Effects of bundle branch block on experimental A-V reentrant tachycardia

The effects of bundle branch block on experimental A-V reentrant tachycardia (PSVT) were studied in 17 dogs using an anomalous pathway simulatory (APS). The APS was a programmable digital electronic circuit with ability for ventricular sensing, retrograde conduction with programmable conduction time, and atrial stimulation. Close bipolar electrodes were positioned at seven contiguous atrial and ventricular sites (V_l) along the A-V ring, these being; anterior, lateral, and posterior right (AR, LR, PR), septal (S), and posterior, lateral and anterior left (PL, LL, AL). Right (R) (seven dogs) and left (L) (10 dogs) bundle branch block (BBB) were produced with transcardiac needle. After BBB, cycle length (CL) of A-V reentrant PSVT was significantly increased only with ipsilateral sites. Thus, with RBBB, CL of PSVT increased by 37 ± 3 msec., 27 ± 3 msec., and 23 ± 4 msec. (P < 0.001), at AR, LR, and PR sites respectively. With LBBB, CL of PSVT increased only with left-sided sites. Thus, CL increased by 34 ± 2.6 msec., 38 ± 4.6 msec., and 32 ± 3.3 msec., (P < 0.001) with PL, LL, and AL sites, respectively. PSVT CL and septal site did not change significantly after either R or LBBB. The increase in CL was explicable in terms of corresponding increases in intraventricular conduction time (H-V_l). There were slight compensatory decreases in A-H intervals for the increases in H-V_l. These studies confirm findings suggested by clinical electrophysiological observation.     

Unmasked superoparaseptal pathway conduction due to atrial fibrillation in a patient with left ventricular dysfunction

We report the case of a 56-year-old woman with newly diagnosed atrial fibrillation (AF) and severe left ventricular (LV) dysfunction caused by rapid conduction via an accessory pathway (AP), mimicking left bundle branch block, as the first clinical manifestation of Wolff–Parkinson–White (WPW) syndrome. Electrical cardioversion of the AF revealed a short PR interval and a delta wave, which was positive in leads I, II, aVL, and V₂ and negative in lead V₁ with a transition zone between V₁ and V₂. Radiofrequency catheter ablation of a superoparaseptal pathway was accompanied by rapid recovery from LV systolic dysfunction.     

Asymmetry of retrograde conduction and reentry within the His-Purkinje system: A comparative analysis of left and right ventricular stimulation

Objectives. The purpose of this study was to delineate retrograde His-Purkinje system conduction and reentry (V₃phenomenon) during left ventricular extrastimulation and compare them with right ventricular extrastimulation.Background. The V₃phenomenon has been well described in the past during right ventricular extrastimulation; however, it has not been studied systematically during left ventricular extrastimulation.Methods. Left and right ventricular pacing were performed in 13 patients. Retrograde and anterograde routes of impulse propagation were determined on the basis of the sequence of His (H) and right bundle (RB) potentials, H-RB intervals, as well as the QRS configuration and axis of V₃beats.Results. During right ventricular pacing, retrograde conduction of V₂, when discernible, occurred exclusively through the left bundle at all coupling intervals equal to or shorter than the His-Purkinje relative refractory period, with the exception of two isolated beats. During left ventricular extrastimulation, His bundle activation was through the left bundle in nine patients and through the right or left bundle in three other patients. In one patient, the route could not be determined. The V₃phenomena occurred in eight patients during right ventricular pacing. Seven patients had a left bundle branch block pattern QRS configuration, and one had a right bundle branch block pattern configuration. V₃beats occurred in five patients during left ventricular apex pacing: left bundle branch block pattern configuration in one patient and right bundle branch block pattern configuration in four. In three of these four patients, the reentry was interfascicular and limited to the left bundle branch system.Conclusions. The left-sided His-Purkinje system is the preferred retrograde route of impulse propagation during both left and right ventricular extrastimulation. Reentry within the His-Purkinje system elicited by right ventricular extrastimulation involves both bundle branches, whereas this reentry tends to occur within the left-sided His-Purkinje system during left ventricular pacing.     

