QT Interval Research Articles

6966 A Rhythmic Life-Threatening Enigma Unveiled: KCNH2 Mutation-Associated Torsades de Points Unmasking Primary Hyperaldosteronism in Cardiological Realm

Abstract Disclosure: S. Dejprapasorn: None. N. Nopparatana: None. S. Soonthornpun: None. R. Leelawattana: None. N. Kietsiriroje: None. S. Limumpornpetch: None. T. Nilmoje: None. W. Lohawijarn: None. T. Wongsuttipakorn: None. P. Choochuen: None. P. Limumpornpetch: None. Introduction: Primary hyperaldosteronism (PA) is characterized by hypertension and hypokalemia. However, its ability to masquerade life-threatening Torsades de Pointes makes it an unusual and dismissed diagnosis, revealing the link between PA and serious arrythmia. Clinical Case A 30-year-old female experienced three episodes of palpitations, followed by syncope. Upon admission, her blood pressure was 147/87 mmHg. ECG showed prolonged QT intervals with potassium level was 2.6 mmol/L (3.5-5.0 mmol/L). Continuous cardiac monitoring captured Torsades de Pointes. Despite potassium replacement, long QT still persisted. Pathogenic variant, c.2592+1G>A, within KCNH2 was discovered. Aldosterone concentration showed 69.65 ng/dL (9.70-62.60 ng/dL) and plasma renin activity was 0.12 ng/mL/h (1.50-5.70 ng/mL/h). Aldosterone-to-renin ratio was 580. Aldosterone post 4-h saline infusion test was 31.71 ng/dL which were consistent with PA. Adrenal unenhanced CT scan identified bilateral adrenal nodules (right 1.3 cm, left 1.1 cm). After receiving a cardioverter-defibrillator and spironolactone, the patient has had no palpitations, and their potassium level has remained normal. Clinical lessons: PA rarely presents ventricular arrhythmia. KCNH2 mutation may link between long QT syndrome (LQTS) and PA arises. LQTS type 2 is attributable to KCNH2 mutations, impacting potassium channel subunits crucial for adjusting currents during sympathetic activation. This is essential for shortening the QT interval with increasing heart rate. KCNH2 mutations disrupt this process, prolonging the QT interval and heightening the risk of arrhythmias. Aldosterone synthesis relies on calcium signaling triggered by potassium currents. Adrenal cortex hosts approximately 90 potassium channels genes, including KCNJ5 and KCNH2. Mutations in gene can disrupt the calcium signaling cascade, leading to excessive aldosterone production. While KCNJ5 mutation is well-documented in PA, the potential correlation between KCNH2 mutations and a similar mechanism remains unexplored in clinical reports to date. This case highlights the importance of a thorough comprehension of genetic cause contributing to pathogenesis of PA with complex clinical presentations. Presentation: 6/1/2024

