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Hypertonic sodium bicarbonate is advocated for the treatment of sodium channel blocker poisoning, but its efficacy varies amongst different sodium channel blockers. This Commentary addresses common pitfalls and appropriate usage of hypertonic sodium bicarbonate therapy in cardiotoxic drug poisonings. Serum alkalinization is best achieved by the synergistic effect of hypertonic sodium bicarbonate and hyperventilation (PCO2 ∼ 30–35 mmHg [0.47–0.6 kPa]). This reduces the dose of sodium bicarbonate required to achieve serum alkalinization (pH ∼ 7.45–7.55) and avoids adverse effects from excessive doses of hypertonic sodium bicarbonate. Tricyclic antidepressant poisoning responds well to sodium bicarbonate therapy, but many other sodium channel blockers may not. For instance, drugs that block the intercellular gap junctions, such as bupropion, do not respond well to alkalinization. For sodium channel blocker poisonings in which the expected response is unknown, a bolus of 1–2 mmol/kg sodium bicarbonate can be used to assess the response to alkalinization. Hypertonic sodium bicarbonate can cause electrolyte abnormalities such as hypokalaemia and hypocalcaemia, leading to QT interval prolongation and torsade de pointes in poisonings with drugs that have mixed sodium and potassium cardiac channel properties, such as hydroxychloroquine and flecainide. Excessive doses of hypertonic sodium bicarbonate commonly occur if it is administered until the QRS complex duration is < 100 ms. A prolonged QRS complex duration is not specific for sodium channel blocker toxicity. Some sodium channel blockers do not respond, and even when there is a response, it takes a few hours for the QRS complex duration to return completely to normal. In addition, QRS complex prolongation can be due to a rate-dependent bundle branch block. So, no further doses should be given after achieving serum alkalinization (pH ∼ 7.45–7.55). A further strategy to avoid overdosing patients with hypertonic sodium bicarbonate is to set maximum doses. Exceeding 6 mmol/kg is likely to cause hypernatremia, fluid overload, metabolic alkalosis, and cerebral oedema in many patients and potentially be lethal. We propose that hypertonic sodium bicarbonate therapy be used in patients with sodium channel blocker poisoning who have clinically significant toxicities such as seizures, shock (systolic blood pressure < 90 mmHg, mean arterial pressure <65 mmHg) or ventricular dysrhythmia. We recommend initial bolus dosing of hypertonic sodium bicarbonate of 1–2 mmol/kg, which can be repeated if the patient remains unstable, up to a maximum dose of 6 mmol/kg. This is recommended to be administered in conjunction with mechanical ventilation and hyperventilation to achieve serum alkalinization (PCO2∼30–35 mmHg [4-4.7 kPa]) and a pH of ∼7.45–7.55. With repeated bolus doses of hypertonic sodium bicarbonate, it is imperative to monitor and correct potassium and sodium abnormalities and observe changes in serum pH and on the electrocardiogram. Hypertonic sodium bicarbonate is an effective antidote for certain sodium channel blocker poisonings, such as tricyclic antidepressants, and when used in appropriate dosing, it works synergistically with hyperventilation to achieve serum alkalinization and to reduce sodium channel blockade. However, there are many pitfalls that can lead to excessive sodium bicarbonate therapy and severe adverse effects. [ABSTRACT FROM AUTHOR]

Hydroxychloroquine overdose is associated with myocardial toxicity and conduction disorders. We report a case of hydroxychloroquine overdose that demonstrated a rapid progressive intraventricular conduction delay and QT prolongation resulting in significant bradycardia and shock despite aggressive treatment. We describe the rare capture of abrupt abnormalities of this overdose in sequential electrocardiograms in the immediate hours post-ingestion. [ABSTRACT FROM AUTHOR]

