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Repolarization
Kinds of Repolarization Terms modified by Repolarization Selected AbstractsRepolarization of the cardiac action potential.ACTA PHYSIOLOGICA, Issue 2010Does an increase in repolarization capacity constitute a new anti-arrhythmic principle? Abstract The cardiac action potential can be divided into five distinct phases designated phases 0,4. The exact shape of the action potential comes about primarily as an orchestrated function of ion channels. The present review will give an overview of ion channels involved in generating the cardiac action potential with special emphasis on potassium channels involved in phase 3 repolarization. In humans, these channels are primarily Kv11.1 (hERG1), Kv7.1 (KCNQ1) and Kir2.1 (KCNJ2) being the responsible ,-subunits for conducting IKr, IKs and IK1. An account will be given about molecular components, biophysical properties, regulation, interaction with other proteins and involvement in diseases. Both loss and gain of function of these currents are associated with different arrhythmogenic diseases. The second part of this review will therefore elucidate arrhythmias and subsequently focus on newly developed chemical entities having the ability to increase the activity of IKr, IKs and IK1. An evaluation will be given addressing the possibility that this novel class of compounds have the ability to constitute a new anti-arrhythmic principle. Experimental evidence from in vitro, ex vivo and in vivo settings will be included. Furthermore, conceptual differences between the short QT syndrome and IKr activation will be accounted for. [source] Electrocardiogram Differentiation of Benign Early Repolarization Versus Acute Myocardial Infarction by Emergency Physicians and CardiologistsACADEMIC EMERGENCY MEDICINE, Issue 9 2006Samuel D. Turnipseed MD Abstract Objectives: ST-segment elevation (STE) related to benign early repolarization (BER), a common normal variant, can be difficult to distinguish from acute myocardial infarction (AMI). The authors compared the electrocardiogram (ECG) interpretations of these two entities by emergency physicians (EPs) and cardiologists. Methods: Twenty-five cases (13 BER, 12 AMI) of patients presenting to the emergency department with chest pain were identified. Criteria for BER required four of the following: 1) widespread STE (precordial greater than limb leads), 2) J-point elevation, 3) concavity of initial up-sloping portion of ST segment, 4) notching or irregular contour of J point, and 5) prominent, concordant T waves. Additional BER criteria were 1) stable ECG pattern, 2) negative cardiac injury markers, and 3) normal cardiac stress test or angiography. AMI criteria were 1) regional STE, 2) positive cardiac injury markers, and 3) identification of culprit coronary artery by angiography in less than eight hours of presentation. The 25 ECGs were distributed to 12 EPs and 12 cardiologists (four in academic medicine, four in community practice, and four in community academics [health maintenance organization] in each physician group). The physicians were informed of the patients' age, gender, and race, and they then interpreted the ECGs as BER or AMI. Undercalls (AMI misdiagnosed as BER) and overcalls (BER misdiagnosed as AMI) were calculated for each physician group. Results: Cardiologists correctly interpreted 90% of ECGs, and EPs correctly interpreted 81% of ECGs. The proportion of undercalls (missed AMI/total AMI) was 2.8% for cardiologists (95% confidence interval [CI] = 0.09% to 5.5%) compared with 9.7% for EPs (95% CI = 4.8% to 14.6%) (p = 0.02). The proportion of overcalls (missed BER/total BER) was 17.3% for cardiologists (95% CI = 11.4% to 23.3%) versus 27.6% for EPs (95% CI = 20.6% to 34.6%) (p = 0.03). The mean number of years in practice was 19.8 for cardiologists (95% CI = 19 to 20.5) and 11 years for EPs (95% CI = 10.5 to 12.0) (p < 0.001). Conclusions: Although correct interpretation was high in both groups, cardiologists, who had significantly more years of practice, had fewer misinterpretations than EPs in distinguishing BER from AMI electrocardiographically. [source] The Effect of Antihistamine Cetirizine on Ventricular Repolarization in Congenital Long QT SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2007ANNA-MARI HEKKALA M.D. Introduction: Many drugs are known to block cardiac potassium channels, thus prolonging QT interval and predisposing to malignant arrhythmias. Patients with congenital long QT syndrome are particularly vulnerable, but usually electrophysiological effects of drugs have not been assessed in these patients at risk. Methods: Fifteen asymptomatic patients with type 1 (LQT1), 15 patients with type 2 (LQT2) long QT syndrome, and 15 healthy volunteers took a placebo and cetirizine 10 mg. In addition, healthy volunteers took cetirizine 50 mg. The study was single-blinded and randomized. Exercise tests were performed during stable plasma concentrations. The electrocardiogram was recorded with a body surface potential mapping system (BSPM). Data were analyzed with an automated analyze program. QT intervals to the T wave apex and T wave end and their difference (Tp-e) were determined at rest and at specified heart rates during and after exercise. Results: Cetirizine did not lengthen the QT intervals at rest or during exercise and recovery in any group. It shortened Tp-e at rest in LQT1 and LQT2 patients and during exercise test in LQT1 patients, thus slightly decreasing electrocardiographic transmural dispersion of repolarization. Conclusions: Cetirizine does not adversely modify ventricular repolarization in types 1 and 2 long QT syndrome, suggesting that it might be used safely in these long QT syndrome patients. [source] Proarrhythmia as a Class Effect of Quinolones: Increased Dispersion of Repolarization and Triangulation of Action Potential Predict Torsades de PointesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2007PETER MILBERG M.D. Background: Numerous noncardiovascular drugs prolong repolarization and thereby increase the risk for patients to develop life-threatening tachyarrhythmias of the torsade de pointes (TdP) type. The development of TdP is an individual, patient-specific response to a repolarization-prolonging drug, depending on the repolarization reserve. The aim of the present study was to analyze the underlying mechanisms that discriminate hearts that will develop TdP from hearts that will not develop TdP. We therefore investigated the group of quinolone antibiotics that reduce repolarization reserve via IKr blockade