12344 Four-Month Delay In Denosumab Induced Severe Hypocalcemia And Hypophosphatemia. Case Report

Abstract Disclosure: M.M. Eid: None. S. Reutrakul: None. Introduction: Denosumab is a fully human monoclonal antibody that binds to the receptor activator of nuclear factor kappa Β ligand, blocks osteoclast function and reduces bone resorption. Case: A 91 year old male with history of osteoporosis, type 2 diabetes, chronic kidney disease (CKD) and prostate cancer. Presented with fatigue and cold intolerance. Denied confusion, muscle cramp, perioral numbness/tingling, bowel habit change. Medications included empagliflozin 12.5 mg/day, leuprorelin 45 mg every 6 months since 2021 and cholecalciferol 1000IU/day. On examination, he was alert and oriented x 3 with stable vital signs. No thyromegaly. Chvostek's sign was negative. Labs: serum calcium (Ca) 6.5 mg/dl, corrected Ca (Co Ca) 6.7mg/dl(N 8.7-10.4), ionized Ca 0.7mMol/l (N 1.13-1.32), TSH 131uIU/ml (N 0.55-4.78), free T4 0.72ng/dl (N 0.89-1.76), creatinine 1.55mg/dl, GFR 42ml/min/1.73m2, HbA1C 6.1%. EKG with corrected QT interval of 499 msec. Hypocalcemia work up : parathyroid hormone (PTH) 762 pg/ml (N 18.4-80.1), 25 OH vitamin D (Vit D) 37ng/ml (N 30-100), 1,25 OH Vit D 77pg/ml (N 18-72), phosphorus (Phos) 1mg/dl (N 2.4-5.1), magnesium (Mag) 1.7mg/dl (N 1.6-2.6),ALP 59U/L(N 45-117). Clinical impressions were a new diagnosis of primary hypothyroidism and non PTH mediated hypocalcemia with secondary hyperparathyroidism. A thorough review of medication revealed that he received the first dose of denosumab 60 mg 4 months prior to this presentation. Baseline labs 1 month prior to denosumab: Ca/Co Ca 9.1/9.2mg/dl, Phos 4.5mg/dl, PTH 199.6pg/ml, Mag 2.1mg/dl,TSH 2.72 uIU/ml. 2 months after denosumab administration, serum Ca/Co Ca 8.8/8.6mg/dl. He was admitted and received Ca gluconate 2gm IV pushes, calcitriol 0.5 mcg/day and levothyroxine 50 mcg/day and kept on cardiac monitoring. He remained asymptomatic. On the 5th day, serum Ca/Co Ca 8.4/8.6mg/dl, Phos 3mg/dl, Mag 2mg/dl. He was discharged on oral Ca Carbonate, calcitriol and levothyroxine. The second denosumab dose was cancelled. Conclusion: Denosumab is an effective anti-osteoporotic medication but can cause hypocalcemia. The risks for denosumab induced hypocalcemia include renal impairment, Vit D deficiency and lack of Ca/Vit D supplementation. Hypocalcemia usually occurs 1 - 2 weeks after denosumab, corresponding to its peak of action. Checking serum Ca and Vit D with correction of deficiencies before starting denosumab is recommended. In high risk patients with CKD, daily Ca and Vit D supplements are recommended (1). Our case has CKD and developed severe hypocalcemia and hypophosphatemia 4 months after receiving denosumab without other apparent causes for hypocalcemia. Hypothyroidism is likely an incidental diagnosis and not contributing to hypocalcemia in the absence of rhabdomyolysis. Reference: 1.Jalleh R, Basu G, Leu RL, Jesudason S: Denosumab induced severe hypocalcemia in chronic kidney disease. Case Rep Nephrol.2018 Presentation: 6/2/2024

5074 Licorice Root Supplement As A Cause Of Hypokalemic Hypertension

Abstract Disclosure: G. Gill: None. S.M. Harman: None. L.A. Robles: None. A 67-year-old female Veteran presented to an emergency room with a one-day history of high blood pressure, chest tightness, and exertional dyspnea. Her blood pressure was 162/90 mm Hg, pulse regular at 71 BPM, and pain level 5/10. She had a history of hypertension, stable on hydrochlorothiazide alone, hyperlipidemia, anxiety, and depression. Physical exam was benign. EKG revealed normal sinus rhythm at 60 BPM, normal axis, a prolonged QT interval of 510 ms, and no ST changes. Lab evaluation showed a low potassium of 2.4 mEq/L, sodium 145 mEq/L. Other lab measurements (CBC, liver function tests and cardiac enzymes) were within laboratory reference ranges. Medications included topiramate for migraine and over-the-counter supplements for constipation, “thyroid health,” and a topical “testosterone booster” prescribed by a non-allopathic practitioner. Her hypokalemia was attributed to hydrochlorothiazide and topiramate and both were discontinued. She was started on nifedipine for blood pressure control and 40 mEq/day of potassium for hypokalemia. Within 2 weeks of discharge, she presented again with elevated blood pressure and a plasma potassium of 4.0 mMol/L. Further history revealed that her constipation supplement consisted of licorice root (glycyrrhiza glabra) extract 900 mg per capsule, of which she took 3 to 4 capsules daily. The patient was advised to discontinue all supplements. Thyroid function tests were within normal limits. Due to a suspicion of hyperaldosteronism, the ED physician requested an abdominal CT scan which showed a 1 cm, -17.5 Hounsfield unit, right adrenal nodule. Also consistent with hyperaldosteronism, plasma renin activity (PRA) was suppressed at 0.07 ng/mL/hr. However, a serum aldosterone level was less than 1 ng/dL. Her 24-hour urinary metanephrines were normal and a 24-hour urine free cortisol was 31.6 mcg/dL. Morning plasma cortisol was 5.1 mcg/dL. A tentative diagnosis of licorice-induced hyperaldosteronism was made and the patient was treated with a taper of spironolactone. After discontinuing spironolactone, blood pressure was 116/70mmHg and serum potassium was 4.5 mMol/L with a PRA of 0.66 ng/mL/hr and serum aldosterone of <5.0 ng/dL. The syndrome of factitious hyperaldosteronism due to licorice consumption has been well described. The mechanism, inhibition of renal (type 2) 11-beta-hydroxysteroid dehydrogenase by glycyrrhizic acid, allowing cortisol to exercise its considerable mineralocorticoid action, is well understood. Most prior reports have been in patients habitually consuming licorice candy, usually imported, since conventional licorice sold in the U.S. is artificially flavored. Our report illustrates the importance of obtaining a history of use of over-the-counter supplements and assessing their ingredients and the fact that presence of an adrenal nodule and a low PRA does not always indicate endogenous hyperaldosteronism. Presentation: 6/2/2024

