Prolonged QRS Research Articles

Assessment of QT interval in ventricular paced rhythm: Derivation of a novel formula

ObjectiveThe objective of the study was to determine the optimal formula to estimate QT interval adjusting for QRS prolongation during right ventricular (RV) pacing. MethodsThis observational study included individuals (n = 43) with a newly implanted permanent ventricular pacemaker, who had a narrow QRS complex before pacemaker insertion. QT interval with RV pacing was related to QT interval before pacemaker implantation. The validation cohort (n = 442) had permanent RV pacing in DDD mode. ResultsA new QTc formula was derived utilizing the constants from the relationship between the spline heart rate QT correction (QTcRBK) before and after pacing; specifically, QTcRBKPACED = QTcRBK × 0.86. The JT interval from paced complexes was highly heart rate (HR) dependent and was not accurate for QT assessment. Previous, QTc formula for paced complexes were not highly correlated with QT before pacing unless a robust HR correction is added. Formulae subtracting a fixed amount from QTcPACED markedly overestimated QTc before pacing. ConclusionWe proposed a new, simple formula for QT estimation in RV pacing. JT interval in paced complexes is highly HR dependent and is not accurate for QT assessment. The new spline approach for HR correction for the QT, once incorporated into some previously proposed formulae, blunts HR dependency and improves prediction of QT before pacing. QTcRBKPACED*0.86 and QTcRBKPACED – (QRS*0.5) demonstrated the best balance of relatively strong correlation to QTc before pacing and accurate QTc prolongation identification. Abnormal QT for QTcRBKPACED*0.86 as defined by the 97.5th and 99th percentile are 469 and 479 ms respectively.

Permanent pacing and conduction recovery in patients undergoing cardiac surgery for active infective endocarditis in an Australian Tertiary Center.

Postoperative heart block is common among patients undergoing surgery for infective endocarditis (IE). Limited data exists allowing cardiologists to predict who will require permanent pacemaker (PPM) implantation postoperatively. We aimed to determine the rate of postoperative PPM insertion, predictors for postoperative PPM, and describe PPM utilization and rates of device-related infection during follow-up. A retrospective analysis was performed of 191 consecutive patients from a single institution who underwent cardiac surgery for IE between 2001 and 2017. Preoperative and operative predictors for postoperative PPM were evaluated using univariate and multivariate logistic regression. The rate of postoperative PPM implantation was 11% (17/154). The PPM group had more preoperative prolonged PR interval alone (33% vs 12%; P = .03), coexistent prolonged PR and QRS durations (13% vs 2%; P = .01), infection beyond the valve leaflets (82% vs 41%; P = .001), aortic root debridement (65% vs 23%; P = <.001), patch repair (47% vs 20%; P = .01), postoperative prolonged PR interval (50% vs 24%; P = .01), and prolonged QRS duration (47% vs 15%; P = .001). On multivariate analysis, infection beyond the valve leaflets emerged as an independent predictor for postoperative PPM (odds ratio, 1.94, 95% confidence interval, 1.14-3.28; P = .014). A reduction in PPM utilization was observed in five patients while eight patients continued to show significant ventricular pacing with no underlying rhythm at 12 months. There were no device-related infections. Postoperative PPM was required in 11% of patients undergoing surgery for IE over a 16-year period. Infection beyond the valve leaflet was an independent predictor for postoperative PPM insertion.

Electrophysiologic and molecular mechanisms of a frameshift NPPA mutation linked with familial atrial fibrillation

