhythmia that occurs after the release of aortic cross-clamp (ACC) in patients undergoing cardiopulmonary bypass (CPB) surgery. Repeated defibrillation and long duration of VF could increase myocardial injuries. In patients with left ventricular hypertrophy (LVH), VF is easier to occur and more difficult to be terminated. Amiodarone, known as class III antiarrhythmic agent, has the prominent properties of converting VF and restoring the sinus rhythm. Before ACC release, administration of amiodarone has been confirmed useful to reduce occurrence of VF. However, few studies are focused on the effect of amiodarone before ACC release on reducing VF in patients with LVH. This study aimed at determining the efficacy of prophylactic intravenous amiodarone administration on reperfusion VF after release of ACC in patients with LVH undergoing CPB surgery. This will be a prospective, randomized, double-blind, placebo-controlled trial. The trial will enroll 54 patients with LVH aged 18-75 years who will undergo CPB surgery. All eligible participants will be randomly allocated to either the amiodarone or placebo group by using the block randomization in a 1:1 ratio. The primary end point will be the incidence rate of VF 30 minutes after ACC release and be assessed using the Fisher exact test. All data will be analyzed in accordance with the intention-to-treat principle. The study began in August 2022, and the data collection will take place for the next 2 academic years. As of this writing, 21 participants have already been recruited for the study. With this trial, we are hoping to demonstrate that prophylactic infusion of amiodarone before ACC release could reduce the occurrence of reperfusion VF in patients with LVH. ClinicalTrials.gov ChiCTR2000035057; https://www.chictr.org.cn/showprojen.aspx?proj=57145. DERR1-10.2196/40115.

Antiarrhythmic properties of N-Deacetyllappaconitine Hydrochloride

The aim of the investigation was the research of the N-deacetyllappaconitine hydrochloride antiarrhythmic properties. It was found that the studied substance was effective on the cardiac arrhythmias model caused by aconitine hydrochloride, but does not act on the models of calciume chlorideinduced arrhythmias and reperfusion ventricular fibrillation. The studied compound is less toxic than the comparison drug lappaconitine hydrobromide and acts in lower doses on the aconitine model of arrhythmias. N-Deacetyllappaconitine hydrochloride appears to be a Class I antiarrhythmic agent according to the Vaughan Williams classification.

Terminal T-wave inversion predicts reperfusion tachyarrhythmias in STEMI

IntroductionA reliable electrocardiographic predictor of ventricular fibrillation (VF) in patients with ST elevation myocardial infarction (STEMI) is lacking so far. Previous experimental/simulation study suggested a terminal T-wave inversion (TTWI) in ischemia-related ECG leads corresponding to anterior infarct localization as an independent predictor of reperfusion VF (rVF). This T-wave characteristic has never been tested as a rVF predictor in clinical settings. The aim of this study was to test if terminal T-wave inversion (TTWI) at admission ECG (before reperfusion) can serve as a predictor of ventricular fibrillation during reperfusion (rVF) in patients with anterior STEMI undergoing primary PCI. Methods and resultsStudy population included consecutive patients with anterior infarct localization admitted for primary PCI (n = 181, age 65 [57; 76] years, 66% male). Of those, 14 patients had rVF (rVF group, age 59 [47; 76] years, 64% male) and patients without rVF comprised the No-rVF group (n = 167, age 65 [57; 76] years, 66% male). Association of TTWI with rVF was analyzed using logistic regression analysis adjusted for relevant clinical and electrocardiographic covariates. The prevalence of TTWI in rVF group was 62% comparing to 23% in the No-rVF group, p = 0.005. TTWI was associated with increased risk of rVF (OR 5.51; 95% CI 1.70–17.89; p = 0.004) and remained a significant predictor after adjustment for age, gender, history of MI prior to index admission, VF before reperfusion, Tpeak-Tend, maximal ST elevation, and QRS duration (OR 23.49; 95% CI 3.14–175.91; p = 0.002). ConclusionsThe terminal T-wave inversion in anterior leads before PCI independently predicted rVF in patients with anterior MI thus confirming the previous experimental/simulation findings.

Cardioprotective and Vasoprotective Effects of Corticotropin-Releasing Hormone and Urocortins: Receptors and Signaling.