Design, synthesis and biological evaluation of arylpropylamine derivatives as potential multi-target antidepressants

In this study, a series of novel arylpropylamine derivatives were designed, synthesized and evaluated as potential multi-target antidepressants. Among them, compound (R)-13j displayed unique pharmacological features, exhibiting excellent inhibitory potency against serotonin and noradrenaline transporters (SERT/NET) and high affinity for 5-HT2A/2C receptor, and showing low affinity for histamine H1, adrenergic α1 receptors and hERG channels (to reduce QT interval prolongation). Molecular docking studies provided a rational binding model of (R)-13j in complex with SERT and 5-HT2A/2C receptor. In animal models, compound (R)-13j dose-dependently reduced the immobility time in the tail suspension test (TST) and the forced swimming test (FST) in mice, with higher efficacy when compared to duloxetine, and showed no stimulatory effect on the locomotor activity. Moreover, compound (R)-13j significantly shortened the immobility time in the ACTH-induced rat model of treatment-resistant depression (TRD). Furthermore, compound (R)-13j also exhibited a higher threshold for acute toxicity than duloxetine. In addition, compound (R)-13j possessed a favorable pharmacokinetic profile in mice. Taken together, compound (R)-13j may constitute a novel class of drugs for the treatment of depression.

6692 Proarrhythmic Risk Of Hypoglycemia; A Case Of Insulin-Induced Hypoglycemia Provoking Torsade De Pointes-Cardiac Arrest

Abstract Disclosure: A.M. San Hernandez: None. A. Adelkhanova: None. H. Ashraf: None. J. Aguayo Herrera: None. M.F. Siddiqui: None. Introduction: Torsade de Pointes is a life-threatening polymorphic ventricular tachycardia which is associated with QTc prolongation caused by medications, metabolic and electrolyte abnormalities. Very few cases of hypoglycemia causing QTc prolongation and Torsades de Pointes have been reported in the literature. Although the mechanism is unclear, the effects of low blood glucose have been proposed to induce a sympathetic response, hypokalemia and calcium disturbances. We report a case of an insulin-induced hypoglycemia causing Torsades de Pointes cardiac arrest, highlighting the proarrhythmic risk of hypoglycemia. Case presentation: A 57-year-old female with a history of Insulin-dependent Type 2 Diabetes Mellitus (DM) was brought in by EMS due to severe symptomatic hypoglycemia (POC blood glucose of 30 mg/dL), requiring treatment with dextrose. Patient reported reduced oral intake due to vomiting for 1 week and continued insulin administration without self-monitoring of blood glucose. Laboratory work up on presentation revealed severe hypoglycemia VBG= 55 mg/dL and mild hypomagnesemia Mg=1.4mg/dL (Ref Range 1.7-2.2mg/dl) which was treated. There was no hypokalemia or hypocalcemia. ECG showed sinus rhythm with prolonged QTc interval of 573ms and non-specific ST changes.Few hours later, patient developed torsades de pointes, requiring ACLS resuscitation. ROSC was achieved after two rounds of CPR. Patient received dextrose infusion to maintain euglycemic state. She was not taking any QTc prolonging medication. There was no history of autoimmune disease. Except for hypoglycemia, no other metabolic abnormality could be identified. Cardiac and pulmonary etiologies of cardiac arrest were ruled out. Post-ROSC ECG showed sinus tachycardia with normalization of QTc to 454ms. Thus, Insulin-induced hypoglycemia was appointed as the main culprit for her cardiac arrest, in the setting of QTc prolongation. Patient received diabetes self-management and hypoglycemia education. Conclusion: Several studies support strong correlation between hypoglycemia and arrhythmic events during bedtime in people with diabetes “The dead in bed syndrome”. Hypoglycemia causes an acquired long QT syndrome independent of other risk factors such as cardiac autonomic neuropathy. Possible mechanisms include; sympathoadrenal activation, which regulates potassium, calcium and chloride channels or altered autonomic regulation caused by hypoglycemia itself regardless of the effect of insulin or hypokalemia. QT prolongation is a risk factor for sudden cardiac death by causing torsades de pointes ventricular tachycardia (VT).People with insulin dependent diabetes are at high risk of hypoglycemia and should be cautioned about the proarrhythmic risk of hypoglycemia. Education is crucial, and Continuous glucose monitor (CGM) is a valuable tool to be use in such a patient population. Presentation: 6/3/2024

