Number Of Premature Ventricular Complexes Research Articles

The analysis of the parameters of 24-hr ECG Holter monitoring in patients with blood neoplasms undergoing high-dose chemotherapy and stem cell transplantation.

Hematopoietic stem cell transplantation (HSCT) is a widely used procedure in the treatment of malignant diseases, including blood neoplasms and has increased survival in hematological diseases. The aim of the study was to analyze parameters of 24-hr ECG monitoring in patients with selected blood neoplasms in whom the procedure of hematopoietic stem cell transplantation was performed. The study group consisted of 64 adults diagnosed with hematologic cancer qualified for HSCT with the previous high dose chemotherapy (HDC). In all patients 24-hr Holter monitoring was carried out twice. First examination took place prior to the HSCT procedure, and the second after finishing the procedure of HSCT. The minimal and mean heart rate (HR min and HR max) from 24-hr ECG recording was statistically significantly higher after the transplantation in comparison with the first test. The number of premature ventricular complexes (PVCs) was higher in the test after HSCT. In the second examination there was significantly higher percentage of premature ventricular complexes, incidents of tachycardia, and Mobitz type 1 second degree atrioventricular block. In regression analysis, in a group of patients with blood neoplasms after HSCT and HDC, administration of cyclophosphamide, fludarabine and total body irradiation were independent risk factors for electrocardiographic abnormalities in 24-hr Holter monitoring, that is, the increase in HR min, HR mean and PVCs. In patients with blood neoplasms undergoing HSCT more electrocardiographic abnormalities may be found after this procedure in comparison with the 24-hr Holter monitoring before transplantation.

Effects of Traditional Chinese Medicine Shensong Yangxin Capsules on Heart Rhythm and Function in Congestive Heart Failure Patients with Frequent Ventricular Premature Complexes: A Randomized, Double-blind, Multicenter Clinical Trial.

Background:Pharmacological therapy for congestive heart failure (CHF) with ventricular arrhythmia is limited. In the study, our aim was to evaluate the effects of Chinese traditional medicine Shensong Yangxin capsules (SSYX) on heart rhythm and function in CHF patients with frequent ventricular premature complexes (VPCs).Methods:This double-blind, placebo-controlled, multicenter study randomized 465 CHF patients with frequent VPCs to the SSYX (n = 232) and placebo groups (n = 233) for 12 weeks of treatment. The primary endpoint was the VPCs monitored by a 24-h ambulatory electrocardiogram. The secondary endpoints included the left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter, N-terminal pro-brain natriuretic peptide (NT-proBNP), New York Heart Association (NYHA) classification, 6-min walking distance (6MWD), Minnesota Living with Heart Failure Questionnaire (MLHFQ) scores, and composite cardiac events (CCEs).Results:The clinical characteristics were similar at baseline. SSYX caused a significantly greater decline in the total number of VPCs than the placebo did (−2145 ± 2848 vs. −841 ± 3411, P < 0.05). The secondary endpoints of the LVEF, NYHA classification, NT-proBNP, 6MWD, and MLHFQ scores showed a greater improvements in the SSYX group than in the placebo group (ΔLVEF at 12th week: 4.75 ± 7.13 vs. 3.30 ± 6.53; NYHA improvement rate at the 8th and 12th week: 32.6% vs. 21.8%, 40.5% vs. 25.7%; mean level of NT-proBNP in patients with NT-proBNP ≥125 pg/ml at 12th week: −122 [Q1, Q3: −524, 0] vs. −75 [Q1, Q3: −245, 0]; Δ6MWD at 12th week: 35.1 ± 38.6 vs. 17.2 ± 45.6; ΔMLHFQ at the 4th, 8th, and 12th week: −4.24 ± 6.15 vs. −2.31 ± 6.96, −8.19 ± 8.41 vs. −3.25 ± 9.40, −10.60 ± 9.41 vs. −4.83 ± 11.23, all P < 0.05). CCEs were not different between the groups during the study period.Conclusions:In this 12-week pilot study, SSYX was demonstrated to have the benefits of VPCs suppression and cardiac function improvement with good compliance on a background of standard treatment for CHF.Trial Registration:www.chictr.org.cn, ChiCTR-TRC-12002061 (http://www.chictr.org.cn/showproj.aspx?proj=7487) and Clinicaltrials.gov, NCT01612260 (https://clinicaltrials.gov/ct2/show/NCT01612260).

