Systemic primary carnitine deficiency induces severe arrhythmia due to shortening of QT interval.

BACKGROUND: Systemic primary carnitine deficiency (PCD) is characterized by cardiomyopathy and arrhythmia. Without carnitine supplementation, progression is usually towards fatal cardiac decompensation. While the cardiomyopathy is most likely secondary to energy deficiency, the mechanism of arrhythmia is unclear, and may be related to a short QT interval. OBJECTIVE: We aim to describe rhythmic manifestations at diagnosis and with carnitine supplementation. METHODS: French patients diagnosed for PCD were retrospectively included. Clinical and para clinical data at diagnosis and during follow-up were collected. Electrocardiograms with QT interval measurements were blinded reviewed by two paediatric cardiologists. RESULTS: Nineteen patients (median age at diagnosis 2.3 years (extremes 0.3-28.9)) followed in 8 French centres were included. At diagnosis, 21% of patients (4/19) had arrhythmia (2 ventricular fibrillations, 1 ventricular tachycardia and 1 sudden death), and 84% (16/19) had cardiomyopathy. Six electrocardiograms before treatment out of 11 available displayed a short QT (QTc < 340 ms). Median corrected QTc after carnitine supplementation was 404 ms (extremes 341-447) versus 350 ms (extremes 282-421) before treatment (p < 0.001). The whole QTc was prolonged, and no patient reached the criterion of short QT syndrome with carnitine supplementation. Three patients died, probably from rhythmic cause without carnitine supplementation (two extra-hospital sudden deaths and one non-recoverable rhythmic storm before carnitine supplementation), whereas no rhythmic complication occurred in patients with carnitine supplementation. CONCLUSION: PCD is associated with shortening of the QT interval inducing severe arrhythmia. A potential explanation would be a toxic effect of accumulated fatty acid and metabolites on ionic channels embedded in the cell membrane. Carnitine supplementation normalizes the QTc and prevents arrhythmia. Newborn screening of primary carnitine deficiency would prevent avoidable deaths.

Evaluation of the effect of sodium zirconium cyclosilicate on arrhythmia-related cardiovascular outcomes in patients receiving chronic haemodialysis with hyperkalaemia: protocol for the multicentre, randomised, controlled DIALIZE-Outcomes study.

INTRODUCTION: Patients with kidney failure receiving chronic haemodialysis have elevated risk of arrhythmias potentially increasing the likelihood of sudden cardiac death, stroke and hospitalisation. The DIALIZE study (NCT03303521) demonstrated that sodium zirconium cyclosilicate (SZC) was an efficacious and well-tolerated treatment for predialysis hyperkalaemia in patients undergoing haemodialysis. The DIALIZE-Outcomes study evaluates the effect of SZC on sudden cardiac death and arrhythmia-related cardiovascular outcomes in patients receiving chronic haemodialysis with recurrent hyperkalaemia. METHODS AND ANALYSIS: International, multicentre, randomised, double-blind, placebo-controlled study conducted at 357 study sites across 25 countries. Adults (≥18 years) receiving chronic haemodialysis three times per week with recurrent predialysis serum potassium (K+) ≥5.5 mmol/L post long interdialytic interval (LIDI) are eligible. Patients (~2800) will be randomised 1:1 to SZC or placebo, starting at 5 g orally once daily on non-dialysis days and titrated weekly in 5 g increments (maximum 15 g) to target predialysis serum K+ 4.0-5.0 mmol/L post LIDI. The primary objective is to evaluate efficacy of SZC versus placebo in reducing occurrence of the primary composite endpoint of sudden cardiac death, stroke or arrhythmia-related hospitalisation, intervention or emergency department visit. Secondary endpoints include efficacy of SZC versus placebo in maintaining normokalaemia (serum K+ 4.0-5.5 mmol/L post LIDI) at the 12-month visit, preventing severe hyperkalaemia (serum K+ ≥6.5 mmol/L post LIDI) at the 12-month visit and reducing the incidence of individual cardiovascular outcomes. Safety of SZC will be evaluated. The study is event driven, with participants remaining in the study until 770 primary endpoint events have occurred. Average time in the study is expected to be ~25 months. ETHICS AND DISSEMINATION: Approval was obtained from the relevant institutional review board/independent ethics committee from each participating site (approving bodies in supplementary information). The results will be submitted to a peer-reviewed journal. TRIAL REGISTRATION NUMBERS: EudraCT 2020-005561-14 and clinicaltrials.gov identifier NCT04847232.