Maternal hypertensive disorders of pregnancy and electrocardiographic findings among newborns: The Copenhagen Baby Heart Study.

Maternal preeclampsia is associated with both congenital heart defects and changes in left ventricular structure and function in the offspring. Whether preeclampsia and gestational hypertension also affect the offspring's cardiac conduction system is unknown. This study assesses whether infants exposed to maternal hypertensive disorders of pregnancy (HDPs) exhibit changes in their electrocardiogram (ECG) compared with infants unexposed to HDPs. This population-based cohort study included newborns from the Copenhagen Baby Heart Study who had an ECG performed within 30 days of birth and had available obstetric information. ECG parameters of newborns exposed to maternal HDPs were compared with those of unexposed newborns using linear regression. Our study cohort included 11,826 newborns, including 441 exposed to maternal preeclampsia and 320 exposed to gestational hypertension. Infants exposed to preeclampsia had prolonged QRS durations (adjusted mean difference 0.6 ms, 95% confidence interval [CI] 0.04, 1.16) and lower maximum amplitudes of the R-wave in V1 (adjusted mean difference, linear scale 0.95, 95% CI 0.90, 1.00), compared with unexposed infants. Exposure to maternal preeclampsia was not associated with changes in other ECG parameters. Exposure to gestational hypertension was associated with increased QT interval durations (QTc Bazett, adjusted mean difference 2.48 ms, 95% CI -0.23, 5.20; QTc Fridericia, adjusted mean difference 2.32 ms, 95% CI -0.19, 4.83). Our findings suggest that the newborn cardiac conduction system is affected by exposure to maternal preeclampsia. This could reflect the previously described thickening of the left ventricular myocardium in infants exposed to preeclampsia.

Clinical Outcomes of Benzodiazepine Prescribing for People Receiving Opioid Agonist Treatment: A Systematic Review of the Evidence.

Many countries are experiencing an increased use of unregulated benzodiazepines in combination with opioids and other drugs, which contributes to drug-related harm. This descriptive review identifies and synthesises the outcomes of studies co-prescribing benzodiazepines and opioids. A systematic review was undertaken in Medline, CINAHL, PsychInfo, Embase, and the Cochrane databases covering publications from 1 January 1991 to 18 November 2021. Inclusion criteria were peer reviewed, English language studies of adults prescribed opioid agonist treatment (OAT) and a concurrent benzodiazepine, and reporting outcome data. Of the 4370 titles screened, 18 papers were included. The main outcomes identified covered all-cause mortality (ACM) (n = 5); overdose death (n = 3); retention in treatment (n = 7); and hospitalisation/emergency department encounters (n = 2). Other outcomes included QTc interval, cognitive function, illicit drug use, and mental health. The prescription of benzodiazepines alongside OAT increased the ACM by 75-90%, while evidence on overdose death was less robust but indicative of increased risk (40-334%). There was an indicative positive effect on treatment retention, with increased retention in those prescribed a benzodiazepine with OAT compared to those not prescribed or taking non-prescribed benzodiazepines. In conclusion, methodologically robust epidemiological studies found increased ACM and overdose death but possibly improved retention. However confounders (e.g., psychiatric comorbidity) exist, so a trial is recommended.

Evaluation of Frontal QRS-T Angle in Children With ADHD and Healthy Controls.