Doppler Echocardiographic Analysis of Left Ventricular Diastolic Blood Flow

We analyzed the diastolic flow pattern in the left ventricle by means of pulsed Doppler echocardiography in 150 consecutive patients (51 ± 14 years old) with various cardiac conditions. The flow pattern typical of the left ventricular inflow tract (E and A) was duplicated in the outflow tract and on the lateral wall in the form of a reversed biphasic pattern (E* and A*) extended into the phase ofisovolumic contraction. E* was delayed by 72 ± 44 msec compared to E, A* was only delayed by 47 ± 31 msec compared to A (a significant difference in the delays, P < 0.0001). In patients with left ventricular hypertrophy (n= 23), the delay of E* compared to E was greater than in normal subjects (n= 60) (91 ± 52 as compared to 66 ± 37 msec; P < 0.01). In three patients with constrictive pericarditis, the delay A/A* was greater than the delay E/E*, in contrast to the situation in normal subjects and patients with left ventricular hypertrophy. During isovolumic relaxation, acceleration of flow toward the apex was found near the septum in 77% of the patients. In 20 patients, an intraobserver, interob-server, cycle-to-cycle, technician-to-technician, and day-to-day test of the variability of 19 Doppler parameters was carried out. In general, the largest differences were shown in the day-to-day and the technician-to-technician testing. Of the inflow tract measurements, V_maxE and V_max A and their time-velocity integrals were readily reproducible. The reproducibility of acceleration and deceleration slope measurement was not so good. In the outflow tract, V_maxE*, the time-velocity integral of E* and the delay between A and A* were well reproducible. No sources of variability specific to individual patients were shown for the flow during the isovolumic relaxation phase, but there were significant differences in the technician-to-technician and interobserver variability testing. Thus, information on diastolic flow behavior in the left ventricle may be obtained by Doppler echocardiography. This provides more information than that obtainable by analysis of the inflow profile alone. The addition of these parameters to analysis of transmural flow patterns might allow enhanced appraisal of abnormalities not only in muscular relaxation but also in chamber compliance. (ECHOCARDIOGRAPHY, Volume 8, September 1991)     

12-Kanal-Elektrokardiogramm

The surface electrocardiogram (ECG) is an important diagnostic tool for the diagnosis of arrhythmias and acute coronary syndrome. Supraventricular tachycardias (SVT) are paroxysmal tachycardias as are sinus tachycardia, atrial tachycardia, AV nodal reentry tachycardia, and tachycardia due to accessory pathways. All SVT are characterized by a ventricular heart rate >100/min and small QRS complexes (QRS width <0.12 s) during tachycardia. It is important to analyze the relation between P wave and QRS complex to look for an electrical alternans as a leading finding for an accessory pathway. Wide QRS complex tachycardias (QRS width ≥ 0.12 s) occur in SVT with aberrant conduction and SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardias, AV dissociation, negative or positive concordant pattern in V₁–V₆, a notch in V₁ and QR complexes in V₆ in tachycardias with left bundle branch block morphologies are findings indicating VT. In addition, an R/S relation <1 in V₆ favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the right way with a systematic approach, the specificity and sensitivity of correctly identifying a SVT or VT can be raised by >95%. The 12-lead surface ECG allows the coronary culprit lesion to be located in 97% due to determination of the 12-lead ST segment deviation score.     

Bundle Branch Reentrant Ventricular Tachycardia:

Sustained Bundle Branch Reentrant Tachycardia. introduction: The clinical, electrophysiologic features and follow-up of 48 patients with inducible bundle branch reentrant (BBR) tachycardia are presented. Methods and Results: Forty-eight patients were identified in whom a diagnosis of BBR tachycardia was made during electrophysiologic evaluation. The clinical presentation was syncope or sudden death in 38 patients, and sustained palpitations during wide QRS complex tachycardia in 5 patients. Electrophysiologic studies were performed in 5 additional patients for various other reasons. Structural heart disease was present in 45 patients. Idiopathic dilated cardiomyopathy and coronary artery disease were the anatomical substrates in 19 (39%) and 24 (50%) patients, respectively, severe aortic regurgitation was present in 2 patients, and no organic heart disease was identified in 3. All 48 patients had evidence of His-Purkinje system disease. BBR tachycardia with left and right bundle branch block morphologies was induced in 46 and 5 patients, respectively, and interfascicular BBR tachycardia was initiated in 2 patients. Ventricular tachycardia of a myocardial origin was induced in 11 patients. Management of BBR tachycardia included transcatheter bundle branch ablation in 28 patients, and antiarrhythmic drug therapy in 16 patients. Four patients were treated with implantablc defibrillators. After a mean follow-up of 15.8 months in 42 patients, there were 13 deaths due to congestive heart failure, 4 sudden cardiac deaths, 3 nonsudden cardiac deaths, and 3 noncardiac related deaths. Conclusion: Sustained BBR, a form of monomorphic ventricular tachycardia, is a highly malignant arrhythmia usually seen in patients with structural heart disease. Three different types of BBR tachycardia are described. If distinguished from ventricular tachycardia of a myocardial origin, catheter ablation of the right bundle branch can be easily performed and effectively eliminates BBR. During follow-up, congestive heart failure is the most common cause of death in this population.     

