Cardiac Electrical Instability Research Articles

An Ominous ECG: What Is the Mechanism? Specific Subtype of Ventricular Separation

Homologous ventricular electrical separation is a rare electrocardiogram manifestation; it is defined as a specific subtype of ventricular separation caused by excitation that originates from the supraventricular rhythm and travels through the His-Pukenje system, resulting in severe asynchrony of biventricular depolarization and production of 2 QRS complexes. It always indicates irreversible cardiac impairment and electrical instability. (Level of Difficulty: Advanced.)

Individuals with chronic epilepsy have elevated P-wave heterogeneity comparable to patients with atrial fibrillation.

Identification of epilepsy patients with elevated risk for atrial fibrillation (AF) is critical given the heightened morbidity and premature mortality associated with this arrhythmia. Epilepsy is a worldwide health problem affecting nearly 3.4 million people in the United States alone. The potential for increased risk for AF in patients with epilepsy is not well appreciated, despite recent evidence from a national survey of 1.4 million hospitalizations indicating that AF is the most common arrhythmia in people with epilepsy. We analyzed inter-lead heterogeneity of P-wave morphology, a marker reflecting arrhythmogenic nonuniformities of activation/conduction in atrial tissue. The study groups consisted of 96 patients with epilepsy and 44 consecutive patients with AF in sinus rhythm before clinically indicated ablation. Individuals without cardiovascular or neurological conditions (n = 77) were also assessed. We calculated P-wave heterogeneity (PWH) by second central moment analysis of simultaneous beats from leads II, III, and aVR ("atrial dedicated leads") from standard 12-lead electrocardiography (ECG) recordings from admission day to the epilepsy monitoring unit (EMU). Female patients composed 62.5%, 59.6%, and 57.1% of the epilepsy, AF, and control subjects, respectively. The AF cohort was older (66 ± 1.1 years) than the epilepsy group (44 ± 1.8 years, p < .001). The level of PWH was greater in the epilepsy group than in the control group (67 ± 2.6 vs. 57 ± 2.5 μV, p = .046) and reached levels observed in AF patients (67 ± 2.6 vs. 68 ± 4.9 μV, p = .99). In multiple linear regression analysis, PWH levels in individuals with epilepsy were mainly correlated with the PR interval and could be related to sympathetic tone. Epilepsy remained associated with PWH after adjustments for cardiac risk factors, age, and sex. Patients with chronic epilepsy have increased PWH comparable to levels observed in patients with AF, while being ~20 years younger, suggesting an acceleration in structural change and/or cardiac electrical instability. These observations are consistent with emerging evidence of an "epileptic heart" condition.

P9 INCESSANT ARRHYTHMIC STORM, EFFECTIVELY TREATED BY VENTRICULOPLASTY

Abstract Arrhythmic storm is an emergency characterized by cardiac electrical instability leading to multiple episodes of sustained ventricular arrhythmias in a short period of time. Patients have multiple comorbidities that require multidisciplinary interventions to achieve clinical stability. The genesis of arrhythmic storm involves a complex interaction between a predisposing arrhythmogenic substrate, triggering factors, autonomic nervous system, and patient comorbidities. Antiarrhythmic drug therapy plays a key role and has been shown to be associated with a significant reduction in VT recurrence. Transcatheter ablation in patients refractory to drug therapy has been shown to reduce arrhythmic recurrences, ICD shocks, and improve patients‘ cumulative survival over time. Rare cases of arrhythmic storm refractoriness treated by plastic ventricle for the purpose of excluding scar are reported in the literature. We present the case of a 62–year–old man, Caucasian race, suffering from chronic ischemic heart disease with hypokinetic–dilated evolution carrying CRT–D, diabetic, obese, dyslipidemic, undergoing multiple percutaneous revascularizations. Sent to our hospital from a peripheral hospital for arrhythmic storm refractory to maximal antiarrhythmic therapy treated with multiple internal and external DC shocks. During hospitalization, the patient underwent SEF and attempted ATC which was ineffective in the following days due to recurrence of numerous episodes of TVS. In view of the clinical picture and refractoriness to therapy, it was decided to perform coronary examination which found subocclusion of the 1st diagonal branch treated by implantation of medicated stent. On ventriculography, the presence of severe pseudoaneurysmal formation supplied at the level of the anterior wall of the left ventricle was confirmed. It was decided to transfer the patient to cardiac surgery to perform ventriculoplasty surgery. In the following days, the patient underwent surgery through exclusion of the aneurysm by patching in pericardium in CEC. Procedure was free of complications. On follow–up echocardiogram dilated left ventricle with severe left ventricular dysfunction with findings of cardiac aneurysm exclusion. In the following days, the patient presented no further arrhythmic episodes.