Despite the recent progress in research and therapy, cardiovascular diseases are still the most common cause of death worldwide, thus new approaches are still needed. The aim of this review is to highlight the cardioprotective potential of urocortins and corticotropin-releasing hormone (CRH) and their signaling. It has been documented that urocortins and CRH reduce ischemic and reperfusion (I/R) injury, prevent reperfusion ventricular tachycardia and fibrillation, and improve cardiac contractility during reperfusion. Urocortin-induced increase in cardiac tolerance to I/R depends mainly on the activation of corticotropin-releasing hormone receptor-2 (CRHR2) and its downstream pathways including tyrosine kinase Src, protein kinase A and C (PKA, PKCε) and extracellular signal-regulated kinase (ERK1/2). It was discussed the possibility of the involvement of interleukin-6, Janus kinase-2 and signal transducer and activator of transcription 3 (STAT3) and microRNAs in the cardioprotective effect of urocortins. Additionally, phospholipase-A2 inhibition, mitochondrial permeability transition pore (MPT-pore) blockade and suppression of apoptosis are involved in urocortin-elicited cardioprotection. Chronic administration of urocortin-2 prevents the development of postinfarction cardiac remodeling. Urocortin possesses vasoprotective and vasodilator effect; the former is mediated by PKC activation and prevents an impairment of endothelium-dependent coronary vasodilation after I/R in the isolated heart, while the latter includes both cAMP and cGMP signaling and its downstream targets. As CRHR2 is expressed by both cardiomyocytes and vascular endothelial cells. Urocortins mediate both endothelium-dependent and -independent relaxation of coronary arteries.

P2Y12 inhibition in macrophages reduces ventricular arrhythmias in rats after myocardial ischemia-reperfusion.

Myocardial ischemia-reperfusion (I/R) injury is still thought to be an unsolved puzzle that may lead to reperfusion arrhythmias and sudden cardiac death. Inflammation plays a key role in myocardial I/R. Studies have indicated that purinoceptor 2Y12 (P2Y12) antagonists have anti-inflammatory properties that are cardioprotective. In this study, we explored whether inhibition of P2Y12 in macrophages could reduce cardiac inflammation and attenuate reperfusion arrhythmias after myocardial I/R. Rats were randomly divided into 4 groups: group A (control + vehicle); group B (control + P2Y12 shRNA lentiviral vector); group C (myocardial I/R + vehicle); and group D (myocardial I/R + P2Y12 shRNA lentiviral vector). Infarct size, reperfusion arrhythmias, and P2Y12 and platelet endothelial cell adhesion molecule-1 (CD31) protein expression were measured. The incidence of reperfusion ventricular tachycardia and fibrillation (VT/VF) was 90% in the I/R group, while it was reduced to 50% by P2Y12 shRNA treatment. Ionized calcium binding adapter molecule 1 and P2Y12 immunoreactivity in the myocardial I/R + P2Y12 shRNA group was lower compared to the myocardial I/R group. P2Y12 shRNA treatment increased α-smooth muscle actin (α-SMA) and CD31 protein expression, as evidence by western blot and immunohistochemistry analyses (0.31 ±0.01 compared to 0.26 ±0.008, group D compared to group C, p < 0.05). Inhibition of P2Y12 in macrophages improved reperfusion arrhythmias in our rat I/R model, suggesting that blocking P2Y12 could decrease the inflammatory response after cardiac perfusion.

P2661Ventricular fibrillation during acute STEMI is not associated with early repolarization pattern on ECG recorded prior to the index ischemic episode

