Incidence Of Tachyarrhythmias Research Articles

Abstract 12013: Cardiac Arrhythmia After COVID-19 Vaccination versus Non-COVID-19 Vaccination: A Systematic Review and Meta-Analysis

Introduction: Arrhythmia after COVID-19 vaccination is increasingly reported. Whether the risk from COVID-19 vaccines exceeds that of non–COVID-19 vaccines remains controversial. In this study, the incidence of arrhythmia after COVID-19 versus non–COVID-19 vaccination were investigated. Methods: Medline (via PubMed), Scopus, Cochrane Library, and Embase databases were searched for observational studies reporting the incidence of postvaccination arrhythmias from January 1, 1947 to November 27, 2022. Secondary endpoints included tachyarrhythmia incidence and all-cause mortality. Arrhythmia incidence by age, vaccine type, sex, and COVID-19 vaccine dose were analysed, and intrastudy risk for bias and certainty of evidence were evaluated. Results: The overall incidence of arrhythmia (1,528,500,116 vaccine doses, 43 studies) was 561·3 cases per million doses. Arrhythmias were more common after COVID-19 vaccination than non–COVID-19 vaccination (3790·4 vs 13·7 cases per million doses; p<0·001). Compared with COVID-19 vaccines, the influenza, pertussis, and human papillomavirus vaccines were associated with fewer cases of arrhythmia. The overall incidence of tachyarrhythmia was 910·5 cases per million doses; it was higher after COVID-19 vaccination than non-COVID-19 vaccination (6681·8 vs 34·3 cases per million doses; p<0·001). Pooled all-cause mortality postvaccination was 2·4 deaths per million doses. Mortality was comparable between COVID-19 and non–COVID-19 vaccination groups. Conclusions: Although arrhythmia was more frequent after COVID-19 vaccination than after non-COVID-19 vaccination, it was still uncommon. The safety and efficacy of COVID-19 vaccines should be assessed in light of other important factors as well, such as the incidence of regional outbreaks and effects from the COVID-19 infection itself.

Tachyarrhythmia after the total cavopulmonary connection: incidence, prognosis, and risk factors.

The purpose of this study is to evaluate the incidence and outcomes regarding tachyarrhythmia in patients after total cavopulmonary connection. A retrospective analysis of 620 patients who underwent total cavopulmonary connection between 1994 and 2021 at our institution was performed. Incidence of tachyarrhythmia was depicted, and results after onset of tachyarrhythmia were evaluated. Factors associated with the onset of tachyarrhythmia were identified. A total of 52 (8%) patients presented with tachyarrhythmia that required medical therapy. Onset during hospital stay was observed in 27 patients, and onset after hospital discharge was observed in 32 patients. Freedom from late tachyarrhythmia following total cavopulmonary connection at 5, 10, and 15 years was 97, 95, and 91%, respectively. The most prevalent late tachyarrhythmia was atrial flutter (50%), followed by supraventricular tachycardia (25%) and ventricular tachycardia (25%). Direct current cardioversion was required in 12 patients, and 7 patients underwent electrophysiological study. Freedom from Fontan circulatory failure after onset of tachyarrhythmia at 10 and 15 years was 78% and 49%, respectively. Freedom from occurrence of decreased ventricular systolic function after the onset of tachyarrhythmia at 5 years was 85%. Independent factors associated with late tachyarrhythmia were dominant right ventricle (hazard ratio, 2.52, p = 0.02) and weight at total cavopulmonary connection (hazard ratio, 1.03 per kilogram; p = 0.04). Type of total cavopulmonary connection at total cavopulmonary connection was not identified as risk. In our large cohort of 620 patients following total cavopulmonary connection, the incidence of late tachyarrhythmia was low. Patients with dominant right ventricle and late total cavopulmonary connection were at increased risk for late tachyarrhythmia following total cavopulmonary connection.

Tachyarrhythmias after extracardiac conduit Fontan procedure in the long-term follow-up: may native anatomy of single ventricle predict their occurrence?

