[The risk patient in anesthesia. Arrhythmia as a risk factor].
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Anesthesia↗
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Kv11.1 (hERG) Protein Interaction Networks Connect Endocytic Trafficking to Polygenic Influences on Cardiac Repolarization.
Polygenic scores (PGS) capture the combined effect of many common genetic variants on quantitative traits and disease risk, yet their functional consequences at the protein level remain poorly defined. Here, we integrated quantitative and interaction proteomics to resolve how polygenic liability for cardiac repolarization manifests in human cells. We studied human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from donors with extreme PGS for QT interval duration, a clinically relevant electrophysiologic trait associated with arrhythmia risk. Global quantitative proteomics revealed increased abundance of mitochondrial proteins in high-PGS cardiomyocytes. To define protein network-level effects on a key repolarizing ion channel, we performed multiplexed affinity purification-mass spectrometry (AP-MS) of Kv11.1. While mitochondrial changes did not directly explain Kv11.1-associated complexes, interactome analysis revealed increased association of Kv11.1 with myosin motor proteins and endosomal recycling machinery in high-PGS cells. These findings suggest altered channel trafficking dynamics of Kv11.1, distinct from the trafficking defects observed in monogenic Kv11.1 variants. Together, these data show that integrating global and interaction proteomics can resolve how polygenic variation reshapes protein networks. Future work using these methods could connect genomic risk to subcellular remodeling and our work provides a generalizable framework to probe the proteomic basis of complex traits. SIGNIFICANCE STATEMENT: Polygenic scores (PGS) predict disease risk, but how biological pathways are influenced by these common variants remains difficult to define. We generated human induced pluripotent stem cells from individuals with extreme high- and low- PGS for QT interval, a key electrocardiographic measure linked to arrhythmia risk. By combining global proteomics and interactomics for a common ion channel involved in regulating the QT interval (Kv11.1) we found potential mechanisms that are influenced by common genetic traits in patients. Our work provides an approach to connect polygenic scores to pathway-level molecular mechanisms in human cells and a general framework for uncovering how complex genetic architecture drives disease-relevant biology.
AP-MS↗
Arrhythmia and cardiomyopathy risk in Taiwan with complementary biobank evidence on thyroid genetic susceptibility: an integrative population-based framework.
BACKGROUND: Arrhythmia-induced cardiomyopathy (AiCM) is a potentially reversible cause of ventricular dysfunction; however, only a subset of patients with arrhythmia develop cardiomyopathy. Emerging evidence suggests that endocrine factors, particularly thyroid dysfunction with genetic susceptibility, may contribute to inter-individual variability in arrhythmia-related myocardial outcomes. METHODS: We performed a dual-cohort population-based study using the National Health Insurance Research Database (NHIRD, 2000-2015) and the Taiwan Biobank (TWB). In NHIRD, we examined the association between newly diagnosed arrhythmia and incident cardiomyopathy using Cox proportional hazards models. In TWB, genome-wide data, thyroid-stimulating hormone (TSH), polygenic risk scores (PRSs), lifestyle factors, and metabolic comorbidities were analyzed using multivariable regression and interaction models to assess determinants of thyroid dysfunction. RESULTS: In the NHIRD cohort, arrhythmia was associated with a significantly increased risk of incident cardiomyopathy (adjusted hazard ratio (aHR): 2.49, 95% CI: 1.94-2.96), with atrial fibrillation showing the strongest association among arrhythmia subtypes. In the TWB cohort, a higher thyroid polygenic risk score was strongly associated with thyroid dysfunction (adjusted odds ratio (aOR): 6.64, 95% CI: 5.86-7.52). The association between genetic susceptibility and thyroid dysfunction was further modified by metabolic and lifestyle factors, including diabetes, hyperlipidemia, and dietary patterns. Genome-wide analysis identified multiple loci associated with thyroid-stimulating hormone regulation, consistent with a polygenic architecture of thyroid endocrine traits. CONCLUSION: Arrhythmia was associated with an increased risk of cardiomyopathy in a nationwide cohort, while thyroid genetic susceptibility was strongly associated with thyroid dysfunction in a biobank cohort and modified by metabolic and lifestyle factors. These findings provide complementary population-level evidence of parallel cardiovascular and endocrine-genetic associations. Because the two cohorts were not individually linked, causal inference cannot be established. The results support a systems-level framework of endocrine-cardiac interaction and suggest that integrated clinical and genetic risk assessment may help identify individuals who warrant closer monitoring.
arrhythmia↗
The electrocardiographic recognition of cardiac states at high risk of ventricular arrhythmias. An experimental study in dogs.