Conflicting findings exist regarding the link between attention deficit hyperactivity disorder (ADHD) and cardiovascular diseases. This study aimed to evaluate the frontal QRS-T (fQRS-T) angle and its correlation with symptom severity in children diagnosed with ADHD. The study population consisted of 172 patients diagnosed with ADHD (120 drug naive and 52 drug positive) and 82 healthy controls. ADHD symptoms were assessed using the Atilla Turgay DSM-IV-Based Screening and Assessment Scale for Disruptive Conduct Disorders (T-DSM-IV-Scale). The fQRS-T angle and corrected QT (QTc) interval were obtained from the automated reports of 12-lead electrocardiography device for each patient. QTc interval and fQRS-T angle were significantly different among the groups. Post hoc analyses showed that QTc interval and fQRS-T angle of ADHD drug naive and ADHD drug positive patients were significantly higher than the healthy control groups. However, there was no significant difference between drug naive and drug positive patients regarding QTc interval and fQRS-T angle. Both QTc interval and fQRS-T angle showed positive correlations with the severity of ADHD symptoms (r = 0.263, p = .001 and r = 0.175, p = .023 respectively). We found that fQRS-T angle was significantly wider in children with ADHD. Therefore, we suggest that fQRS-T angle may help in cardiovascular risk assessment in children with ADHD.

Electrocardiographic abnormalities are frequently detected in healthy adult Borzoi with a normal echocardiogram.

Borzoi reportedly experience sudden death. The objective of this study was to report ECG intervals, amplitudes, and frequency of ECG abnormalities in clinically healthy Borzoi. 98 clinically healthy Borzoi were prospectively recruited and underwent echocardiogram, ECG, and cardiac troponin I testing between October 2020 and December 2022. Standard ECG measurements were obtained. Early repolarization notches and slurs were recorded. Of 82 Borzoi with a structurally normal echocardiogram, ventricular arrhythmias were documented in 8 (10%) dogs, all of which had normal cardiac troponin I concentrations. Median P wave duration was 55 milliseconds (range, 45 to 70 milliseconds). Median PR interval was 125 milliseconds (range, 80 to 175 milliseconds). Thirty-one (38%) Borzoi had first-degree atrioventricular block (PR interval > 130 milliseconds). Median QRS duration was 65 milliseconds (range, 48 to 90 milliseconds). Median QT interval was 235 milliseconds (range, 185 to 275 milliseconds). Twenty-nine (35%) and 15 (18%) of 82 Borzoi had QT intervals > 240 or > 250 milliseconds, respectively. Sixty-seven of 82 (82%) Borzoi had early repolarization notches or slurs. Seventeen of 82 (21%) Borzoi had an abnormality of the ST segment, most commonly convexity/doming. Convexity of the ST segment was intermittent (n = 9) or persistent (4). Ventricular arrhythmias, early repolarization, prolonged QT intervals, and ST segment abnormalities are not infrequent in clinically healthy Borzoi. P, PR, and QRS durations are commonly prolonged compared to general canine reference intervals. Future study into heritable channelopathies in Borzoi is warranted given the frequency of ventricular arrhythmias, repolarization abnormalities, and sudden death in the breed. Breed-specific ECG reference intervals are needed.

Study of the Arrhythmogenic Profile of Dogs with Myxomatous Mitral Valve Disease in Stages B1 and B2.

Myxomatous mitral valve disease (MMVD) is the most prevalent cardiac disease in dogs. This study aimed to compare the arrhythmogenic profile and heart rate variability (HRV) of dogs with MMVD in stages B1 and B2. Electrocardiographic exams and the medical records of 60 dogs were analyzed, and HRV, P wave dispersion, QT interval dispersion, and QT interval instability parameters were determined. The results showed significantly increased values in stage B2 compared with stage B1 (p < 0.05) regarding P wave maximum and minimum duration (Pmax and Pmin) and short-term instability (STI). In contrast, no statistically significant differences were observed regarding HRV parameters, P wave dispersion, or QT interval dispersion. Our findings showed that cardiac remodeling in stage B2 could not significantly alter the sympathovagal balance and showed little interference with the predisposition of arrhythmias in dogs with MMVD.