Right ventricular epicardial arrhythmogenic substrate in long-QT syndrome patients at risk of sudden death.

AIMS: The long-QT syndrome (LQTS) represents a leading cause of sudden cardiac death (SCD). The aim of this study was to assess the presence of an underlying electroanatomical arrhythmogenic substrate in high-risk LQTS patients. METHODS AND RESULTS: The present study enrolled 11 consecutive LQTS patients who had experienced frequent implantable cardioverter-defibrillator (ICD discharges triggered by ventricular fibrillation (VF). We acquired electroanatomical biventricular maps of both endo and epicardial regions for all patients and analyzed electrograms sampled from several myocardial regions. Abnormal electrical activities were targeted and eliminated by the means of radiofrequency catheter ablation. VF episodes caused a median of four ICD discharges in eleven patients (6 male, 54.5%; mean age 44.0 ± 7.8 years, range 22-53) prior to our mapping and ablation procedures. The average QTc interval was 500.0 ± 30.2 ms. Endo-epicardial biventricular maps displayed abnormally fragmented, low-voltage (0.9 ± 0.2 mV) and prolonged electrograms (89.9 ± 24.1 ms) exclusively localized in the right ventricular epicardium. We found electrical abnormalities extending over a mean epicardial area of 15.7 ± 3.1 cm2. Catheter ablation of the abnormal epicardial area completely suppressed malignant arrhythmias over a mean 12 months of follow-up (median VF episodes before vs. after ablation, 4 vs. 0; P = 0.003). After the procedure, the QTc interval measured in a 12-lead ECG analysis shortened to a mean of 461.8 ± 23.6 ms (P = 0.004). CONCLUSION: This study reveals that, among high-risk LQTS patients, regions localized in the epicardium of the right ventricle harbour structural electrophysiological abnormalities. Elimination of these abnormal electrical activities successfully prevented malignant ventricular arrhythmia recurrences.

A survey study of the use of a subcutaneous implantable cardioverter-defibrillator in various clinical scenarios by expert electrophysiologists in Poland.

BACKGROUND: A subcutaneous implantable cardioverter-defibrillator (S-ICD) has become a recognized alternative to a traditional transvenous implantable cardioverter-defibrillator (T-ICD). Despite the growing evidence of non-inferiority of S-ICD, there are no clear clinical guidelines for selection of either of the two available systems. The aim of the study was to analyze the decisions made in predefined typical clinical scenarios by Polish cardiologists experienced in the use of both S-ICDs and T-ICDs. METHODS: A group of 30 experts of cardiac electrotherapy experienced in the use of S-ICDs was recruited and invited to participate in a web-based anonymous survey. The survey questions regarded the proposed therapy in various but typical clinical scenarios. RESULTS: From the invited 30 experts representing 18 clinical centers, 25 completed the survey. 72% of them declared that the number of S-ICDs implanted at their center during the preceding 12 months exceeded 10, and 40% - that it was over 20. Rates of responders preferring S-ICD or T-ICD in various clinical scenarios are reported and discussed in detail. CONCLUSIONS: Significant divergence of opinion exists among Polish experts regarding the use of a subcutaneous cardioverter-defibrillator. It is especially pronounced on the issue of the use of the system in middle-age patients, in case of complications of the hitherto ICD therapy, or the need of upgrading the existing cardiac implantable electronic device.

Myocardial ATP depletion detected noninvasively predicts sudden cardiac death risk in patients with heart failure.