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Animals↗
Monitoring for serious arrhythmias and high risk of sudden death.
Ventricular premature beats (VPBs) are present in 85% of patients with coronary heart disease (CHD). A classification of VPBs based on frequency, multiformity, repetitive pattern, and degree of prematurity promises to aid in identifying patients at high risk of sudden death. Advanced grade or repetitive forms of VPBs are observed in 41% of patients with CHD who are monitored for 24 hours while ambulatory. Exercise stress is less effective than monitoring, but when advanced grades are exposed by exercise, they are likely to be persistent for two or more hours during monitoring. Such persistent and advanced grades characterize patients with multivessel coronary artery disease. Diurnal variations occur in VPB frequency and pattern with significant reduction during sleep. This as well as other facts suggest a primary role for neural activity in the genesis of ventricular ectopy. The relevance of these observations to sudden death is considered.
Aged↗
[Indications and risks of anti-arrhythmia treatment with propafenone (author's transl)].
Propafenone, a new anti-arrhythmia drug, was given at an average dose of 70-140 mg (1-2 mg/kg body-weight) to 124 patients with various types of cardiac arrhythmias. It proved successful in patients with ectopic beats and tachycardias of atrial or ventricular origin. Ectopic beats were suppressed in 40 of 81 patients, while sinus rhythm was restored in 15 of 19 patients with paroxysmal tachycardias. On the other hand, sinus rhythm was restored in only 5 of 22 patients with atrial tachy-arrhythmias, while in most of the others in this group the heart rate decreased markedly during propafenone injection. The effect of propafenone was on atrial and ventricular myocardium and on the conduction system, lowering the discharge rate of sinus node and ectopic pacemakers. ECG signs of pre-excitation disappeared in 4 of 9 patients with WPW syndrome given the drug. Propafenone may prolong atrioventricular and intraventricular conduction, as well as cause a transitory decrease in cardiac function and a fall in systemic arterial blood pressure. It should, therefore, not be given to patients in severe heart failure, hypotension or shock, or with high-degree atrioventricular, intraventricular or sinoatrial block.
Adult↗
Risk stratification in short QT syndrome: Findings from a pooled analysis.
BACKGROUND: In long QT syndrome, longer QT intervals indicate increased arrhythmic risk, and a rate-corrected QT interval (QTc) of ≥500 ms denotes high risk. Establishing similar associations in short QT syndrome (SQTS) remains elusive. OBJECTIVE: This study aimed to demonstrate that shorter QT intervals denote a higher risk of malignant arrhythmias in SQTS and to define the "high-risk" QTc value in SQTS. METHODS: Pooled analysis of patients treated in our institutions or those reported in the literature revealed 162 patients with SQTS and known symptomatic status; 57 of them (35.2%) had arrhythmic symptoms (sudden death, cardiac arrest, or malignant syncope). RESULTS: There was a significant inverse association between the QTc and arrhythmic symptoms (with a median QTc of 315.0 ms [interquartile range 300.5-338.0] among symptomatic patients vs 330.0 ms [interquartile range 312.5-355.0] among asymptomatic patients; P = .0023). Receiver operator characteristics analysis showed that shorter QTc values were associated with a higher risk (area under the curve 0.64 ± 0.04; P = .0024). When patients were grouped by QTc range, most of those with a QTc of ≤320 ms had malignant arrhythmic symptoms, whereas the reverse was true for those with a QTc of ≥320 ms. Male patients were overrepresented in the SQTS cohort and more so in the subgroup with malignant symptoms. CONCLUSION: This pooled analysis of patients with SQTS demonstrates that, among patients with congenital SQTS, a shorter QTc is associated with a higher risk of malignant ventricular arrhythmias. A QTc shorter than 320 ms correlates with a higher arrhythmic risk. Men seem to be at higher risk.