Introduction: Patients with Fontan anatomy are at increased risk for exercise intolerance and early morbidity and mortality. QRS complex fragmentation (fQRS) and prolongation have been studied in multiple heart diseases, but their clinical importance is unknown in the Fontan population. Methods: A retrospective cross‐sectional study was performed. ECGs were evaluated for QRS prolongation (>98 percentile for age) and fQRS (≥3 R‐waves/notches in the R/S complex [more than two in RBBB] in ≥2 contiguous leads). The primary outcome measures were CPET performance. Results: Total 90 patients (median age 18 years, 57% male, 59% RV dominant) were included; 13% had fQRS and 31% had prolonged QRS. Demographically, patients with fQRS or prolonged QRS were like those without. Peak VO2 (64% vs. 63%, p.45), VE/VCO2 slope (85% vs. 88%, p =.74), and O2 pulse (149% vs. 129%, p =.83) were similar in the fQRS group versus those without. Upon multi‐variable regression, body mass index (β = ‐0.38, p <.01) and QRS duration (β = ‐0.29, p <.01) were independently associated with % predicted VO2; fQRS was not. Lower cardiac index (2.2 vs. 2.8 L/min/m2, p =.03) and higher ventricular end‐diastolic pressure (13 vs. 10 mmHg, p =.02) was seen with fQRS. Conclusions: QRS fragmentation is present in patients with Fontan physiology. fQRS showed no association with CPET performance but was related to invasive hemodynamic markers of ventricular performance. QRS duration may be a better predictor of exercise function following Fontan. [ABSTRACT FROM AUTHOR]

Introduction: The electrocardiogram (ECG) is often used to identify which hyperkalemic patients are atrisk for adverse events. However, there is a paucity of evidence to support this practice. This studyanalyzes the association between specific hyperkalemic ECG abnormalities and the development ofshort-term adverse events in patients with severe hyperkalemia.Methods: We collected records of all adult patients with potassium (K+) ≥6.5 mEq/L in the hospitallaboratory database from August 15, 2010, through January 30, 2015. A chart review identified patientdemographics, concurrent laboratory values, ECG within one hour of K+ measurement, treatments andoccurrence of adverse events within six hours of ECG. We defined adverse events as symptomaticbradycardia, ventricular tachycardia, ventricular fibrillation, cardiopulmonary resuscitation (CPR) and/ordeath. Two emergency physicians blinded to study objective independently examined each ECG forrate, rhythm, peaked T wave, PR interval duration and QRS complex duration. Relative risk wascalculated to determine the association between specific hyperkalemic ECG abnormalities and shorttermadverse events.Results: We included a total of 188 patients with severe hyperkalemia in the final study group. Adverseevents occurred within six hours in 28 patients (15%): symptomatic bradycardia (n=22), death (n=4),ventricular tachycardia (n=2) and CPR (n=2). All adverse events occurred prior to treatment with calciumand all but one occurred prior to K+-lowering intervention. All patients who had a short-term adverse eventhad a preceding ECG that demonstrated at least one hyperkalemic abnormality (100%, 95% confidenceinterval [CI] [85.7-100%]). An increased likelihood of short-term adverse event was found forhyperkalemic patients whose ECG demonstrated QRS prolongation (relative risk [RR] 4.74, 95% CI[2.01-11.15]), bradycardia (HR

Bupropion is an antidepressant used in the treatment of major depressive disorder, seasonal affective disorder, nicotine addiction, and weight loss. It primarily functions via norepinephrine and dopamine reuptake inhibition. At toxic doses, bupropion can elicit seizures, as well as precipitate corrected QT interval (QTc) and QRS prolongation. We describe a case of an 18-year-old female who reportedly ingested 28 grams of extended-release bupropion, a dose much higher than in previously reported cases. Toxic ingestion precipitated status epilepticus, prolonged QTc, widened QRS, pulseless ventricular tachycardia (pVT), and subsequent cardiovascular collapse necessitating veno-arterial extracorporeal membrane oxygenation (ECMO) and Impella support. Historically, the cardiotoxic effects of bupropion toxicity have largely been treated with supportive care, sometimes requiring ECMO. This patient's course was complicated by a widening QRS despite aggressive bicarbonate therapy and recurrent pVT, which was ultimately aborted with lidocaine. Neurological prognostication was further complicated by a lack of brainstem reflexes on the exam. With maximal supportive care, the patient was liberated from Impella, ECMO, and the ventilator by hospital day seven. At discharge, she was neurologically intact with full recovery of cardiac function. This case emphasizes the need for early consideration of transfer to an ECMO center in the setting of a bupropion overdose and offers a potentially effective treatment option for bupropion-induced ventricular arrhythmia., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Reinsch et al.)

