The effects of a music intervention on the autonomic nervous system during recovery from strenuous exercise.

OBJECTIVE: To investigate the effect of music on heart rate recovery (HRR) and heart rate variability (HRV) after intense exertion. METHODS: Five hundred male students enrolled at Yongin University, Korea, underwent a cycling test to assess aerobic capacity; 180 students with equal scores were selected for a music intervention, which was conducted after vigorous exercise. The 180 participants were randomized into three music groups and a control group; the participants in each music group listened to music at three different tempos: slow (lento) (n = 45), moderate (moderato) (n = 45), and fast (allegretto) (n = 45). The control group did not listen to music (n = 45). After the test, data on cardiac recovery and HRV were gathered and modeled. RESULTS: The results revealed no significant variation in HRR and HRV indexes between the four cohorts (p > .05), and no significant differences were observed in the anaerobic power cycling indexes during strenuous exercise (p > .05). The music intervention had a significant impact on HR, low-frequency power (LF), high-frequency power (HF), normalized LF (LFnorm ), normalized HF (HFnorm ), and the LF/HF ratio during recovery (p < .05). CONCLUSION: After rigorous activity, listening to allegretto music improved HRR and restored HRV equilibrium, which is critical to preventing and minimizing arrhythmias and sudden cardiac death.

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.

Diet and Sudden Death: How to Reduce the Risk.

In addition to the association of dietary patterns, specific foods and nutrients with several diseases, including cardiovascular disease and mortality, there is also strong emerging evidence of an association of dietary patterns with the risk of sudden cardiac death (SCD). In this comprehensive review, data are presented and analyzed about foods and diets that mitigate the risk of ventricular arrhythmias (VAs) and SCD, but also about arrhythmogenic nutritional elements and patterns that seem to enhance or facilitate potentially malignant VAs and SCD. The antiarrhythmic or protective group comprises fish, nuts and other foods enriched in omega-3 polyunsaturated fatty acids, the Mediterranean and other healthy diets, vitamins E, A and D and certain minerals (magnesium, potassium, selenium). The arrhythmogenic-food group includes saturated fat, trans fats, ketogenic and liquid protein diets, the Southern and other unhealthy diets, energy drinks and excessive caffeine intake, as well as heavy alcohol drinking. Relevant antiarrhythmic mechanisms include modification of cell membrane structure by n-3 polyunsaturated fatty acids, their direct effect on calcium channels and cardiomyocytes and their important role in eicosanoid metabolism, enhancing myocyte electric stability, reducing vulnerability to VAs, lowering heart rate, and improving heart rate variability, each of which is a risk factor for SCD. Contrarily, saturated fat causes calcium handling abnormalities and calcium overload in cardiomyocytes, while a high-fat diet causes mitochondrial dysfunction that dysregulates a variety of ion channels promoting VAs and SCD. Free fatty acids have been considered proarrhythmic and implicated in facilitating SCD; thus, diets increasing free fatty acids, e.g., ketogenic diets, should be discouraged and replaced with diets enriched with polyunsaturated fatty acids, which can also reduce free fatty acids. All available relevant data on this important topic are herein reviewed, large studies and meta-analyses and pertinent advisories are tabulated, while protective (antiarrhythmic) and arrhythmogenic specific diet constituents are pictorially illustrated.

Computational Model for Therapy Optimization of Wearable Cardioverter Defibrillator: Shockable Rhythm Detection and Optimal Electrotherapy.