Rare Association: Chagas' Disease and Hypertrophic Cardiomyopathy

A woman (49 years) with Chagas’ disease showed: ECG, right bundle‐branch block and left anterior–superior fascicular block; V₁ has unusual R > R’, and elevated ST segment from V₂ to V₆. Additional imaging revealed concomitant HCM and Chagas, which is uncommon. Overlapping of ECG findings can be explained by this rare association of diseases.     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

Depressed inotropic state and reduced myocardial oxygen consumption in the human heart

The relation between myocardial oxygen uptake (MVO₂) and the mechanical properties of left ventricular contraction were studied in 14 patients with and without left ventricular dysfunction. Coronary blood flow was estimated by helium washout, and left ventricular inotropic state was characterized from the mean left ventricular circumferential fiber shortening velocity in the minor equator (mean V_CF) and the value at peak tension (V_CF at max T). Ten patients with left ventricular dysfunction whose mean V_CF values were less than 1 circumference/sec were compared with patients whose mean V_CF values fell within the normal range. Patients with depressed shortening velocity had lower than normal average coronary blood tlow values (53 ± 3 vs. 70 ± 3 ml/100 g per min, respectively, P < 0.005) and reduced MVO₂ (75 ± 5 vs. 120 ± 6 μl/100 g per beat, P < 0.001). Coronary venous washout curves were well fitted by mono-exponential functions in normal patients but deviated appreciably from a single exponential in patients with left ventricular dysfunction, thereby indicating nonuniform distribution of coronary blood flow in the latter group. Peak and mean developed tension at the minor circumference, tension-time index, stroke work and fiber-shortening work per myocardial volume correlated poorly with MVO₂. However, mean V_CF and V_CF at max T correlated significantly with MVO₂ (r = 0.63, P < 0.02). These findings are in agreement with previous experimental findings demonstrating the importance of the contractile state as a determinant of myocardial oxygen consumption.     

Tissue Doppler Imaging: A New Technique for Assessment of Pseudonormalization of the Mitral Inflow Pattern

Left ventricular diastolic dysfunction (LVDD) is a frequent cause of heart failure. Doppler echocardiography has become the method of choice for the noninvasive evaluation of LVDD. However, pseudonormalization (PN) of the mitral inflow often presents a diagnostic challenge in clinical practice. In this setting, we sought to define the role of tissue Doppler imaging (TDI) of the septal mitral annulus. Echocardiography was performed in 36 consecutive subjects (age 59 ± 10 years). Eighteen of these had diagnosed coronary artery disease (CAD) with recent onset of symptoms (within 3 months), 18 had clinical suspicion of CAD, and 15 had symptoms of heart failure (New York Heart Association [NYHA] Class 2.4 ± 0.5 ). The mitral inflow profile (E, A, E/A) was measured by pulsed Doppler, and the deceleration time (DT) and the isovolumic relaxation time (IVRT) were calculated. Peak diastolic velocities of the septal mitral annulus (E_T, A_T, E_T/A_T) and the time interval from Q in the ECG to the onset of E_T were derived from pulsed TDI. Left heart catheterization was performed for direct measurement of left ventricular end‐diastolic pressure (LVEDP). PN defined by an E/A ratio > 1 and an LVEDP ≥ 16 mmHg was found in nine patients. All patients with PN had symptoms of heart failure (NYHA Class 2.8 ± 0.5 ). Patients with and without PN did not differ with respect to the E/A ratio (1.29 ± 0.44 vs 1.16 ± 0.23, P = ns ), DT (182 ± 38 msec vs 205 ± 42 msec, P = ns ), and IVRT (88 ± 24 msec vs 92 ± 18 msec, P = ns ). In the group with PN, a significant reduction of E_T (5.6 ± 1.8 cm/sec vs 8.8 ± 2.9 cm/sec, P < 0.05 ) and E_T/A_T (0.5 ± 0.16 vs 0.82 ± 0.37, P < 0.05 ) was detected. In the PN group, the Q‐E_T interval was prolonged (404 ± 48 msec vs 346 ± 50 msec, P < 0.05 ). Receiver operating characteristic curve analysis for E_Tyielded an area under the curve of 0.78 ± 0.06 (P = 0.034 ) for separating patients with versus without PN. When the combination of E_T < 7 cm/sec and E_T/A_T < 1 was used as cutpoint, PN could be identified with a sensitivity of 83% and a specificity of 79%. There was no significant relation between LVEDP and either E_T (r = 0.32, P > 0.2 ) or the Q‐E_T interval (r = 0.14, P > 0.5 ). In conclusion, E_T and the Q‐E_T interval appear to be useful parameters for assessing LV diastolic dysfunction in symptomatic patients with a pseudonormal mitral inflow pattern and elevated filling pressures.     