Twenty-four hour Holter monitoring in finishing cattle housed outdoors

IntroductionAtrial premature complexes have been reported to be the most common arrhythmia in cattle and is suspected to be secondary to systemic disease, especially gastrointestinal disease. In order to properly identify pathologic arrhythmia in cattle, the normal rhythm and arrhythmia prevalence should be defined. The objective of this study was to determine the normal heart rate, rhythm, number of ventricular premature complexes (VPCs), and atrial premature complexes (APCs) in unrestrained Angus steers. AnimalsTwenty-seven client owned steers with unremarkable physical examinations and serum biochemical analyses were used. Materials and methodsTwenty-four hour Holter monitors, attached by a custom-made harness, were retrospectively evaluated. Three lead electrocardiographic registrations of good quality and normal sinus rhythm were obtained from all steers in the study. ResultsThe mean heart rate was 66.8 bpm ± 16.4 bpm. Ventricular premature complexes were rare (noted in 14.8% of steers), and APCs were common (noted in 85% of the steers). Simple second degree AV block was observed in 18.5% of the steers. ConclusionIn summary, healthy steers have rare single VPCs, although it is possible for an individual animal to have apparent more frequent VPCs. Mean heart rate varies with a diurnal pattern similar to other species. Atrial premature complexes are the most prevalent abnormality observed in feedlot steers.

Ambulatory electrocardiogram recordings in cats with primary asymptomatic hypertrophic cardiomyopathy.

Objectives The aims of the study were to determine the heart rate, rhythm, number of ventricular premature complexes (VPCs) and atrial premature complexes (APCs) in unsedated cats with asymptomatic hypertrophic cardiomyopathy (HCM), using 24 h ambulatory electrocardiogram (ECG) (Holter) in the home environment and to compare the results with those from healthy control cats. Methods Fifteen privately owned cats with asymptomatic HCM entered the study. Data from 23 healthy cats, previously published by our group, were used as the control. Clinical examination, measurement of blood pressure, echocardiographic examination, Holter recordings and biochemical analyses were performed in all cats. Holter recordings were obtained in the home environment. Results Three-lead ECGs of good quality were obtained from 15 cats with HCM. The median heart rate was 145 (interquartile range [IQR] 137-184) beats per minute for the cats with HCM. All cats with HCM presented with normal sinus rhythm; 60% of cats had intermittent sinus arrhythmia. Median number of VPCs was 3 (IQR 1-17). Three cats had APCs and three cats had both escape beats and intermittent sinus arrhythmia. Conclusions and relevance Asymptomatic cats with HCM had few VPCs and APCs on 24 h ambulatory ECG in the home environment. Intermittent sinus arrhythmia was observed in 60% of cats with HCM. The present study shows that the heart rate and the number of VPCs and APCs in cats with asymptomatic HCM are similar to that found in healthy control cats.

Supine Frequent Ventricular Extrasystoles in a Pregnant Woman without Structural Heart Disease.

Arrhythmias are the most common cardiac complication during gestational period and may occur in women with or without known structural heart disease. Premature extra beats and sustained tachyarrhythmias are the most common arrhythmias in pregnancy. Symptomatic episodes occur in 20–44% of pregnant women, usually as palpitations, dizziness, or syncope. We searched on Pubmed for ventricular premature complexes (VPC) in pregnant women and found no case reporting increased incidence of this arrhythmia while supine. The aim of this study is to report a case of a pregnant woman without previous structural heart disease that presented a great number of VPC when supine. The arrhythmogenesis increase during pregnancy is multifactorial. In the reported case, we believe that augmented venous return was the most important pathophysiologic process. When the patient changes to left lateral decubitus, there could be a sudden release of the inferior vena cava, causing an abrupt augmentation of venous return to the right heart chambers and increasing the risk of arrhythmias. Obstetricians and primary care physicians should be aware of palpitations and related patient complains while they are asleep or supine.