in an intact heart model of proarrhythmia. Methods and Results: In 47 Langendorff-perfused, AV-blocked rabbit hearts, ciprofloxacin (n = 10), ofloxacin (n = 14), levofloxacin (n = 10), and moxifloxacin (n = 13) in concentrations from 100 ,M to 1,000 ,M were infused. Eight monophasic action potentials (MAPs) and an ECG were recorded simultaneously. After incremental pacing at cycle lengths from 900 ms to 300 ms to compare the action potential duration, potassium concentration was lowered to provoke TdP. All antibiotics led to a significant increase in QT interval and MAP duration, and exhibited reverse-use dependence. Eight simultaneously recorded MAPs demonstrated an increase in dispersion of repolarization in the presence of all antibiotics. MAP triangulation (ratio: MAP90/50) and fluctuation of consecutive action potentials were increased for all tested drugs at high concentrations. In the presence of low potassium concentration, all quinolones led to TdP: ciprofloxacin, 4 out of 10 (40%); ofloxacin, 3 out of 14 (21%); moxifloxacin, 9 out of 13 (69%); and levofloxacin, 2 out of 10 (20%). Hearts that developed TdP demonstrated a significant greater influence on dispersion of repolarization and on triangulation as compared with hearts without TdP. Conclusion: Quinolone antibiotics may be proarrhythmic due to a significant effect on myocardial repolarization. The individual response of a heart to develop TdP in this experimental model is characterized by a greater effect on dispersion of repolarization and on triangulation of action potential as compared with hearts that do not develop TdP. [source] Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Michael H. Swann M.SC. Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source] Adrenergic-Cholinergic Interaction that Modulates Repolarization in the Atrium is Altered with AgingJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2002EUGENE A. SOSUNOV Ph.D. Autonomic Modulation of Atrial Repolarization.Introduction: Aging is associated with involution of both limbs of the autonomic nervous system, and the prejunctional and postjunctional effects of adrenergic and cholinergic stimulation are altered with senescence. Hence, postjunctional age-related changes in adrenergic-cholinergic interaction are a likely occurrence and may contribute to an altered substrate for arrhythmias. Methods and Results: Microelectrode techniques were used to record action potentials from epicardial slices of Bachmann's bundles of dogs aged 3 to 5 years (adult) and 8 to 12 years (old) in the absence or presence of acetylcholine and isoproterenol (separately and in combination). In control, action potential duration to 90% repolarization (APD) was longer in old atria. Acetylcholine (10,8 to 10,5 mol/L) in a concentration-dependent manner hyperpolarized and shortened APD in both tissues, with more prominent effects in the old. The effects of isoproterenol (10,9 to 10,6 mol/L) to elevate the plateau and shorten APD were about the same in both adult and old tissues. In adults, low concentrations of isoproterenol (10,9 and 10,8 mol/L) significantly prolonged APD, which had been first shortened by acetylcholine. This effect of isoproterenol was decreased in old atrial tissue, resulting in shorter APD in old than adult atria in the combined presence of beta-adrenergic and muscarinic agonists. Conclusion: In adult Bachmann's bundle, beta-adrenergic stimulation effectively operates as a "brake" to decrease the extent of cholinergic-induced APD shortening. The action of beta-adrenergic stimulation to antagonize acetylcholine-induced acceleration of repolarization declines with age, which may contribute to an altered arrhythmogenic substrate. [source] Atrial Fibrillation in the Goat Induces Changes in Monophasic Action Potential and mRNA Expression of Ion Channels Involved in RepolarizationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000HUUB M.W. VAN DER VELDEN PH.D. MAP Changes and Ion Channel Expression in Goat AF. Introduction: Sustained atrial fibrillation (AF) is characterized by a marked shortening of the atrial effective refractory period (AKRP) and a decrease or reversal of its physiolonic adaptation to heart rate. The aim of the present study was to investigate whether the AF-induced changes in AKKP in the goat are associated with changes in the atrial monophasic action potential (MAP) and whether an abnormal expression of specific ion channels underlies such changes. Methods and Results: Following thoracotomy, MAPs were recorded from the free wall of the right atrium hoth before induction of AF (control) and after cardioversion of sustained AF (>2 months) in chronically instrumented goats. In control goats. MAP duration at 80% repolarization (MAPD80) shortened (P < 0.01) from 132 ± 4 msec during slow pacing (400-msec interval) to 86 ± 10 msec during fast pacing (180 msec). After cardioversion of sustained AF, the MAPD80, during slow pacing was as short as 67 ± 5 msec (electrical remodeling). Increasing the pacing rate resulted in prolongation (P = 0.02) of the MAPD80 to 91 ± 6 msec. Also. MAPD20 (20% repolarization) shortened (P = 0.05) from 32 ± 4 msec (400 msec) to 14 ± 7 msec (180 msec) in the control goats, whereas it prolonged (P = 0.03) from 20 ± 3 msec (400 msec) to 33 ± 5 msec (180 msec) in sustained AF, mRNA expression of the L-type Ca2+ channel ,1c gene and Kv1.5 potassium channel gene, which underlie Ica, and Ikur respectively, was reduced in sustained.AF compared with sinus rhythm hy 32% (P = 0.01) and 45% (P < 0.01). respectively. No significant changes were found in the mRNA levels of the rapid Na+ channel, the Na+/Ca2+ exchanger, or the Kv4.2/4.3 channels responsible for I10. Conclusion: AF-induced electrical remodeling in the goat comprises shortening of MAPD and reversal of its physiologic rate adaptation. Changes in the time course of reploarization of the action potential are associated with changes in mRNA expression of the , subunit genes of the L.-type Ca2+ channel and the Kvl.5 potassium channel. [source] QT Dispersion Does Not Represent Electrocardiographic Interlead Heterogeneity of Ventricular RepolarizationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000MAREK MALIK Ph.D. QT Dispersion and Repolarization Heterogeneity. Introduction: QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than "nondipolar" signals. Methods and Results: Seventy-eight normal subjects (47 ± 16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38 ± 15 years. 