T-wave Heterogeneity is Superior to QTc in 12-Lead ECG in Detection of Cardiac Electrical Instability at EMU Admission (S35.004)

T-wave Heterogeneity is Superior to QTc in 12-Lead ECG in Detection of Cardiac Electrical Instability at EMU Admission (S35.004)

Habitual physical activity improves vagal cardiac modulation and carotid baroreflex function in elderly women.

The impact of habitual physical activity on vagal-cardiac function and baroreflex sensitivity in elderly women is poorly characterized. This study compared vagal-cardiac modulation and carotid baroreflex (CBR) function in eight physically active (67.6 ± 1.9 years; peak O2 uptake 29.1 ± 2.5 mL/min/kg) versus eight sedentary (67.3 ± 1.8 years; peak O2 uptake 18.6 ± 0.9 mL/min/kg) elderly women. Heart rate (HR) variabilities and maximal changes of HR and mean arterial pressure (MAP) elicited by 5-s pressure pulses between +40 and -80 mmHg applied to the carotid sinus were measured at rest and during carotid baroreceptor unloading effected by -15 mmHg lower-body negative pressure (LBNP). HR variability was greater in active than sedentary women in both low (0.998 ± 0.286 versus 0.255 ± 0.063 bpm2; P = 0.036) and high (0.895 ± 0.301 versus 0.156 ± 0.045 bpm2; P = 0.044) frequency domains. CBR-HR gains (bpm/mmHg) were greater (fitness factor P < 0.001) in active versus sedentary women at rest (-0.146 ± 0.014 versus -0.088 ± 0.011) and during LBNP (-0.105 ± 0.014 versus -0.065 ± 0.008). CBR-MAP gains (mmHg/mmHg) tended to be greater (fitness factor P = 0.077) in active versus sedentary women at rest (-0.132 ± 0.013 versus -0.110 ± 0.011) and during LBNP (-0.129 ± 0.015 versus -0.113 ± 0.013). However, LBNP did not potentiate CBR-MAP gains in either sedentary or active women (LBNP factor P = 0.94), and it depressed CBR-HR gains in both groups (LBNP factor P = 0.003). CBR-HR gains in the sedentary women did not differ (sex factor P = 0.65) from gains reported in age-matched sedentary men, although CBR-MAP gains tended to be greater (sex factor P = 0.109) in the men. Thus, tonic vagal modulation indicated by HR variability and dynamic vagal responses assessed by CBR-HR gain were augmented in physically active women. Enhanced vagal-cardiac function may protect against senescence-associated cardiac electrical and hemodynamic instability in elderly women.

Ventricular Tachycardia Storm Management in Acute Cardiac Care: Prompt response to life-threatening conditions