Abstract Background Generally considered as benign, ECG early repolarization (ER) pattern was recently claimed to be an indicator of increased susceptibility to fatal arrhythmias during acute ischemia. The victims of sudden cardiac death have been reported to have high prevalence of ER comparing with survivors of acute coronary event. We aimed to test the association between the ER pattern on resting ECG recorded prior to ST-elevation myocardial infarction (STEMI) and the risk of ventricular fibrillation (VF) during acute phase of STEMI in non-selected population of STEMI patients. Methods For STEMI patients admitted to a tertiary care hospital for primary PCI during 2007–2010 (n=2286), all ECGs recorded prior to the date of admission with STEMI were extracted from a digital archive. The latest ECG recorded prior to the index STEMI was used for analysis. After excluding ECGs with paced rhythm and intraventricular blocks with QRS duration ≥120ms, the remaining ECGs were processed using the Glasgow algorithm allowing automatic ER detection. The association between ER-pattern on historical ECG and VF during the first 48 hours of STEMI was tested using logistic regression. Results Historical ECGs were available for 1584 patients; 124 of them were excluded due to a paced rhythm or wide QRS, leaving 1460 patients available for analysis (age 68±12 years, 67% male). The time from historical ECG to STEMI was 16 (IQR 4–49) months. ER pattern was present on historical ECG in 272 of 1460 (18.6%) (ER+ group), among them in 90 (33%) – in inferior leads, in 116 (43%) – in lateral leads, in 66 (24%) – both in inferior and lateral leads. ER+ patients were younger both at the time of historical ECG (64±13 vs 66±19; p=0.041) and at the time of STEMI (67±12 vs 68±12; p=0.033), and had lower heart rate on historical ECG (68±12 vs 73±15; p&lt;0.001) than ER- patients. ER+ and ER- groups did not differ regarding clinical characteristics and conventional ECG measurements. The course of STEMI was complicated by VF in 106 patients (17 of them from ER+ group). The occurrence of VF during STEMI was not associated with ER-pattern on historical ECG (OR 0.875 95% CI 0.518–1.479; p=0.618). There was no association of ER pattern with VF before reperfusion (OR 0.54 95% CI 0.25–1.21; p=0.135) or reperfusion VF (OR 1.28 95% CI 0.55–3.01; p=0.569). No association was observed with regard to localization (inferior or lateral) of ER-pattern either. Conclusion In a non-selected population of STEMI patients the presence of ER-pattern on ECG recorded prior to the acute coronary event was not associated with VF during the first 48 hours of STEMI.

Prophylactic Effect of Amiodarone Infusion on Reperfusion Ventricular Fibrillation After Release of Aortic Cross-Clamp in Patients with Left Ventricular Hypertrophy Undergoing Aortic Valve Replacement: ARandomized Controlled Trial

To investigate whether prophylactic amiodarone infusion prevents ventricular fibrillation after aortic cross-clamp release and attenuates cytokine production in patients with left ventricular hypertrophy undergoing cardiac surgery. Prospective, randomized controlled trial. A public hospital. The study comprised 68 patients undergoing aortic valve replacement for severe aortic stenosis. Patients were randomly assigned to receive a 150mg bolus then 30mg/h continuous infusion of amiodarone (amiodarone group) or a 1 mg/kg bolus then 1 mg/kg/h continuous infusion of lidocaine (lidocaine group). The primary outcome was the ventricular fibrillation incidence rate after aortic cross-clamp release. Secondary outcomes included perioperative serum interleukin-6 and tumor necrosis factor-alpha levels. The ventricular fibrillation incidence rate was significantly lower in the amiodarone than in the lidocaine group (20.6% v 50%, relative risk 0.41; 95% confidence interval [CI] 0.20-0.86; p = 0.021). Interleukin-6 levels 1hour after aortic cross-clamp release and at intensive care unit admission were significantly lower in the amiodarone than in the lidocaine group (geometric mean [95% CI] 117.4pg/mL [87.1-158.4] v 339.5pg/mL [210.6-547.2]; p < 0.01 and 211.1pg/mL [162.8-73.6] v 434.1pg/mL [293.7-641.5]; p < 0.01, respectively). Tumor necrosis factor-alpha levels 1hour after aortic cross-clamp release were significantly lower in the amiodarone than in the lidocaine group (geometric mean [95% CI] 1.624pg/mL [1.359-1.940] v 2.283pg/mL [1.910-2.731]; p = 0.02). Amiodarone prevented reperfusion ventricular fibrillation in patients with left ventricular hypertrophy undergoing aortic valve replacement to a greater extent than did lidocaine. Furthermore, amiodarone inhibited postoperative interleukin-6 and tumor necrosis factor-alpha production.