A new ECG algorithm for the localization of accessory pathways using only the polarity of the QRS complex

A new algorithm is proposed for localization of accessory atrioventricular pathways by use of a 12-lead electrocardiogram (ECG). The polarity of the QRS complex in leads III, V₁, and V₂ from 102 patients with Wolff-Parkinson-White syndrome with manifested preexcitation who underwent successful radiofrequency catheter ablation was analyzed. Accessory pathways on the right side of the heart were localized to three regions around the tricuspid annulus, and left-sided pathways were localized to two regions around the mitral valve annulus. In 42 of 46 patients (91%) with left posterolateral accessory pathways, a common characteristic of the ECG was a positive QRS complex in leads III and V₁ (sensitivity 91%, specificity 95%). Of 19 patients with left inferior paraseptal or inferior accessory pathways, 16 (84%) had a negative QRS complex in lead III and a positive QRS complex in lead V₁ (sensitivity 84%, specificity 98%). All six patients with right anterosuperior paraseptal accessory pathways had a positive QRS complex in lead III but a negative QRS complex in lead V₁ (sensitivity 100%, specificity 97%). The 25 patients with right inferior paraseptal or inferior accessory pathways had a negative or isodiphasic QRS complex in leads III and V₁, but the QRS complex was positive in lead V₂ in 21 (84%) of these patients (sensitivity 84%, specificity 100%). Finally, five of the six patients (83%) with right anterior accessory pathways had a negative QRS complex in leads III, V₁, and V₂ (sensitivity 83%, specificity 96%). With the algorithm, the localization of accessory pathways was thus identified in 90 of the 102 patients (88%).     

Prophylactic permanent pacemakers for patients with chronic bundle branch block.

His bundle recordings were obtained in 189 patients with chronic bundle branch block, and the patients were followed for a mean of approximately 20 months. Forty patients underwent prophylactic pacemaker insertion (group II) and 149 did not (group I). There was no significant difference between the two groups at the time of entry into the study with regard to mean age, serum cholesterol or the incidence of smoking, diabetes, hypertension, coronary artery disease or congestive heart failure. The patients in group II had a significantly higher incidence of transient neurologic symptoms (30 of 40,75 per cent, versus 79 of 149, 53 per cent, p < 0.05) and longer mean infranodal conduction time (79 ± 25 versus 61 ± 20 msec, p < 0.001). Eleven patients died before symptom relief could be assessed. More paced patients (group II) had relief of neurologic symptoms compared with the unpaced group (18 of 25, 72 per cent, versus 36 of 73, 49 per cent), but the difference was not quite statistically significant (0.1 <p > 0.05). There was no significant difference between the two groups in the total mortality or the incidence of sudden death. Nineteen of 21 sudden deaths occurred in patients with coronary artery disease and/or congestive heart failure.In conclusion, (1) prophylactic pacemaker insertion in a subset of largely symptomatic patients with chronic bundle branch block and long H-Q time did not protect against sudden death; the incidence of this complication appears to be related to the type and severity of underlying heart disease; (2) presenting neurologic symptoms may be an inadequate guide to assess the need for permanent pacing in bundle branch block.     