Abstract Funding Acknowledgements Type of funding sources: None. Background Arrhythmic complications, especially tachycardias, represent a common and important comorbidity during long-term follow up (FU) in patients with Fontan palliation for complexes congenital heart diseases (CHDs) with univentricular hearts. Surgical Fontan technique has evolved from direct atrio-pulmonary connection via the intracardiac lateral tunnel to the latest extracardiac conduit (ECC) procedure. Despite its shorter FU compared to previous techniques, the ECC variation is nowadays the main approach for many improvements, including lower incidence of arrhythmic complications (especially atrial arrhythmias). Purpose The aim of this study was to evaluate, during a long-term FU, the incidence of tachyarrhythmias and their correlation with the morphology of CHDs’ single ventricle native anatomy in a large cohort of patients with previous ECC Fontan procedure. Methods In this single centre observational cohort study, we retrospectively evaluated 351 patients treated with ECC Fontan palliation in our Institution between January 1987 and October 2017. Exclusion criteria were ECC Fontan take-down and a FU less than 5 years. CHD diagnosis, single ventricle native anatomy and surgical history were reviewed. Patients had cardiac examination once a year. We divided the overall study population in 2 groups based on unique ventricle's morphology: left-type (LV group) or right-type (RV group). Results A total of 303 patients [56% males; mean age at last FU 20 (IQR 15-28) years; 64.7% LV group] with ECC Fontan were enrolled. The mean FU was 16 (IQR 11-20, the longest 33) years. No sudden arrhythmic cardiac death occurred. Ten patients (6 of the LV group) underwent cardiac transplantation for Fontan failure. During FU, 34 patients of the LV (17.3%) and 22 of the RV group (20.2%) showed at least one tachyarrhythmia after a mean time of 12.1 and 12.9 years from ECC procedure, respectively. One patient (LV group) had one tachyarrhythmia in the early time period, <30 days from procedure. LV group showed a higher incidence of supraventricular tachyarrhythmias (SVTs) than RV group (68% vs 41% of total arrhythmias, p=0.08); in contrast, in RV group we found a higher number of ventricular tachyarrhythmias (VTs) compared to the other group (73% vs 41%, p=0.04). We observed both types of tachyarrhythmias (SVT and VT) in 3 patients of LV and 2 of RV group. Conclusions This study, with one of the largest cohort and longest FU after ECC Fontan, shows that ECC is associated with higher arrhythmic complications than previously reported, even though with longer latency period than other Fontan procedures. Moreover, our results suggest that patients with right-type single ventricle native anatomy are significantly more prone to develop VTs compared to those with left-type ventricle. This may reflect the drawbacks of the right ventricle physiology within Fontan circulation where the right ventricle acts for long time as the main pump of the circulatory system.

Preexcitation with Multiple Accessory Pathways as a First Presentation of Undiagnosed Late Stage Ebstein’s Anomaly in an Adult

Ebstein’s anomaly (EA) is a relatively rare congenital heart disease that has long been a challenge both to cardiac surgeons and electrophysiologists. In addition to the hemodynamic burden of the tricuspid valve defect itself, the electrocardiogram (ECG) is abnormal in most cases with a high incidence of tachyarrhythmias, that can often be imputable to accessory atrioventricular pathways mostly located along the tricuspid posterior and septal valve leaflets, and rarely, to multiple accessory pathways. We here report the case of a 19-year-old girl with no known cardiac history, in whom a late stage EA with Eisenmenger syndrome, was diagnosed following a syncopal episode attributed to preexcited atrial tachy-fibrillation with an aspect consistant with multiple accessory pathways with at least one of them being right postero-septal. The patient’s management was very challenging for the heart team considering the fixed pulmonary hypertension and the fact she was reluctant to catheter ablation. This case report underlines the importance of early diagnosis and treatment of EA and its rhythmic complications and explores the anatomic peculiarities of this disease with attention to features that could be important to both arrhythmogenesis and ablation therapy in this unique population.

Association between tachyarrhythmia and mortality in a cohort of critically ill patients with coronavirus disease 2019 (COVID-19).

BackgroundCardiovascular involvement manifesting as arrhythmias has been confirmed in patients with coronavirus disease 2019 (COVID-19), so we aimed to explore the association between primary tachyarrhythmia and death in critically ill patients with COVID-19 in this retrospective study.MethodsA total of 79 critically ill patients with COVID-19 were included. Demographic characteristics, clinical data (past history, vital signs, therapeutic management, and outcomes), and results of laboratory findings and cardiac investigations were collected. All statistical analyses were performed using SPSS 23.0 software (IBM, Armonk, NY, USA).ResultsThe median age was 65±12 years, and 53 patients (67%) were male. A total of 57 (72%) patients died, and compared with survivors, these patients were older and had significantly higher Acute Physiology and Chronic Health Evaluation (APACHE) II score, Sequential Organ Failure Assessment (SOFA) score and fewer lymphocytes as well as higher heart rate (P<0.05). Autopsy findings did not suggest severe myocarditis. A total of 19 (24%) patients had tachyarrhythmias, including 10 (13%) with atrial fibrillation (AF) and 9 (11%) with ventricular tachycardia or fibrillation. The incidence of tachyarrhythmias in non-survivor was much higher than in survivors (P=0.04). In a Cox regression model, older patients with ventricular tachyarrhythmias (VTAs) age were at a higher risk of death, with hazard ratio (HR) of 3.302 [95% confidence interval (CI), 1.524–7.154, P=0.002] and 1.045 (95% CI, 1.020–1.071, P=0.000), respectively. The use of beta-blockers [HR, 0.219 (95% CI, 0.066–0.722); P=0.013] was associated with a lower risk of death.ConclusionsCritically ill patients with COVID-19 had a poor prognosis. VTA and older age were independent prognostic factors of death. Beta-blockers might be an effective therapy to improve survival.