Abuse of the common anti-diarrheal loperamide is associated with QT interval prolongation as well as development of the potentially fatal arrhythmia torsades de pointes. The mechanism underlying this cardiotoxicity is high affinity inhibition of the human ether-a-go-go-related gene (hERG) cardiac K+ channel. N -Desmethyl loperamide is the major metabolite of loperamide and is a close structural relative of the parent molecule. To date no information is available regarding the affinity of N -desmethyl loperamide for human cardiac ion channels. The effects of N -desmethyl loperamide on various cloned human cardiac ion channels including hERG, KvLQT1/mink and Na v 1.5 were studied and compared to that of the parent. N -Desmethyl loperamide was a much weaker (7.5-fold) inhibitor of hERG compared to loperamide. However, given the higher plasma levels of the metabolite relative to the parent, it is likely that N -desmethyl loperamide can contribute, at least secondarily, to the cardiotoxicity observed with loperamide abuse. We used the recently solved cryo-EM structure of the hERG channel together with previously published inhibitors, to understand the basis of the interactions as well as the difference that a single methyl plays in the hERG channel blocking affinities of these two compounds. [ABSTRACT FROM AUTHOR]

Background: We sought to develop an improved 12 lead ECG model to diagnose hyperkalemia by use of traditional and novel parameters.Methods: We retrospectively analyzed ECGs in consecutive hyperkalemic patients (serum potassium (K)>5.3mEq/L) by blinded investigators with normokalemic ECGs as internal controls. Potassium levels were modeled using general linear mixed models followed by refit with standardized variables. Optimum sensitivity and specificity were determined using cut point analysis of ROC-AUC.Results: The training set included 236 ECGs (84 patients) and validation set 97 ECGs (23 patients). Predicted K=(5.2354)+(0.03434*descending T slope)+(-0.2329*T width)+(-0.9652*reciprocal of new QRS width>100msec). ROC-AUC in the validation set was 0.78 (95% CI 0.69-0.88). Maximum specificity of the model was 84% for K>5.91 with sensitivity of 63%.Conclusion: ECG model incorporating T-wave width, descending T-wave slope and new QRS prolongation improved hyperkalemia diagnosis over traditional ECG analysis. [ABSTRACT FROM AUTHOR]

Purpose: Prolonged QRS duration is the main selection criterion for cardiac resynchronization therapy (CRT) which ameliorates left ventricular mechanical dyssynchrony (MD). However, consequences of post-CRT QRS prolongation and residual MD have been poorly evaluated. We aimed to define the predictors of persistent MD and hypothesized that CRT-induced QRS change (ΔQRS) might have an impact on residual MD after CRT.Methods: A total of 80 patients receiving CRT were included in the study. ΔQRS was calculated as the difference between the baseline and paced QRS intervals. Residual MD was assessed early after device implantation with a longitudinal dyssynchrony index (Yu index). Significant MD was defined as a Yu index ≥ 33 msec. Two groups were created based on residual MD and compared according to clinical, electrocardiographic and echocardiographic features.Results: Patients with persistent MD had longer paced QRS durations (182.5 ± 16.2 vs. 165.4 ± 22.5 msec, p = 0.03) and were less likely to have left ventricular (LV) leads located in the posterolateral vein (53 % vs. 85 %, p = 0.002). The linear correlation between the ΔQRS and the Yu index values was modest (Spearman's rho = -0.341, p = 0.002); additionally, a prolonged QRS was strongly associated with MD after CRT (p = 0.00008). Both LV lead localization and CRT-induced QRS prolongation emerged as the significant predictors of persistent MD. A biventricularly paced QRS more than 10 msec longer than the pre-paced QRS width was predictive of persistent MD after CRT (sensitivity = 80 %, specificity = 62 %).Conclusions: ΔQRS was found to be associated with residual MD after CRT. Ten milliseconds of QRS prolongation predicted persistent MD after CRT. [ABSTRACT FROM AUTHOR]

