Bifid T waves in leads V2 and V3 in children: a normal variant

<p>Abstract</p> <p>Introduction</p> <p>The T wave is rarely bifid, apart from patients with long QT syndrome or subjects treated with antiarrhythmic drugs. At times, a U wave partially superimposed upon the T wave is responsible for an apparently bifid T wave. Bifid T waves, in contrast, have been described in normal children in the past, but the phenomenon has not received any attention in recent years, to the extent that it is not mentioned in current textbooks of paediatric cardiology. Aim of the present study was to determine the incidence and clinical counterpart of bifid T waves in a paediatric population.</p> <p>Methods</p> <p>We selected 604 consecutive children free from clinically detectable heart disease; subjects whose electrocardiogram showed a bifid T wave underwent a complete clinical and echocardiographic examination. In addition, the electrocardiograms of 110 consecutive adults have also been analyzed. A T wave was considered as bifid whenever it was notched, being the 2 peaks separated from each other by a notch with duration ≥ 0.02 sec and voltage ≥ 0.05 mV. Moreover, in 7 children with bifid T wave in lead V2 further precordial recordings were obtained: a small electrode was gradually moved from V1 to V3, and 4 additional leads were recorded: 2 between V1 an V2, and 2 between V2 and V3.</p> <p>Results</p> <p>A bifid T wave was observed in 110 children (18,3%), with a relatively age-related incidence; the highest rate of bifid T waves (53%) occurred in the group of 5-year-old children. The bifid T wave was detected only in lead V2 in 51 cases (46,4%), only in lead V3 in 5 cases (4,6%), in both leads V2 and V3 in 50 cases (45,4%), and in leads other than V2 and V3 in 4 cases (3,6%). In the adult group, none of the examined electrocardiograms showed bifid T waves in any lead.</p> <p>In the bifid T wave paediatric population, the echocardiogram did not reveal any abnormality, apart from 3 subjects which had an asymptomatic mitral valve prolapse; a trivial mitral and/or tricuspid regurgitation detected by color Doppler, as well as a patent foramen ovale in infants, were not considered as abnormal findings. The QTc interval was normal in all of the subjects; the average QTc interval was not different in the bifid T wave population (402 ± 46 msec) with respect to the control group (407 ± 39 msec).</p> <p>Conclusion</p> <p>The incidence of bifid T waves in leads V2 and V3 in normal children is high, and awareness of this phenomenon avoids possible misinterpretations leading to a diagnosis of ECG abnormalities.</p

The effects of gender on electrical therapies for the heart: physiology, epidemiology, and access to therapies: A report from the XII Congress of the Italian Association on Arrhythmology and Cardiostimulation (AIAC)

The difference between men and women is clear even just by looking at an electrocardiogram: females present higher resting heart rate, a shorter QRS complex length and greater corrected QT interval. The development of these differences from pubertal age onward suggests that sexual hormones play a key role, although their effect is far from being completely understood. Different incidences between sexes have been reported for many arrhythmias, both ventricular and supraventricular, and also for sudden cardiac death. Moreover, arrhythmias are an important issue during pregnancy, both for diagnosis and treatment. Interestingly, cardiovascular structural and electrophysiological remodelling promoted by exercise training enhances this 'gender effect'. Despite all these relevant issues, we lack gender specific recommendations in the current guidelines for electrical therapies for heart rhythm disorders and heart failure. Even more, we continue to see that fewer women are included in clinical trials and are less referred than men for these treatments

Sustained ventricular fusion simulating a biventricular pacing

An electrocardiogram from a patient implanted with a dual-chamber DDD pacemaker showed paced QRS complexes whose morphology and frontal-plane axis were consistent with biventricular stimulation with right ventricular lead located at the apex. However, some electrocardiographic findings were suggestive, rather, of univentricular right apical pacing and sustained ventricular fusion with competing native atrioventricular conduction in the presence of patient's spontaneous QRS showing right bundle branch block plus left anterior hemiblock. Shortening atrioventricular delay with magnet application advanced right ventricle stimulation and prevented the supraventricular impulse to contribute to ventricular depolarization, thereby making clear the mechanism of right ventricular apical pacing

Quantitative comparison between amyloid deposition detected by (99m)Tc-Diphosphonate imaging and myocardial deformation evaluated by strain echocardiography in transthyretin-related cardiac amyloidosis.