Background: Ventricular Tachycardia (VT) storm or electrical storm (ES) is defined as cardiac electrical instability and refers to the occurrence of three or more ventricular tachyarrhythmias (VT and or ventricular fibrillation (VF)) in a 24-hour period, or VT recurring soon (within five minutes) after termination of another VT episode, or sustained or no sustained VT with total ectopic beats greater than sinus beats in a 24-hour period. The frequency of VT storms varies on population. When ICDs are implanted for primary prevention (4 percent), it is lower than when they are implanted for secondary prevention (20 percent). Case Summary: We presented patient with Ventricular Tachycardia (VT) storm. A 63-year old woman was admitted to emergency room with chief complaint frequent episodes of palpitation. She was found to have monomorphic VT with unstable hemodynamic. Then she got cardioversion 100 Joule, continued with lidocaine drip and VT reverted to sinus rhythm. Patient admitted to cardiovascular care unit, but she had VT refractory. She got complete revascularization for coronary artery before, but the episodic of VT still occurred with cardiogenic shock (CS) and pulmonary edema. She got cardioversion, amiodarone iv and inotropes, then observed this patient at CVCU. After the condition stable, this patient was discharged and planned for ICD insertion at the next admission. Discussion: We discuss the various available treatment options for VT storm and practical challenges faced in management of hemodynamically unstable VT storm. Initial management involves identifying and correcting the underlying ischemia, electrolyte imbalances, or other inciting factors.

Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats.

Recent epidemiological findings link asthma to adverse cardiovascular responses. Yet, the precise cardiovascular impacts of asthma have been challenging to disentangle from the potential cardiovascular effects caused by asthma medication. The purpose of this study was to determine the impacts of allergic airways disease alone on cardiovascular function in an experimental model. Female Wistar rats were intranasally sensitized and then challenged once per week for 5 weeks with saline vehicle or a mixture of environmental allergens (ragweed, house dust mite, and Aspergillus fumigatus). Ventilatory and cardiovascular function, measured using double-chamber plethysmography and implantable blood pressure (BP) telemetry and cardiovascular ultrasound, respectively, were assessed before sensitization and after single and final allergen challenge. Responses to a single 0.5 ppm ozone exposure and to the cardiac arrhythmogenic agent aconitine were also assessed after final challenge. A single allergen challenge in sensitized rats increased tidal volume and specific airways resistance in response to provocation with methacholine and increased bronchoalveolar lavage fluid (BALF) eosinophils, neutrophils, lymphocytes, cytokines interleukin (IL)-4, IL-5, IL-10, IL-1β, tumor necrosis factor-α, and keratinocyte chemoattract-growth-related oncogene characteristic of allergic airways responses. Lung responses after final allergen challenge in sensitized rats were diminished, although ozone exposure increased BALF IL-6, IL-13, IL-1 β, and interferon-γ and modified ventilatory responses only in the allergen group. Final allergen challenge also increased systolic and mean arterial BP, stroke volume, cardiac output, end-diastolic volume, sensitivity to aconitine-induced cardiac arrhythmia, and cardiac gene expression with lesser effects after a single challenge. These findings demonstrate that allergic airways responses may increase cardiovascular risk in part by altering BP and myocardial function and by causing cardiac electrical instability.

Epileptic seizures and Epilepsy Monitoring Unit admission disclose latent cardiac electrical instability