Peculiarities of Cardiohemodynamics and its Autonomic Regulation in Elderly People

The study was aimed to the experimental verification of the authors’ hypothesis that in elderly people an endogenous functional mechanism develops during late ontogeny to protect muscle effectors of the cardiovascular system (CVS) against negative effects of excessive activity of the sympathetic nervous system by partial replacement of its neurotransmitter norepinephrine with humoral catecholamines. Experiments were carried out using our original method of arterial piezopulsometry which allows evaluation of cardiohemodynamic parameters, as well as the spectral power of oscillations of VmaxPP and TNN parameters of arterial blood pressure pulse waves caused by regulatory effects of the autonomic nervous and endocrine systems. Such a replacement is assumed to be crucial for raising the metabolic tolerance of the CVS in elderly people to an age-related increase in oxygen deficiency, as well as for reducing the incidence of tachyarrhythmia, stenocardia and other cardiac pathological conditions under the influence of psychoemotional and physical stressors.

Behavioural patterns of electrolyte repletion in intensive care units: lessons from a large electronic dataset

Repletion of electrolytes often depends on provider-specific behavior and hospital policy. We examined the pattern of electrolyte repletion across several intensive care units (ICU) in a large healthcare system from 2010–2015. This included 109 723 potassium repletions, 51 833 magnesium repletions, 2 306 calcium repletions, 8 770 phosphate repletions, and 3 128 249 visit-days over 332 018 visits. Potassium, magnesium, and calcium were usually repleted within the institutional reference range. In contrast, the bulk of phosphate repletion was done with pre-repletion serum level below the reference range. The impact of repletion on post-repletion levels was significant but uniformly small. The pre-repletion serum level had a significant inverse correlation with the post-repletion level of each electrolyte. Potassium, magnesium and phosphate follow-up labs were scheduled in 9–10 hours after their repletion. In contrast, calcium was rechecked in less than 20 minutes. Routine repletion of potassium, magnesium and calcium had no effect on the incidence of tachyarrhythmias. We estimated the expense from electrolyte repletion within the reference range was approximately $1.25 million. Absent a specific clinical indication, repleting electrolytes when the serum concentration are within normative values may represent an avenue for cost savings, staff burden unload and potential reduction in frequency of complications in the ICUs.

Human Cardiomyocyte Progenitor Cells in Co-culture with Rat Cardiomyocytes Form a Pro-arrhythmic Substrate: Evidence for Two Different Arrhythmogenic Mechanisms.

Background: Cardiomyocyte progenitor cells (CMPCs) are a promising cell source for regenerative cell therapy to improve cardiac function after myocardial infarction. However, it is unknown whether undifferentiated CMPCs have arrhythmogenic risks. We investigate whether undifferentiated, regionally applied, human fetal CMPCs form a pro-arrhythmic substrate in co-culture with neonatal rat ventricular myocytes (NRVMs).Method: Unipolar extracellular electrograms, derived from micro-electrode arrays (8 × 8 electrodes) containing monolayers of NRVMs (control), or co-cultures of NRVMs and locally seeded CMPCs were used to determine conduction velocity and the incidence of tachy-arrhythmias. Micro-electrodes were used to record action potentials. Conditioned medium (Cme) of CMPCs was used to distinguish between coupling or paracrine effects.Results: Co-cultures demonstrated conduction slowing (5.6 ± 0.3 cm/s, n = 50) compared to control monolayers (13.4 ± 0.4 cm/s, n = 26) and monolayers subjected to Cme (13.7 ± 0.6 cm/s, n = 11, all p < 0.001). Furthermore, co-cultures had a more depolarized resting membrane than control monolayers (−47.3 ± 17.4 vs. −64.8 ± 7.7 mV, p < 0.001) and monolayers subjected to Cme (−64.4 ± 8.1 mV, p < 0.001). Upstroke velocity was significantly decreased in co-cultures and action potential duration was prolonged. The CMPC region was characterized by local ST-elevation in the recorded electrograms. The spontaneous rhythm was faster and tachy-arrhythmias occurred more often in co-cultured monolayers than in control monolayers (42.0 vs. 5.4%, p < 0.001).Conclusion: CMPCs form a pro-arrhythmic substrate when co-cultured with neonatal cardiomyocytes. Electrical coupling between both cell types leads to current flow between a, slowly conducting, depolarized and the normal region leading to local ST-elevations and the occurrence of tachy-arrhythmias originating from the non-depolarized zone.