21 women), 72 dilated cardiomyopathy patients (DCM; 48 ± 15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63 ± 12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). OTd was 33.6 ± 18.3, 47.0 ± 19.3, 34.8 ± 21.2, and 57.5 ± 25.3 msec in normals, HCM, CM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%± 0.031%, 0.067%± 0.067%, 0.112%± 0.154%, and 0.186%± 0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS. other P < 0.006), The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. Conclusion: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it. [source] Changes in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized DogsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000MICHAEL RUBART M.D. Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid-myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ,6 and ,3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing-induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4-aminopyridine-sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ,30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L-type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+ -activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency-dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl. [source] Ionic Basis for Action Potential Prolongation by Phenylephrine in Canine Epicardial MyocytesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2000RICHARD B. ROBINSON Ph.D. Phenylephrine Action on Repolarization. Introduction: In canine ventricle, ,-adrenergic agonists prolong action potential duration (APD) without any effect on the action potential notch, suggesting that, in this species, the effect on repolarization might he independent of inhibition of Ito. The present study investigated the action of the ,-adrenergic agonist phenylephrine on the action potential and the repolarizing currents Ito and IK in isolated canine epicardial myocytes. Methods and Results: Isolated cells from canine epicardial tissue, and Purkinje fibers, were studied with the whole cell, voltage clamp method. Phenylephrine 0.1 ,M increased APD by 13%± 4% at 90% repolarization without affecting the notch or amplitude. Under voltage clamp, concentrations of phenylephrine as high as 10 ,M had no effect on Itp in canine epicardial myocytes. However, Ito of isolated canine Purkinje myocytes was reduced to 69%± 7% of control by 1 ,M phenylephrine. Further studies in canine epicardial myocytes revealed an action of phenylephrine to inhibit Ik, and in particular IKs Using a voltage protocol that included a two-step repolarization to separate IKs and IKr tail components, the largely 1Ke, component was not significantly affected by 1 ,M phenylephrine, whereas the largely IKs component was reduced to 81%± 5% of control value. Conclusion: ,-Adrenergic prolongation of repolarization in canine epicardium does not result from inhibition of Ito. Rather, it appears that reduction of IKs contributes to the action of phenylephrine. The unresponsiveness of epicardial Ito is not a general characteristic of the canine heart, because Purkinje myocyte Ito was inhibited, suggesting regional differences in the molecular basis of lto, and/or a-adrenergic signaling in the canine heart. [source] Myocardial Repolarization: From Gene to BedsideJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 2 2003Jean T Barbey M.D. No abstract is available for this article. [source] Acute Effects of Low Doses of Red Wine on Cardiac Conduction and Repolarization in Young Healthy SubjectsALCOHOLISM, Issue 12 2009Matteo Cameli Background:, Moderate to high blood concentrations of ethanol have been shown to yield acute changes in cardiac electrophysiological properties, but the effect of low concentrations have never been assessed. The role of concomitant changes in clinical variables or cardiac dimensions is also still unknown. This study aimed at exploring the acute effects of low doses of ethanol, administered as Italian red wine, on conduction, depolarization, and repolarization electrocardiographic (ECG) intervals in a population of healthy subjects. Methods:, Forty healthy young volunteers drank a low quantity of red wine (5 ml/kg), and an equal volume of fruit juice in separate experiments. Heart rate, P-wave duration, PR interval, QRS duration, QT interval, corrected QT interval, QT dispersion, and corrected QT dispersion were assessed at baseline and after 60 minutes from challenge. Results:, Mean blood ethanol concentration after drinking was 0.48 ± 0.06 g/l. Compared to the control challenge, significant changes after red wine intake were observed in P-wave duration (from 101 ± 11 to 108 ± 14 milliseconds, p = 0.0006), PR interval (from 153 ± 15 to 167 ± 17 milliseconds, p < 0.0001), QT interval (from 346 ± 28 to 361 ± 24 milliseconds, p < 0.0001), and corrected QT interval (from 388 ± 24 to 402 ± 30 milliseconds, p = 0.0006). None of these changes showed correlations with modifications in clinical or echocardiographic variables. In multivariate analyses aimed at exploring predictors of ECG changes, none of the variables entered the final models. Conclusions:, Low doses of red wine acutely slow cardiac conduction and prolong repolarization in normal individuals. These changes are poorly predictable. The potential arrhythmogenic impact of these effects is worthy of exploration. [source] Effects of Ischemia on Repolarization in Patients with Single and Multivessel Coronary DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003DALIA GIEDRIMIENE GIEDRIMIENE, D., et al.: Effects of Ischemia on Repolarization in Patients with Single and Multivessel Coronary Disease. To evaluate if QT dispersion (QTd) may be affected by the number of obstructed coronary arteries (CAs) in patients with acute myocardial infarction (MI) and undergoing angioplasty, and to evaluate if QTd may be affected by ejection function of the heart. The infarct related CA was identified by coronary angiography in 141 patients (97 men, mean age61.6 ± 12.9years) with acute MI undergoing percutaneous angioplasty. Successful reperfusion was defined as TIMI III flow with <20% residual stenosis. QTd, calculated by subtracting the shortest from the longest QT interval on 12-lead electrocardiograms, was examined immediately before and after angioplasty, at 24 hours, and 3 days after angioplasty. Successful reperfusion was achieved in 98 (69.5%) patients. Prolonged QTd at baseline was found in all patients with ischemia. A trend toward a decrease in QTd was observed immediately after angioplasty and at 24 hours, and a significant decrease at 3 days in patients with successful reperfusion regardless of the number of occluded CAs. There was no change in QTd found in patients with no reperfusion. An increase in QTd was observed in patients with acute ischemia due to single or multivessel disease. (PACE 2003; 26[Pt. II]:390,393) [source] Dispersion of QT Intervals: A Measure of Dispersion of Repolarization or Simply a Projection Effect?