Background. QRS duration has long been established as a strong predic-tor of sudden cardiac death in patients after surgical correction of Tetral-ogy of Fallot (TOF). Several factors has been correlated to QRS duration, i.e severity of pulmonal regurgitation and right ventricular volume after TOF correction. But there is no established relation between right ven-tricular function and QRS duration after surgical correction TOF. Objectives. We aimed to investigate the relation between QRS duration and right ventricular function and whether patients after TOF repair with right bundle branch block have left ventricular dissynchrony. Methods.50 patients with repaired TOF were studied. Right ventricular function were derived from tissue Doppler imaging Tei index. Left ven-tricular dissynchrony were derived from tissue Doppler imaging. The time interval between the onset of QRS complex and the onset of systolic ejec-tion was measured for six left ventricular basal wall, i.e septal, lateral, anteroseptal, posterior, anterior and inferior wall. Mechanical delay from septal to lateral wall, antero-septal to posterior wall and anterior to infe-rior wall was calculated. Measured data were correlated with QRS dura-tion. Results.There was relation between QRS duration and right ventricular function (P = 0.028, r = 0.44). Ten (20%) of the examined patients after TOF repair had LV dissnynchrony particularly in patients with RBBB and prolonged QRS duration (160 9 ms). Conclusions.There is correlation between right ventricular function and QRS duration. Left ventricular dissynchrony may exist in patients after TOF repair with RBBB.

The article presents a study to investigate the effects of endothelin type B (ETB) receptor antagonist BQ-788 on amitriptyline-induced cardiotoxicity and the role of ETB receptors cardiovascular depression induced by amitriptyline. The study uses male Wistar rats that were anaesthetized with urethane/chloralose. Results of the study show that : Amitriptyline caused a significant decrease in mean arterial pressure (MAP) and decreased heart rate (HR).

Background: The benefits of cardiac resynchronization in inducing reverse ventricular remodeling in patients with left ventricular (LV) systolic dysfunction have been well established. Still, up to 30% of the patients fail to derive significant improvement from this therapy. A subset of “nonresponders” experience deterioration in LV function following cardiac resynchronization therapy (CRT). Characteristics of this patient population, however, have not been studied. Objective: To determine characteristics of patients who experience deterioration in LV function following CRT. Methods: Clinical, electrocardiographic, and echocardiographic data were collected in 856 consecutive patients presenting for a new CRT device. For inclusion, all patients had an LV ejection fraction ''40%, a QRS duration ''120 ms, and available baseline and follow-up echocardiograms and electrocardiograms. Deterioration in LV function was defined as an absolute decrease of 5% or greater in ejection fraction from baseline. Multivariate models were constructed to identify variables significantly associated with deterioration. Results: A total of 507 patients met inclusion criteria, of which 60 (11.8%) met criteria for deterioration. Patients with deterioration were more likely to be men (86.7% vs 66.9%; P = .002), have a non–left bundle branch block morphology (41.7% vs 23.7%; P = .001), and a history of atrial fibrillation (66.7% vs 51.7%; P = .03). On comparing the pre-CRT QRS duration with the first biventricular-paced QRS duration post-CRT implant, it was found that patients with LV deterioration had significant QRS widening than did those without deterioration (ms) (+3.9 ± 34.1 vs −9.0 ± 27.4, P = .007, respectively). In multivariate analysis, QRS widening indexed to the baseline QRS duration was significantly associated with LV deterioration (odds ratio 1.14 [1.06–1.23]; P = .001). Conclusion: QRS widening is associated with deterioration in LV function following CRT. [Copyright &y& Elsevier]