BACKGROUNDSudden cardiac death (SCD) remains a worldwide public health problem in need of better noninvasive predictive tools. Current guidelines for primary preventive SCD therapies, such as implantable cardioverter defibrillators (ICDs), are based on left ventricular ejection fraction (LVEF), but these guidelines are imprecise: fewer than 5% of ICDs deliver lifesaving therapy per year. Impaired cardiac metabolism and ATP depletion cause arrhythmias in experimental models, but to our knowledge a link between arrhythmias and cardiac energetic abnormalities in people has not been explored, nor has the potential for metabolically predicting clinical SCD risk.METHODSWe prospectively measured myocardial energy metabolism noninvasively with phosphorus magnetic resonance spectroscopy in patients with no history of significant arrhythmias prior to scheduled ICD implantation for primary prevention in the setting of reduced LVEF (≤35%).RESULTSBy 2 different analyses, low myocardial ATP significantly predicted the composite of subsequent appropriate ICD firings for life-threatening arrhythmias and cardiac death over approximately 10 years. Life-threatening arrhythmia risk was approximately 3-fold higher in patients with low ATP and independent of established risk factors, including LVEF. In patients with normal ATP, rates of appropriate ICD firings were several-fold lower than reported rates of ICD complications and inappropriate firings.CONCLUSIONTo the best of our knowledge, these are the first data linking in vivo myocardial ATP depletion and subsequent significant arrhythmic events in people, suggesting an energetic component to clinical life-threatening ventricular arrhythmogenesis. The findings support investigation of metabolic strategies that limit ATP loss to treat or prevent life-threatening cardiac arrhythmias and herald noninvasive metabolic imaging as a complementary SCD risk stratification tool.TRIAL REGISTRATIONClinicalTrials.gov NCT00181233.FUNDINGThis work was supported by the DW Reynolds Foundation, the NIH (grants HL61912, HL056882, HL103812, HL132181, HL140034), and Russell H. Morgan and Clarence Doodeman endowments at Johns Hopkins.

Circadian rhythms, cardiac arrhythmias and sudden death.

The heart, like most mammalian organs, is influenced by circadian patterns. The suprachiasmatic nucleus in the hypothalamus has a key role in this influence, via various neurohumoral factors, particularly the autonomic nervous system. In addition, a local cardiac peripheral clock might drive a circadian rhythm related to the expression of ion channels. Several myocardial functions are influenced by these circadian cycles including activity/rest, regeneration, nutrient storage, growth, and myocardial repair. Numerous circadian genes have been identified in basic studies, and both biological factors and environmental features (including epigenetic) influence the human circadian rhythm. A normal circadian rhythm is important to maintain a normal heart rhythm and circadian rhythm disturbances can predispose to the development of cardiac arrhythmias. The normal heart rate presents a daily variability with a morning peak and nocturnal bradycardization. Ventricular arrhythmias and sudden death are more likely to occur in the morning after waking, while atrial fibrillation and heart blocks most commonly occur at night. Drugs such as beta-blockers might modify the chronobiology of some of these arrhythmias. On the other hand, drugs that influence circadian rhythm, like the circadian hormone melatonin, have demonstrated pleiotropic properties and show promising results as antiarrhythmics. This review is focused on the current understanding of the basic mechanism and clinical implications of the association circadian rhythms-cardiac arrhythmias/sudden death. The close relationship between circadian patterns and arrhythmias may provide us with the possibility of novel interventions to decrease the arrhythmic risk in some patients.

A Multicenter External Validation of a Score Model to Predict Risk of Events in Patients With Brugada Syndrome.

A multivariate risk score model was proposed by Sieira et al in 2017 for sudden death in Brugada syndrome; their validation in 150 patients was highly encouraging, with a C-index of 0.81; however, this score is yet to be validated by an independent group. A total of 192 records of patients with Brugada syndrome were collected from 2 centers in the United Kingdom and retrospectively scored according to a score model by Sieira et al. Data were compiled summatively over follow-up to mimic regular risk re-evaluation as per current guidelines. Sudden cardiac death survivor data were considered perievent to ascertain the utility of the score before cardiac arrest. Scores were compared with actual outcomes. Sensitivity in our cohort was 22.7%, specificity was 57.6%, and C-index was 0.58. In conclusion, up to 75% of cardiac arrest survivors in this cohort would not have been offered a defibrillator if evaluated before their event. This casts doubt on the utility of the score model for primary prevention of sudden death. Inherent issues with modern risk scoring strategies decrease the likelihood of success even in robustly designed tools such as the Sieira score model.

Heart Rate Variability and Long Chain n-3 Polyunsaturated Fatty Acids in Chronic Kidney Disease Patients on Haemodialysis: A Cross-Sectional Pilot Study.