Functional bundle branch block: Discordant response of right and left bundle branches to changes in heart rate

Faster heart rates shorten refractoriness more in some tissues than in others. This study investigates whether faster heart rates shorten relative refractoriness more in the right than left bundle branch in humans. Premature atrial stimulation at 2 or more basic cycle lengths was performed in 314 patients with no evidence of atrioventricular conduction system disease. In 10 patients, both functional right and left bundle branch block (BBB) developed with premature atrial stimulation. Functional right BBB occurred at the longer basic cycle length, and functional left BBB at the shorter cycle length in 8 patients. In 2 patients functional right and functional left BBB were present at the same cycle length, but functional left BBB occurred at a shorter premature atrial coupling interval. For all patients, the mean functional right bundle branch relative refractoriness was 438 ms at a basic cycle length of 847 ms, and functional left bundle branch relative refractoriness was 357 ms at a cycle length of 622 ms (p <0.01). The HV interval was 45 ± 15 ms at control and increased with functional left BBB to 77 ± 19 ms (p <0.01), but not with functional right BBB. Thus, relative refractoriness of the right and left bundle branches are rate-dependent and discordant. At longer cycle lengths, relative refractoriness of the right bundle branch is greater than that of the left bundle branch, and at shorter cycle lengths relative refractoriness of the left bundle branch is greater than that of the right bundle branch. The relative refractory period curves “cross over” and can explain the presence of both functional right and left BBB in the same patient.     

Ectopic Ventricular Beats Originating in Ischemically-Injured Left Ventricular Epicardium, 24 Hours Following Coronary Artery Occlusion in the Dog

Epicardial Ectopics. Introduction: Ventricular ectopic beats demonstrating: (1) depolarization in ischemically-injured anterior epicardium preceding His-Purkinje activation by more than 25 msec; (2) initial delta waves on the anterior chest leads of the surface ECG coincident with presystolic epicardial activation; and (3) a left bundle branch block morphology were observed in 46 of 256 anesthetized dogs evaluated 18–24 hours following anterior descending coronary artery occlusion. Methods and Results: In 18 experiments, endocardial and epicardial recordings, and signal-averaged recordings from the left ventricle were used to determine the earliest activation time/site for epicardial ectopic beats. In these ventricular ectopic beats, early epicardial activation was coupled to the preceding beat by a constant, fixed coupling interval. Electrical activity during the interectopic interval was not detected with composite or multiple bipolar recordings, or with signal averaging from the heart. The mean coupling interval was prolonged by lidocaine from 385 ± 24to 409 ± 45 msec (P < 0.01), and was decreased by epinephrine (364 ± 7 msec) and D-600 (324 ± 32 msec)(P < 0.05). Spontaneous ventricular beats of epicardial origin could be reversibly suppressed by epicardial lidocaine administration or permanently suppressed with intracoronary latex injection, eliminating presystolic potentials. Histologic examination of the epicardium revealed surviving tissue bands (0.5–2.0 mm) distributed throughout transmural infarcted epicardium. Conclusion: The present experiments demonstrate constant-coupled ectopic ventricular beats of epicardial origin, 18–24 hours following myocardial infarction. The ventricular ectopic beats may result from abnormal automaticity or electrotonic excitation from an initiating beat across an unexcitable gap with slow conduction from the “site of origin’ to reactivate the left ventricle. (JCardiovasc Electrophysiol, Vol. 3, pp. 315–333, August 1992)     

Effect of Sustained Load on Dispersion of Ventricular Repolarization and Conduction Time in the Isolated Intact Rabbit Heart