Decreased prevalence of cardiac arrhythmias during and after vigorous and prolonged exercise in healthy male marathon runners

Vigorous exercise such as marathon running results in an increased risk of sudden cardiac death. Malignant arrhythmias seem to be the primary cause. However, continuous electrocardiographic monitoring for detection of arrhythmias during a marathon race has not been performed yet. Twenty male marathon runners (age 45 ± 8 years) free of cardiovascular disease underwent 24-hour Holter monitoring 5 weeks before a marathon race (baseline). Subsequently, wireless Holter monitoring started immediately before the race, recorded up to 70 hours postrace. Electrocardiograms were analyzed for the presence of arrhythmias. Additionally, cardiac troponin, interleukin-6 (IL-6), and electrolytes were assessed prerace and postrace. At baseline Holter recordings, runners showed a median of 9 (interquartile range 3-25) atrial premature complexes (APCs) and 4 (2-16) ventricular premature complexes (VPCs) per 100,000 beats. Compared to baseline, the number of APCs decreased significantly during and 1 hour after the marathon race (0 [0-3] and 0 [0-0], all P < .001) as well as the number of VPCs during the race (0 [0-0], P = .008). No malignant arrhythmias occurred. Mean postrace levels for troponin and IL-6 were significantly augmented after the race (prerace to postrace: troponin 4 times, IL-6 17 times, all P < .001); however, no significant influence of these biomarkers or electrolytes on the prevalence of arrhythmias was observed (all P > .05). In this cohort of male runners free of cardiovascular disease, the prevalence of arrhythmias during and after a marathon race was decreased. Arrhythmogenic risk was independent of changes in biomarkers assessing cardiac injury, inflammation, and changes in electrolytes.

Long-Term Effect of Continuing Sports Activity in Competitive Athletes With Frequent Ventricular Premature Complexes and Apparently Normal Heart

The long-term outcome of athletes with frequent ventricular premature complexes (VPCs) and apparently normal heart has not been fully clarified. To evaluate the clinical and prognostic significance of VPCs and the influence of continuing sports activity during follow-up, we studied 120 healthy athletes (96 men; median age 16 years) in whom frequent VPCs (>100 VPCs/24 hours) were discovered by chance during preparticipation screening. All athletes were followed up for a median of 84 months. During follow-up, 96 underwent serial 24-hour Holter recording and 62 underwent serial echocardiography. The median number of VPCs/24 hours on basal Holter was 3,760. During follow-up, 81 athletes continued sports activity, whereas 39 did not. No athlete died or developed overt heart disease. The median number of VPCs/24 hours decreased in both athletes who continued sports activity and those who did not (from 3,805 to 1,124, p <0.0001 and from 5,787 to 1,298, p <0.0001, respectively). During follow-up, left ventricular ejection fraction slightly decreased to <55% in 9 of 62 athletes who, in respect to the remaining 53, had more VPCs/24 hours both in the basal state (12,000 vs 3,880) and during follow-up (10,702 vs 1,368), and a longer follow-up (95 vs 36 months). In conclusion, (1) frequent VPCs in athletes without heart disease have a long-term benign prognostic significance, (2) sporting activity does not modify this benign outcome, (3) during follow-up, the burden of VPCs decreases whether or not subjects continue sports activity, and (4) in 14.5% of athletes, ejection fraction slightly decreases over time.