Humans↗
Mechanisms of arrhythmias in chronic obstructive lung disease.
Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.
Aged↗
Prevalence and Prognostic Significance of Exercise-Accentuated J-Point Elevation in Brugada Syndrome.
BACKGROUND: The clinical significance of accentuation of precordial J-point elevation during exercise in Brugada syndrome (BrS) remains unclear. OBJECTIVES: This study sought to determine the prevalence and prognostic significance of accentuation of J-point elevation during exercise in a large single-center BrS cohort. METHODS: In this retrospective study, 141 consecutive patients referred for BrS evaluation (95 with type 1 BrS pattern-BrS1 cohort, 46 without type 1 pattern but with loss-of-function sodium voltage-gated channel alpha subunit 5 variants-SCN5A cohort) who underwent exercise stress testing (EST) from January 1, 2000, through October 31, 2025 were included. Two blinded cardiologists reviewed all tracings. An exercise-accentuated BrS phenotype was defined as J-point elevation increase ≥1 mm in V1/V2 during exercise. Cardiac events included arrhythmic syncope, cardiac arrest, and appropriate implantable cardioverter-defibrillator shocks. Firth penalized logistic regression was used for unadjusted and adjusted analyses. RESULTS: Overall, 41 patients (29%) demonstrated an exercise-accentuated BrS phenotype, emerging near peak exercise (median 90% age-predicted maximum heart rate). The phenotype was highly reproducible on serial testing (88% of follow-up ESTs). Exercise-accentuated phenotype was not associated with overall cardiac events (unadjusted OR: 1.83 [0.84-3.99]; P = 0.13; adjusted OR: 1.22 [0.47-3.21]; P = 0.69). However, it was strongly associated with exertion-triggered cardiac events (unadjusted OR: 10.50 [2.94-37.50]; P < 0.001; adjusted OR: 10.04 [2.76-36.53]; P < 0.001), independent of sex, exercise workload, and baseline type 1 pattern. Consistent results were noted in SCN5A variant-positive patients. CONCLUSIONS: Exercise-induced accentuation of J-point elevation reproducibly identifies a subset of BrS patients at risk for exertional cardiac events. These findings support the inclusion of EST in the evaluation of patients with a clinical diagnosis or genetic susceptibility to BrS and may inform exercise-related risk counseling.
Brugada syndrome↗
Association between plasma homocysteine levels and P-wave dispersion in pediatric patients with hyperhomocysteinemia.
UNLABELLED: Hyperhomocysteinemia has been recognized as a cardiovascular risk factor associated with endothelial dysfunction, oxidative stress, and vascular inflammation. Experimental and clinical studies suggest that elevated homocysteine levels may also influence myocardial electrophysiology and contribute to arrhythmogenesis. However, data regarding the relationship between homocysteine levels and electrocardiographic markers of atrial conduction in pediatric populations remain limited. This study aimed to evaluate the association between plasma homocysteine levels and electrocardiographic parameters, particularly P-wave dispersion, in children. This multicenter retrospective case-control study included pediatric patients evaluated in four tertiary pediatric metabolism centers between January 2023 and December 2025. A total of 47 patients with hyperhomocysteinemia (plasma total homocysteine ≥ 15 µmol/L) and 43 age- and sex-matched controls with normal homocysteine levels were included. Controls were selected from the screened population among children