Acute Stroke of the Insular Cortex Leading to Heart Failure

In humans, the limbic and paralimbic systems, including the insular cortex, are the central autonomic networks responsible for maintaining cardiovascular autonomic control. The right insular cortex plays a predominant role in establishing sympathetic tone while the left insular cortex in establishing parasympathetic tone of the heart. Disturbances in the autonomic system due to cerebrovascular diseases, such as an ischemic stroke in the territory of the middle cerebral artery, could lead to impairment in the cardiovascular balance, consequently increasing the incidence of tachyarrhythmia. Abnormalities of cardiovascular autonomic control may retain prognostic relevance, as they have been associated with adverse clinical outcomes after stroke. Acute ischemic stroke has been shown to increase the rate of cardiac-related mortality as a pathophysiological consequence of an acute stress response in patients with no cardiovascular comorbidities due to the dysfunction of the brain-heart axis. This case report highlights an instance when this axis was disturbed leading to non-ischemic cardiomyopathy. J Med Cases. 2016;7(3):94-97 doi: http://dx.doi.org/10.14740/jmc2426w

32 Influence of Sleep Apnoea on Biventricular Pacing, Heart Rate Trend and Tachyarrhythmia’s in Heart Failure Patients who have undergone Cardiac Resynchronisation Therapy

Introduction Sleep apnoea syndrome (SAS) has been reported in 40–60% of people with heart failure (HF) 1 with varying reports as to whether this is predominantly central or obstructive. Undiagnosed intermittent hypoxia during sleep increases sympathetic activation and endothelial dysfunction so may worsen cardiac outcomes. SAS also prevents the normal drop in heart rate that accompanies the onset of sleep and coupled with reflex increases in central sympathetic outflow could lead to the development of recurrent nocturnal ischaemia and arrhythmias. 2 We compared average heart rate, percentage of Biventricular pacing and logged tachyarrhythmia’s in those with and without recently diagnosed SAS in a specific cohort of HF patients who underwent cardiac resynchronisation therapy (CRT). Method Prospective, cross-sectional study. 37 Consecutive HF patients, 30 males, mean (SD) age= 69.8 (8.4) yrs, BMI 29.3 (8.7) kg/m 2 , and mean LVEF 25 (7)% – who were referred to a UK tertiary cardiac centre for CRT according to National Guidelines. They underwent baseline limited channel sleep studies (Apnea Link TM ResMed, Abingdon, UK) immediately prior to CRT. All patients were deemed on optimal medication at the discretion of a cardiologist. None had known SAS. An apnoea hyopnea index (AHI) >15 events per hour was deemed a positive result for treatable SAS according to UK guidelines. Average heart rate, percentage of biventricular pacing and logged tachyarrhythmias were obtained from six weeks post CRT follow up. Results 20 from 37 (54%) had an AHI >15 events per hour. All 20 patients had predominantly obstructive sleep apnoea, 5 of these 17 patients had some central sleep apnoea, but this was still less than their obstructive episodes. None had predominantly central sleep apnoea. Conclusion There is a high prevalence (54%) of significant SAS in the group of heart failure patients referred for CRT. Unlike other studies we found a relatively low prevalence of central sleep apnoea. There was no difference in average heart rate and percent of biventricular pacing in those with and without SAS. However there is increased incidence of tachyarrhythmias in those with SAS and this might be explained by recurrent hypoxia and increased sympathetic activity in sleep apnoea patients. References Eur Resp J. 2007;29(6):1201-5 Circulation 2003;107:1671-8

Association between perioperative dexmedetomidine and arrhythmias after surgery for congenital heart disease.