Wearable cardioverter defibrillator (WCD) is a life saving, wearable, noninvasive therapeutic device that prevents fatal ventricular arrhythmic propagation that leads to sudden cardiac death (SCD). WCD are frequently prescribed to patients deemed to be at high arrhythmic risk but the underlying pathology is potentially reversible or to those who are awaiting an implantable cardioverter-defibrillator. WCD is programmed to detect appropriate arrhythmic events and generate high energy shock capable of depolarizing the myocardium and thus re-initiating the sinus rhythm. WCD guidelines dictate very high reliability and accuracy to deliver timely and optimal therapy. Computational model-based process validation can verify device performance and benchmark the device setting to suit personalized requirements. In this article, we present a computational pipeline for WCD validation, both in terms of shock classification and shock optimization. For classification, we propose a convolutional neural network-"Long Short Term Memory network (LSTM) full form" (Convolutional neural network- Long short term memory network (CNN-LSTM)) based deep neural architecture for classifying shockable rhythms like Ventricular Fibrillation (VF), Ventricular Tachycardia (VT) vs. other kinds of non-shockable rhythms. The proposed architecture has been evaluated on two open access ECG databases and the classification accuracy achieved is in adherence to American Heart Association standards for WCD. The computational model developed to study optimal electrotherapy response is an in-silico cardiac model integrating cardiac hemodynamics functionality and a 3D volume conductor model encompassing biophysical simulation to compute the effect of shock voltage on myocardial potential distribution. Defibrillation efficacy is simulated for different shocking electrode configurations to assess the best defibrillator outcome with minimal myocardial damage. While the biophysical simulation provides the field distribution through Finite Element Modeling during defibrillation, the hemodynamic module captures the changes in left ventricle functionality during an arrhythmic event. The developed computational model, apart from acting as a device validation test-bed, can also be used for the design and development of personalized WCD vests depending on subject-specific anatomy and pathology.

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.

Anti-Ro/SSA Antibodies and the Autoimmune Long-QT Syndrome.

Autoimmunity is increasingly recognized as a novel pathogenic mechanism for cardiac arrhythmias. Several arrhythmogenic autoantibodies have been identified, cross-reacting with different types of surface proteins critically involved in the cardiomyocyte electrophysiology, primarily ion channels (autoimmune cardiac channelopathies). Specifically, some of these autoantibodies can prolong the action potential duration leading to acquired long-QT syndrome (LQTS), a condition known to increase the risk of life-threatening ventricular arrhythmias, particularly Torsades de Pointes (TdP). The most investigated form of autoimmune LQTS is associated with the presence of circulating anti-Ro/SSA-antibodies, frequently found in patients with autoimmune diseases (AD), but also in a significant proportion of apparently healthy subjects of the general population. Accumulating evidence indicates that anti-Ro/SSA-antibodies can markedly delay the ventricular repolarization via a direct inhibitory cross-reaction with the extracellular pore region of the human-ether-a-go-go-related (hERG) potassium channel, resulting in a higher propensity for anti-Ro/SSA-positive subjects to develop LQTS and ventricular arrhythmias/TdP. Recent population data demonstrate that the risk of LQTS in subjects with circulating anti-Ro/SSA antibodies is significantly increased independent of a history of overt AD, intriguingly suggesting that these autoantibodies may silently contribute to a number of cases of ventricular arrhythmias and cardiac arrest in the general population. In this review, we highlight the current knowledge in this topic providing complementary basic, clinical and population health perspectives.

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.

Clinical Approach to Symptomatic and Asymptomatic Patients with Ventricular Pre-excitation.

Despite extensive knowledge of the physiopathology of ventricular pre-excitation, management of asymptomatic patients with this condition remains controversial.

Cardiac Arrhythmia Prevention in Ischemia and Reperfusion by Low-Dose Dietary Fish Oil Supplementation in Rats.