A frameshift (fs) mutation in the natriuretic peptide precursor A (NPPA) gene, encoding a mutant atrial natriuretic peptide (Mut-ANP), has been linked with familial atrial fibrillation (AF) but the underlying mechanisms by which the mutation causes AF remain unclear. We engineered 2 transgenic (TG) mouse lines expressing the wild-type (WT)-NPPA gene (H-WT-NPPA) and the human fs-Mut-NPPA gene (H-fsMut-NPPA) to test the hypothesis that mice overexpressing the human NPPA mutation are more susceptible to AF and elucidate the underlying electrophysiologic and molecular mechanisms. Transthoracic echocardiography and surface electrocardiography (ECG) were performed in H-fsMut-NPPA, H-WT-NPPA, and Non-TG mice. Invasive electrophysiology, immunohistochemistry, Western blotting and patch clamping of membrane potentials were performed. To examine the role of the Mut-ANP in ion channel remodeling, we measured plasma cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) levels and protein kinase A (PKA) activity in the 3 groups of mice. In H-fsMut-NPPA mice mean arterial pressure (MAP) was reduced when compared to H-WT-NPPA and Non-TG mice. Furthermore, injection of synthetic fs-Mut-ANP lowered the MAP in H-WT-NPPA and Non-TG mice while synthetic WT-ANP had no effect on MAP in the 3 groups of mice. ECG characterization revealed significantly prolonged QRS duration in H-fsMut-NPPA mice when compared to the other two groups. Trans-Esophageal (TE) atrial pacing of H-fsMut-NPPA mice showed increased AF burden and AF episodes when compared with H-WT-NPPA or Non-TG mice. The cardiac Na+ (NaV1.5) and Ca2+ (CaV1.2/CaV1.3) channel expression and currents (INa, ICaL) and action potential durations (APD90/APD50/APD20) were significantly reduced in H-fsMut-NPPA mice while the rectifier K+ channel current (IKs) was markedly increased when compared to the other 2 groups of mice. In addition, plasma cGMP levels were only increased in H-fsMut-NPPA mice with a corresponding reduction in plasma cAMP levels and PKA activity. In summary, we showed that mice overexpressing an AF-linked NPPA mutation are more prone to develop AF and this risk is mediated in part by remodeling of the cardiac Na+, Ca2+ and K+ channels creating an electrophysiologic substrate for reentrant AF.

Polyphenol‐Rich Fraction of Parquetina nigrescens Quenches Dichlorvos‐Induced Cardiorenal Dysfunction through Reduction in Nitrotyrosine/ p38 MAPK pathways

Parquetina nigrescens is commonly used to treat diseases in humans and animals in developing countries, including Nigeria. This study evaluates the effects of its polyphenol‐rich fraction (prf) on dichlorvos‐induced cardio‐ and renal toxicity. There were several factors assessed during this study, including cardiac and renal markers, serum myeloperoxidase and xanthine oxidase, and electrocardiograph (ECG) changes. The changes in electrocardiograph (ECG) were recorded. Immunohistochemistry of cardiac and renal p38 and nitrotyrosine was determined. Dichlorvos exposure caused a significant decrease in L‐glutathione (reduced glutathione) and other antioxidant enzymes with increases in malondialdehyde, myeloperoxidase, advanced oxidation protein products, and protein carbonyl levels. It also brought about alterations in microanatomy of the heart and kidneys accompanied by increases in serum creatinine and urea levels. Exposure to dichlorvos induced prolonged QRS interval and shortened QT durations in rats. Immunohistochemistry revealed lower expressions of cardiac nitrotyrosine and renal p38 (mitogen‐activated protein kinase; MAPK) in rats treated with prf of P. nigrescens. Combining all, prf of P. nigrescens demonstrated antioxidant as well as protective properties in the heart and kidneys of rats exposed to dichlorvos. It ameliorated dichlorvos‐induced cardio‐ and nephrotoxicity giving credence to its use in ethnomedicine.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Akut miyokarditte fragmante QRS kompleksinin prognostik rolü

Aim: Although a fulminant course of the myocarditis is difficult to predict, it may lead to acute heart failure and death. Previous studies have demonstrated that reduced left ventricular systolic function and prolonged QRS duration can predict the fulminant course. This study aimed to identify whether fragmented QRS complex (fQRS) could also be predictive of fulminant disease in this population. Material and Methods: We retrospectively included 156 patients diagnosed with acute myocarditis. They were divided into the fulminant group (n = 18) and the non-fulminant group (n = 138). Multivariate logistic regression analysis was used to identify the independent factors predictive of fulminant disease. Results: Fragmented QRS developed in 11 (61%) in the fulminant group and only 10 patients (7%) in the non-fulminant group (p &amp;lt;0.001). Patients with fulminant myocarditis had a higher mortality rate than those with non-fulminant disease (44.6% vs. 0%, p &amp;lt; 0.001). Multivariate analysis revealed that the presence of fQRS (p=0.019), longer Tpe/qt ratio (p=0.022) and clinical heart failure (&amp;lt;0.001) were significant predictors associated with a fulminant course of myocarditis. Conclusion: The presence of fQRS complex, as a simple and feasible electrocardiographic marker, seems to be a novel predictor fulminant myocarditis. This simpleparameter may be used in identifying patients at high risk for fulminancy and so early mechanical support could provide improved patient outcomes.