with available homocysteine measurements, electrocardiographic and echocardiographic evaluations, and no confirmed inherited metabolic disease or cardiac disorder. Clinical, biochemical, and electrocardiographic parameters, including maximum P-wave duration and P-wave dispersion, were retrospectively analyzed. A total of 90 participants were included, comprising 47 children with hyperhomocysteinemia and 43 healthy controls. P-wave dispersion and maximum P-wave duration were significantly higher in the hyperhomocysteinemia group compared with controls (48.96 [19.48-100.0] vs. 38.57 [10.57-71.19] ms, p < 0.001). Plasma homocysteine levels showed a moderate positive correlation with P-wave dispersion (ρ = 0.441, p < 0.001). These differences were more pronounced in children with higher homocysteine levels and in younger age groups (< 2 years and 2-14 years). In contrast, PR interval (p = 0.790) and QTc interval (p = 0.183) did not differ significantly between groups. Vitamin B12 levels were significantly lower in the hyperhomocysteinemia group (p = 0.013), while folate levels were comparable (p = 0.974). Although sodium, potassium, and magnesium levels differed significantly between groups, all values remained within normal physiological ranges. CONCLUSIONS: Children with hyperhomocysteinemia showed increased P-wave dispersion compared with controls. These findings suggest an association between elevated homocysteine levels and altered atrial conduction parameters in children. Further prospective studies are needed to determine the clinical significance of these findings. WHAT IS KNOWN: • Hyperhomocysteinemia is associated with cardiovascular risk and endothelial dysfunction. • Elevated homocysteine levels have been linked to cardiac electrophysiological alterations in adult populations. WHAT IS NEW: • Elevated homocysteine levels are associated with increased P-wave dispersion in children, with more pronounced effects observed in younger age groups. • These findings support an association between hyperhomocysteinemia and altered atrial conduction parameters in children.
Adolescent↗
Disopyramide kinetics in patients with acute myocardial infarction.
The kinetic behavior of disopyramide was studied in 20 patients with suspected myocardial infarction: in 13 of these, the diagnosis was subsequently confirmed. All received a 400-mg oral loading dose of disopyramide base followed by an oral maintenance regimen of either 100 or 200 mg 4 times daily. The elimination half-life (t1/2beta) was longer (p less than 0.05) in patients with confirmed infarction than in patients with unconfirmed infarction [38.0 +/- 3.7 hr (mean +/- SEM) compared to 24.3 +/- 0.8 hr, and 21.2 +/- 2.1 hr compared to 7.2 +/- 2.4 hr for the 100- and 200-mg maintenance dose regimens, respectively]. The t1/2beta was dose dependent for infarct and noninfarct patients. Two of the patients with confirmed infarction failed to reach trough plasma levels equal to or exceeding the lower end of the manufacturer's recommended therapeutic range (3.3 mug/ml) during the study. For the remaining 11 patients the time taken to achieve trough plasma levels of 3.3 mug/ml varied from 18 to 170 hr; hence plasma disopyramide concentration in these patients was suboptimal at a time when the risk of arrhythmias is high. Modification of existing oral loading dose regimens is therefore required for optimization of oral disopyramide therapy.
Administration, Oral↗
Genome-Wide Association Study of Accessory Atrioventricular Pathways.