TRPM4 channel re-expression after myocardial infarction is essential for survival in mice

Introduction: TRPM4 is a Ca2+-activated non selective cation channel involved in conduction disorders. TRPM4 is expressed in sinoatrial and atrial cells but only poorly in ventricles. However, in vitro studies detected this current in cardiac hypertrophy concomitantly with fetal gene re-expression. The aim of our study was to investigate whether TRPM4 plays a functional role in ventricular cardiomyocytes in hypertrophy following Myocardial Infarction (MI). Methods: MI was induced by left coronary artery ligation in Trpm4-gene knock-out (Trpm4-/-) and Trpm4+/+ mice (23 and 12, respectively). Post-MI heart failure was verified using Doppler-echocardiography. Electrocardiograms (ECGs) were recorded by telemetry during 12h. Left Ventricular (LV) cardiomyocytes were isolated 4 weeks after MI. Action Potential (AP) and TRPM4-current were recorded using the patch-clamp technique. The propensity of cells to trigger spontaneous electrical activities was assessed. Store-Operated Ca2+-Entry (SOCE), negatively regulated by TRPM4, was measured using fluorescence microscopy. TRPM4 transcript and protein expression in left ventricle were studied using qPCR and western blot analysis. Results: Kaplan-Meier analysis evidenced a higher mortality rate for Trpm4-/–MI mice when compared with Trpm4+/+-MI animals (56% vs. 91%, P=0.03). Echocardiograms showed increased LV mass (3.85±0.4 vs. 2.49±0.2 mg/g, P=0.009) while fractional shortening was reduced (15.2±1.5 vs. 22.7±2.2, P=0.013) in Trpm4-/–MI vs. Trpm4+/+-MI mice. The number of premature ventricular complexes was increased in Trpm4-/–MI vs. Trpm4+/+-MI mice (57±5 vs. 35±3, P=0.028). Surprisingly, there was no difference in the lengthening of AP in LV myocytes following MI between Trpm4-/- and Trpm4+/+ (APD90: 94.4±23 vs. 88±15 ms, P=0.58, respectively). However, Trpm4-/–MI cells exhibited more EADs and DADs than Trpm4+/+-MI (EADs: 11/25 vs. 6/30, P=0.02; DADs: 8/25 vs. 2/30, P=0.008). Moreover, an increase of Trpm4 transcript was found in Trpm4+/+-MI ventricle, associated with TRPM4 protein presence (western blot) and function (TRPM4 current: 1.28±0.1 vs. 0.01±0.06 pA/pF at +40 mV, P=0.001). This expression correlated to a decrease of SOCE in cardiomyocytes from MI group vs. sham group (P=0.001). Conclusion: Lack of TRPM4 channel re-expression in the LV worsened the deleterious effects of post-MI cardiac remodeling on survival, hypertrophy, heart function, and arrhythmic events. Negative regulation of SOCE, involved in cardiac remodeling, and occurrence of spontaneous cellular arrhythmias suggests that TRPM4 channel plays a critical role in post-MI adaptations.

Aritmojenik Sağ Ventrikül Kardiyomiyopatili Boxerlarda 24 Saatlik Holter Monitorizasyon ve Troponin I Seviyesi

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is described as a disease that has an autosomal dominant trait with reduced penetrance, that appears in dogs between two and eight years of age. Boxers are predisposed to ARVC. Some of the symptoms of ARVC are fainting, attacks of tachycardia especially vetnricular tachycardia and sudden cardiac death. The aim of the study was to estimate the usefulness of 24-h Holter monitoring and the level of troponin I (cTnl) in examining the treatment of Boxers with ARVC. 24-h Holter monitoring and plasma concentrations of cTnI were carried out every three months after introducing anti-arrhythmic treatment (metoprolol prolongatum, sotalol or amiodaron). There was a significant correlation between the number of ventricular premature complexes (VPC) over a 24-h period and the level of cTnl. No correlation was found between the appearance of monitoring ventricular tachycardia (VT) and the level of cTnl. The presented results show the possibility to use cTnl to evaluate the efficacy of antiarrhythmia treatment in dogs with ARVC.