Background. Cardiac arrest due to lamotrigine (LTG) has been reported after co-ingestion with bupropion, but severe sodium channel blockade in the absence of other toxins has not been described. We report a case of cardiac arrest and status epilepticus following a massive LTG overdose. Case Report. A 48 year-old female was brought to the ED with seizure-like activity subsequent to ingesting 7.5 g of LTG. Vital signs were HR 131, BP 107/68, T 99.4°F, RR 16. She was intubated in the ED for a low GCS. Initial ECG demonstrated a narrow-complex normal sinus rhythm, and her labs were unremarkable. Three hours after intubation she developed status epilepticus, and a pulseless wide-complex tachycardia. She was aggressively resuscitated during which time pulses were periodically reestablished, but lost each time seizures recurred. She was not stabilized until the convulsions were terminated with vecuronium. Her post-resuscitation ECG demonstrated a junctional tachycardia with a 3 mm R-wave in aVR. The LTG level was 74.7 mcg/ml (therapeutic: 3-14 mcg/ml). Comprehensive LC-MS/MS drug screen was negative for all screened compounds. Discussion. This is the first report of cardiovascular collapse due to LTG with the highest drug concentration to date. Conclusion. The degree of neurologic and cardiovascular toxicity seen in this case are novel and illustrate the potential for severe sodium channel blockade after massive LTG poisonings. Drug levels are not clinically relevant in the acute setting due to the time delay in obtaining results, and recurrent seizure activity may be the only clinical finding that precedes severe cardiac toxicity. [ABSTRACT FROM AUTHOR]

We planned this study in order to investigate the effects of theophylline on cardiovascular parameters in an anaesthetized rat model of amitriptyline toxicity. In the preliminary study, we tested theophylline as 1 mg/kg of bolus, followed by a 0.5-mg/kg infusion. Toxicity was induced by the infusion of 0.94 mg/kg/min of amitriptyline up to the point of a 40-45% inhibition of mean arterial pressure (MAP). The rats were randomized to two groups: a group of 5% dextrose bolus followed by 5% dextrose infusion, and another group with theophylline bolus followed by infusion. Amitriptyline caused a significant decrease in MAP and prolongation in QRS; however, it did not alter heart rate (HR). When compared to the dextrose group, theophylline administration increased MAP, shortened prolonged QRS duration, and increased HR ( P < 0.05, respectively). There was no statistically significant difference in the results of arterial blood-gas analyses among the groups ( P > 0.05). Bolus doses followed by a continuous infusion of theophylline were found to be effective in reversing the hypotension and QRS prolongation seen in amitriptyline toxicity. One of the possible explanations of this beneficial effect is nonselective adenosine antagonism of theophylline. Further studies are needed to reveal the exact mechanism of the observed effect. [ABSTRACT FROM AUTHOR]

Abstract: The electrocardiographic diagnosis of left ventricular hypertrophy (LVH) has been centered on improving the diagnostic sensitivity and specificity of the method, using criteria whose precise relationship to increased left ventricular mass are not established. Although the electrocardiogram (ECG) has been displaced to a secondary role in the prediction of left ventricular mass, ECG/LVH has been shown to be a strong predictor of morbidity and early mortality. There are strong clues that each of the parameters in ECG/LVH is related to cardiac contractility and ejection. It is suggested that research be redirected to an exploration of these relationships and predicted that this will lead to both a better understanding of this venerable tool and an improvement in its usefulness to the clinician and patient. [Copyright &y& Elsevier]

Background: Current consensus documents on Brugada syndrome recommend the diagnostic intravenous administration of a Na-channel blocker to be stopped when the QRS prolongs to ≥130% of baseline, presumably because of increased arrhythmic risk. Objective: This study sought to assess QRS prolongation during ajmaline testing and its relation to arrhythmic risk. Methods: We analyzed an electrocardiographic (ECG) database collected during ajmaline testing in 148 patients (92 men, age 36 ± 15 years). The QRS was measured at baseline and during the 1st to 7th, 10th, and 15th minute after the beginning of ajmaline administration. Results: The average QRS prolongation was 36% ± 16% (range 9% to 88%), not significantly different between positive (n = 30) and negative (n = 118) tests. QRS prolonged to ≥130% during 16 (55%) positive and 71 (61%) negative tests (P = .50), with no clinical side effects. The incidence of ventricular arrhythmias was not significantly different between patients with and without QRS prolongation. Short runs (3 to 8 complexes) of nonsustained ventricular tachycardia occurred in 3 patients with QRS prolongation ≥130%. In 40% of positive tests, prolongation ≥130% occurred earlier by >1 minute than diagnostic Brugada ECG changes, i.e., early termination of the test could possibly have resulted in false-negative outcomes. Conclusion: QRS prolongation ≥130% occurs in >50% of all tests. In 40% of positive tests it occurs before diagnostic ECG changes. Always terminating the test when QRS prolongs ≥130% could possibly result in loss of important diagnostic information. It is appropriate to adjust the criteria for early termination of the test to the baseline QRS and possibly other factors. [Copyright &y& Elsevier]