Ischemic QRS prolongation as a predictor of ventricular fibrillation in a canine model

Objectives. An acute coronary occlusion and its possible subsequent complications is one of the most common causes of death. One such complication is ventricular fibrillation (VF) due to myocardial ischemia. The severity of ischemia is related to the amount of coronary arterial collateral flow. In dog studies collateral flow has also been shown to be associated with QRS prolongation. The aim of this study was to investigate whether ischemic QRS prolongation (IQP) is associated with impending VF in an experimental acute ischemia dog model. Methods. Degree of IQP and occurrence of VF were measured in dogs (n = 21) during coronary occlusion for 15 min and also during subsequent reperfusion (experiments conducted in 1984). Results. There was a significant difference in absolute IQP between dogs which developed VF during reperfusion (47 ± 29 ms, mean ± SD) and those which did not (12 ± 10 ms; p = .001). Conclusions. IQP during acute coronary occlusion is associated with reperfusion VF in an experimental dog model and might therefore be a potential predictor of malignant arrhythmias in patients with acute coronary syndrome.

Repolarization in perfused myocardium predicts reperfusion ventricular tachyarrhythmias

BackgroundAim of the study was to find out which myocardial repolarization parameters predict reperfusion ventricular tachycardia and fibrillation (VT/VF) and determine how these parameters express in ECG. MethodsCoronary occlusion and reperfusion (30/30min) was induced in 24 cats. Local activation and end of repolarization times (RT) were measured in 88 intramyocardial leads. Computer simulations of precordial electrograms were performed. ResultsReperfusion VT/VF developed in 10 animals. Arrhythmia-susceptible animals had longer RTs in perfused areas [183(177;202) vs 154(140;170) ms in susceptible and resistant animals, respectively, P<0.05]. In logistic regression analysis, VT/VFs were associated with prolonged RTs in the perfused area (OR 1.068; 95% CI 1.012–1.128; P=0.017). Simulations demonstrated that prolonged repolarization in the perfused/border zone caused precordial terminal T-wave inversion. ConclusionsThe reperfusion VT/VFs were independently predicted by the longer RT in the perfused zone, which was reflected in the terminal negative phase of the electrocardiographic T-wave.

Prophylactic amiodarone in patients with severe aortic stenosis and left ventricular hypertrophy undergoing aortic valve replacement: Silencing the rebels

BackgroundVentricular fibrillation occurs commonly after aortic cross clamp in patients undergoing aortic valve replacement for severe aortic stenosis. Amiodarone is a class III antiarrhythmic drug that can be used as a prophylactic measure to prevent reperfusion ventricular fibrillation as ventricular fibrillation increases myocardial oxygen demand and hence myocardial damage. MethodsA prospective, randomized, triple blinded study conducted in a single institution, Cardio-thoracic Academy, Ain –Shams University, Cairo, Egypt.120 patients with severe AS enrolled for elective aortic valve replacement. 60 patients received 10 ml of normal saline 9% (control group), while the other 60 patients received a single dose of Amiodarone 150 mg in 10 ml of Dextrose 5% through the pump circuit (Case Group). The incidence of post clamp arrhythmia, need of defibrillation, cardiac support was recorded. Results36 patients (60%) of the case group had spontaneous sinus rhythm upon declamping which is significantly lower than control group. The incidence of VF was lower in the case group (P value < 0.001) (highly significant). The number of DC shock required for ventricular defibrillation, total bypass and declamping times were significantly lower in the case group. ConclusionsProphylactic use of a single dose amiodarone through the pump circuit before cross clamp release reduces the incidence of reperfusion induced ventricular fibrillation and subsequent defibrillation therapy needed.

ELECTROCARDIOGRAPHIC MARKERS OF CARDIOMYOCYTES’ ACTION POTENTIALS LENGTHENING IN THE BORDER ZONE OF ISCHEMIA (EXPERIMENTAL AND MODEL STUDY)

Background : Ventricular fibrillation within the first 5 min of reperfusion was observed in the animals with lengthening but not shortening of action potential duration (APD) in the border zone of ischemia. Objective : The objective of the study was to find the electrocardiographic manifestations of the APD changes in the border zone of ischemia as the markers of ventricular fibrillation. Design and methods : The simulations were carried out using the model of the cat heart ventricles. To simulate the ischemia, we decreased activation velocity and modified the durations and the amplitudes of action potentials. Results : The simulations showed that APD’s increase in the border zone of ischemia was detectable in the ECG leads most proximal to the heart (V2,V3). It was manifested by the T-wave lengthening and the change of its polarity in the terminal period of repolarization. The similar T-wave features were observed in the electrograms of cats with the reperfusion ventricular fibrillation Conclusion : The simulation data can be useful for the development of new methods of diagnostics of the most dangerous types of ischemia associated with ventricular fibrillation.