Effect of antihypertensive therapy on development of incident conduction system disease in hypertensive patients.

Previous work has demonstrated that treatment of hypertensive patients with the angiotensin-converting enzyme inhibitor lisinopril was associated with a reduced incidence of a composite conduction system disease endpoint and also left bundle branch block (LBBB) compared with chlorthalidone therapy. The relationship of incident conduction system disease to angiotensin receptor blocker therapy has not been examined. Risk of new right (RBBB) or LBBB in relation to losartan-based vs. atenolol-based treatment was assessed in 8342 hypertensive patients without baseline RBBB or LBBB. Risk of incident intraventricular conduction delay (IVCD), defined as new QRS duration at least 110 ms was assessed in the 7110 patient subset who also had baseline QRS duration less than 110 ms. QRS duration and BBB were determined on in-study ECGs done at 6 months, 1 year and then yearly. During 4.8 ± 1.0 years follow-up, 459 patients developed new LBBB (5.5%), 184 (2.2) new RBBB and 1173 (16.5%) a new IVCD. In univariate Cox analyses, losartan-based treatment was not associated with a significantly reduced risk of either new LBBB (hazard ratio 0.95, 95% CI 0.79-1.14, P = 0.583) or RBBB (hazard ratio 1.02, 95% CI 0.76-1.36, P = 0.903), but resulted in a 15% lower risk of new IVCD (hazard ratio 0.85, 95% CI 0.76-0.95, P = 0.005). In a multivariable Cox model that adjusted for other statistically significant predictors of incident IVCD in this population (age, sex, race, history of ischemic heart disease, MI, heart failure, diabetes or atrial fibrillation, prior antihypertensive treatment, baseline total and HDL cholesterol, serum glucose and creatinine and baseline QRS duration as standard covariates and incident MI and on-treatment systolic and diastolic pressure, BMI and Cornell voltage as time-dependent covariates), losartan treatment remained associated with a 13% lower risk of new IVCD (hazard ratio 0.87, 95% CI 0.77-0.98, P = 0.021). Incident IVCD, but not BBB, is significantly reduced by losartan-based treatment. Further study is warranted to assess the potential differential impact of this therapy on QRS prolongation vs. development of more discrete conduction system block. .

Gender-Based Differences in Cardiac Resynchronization Therapy Response.

Cardiac resynchronization therapy (CRT) has been shown to have a multitude of beneficial effects in select patients with systolic heart failure, by enhancing reverse remodeling, improving quality of life and functional status, reducing risk of heart failure admission, and most importantly, improving survival. Although women were underrepresented in the clinical trials, they were demonstrated to derive greater therapeutic benefit from CRT compared with men. Importantly, women were noted to derive benefit at a lesser degree of QRS prolongation than men, well below the now generally accepted cutoff of QRS ≥150milliseconds.

Automatic diagnosis of strict left bundle branch block using a wavelet-based approach.

Patients with left bundle branch block (LBBB) are known to have a good clinical response to cardiac resynchronization therapy. However, the high number of false positive diagnosis obtained with the conventional LBBB criteria limits the effectiveness of this therapy, which has yielded to the definition of new stricter criteria. They require prolonged QRS duration, a QS or rS pattern in the QRS complexes at leads V1 and V2 and the presence of mid-QRS notch/slurs in 2 leads within V1, V2, V5, V6, I and aVL. The aim of this work was to develop and assess a fully-automatic algorithm for strict LBBB diagnosis based on the wavelet transform. Twelve-lead, high-resolution, 10-second ECGs from 602 patients enrolled in the MADIT-CRT trial were available. Data were labelled for strict LBBB by 2 independent experts and divided into training (n = 300) and validation sets (n = 302) for assessing algorithm performance. After QRS detection, a wavelet-based delineator was used to detect individual QRS waves (Q, R, S), QRS onsets and ends, and to identify the morphological QRS pattern on each standard lead. Then, multilead QRS boundaries were defined in order to compute the global QRS duration. Finally, an automatic algorithm for notch/slur detection within the QRS complex was applied based on the same wavelet approach used for delineation. In the validation set, LBBB was diagnosed with a sensitivity and specificity of Se = 92.9% and Sp = 65.1% (Acc = 79.5%, PPV = 74% and NPV = 89.6%). The results confirmed that diagnosis of strict LBBB can be done based on a fully automatic extraction of temporal and morphological QRS features. However, it became evident that consensus in the definition of QRS duration as well as notch and slurs definitions is necessary in order to guarantee accurate and repeatable diagnosis of complete LBBB.