BackgroundSudden cardiac arrest results from cardiac electrical instability and is 3-fold more frequent in patients with chronic epilepsy than in the general population. We hypothesized that focal to bilateral tonic-clonic seizures (FTBTCS) would acutely impact T-wave alternans (TWA), a marker of cardiac electrical instability linked to an elevated risk for sudden cardiac death, more than focal seizures (FS) [focal aware seizures (FAS) and focal with impaired awareness seizures (FIAS)], due to their greater sympathetic stimulation of the heart. Since stress has been shown to cause significant TWA elevations in patients with heart disease, we also hypothesized that the early days of an inpatient admission to an epilepsy monitoring unit (EMU) would be associated with higher TWA levels compared to later hospital days in patients with chronic epilepsy, presumably due to stress. Design/MethodsWe analyzed the acute effects of seizures [FAS, FIAS, FTBTCS, and nonepileptic seizures (NES)] and day of hospital stay on TWA in 18 patients admitted to the EMU using high-resolution wireless electrocardiographic (ECG) patch monitors. ResultsA total of 5 patients had FTBTCS, 7 patients had FS (2 FAS, 5 FIAS), and 3 patients had NES only during the index hospital stay. Four patients did not have any electroclinical seizures or NES. FTBTCS resulted in marked acute increases in ictal TWA from baseline (2 ± 0.3 µV) to ictal maximum (70 ± 6.1 µV, p < 0.0001), the latter exceeding the 60 µV cut point defined as severely abnormal. By comparison, while FAS and FIAS also provoked significant increases in TWA (from 2 ± 0.5 µV to 30 ± 3.3 µV, p < 0.0001), maximum ictal TWA levels did not reach the 47 µV cut point defined as abnormal. Heart rate increases during FTBTCS from baseline (62 ± 5.8 beats/min) to ictal maximum (134 ± 8.6 beats/min, an increase of 72 ± 7.2 beats/min, p < 0.02) were also greater (p = 0.014) than heart rate increases during FS (from 70 ± 5.2 beats/min to 118 ± 6.2 beats/min, an increase of 48 ± 2.6 beats/min, p < 0.03). In 3 patients with NES, TWA rose mildly during the patients’ typical episodes (from 2 ± 0.6 µV to 14 ± 2.6 µV, p < 0.0004), well below the cut point of abnormality, while heart rate increases were observed (from 75 ± 1.3 to 112 ± 8.7 beats/min, an increase of 37 ± 8.9 beats/min, p = 0.03). Patients with EEG-confirmed electroclinical seizures recorded while in the EMU exhibited significantly elevated interictal TWA maxima (61 ± 3.4 µV) on EMU admission day which were similar in magnitude to ictal maxima seen during FTBTCS (70 ± 6.1 µV, p = 0.21). During subsequent days of hospitalization, daily interictal TWA maxima showed gradual habituation in patients with both FS and FTBTCS but not in patients with NES only. ConclusionsThis is the first study to our knowledge demonstrating that FTBTCS acutely provoke highly significant increases in TWA to levels that have been associated with heightened risk for sudden cardiac death in other patient populations. We speculate that mortality temporally associated with FTBTCS may, in some cases, be due to sudden cardiac death rather than respiratory failure. In patients with EEG-confirmed epilepsy, hospital admission is associated with interictal TWA maxima that approach those seen during FTBTCS, presumably related to stress during the early phase of hospitalization compared to later in the hospitalization, indicating cardiac electrical instability and potential vulnerability to sudden cardiac death related to stress independent of temporal relationships to seizures. The elevated heart rates observed acutely with seizures and on hospital Day 1 are consistent with a hyperadrenergic state and the effect of elevated sympathetic output on a vulnerable cardiac substrate, a phenomenon termed “the Epileptic Heart.”

Spectrum of clinical applications of interlead ECG heterogeneity assessment: From myocardial ischemia detection to sudden cardiac death risk stratification.

Heterogeneity in depolarization and repolarization among regions of cardiac cells has long been recognized as a major factor in cardiac arrhythmogenesis. This fundamental principle has motivated development of noninvasive techniques for quantification of heterogeneity using the surface electrocardiogram (ECG). The initial approaches focused on interval analysis such as interlead QT dispersion and Tpeak–Tend difference. However, because of inherent difficulties in measuring the termination point of the T wave and commonly encountered irregularities in the apex of the T wave, additional techniques have been pursued. The newer methods incorporate assessment of the entire morphology of the T wave and in some cases of the R wave as well. This goal has been accomplished using a number of promising vectorial approaches with the resting 12‐lead ECG. An important limitation of vectorcardiographic analyses is that they require exquisite stability of the recordings and are not inherently suitable for use in exercise tolerance testing (ETT) and/or ambulatory ECG monitoring for provocative stress testing or evaluation of the influence of daily activities on cardiac electrical instability. The objectives of the present review are to describe a technique that has been under clinical evaluation for nearly a decade, termed “interlead ECG heterogeneity.” Preclinical testing data will be briefly reviewed. We will discuss the main clinical findings with regard to sudden cardiac death risk stratification, heart failure evaluation, and myocardial ischemia detection using standard recording platforms including resting 12‐lead ECG, ambulatory ECG monitoring, ETT, and pharmacologic stress testing in conjunction with single‐photon emission computed tomography myocardial perfusion imaging.