Short-Term Fasting Reduces the Extent of Myocardial Infarction and Incidence of Reperfusion Arrhythmias in Rats

The effect of three-day fasting on cardiac ischemic tolerance was investigated in adult male Wistar rats. Anesthetized open-chest animals (pentobarbitone 60 mg/kg, i.p.) were subjected to 20-min left anterior descending coronary artery occlusion and 3-h reperfusion for infarct size determination. Ventricular arrhythmias were monitored during ischemia and at the beginning (3 min) of reperfusion. Myocardial concentrations of beta-hydroxybutyrate and acetoacetate were measured to assess mitochondrial redox state. Short-term fasting limited the infarct size (48.5+/-3.3 % of the area at risk) compared to controls (74.3+/-2.2 %) and reduced the total number of premature ventricular complexes (12.5+/-5.8) compared to controls (194.9+/-21.9) as well as the duration of ventricular tachycardia (0.6+/-0.4 s vs. 18.8+/-2.5 s) occurring at early reperfusion. Additionally, fasting increased the concentration of beta-hydroxybutyrate and beta-hydroxybutyrate/acetoacetate ratio (87.8+/-27.0) compared to controls (7.9+/-1.7), reflecting altered mitochondrial redox state. It is concluded that three-day fasting effectively protected rat hearts against major endpoints of acute I/R injury. Further studies are needed to find out whether these beneficial effects can be linked to altered mitochondrial redox state resulting from increased ketogenesis.

The Effect of Acute Versus Delayed Remote Ischemic Preconditioning on Reperfusion Induced Ventricular Arrhythmias

The effect of remote ischemic preconditioning (RIPC) on arrhythmias in in vivo models is unknown. Our purpose was to determine effects of both acute and delayed RIPC on arrhythmias. In the acute protocol anesthetized open chest rats were exposed to 5 minutes of proximal left coronary artery occlusion (CAO) and 10 minutes of reperfusion. Rats were either untreated (ischemia/reperfusion, IR group, n = 17) or received RIPC (n = 14) with 5 minutes bilateral femoral occlusions followed by 5 minutes of reperfusion times 3, started 30 minutes before CAO. At reperfusion, onset of ventricular tachycardia (VT) was delayed in RIPC group (25.7 seconds) versus IR (8.8 seconds; P = 0.04). Number of episodes of VT was 17.0 in IR versus 3.0 in the RIPC group (P = 0.01) and duration of VT was 54.1 seconds in IR versus 4.9 seconds in RIPC (P = 0.019). Number of ventricular premature complexes (VPC) was 26.0 in IR and 10.0 in RIPC rats (P = 0.04). Levels of reperfusion injury salvage kinases (RISK), that is, phospho-Akt and phospho-p70S6 in the risk area of IR and RIPC hearts were similarly higher compared to the nonischemic areas both at 1 and 10 minutes into reperfusion. Delayed RIPC was induced on day 1 and on day 2, myocardial IR was induced. Delayed RIPC did not affect VT or VPC. Acute RIPC of the lower limbs induced a powerful delay in/and reduction in IR induced ventricular arrhythmias, but without evoking the RISK pathway; a late protective phase of RIPC on arrhythmias did not occur.

Multifocal Ectopic Purkinje-Related Premature Contractions: A New SCN5A-Related Cardiac Channelopathy