Low heart rate variability (HRV) is independently associated with increased risk of sudden cardiac death (SCD) and all cardiac death in haemodialysis patients. Long chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) may exert anti-arrhythmic effects. This study aimed to investigate relationships between dialysis, sleep and 24 h HRV and LC n-3 PUFA status in patients who have recently commenced haemodialysis. A cross-sectional study was conducted in adults aged 40-80 with chronic kidney disease (CKD) stage 5 (n = 45, mean age 58, SD 9, 20 females and 25 males, 39% with type 2 diabetes). Pre-dialysis blood samples were taken to measure erythrocyte and plasma fatty acid composition (wt % fatty acids). Mean erythrocyte omega-3 index was not associated with HRV following adjustment for age, BMI and use of ß-blocker medication. Higher ratios of erythrocyte eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) were associated with lower 24 h vagally-mediated beat-to-beat HRV parameters. Higher plasma EPA and docosapentaenoic acid (DPAn-3) were also associated with lower sleep-time and 24 h beat-to-beat variability. In contrast, higher plasma EPA was significantly related to higher overall and longer phase components of 24 h HRV. Further investigation is required to investigate whether patients commencing haemodialysis may have compromised conversion of EPA to DHA, which may impair vagally-mediated regulation of cardiac autonomic function, increasing risk of SCD.

Impact of Dietary Factors on Brugada Syndrome and Long QT Syndrome.

A healthy regime is fundamental for the prevention of cardiovascular diseases (CVD). In inherited channelopathies, such as Brugada syndrome (BrS) and Long QT syndrome (LQTS), unfortunately, sudden cardiac death could be the first sign for patients affected by these syndromes. Several known factors are used to stratify the risk of developing cardiac arrhythmias, although none are determinative. The risk factors can be affected by adjusting lifestyle habits, such as a particular diet, impacting the risk of arrhythmogenic events and mortality. To date, the importance of understanding the relationship between diet and inherited channelopathies has been underrated. Therefore, we describe herein the effects of dietary factors on the development of arrhythmia in patients affected by BrS and LQTS. Modifying the diet might not be enough to fully prevent arrhythmias, but it can help lower the risk.

Plasma Omega-3 Fatty Acids and the Risk of Cardiovascular Events in Patients After an Acute Coronary Syndrome in MERLIN-TIMI 36.

Background Plasma omega-3 polyunsaturated fatty acids (ω3-PUFAs) have been shown to be inversely correlated with the risk of cardiovascular death in primary prevention. The risk relationship in the setting of an acute coronary syndrome is less well established. Methods and Results Baseline plasma ω3-PUFA composition (α-linolenic acid, eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid) was assessed through gas chromatography with flame ionization detection in a case-cohort study involving 203 patients with cardiovascular death, 325 with myocardial infarction, 271 with ventricular tachycardia, and 161 with atrial fibrillation, and a random sample of 1612 event-free subjects as controls from MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation-Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 36), a trial of patients hospitalized with non-ST-segment-elevation -acute coronary syndrome. After inverse-probability-weighted multivariable adjustment including all traditional risk factors, a higher relative proportion of long-chain ω3-PUFAs (eicosapentaenoic acid, docosapentaenoic acid, docosahexaenoic acid) were associated with 18% lower odds of cardiovascular death (adjusted [adj] odds ratio [OR] per 1 SD, 0.82; 95% CI, 0.68-0.98) that was primarily driven by 27% lower odds of sudden cardiac death (adj OR per 1 SD, 0.73; 95% CI, 0.55-0.97). Long-chain ω3-PUFA levels in the top quartile were associated with 51% lower odds of cardiovascular death (adj OR 0.49; 95% CI, 0.27-0.86) and 63% lower odds of sudden cardiac death (adj OR, 0.37; 95% CI, 0.16-0.56). An attenuated relationship was seen for α-linolenic acid and subsequent odds of cardiovascular (adj OR, 0.92; 95% CI, 0.74-1.14) and sudden cardiac death (adj OR, 0.91; 95% CI, 0.67-1.25). No significant relationship was observed between any ω3-PUFAs and the odds of cardiovascular death unrelated to sudden cardiac death, myocardial infarction, atrial fibrillation, or early post-acute coronary syndrome ventricular tachycardia. Conclusions In patients after non-ST-segment-elevation-acute coronary syndrome, plasma long-chain ω3-PUFAs are inversely associated with lower odds of sudden cardiac death, independent of traditional risk factors and lipids. Registration URL: https://www.clinicaltrials.gov. Unique identifier: NCT00099788.

Public health impact of daily life triggers of sudden cardiac death: A systematic review and comparative risk assessment.