IMPORTANCE: Understanding of the genetics of accessory atrioventricular pathways (APs) and affiliated arrhythmias is limited. OBJECTIVE: To investigate the genetics of APs and affiliated arrhythmias. DESIGN, SETTING, AND PARTICIPANTS: This was a genome-wide association study (GWAS) of APs, defined by International Classification of Diseases (ICD) codes and/or confirmed by electrophysiology (EP) study. Genome-wide significant AP variants were tested for association with AP-affiliated arrhythmias: paroxysmal supraventricular tachycardia (PSVT), atrial fibrillation (AF), ventricular tachycardia, and cardiac arrest. AP variants were also tested in data on other heart diseases and measures of cardiac physiology. Individuals with APs and control individuals from Iceland (deCODE Genetics), Denmark (Copenhagen Hospital Biobank, Danish Blood Donor Study, and SupraGen/the Danish General Suburban Population Study [GESUS]), the US (Intermountain Healthcare), and the United Kingdom (UK Biobank) were included. Time of phenotype data collection ranged from January 1983 to December 2022. Data were analyzed from August 2022 to January 2024. EXPOSURES: Sequence variants. MAIN OUTCOMES AND MEASURES: Genome-wide significant association of sequence variants with APs. RESULTS: The GWAS included 2310 individuals with APs (median [IQR] age, 43 [28-57] years; 1252 [54.2%] male and 1058 [45.8%] female) and 1 206 977 control individuals (median [IQR] year of birth, 1955 [1945-1970]; 632 888 [52.4%] female and 574 089 [47.6%] male). Of the individuals with APs, 909 had been confirmed in EP study. Three common missense variants were associated with APs, in the genes CCDC141 (p.Arg935Trp: adjusted odds ratio [aOR], 1.37; 95% CI, 1.24-1.52, and p.Ala141Val: aOR, 1.55; 95% CI 1.34-1.80) and SCN10A (p.Ala1073Val: OR, 1.22; 95% CI, 1.15-1.30). The 3 variants associated with PSVT and the SCN10A variant associated with AF, supporting an effect on AP-affiliated arrhythmias. All 3 AP risk alleles were associated with higher heart rate and shorter PR interval, and have reported associations with chronotropic response. CONCLUSIONS AND RELEVANCE: Associations were found between sequence variants and APs that were also associated with risk of PSVT, and thus likely atrioventricular reentrant tachycardia, but had allele-specific associations with AF and conduction disorders. Genetic variation in the modulation of heart rate, chronotropic response, and atrial or atrioventricular node conduction velocity may play a role in the risk of AP-affiliated arrhythmias. Further research into CCDC141 could provide insights for antiarrhythmic therapeutic targeting in the presence of an AP.
Humans↗
Sodium Glucose Co-Transporter 2 Inhibitors and Ventricular Arrhythmias in Patients with Type 2 Diabetes: A Systematic Review of Observational Studies.
BACKGROUND: Sodium glucose co-transporter 2 inhibitors (SGLT2i) may exert antiarrhythmic effects, but their association with ventricular arrhythmias remains unclear. OBJECTIVE: We conducted a systematic review to evaluate the association between SGLT2i use and the risk of ventricular arrhythmias, cardiac arrest, and sudden cardiac death compared with other antidiabetic medications or no SGLT2i use among patients with type 2 diabetes mellitus. METHODS: MEDLINE, EMBASE, and CENTRAL were searched for observational studies published between March 2013 and March 2026. Quality was assessed using the Risk of Bias In Non-Randomized Studies of Interventions (ROBINS-I) tool, alongside evaluation of pharmacoepidemiology-specific biases. RESULTS: A total of 17 studies (16 cohort and one nested case-control) were included. Based on ROBINS-I, seven studies had moderate, eight serious, and two critical risks of bias. Eleven studies had at least one pharmacoepidemiology-specific bias. For ventricular arrhythmias, estimates ranged from a protective effect (hazard ratio [HR] 0.20, 95% confidence interval [CI] 0.04-0.97) to a potential increased risk (odds ratio 1.87, 95% CI 0.89-3.95) with SGLT2i use. For cardiac arrest, estimates consistently reported a lower risk with estimates that ranged from HR 0.63 (95% CI 0.59-0.68) to HR 0.85 (95% CI 0.82-0.88). The only study on sudden cardiac death reported a potential risk reduction (HR 0.62, 95% CI 0.38-1.01). CONCLUSIONS: While the association between SGLT2i and ventricular arrhythmias remains inconsistent, the use of SGLT2i likely reduces cardiac arrest and may reduce sudden cardiac death, suggesting a possible protective effect on ventricular arrhythmias among patients with type 2 diabetes.
Journal Article↗
Relation of ventricular repolarization to electrocardiographic T wave-form and arrhythmia vulnerability.