Limited Sanguineous Reperfusion Reduces Ventricular Fibrillation Following Intermittent Cold Crystalloid Cardioplegic Arrest.

SourceURL:file://localhost/Users/alex/Desktop/ICFJ%20VF%20submission/Abstract.doc&lt;p&gt;&lt;strong&gt;Background&lt;/strong&gt;&lt;/p&gt;&lt;p&gt;Cold crystalloid cardioplegic arrest does not allow for a controlled hyperkalaemic sanguineous reperfusate, administered under constant flow and pressure conditions in order to limit reperfusion injury. We investigated the use of intermittent, antegrade cold crystalloid cardioplegia combined with a limited flow normokalaemic sanguineous reperfusion and measured the outcome in terms of the incidence of reperfusion ventricular fibrillation.&lt;/p&gt;&lt;p&gt; &lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods&lt;/strong&gt;&lt;/p&gt;&lt;p&gt;Patients requiring coronary revascularization of at least two coronary arteries, including an internal thoracic artery (ITA) anastomosis, were studied in this prospective randomized trial. Myocardial protection was by intermittent, antegrade cold crystalloid cardioplegia. In the control group (n=100), after completion of the distal anastomoses, the heart was reperfused by releasing the aortic and ITA clamps concomitantly. In the study group (n=100) the ITA was allowed to perfuse the heart for 3 minutes before the aortic cross-clamp was removed. The presence of reperfusion ventricular fibrillation from the moment of reperfusion until weaning from cardiopulmonary bypass was recorded.&lt;/p&gt;&lt;p&gt; &lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results&lt;/strong&gt;&lt;/p&gt;&lt;p&gt;The incidence of ventricular fibrillation decreased with an increase in the number of grafts and was significantly lower in the study group (double grafts 2/9, 22.2% vs 19/25, 76.0% &lt;em&gt;p&lt;/em&gt;=0.004; triple grafts 2/39, 4.9% vs 16/33, 48.5% &lt;em&gt;p&lt;/em&gt;&amp;lt;0.001; and quadruple grafts 2/45, 4.4% vs 13/35, 28.7% &lt;em&gt;p&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;&lt;p&gt; &lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions&lt;/strong&gt;&lt;/p&gt;&lt;p&gt;This strategy of myocardial protection combines the advantages of conventional crystalloid cardioplegia with the added benefit of limited sanguineous reperfusion. The results suggest a beneficial effect with regard to reperfusion-induced injury, as evidenced by a significantly reduced incidence of reperfusion ventricular fibrillation.&lt;/p&gt;

Сравнительное изучение токсичности и антиаритмической активности нового n-замещенного производного бензамида

A promising search direction of modern scientists, involved in antiarrhythmic researchs, is the creation of substances that can suppress the repolarization phase of the action potential of myocardial cells. At the same time, the well-known domestic representative of this group of substances – the Nibentan – has a number of undesirable effects. To correct for these effects, the chemical compound the Nibentan with L-glutamic acid as the anion was created. In experi-ments on mice, it was found that the acute toxicity of the compound is N-substituted Benzamide derivative – Racemate Nibentan with L-glutamic acid is below 1.6 times at the intra-peritoneal injection in comparison with the acute toxicity structural analogue the Nibentan. Studied chemical compound in the range of doses from 1 to 5 % from DL50 suppresses reproduction acontinued disturbances of cardiac rhythm, which may serve as evidence of the ability of compounds to inhibit sodium ion currents through the membrane of cardiomyocytes. The compound of the Racemate Nibentan with L-glutamic acid also has a great therapeutic effect on aconitine arrhythmiac model in rats. On the model of transient ischemic arrhythmias a new compound Nibentan with comparable anti-arrhythmic activity in doses of 5 and 2.5 % from LD50, exceeds the reference product to prevent the formation of occlusion and reperfusion ventricular fibrillation in acute experience on cats. This work was supported by the project (project code - 2859) performed in Mordovia State N.P. Ogarev University under Government job and grant RFBR 14-04-31104.