The aim of this study was to describe a new familial cardiac phenotype and to elucidate the electrophysiological mechanism responsible for the disease. Mutations in several genes encoding ion channels, especially SCN5A, have emerged as the basis for a variety of inherited cardiac arrhythmias. Three unrelated families comprising 21 individuals affected by multifocal ectopic Purkinje-related premature contractions (MEPPC) characterized by narrow junctional and rare sinus beats competing with numerous premature ventricular contractions with right and/or left bundle branch block patterns were identified. Dilated cardiomyopathy was identified in 6 patients, atrial arrhythmias were detected in 9 patients, and sudden death was reported in 5 individuals. Invasive electrophysiological studies demonstrated that premature ventricular complexes originated from the Purkinje tissue. Hydroquinidine treatment dramatically decreased the number of premature ventricular complexes. It normalized the contractile function in 2 patients. All the affected subjects carried the c.665G>A transition in the SCN5A gene. Patch-clamp studies of resulting p.Arg222Gln (R222Q) Nav1.5 revealed a net gain of function of the sodium channel, leading, in silico, to incomplete repolarization in Purkinje cells responsible for premature ventricular action potentials. In vitro and in silico studies recapitulated the normalization of the ventricular action potentials in the presence of quinidine. A new SCN5A-related cardiac syndrome, MEPPC, was identified. The SCN5A mutation leads to a gain of function of the sodium channel responsible for hyperexcitability of the fascicular-Purkinje system. The MEPPC syndrome is responsive to hydroquinidine.

Effect of Cd36 on cardiac ischemic tolerance and adrenergic signaling in spontaneously hypertensive rats

CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long‐chain fatty acids (FA). Spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene. We analyzed the effects of mutant Cd36 on cardiac susceptibility to ischemia‐reperfusion injury in adult SHR‐Cd36 transgenic rats with wild type Cd36 compared to age‐matched SHR controls. Using an open‐chest model of coronary artery occlusion, we found that SHR‐Cd36 showed profound ischemic arrhythmogenesis resulting in significantly increased total number of premature ventricular complexes (2623±517 vs. 849±250) in SHR controls. On the other hand, transgenic SHR showed significantly reduced infarct size (52.6±4.3% vs. 72.4±2.9% of area at risk). Similar differences were observed in isolated perfused hearts and the increased incidence of arrhythmias in transgenic SHR was abolished by reserpine suggesting the involvement of catecholamines. Furthermore, forskolin‐stimulated activity of adenylyl cyclase was increased in the SHR‐Cd36. It can be concluded that Cd36 plays an important role in modulating cardiac susceptibility to ischemia‐reperfusion injury. The proarrhythmic effect of Cd36 transgene appears to be related to increased adrenergic stimulation. Supported by grants: GAAV IAAX01110901, GAUK 429611

CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis.

CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long-chain fatty acids (FA). Previously, we found that the spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene that results in reduced transport of long-chain FA into cardiomyocytes and predisposes the SHR to cardiac hypertrophy. In the current study, we analyzed the effects of mutant Cd36 on susceptibility to ischemic ventricular arrhythmias and myocardial infarction in adult SHR-Cd36 transgenic rats with wild-type Cd36 compared with age-matched SHR controls. Using an open-chest model of coronary artery occlusion, we found that SHR-Cd36 transgenic rats showed profound arrhythmogenesis resulting in significantly increased duration of tachyarrhythmias (207 ± 48 s vs. 55 ± 21 s, P < 0.05), total number of premature ventricular complexes (2,623 ± 517 vs. 849 ± 250, P < 0.05) and arrhythmia score (3.86 ± 0.18 vs. 3.13 ± 0.13, P < 0.001). On the other hand, transgenic SHR compared with SHR controls showed significantly reduced infarct size (52.6 ± 4.3% vs. 72.4 ± 2.9% of area at risk, P < 0.001). Similar differences were observed in isolated perfused hearts, and the increased susceptibility of transgenic SHR to arrhythmias was abolished by reserpine, suggesting the involvement of catecholamines. To further search for possible molecular mechanisms of altered ischemic tolerance, we compared gene expression profiles in left ventricles dissected from 6-wk-old transgenic SHR vs. age-matched controls using Illumina-based sequencing. Circadian rhythms and oxidative phosphorylation were identified as the top KEGG pathways, while circadian rhythms, VDR/RXR activation, IGF1 signaling, and HMGB1 signaling were the top IPA canonical pathways potentially important for Cd36-mediated effects on ischemic tolerance. It can be concluded that transgenic expression of Cd36 plays an important role in modulating the incidence and severity of ischemic and reperfusion ventricular arrhythmias and myocardial infarct size induced by coronary artery occlusion. The proarrhythmic effect of Cd36 transgene appears to be dependent on adrenergic stimulation.