Manifestation of Acute Coronary Syndrome in Critically Aortic Stenosis Patients

The clinical presentation of acute coronary syndromes (ACS) is broad, from cardiac arrest, electrical or haemodynamic instability with cardiogenic shock (CS) due to ongoing ischaemia or mechanical complications such as severe mitral regurgitation, to patients who are already pain free again at the time of presentation. Critical aortic stenosis (AS) can cause inadequate myocardial perfusion and in the absence of demonstrable coronary stenosis or occlusion which resulting in ACS manifestation. Critical AS (defined as valve area &lt;0.5 cm2) has been reported to cause mild increases in cardiac biomarkers such as troponin I. A 56-year-old man was admitted to hospital with chief complaint of typcal chest pain. Electrocardiogram (ECG) shows myocardial infarction in left main (LM) equivalent. Echocardiography revealed critical aortic stenosis. Cardiac marker also shows increasing. However, diagnostic coronary angiography (DCA) did not identify any lesions to account for the patient’s electrocardiographic changes and ongoing symptoms of chest pain. Consultation to cardiothorax surgeon to have urgent aortic valve replacement (AVR) were planned and underwent successful aortic valve (AV) replacement without coronary intervention. The definitive treatment for symptomatic severe AS is AVR. Some of the treatments that can be done are immediate coronary angiography and reperfusion procedure if there is suspicion of coronary artery occlusion or stenosis which may cause myocardial infarction; Intra-Aortic Ballon Pump (IABP) if there are signs of myocardial injury with take caution to the contraindications of IABP placement; Perform intervention procedure as soon as possible on aortic valve; Administration of medical therapy for heart failure in symptomatic severe AS patients. The case emphasizes the importance of initial physical examination, ECG, echocardiography, and cardiac markers as a whole that we do in aortic valve stenosis patient presenting with ACS.

Epileptic heart: A clinical syndromic approach.

Prevention of premature death in patients with chronic epilepsy remains a major challenge. Multiple pathophysiologic factors have been implicated, with intense investigation of cardiorespiratory mechanisms. Up to four in five patients with chronic epilepsy exhibit cardiovascular comorbidities. These findings led us to propose the concept of an "epileptic heart," defined as "a heart and coronary vasculature damaged by chronic epilepsy as a result of repeated surges in catecholamines and hypoxemia leading to electrical and mechanical dysfunction." Among the most prominent changes documented in the literature are high incidence of myocardial infarction and arrhythmia, altered autonomic tone, diastolic dysfunction, hyperlipidemia, and accelerated atherosclerosis. This suite of pathologic changes prompted us to propose for the first time in this review a syndromic approach for improved clinical detection of the epileptic heart condition. In this review, we discuss the key pathophysiologic mechanisms underlying the candidate criteria along with standard and novel techniques that permit evaluation of each of these factors. Specifically, we present evidence of the utility of standard 12-lead, ambulatory, and multiday patch-based electrocardiograms, along with measures of cardiac electrical instability, including T-wave alternans, heart rate variability to detect altered autonomic tone, echocardiography to detect diastolic dysfunction, and plasma biomarkers for assessing hyperlipidemia and accelerated atherosclerosis. Ultimately, the proposed clinical syndromic approach is intended to improve monitoring and evaluation of cardiac risk in patients with chronic epilepsy to foster improved therapeutic strategies to reduce premature cardiac death.

Wavelet-based entropy and complexity to identify cardiac electrical instability in patients post myocardial infarction