Dexmedetomidine is commonly used after congenital heart surgery and may be associated with a decreased incidence of postoperative tachyarrhythmias. Using a large cohort of patients undergoing congenital heart surgery, we examined for an association between dexmedetomidine use in the immediate postoperative period and subsequent arrhythmia development. A total of 1593 surgical procedures for congenital heart disease were performed. Dexmedetomidine was administered in the immediate postoperative period after 468 (29%) surgical procedures. When compared with 1125 controls, the group receiving dexmedetomidine demonstrated significantly fewer tachyarrhythmias (29% versus 38%; P<0.001), tachyarrhythmias receiving intervention (14% versus 23%; P<0.001), bradyarrhythmias (18% versus 22%; P=0.03), and bradyarrhythmias receiving intervention (12% versus 16%; P=0.04). After propensity score matching with 468 controls, the arrhythmia incidence between groups became similar: tachyarrhythmias (29% versus 31%; P=0.66), tachyarrhythmias receiving intervention (14% versus 17%; P=0.16), bradyarrhythmias (18% versus 15%; P=0.44), and bradyarrhythmias receiving intervention (12% versus 9%; P=0.17). After excluding controls exposed to dexmedetomidine at a later time in the hospitalization, dexmedetomidine was associated with increased odds of bradyarrhythmias receiving intervention (odds ratio, 2.18; 95% confidence interval, 1.02-4.65). Furthermore, there was a dose-dependent increase in the odds of bradyarrhythmias (odds ratio, 1.04; 95% confidence interval, 1.01-1.07) and bradyarrhythmias receiving intervention (odds ratio, 1.05; 95% confidence interval, 1.01-1.08). Although dexmedetomidine exposure in the immediate postoperative period is not associated with a clinically meaningful difference in the incidence of tachyarrhythmias after congenital heart surgery, it may be associated with increased odds of bradyarrhythmias.

Patient-prosthesis mismatch after mitral valve-in-valve procedure - at the cost of life or serious consequence?

An 81-year-old man, who had undergone a complex cardiosurgical procedure 8 years previously (aortic valve replacement by Medtronic Hancock II 23 mm and mitral valve replacement by Medtronic Hancock II 31 mm, tricuspid valve repair using the Kay technique, and coronary artery bypass surgery with left internal mammary artery (LIMA) to left anterior descending (LAD)), was admitted to the hospital with symptoms suggestive of acute heart failure (NYHA IV). Echocardiographic examination revealed satisfactory function of the aortic prosthesis, and massive regurgitation of the degenerative mitral prosthesis. Left ventricle ejection fraction was estimated at approximately 30% with left ventricle (LV) thinning, an akinetic and thin apex, and mild tricuspid valve insufficiency. Due to these findings cardiopulmonary bypass was used. An intra-aortic balloon pump (IABP) was not introduced due to limited femoral access. The patient, in spite of a very high operative risk (STS 29.8%), was referred for urgent redo cardiac surgery. With this in mind, the patient was qualified for transcatheter mitral valve-in-valve (VIV) implantation. The procedure was performed on-pump with the cardiopulmonary bypass connected via femoral vessels. A transapical approach for delivering the 29 mm Edwards Sapien valve into the mitral position was chosen. Significant efforts were made to protect the scarred apex (pericardium was not dissected). Intraoperative transesophageal echocardiogram (TEE) and fluoroscopy demonstrated precise landing of the new prosthesis, as well as resolution of prior regurgitation and absence of perivalvular leakage. Unfortunately, the initially high mean gradient through the valve remained elevated. The postoperative course was uneventful. On postoperative day 5 in the Cardiology Department due to left ventricular end-diastolic diameter (LVED) > 70 mm and one incidence of tachyarrhythmia, a cardioverter-defibrillator was implanted prophylactically. The patient was discharged home 2 weeks after the procedure. The patient remains in stable condition in class II/III NYHA after 10 months of follow-up. Control echocardiography showed moderate/severe stenosis (mitral valve area 1.0 cm2, mean diastolic pressure gradient (PG) 9 mm Hg) of the implanted VIV prosthesis with no perivalvular leakage and degenerative changes of the leaflets (Figure 1). Figure 1 A, B – Angio-CT – internal diameter sizing of the bioprosthesis annulus (A – 2.58 cm, B – 2.78 cm). C – Doppler showing no regurgitation, but the orifice area is still not optimal. D – Angiography after ... Though the problem of low mitral valve orifice after transcatheter VIV implantation has been deliberated in the literature, in our opinion it has not been outlined in sufficient detail [1]. It is not entirely clear if the patient-prosthesis mismatch (PPM) in our case was influenced by the anatomy of this particular patient, or is rather caused by the atypical position of the bioprosthesis, which was originally designed for the aortic position [2]. From a technical point of view the procedure was executed correctly with maximum balloon inflation during implantation and precise prosthesis positioning. The range of mean diastolic pressure gradients through the mitral orifice after VIV procedures is expansive in available data. We presume, according to our experience, that the rigidity of the biological tissue of which the leaflets are made does not allow complete opening under the diastolic pressure gradients between the left atrium (LA) and LV, which are physiologically much lower than that of the aortic valve [3]. Although VIV has been performed approximately a few hundred times worldwide, there are still quite limited data regarding follow-up of these patients after this procedure [4].