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2000DIEGO DI BERNARDO QT interval dispersion may provide little information about repolarization dispersion. Some clinical measurements demonstrate an association between high QT interval dispersion and high morbidity and mortality, but what is being measured is not clear. This study was designed to help resolve this dilemma. We compared the association between different clinical measures of QT interval dispersion and the ECG lead amplitudes derived from a heart vector model of repolarization with no repolarization dispersion whatsoever. We compared our clinical QT interval dispersion data obtained from 25 subjects without cardiac disease with similar data from published studies, and correlated these QT dispersion results with the distribution of lead amplitudes derived from the projection of the heart vector onto the body surface during repolarization. Published results were available for mean relative QT intervals and mean differences from the maximum QT interval. The leads were derived from Uijen and Dower lead vector data. Using the Uijen lead vector data, the correlation between measurements of dispersion and derived lead amplitudes ranged from 0.78 to 0.99 for limb leads, and using the Dower values ranged from 0.81 to 0.94 for the precordial leads. These results show a clear association between the measured QT interval dispersion and the variation in ECG lead amplitudes derived from a simple heart vector model of repolarization with no regional information. Therefore, measured QT dispersion is related mostly to a projection effect and is not a true measure of repolarization dispersion. Our existing interpretation of QT dispersion must be reexamined, and other measurements that provide true repolarization dispersion data investigated. [source] Chronic Amiodarone Effects on Epicardial Conduction and Repolarization in the Isolated Porcine HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2000DOMINIQUE LACROIX Amiodarone is a potent antiarrhythmic agent with complex chronic effects, notably on repolarization and conduction, that are not fully understood. Its low arrhythmogenic potential has been related to a lack of increase in repolarizution dispersion. Since its effects are not documented in pigs we conducted a mapping study of activation and repolarization in isolated perfused porcine hearts. Amio20 female pigs (n = 7) received amiodarone 20 mg/kg per day over 4 weeks while Amio 5O female pigs (n = 7) received 50 mg/kg per day over 4 weeks. Concentrations of the drug encompassed values found in clinical studies. Then, activation patterns and activation-to-recovery intervals (ARI) were mapped epicardially from 128 unipolar electrograms in isolated perfused hearts in corroboration of epicardial action potential recordings. Mean ARI was longer in Amio20 experiments compared to the seven control hearts (325 ±11 ms vs 288 ± 5 m.s at 1,000 ms), whereas ARI dispersion was not different, being comprised between 7 and 11 ms and generating smooth gradients. In Amio5O experiments, mean ARI was further prolonged (390 ±10 ms at 1,500 ms) with an exaggerated reverse rate dependence concomitant with a depressant effect on the plateau of the action potential. Again, ARI dispersion did not differ from controls. Finally, the drug depressed the maximal rate of depolarization (Vmax) and slowed conduction in a rate dependent and concentration dependent fashion. In conclusion, chronic amiodarone induces Class I and Class HI antiarrhythmic effects in ventricular porcine epicardium that are concentration dependent but does not affect dispersion of repolarization. This may partly explain its low arrhythmogenic potential. [source] Circadian and Gender Effects on Repolarization in Healthy Adults: A Study Using Harmonic Regression AnalysisANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2010Kenneth A. Mayuga M.D. Background: Sudden cardiac death and myocardial infarction have a circadian variation with a peak incidence in the early morning hours. Increased dispersion of repolarization facilitates the development of conduction delay necessary to induce sustained arrhythmia. Both QT-dispersion and T-wave peak to T-wave end (TpTe) have been proposed as markers of dispersion of myocardial repolarization. Methods: Forty healthy adults (20 women), age 35,67 years old, with normal EKGs, echocardiograms, stress tests, and tilt-table tests were analyzed during a 27-hour hospital stay. EKGs were done at eight different time points. QT-intervals, QT-dispersion, and TpTe were measured at each time point. Harmonic regression was used to model circadian periodicity, P < 0.05 was considered significant. Results: The composite QT-interval was longer in women than in men (416 ± 17 msec vs 411 ± 20 msec, respectively, P = 0.006). The QT-dispersion among all leads was greater in men than women (37 ± 13 msec vs 30 ± 11 msec, respectively, P < 0.0001); a similar difference was found in the precordial leads. Harmonic regression showed that QT-dispersion had a significant circadian variation, primarily in men. In men, the maximum QT-dispersion occurred at 6 AM (45 ± 15 msec). TpTe also had a significant circadian variation that was not affected by gender in the majority of leads. Conclusions: A circadian variation exists in the dispersion of myocardial repolarization, as measured by both TpTe and QT-dispersion. Men and women have a different circadian variation pattern. Further studies regarding the mechanisms and clinical implications are needed. Ann Noninvasive Electrocardiol 2010;15(1):3,10 [source] Optimization of Repolarization during Biventricular Pacing: A New Target in Patients with Biventricular Devices?ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2010Cengizhan Türko, lu M.D. Background: Evaluation of repolarization during sequentional biventricular pacing. Methods: Patients with biventricular devices, and left ventricular leads placed to the basal part of lateral left ventricular wall were enrolled. QRS, QTc, JTc, and corrected Tpeak-Tend intervals were compared during sequentional biventricular, left ventricular, and right ventricular pacing. Results: Five patients with nonischemic and five with ischemic cardiomyopathy due to anterior myocardial infarction were enrolled. No correlation was observed between values of repolarization among patients. The optimal values of repolarization were significantly different from values of echocardiographically guided hemodynamic optimization. Two patients with biventricular pacing-induced ventricular fibrillation were successfully treated by reprogramming of V-V delay according to interventricular delay resulting in shorter Tpeak-Tend interval, although delayed effect of amiodarone in one of these patients cannot be ruled out. Conclusions: Patients with biventricular devices may be prone to development of ventricular arrhythmias depending on programmed V-V interval. We suggest that optimization of repolarization may be performed in patients with biventricular pacemakers in the absence of backup ICD and those with frequent episodes of ventricular tachyarrhythmias, although this finding deserves further study. Ann Noninvasive Electrocardiol 2010;15(1):36,42 [source] T-Wave Variability Detects Abnormalities in Ventricular Repolarization: A Prospective Study Comparing Healthy Persons and Olympic AthletesANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009Lara Heinz M.D. Background: Sudden cardiac death in athletes is more common than in the general population. Routine screening procedures are performed to identify competitors at risk. A new Holter-based parameter analyzes variation of the ventricular repolarization (TVar). The aim of this study was to evaluate differences in electrocardiogram (ECG), Echo, and Holter (H) in competitive athletes compared to a healthy control group consisting of medical students (MS). Methods: A total of 40 athletes (19 females, Olympic team, Luxembourg) and 40 MS (22 females) were examined by means of a resting ECG, treadmill exercise (TE), echocardiogram (Echo), as well as H recordings during a routine screening visit. To analyze TVar, a 20-minute H recording at rest (sampling rate 1000 per second) was performed. Moreover, heart rate variability (HRV) as well as HR turbulence (HRT) was computed. Results: No differences in demographic variables were detected. Quantification of HRV detected a significant increase in the vagal component of autonomic cardiac modulation. In contrast, no differences for HRT were found. Echo parameter demonstrated a thicker septal wall without differences of the posterior wall. TVar values were normal in range, but did differ significantly between the two groups. No correlation between TVar and echo as well as Holter parameters was detected. Conclusions: TVar was able to demonstrate significant differences in terms of alterations of ventricular activation. This might indicate an early change of myocardial repolarization representing a substrate for life-threatening arrhythmia. Larger studies on the predictive value of TVar including follow-up are necessary to confirm this preliminary finding. [source] Detailed ECG Analysis of Atrial Repolarization in HumansANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009Fredrik Holmqvist M.D., Ph.D. Introduction: Data on human atrial repolarization are scarce since the QRS complex normally obscures its ECG trace. In the present study, consecutive patients with third-degree AV block were studied to better describe the human Ta wave. Methods and Results: Forty patients (mean age 75 years, 17 men) were included. All anti-arrhythmic drugs were discontinued before ECG recording. Standard 12-lead ECGs were recorded, transformed to orthogonal leads and studied using signal-averaged P wave analysis. The average P wave duration was 124 ± 16 ms. The PTa duration was 449 ± 55 ms (corrected PTa 512 ± 60 ms) and the Ta duration (P wave end to Ta wave end) was 323 ± 56 ms. The polarity of the Ta wave was opposite to that of the P wave in all leads. The Ta peaks were located at 196 ± 55 ms in Lead Y, 216 ± 50 ms in Lead X, and 335 ± 92 in Lead Z. No correlation was found between P wave duration and Ta duration, or between Ta peak amplitude and Ta duration. The morphology of the Ta wave was similar regardless of the interatrial conduction. Conclusions: The Ta wave has the opposite polarity, and the duration is generally two to three times that, of the P wave. Although the Ta peak may occasionally be located in the PQ interval during normal AV conduction, it is unlikely that enough information can be obtained from analysis of this segment to differentiate normal from abnormal atrial repolarization. Hence, an algorithm for QRST cancellation during sinus rhythm is needed to further improve analysis. [source] Electrocardiographic Transmural Dispersion of Repolarization in Patients with Inherited Short QT SyndromeANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2008Olli Anttonen M.D. Background: Short QT syndrome (SQTS) carries an increased risk for sudden cardiac death. However, only a short QT interval does not express the risk of ventricular arrhythmias. Thus, additional evaluation of the repolarization abnormality in SQTS patients is essential. In experimental models of SQTS, increased transmural dispersion of repolarization (TDR) and its electrocardiographic counterpart T-wave peak to T-wave end interval (TPE) appeared critical for induction of polymorphic ventricular tachycardia (PMVT). In a clinical study with acquired long QT syndrome patients, TPE/QT ratio > 0.28 indicated arrhythmia risk. We hypothesized that the TPE/QT ratio would be greater in SQTS patients than in control subjects. Methods and Results: We compared the behavior of the electrocardiographic TDR in three seriously symptomatic SQTS patients of unknown genotype presenting baseline QTc values <320 ms and in nine healthy age-matched control subjects. We determined QT and TPE intervals as well as TPE/QT ratio from 24-hour ECG recordings using a computer-assisted program. Diurnal average of TPE/QT ratio was 0.28 ± 0.03 in SQTS patients and 0.21 ± 0.02 in control subjects (P = 0.01). SQTS patients had also lesser capacity to change TPE intervals from steady-state conditions to abrupt maximal values than control subjects. Conclusion: SQTS patients have increased and autonomically uncontrolled electrocardiographic TDR. According to experimental SQTS models, the present results may in part explain increased vulnerability of SQTS patients to ventricular arrhythmias. [source] Dynamics of Ventricular Repolarization in Patients with Dilated Cardiomyopathy Versus Healthy SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2005Jose Luis Alonso M.D. Background: Patients with impaired left ventricular function have a high risk of developing ventricular arrhythmias and sudden