Amiodarone versus lidocaine for the prevention of reperfusion ventricular fibrillation: A randomized clinical trial.

Reperfusion ventricular fibrillation after aortic cross clamp is one of the important complications of open cardiac surgery and its prevention could reduce myocardial injuries. This study aimed to evaluate the efficacy of single dose of amiodarone or lidocaine by the way of pump circuit three minutes before aortic cross clamp release and compare the results with normal saline as placebo in a randomized double blinded controlled trial. One hundred fifty patients scheduled for first time elective coronary artery bypass graft surgery were randomly assigned to receive either single dose of amiodarone (150 mg), lidocaine (100 mg), or normal saline (5 ml) three minutes before aortic cross clamp release. The incidence of ventricular fibrillation and the need for reuse of drug were compared between these groups by chi-square, Student's t-test, Mann-Whitney test, and One-way ANOVA. SPSS software was used for statistical analysis. The incidence of ventricular fibrillation is higher in the placebo group (15.9%) compare to lidocaine (11.8%) and amiodarone (8.9%) groups; however, there was no statistical difference among the three groups (P = 0.41). Moreover, the reuse of amiodarone (22.7%) was statistically higher (P < 0.05) than lidocaine (5.9%). This study showed no difference among lidocaine, amiodarone, and placebo in preventing ventricular fibrillation after aortic cross clamp release.

Continuous infusion of magnesium–lidocaine mixture for prevention of ventricular arrhythmias during on-pump coronary artery bypass grafting surgery

BackgroundDuring on-pump coronary artery bypass grafting (CABG) surgery, the incidence of reperfusion ventricular fibrillation (VF) is high and post-bypass ventricular arrhythmias are common. Both reperfusion VF and ventricular arrhythmias can cause additional myocardial injury to the already ischemic myocardium. This trial aimed to test the assumption that continuous combined magnesium and lidocaine infusion would be efficient and long lasting for the prevention of post-myocardial vascularization ventricular arrhythmias including VF.MethodsEighty ASA III patients, who were candidates for CABG surgery, were randomly assigned into two groups: Group I (control group, n = 40) and Group II (Group ML, n = 40). After endotracheal intubation, patients of control group were infused with plain normal saline in a volume equivalent to study drugs’ mixture volume. Patients of Group ML were infused with magnesium–lidocaine mixture to achieve a bolus of magnesium sulfate 2 g and lidocaine 100 mg followed by continuous infusion of Mg sulfate 500 mg/h and lidocaine 1 mg/min. The initial cardiac rhythm after aortic cross clamp (ACC) release and the occurrence of post-CPB significant ventricular arrhythmias were recorded.ResultsThe incidences of reperfusion VF and post-CPB ventricular arrhythmias in Group ML were significantly lower than that in control group (22.5% vs. 72.5%) (P < 0.001) and (7.5% vs. 25%) (P < 0.05), respectively. However, in Group ML, this beneficial effect was associated with higher incidence of sinus bradycardia (72.5% vs. 17.5%) and hence pacing needs (22.5% vs. 0.0%) when compared with control group.ConclusionOur study concluded that, during on-pump CABG surgery, the combined administration of magnesium and lidocaine as a bolus dose starting after intubation followed by continuous infusion reduced the incidence of reperfusion VF by 62% and post-CPB ventricular arrhythmias by 70% on expense of increased the incidence of sinus bradycardia and pacing.

Establishment and evaluation of a swine model of acute myocardial infarction and reperfusion–ventricular fibrillation–cardiac arrest using the interventional technique

BackgroundVentricular fibrillation is the main cause of sudden cardiac death among patients with acute myocardial infarction (AMI). Substantial benefits could be obtained by both researchers and practitioners if an AMI reperfusion-ventricular fibrillation-cardiac arrest model were established. MethodsTwenty swine were anesthetized and underwent occlusion of the left anterior descending branch for 90 minutes prior to blood reperfusion. Throughout this process, continuous 12-lead electrocardiography (ECG) was used to monitor heart rate, rhythm, and electrocardiogram alteration. Thereafter, AMI was confirmed by ECG and left ventricular angiography. Heart tissue was collected for pathological analysis, and for evaluation of the establishment of a model of AMI reperfusion. ResultsSeven swine died during the model establishment, and the 13 surviving swine were proven to have myocardial infarction; nine of those survivors had ventricular fibrillation–cardiac arrest after reperfusion based on the electrocardiograph and pathological examination. ConclusionBlocking the left anterior descending branch by inflation of an over-the-wire coronary balloon catheter in swine can result in successful establishment of a swine model of AMI and reperfusion–ventricular fibrillation–cardiac arrest, with good reproducibility and a high survival rate.