Cross-sex hormonal replacement: is this really effective? an experimental clue

Castrated rats of either sex were used in this work, and sex hormones of their own gender or cross-sex hormones were administered for 4 months. Animals were then put through 5 min of myocardial ischemia followed by a 5-min reperfusion injury. Electrocardiographic recordings were made and serum was obtained. Sex hormone levels were measured. Cardiac frequency was calculated, arterial pressure was determined, and the levels of lactate dehydrogenase (LDH), creatinine kinase (CK), and thiobarbituric acid reactive species (TBARs) were analyzed. Proinflammatory cytokine levels were measured in homogenized hearts; besides this, five hearts of each experimental group were obtained and fixed for histopathologic analysis. In male rats with estradiol replacement, the incidence of tachyarrhythmias and CK levels were higher when compared to the rest of the animals. Their cytokine levels were also elevated when compared to the group that received testosterone. Estradiol replacement protected female rats from variations in all of the parameters evaluated, whereas testosterone did not show a protective effect. In the presence of testosterone, the incidence of tachyarrhythmia was higher and TBARs, cytokines, CK, and LDH levels were also elevated. The results shown reinforce the idea that cross-sex hormone administration can damage the cardiovascular system.

AS-135 Incidence of Tachyarrhythmia and its Impact on Two-Year Clinical Outcomes in Patients with ST Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention with Drug-Eluting Stents

Results: The STEMI group showed higher incidence of sustained ventricular tachycardia (VT), non-sustained VT, ventricular fibrillation (VF) and atrial fibrillation (AF) compared with those of other two groups. The baseline clinical and procedural characteristics were similar between pts with tachyarrhythmia and those of control group. Six-month angiographic and cumulative clinical outcomes up to 2 years were similar between the two groups except pts with tachyarrhythmia showed higher incidence of cardiac death within 1 month compared with control group but not at 6 to 24 months (Table 1). Tachyarrhythmia itself was not an independent predictor of cardiac death (Adjusted OR: 1.711, 95% CI: 0.443-6.616, p-value=0.436) within 1 month.

Ischaemic tolerance in aged mouse myocardium: the role of adenosine and effects of A1 adenosine receptor overexpression.

The genesis of the ischaemia intolerant phenotype in aged myocardium is poorly understood. We tested the hypothesis that impaired adenosine-mediated protection contributes to ischaemic intolerance, and examined whether this is countered by A1 adenosine receptor (A1AR) overexpression. Responses to 20 min ischaemia and 45 min reperfusion were assessed in perfused hearts from young (2-4 months) and moderately aged (16-18 months) mice. Post-ischaemic contractility was impaired by ageing with elevated ventricular diastolic (32 +/- 2 vs. 18 +/- 2 mmHg in young) and reduced developed (37 +/- 3 vs. 83 +/- 6 mmHg in young) pressures. Lactate dehydrogenase (LDH) loss was exaggerated (27 +/- 2 vs. 16 +/- 2 IU g-1 in young) whereas the incidence of tachyarrhythmias was similar in young (15 +/- 1 %) and aged hearts (16 +/- 1 %). Functional analysis confirmed equipotent effects of 50 micro M adenosine at A1 and A2 receptors in young and aged hearts. Nonetheless, while 50 micro M adenosine improved diastolic (5 +/- 1 mmHg) and developed pressures (134 +/- 7 mmHg) and LDH loss (6 +/- 2 IU g-1) in young hearts, it did not alter these variables in the aged group. Adenosine did attenuate arrhythmogenesis for both ages (to ~10 %). In contrast to adenosine, 50 micro M diazoxide reduced ischaemic damage and arrhythmogenesis for both ages. Contractile and anti-necrotic effects of adenosine were limited by 100 micro M 5-hydroxydecanoate (5-HD) and 3 micro M chelerythrine. Anti-arrhythmic effects were limited by 5-HD but not chelerythrine. Non-selective (100 micro M 8-sulfophenyltheophylline) and A1-selective (150 nM 8-cyclopentyl-1,3-dipropylxanthine) adenosine receptor antagonism impaired ischaemic tolerance in young but not aged hearts. Quantitative real-time PCR and radioligand analysis indicated that impaired protection is unrelated to changes in A1AR mRNA transcription, or receptor density (~8 fmol mg-1 protein in both age groups). However, A1AR overexpression improved tolerance for both ages, restoring adenosine-mediated protection. These data reveal impaired protection via exogenous and endogenous adenosine contributes to ischaemic intolerance with ageing. This is independent of A1AR expression, and involves ineffective activation of a 5-HD-/diazoxide-sensitive process. The effects of A1AR overexpression indicate that the age-related failure in signalling can be overcome.