Pacing to Reduce Refractory Angina in Patients with Severe Coronary Artery Disease: A Crossover Pilot Trial

Biventricular pacing (BiV) has been shown to reduce wall stress and workload in regions near the pacing sites. This trial investigated if BiV near the ischemic region would reduce chest pain in patients with refractory angina due to severe coronary artery disease (CAD). Eleven patients were implanted with BiV devices with leads positioned at or adjacent to their ischemic regions as detected by single-photon emission computed tomography (SPECT) and randomized to either pacing turned ON or OFF for 3 months, and then crossed over for 3 months. With pacing turned ON, a Dynamic atrioventricular (AV) delay was set for approximately 90% and 70% of the intrinsic AV delay at the resting heart rate and at the onset of symptoms, respectively. One patient was excluded from the analysis due to a large amount of RV pacing during the OFF periods (24-64%) and due to an inability to properly deliver therapy because of an excessive number of ventricular premature complexes. Overall, with the device ON vs. OFF, the number of angina episodes (0.8 ± 0.4 vs. 1.2 ± 0.7 per week, P = 0.03) and amount of nitroglycerin used (0.2 ± 0.1 vs. 1.0 ± 0.7 per week, P = 0.11) was lower with BiV pacing. Furthermore, the treadmill exercise time to symptoms trended higher (427 ± 65 vs. 408 ± 64 s, P = 0.19), and the sum of fluorodeoxyglucose-positron emission tomography (FDG-PET) scores trended lower (7.9 ± 3.5 vs. 12.0 ± 4.0, P = 0.11) with the device ON vs. OFF. Nevertheless, there were no significant differences in SPECT myocardial perfusion scores, left ventricle ejection fraction, wall motion score index, and quality of life scores with device programmed ON vs. OFF (all P > 0.05). In conclusion, this pilot study demonstrated that BiV-P at or near the ischemic region was feasible and associated with significant reductions in angina in patients with severe CAD. Adequately powered prospective studies are needed to confirm these findings.

Coupled pacing controls rapid heart rates better than paired pacing during atrial fibrillation

Delivery of a ventricular extrastimulus shortly after the effective refractory period (ERP) of a sensed (coupled pacing; CP) or a paced (paired pacing; PP) ventricular event can instantly decrease the mechanical pulse rate (MPR) during rapidly conducting atrial fibrillation (AF). We compared the short-term rate-controlling effects of CP and PP during AF with rapid ventricular rates. Sixteen patients with ongoing, spontaneous AF were examined. Mechanical pulse rate was registered via arterial pressure tracings. During CP a coupling interval (CI) of ERP+20 ms was used to reach an optimal haemodynamic effect. Paired pacing was started at a basic cycle length (CL) of 500 ms followed by an extrastimulus with an CI of ERP+20 ms. Drive train was changed at 50 ms increments until the lowest MPR was reached. Proarrhythmic effects were characterized by the number of premature ventricular complexes (PVCs). Mechanical pulse rate significantly decreased in all patients during CP (113 ± 9 vs. 58 ± 4/min). Using CP the controlled rhythm remained irregular (CL range: 896 ± 24-1452 ± 67 ms) while no PVCs were observed. With different drive trains PP resulted in different regular MPRs (range 62 ± 6-80 ± 4/min), but the lowest MPR achieved was significantly higher in the PP group than in the CP. Paired pacing caused premature beats in nine patients (56%) resulting in loss of continuous MPR control. Both CP and PP can reduce the MPR during rapidly conducting AF. Coupled pacing is more applicable, but PP has the advantage to achieve different target heart rates. Paired pacing has more proarrhythmic effects as compared with CP.

Ventricular Arrhythmia Suppression by Magnesium Treatment after Coronary Artery Bypass Surgery.