The normal sequence of ventricular recovery proceeds from epicardium to endocardium, but on the epicardium the pattern of ventricular recovery is similar to the pattern of activation. Data concerning ventricular repolarization have been obtained from analyses of electrocardiographic recordings, suction potential recordings, a limited number of recordings of transmembrane action potentials, and from measurements of refractory periods. Normal ventricular repolarization has now been characterized in sufficient detail that it can be used with theoretic models to derive T waves with forms that correspond closely to recorded T waves. These models provide insights concerning the body surface manifestations of the electrophysiologic events of ventricular repolarization and should contribute to a more physiologic approach to interpreting T wave abnormalities in clinical electrocardiograms. A relationship between inhomogeneity of ventricular refractory period duration and arrhythmia vulnerability has also been documented. Because inhomogeneity of ventricular repolarization is a factor in both T wave-form and arrhythmia vulnerability, methods of analysis of the T wave for determining patients at risk of developing arrhythmias should be possible. One such analysis is presented. The method has been tested on experimental animals before and after interventions designed to increase arrhythmia vulnerability and in a limited number of patient studies. The results to date are encouraging and suggest that in the future electrocardiographic examination will be used as a prognostic tool in addition to its already established diagnostic function.
Action Potentials↗
Ventricular arrhythmias during unstable angina pectoris.
In order to study the occurrence and frequency of ischemia-induced ventricular arrhythmias, we analyzed 105 episodes of spontaneous angina pectoris occurring at rest in 28 hospitalized patients with unstable angina pectoris and proved coronary artery disease. Of 24 patients with serious ventricular arrhythmias during pain, 17 (57%) were arrhythmia-free during monitoring. In the other four patients, 17 of 29 (59%) pain episodes were associated with serious ventricular arrhythmias, and three of these four had serious ventricular arrhythmias during pain-free periods. Each patient tended to manifest the same type of arrhythmia during repeat episodes of pain. It appears that continuous electrocardiogram (ECG) monitoring is important during the initial hospitalization of the patient with unstable angina. The presence of ventricular arrhythmias during pain-free periods indicates a high risk for serious ventricular arrhythmias during episodes of spontaneous pain. These patients should be considered for continued ECG monitoring and antiarrhythmic therapy.
Adult↗
Effects of disopyramide and aprindine on arrhythmias after acute myocardial infarction.
The incidence of ventricular arrhythmias after myocardial infarction was compared in a double blind study of disopyramide (33 patients), aprindine (34 patients) and placebo (31 patients). Total ventricular arrhythmias were less frequent in the aprindine group than in the disopyramide group (P less than 0.05) or than in the combined disopyramide and placebo groups (P less than 0.05). The incidence of life-threatening arrhythmias and of ventricular arrhythmias in high risk patients was also reduced by aprindine compared to disopyramide (P less than 0.001) or placebo (P less than 0.001). It is concluded that aprindine is effective in reducing ventricular arrhythmias and that further investigations on its preventive use after the onset of myocardial infarction are justified.
Acute Disease↗
Cardiac arrhythmias in the anesthetized patient.
Continuous monitoring of the electrocardiogram provides an opportunity for the veterinary surgeon to perform the surgical procedure in a safe and controlled manner. Arrhythmias can usually be eliminated by lowering the concentration of anesthetic and administering additional oxygen. Antiarrhythmic drugs are required when these measures do not control the problem and when surgery cannot be stopped. If a disturbance cannot be abolished or controlled with medication, the surgeon must weigh the potential gain of surgery against the potential risks of the arrhythmia.
Anesthesia↗
[Value of continous electrocardiography (Holter monitoring) in mitral valve prolapse].
Twenty three patients with mitral valve prolapse underwent ambulatory 20 to 24 hour electrocardiography to study the incidence and severity of ventricular arrhythmias. These arrhythmias were found in 20 cases (87 p. 100). Ventricular extrasystoles were usually grouped (14 cases) causing doublets in 8 cases and bursts of ventricular tachycardia in the 6 others. The importance of the information obtained by Holter monitoring should not detract from the value of the standard resting electrocardiogramme. In fact, there appears to be a good correlation between the severity of the ventricular arrhythmia and the presence of ST changes over the postero-inferior zones. These abnormalities were never present in patients without ventricular extrasystoles but on the other hand they were observed in 5 of the 6 patients with ventricular tachycardia. From a practical point of view this may represent a simple means of identifying patients at high risk of dangerous arrhythmias.
Adolescent↗