BACKGROUND: Supplementing animal diets with fish oil increases myocardial omega-3 polyunsaturated fatty acids [ω-3 (n-3) PUFA], lowers heart rate, and prevents malignant cardiac arrhythmias. In contrast to epidemiological reports, results of some human clinical trials and of unphysiologically high doses employed in animal studies call into question the application of dietary ω-3 PUFA for cardioprotection. OBJECTIVE: This study tested the hypothesis that low ω-3 PUFA dietary thresholds for myocardial incorporation in rats, equivalent in dose to what humans derive from eating fish, can reduce heart rate and arrhythmia vulnerability. METHODS: Male Sprague-Dawley rats (12-15 wk old) were fed isoenergetic diets containing 10% fat for 4-5 wk. The control diet (CON) contained 5.5% beef tallow, 2.5% sunflower seed oil, and 2% olive oil. Fish oil diets contained high-DHA tuna oil, exchanged for olive oil: 0.31% [fish oil group 1 (FO1)] (human equivalent EPA + DHA 570 mg/d); 1.25% [fish oil group 2 (FO2)] (equivalent EPA + DHA 2.3 g/d). Anaesthetized rats (pentobarbital, 60 mg/kg intraperitoneally) were subjected in vivo to 15-min cardiac ischemia by left coronary artery occlusion and then reperfusion, with arrhythmias detected by electrocardiogram. RESULTS: Fish oil dose dependently modulated myocardial membrane fatty acids (DHA mean ± SEM: CON, 5.0 ± 0.2%; FO1, 13.1 ± 0.9%; FO2, 18.3 ± 0.4%; n = 4-5; P-trend < 0.001 ANOVA); resting heart rate (CON, 453 ± 6; FO1, 432 ± 4; FO2, 422 ± 5 bpm; n = 15-18; P-trend < 0.001); reduced ventricular fibrillation (VF) (CON, 89%; FO1, 60%; P = 0.052; FO2, 50%; n = 15-18; P = 0.013 chi square); and total arrhythmia severity (arrhythmia score: CON, 6.1 ± 0.4; FO1, 4.6 ± 0.5; FO2, 3.1 ± 0.7; n = 15-18; P-trend < 0.01) during ischemia and reperfusion (VF: Con, 86%; FO1, 22% P = 0.011; FO2, 8% P = 0.001; n = 7-12); (arrhythmia score: CON, 4.6 ± 0.3; FO1, 3.1 ± 0.3; FO2, 1.3 ± 0.3; n = 7-12; P-trend < 0.001). CONCLUSIONS: Ventricular arrhythmias were prevented and heart rate was slowed by lower ω-3 PUFA intake in rats than previously reported, equivalent to human fish consumption and associated with increased myocardial DHA. The efficacy of low-dose fish oil demonstrates biological plausibility for nutritional ω-3 fatty acid-mediated cardioprotection and suggests that effectiveness in human clinical trials may be obscured by failure to exclude fish eaters.

Ventricular Fibrillation Caused by Primary Carnitine Deficiency.

BACKGROUND: Primary carnitine deficiency (PCD) is a rare but potentially life-threatening genetic disorder if left untreated. Although some patients remain asymptomatic lifelong, a few patients present with hepatic encephalopathy, hypoglycemia, cardiomyopathy, dysrhythmia, and even sudden death. CASE REPORT: A 25-year-old woman with PCD collapsed suddenly while eating lunch. Bystander cardiopulmonary resuscitation (CPR) was performed for 8 min, with automated external defibrillation once before admission. Upon arrival at our emergency department (ED), she was unresponsive without a pulse or spontaneous breathing. The initial heart rhythm on the electrocardiogram monitor was ventricular fibrillation (VF). The medical staff continued CPR with defibrillation for sustained VF. Return of spontaneous circulation (ROSC) was achieved after a total resuscitation time of 14 min, with defibrillation twice after cardiac arrest. The heart rhythm after ROSC was atrial fibrillation, with a rapid ventricular rate initially and subsequent progression to sinus tachycardia with diffuse ST segment depression and a prolonged QT interval. Her low carnitine level was consistent with her underlying disease. Cardiac magnetic resonance imaging and sonography for detection of cardiomyopathy showed no significant findings. With carnitine supplementation for a few days, her plasma carnitine level returned to 30 µM, with no recurrence of ventricular dysrhythmia. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: PCD is rare but could be life-threatening, and compiling detailed histories may help emergency physicians to determine the cause of sudden cardiac death after resuscitation. This information may be used to correct potential underlying problems and prevent recurrence of the condition after treatment.

Effect of the antipsychotic drug haloperidol on arrhythmias during acute myocardial infarction in a porcine model.

Patients receiving psychiatric medication, like the antipsychotic drug haloperidol, are at an increased risk of sudden cardiac death (SCD). Haloperidol blocks the cardiac rapidly-activating delayed rectifier potassium current, thereby increasing electrical dispersion of repolarization which can potentially lead to arrhythmias. Whether these patients are also at a higher risk to develop SCD during an acute myocardial infarction (AMI) is unknown. AMI locally shortens action potential duration, which might further increase repolarization dispersion and increase the risk of arrhythmia in the presence of haloperidol compared to without. Our aim was to test whether treatment with haloperidol implies an increased risk of SCD when eventually experiencing AMI. Twenty-eight female Danish Landrace pigs were randomized into three groups: low dose haloperidol (0.1 mg/kg), high dose (1.0 mg/kg) or vehicle-control group. One hour after haloperidol/vehicle infusion, AMI was induced by balloon-occlusion of the mid-left anterior descending coronary artery and maintained for 120 min, followed by 60 min of reperfusion. VF occurred during occlusion in 7/11 pigs in the control group, 3/11 in the low dose (p = 0.198) and 2/6 in the high dose group (p = 0.335). High dose haloperidol significantly prolonged QT, and reduced heart rate, vascular resistance and blood pressure before and during AMI. Premature ventricular contractions in phase 1b during AMI were reduced with high dose haloperidol. AMI-induced arrhythmia was not aggravated in pigs with haloperidol treatment. Our results do not suggest that AMI is contributing to the excess mortality in patients treated with antipsychotic drugs seen in epidemiological studies.