Ventricular arrhythmias occur frequently shortly after coronary artery bypass grafting (CABG), and their occurrence coincides with the postoperative decline in serum magnesium (Mg) levels. To examine if this decline causes ventricular arrhythmias and if their appearance could be reduced by intravenous Mg administration, 140 consecutive CABG patients were randomized to receive 70 mmol of Mg sulphate (N = 69) or placebo (N = 71) over two days. Serum Mg concentration fell to 0.77 mmol/l in the control group but rose to 1.09 mmol/l in the Mg group (p < 0.001). On 48 h Holter, the number of ventricular premature complexes (VPC) on the third postoperative day was reduced in the Mg group (4 +/- 5 vs 12 +/- 21 VPCs/h; p < 0.05) and the incidence of complex ventricular arrhythmias (Lown grade 2-5) was significantly diminished (19% vs 41% of the patients; p < 0.05). In multivariate analysis, high risk ventricular arrhythmias (repetitive polymorphic ventricular complexes, couplets, R-on-T complexes or operative tachycardia) were independently predicted by high number of bypassed vessels (p = 0.01), poor NYHA functional class (p = 0.06), preoperative diuretic use (p = 0.07), and low postoperative Mg levels (p = 0.08). In conclusion, correction of the postoperative decline in serum Mg concentration decreases the occurrence of early VPCs and complex ventricular arrhythmias. Patients with extensive underlying coronary artery disease and prior diuretic therapy appear to benefit greatest from Mg treatment.http://link.springer-ny.com/link/service/journals/00547/bibs/8n3p165.html

14 Diazoxide-induced antiarrhythmic protection in the non-diabetic and diabetic rat heart does not require activation of PI3-kinase/AKT

Mitochondrial KATP channels (mitoKATP) activation interacting with phosphatidylinositol 3-kinase (PI3K)/Akt has been suggested as a key element in preconditioning protection against lethal myocardial ischaemia/reperfusion injury in healthy heart,1 while its...

07 Use of the dog-isolated cardiac Purkinje fibre assay to investigate a compound with in vivo proarrhythmic activity

The dog-isolated cardiac Purkinje fibre assay is commonly used to assess the electrophysiologic effects of drugs known to prolong the QT interval. Drug-induced QT prolongation can be associated with Torsade...

Combination therapy with mexiletine and sotalol suppresses inherited ventricular arrhythmias in German shepherd dogs better than mexiletine or sotalol monotherapy: A randomized cross-over study

Objectives To determine the spontaneous variability of ventricular arrhythmias (VA) and evaluate anti-arrhythmic efficacy of mexiletine, sotalol, and a mexiletine–sotalol combination in German shepherd dogs (GSD) with inherited arrhythmias. Animals, materials and methods 12 affected GSD, median age 20 weeks, received mexiletine (8 mg/kg PO q8 h), sotalol (2.5 mg/kg PO q12 h), and combination therapy for 6 days in random order. Pre- and post-treatment 24 h Holter recordings were acquired, allowing determination of VA variability and reduction in 24 h VA for each treatment. Drug concentrations during each arm were measured. Results An anti-arrhythmic effect could be inferred if ventricular premature complexes (VPC), ventricular couplets (V cpl), ventricular tachycardia runs (VT runs) and total ventricular ectopy (VE tot) frequency were reduced by 61%, 97%, 98%, and 63% (1 control Holter model), by 53%, 94%, 95%, and 54% (4 control Holter model) and by 54%, 95%, 96% and 56% (3 control Holter model). Combination therapy reduced VPC and VE tot in more dogs (5/12 and 6/12) than mexiletine (1/11 and 2/11) or sotalol (2/9 and 1/9) ( p < 0.05). The combination therapy reduced the mean number of VPC, V cpl, and VE tot. Sotalol monotherapy produced an increase in VT runs. Plasma mexiletine concentration was higher during combination therapy than with monotherapy. Conclusions Combination therapy reduced VPC in affected GSD. Sotalol monotherapy increased VT runs. Combination therapy increased plasma mexiletine concentrations.