BACKGROUND: Sudden cardiac death (SCD) may be triggered by daily circumstances and activities such as stressful psycho-emotional events, physical exertion or substance misuse. We calculated population attributable fractions (PAFs) to estimate the public health relevance of daily life triggers of SCD and to compare their population impacts. METHODS: We searched PubMed, Scopus and the Web of Science citation databases to retrieve studies of triggers of SCD and cardiac arrest that would enable a computation of PAFs. When more studies investigated the same trigger, a meta-analytical pooled risk random-effect estimate was used. RESULTS: Of the retrieved studies, eight provided data enabling computation of PAFs. The prevalence of exposure within population for SCD triggers in the control periods ranged from 1.06% for influenza infection to 8.73% for recent use of cannabis. Triggers ordered from the highest to the lowest risk increase were: physical exertion, recent cocaine use, episodic alcohol consumption, recent amphetamine use, episodic coffee consumption, psycho-emotional stress within the previous month, influenza infection, and recent cannabis use. The relative risk increase ranged from 1.10 to 4.98. By accounting for both the magnitude of the risk increase and the prevalence in the population, the present estimates of PAF assign 14.5% (95% confidence interval [CI] 4.9-28.5) of all SCDs to episodic alcohol consumption, 9.4% (95% CI 1.2-29.3) to physical exertion, 6.9% (95% CI 0.3-25.0) to cocaine, 6% (95% CI 1.2-14.6) to episodic coffee consumption, 3% (95% CI 0.4-6.8) to psycho-emotional stress in the previous month, 1.7% (95% CI -0.9 to 12.9) to amphetamines, 0.9% (95% CI -4.9 to 12.5) to cannabis, and 0.3% (95% CI 0.2-0.4) to influenza infections. CONCLUSIONS: In addition to episodic alcohol consumption, a trigger with the greatest public health importance for SCD, episodic physical exertion, cocaine use and coffee consumption also show a considerable population impact.

Machine Learned Cellular Phenotypes in Cardiomyopathy Predict Sudden Death.

RATIONALE: Susceptibility to VT/VF (ventricular tachycardia/fibrillation) is difficult to predict in patients with ischemic cardiomyopathy either by clinical tools or by attempting to translate cellular mechanisms to the bedside. OBJECTIVE: To develop computational phenotypes of patients with ischemic cardiomyopathy, by training then interpreting machine learning of ventricular monophasic action potentials (MAPs) to reveal phenotypes that predict long-term outcomes. METHODS AND RESULTS: We recorded 5706 ventricular MAPs in 42 patients with coronary artery disease and left ventricular ejection fraction ≤40% during steady-state pacing. Patients were randomly allocated to independent training and testing cohorts in a 70:30 ratio, repeated K=10-fold. Support vector machines and convolutional neural networks were trained to 2 end points: (1) sustained VT/VF or (2) mortality at 3 years. Support vector machines provided superior classification. For patient-level predictions, we computed personalized MAP scores as the proportion of MAP beats predicting each end point. Patient-level predictions in independent test cohorts yielded c-statistics of 0.90 for sustained VT/VF (95% CI, 0.76-1.00) and 0.91 for mortality (95% CI, 0.83-1.00) and were the most significant multivariate predictors. Interpreting trained support vector machine revealed MAP morphologies that, using in silico modeling, revealed higher L-type calcium current or sodium-calcium exchanger as predominant phenotypes for VT/VF. CONCLUSIONS: Machine learning of action potential recordings in patients revealed novel phenotypes for long-term outcomes in ischemic cardiomyopathy. Such computational phenotypes provide an approach which may reveal cellular mechanisms for clinical outcomes and could be applied to other conditions.

[Influence of Omega-3 PUFA on Non-invasive factors determining the risk of arrhYthmias eXcess and sudden cardiac death in patients with HFpEF with ischemic etiology (ONYX)].