Ellagic Acid Protects Cardiac Arrhythmias Following Global Cerebral Ischemia/Reperfusion Model.

Background: Cerebral ischemia/reperfusion (I/R) could increase the reactive oxidative stress in the cardiomyocytes. Also, some studies report cardiac arrhythmias following oxidative stressor such as I/R. Hence, this study was aimed to investigate the effects of ellagic acid (EA) against arrhythmias in a cerebral I/R model. Materials and Methods: Thirty-two male rats were randomly allocated into four groups: Sham (normal saline, 10 days), EA (100 mg/kg EA, 10 days), I/R (20 min ischemia followed by 30 min reperfusion, 10 days), and EA + I/R (100 mg/kg EA before I/R). In all animals, electrocardiogram (ECG) was recorded pre-ischemia and postischemia on the first and 11th days, respectively. Results: The I/R group showed an abnormally prolonged QTc interval after ischemia compared to the preischemia and control groups. EA administration in the EA+I/R group significantly reduced this prolonged QTc interval (P< 0.01). In the I/R group, ischemic/reperfusion resulted in a prolonged QRS complex and an elevated ST, which EA significantly prevented (P<0.01). In addition, EA significantly prevented the dramatically shortened RR interval induced by reperfusion (P<0.01). The incidence of ventricular fibrillation significantly increased in the I/R group; then it dramatically decreased following the administration of EA (P<0.0001). Conclusion: EA pretreatment repaired the adverse effects of I/R on the ECG parameters, which can be attributed to its negative chronotropic effects. EA pretreatment can prevent the cerebral I/R-induced heart arrhythmias.

Ellagic Acid Protects Cardiac Arrhythmias Following Global Cerebral Ischemia/Reperfusion Model

Background: Cerebral ischemia/reperfusion (I/R) could increase the reactive oxidative stress in the cardiomyocytes. Also, some studies report cardiac arrhythmias following oxidative stressor such as I/R. Hence, this study was aimed to investigate the effects of ellagic acid (EA) against arrhythmias in a cerebral I/R model. Materials and Methods: Thirty-two male rats were randomly allocated into four groups: Sham (normal saline, 10 days), EA (100 mg/kg EA, 10 days), I/R (20 min ischemia followed by 30 min reperfusion, 10 days), and EA + I/R (100 mg/kg EA before I/R). In all animals, electrocardiogram (ECG) was recorded pre-ischemia and postischemia on the first and 11th days, respectively. Result: The I/R group showed an abnormally prolonged QTc interval after ischemia compared to the preischemia and control groups. EA administration in the EA+I/R group significantly reduced this prolonged QTc interval (P&lt; 0.01). In the I/R group, ischemic/reperfusion resulted in a prolonged QRS complex and an elevated ST, which EA significantly prevented (P&lt;0.01). In addition, EA significantly prevented the dramatically shortened RR interval induced by reperfusion (P&lt;0.01). The incidence of ventricular fibrillation significantly increased in the I/R group; then it dramatically decreased following the administration of EA (P&lt;0.0001). Conclusion: EA pretreatment repaired the adverse effects of I/R on the ECG parameters, which can be attributed to its negative chronotropic effects. EA pretreatment can prevent the cerebral I/R-induced heart arrhythmias.[GMJ. 2019;inpress:e1235]

Ellagic Acid Protects Cardiac Arrhythmias Following Global Cerebral Ischemia/Reperfusion Model