Myocardial infarction (MI) has been long recognized as the main cause of malignant ventricular arrhythmia and/or sudden cardiac death. The region of myocardial scars is related to conduction abnormalities that are rejected as fragmentation of the QRS complexes, which could persist several months after the acute event. In the present work, we evaluated the normalized entropy (H) and the statistical complexity (C) of QRS complexes, by using the continuous wavelet transform, as an effective method to quantify abnormal alterations in cardiac electrical activity in post-MI patients.We have included the standard 12-leads electrocardiogram (ECG) records of healthy subjects (CTRL), n = 48, and MI patients without ventricular tachycardia (VT) and/or fibrillation (VF), grouped in MI healing (MI7), n = 84, and healed (MI60), n = 41, phases.The mean H and C values (H‾ and C‾) of each subject were calculated. H‾ significantly increased and C‾ significantly decreased (p < 0.05) for MI7, and were sustained in MI60, with respect to CTRL. We integrated all the ECG leads in a single multi-lead criteria (H‾ML and C‾ML). Moreover, we separated MI patients according to the infarcted area in anterior and inferior subsets. H‾ML and C‾ML showed the same trends as H‾ and C‾ for total patients and both infarcted areas subsets, with the advantage that higher values of sensitivity and specificity were obtained.In conclusion, wavelet entropy and statistical complexity applied to ECG records give new insight into the analysis of patients post-MI, who have not suffered VT/VF, in both MI stages, independently of the infarction areas analyzed.

Associations between PM2.5 metal components and QT interval length in the Normative Aging Study

BackgroundSeveral studies have found associations between increases in QT interval length, a marker of cardiac electrical instability, and short-term fine particulate matter (PM2.5) exposures. To our knowledge, this is the first study to examine the association between specific PM2.5 metal components and QT interval length. MethodsWe measured heart-rate corrected QT interval (QTc) duration among 630 participants in the Normative Aging Study (NAS) based in Eastern Massachusetts between 2000 and 2011. We utilized time-varying linear mixed-effects regressions with a random intercept for each participant to analyze associations between QTc interval and moving averages (0–7 day moving averages) of 24-h mean concentrations of PM2.5 metal components (vanadium, nickel, copper, zinc and lead) measured at the Harvard Supersite monitoring station. Models were adjusted for daily PM2.5 mass estimated at a 1 km × 1 km grid cell from a previously validated prediction model and other covariates. Bayesian kernel machine regression (BKMR) was utilized to assess the overall joint effect of the PM2.5 metal components. ResultsWe found consistent results with higher lead (Pb) associated with significant higher QTc intervals for both the multi-pollutant and the two pollutant (PM2.5 mass and a PM2.5 component) models across the moving averages. The greatest effect of lead on QTc interval was detected for the 4-day moving average lead exposure. In the multi-pollutant model, each 2.72 ng/m3 increase in daily lead levels for a 4-day moving average was associated with a 7.91 ms (95% CI: 3.63, 12.18) increase in QTc interval. In the two-pollutant models with PM2.5 mass and lead, each 2.72 ng/m3 increase in daily lead levels for a 4-day moving average was associated with an 8.50 ms (95% CI: 4.59, 12.41) increase in QTc interval. We found that 4-day moving average of copper has a negative association with QTc interval when compared to the other PM2.5 metal components. In the multi-pollutant model, each 1.81 ng/m3 increase in daily copper levels for a 4-day moving average was associated with an −3.89 ms (95% CI: -6.98, −0.79) increase in QTc interval. Copper's essential function inside the human body could mediate its cardiotoxicity on cardiac conductivity and explain why we found that copper in comparison to the other metals was less harmful for QTc interval. ConclusionsExposure to metals contained in PM2.5 are associated with acute changes in ventricular repolarization as indicated by QT interval characteristics.

Multi-year improvement in autonomic tone, baroreceptor sensitivity, and cardiac electrical stability using vagus nerve stimulation in patients with HFrEF in the ANTHEM-HF study