Methods and results 28 patients with transthyretin mutation and a group of 14 controls underwent echocardiography to quantify left ventricular (LV) dimensions and function, and global (G) longitudinal (L), radial (R) and circumferential (C) strain (S). 99mTc-3, 3-diphosphono-1, 2-propanodicarboxylic-acid-scintigraphy (99mTc-DPD) was used to quantify cardiac amyloidosis (CA). 99mTc-DPD revealed accumulation in 14 of 28 patients (CA-group) and no accumulation (no CA-group) in 14 patients. Cardiac accumulation was mild-moderate in 5 (Mild-Moderate CA-group) and severe in 9 patients (Severe CA-group). Severe CA-group showed higher values of LV septal thickness (LVST), posterior wall thickness and E/E' ratio than the no CA-group and the control group (adj. p<0.05). Ejection fraction was similar among groups (p=0.65). GLS was lower (p=<0.001) in severe CA-group (-12.2 ± 4.5) respect to no CA-group (-19.3 ± 3.0) and to the control group (-20.9 ± 2.5). On the contrary, GCS and GRS were lower (p=<0.05) in mild-moderate CA-group (-10.8 ± 4.1 and 9.5 ± 5.7, respectively) respect to the severe CA-group (-18.9 ± 5.1 and 23.9 ± 6.3 respectively), no CA-group (-19.2 ± 4.1 and 28.4 ± 10.2 respectively) and the control group (-23.9 ± 4.4 and 29.9 ± 8.7 respectively). A correlation was found between the scintigraphic heart retention (HR) index and LVST (r=0.72; p<0.001) and E/E' (r=0.46; p=0.03). An inverse tendency was observed between HR and GLS (r=−0.40; p=0.06)

Presumptive myocarditis with ST-Elevation myocardial infarction presentation in young males as a new syndrome. Clinical significance and long term follow up

<p>Abstract</p> <p>Background</p> <p>Acute myocarditis may mimic myocardial infarction, since affected patients complain of "typical" chest pain, the ECG changes are identical to those observed in acute coronary syndromes, and serum markers are increased. We describe a case series of presumptive myocarditis with ST segment elevation on admission ECG.</p> <p>Methods and Results</p> <p>From 1998 to 2009, 21 patients (20 males; age 17-42 years) were admitted with chest pain, persistent ST segment elevation, serum enzyme and troponine release. All but one patients had fever and flu-like symptoms prior to admission. No abnormal Q wave appeared in any ECG tracing, and angiography did not show significant coronary artery disease. Patients remained asymptomatic at long term follow-up, except 2 who experienced a late relapse, with the same clinical, electrocardiographic and serum findings as in the first clinical presentation.</p> <p>Conclusion</p> <p>Presumptive myocarditis of possible viral origin characterized by ST elevation mimicking myocardial infarction, good short term prognosis and some risk for recurrence is relatively frequent in young males and appears as a distinct clinical condition.</p

Supraventricular Tachycardia Initiated by Couplets of Atrial Extrasystoles but Not by Single Premature Atrial Beats: What Is the Mechanism?

The reported electrocardiogram shows several atrial extrasystoles (AEs) sometimes occurring in couplets. The former beat of each couplet is nonconducted, whereas the latter triggers a supraventricular tachycardia with negative P waves in inferior leads and RP &gt; PR. This suggests an atypical atrioventricular nodal reentrant tachycardia involving the fast pathway anterogradely and the slow pathway retrogradely. The tachycardia is never precipitated by single AEs. The blocked AE of each pair is pivotal in tachycardia initiation, allowing the subsequent impulse to conduct down the fast pathway. A concealed slow pathway penetration during the blocked AE is invoked as the key mechanism