Abstract: Aims: To investigate the role of beta receptor blockade via adenosine A1 receptor stimulation on amitriptyline-induced QRS prolongation. Methods: Isolated rat hearts were randomized into three groups (n =8 for each group). After pretreatment with 5% dextrose (control) or DPCPX (8-cyclopentyl-1,3-dipropylxanthine), or propranolol+DPCPX, amitriptyline infusion was given to all groups. Intact beta adrenergic receptor response was verified with a bolus dose of isoproteranol (3×10−5 M). Results: Amitriptyline (5.5×10−5 M) infusion following pretreatment with 5% dextrose or 10−4 M DPCPX prolonged QRS by 40–110% and 30–75%, respectively. After the beta receptor blockade with 10−2 M propranolol bolus, amitriptyline infusion following pretreatment with DPCPX prolonged QRS by 40–130%. Amitriptyline infusion following pretreatment with DPCPX (10−4 M) shortened the QRS at 40, 50 and 60 min significantly when compared to propranolol+DPCPX group (168.8±4.9%, p <0.05; 170.8±6.9%, p <0.01; 174.0±6.9%, p <0.01, respectively). Amitriptyline infusion following pretreatment with 5% dextrose prolonged QRS duration significantly at 50th minutes (209.5±6.1%, p <0.05) compared to DPCPX pretreatment group. Conclusion: DPCPX pretreatment shortened amitriptyline-induced QRS prolongation. Beta adrenergic receptor blockade enhanced QRS prolongation shortened by DPCPX pretreatment. Adenosine A1 receptor stimulation related to beta adrenergic receptor blockade may play a role in amitriptyline-induced QRS prolongation in isolated rat hearts. [Copyright &y& Elsevier]

The aim of this study was to investigate the effect of glucagon on cardiovascular parameters in anesthetized rat model of tricyclic antidepressant overdose. Toxicity was induced by infusion of amitriptyline 0.94 mg/kg/mm until a 40-45% of reduction in mean arterial pressure was observed. Amitriptyline infusion rats were then randomized into three groups. Control group of rats (group 1) received a bolus of 5% dextrose followed by the continuous infusion of dextrose, whereas treatment groups received 1 mg/kg (group 2) or 2 mg/kg (group 3) bolus doses of glucagon followed by continuous infusion (0.1 mg/kg/mm) of glucagons for 60 mm. Mean arterial pressure, heart rate, and electrocardiogram were recorded. Amitriptyline caused a significant decrease in mean arterial pressure and a prolongation in QRS, yet it did not change the heart rate. High.bolus dose of glucagon (2 mg/kg) followed by glucagon inftision significantly increased mean arterial pressure at 40, 50, and 60 mm (P < 0.05) and shortened the prolonged QRS at 50 and 60 mm (P < 0.05) when compared with control group. There was also a significant increase in heart rate. In conclusion, bolus doses followed by a continuous infusion of glucagon were found to be effective in reversing the hypotension and QRS prolongation in the rat model of amitriptyline toxicity. Further studies are needed to reveal the exact mechanism of the proposed effect. [ABSTRACT FROM AUTHOR]

Lamotrigine and felbamate are 2 newer anticonvulsant medications used to control refractory partial and generalized seizures. Although several cases of lamotrigine toxicity secondary to acute intentional or unintentional overdose have been described, there is little published information related to potential side-effects associated with the therapeutic use of these agents. Described is a case of a 22-year-old woman who presented to the emergency department after experiencing 2 seizure-like episodes. Findings on evaluation included nystagmus, ataxia, widening of the QRS complex and right-axis deviation on ECG. The patient reported only therapeutic use of her medications. The lamotrigine level was 14.8 mgIL. The mechanism of action for lamotrigine is blockade of the sodium channels; therefore, the patient was treated with intravenous sodium bicarbonate with resultant QRS narrowing following administration. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to evaluate the contribution of QRS prolongation in the diagnosis of coronary artery disease (CAD) in patients with exercise-induced ST-segment depression exclusively during the recovery period. Methods: The study population consisted of 107 patients (90 males and 17 females) aged 39–70 (mean 59 ± 7) years who underwent a treadmill exercise test using Bruce protocol and presented ST-segment depression limited to the recovery period. Angiographic data were available for all studied patients. Results: Among studied patients, 74 (69%) were found to have hemodynamically significant CAD, while the remaining 33 (31%) had normal coronary arteries. Concomitant QRS prolongation was revealed in 61 (82%) of the patients with angiographically documented CAD, while in 13 (18%) patients QRS duration remained unchanged. On the contrary, only 4 (12%) of the 33 patients with normal coronary arteries showed prolonged QRS duration during ST depression, while in the remaining 29 (88%) QRS duration remained unchanged. Conclusions: The evaluation of the concomitant QRS duration changes may discriminate patients with truly ischemia-induced ST-segment depression limited to the recovery period. [ABSTRACT FROM AUTHOR]