Abstract Background HFrEF patients experience long-term deterioration of autonomic function and cardiac electrical stability linked to increased sudden cardiac death risk. ANTHEM-HF (NCT01823887) reported improved baroreceptor sensitivity (heart rate turbulence, HRT), heart rate variability (rMSSD), and reduced cardiac electrical instability (T-wave alternans, TWA) after 12 months of chronic vagus nerve stimulation (VNS). It is unknown whether these benefits persist long-term. Methods HRT, rMSSD, TWA, and VT occurrence were evaluated during chronic VNS in all patients with symptomatic HFrEF with available 36-month follow-up data (n=25). ECGs were analyzed before Autonomic Regulation Therapy system implantation (LivaNova USA) and after chronic cervical VNS. Results Improvement in HRT slope persisted at 24 months (8.1±1.2 ms/RR interval, p=0.02) and 36 months (7.9±0.9 ms/RR interval, p=0.03) of VNS compared to baseline. RMSSD increase continued at 24 months (34.6±2.7 ms2, p&amp;lt;0.02) and 36 months (36.4±2.0 ms2, p=0.002). Peak TWA levels remained reduced at 24 months (47.8±1.3 μV, p&amp;lt;0.0001) and 36 months (46.1±1.6 μV, p&amp;lt;0.0001). No sudden death, VF, or sustained VT occurred, and patients with nonsustained VT decreased from 11 (44%) at baseline to 1 (5%) at 24 months (p&amp;lt;0.003) and 2 (11%) at 36 months (p&amp;lt;0.02). Conclusion In patients with HFrEF, chronic VNS appears to confer persistent 3-year improvements in autonomic tone, baroreceptor sensitivity, and cardiac electrical stability. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): LivaNova PLC

Associations between PM2.5 metal components and QT interval length

Background/Aim: Several studies have found associations between increases in QT interval length, a marker of cardiac electrical instability, and short-term fine particulate matter (PM2.5). To our knowledge, this is the first study to examine the association between specific PM metal components and QT interval length. Methods: We measured heart-rate corrected QT interval (QTc) duration among 630 participants in the Normative Aging Cohort (NAS) based in Eastern Massachusetts between 2000 to 2012. We utilized time-varying linear mixed-effects regressions with a random intercept to analyze associations between QTc interval and moving averages (0 to 7-day moving averages) of 24-hour mean concentrations of PM metal components (vanadium, nickel, copper, zinc and lead) measured at the Harvard Supersite monitoring station. Models were adjusted for daily PM2.5 mass estimated at a 1 km x 1 km grid cell from a previously validated prediction model and other covariates. Bayesian kernel machine regression (BKMR) was utilized to assess the overall effect of the PM components and the exposure-dose response curves. Results: We found consistent results with higher lead (Pb) associated with significant higher QTc intervals for both the multi-pollutant and the two pollutant (PM2.5 and a PM component) models across the moving averages. The greatest effect of lead on QTc interval was detected for the 4-day moving average lead exposure. In the multi-pollutant model, each 2.72 ng/m3 increase in daily lead levels for a 4-day moving average was associated with an 8.77 ms (95% CI: 4.25,13.29) increase in QTc interval. In the two-pollutant models with PM2.5 mass and lead, each 2.72 ng/m3 increase in daily lead levels for a 4-day moving average was associated with a 9.19 ms (95% CI: 5.09,13.30) increase in QTc interval. Conclusions: Our findings suggest that metals contained in PM2.5 are associated with acute changes (0 to 7-day moving averages) in ventricular repolarization.

In Memoriam: Lionel H. Opie, MD (1933-2020).

In Memoriam: Lionel H. Opie, MD (1933-2020).

Comparative Acute Impact of Focal and Generalized Tonic-clonic Seizures on Cardiac Electrical Instability in the Epilepsy Monitoring Unit (1493)

Comparative Acute Impact of Focal and Generalized Tonic-clonic Seizures on Cardiac Electrical Instability in the Epilepsy Monitoring Unit (1493)

Electrical Storm in Patients with Inappropriate Implantable Cardioverter-Defibrillator Therapy: Current Trends in Clinical Practice between Guidelines and Technology Progress