Selective heart rate reduction with ivabradine slows ischaemia-induced electrophysiological changes and reduces ischaemia–reperfusion-induced ventricular arrhythmias

Heart rates during ischaemia and reperfusion are possible determinants of reperfusion arrhythmias. We used ivabradine, a selective If current inhibitor, to assess the effects of heart rate reduction (HRR) during ischaemia–reperfusion on reperfusion ventricular arrhythmias and assessed potential anti-arrhythmic mechanisms by optical mapping. Five groups of rat hearts were subjected to regional ischaemia by left anterior descending artery occlusion for 8min followed by 10min of reperfusion: (1) Control n=10; (2) 1μM of ivabradine perfusion n=10; (3) 1μM of ivabradine+5Hz atrial pacing throughout ischaemia–reperfusion n=5; (4) 1μM of ivabradine+5Hz pacing only at reperfusion; (5) 100μM of ivabradine was used as a 1ml bolus upon reperfusion. For optical mapping, 10 hearts (ivabradine n=5; 5Hz pacing n=5) were subjected to global ischaemia whilst transmembrane voltage transients were recorded. Epicardial activation was mapped, and the rate of development of ischaemia-induced electrophysiological changes was assessed. HRR observed in the ivabradine group during both ischaemia (195±11bpm vs. control 272±14bpm, p<0.05) and at reperfusion (168±13bpm vs. 276±14bpm, p<0.05) was associated with reduced reperfusion ventricular fibrillation (VF) incidence (20% vs. 90%, p<0.05). Pacing throughout ischaemia–reperfusion abolished the protective effects of ivabradine (100% VF), whereas pacing at reperfusion only partially attenuated this effect (40% VF). Ivabradine, given as a bolus at reperfusion, did not significantly affect VF incidence (80% VF). Optical mapping experiments showed a delay to ischaemia-induced conduction slowing (time to 50% conduction slowing: 10.2±1.3min vs. 5.1±0.7min, p<0.05) and to loss of electrical excitability in ivabradine-perfused hearts (27.7±4.3min vs. 14.5±0.6min, p<0.05). Ivabradine administered throughout ischaemia and reperfusion reduced reperfusion VF incidence through HRR. Heart rate during ischaemia is a major determinant of reperfusion arrhythmias. Heart rate at reperfusion alone was not a determinant of reperfusion VF, as neither a bolus of ivabradine nor pacing immediately prior to reperfusion significantly altered reperfusion VF incidence. This anti-arrhythmic effect of heart rate reduction during ischaemia may reflect slower development of ischaemia-induced electrophysiological changes.

Sudden cardiac death secondary to demonstrated reperfusion ventricular fibrillation in a woman with Takotsubo cardiomyopathy

Takotsubo cardiomyopathy is a left ventricle cardiomyopathy characterized by a reversible dyskinesia responsible for the typical apical ballooning aspect. The disease is considered benignant with a full recovery within a few weeks. We present the case of a 52-year-old woman who presented with angina diagnosed with Takotsubo cardiomyopathy on the basis of both noninvasive (electrocardiography, echocardiography) and invasive (angiography) exams. At discharge, a Holter monitor was fitted to the patient. During the recording the patient faced sudden cardiac death. The analysis of the Holter traces allowed some speculations on the mechanism of this unexpected arrhythmic death. The cause of the fatal ventricular fibrillation appears to be the fast reperfusion following a short occlusion of an epicardial coronary artery. This case highlights the epicardial vasospasm as an important pathogenic mechanism of the syndrome and the possible usefulness of diagnostic tests able to elicit the spasm susceptibility and guide a more targeted pharmacological therapy. Some considerations are also possible on the cellular processes linking the rapid reperfusion and the arrhythmias onset.