Aim Patients with heart failure with reduced left ventricular (LV) ejection fraction (HFrEF) who have had acute myocardial infarction have an unfavorable prognosis, largely due to ventricular arrhythmias (VA) and risk of sudden cardiac death (SCD). The optimal treatment (triple neurohormonal blockade plus implantable cardioverter defibrillator and cardiac resynchronization therapy) reduced the risk of SCD primarily due to reverse cardiac remodeling, but has not solved this problem completely. Efficacy of purified ω-3 polyunsaturated fatty acid esters (PUFA) in low doses (1 g/day) in reducing VA and risk of SCD in HFrEF patients was demonstrated in two large randomized clinical trials. The PUFA effects was suggested to be related also with increased heart rhythm variability (HRV) and chronotropic action, which might depend on the drug dose. The present open, prospective, randomized, comparative study in parallel groups evaluated the effect of Omacor in different doses on noninvasive markers of SCD risk in patients with ischemic HFrEF receiving the optimal drug therapy.Methods Patients (n=40) were randomized at a 1:1:2 ratio to the control group (n=10), the Omacor 1 g/day treatment group (n=10), and the Omacor 2 g/day treatment group (n=20) and were followed up for 12 months. Clinical evaluation included changes in the CHF functional class (FC) and Clinical Condition Scale (CCS) score; concentration of N-terminal pro-hormone brain natriuretic peptide (NT-proBNP); and peak oxygen consumption during exercise (peak VO2). The LV function was evaluated by LVEF. Holter ECG monitoring was used for evaluation of HRV (SDNN), average 24-h heart rate (HR), number of ventricular extrasystoles (VE) per hour and severity of VA, and presence of paired VE and VT runs.Results Improvement of CHF FC became significant only with the high-dose Omacor treatment (2 g/day). The CCS score showed a tendency towards decrease also with a lower dose (1 g/day) whereas the level of NT-proBNP significantly decreased with both Omacor doses. The increase in LV EF was significant only with the use of Omacor 2 g/day (+3 %, р=0.002). A negative chronotropic effect of ω-3 PUFA was observed. Average 24-h HR decreased by 8 bpm (р=0.05) and 11 bpm (р<0.001) with Omacor 1 g/day and 2 g/day, respectively. Either dose of ω-3 PUFA significantly improved VO2, which directly correlated with LV EF and inversely correlated with HR. The decrease in number of VE was associated not only with improved HRV (SDNN) but also with the decrease in 24-h HR, and thus Omacor 2 g/day significantly decreased the number of VE (by 16 per hour) and dangerous VA (paired VE and VT runs ceased to be detected in 40 % of patients).Conclusion Since HR, HRV, and VA are closely interrelated, the effect of ω-3 PUFA specifically on these noninvasive markers apparently determines its ability to decrease the risk of SCD in patients with ischemic HFrEF. The antiarrhythmic effect of Omacor was greater with higher doses of this drug.

Resuscitated sudden cardiac death due to severe hypokalemia caused by teff grain herbal tea: A case report.

Obesity is a common health problem and the prevalence is increasing worldwide. The improper and unregulated use of unconventional therapies, especially herbal treatment methods, has grown due to widespread availability. In our case, a 41-year-old male patient developed palpitation, confusion, loss of consciousness, and cardiac arrest while at home. An emergency medical team was called and chest compressions were performed by his wife until the medical team arrived. Ventricular fibrillation was detected on the monitor 5 minutes after the cardiac arrest occurred and the patient was defibrillated. A physical evaluation revealed hypotension and tachycardia. Electrocardiography (ECG) showed a fast idioventricular rhythm with capture and fusion beats and evident J waves in leads DII, DIII, and aVF. Brain magnetic resonance imaging and thoracic tomography revealed no pathology to explain his clinical condition and the coronary angiography results were not significant. The laboratory parameters included potassium (K): 2.23 mEq/L, ionized K (arterial blood): 2.43 mEq/L, sodium: 142 mEq/L, calcium: 9.3 mg/dL, creatinine: 1.6 mg/dL, pH: 7.29, cardiac troponin I: 0.12 (normal range: 0-0.11 ng/mL) and creatinine kinase mass: 8.3 (normal range: 0-3.23 ng/mL). After fluids and electrolyte replacement therapy were administered, the ECG results revealed narrow QRS complex atrial fibrillation followed by a normal sinus rhythm with a 490 ms corrected QT interval. The patient was extubated in follow-up. There were no risk factors for coronary artery disease, no history of drug or other substance use, and no exposure to excessive emotional or physical stress. The patient said that he had been consuming a large quantity of teff tea for 5 days to lose weight. He was discharged without any complications and has been asymptomatic in 9 months of follow-up. The inappropriate use of weight loss alternatives, especially herbal therapies such as teff tea, and the incidence of associated side effects are increasing due to wide availability and easy access. The general population should be warned about this issue.