Background: Cerebral ischemia/reperfusion (I/R) could increase the reactive oxidative stress in the cardiomyocytes. Also, some studies report cardiac arrhythmias following oxidative stressor such as I/R. Hence, this study was aimed to investigate the effects of ellagic acid (EA) against arrhythmias in a cerebral I/R model. Materials and Methods: Thirty-two male rats were randomly allocated into four groups: Sham (normal saline, 10 days), EA (100 mg/kg EA, 10 days), I/R (20 min ischemia followed by 30 min reperfusion, 10 days), and EA + I/R (100 mg/kg EA before I/R). In all animals, electrocardiogram (ECG) was recorded pre-ischemia and postischemia on the first and 11th days, respectively. Results: The I/R group showed an abnormally prolonged QTc interval after ischemia compared to the preischemia and control groups. EA administration in the EA+I/R group significantly reduced this prolonged QTc interval (P&lt; 0.01). In the I/R group, ischemic/reperfusion resulted in a prolonged QRS complex and an elevated ST, which EA significantly prevented (P&lt;0.01). In addition, EA significantly prevented the dramatically shortened RR interval induced by reperfusion (P&lt;0.01). The incidence of ventricular fibrillation significantly increased in the I/R group; then it dramatically decreased following the administration of EA (P&lt;0.0001). Conclusion: EA pretreatment repaired the adverse effects of I/R on the ECG parameters, which can be attributed to its negative chronotropic effects. EA pretreatment can prevent the cerebral I/R-induced heart arrhythmias. [GMJ.2019;8:e1235]

Correction of the QRS duration for heart rate

ObjectiveTo determine the clinical value of correcting the QRS duration for heart rate. BackgroundWe recently observed [1] that the QRS duration shortens during spontaneous increases in heart rate. In the current study, we analyzed ECG and pharmacokinetic data of 21 subjects who received quinidine in a recent study [2]. They experienced the expected post-quinidine increase in heart rate, allowing us to determine if quinidine's well-known QRS prolongation might be attenuated due to the concomitant rate increase. MethodsIn a crossover-designed study, after baseline ECG recording, the subjects received quinidine 400 mg orally or placebo, and ECGs and quinidine plasma concentrations were then obtained at 15 prespecified timepoints over 24 h. The previously determined QRS-RR regression slope (0.0125) [1] was used to rate-correct QRS. Change in QRS from baseline (dQRS) and rate-corrected change in QRS from baseline (dQRSc) over time were plotted with the mean quinidine concentration and the correlation of plasma concentration with dQRS and dQRSc was assessed by pairwise correlation and linear regression. ResultsThere was a statistically significantly greater increase in heart rate at all timepoints combined in the quinidine arm compared with the placebo arm (9.9 ± 6.80 vs. 5.2 ± 7.42, respectively, p < 0.0001). dQRSc was significantly greater at all timepoints combined compared with dQRS (1.99 ± 4.824 vs −0.68 ± 4.640 msec, respectively, p < 0.0001). dQRS correlated poorly with quinidine plasma concentration (p = 0.127), with no clear change in QRS observed. On the other hand, dQRSc correlated well with quinidine concentration (p = 0.010), with a clear rise and fall in dQRSc that mirrored the rise and fall of quinidine concentration. ConclusionRate correction of the QRS duration improves detection of QRS prolongation in the presence of heart rate change. Condensed abstractUsing the mean QRS – RR slope determined previously in normal volunteers [1], we corrected the QRS duration for its known dependency on heart rate in 21 subjects who received quinidine and experienced the expected post-quinidine increase in heart rate in a recent clinical trial [2]. We found that uncorrected QRS did not correlate with quinidine concentration (p = 0.127), while rate-corrected QRS correlated well (p = 0.010) and mirrored the rise and fall of quinidine concentration. Rate correction of the QRS duration improves detection of QRS prolongation in the presence of heart rate change.

Adverse Effects of Physostigmine.