death. Among different markers of risk, the prolongation and regional heterogeneity of repolarization are of increasing interest. However, there are limited data regarding feasibility of analyzing repolarization parameters and their dynamics in 24-hour Holter ECG recordings. Methods: Dynamic behavior of repolarization parameters was studied with a new automatic algorithm in digital 24-hour Holter recordings of 60 healthy subjects and 55 patients with idiopathic dilated cardiomyopathy (IDC). Repolarization parameters included the mean value of QT and QTc durations, QT dispersion, and peaks of QT duration and QT dispersion above prespecified thresholds. Results: In comparison to healthy subjects, patients with IDC had lower heart rate variability, longer mean QT and QTc durations, higher content of QTc peaks >500 ms, longer QT dispersion and its standard deviation, and a higher content of peaks >100 ms of QT dispersion (P < 0.01 for all comparisons). These repolarization parameters were significantly higher in IDC patients after adjustment for age, sex, and heart rate variability. The parameters of repolarization dynamics correlated with SDNN in healthy subjects but not in dilated cardiomyopathy patients. Conclusions: The automatic assessment of repolarization parameters in 24-hour digital ECG recordings is feasible and differentiates dilated cardiomyopathy patients from healthy subjects. Patients with dilated cardiomyopathy have increased QT duration, QT dispersion, and increased variability of QT dispersion reflecting variations in T-wave morphology, the factors which might predispose them to the development of arrhythmic events. [source] Differences between Ventricular Repolarization in Men and Women: Description, Mechanism and ImplicationsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2003Borys Surawicz M.D., M.A.C.C. The purpose of this review article is to discuss the differences between ventricular repolarization in males and females in terms of morphology, possible mechanism, and practical significance. The interest in the subject increased when it became known that in comparison to men, women have a higher incidence of torsade de pointes (tdp) and a greater lengthening of QT-interval after administration of class III antiarrhythmic drugs. Before puberty, the QT intervals and the patterns of ventricular repolarization in boys and girls are similar. At puberty, in boys the QT interval shortens, and a typical male pattern of ventricular repolarization develops. This pattern is characterized by a higher amplitude of the J-point, a shorter and steeper ST segment course, a steeper ascent, and a higher amplitude of the T wave. This pattern is prevalent in >90% of young males. With increasing age the prevalence of the male pattern in males declines gradually and drops to 14% in the oldest age group. The rise and fall of the prevalence of the male pattern appears to parallel the rise and decline of testosterone in males. The female pattern of ventricular repolarization is prevalent in about 80% of females in all age groups. The hormonal effects on ventricular repolarization have been studied in normal and castrated rabbits of both sexes. The available evidence indicates that the females have greater divergence of L calcium current among different layers of the myocardium and a lower density of the repolarizing Kr and Ks currents. The clinical significance of the repolarization differences among genders remains to be determined. Of particular interest is the question whether the males with female pattern are at the same risk of tdp as the females or whether the females with male pattern are at lower risk of tdp than the females with female pattern. [source] Electrocardiographic Quantitation of Heterogeneity of Ventricular RepolarizationANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2000Peter M. Okin M.D. Background:QT interval dispersion (QTd) measured from the surface ECG has emerged as the most common noninvasive method for assessing heterogeneity of ventricular repolarization. Although QTd correlates with dispersion of monophasic action potential duration at 90% repolarization and with dispersion of recovery time recorded from the epicardium, total T-wave area, representing a summation of vectors during this time interval, has been shown to have the highest correlation with these invasive measures of dispersion of repolarization. However, recent clinical studies suggest that the ratio of the second to first eigenvalues of the spatial T-wave vector using principal component analysis (PCA ratio) may more accurately reflect heterogeneity of ventricular repolarization. Methods:To better characterize the ECG correlates of surface ECG measures of heterogeneity of ventricular repolarization and to establish normal values of these criteria using an automated measurement method, the relations of QRS onset to T-wave offset (QTod) and to T-wave peak (QTpd) dispersion and the PCA ratio to T-wave area and amplitude, heart rate, QRS axis and duration, and the QTo interval were examined in 163 asymptomatic subjects with normal resting ECGs and normal left ventricular mass and function. QTod and QTpd were measured by computer from digitized ECGs as the difference between the maximum and minimum QTo and QTp intervals, respectively. Results:In univariate analyses, a significant correlation was found between the sum of the T-wave area and the PCA ratio (R =,0.46, P < 0.001), but there was no significant correlation of the sum of T-wave area with QTod (R = 0.11, P = NS) or QTpd (R=0.09, P = NS). There were only modest correlations between QTod and QTpd (R = 0.45) and between the PCA ratio and QTod (R = 0.29) and QTpd (R = 0.49) (each P < 0.001). In stepwise multivariate linear regression analyses, the PCA ratio was significantly related to the sum of T-wave area, T-wave amplitude in aVL, and to female gender (overall R = 0.54, P < 0.001), QTod correlated only with the maximum QTo0 interval (R = 0.39, P < 0.001), and QTpd was related to heart rate and QRS axis (overall R = 0.36, P <0.001). In addition, the normal interlead dispersion of repolarization as measured by QTod was significantly greater than dispersion measured by QTod (23.5 ± 11.5 ms vs 18.3 ± 11.2 ms, P < 0.001). Conclusions: These findings provide new information on ECG measures of heterogeneity of repolarization in normal subjects, with a significantly higher intrinsic variability of Q to T-peak than Q to T-offset dispersion and only modest correlation between these wo measures. The independent relation of the PCA ratio to the sum of T-wave area