2020 Canadian Cardiovascular Society/Canadian Heart Rhythm Society Position Statement on the Management of Ventricular Tachycardia and Fibrillation in Patients With Structural Heart Disease.

This Canadian Cardiovascular Society position statement is focused on the management of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) that occurs in patients with structural heart disease (SHD), including previous myocardial infarction, dilated cardiomyopathy, and other forms of nonischemic cardiomyopathy. This patient population is rapidly increasing because of advances in care and improved overall survival of patients with all forms of SHD. In this position statement, the acute and long-term management of VT/VF are outlined, and the many unique aspects of care in this population are emphasized. The initial evaluation, acute therapy, indications for chronic suppressive therapy, choices of chronic suppressive therapy, implantable cardioverter-defibrillator programming, alternative therapies, and psychosocial care are reviewed and recommendations for optimal care are provided. The target audience for this statement includes all health professionals involved in the continuum of care of patients with SHD and VT/VF.

Islets of heterogeneous myocardium within the scar in cardiac magnetic resonance predict ventricular tachycardia after myocardial infarction.

INTRODUCTION: We assessed findings in cardiac magnetic resonance (CMR) as predictors of ventricular tachycardia (VT) after myocardial infarction (MI), which could allow for more precise identification of patients at risk of sudden cardiac death. METHODS: Forty-eight patients after prior MI were enrolled and divided into two groups: with (n = 24) and without (n = 24) VT. VT was confirmed by electrophysiological study and exit site was estimated based on 12-lead electrocardiogram. All patients underwent CMR with late gadolinium enhancement. RESULTS: The examined groups did not differ significantly in clinical and demographical parameters (including LV ejection fraction). There was a significant difference in the infarct age between the VT and non-VT group (15.8 ± 8.4 vs 7.1 ± 6.7 years, respectively; P = .002), with the cut-off point at the level of 12 years. In the scar core, islets of heterogeneous myocardium were revealed. They were defined as areas of potentially viable myocardium within or adjacent to the core scar. The number of islets was the strongest independent predictor of VT (odds ratio [OR], 1.42; confidence interval [CI], 1.17-1.73), but total islet size and the largest islet area were also significantly higher in the VT group (OR, 1.04; CI, 1.02-1.07 and OR, 1.16; CI, 1.01-1.27, respectively). Myocardial segments with fibrosis forming 25%-75% of the ventricular wall were associated with a higher incidence of VT (7.5 ± 2.1 vs 5.7 ± 2.6; P = .014). Three-dimension CMR reconstruction confirmed good correlation of the location of the islets/channels with VT exit site during electroanatomical mapping in five cases. CONCLUSIONS: The identification and quantification of islets of heterogeneous myocardium within the scar might be useful for predicting VT in patients after MI.

Sex Differences in Electrophysiology, Ventricular Tachyarrhythmia, Cardiac Arrest and Sudden Cardiac Death Following Acute Myocardial Infarction.

BACKGROUND: Women experience less appropriate implantable cardioverter-defibrillator (ICD) interventions and are underrepresented in randomised ICD trials. Sex-differences in inducible and spontaneous ventricular tachycardia/fibrillation (VT/VF), cardiac arrest and sudden cardiac death (SCD) early post-myocardial infarction (MI) require further study. METHODS: Consecutive ST-elevation MI patients with left ventricular ejection fraction (LVEF)≤40% underwent electrophysiology study (EPS) to target early prevention of SCD. An ICD was implanted for a positive (inducible monomorphic VT) but not a negative (no arrhythmia or inducible VF) EPS. The combined primary endpoint of VT/VF (spontaneous or ICD-treated), cardiac arrest or SCD was assessed using competing risk survival analysis in women versus men with adjustment for confounders. Logistic regression was used to determine independent predictors of inducible VT at EPS. RESULTS: A total of 403 patients (16.9% female) underwent EPS. Women were significantly older than men but with similar LVEF (31.5 ± 6.3 versus 31.6 ± 6.4%, p = 0.91). Electrophysiology study was positive for inducible VT in 22.1% and 33.4% (p = 0.066) and an ICD implanted in 25.0% and 33.4% (p = 0.356) of women versus men. Appropriate ICD activations (VT/VF) occurred in 5.9% of women and 36.6% of men (p = 0.012). The adjusted cumulative primary endpoint incidence was significantly lower in women than men (1.6% versus 26.5%, p = 0.03). Female sex was not an independent predictor of inducible VT at EPS (HR 0.63, 95% CI 0.33-1.23, p = 0.178). CONCLUSIONS: Women with early post-MI cardiomyopathy had lower VT/VF, cardiac arrest and SCD, compared to men. In ICD recipients the rate of appropriate activations was six-fold less in women compared to men.