Effect of CYP3A5*3 genotype on exposure and efficacy of quetiapine: A retrospective, cohort study

BackgroundThe involvement of cytochrome P450 3A5 (CYP3A5) in the metabolism of quetiapine has been proposed, though conclusive evidence is lacking. This study aimed to quantitatively assess the impact of CYP3A5 genetic variability on quetiapine exposure in a Chinese patient population. MethodsPatient data were retrospectively collected from the database of the Mental Health Centre at the First Hospital of Hebei Medical University, covering the period from September 1, 2019, to July 1, 2023. The study included patients genotyped for CYP3A5 who were treated with quetiapine. Inclusion criteria for the analysis of pharmacokinetic parameters, such as serum concentrations of the drug and its metabolites, included oral administration of quetiapine, availability of information on the prescribed daily dose and concomitant medications, and the determination of steady-state blood levels at the time of sampling (after at least 3 days of continuous administration at the same dose). Exclusion criteria comprised polypharmacy with known CYP3A4 inducers or inhibitors, as well as patients with hepatic or renal insufficiency. The primary endpoint was the exposure to quetiapine and N-dealkylquetiapine, measured using dose-corrected concentrations (C/D). The secondary endpoint was the metabolism of quetiapine to N-dealkylquetiapine, assessed by the ratio of metabolite to parent drug concentrations. The third endpoint is the differences in adverse reactions, QTc intervals, and biochemical parameters among patients with different CYP3A5 genotypes. ResultBased on the inclusion and exclusion criteria, clinical data from 207 patients were ultimately included in the study. Of these, 20 patients had the CYP3A5*1/*1 genotype, 78 had the CYP3A5*1/*3 genotype, and 109 had the CYP3A5*3/*3 genotype.The CYP3A5*3 variant was found to significantly impact the metabolism of quetiapine. The C/D values for both quetiapine and dealkylated quetiapine were notably higher in individuals with the *3/*3 genotype compared to those with the *1/*1 and *1/*3 genotypes (P1 <0.001 and P2 = 0.002, respectively). A comparison of the variability in metabolic ratios among different genotype groups revealed no significant difference (P = 0.067). However, a post hoc analysis indicated that the metabolic ratio in poor metabolizers was significantly lower than that in intermediate metabolizers (P = 0.021). The analysis of adverse reaction incidence and QTc intervals among different genotypes showed no statistically significant differences (P = 0.652, P = 0.486). However, comparison of biochemical parameters across different genotype groups revealed that alanine aminotransferase, uric acid, hemoglobin, and gamma-glutamyl transferase levels were significantly higher in patients with the CYP3A5*3/*3 genotype compared to those with the CYP3A5*1/*1 and CYP3A5*1/*3 genotypes. ConclusionThe results indicated that the genetic polymorphism of CYP3A5*3 significantly influences the metabolism of quetiapine. Specifically, carriers of the CYP3A5*3/*3 genotype exhibited higher blood levels of quetiapine, with a greater likelihood of these levels exceeding the therapeutic range. This finding underscores the need for clinicians to carefully monitor and potentially adjust the dosage for patients with this genotype to avoid adverse effects. This finding underscores the need for clinicians to pay special attention to the efficacy and occurrence of adverse reactions when prescribing quetiapine to patients carrying the CYP3A5*3/*3 genotype.

Comparing the effects of three local anaesthetic agents on cardiac conduction system - A randomised study.

This study aimed to compare the effects of three local anaesthetic (LA) agents, namely bupivacaine, levobupivacaine, and ropivacaine, on the cardiac conduction system as assessed by corrected QT (QTc) and P wave dispersion (PWD) intervals in lower limb orthopaedic surgeries and to find the most suitable LA agent that can be used for a long duration. The study included 75 patients with American Society of Anesthesiologists physical status I and II of either gender in the age group of 18-65 years undergoing elective lower limb orthopaedic surgeries under epidural anaesthesia. These were allocated to groups B (bupivacaine), L (levobupivacaine), and R (ropivacaine). We observed blood pressure, heart rate, respiratory rate, PWD, and QTc intervals from baseline value through Holter monitoring, pain assessment by visual analogue scale, and demand and total volume of LA consumed by patient-controlled analgesia devices. The repeated measures of ANOVA were carried out to find the effect of time and time-to-group interaction among the groups across the periods. On intergroup comparison of QTc and PWD, no significant difference among groups was observed, but on intragroup analysis, a statistically significant increase in QTc and PWD from baseline was observed for each of groups B, L, and R at all time intervals. However, the mean increase in QTc and PWD recorded for Group B was higher than in groups L and R. Bupivacaine has the maximal tendency to prolong QTc and PWD. All three agents showed comparable haemodynamic effects and time to onset of sensory and motor blockade.