Energy Transfer in Acute Diabetic Rat Hearts

Hearts of rats with diabetes mellitus (DM) are characterized by energy demands exceeding their energy production, but they might also exhibit decreased vulnerability to ischemia and calcium overload. This indicates adaptation in cardiac energetics (CE), where energy transport is not rate-limiting. Aim-This study was designed to elucidate the functional significance of the DM-induced adaptation in CE by investigating the formation of mitochondrial contact sites (MiCS), facilitating the Ca-dependent/high-capacity energy transfer from mitochondria, in conjunction with testing the ischemic tolerance (IT) of hearts. After 1 week of streptozotocin-induced DM (45 mg/kg iv), the hearts of male diabetic and age-matched control rats (C) were isolated and Langendorff-perfused with either 1.6 or 2.2 mmol/L of CaCl(2). MiCS formation was assessed by cytochemical detection of mCPK octamers and was quantified stereologically as MiCS to mitochondrial surface ratio (S(S)). IT was evaluated in anesthetized open-chest animals subjected to 30-min occlusion of the LAD coronary artery followed by 4-h reperfusion, by monitoring ischemic arrhythmias and by measuring the size of infarction (tetrazolium double staining). In C hearts, increasing Ca2+ induced both positive inotropic response (dP/dt increase from 2270 +/- 220 to 2955 +/- 229, p < 0.01) and elevated MiCS formation (S(S) increase from 0.070 +/- 0.011 to 0.123 +/- 0.012, p < 0.01). In DM hearts, basic MiCS formation was already comparable with that induced by elevated Ca2+ in C hearts and could not be further stimulated by Ca2+. In C, ventricular tachycardia represented 55.4% of the total arrhythmias and occurred in 90% of the animals. In DM rats, the arrhythmia profile was similar to that in C, and the incidence of tachyarrhythmias and their severity were not enhanced (arrhythmia score: 3.18 +/- 0.4 vs. 3.30 +/- 0.3 in C). The infarct size normalized to the size of area at risk was smaller in the DM than in C hearts (52.3 +/- 5.8% vs. 69.2 +/- 2.2%, respectively; p < 0.05). Ca-signaling represents the link between energy delivery from mitochondria (via MiCS) and energy requirements of the heart. In DM hearts, energy transport via MiCS is elevated to the maximum value. This contributes to increased resistance of DM hearts to irreversible cell damage.

Prostaglandins and the antiarrhythmic effect of preconditioning in the isolated rat heart.

Our study evaluated the relationship between the endogenous production of prostacyclin and the antiarrhythmic effect of ischemic preconditioning against ischemic and reperfusion-induced tachyarrhythmia. Langendorff perfused rat hearts underwent 30 min regional ischemia with reperfusion. Preconditioning was induced by a single episode of 5 min ischemia and 15 min reperfusion. Prostaglandin 6-keto F1 alpha (a stable metabolite of prostacyclin) was determined in the coronary effluent. In the control group the incidence of tachyarrhythmia was 31% during ischemia and 67% during reperfusion. Preconditioning did not affect ischemic arrhythmias but attenuated arrhythmias a reperfusion (8%, p < 0.01) and was associated with increased release of prostacyclin prior to reperfusion. Aspirin abolished the antiarrhythmic effect of preconditioning against reperfusion tachyarrhythmias. However, no relationship was found between suppression of prostacyclin production and the occurrence of arrhythmia in individual hearts. Thus, our findings suggest that metabolites of arachidonic acid via the cyclooxygenase pathway are involved in the protective effect of ischemic preconditioning against reperfusion-induced tachyarrhythmias.