Physostigmine is a tertiary amine carbamate acetylcholinesterase inhibitor. Its ability to cross the blood-brain barrier makes it an effective antidote to reverse anticholinergic delirium. Physostigmine is underutilized following the publication of patients with sudden cardiac arrest after physostigmine administration in patients with tricyclic antidepressant (TCA) overdoses. We completed a narrative literature review to identify reported adverse effects associated with physostigmine administration. One hundred sixty-one articles and a total of 2299 patients were included. Adverse effects occurred in 415 (18.1%) patients. Hypersalivation (206; 9.0%) and nausea and vomiting (96; 4.2%) were the most common adverse effects. Fifteen (0.61%) patients had seizures, all of which were self-limited or treated successfully without complication. Symptomatic bradycardia occurred in 8 (0.35%) patients including 3 patients with bradyasystolic arrests. Ventricular fibrillation occurred in one (0.04%) patient with underlying coronary artery disease. Of the 394 patients with TCA overdose, adverse effects were described in 14 (3.6%). Adverse effects occurred in 7.7% of patients treated with an overdose of an anticholinergic agent compared with 20.6% of patients with non-anticholinergic agents. Five (0.22%) fatalities were identified. In conclusion, significant adverse effects associated with the use of physostigmine were infrequently reported. Seizures were self-limited or resolved with benzodiazepines, and all patients recovered neurologically intact. Physostigmine should be avoided in patients with QRS prolongation on EKG, and caution should be used in patients with a history of coronary artery disease and overdoses with QRS prolonging medications. Based upon our review, physostigmine is a safe antidote to treat anticholinergic overdose.

Ferulic acid ameliorates doxorubicin-induced cardiac toxicity in rats.

Ferulic acid (FA) is a phenolic compound with potent antioxidant activity. The objective of the study was to study the protective effects of FA on doxorubicin (Dox)-induced myocardial toxicity in rats. Wistar rats received vehicle (control) or Dox (20 mg/kg, i.p.) or telmisartan (Tel; 10 mg/kg, p.o.) or ferulic acid (20 mg/kg and 40 mg/kg, p.o.) for 7 days followed by treatment with Dox (20) on the fifth day of treatment, except the control group. On day 8, electrocardiographic parameters were recorded followed by blood withdrawal and then the animals were sacrificed for histopathology. Administration of Dox showed prolonged RR, QTc interval, and QRS complex. The levels of serum CK-MB, LDH, IL-1β, and IL-6 were significantly increased (p < 0.01). Similarly, levels of Ca+2, Mg+2 ATPase, and Ca+2 ATPase and expression of ANP and BNP were significantly higher as compared to the control. In the FA-treated group, ECG was normal. The serum levels of CK-MB, LDH, IL-1β, and IL-6 were not elevated. Heart tissue Ca+2, Mg+2 ATPase, and Ca+2 ATPase did not show a statistical difference compared to the control group. The FA treatment attenuated the expression of ANP and BNP. FA (20 and 40) augmented myocardial GSH and Na+/K+ ATPase. Histopathology of the heart confirmed the cardioprotective effect of FA.

Characterization of microminipig as a laboratory animal for safety pharmacology study by analyzing fluvoxamine-induced cardiovascular and dermatological adverse reactions.

Fluvoxamine is a selective serotonin-reuptake inhibitor, of which IC50 values for serotonin- and noradrenaline-uptake process were reported to be 3.8 and 620nmol/L, respectively, also known to directly inhibit cardiac Na+, Ca2+, and K+ channels. We characterized microminipig as a laboratory animal by analyzing fluvoxamine-induced cardiovascular and dermatological responses under halothane anesthesia. Fluvoxamine maleate was infused in doses of 0.1, 1, and 10mg/kg over 10min with a pause of 20min (n = 4). The peak plasma concentrations were 35, 320, and 1906ng/mL, of which free plasma concentrations were estimated as 20, 187, and 1108nmol/L, respectively. The low and middle doses did not alter any cardiovascular variable. The high dose increased heart rate and mean blood pressure, prolonged QRS width, but shortened QT interval, whereas no significant change was detected in PR interval or QTcF. Moreover, it induced systemic erythema on the skin. Pretreatment of H1/5-HT2A antagonist cyproheptadine hydrochloride sesquihydrate in a dose of 0.3mg/kg significantly attenuated the fluvoxamine-induced pressor response; but tended to further enhance sinus automaticity, atrioventricular nodal conduction; and ventricular repolarization in addition to intraventricular conduction delay; whereas it markedly suppressed onset of systemic erythema (n = 4). In microminipigs, cardiovascular adverse effects of the high dose may be manifested as a sum of its inhibitory action on the cardiac ionic channels and its stimulatory effects on serotonergic and adrenergic systems, whereas dermatologic reaction can be induced primarily through H1/5-HT2A receptor-dependent mechanism. Thus, microminipigs may be used for analyzing such multifarious adverse events of clinical serotonergic pharmacotherapy.