Serum N-6 polyunsaturated fatty acid concentrations and heart rate- corrected QT and JT intervals

Serum N-6 polyunsaturated fatty acid concentrations and heart rate- corrected QT and JT intervals

Risk of renal impairment in atypical antipsychotics: a systematic review and meta-analysis.

Atypical antipsychotics are associated with several adverse effects including metabolic syndrome, weight gain, QTc interval prolongation, and extrapyramidal effects. This study aims to investigate the risk of renal impairment in patients receiving atypical antipsychotics. A systematic literature search was conducted via PubMed and Ovid SP and Web of Science to retrieve studies reporting the risk of renal impairment in patients receiving atypical antipsychotic treatment. The pooled risk ratio (RR) of renal impairment and the subgroup analysis was calculated using the random-effects generic inverse variance method in Cochrane Review Manager. A total of 4 studies involving 514,710 patients (221, 873 patients on atypical antipsychotics/CKD and 292, 837 controls) were included in this meta-analysis. Patients on atypical antipsychotics exhibited an increased risk of renal impairment, with a pooled risk ratio of 1.34 (95%CI 1.23-1.47). Subgroup analysis demonstrated that atypical antipsychotic use was associated with an increased risk of both acute kidney injury (AKI) (RR 1.51, 95%CI 1.34-1.71) and chronic kidney disease (CKD) (RR: 1.23, 95%CI 1.12-1.35). Patients receiving atypical antipsychotics have an increased risk of renal impairment. Quetiapine carries the highest risk of renal impairment encompassing both AKI and CKD.

9307 Significance of Assessing QTc Interval in Chronic Hypoparathyroidism and its Clinical and Biochemical Correlates

9307 Significance of Assessing QTc Interval in Chronic Hypoparathyroidism and its Clinical and Biochemical Correlates

7807 Significance of Assessing QTc Interval in Chronic Hypoparathyroidism and its Clinical and Biochemical Correlates

7807 Significance of Assessing QTc Interval in Chronic Hypoparathyroidism and its Clinical and Biochemical Correlates

Prognostic significance of global electrical heterogeneity (GEH) parameters between coronary microvascular dysfunction (CMD) and obstructive coronary artery disease (OCAD): a retrospective cohort study

BackgroundBoth coronary microvascular dysfunction (CMD) and obstructive coronary artery disease (OCAD) cause myocardial ischemia, making accurate diagnosis of CMD an unmet challenge. AimWe investigate whether electrocardiogram (ECG)-constructed global electrical heterogeneity (GEH) can differentiate CMD and OCAD. MethodsThis retrospective study comprised 74 OCAD and 77 CMD patients with their clinical characteristics and ECGs. QRS onset and offset, R-peak, and T-wave offset were marked on vector-magnitude (VM) derived from ECG-constructed time-coherent global XYZ median beats. 22 GEH parameters (i.e., QT Interval, area and peak QRS-T angles, the area under curve of QT interval on VM (AUC_QT_VM), the direction (azimuth and elevation) and magnitudes of the spatial peak and area vectors for QRS, T, and spatial ventricular gradient (SVG) were calculated and tested using logistic regression analyses to identify significant predictors. ResultsSix GEH parameters (i.e., QT Interval, Peak QRS Azimuth, Area QRS Azimuth, Area T Elevation, Area T, and Area SVG Elevation) were identified as significant predictors. After multivariable adjustment, AUC_QT_VM (odds ratio (OR) = 0.979, [95 % confidence interval (CI) 0.964–0.995], P = 0.009), Area SVG Elevation (OR = 0.978, [95 % CI 0.959–0.998], P = 0.031), and QT Interval (OR = 1.014, [95 % CI 1.000–1.024], P = 0.010) were selected, with the area under curve (AUC) of 0.717 ([95 % CI 0.636–0.798], P < 0.0001) and accuracy of 0.645 on the training dataset and accuracy of 0.608 on the validation dataset. ConclusionsArea SVG Elevation and QT Interval could differentiate CMD and OCAD, indicating that our proposed GEH-based method may offer a new possibility and pathway for non-invasive detection of CMD.