suggests that the PCA ratio may be a more accurate surface ECG reflection of the heterogeneity of ventricular repolarizat on. A.N.E. 2000;5(1):79,87 [source] Electrophysiological Effects of the Anti-Cancer Drug Lapatinib on Cardiac RepolarizationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2010Hyang-Ae Lee Although lapatinib is associated with a risk of QT prolongation, the effects of the drug on cellular cardiac electrical properties and on action potential duration (APD) have not been studied. To evaluate the potential effects of lapatinib on cardiac repolarization, we investigated its electrophysiological effects using a whole-cell patch,clamp technique in transiently transfected HEK293 cells expressing human ether-à-go-go (hERG; to examine the rapidly activating delayed rectifier K+ current, IKr), KCNQ1/KCNE1 (to examine the slowly activating delayed rectifier K+ current, IKs), KCNJ2 (to examine the inwardly rectifying K+ current, IK1), or SCN5A (to examine the inward Na+ current, INa) and in rat cardiac myocytes (to examine the inward Ca2+ current, ICa). We also examined its effects on the APD at 90% (APD90) in isolated rabbit Purkinje fibres. In ion channel studies, lapatinib inhibited the hERG current in a concentration-dependent manner, with a half-maximum inhibition concentration (IC50) of 0.8 ± 0.09 ,m. In contrast, at concentrations up to 3 ,m, lapatinib did not significantly reduce the INa, IK1 or ICa amplitudes; at 3 ,m, it did slightly inhibit the IKs amplitude (by 19.4 ± 4.7%; p < 0.05). At 5 ,m, lapatinib induced prolongation of APD90 by 16.1% (p < 0.05). These results suggest that the APD90 -prolonging effect of lapatinib on rabbit Purkinje fibres is primarily a result of inhibition of the hERG current and IKs, but not INa, IK1 or ICa. [source] Differences in sino-atrial and atrio-ventricular function with age and sex attributable to the Scn5a+/, mutation in a murine cardiac modelACTA PHYSIOLOGICA, Issue 1 2010K. Jeevaratnam Abstract Aim:, To investigate the interacting effects of age and sex on electrocardiographic (ECG) features of Scn5a+/, mice modelling Brugada syndrome. Methods:, Recordings were performed on anaesthetized wild-type (WT) and Scn5a+/, mice and differences attributable to these risk factors statistically stratified. Results:,Scn5a+/, exerted sex-dependent effects upon sino-atrial function that only became apparent with age. RR intervals were greater in old male than in old female Scn5a+/,. Atrio-ventricular (AV) conduction was slower in young female mice, whether WT and Scn5a+/,, than the corresponding young male WT and Scn5a+/,. However, PR intervals lengthened with age in male but not in female Scn5a+/, giving the greatest PR intervals in old male Scn5a+/, compared with either old male WT or young male Scn5a+/, mice. In contrast, PR intervals were similar in old female Scn5a+/, and in old female WT. QTc was prolonged in Scn5a+/, compared with WT, and female Scn5a+/, compared with female WT. Age-dependent alterations in durations of ventricular repolarization relative to WT affected male but not female Scn5a+/,. Thus, T-wave durations were greater in old male Scn5a+/, compared with old male WT, but indistinguishable between old female Scn5a+/, and old female WT. Finally, analysis for combined interactions of genotype, age and sex demonstrated no effects on P wave and QRS durations and QTc intervals. Conclusion:, We demonstrate for the first time that age, sex and genotype exert both independent and interacting ECG effects. The latter suggest alterations in cardiac pacemaker function, atrio-ventricular conduction and ventricular repolarization greatest in ageing male Scn5a+/,. [source] Repolarization of the cardiac action potential.ACTA PHYSIOLOGICA, Issue 2010Does an increase in repolarization capacity constitute a new anti-arrhythmic principle? Abstract The cardiac action potential can be divided into five distinct phases designated phases 0,4. The exact shape of the action potential comes about primarily as an orchestrated function of ion channels. The present review will give an overview of ion channels involved in generating the cardiac action potential with special emphasis on potassium channels involved in phase 3 repolarization. In humans, these channels are primarily Kv11.1 (hERG1), Kv7.1 (KCNQ1) and Kir2.1 (KCNJ2) being the responsible ,-subunits for conducting IKr, IKs and IK1. An account will be given about molecular components, biophysical properties, regulation, interaction with other proteins and involvement in diseases. Both loss and gain of function of these currents are associated with different arrhythmogenic diseases. The second part of this review will therefore elucidate arrhythmias and subsequently focus on newly developed chemical entities having the ability to increase the activity of IKr, IKs and IK1. An evaluation will be given addressing the possibility that this novel class of compounds have the ability to constitute a new anti-arrhythmic principle. Experimental evidence from in vitro, ex vivo and in vivo settings will be included. Furthermore, conceptual differences between the short QT syndrome and IKr activation will be accounted for. [source] Electrophysiological determinants of hypokalaemia-induced arrhythmogenicity in the guinea-pig heartACTA PHYSIOLOGICA, Issue 4 2009O. E. Osadchii Abstract Aim:, Hypokalaemia is an independent risk factor contributing to arrhythmic death in cardiac patients. In the present study, we explored the mechanisms of hypokalaemia-induced tachyarrhythmias by measuring ventricular refractoriness, spatial repolarization gradients, and ventricular conduction time in isolated, perfused guinea-pig heart preparations. Methods:, Epicardial and endocardial monophasic action potentials from distinct left ventricular (LV) and right ventricular (RV) recording sites were monitored simultaneously with volume-conducted electrocardiogram (ECG) during steady-state pacing and following a premature extrastimulus application at progressively reducing coupling stimulation intervals in normokalaemic and hypokalaemic conditions. Results:, Hypokalaemic perfusion (2.5 mm K+ for 30 min) markedly increased the inducibility of tachyarrhythmias by programmed ventricular stimulation and rapid pacing, prolonged ventricular repolarization and shortened LV epicardial and endocardial effective refractory periods, thereby increasing the critical interval for LV re-excitation. Hypokalaemia increased the RV-to-LV transepicardial repolarization gradients but had no effect on transmural dispersion of APD90 and refractoriness across