Evaluation using a four-dimensional imaging tool before and after pulmonary valve replacement in a patient with tetralogy of Fallot: a\xa0case report

BackgroundPulmonary regurgitation is a common complication after tetralogy of Fallot repair, resulting in right ventricular dysfunction, arrhythmia, and sudden death. However, the indications and optimal timing for pulmonary valve replacement are not fully known. We describe a case in which a four-dimensional imaging tool was useful in the decision to re-operate, thus resulting in decreased energy loss and improved right ventricular function after the re-operation for tetralogy of Fallot.Case presentationA 54-year-old Japanese woman visited our hospital due to palpitations and wide QRS tachycardia with persistent tiredness for several months. She underwent repair of tetralogy of Fallot when she was 2-years old. An electrocardiogram showed prolonged QRS duration (199 msec) with a complete right bundle branch block and an echocardiograph demonstrated that her right ventricle was highly enlarged and had poor contraction, and severe pulmonary valve regurgitation with one leaflet flail. Four-dimensional flow magnetic resonance imaging demonstrated that regurgitant volumes and regurgitant fractions of pulmonary regurgitation were calculated as 63.12 ml and 54.0%, respectively. Right ventricular end-diastolic/end-systolic volume index was 169.54/99.76 mL/m2, and the cardiac index was 1.78 L/minute per m2. Flow energy loss was 2.93 mW, which is estimated to be three times higher than normal controls. An electrophysiological study showed an intact anterior internodal pathway and a slow pathway just through the outside of the right atriotomy line scar, which is supposed to cause a re-entry circuit. We decided to perform a pulmonary valve replacement and a right maze procedure. A 27 mm bioprosthetic valve was implanted in the native pulmonary annulus with a supra-annular position. Concomitantly, the right maze procedure was performed. A four-dimensional flow magnetic resonance imaging done 3 months later showed that right ventricular end-diastolic/end-systolic volume index had significantly reduced to 85.24/55.41 mL/m2 and the cardiac index had increased from 1.78 to 2.58 L/minute per m2. Energy loss had greatly improved from 2.93 to 1.48 mW.ConclusionsA four-dimensional imaging tool was useful in the decision to re-operate, thus resulting in decreased energy loss and improved right ventricular function after the re-operation for tetralogy of Fallot.

Certification Is for You ….

Certification Is for You ….

Changes in ECG among patients with drug induced poisoning in a tertiary care hospital

Background: A wide variety of ECG changes can be seen with cardiac and noncardiac agents and may occur at therapeutic or toxic levels. Wide QRS and QT prolongation may be seen in poisoning cases; are potentially dangerous and indicate the necessity of continuous cardiac monitoring.The objective of this study was to determine the changes in ECG among patients admitted with pharmaceutical drug induced poisoning in a tertiary care hospital in Dhaka.&#x0D; Methods: This cross sectional study was carried out at the Department of Medicine, Dhaka Medical College Hospital (DMCH) during July-December, 2013. Detailed information were obtained; clinical examination and relevant investigations including ECG were done in each case according to protocol.&#x0D; Results: Among 66 cases mean age was 22.9 (±6.47) years and male to female ratio was 1: 2.14 (21 Vs 45). Common drug groups taken by the study population were benzodiazepines in 31(47.0%) and tricyclic antidepressants (TCA) in 18(27.3%) cases.Normal ECG findings were found in 28 (42.4%) cases, 18 (27.3%) cases revealed sinus tachycardia, 11(16.7%) showed prolong QT Interval, 6(9.1%) had atrial tachycardia, 5(7.6%) showed wide QRS and 3(4.6%) cases revealed prolong PR interval. Patients withTCA poisoning developedsinus tachycardia in 11(61.1%), prolong QT Interval in 6(33.3%), wide QRS in 5(27.8%),atrial tachycardia in 5(27.8%), prolong PR Interval in 2(11.1%), and Tall R in aVRin 2(11.1%) cases. Prolong QT Interval were found among 3 (75.0%) patients with K+ efflux channel blockers (chlorpromazine, chlorpheniramine and quetiapine) overdose.Patients with beta blocker overdose developed sinus bradycardia in 4 (100.0%) and prolong PR Interval in 1(25.0%) cases.&#x0D; Conclusion: Common drugs taken by the patients were amitriptyline sedatives. Wide QRS, prolong QT interval and some other ECG changes were observed by TCA poisoning in higher doses. TCA, benzodiazepines and K channel blockers induced prolong QT Interval in higher doses.Careful interpretation of ECG findings can provide key information to guide management of the poisoned patients.&#x0D; Bangladesh Med Res Counc Bull 2018; 44: 160-167