Effect of Different Levofloxacin Doses on QTc Interval Prolongation in Multidrug-Resistant Tuberculosis Patients Treated with the 9-Month All-Oral Regimen

Introduction: The World Health Organization (WHO) has recommended the 9-month all-oral regimen for multidrug-resistant tuberculosis (MDR-TB) treatment. This regimen is expected to increase the treatment success rate. Bedaquiline, levofloxacin, and clofazimine are QT-prolonging drugs included in the 9-month all-oral regimen. Bedaquiline and clofazimine are given at the same dose for all patients, while levofloxacine dose is given in 750 mg and 1,000 mg based on the body weight. This study analyzed the correlation between different levofloxacin doses and certain factors on QTc interval prolongation. Methods: This observational retrospective study used the medical records of MDR-TB patients who underwent the 9-month all-oral regimen. Electrocardiography (ECG) for QTc interval measurement was recorded at the baseline before and 2 weeks after treatment. The measured variables included patient demographic data, body mass index (BMI), electrolyte levels, and comorbidities. Results: Thirty MDR-TB patients were included in this study. Gender, diabetes mellitus (DM), and levofloxacin dose did not correlate with QTc interval prolongation at 2 weeks after drug administration (p-values of 0.558, 0.197, and 0.134, respectively). Age, potassium level, magnesium level, calcium level, and baseline QTc interval also did not correlate with QTc interval prolongation at 2 weeks after drug administration (p-values of 0.433, 0.479, 0.705, 0.746, and 0.333, respectively). Multivariate analysis showed that the risk factor associated with QTc interval prolongation at 2 weeks after drug administration was a BMI of 0.013. Conclusion: Different levofloxacin doses did not correlate with QTc interval prolongation in MDR-TB patients treated with the 9-month all-oral regimen. The incidence of QTc interval prolongation was significantly associated with the lower BMI level.

Preoperative electrocardiogram in prediction of 90-day postoperative mortality: retrospective cohort study

BackgroundThere are conflicting data on the relationship between preoperative electrocardiogram and postoperative mortality. We aimed to assess the predictive value of preoperative ECG on postoperative all-cause mortality in patients undergoing non-cardiac surgery (NCS).MethodsWe retrospectively reviewed records of hospitalized patients who underwent an internal preoperative examination and subsequent NCS in the years 2015–2021. We recorded patient comorbidities, vital functions, results of biochemical tests, ECG. The primary end point was 90-day postoperative all-cause mortality, acquired from the hospital records and the nationwide registry run by the Institute of Health Information and Statistics of the Czech Republic.ResultsWe enrolled a total of 2219 patients of mean age 63 years (48% women). Of these, 152 (6.8%) died during the 90-day postoperative period. There were statistically significant associations between increased 90-day postoperative all-cause mortality and abnormal ECG findings in resting heart rate (≥ 80 bpm, relative risk [RR] = 1.82 and ≥ 100 bpm, RR = 2.57), presence of atrial fibrillation (RR = 4.51), intraventricular conduction delay (QRS > 0.12 s, RR = 2.57), ST segment changes and T wave alterations, left bundle branch hemiblock (RR = 1.64), and right (RR = 2.04) and left bundle branch block (RR = 4.13), but not abnormal PQ and QT intervals, paced rhythm, incomplete right bundle branch block, or other ECG abnormalities. A resting heart rate (≥ 80 bpm, relative risk [RR] = 1.95 and ≥ 100 bpm, RR = 2.20), atrial fibrillation (RR = 2.10), and right bundle branch block (RR = 2.52) were significantly associated with 90-day postoperative all-cause mortality even in subgroup of patients with pre-existing cardiac comorbidities.ConclusionsPatients with abnormal preoperative ECG findings face an elevated risk of all-cause mortality within 90 days after surgery. The highest mortality risk is observed in patients with atrial fibrillation and left bundle branch block. Additionally, an elevated heart rate, right bundle branch block, and atrial fibrillation further increase the risk of death in patients with pre-existing cardiac conditions.

Cruel surprise — stroke in the shadow of chloroquine and prolonged QT interval: a case report

Cruel surprise — stroke in the shadow of chloroquine and prolonged QT interval: a case report