Subcutaneous nerve stimulation reduces sympathetic nerve activity in ambulatory dogs with myocardial infarction.

BACKGROUND: Subcutaneous nerve stimulation (ScNS) remodels the stellate ganglion and reduces stellate ganglion nerve activity (SGNA) in dogs. Acute myocardial infarction (MI) increases SGNA through nerve sprouting. OBJECTIVE: The purpose of this study was to test the hypothesis that ScNS remodels the stellate ganglion and reduces SGNA in ambulatory dogs with acute MI. METHODS: In the experimental group, a radio transmitter was implanted during the first sterile surgery to record nerve activity and an electrocardiogram, followed by a second sterile surgery to create MI. Dogs then underwent ScNS for 2 months. The average SGNA (aSGNA) was compared with that in a historical control group (n = 9), with acute MI monitored for 2 months without ScNS. RESULTS: In the experimental group, the baseline aSGNA and heart rate were 4.08±0.35 µV and 98±12 beats/min, respectively. They increased within 1 week after MI to 6.91±1.91 µV (P=.007) and 107±10 beats/min (P=.028), respectively. ScNS reduced aSGNA to 3.46±0.44 µV (P<.039) and 2.14±0.50 µV (P<.001) at 4 and 8 weeks, respectively, after MI. In comparison, aSGNA at 4 and 8 weeks in dogs with MI but no ScNS was 8.26±6.31 µV (P=.005) and 10.82±7.86 µV (P=0002), respectively. Immunostaining showed confluent areas of remodeling in bilateral stellate ganglia and a high percentage of tyrosine hydroxylase-negative ganglion cells. Terminal deoxynucleotidyl transferase dUTP nick end labeling was positive in 26.61%±11.54% of ganglion cells in the left stellate ganglion and 15.94%±3.62% of ganglion cells in the right stellate ganglion. CONCLUSION: ScNS remodels the stellate ganglion, reduces SGNA, and suppresses cardiac nerve sprouting after acute MI.

Association of Dietary Magnesium Intake with Fatal Coronary Heart Disease and Sudden Cardiac Death.

Background: Postmenopausal women represent the highest population-based burden of cardiovascular disease, including sudden cardiac death (SCD). Our understanding of the etiology and risk factors contributing to fatal coronary heart disease (CHD) and SCD, particularly among women, is limited. This study examines the association between dietary magnesium intake and fatal CHD and SCD. Materials and Methods: We examined 153,569 postmenopausal women who participated in the Women's Health Initiative recruited between 1993 and 1998. Magnesium intake at baseline was assessed using a validated food frequency questionnaire, adjusting for energy via the residual method. Fatal CHD and SCD were identified over an average follow-up of 10.5 years. Results: For every standard deviation increase in magnesium intake, there was statistically significant risk reduction, after adjustment for confounders, of 7% for fatal CHD (hazard ratio [HR] 0.93, 95% confidence interval [CI] 0.89-0.97), and 18% risk reduction for SCD (HR 0.82, 95% CI 0.58-1.15) the latter of which did not reach statistical significance. In age-adjusted quartile analysis, women with the lowest magnesium intake (189 mg/day) had the greatest risk for fatal CHD (HR 1.54, 95% CI 1.40-1.69) and SCD (HR 1.70, 95% CI 0.94-3.07). This association was attenuated in the fully adjusted model, with HRs of 1.19 (95% CI 1.06-1.34) for CHD and 1.24 (95% CI 0.58-2.65) for SCD for the lowest quartile of magnesium intake. Conclusions: This study provides evidence of a potential inverse association between dietary magnesium and fatal CHD and a trend of magnesium with SCD in postmenopausal women. Future studies should confirm this association and consider clinical trials to test whether magnesium supplementation could reduce fatal CHD in high-risk individuals.

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.