Can QRS duration predict microvascular reperfusion after primary percutaneous coronary intervention?

Background: In patients with ST-segment elevation myocardial infarction (STEMI), primary percutaneous coronary intervention (PCI) was associated with early and sustained restoration of blood flow compared to fibrinolytic therapy. Impaired myocardial blush grade (MBG) may be present in many after successful PCI. Prolonged QRS was found to be associated with an increased morbidity and mortality after STEMI. Aim: This study aims to find out if prolonged QRS in STEMI patients can predict low MBG after primary PCI. Patients and Methods: Sixty STEMI patients were included in our study. History taking, clinical examination, electrocardiography with measuring of QRS duration, primary PCI, and echocardiography were done to them. QRS duration was measured before and after PCI, and the change was calculated. Results: Patients with low MBG (0–1) had significantly higher QRS duration before and after PCI and significantly lower change after PCI (P < 0.00001 for each). Independent predictors for MBG were in order of significance: QRS duration before PCI (P < 0.00001), QRS duration after PCI (P < 0.00001), troponin level (P < 0.00001), symptom to balloon time (P = 0.0063), and creatine kinase MB level (P = 0.015). QRS duration 89 ms could predict low MBG with sensitivity 82.6%, specificity 86.5%, positive predictive value 79.2%, and negative predictive value 88.9%. Conclusion: In STEMI patients undergoing primary PCI, prolonged QRS duration was associated with a low MBG, a sign of impaired microvascular reperfusion. QRS duration before and after PCI were found to be independent predictors for low MBG (0–1).

Prognostic Implication of Ventricular Conduction Disturbance Pattern in Hospitalized Patients with Acute Heart Failure Syndrome.

Background and ObjectivesConflicting data exist regarding the prognostic implication of ventricular conduction disturbance pattern in patients with heart failure (HF). This study investigated the prognostic impact of ventricular conduction pattern in hospitalized patients with acute HF.MethodsData from the Korean Acute Heart Failure registry were used. Patients were categorized into four groups: narrow QRS (<120 ms), right bundle branch block (RBBB), left bundle branch block (LBBB), and nonspecific intraventricular conduction delay (NICD). The NICD was defined as prolonged QRS (≥120 ms) without typical features of LBBB or RBBB. The primary endpoint was the composite of all-cause mortality or rehospitalization for HF aggravation within 1 year after discharge.ResultsThis study included 5,157 patients. The primary endpoint occurred in 39.7% of study population. The LBBB group showed the highest incidence of primary endpoint followed by NICD, RBBB, and narrow QRS groups (52.5% vs. 49.7% vs. 44.4% vs. 37.5%, p<0.001). In a multivariable Cox-proportional hazards regression analysis, LBBB and NICD were associated with 39% and 28% increased risk for primary endpoint (LBBB hazard ratio [HR], 1.392; 95% confidence interval [CI], 1.152–1.681; NICD HR, 1.278; 95% CI, 1.074–1.520) compared with narrow QRS group. The HR of RBBB for the primary endpoint was 1.103 (95% CI, 0.915–1.329).ConclusionsLBBB and NICD were independently associated with an increased risk of 1-year adverse event in hospitalized patients with HF, whereas the prognostic impacts of RBBB were limited.Trial RegistrationClinicalTrials.gov Identifier: NCT01389843