Arrhythmia and Delayed Recovery of Cardiac Action Potential During Reperfusion After Ischemia

The role of reactive metabolites of oxygen, oxygen radicals (O-Rs), as mediators of potentially arrhythmogenic alterations in cellular electrical properties and contractile dysfunction of cardiac muscle during reperfusion after ischemia was investigated. Electrical and mechanical activities of arterially perfused guinea pig right ventricular walls were recorded simultaneously with intracellular microelectrodes and a force transducer. Preparations were maintained in Krebs-Henseleit solution (perfusion rate, 1.5 mL/min) and subjected to 30 minutes of no-flow ischemia followed by 60 minutes of reperfusion or pretreated with O-R scavengers (superoxide dismutase, 50 U/mL; catalase, 600 U/mL; and mannitol, 2 mmol/L) for 10 to 20 minutes, followed by 30 minutes of ischemia and 60 minutes of reperfusion. Reperfusion in untreated preparations caused (1) depolarization of resting membrane potential by 8 to 10 mV and slow recovery of action potential duration requiring 60 minutes to attain the preischemic duration, (2) tachyarrhythmias and premature action potentials, (3) postischemic contractile dysfunction, and (4) increased coronary perfusion pressure in untreated preparations. Pretreatment with scavenger cocktail affected neither electrical nor contractile activity before or during no-flow ischemia, but it (1) accelerated recovery of resting membrane potential and action potential duration, (2) reduced the incidence of tachyarrhythmia, (3) improved contractile function, and (4) inhibited the rise in perfusion pressure on reflow. Reperfusion with an exogenous O-R-generating system containing xanthine/xanthine oxidase (X/XO, 2 mmol/L:10 mU/mL) inhibited recovery of action potential duration and contractility. Treatment of normoxic arterially perfused right ventricular walls with X/XO caused a decline in action potential duration by approximately 20% within 30 minutes. In contrast, X/XO caused a 30% increase in the duration of action potentials in superfused papillary muscles or small strips of right ventricular walls over the same time period. Pretreatment with sodium nitroprusside (10 mumol/L) inhibited the decline in duration induced by X/XO in normoxic right ventricular walls but was without effect on prolongation due to X/XO in papillary muscles. Reperfusion with nitroprusside after no-flow ischemia caused (1) accelerated recovery of preischemic action potential configuration, (2) a significant decline in the incidence of reperfusion arrhythmias, (3) improved postischemic contractile performance, and (4) inhibition of the increase in perfusion pressure associated with reflow. The data indicate that slow recovery of the action potential duration caused by O-Rs in reperfusion cannot be explained by the direct effects of O-Rs on cardiac myocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Does Your Wolff-Parkinson-White Patient Need to Slow Down?

In brief Two healthy young athletes, a 22-year-old college football player and a 31-year-old elite runner, were evaluated for paroxysmal tachycardia. The football player's resting ECG showed the short PR interval and delta wave characteristic of Wolff-Parkinson-White syndrome. Electrophysiologic studies were required to diagnose accessory-pathway conduction in the runner. The high incidence of tachyarrhythmias seen among people who have this preexcitation syndrome makes detection essential. When such arrhythmias cannot be controlled with drug therapy, catheter ablation helps.

Myo‐electrical and motor activity of the stomach in the first days after abdominal surgery: Evaluation by electrogastrography and impedance gastrography

The electrical and motor activities of the stomach were studied in the early postoperative phase after abdominal surgery by means of surface recording techniques: electrogastrography (EGG) and impedance gastrography (IGG). EGG and IGG recordings were made pre-operatively and on the first and second postoperative days. Physical signs and symptoms related to gastrointestinal motility were assessed. Two patient groups were studied; a group of patients undergoing cholecystectomy (n = 9) was compared with a group with major colonic surgery (n = 14). After colonic surgery, resumption of a normal oral diet was later and nausea and vomiting were seen more frequently than after cholecystectomy. Other physical signs concerning intestinal motility did not differ between the groups. Gastric myo-electrical activity (0.04-0.06 Hz), recorded electrogastrographically, tended to decrease in the postoperative phase in both groups, and return to pre-operative values later in the colonic surgery group. However, none of the differences reached statistical significance. Abnormal gastric activity (tachyarrhythmia) was observed in one pre-operative patient but in 6 patients (2 cholecystectomy, 4 colonic surgery) after operation. IGG variables were not significantly affected by the operation and were not significantly different between the groups. No correlation between the symptoms nausea and vomiting in the postoperative phase and the incidence of tachyarrhythmias could be demonstrated in this study. It is concluded that antral myo-electrical and motor activity, measured with non-invasive techniques (EGG and IGG), are not grossly abnormal on the first and second postoperative day after abdominal surgery. It is further concluded that abnormal gastric frequencies do not appear to play a major role in the genesis of postoperative nausea and vomiting.