Difficulties with invasive risk stratification performed under anesthesia in pediatric Wolff-Parkinson-White Syndrome.

BACKGROUND: Children with Wolff-Parkinson-White Syndrome (WPW) are at risk for sudden death. The gold standard for risk stratification in this population is the shortest pre-excited RR interval during atrial fibrillation (SPERRI). OBJECTIVE: The purpose of this study was to determine how closely measurements made in the electrophysiology laboratory in patients with WPW compared to SPERRI obtained during an episode of clinical pre-excited atrial fibrillation (Clinical-SPERRI). METHODS: This was a subgroup analysis of a multicenter study of children with WPW. Subjects in our study (N = 49) were included if they had Clinical-SPERRI measured in addition to 1 or more of 3 surrogate measurements: SPERRI obtained during electrophysiological study (EP-SPERRI), accessory pathway effective refractory period (APERP), or shortest pre-excited paced cycle length with 1:1 conduction (SPPCL). RESULTS: Seventy percent of electrophysiological measurements were made with patients under general anesthesia. Clinical-SPERRI moderately correlated with EP-SPERRI (r = 0.495; P = .012). However, 24% of our patients with Clinical-SPERRI ≤250 ms would have been misclassified as having a low-risk pathway based on EP-SPERRI >250 ms. Clinical-SPERRI did not correlate with APERP or SPPCL (r < 0.3; P >.1). Mean EP-SPERRI, APERP, and SPPCL all were greater than Clinical-SPERRI. CONCLUSION: Electrophysiology laboratory measurements of pathway characteristics made with patients under general anesthesia do not correlate well with Clinical-SPERRI. Of APERP, SPPCL, and EP-SPERRI, only EP-SPERRI had moderate correlation with Clinical-SPERRI. This study questions the predictive ability of invasive risk stratification with patients under general anesthesia, given that 24% of patients with high-risk Clinical-SPERRI (≤250 ms) had EP-SPERRI that may be considered low risk (>250 ms).

The Spectrum of Idiopathic Ventricular Fibrillation and J-Wave Syndromes: Novel Mapping Insights.

Idiopathic ventricular fibrillation and J-wave syndromes are causes of sudden cardiac death (SCD) without any identified structural cardiac disease after extensive investigations. Recent data show that high-density electrophysiological mapping may ultimately offer diagnoses of subclinical diseases in most patients including those termed "unexplained" SCD. Three major conditions can underlie the occurrence of SCD: (1) localized depolarization abnormalities (due to microstructural myocardial alteration), (2) Purkinje abnormalities manifesting as triggering ectopy and inducible reentry; or (3) repolarization heterogeneities. Each condition may result from a spectrum of pathophysiologic processes with implications for individual therapy.

Clinical characteristics and long-term clinical course of patients with Brugada syndrome without previous cardiac arrest: a multiparametric risk stratification approach.

AIMS: Risk stratification in Brugada syndrome (BrS) still represents an unsettled issue. In this multicentre study, we aimed to evaluate the clinical characteristics and the long-term clinical course of patients with BrS. METHODS AND RESULTS: A total of 111 consecutive patients (86 males; aged 45.3 ± 13.3 years) diagnosed with BrS were included and followed-up in a prospective fashion. Thirty-seven patients (33.3%) were symptomatic at enrolment (arrhythmic syncope). An electrophysiological study (EPS) was performed in 59 patients (53.2%), and ventricular arrhythmias were induced in 32 (54.2%). A cardioverter defibrillator was implanted in 34 cases (30.6%). During a mean follow-up period of 4.6 ± 3.5 years, appropriate device therapies occurred in seven patients. Event-free survival analysis (log-rank test) showed that spontaneous type-1 electrocardiogram pattern (P = 0.008), symptoms at presentation (syncope) (P = 0.012), family history of sudden cardiac death (P < 0.001), positive EPS (P = 0.024), fragmented QRS (P = 0.004), and QRS duration in lead V2 > 113 ms (P < 0.001) are predictors of future arrhythmic events. Event rates were 0%, 4%, and 60% among patients with 0-1 risk factor, 2-3 risk factors, and 4-5 risk factors, respectively (P < 0.001). Current multiparametric score models exhibit an excellent negative predictive value and perform well in risk stratification of BrS patients. CONCLUSIONS: Multiparametric models including common risk factors appear to provide better risk stratification of BrS patients than single factors alone.