The term “Electrical Storm” (ES) indicates cardiac electrical instability manifested by several episodes of ventricular tachyarrhythmias within a short time. In the contemporary implantable cardioverter-defibrillator (ICD) era, ES is defined as recurrent (three or more separate episodes) of ICD discharges over 24 hours. Some ESs are due to inappropriate repetitive shock and are potentially lethal for the patient. The most common causes of inappropriate ICD shock include supraventricular tachycardia with high ventricular response and oversening of peaked T waves or R wave, myopotentials or electrical noise. Appropriate diagnosis and treatment are critical in the Emergency Department. To approach these patients systematically, it is important to understand, that there are four causes of shock. Modern ICD incorporate sophisticated tachycardia detection algorithms within their programming designed to minimize devices’ detection mistakes and ICD-related information can also be checked using remote home monitoring systems. However, these opportunities are often not utilized to their full benefit. Thus, careful attention should be paid to the programming of the device. Fine tuning of the detection and differentiation algorithms is critical, and best done by a practitioner who understands the subtle differences among the different manufacturers. The racommendations for those problems should be revised.

Intrapericardial administration of anti-arrhythmic medications in patients with electrical storm

IntroductionElectrical storm (ES) is cardiac electrical instability characterized by recurrent episodes of ventricular tachyarrhythmias. ES is associated with increased mortality and morbidity, hence requires prompt intervention. Treatment of underlying etiology is of prime importance in termination of ES. Anti-arrhythmic medications serve as an adjunctive therapy in suppression of ES by reducing myocardial excitability. The anti-arrhythmic conventionally employed is amiodarone in combination with non-selective beta-blockers to reduce the adrenergic input to myocardium. However, anti-arrhythmics at increased concentrations can lead to adverse systemic effects including hemodynamic instability. HypothesisWe hypothesize 1. The use of intravenous or oral anti-arrhythmic therapy for patients in electrical storm is limited by their toxicities and blood pressure lowering effect. Corollary 1. Injection of anti-arrhythmic medications into the pericardial space, an extra-vascular structure encasing the heart, provides an option for use of higher concentration of anti-arrhythmic while limiting systemic absorption. Corollary 2. The pericardial space has direct communication to the epicardium, the outer most layer of cardiac muscle, spatial proximity may allow for effective therapeutic options in electrical storm. We present experimental and clinical evidence in support of these hypothesis.

The effect of ivabradine as part of standard therapy on vascular endothelial function and cardiac electrical instability in patients with post-infarction cardiosclerosis and heart failure

Aim. To reveal the equivalence of nebivolol replacement with ivabradine in the prevention of endothelial dysfunction and cardiac electrical instability in patients with heart failure with reduced ejection fraction (HFrEF).Material and methods. In current observational study, 126 patients with HFrEF in the postinfarction period were randomized into two groups for six-month treatment: group 1 (n=62) — standard therapy (acetylsalicylic acid 0,1 g/day, clopidogrel 75 mg/day, veroshpiron 50 mg/day, nebivolol 5 mg/day, perindopril 5 mg/day and rosuvastatin 20 mg/day; group 2 (n=66) — the same therapy with nebivolol replacement with ivabradine 10 mg/day. Initially and after 6 months, 24-hour Holter monitoring was performed, heart rate variability was determined. We also investigated endothelial dysfunction using the photoplethysmographic technique with post-occlusive reactive hyperemia (PORH) test.Results. The heart rate, the number of episodes and the duration of symptomatic and silent myocardial ischemia, total myocardial ischemia were significantly decreased in both groups (p&lt;0,001). The decrease of supraventricular extrasystole frequency in both groups had not statistical significance (p&gt;0,05). In both groups, after therapy, parameters of heart rate variability were improved with the parasympathetic predominance (p&lt;0,01). In both groups, the PORH test revealed the increase of brachial artery diameter (group 1 — 5,90Ѓ}3,15% and group 2 — 5,88Ѓ}1,82%) and pulse wave amplitude (group 1 — 1,81Ѓ}0,78 and group 2 — 1,73Ѓ}0,90 times), which indicates a trend towards an improvement in endothelial function. Intergroup comparisons did not reveal significant differences.Conclusion. Ivabradine is equivalent to nebivolol in preventing ventricular extrasystole and reducing heart rate, number of episodes of symptomatic and silent ischemia and the duration of total myocardial ischemia in patients with HFrEF. Ivabradine equivalently to nebivolol improves endothelial function and heart rate variability with reducing the sympathetic activity.