Introduction: T wave alternans (TWA) is a promising new noninvasive marker of arrhythmia vulnerability that quantifies beat-to-beat changes in ventricular repolarization. Secondary repolarization abnormalities are common in subjects with wide QRS complexes. However, the relationship between TWA and QRS prolongation has not been evaluated. The goal of this study was to determine if QRS prolongation influences the prevalence or prognostic value of TWA. Methods and Results: The study consisted of 108 consecutive patients with coronary artery disease and left ventricular ejection fraction ≤40% who were referred for electrophysiologic studies. Patients underwent TWA testing using bicycle ergometry in the absence of beta-blockers or antiarrhythmic drugs. The primary endpoint was the combined incidence of death, sustained ventricular arrhythmias, and appropriate implantable cardioverter defibrillator therapy. The prognostic value of TWA was assessed in the entire cohort and in two subgroups: QRS < 120 msec (normal, n = 62) and QRS ≥ 120 msec (prolonged, n = 46). TWA (hazard ratio 2.2, P = 0.03) and QRS prolongation (hazard ratio 2.2, P = 0.01) were both significant and independent predictors of arrhythmic events. QRS prolongation had no effect on the prevalence of positive TWA tests (QRS < 120 msec: 48%, QRS ≥ 120 msec: 50%, P = NS). TWA was a highly significant predictor of events in patients with a normal QRS (hazard ratio 5.8, P = 0.02). In contrast, TWA was not useful for risk stratitication in subjects with QRS prolongation (hazard ratio 1.1, P = 0.8). Conclusion: TWA is useful only for risk stratification in the absence of QRS prolongation. The presence of QRS prolongation and left ventricular ejection fraction ≤ 40% may be sufficient evidence of an adverse prognosis that additional risk stratification is not useful or necessary. [ABSTRACT FROM AUTHOR]

We investigated the interaction of class-I aniiarrhythmic drugs as they affect intraventricular conduction of human hearts in vivo. QRS duration in signal-averaged electrocardiograms and standard electrocardiograms were measured as an index of intraventricular conduction time in 17 patients with implanted pacemakers at various pacing rates (100–180 ppm, VVI mode). Single intravenous administration of lidocaine, disopyramide or aprindine prolonged the QRS of signal-averaged electrocardiograms in a frequency-dependent manner. Lidocaine (n = 17) produced sign QRS prolongation from pre-drug control at rates ≥120 ppm (6·2 ± 1·4% at 180 ppm), whereas disopyramide (n = 17) and aprindine (n = 17) did so from the lowest rate (8·9 ±1·8% to 12·3 ± 2·9% at 100–180 ppm with disopyramide; 14·7 ± 1·3% to 19·3 ± 22% at 100–180 ppm with aprindine). Addition of lidocaine to disopyramide (n=17) showed an additive effect; QRS prolongation was enhanced significantly by 1·4–2·8% at rates ≥ 150 ppm. In contrast, addition of lidocaine to aprindine (n =17) showed a subtractive effect; the QRS prolongation was attenuated significantly by 1·6–2·4% at rates 150 ppm. Combined intravenous administration of class-I antiarrhythmic drugs causes not only additive but also subtractive effects on the intra ventricular conduction of the human heart, probably through their interaction on the sodium channel receptor. [ABSTRACT FROM PUBLISHER]