the LV wall. As determined by local activation time recordings, the LV-to-RV transepicardial conduction and the LV transmural (epicardial-to-endocardial) conduction were slowed in hypokalaemic heart preparations. This change was attributed to depressed diastolic excitability as evidenced by increased ventricular pacing thresholds. Conclusion:, These findings suggest that hypokalaemia-induced arrhythmogenicity is attributed to shortened LV refractoriness, increased critical intervals for LV re-excitation, amplified RV-to-LV transepicardial repolarization gradients and slowed ventricular conduction in the guinea-pig heart. [source] Adenosine induces prolonged anti-,-adrenergic effects in guinea-pig papillary muscleACTA PHYSIOLOGICA, Issue 1 2002L. ARVOLA ABSTRACT A sustained anti- , -adrenergic effect of adenosine has been reported. This study was initiated to investigate this topic and especially elucidate the role of protein kinase C (PKC). Contractile force amplitude and action potential duration at 90% repolarization (APD90) were measured in guinea-pig papillary muscles before and after 5 min challenge with 5 nm isoproterenol. Protocols contained 30 min exposure to the test agents adenosine 33 ,m (ado), adenosine + PKC-inhibitor bisindolylmaleimide 20 nM (ado + BIM), PKC-activator 1,2-dioctanoyl-sn-glycerol 10 ,m (DOG) and , -agonist phenylephrine 5 ,m (phe). Isoproterenol was given at the end of test exposure and after 15 min washout. Results are mean ± SEM of percentage-change, P , 0.05 considered significant and labelled *. The first isoproterenol challenge significantly increased contractile force (27 ± 7%*) in the control group. Responses in the test groups were 2 ± 4 (ado), 1 ± 5 (ado + BIM), 14 ± 4* (DOG), 0 ± 2% (phe). After washout of adenosine, DOG and phenylephrine, isoproterenol induced 3 ± 8 (ado), 23 ± 5* (ado + BIM), 13 ± 5* (DOG), 15 ± 7% (phe) increase in test groups compared with 22 ± 5%* increase in contractile force in the control group. After 45 min washout of adenosine the inotropic response was still significantly reduced compared with control (29 ± 4 vs. 79 ± 8%*). Isoproterenol stimulation shortened APD90 in controls at both time points (5 ± 1%* and 4 ± 1%*), with no significant shortening in test groups. Adenosine induces sustained anti- , -adrenergic effects on contractile force as well as APD90. A role for PKC in signal transduction is supported with respect to contractile force. [source] Electrocardiogram Differentiation of Benign Early Repolarization Versus Acute Myocardial Infarction by Emergency Physicians and CardiologistsACADEMIC EMERGENCY MEDICINE, Issue 9 2006Samuel D. Turnipseed MD Abstract Objectives: ST-segment elevation (STE) related to benign early repolarization (BER), a common normal variant, can be difficult to distinguish from acute myocardial infarction (AMI). The authors compared the electrocardiogram (ECG) interpretations of these two entities by emergency physicians (EPs) and cardiologists. Methods: Twenty-five cases (13 BER, 12 AMI) of patients presenting to the emergency department with chest pain were identified. Criteria for BER required four of the following: 1) widespread STE (precordial greater than limb leads), 2) J-point elevation, 3) concavity of initial up-sloping portion of ST segment, 4) notching or irregular contour of J point, and 5) prominent, concordant T waves. Additional BER criteria were 1) stable ECG pattern, 2) negative cardiac injury markers, and 3) normal cardiac stress test or angiography. AMI criteria were 1) regional STE, 2) positive cardiac injury markers, and 3) identification of culprit coronary artery by angiography in less than eight hours of presentation. The 25 ECGs were distributed to 12 EPs and 12 cardiologists (four in academic medicine, four in community practice, and four in community academics [health maintenance organization] in each physician group). The physicians were informed of the patients' age, gender, and race, and they then interpreted the ECGs as BER or AMI. Undercalls (AMI misdiagnosed as BER) and overcalls (BER misdiagnosed as AMI) were calculated for each physician group. Results: Cardiologists correctly interpreted 90% of ECGs, and EPs correctly interpreted 81% of ECGs. The proportion of undercalls (missed AMI/total AMI) was 2.8% for cardiologists (95% confidence interval [CI] = 0.09% to 5.5%) compared with 9.7% for EPs (95% CI = 4.8% to 14.6%) (p = 0.02). The proportion of overcalls (missed BER/total BER) was 17.3% for cardiologists (95% CI = 11.4% to 23.3%) versus 27.6% for EPs (95% CI = 20.6% to 34.6%) (p = 0.03). The mean number of years in practice was 19.8 for cardiologists (95% CI = 19 to 20.5) and 11 years for EPs (95% CI = 10.5 to 12.0) (p < 0.001). Conclusions: Although correct interpretation was high in both groups, cardiologists, who had significantly more years of practice, had fewer misinterpretations than EPs in distinguishing BER from AMI electrocardiographically. [source] Left Ventricular Function in Male Patients with Secondary HypogonadismECHOCARDIOGRAPHY, Issue 3 2007Oben Baysan M.D. Background: In addition to the effects on ventricular repolarization, testosterone could also affect left ventricular performance. The enhancement of left ventricular contractility in testosterone-deficient rats following testosterone replacement implies to the possible testosterone effect. Objectives: The aim of the current study is to reveal the alterations of left ventricular functions, if any, in secondary hypogonadal male patients. Methods: Thirty-four males with secondary hypogonadism comprised the study group. The control group consisted of 30 healthy subjects. Echocardiographic measurements including left ventricular dimensions, ejection fraction, mitral inflow, and left ventricular outflow parameters were obtained from all subjects. Tissue Doppler parameters were also measured from left ventricular lateral wall and interventricular septum. Results: Left ventricular diameters, wall thicknesses, and performance parameters were similar in both groups. Mitral inflow parameters showed a statistically insignificant difference. Pulse-wave tissue Doppler interpretation of hypogonadal and healthy subjects were similar in terms of lateral and septal basal segment Sm, Em, and Am wave velocities. Conclusions: Regarding the findings of previous studies that showed impaired myocardial contractility and lusitropy in testosterone deficient rats and our study results, further studies are needed for better understanding of testosterone's effects on human myocardium. [source] | |||||||||||||||||||||||||||||||