Association of Vitamin D Deficiency with Profound Cardiogenic Shock in Patients Resuscitated From Sudden Cardiac Arrest.

BACKGROUND: Vitamin D deficiency is associated with various cardiovascular diseases, including sudden cardiac arrest (SCA). Profound cardiogenic shock is associated with morbidity and mortality in patients with SCA. This study investigated the association of vitamin D deficiency with profound cardiogenic shock in patients resuscitated from SCA. PATIENTS AND METHODS: We enrolled patients who were successfully resuscitated from out-of-hospital cardiac arrests of a presumed cardiac cause. Profound cardiogenic shock was defined as refractory hypotension requiring high-dose vasopressor infusion (norepinephrine >0.5 mcg/kg/min) despite adequate intravascular volume replacement. Vitamin D levels were measured as plasma 25(OH)D concentrations and severe vitamin D deficiency was defined as 25(OH)D <10 ng/mL. RESULTS: A total of 237 subjects (179 men (76%), mean age 56.5 ±â€Š16.5 years) were included in this study. The first monitored rhythm was shockable in 160 subjects (68%). Mean arrest time and CPR times were 25.6 ±â€Š15.7 and 22.8 ±â€Š15.0 min, respectively. Profound cardiogenic shock was observed in 100 subjects (42%). The mean vitamin D level was 12.3 ±â€Š6.7 ng/mL, and vitamin D deficiency was diagnosed in 109 subjects (46%). In profound cardiogenic shock subjects, vitamin D levels were significantly lower (10.7 ±â€Š7.0 vs. 13.4 ±â€Š6.2 ng/mL, P = 0.002) and severe vitamin D deficiency was observed more frequently (63% vs. 34%, P < 0.001). Subjects with profound cardiogenic shock were likely to have longer arrest times (29.5 ±â€Š17.0 vs. 22.7 ±â€Š14.0 min, P = 0.001), left ventricular systolic dysfunction (LVEF < 40%, 73% vs. 38%, P < 0.001), and baseline renal dysfunction (65% vs. 37%, P < 0.001). Multivariate logistic analysis indicated that vitamin D deficiency was significantly associated with profound cardiogenic shock after SCA (OR 2.71, 95% CI 1.42-5.18, P = 0.003) after adjusting for confounding variables. CONCLUSIONS: Severe vitamin D deficiency was strongly associated with profound cardiogenic shock and mortality in patients resuscitated from SCA.

The Effect of Marine n-3 Polyunsaturated Fatty Acids on Heart Rate Variability in Renal Transplant Recipients: A Randomized Controlled Trial.

Resting heart rate (rHR) and heart rate variability (HRV) are non-invasive measurements that predict the risk of sudden cardiac death (SCD). Marine n-3 polyunsaturated fatty acid (PUFA) supplementation may decrease rHR, increase HRV, and reduce the risk of SCD. To date, no studies have investigated the effect of marine n-3 PUFA on HRV in renal transplant recipients. In a randomized controlled trial, 132 renal transplant recipients were randomized to receive either three 1 g capsules of marine n-3 PUFA, each containing 460 mg/g EPA and 380 mg/g DHA, or control (olive oil) for 44 weeks. HRV was calculated in the time and frequency domains during a conventional cardiovascular reflex test (response to standing, deep breathing, and Valsalva maneuver) and during 2 min of resting in the supine position. There was no significant effect of marine n-3 PUFA supplementation on time-domain HRV compared with controls. rHR decreased 3.1 bpm (± 13.1) for patients receiving marine n-3 PUFA compared to 0.8 (± 11.0) in controls (p = 0.28). In the frequency domain HRV analyses, there was a significant change in response to standing in both high and low frequency measures, 2.9 (p = 0.04, 95% CI (1.1;8)) and 2.7 (p = 0.04, 95% CI (1.1;6.5)), respectively. In conclusion, 44 weeks of supplemental marine n-3 PUFAs in renal transplant recipients significantly improved the cardiac autonomic function, assessed by measuring HRV during conventional cardiovascular reflex tests.