Effect of Sustained Load on EP Parameters. Introduction: It is well known that myocardial stretch can elicit ventricular arrhythmias in experimental models. However, previous reports have predominantly documented stretch-induced arrhythmias during short, pulsatile stretch. The arrhythmogenic mechanism of sustained static stretch is incompletely understood. Methods and Results: To examine the influence of sustained load on several electrophysiologic parameters, a latex balloon was placed into the left ventricle of ten isolated Langendorffperfused rabbit hearts and filled with a neutral volume of fluid. The heart was paced from a catheter inside the right ventricle (apicoseptal endocardial position), and the following parameters were studied during steady-state pacing with a cycle length of 500 msec (S1) and during extrastimulation (S2, base drive of 8 beats): monophasic action potential (MAP) durations at 90% repolarization (APD₉₀) from 5 to 6 epicardial electrodes located on both ventricles and one right ventricular endocardial contact electrode; dispersion of APD₉₀ (range of MAP durations from all electrodes); effective refractory period (ERP) and longest activation time (pacing stimulus to MAP upstroke). After baseline recordings, the balloon inside the left ventricle was filled with a volume of 1.0 mL of fluid by means of a servo-controlled pump. The ERP was significantly shortened from 198 ± 9 msec at baseline to 183 ± 8 msec during sustained load (P < 0.03). Similarly, the average APD₉₀ was shortened from 180 ± 5 msec at baseline to 175 ± 6 msec during sustained load (P < 0.006) with steady-state pacing and from 178 ± 6 msec to 170 ± 8 msec during premature extrastimulation (P < 0.03). At the same time, dispersion of APD₉₀ was increased from 27 ± 5 msec to 38 ± 6 msec (P < 0.002) during steady-state pacing and from 28 ± 4 msec to 38 ± 6 msec (P = 0.013) during premature extrastimulation. The longest activation time among all MAP recordings was increased from 39 ± 2 msec to 43 ± 3 msec (P = 0.003) during steady-state pacing and from 56 ± 6 msec to 69 ± 6 msec during premature extrastimulation (P < 0.003). Conclusions: Sustained load shortens the ERP and the mean APD₉₀ and at the same time increases dispersion of APD₉₀ and prolongs activation times. These findings provide additional insight into the arrhythmogenic mechanisms of sustained mechanical load.     

Radiation exposure to patient and operator during radiofrequency ablation for supraventricular tachycardia

Abstract Background: Radiofrequency (RF) ablation has become the primary method of treatment for supraventricular tachycardia and often requires prolonged fluoroscopy times. Aim: To quantitate radiation exposure to patient and operator during RF ablation for supraventricular tachycardia. Methods: Thermoluminescent dosemeters were used to monitor radiation at seven sites. Positions were: patient's thyroid, left scapula, T9 vertebra, right scapula and L4-L5 vertebra and the operator's thyroid and left hand. Monitoring was performed during 22 procedures. Of the patients studied 10 (45%) had atrioventricular junctional re-entry tachycardia (AVJRT) and 12 (55%) had accessory pathway tachycardia. Results: The median fluoroscopy times (minutes) and inter-quartile ranges were 46 (39–65) for AVJRT, 55 (52–60) for left free wall accessory pathway (LFW), 107 (89–140) for septal and 166 (128–176) for RFW pathways. The mean radiation doses (mGy) to the chest wall were 50 for AVJRT, 47 for LFW, 87 for septal and 151 for RFW pathways. The mean radiation to the chest wall of the patient per case was found to be 3.9 times that reported for diagnostic cardiac catheter-isation and 1.5 times that reported for angioplasty. Conclusions: Radiofrequency ablation is associated with significant irradiation of the patient and operator. All precautions should be taken to decrease this exposure. If eye irradiation is assumed to be equal to that to the thyroid, more than 45 procedures per month by a single operator (using ceiling-suspended lead glass shielding) may result in exceeding the recommended dose limit to the eye. (Aust NZ J Med 1995; 25; 490–495.)     

Electrocardiogram of the athlete: An analysis of 289 professional football players

The electrocardiogram (EGG) of athletes reflects physiologic cardiovascular adaptations that occur in well-conditioned individuals. To more clearly define electrocardiographic changes seen in predominantly power-trained athletes, the ECGs of 289 apparently healthy professional football players were analyzed in detail. The players, aged 21 to 35 years, one-third of whom were black, had a mean body surface area of 2.24 m², a mean heart rate at rest of 56 ± 9 beats/min (with 77% (223) having a rate of less than 60 beats/min), and a mean P axis of 30 ± 25 °. A wide QRS-T angle (>60 °) was present in 14% (41 players) of the group. The mean PR interval was 0.18 ± 0.02 second (>0.21 in 9% [26 players]). Although two-thirds of the players had a QRS duration of 0.10 second, only 1 had right bundle branch block and none had left bundle branch block. The sum of S in lead V₁ plus R in lead V₅ averaged 37 ± 9 mm, with 35% (101 players) demonstrating voltage criteria for left ventricular hypertrophy. The S + R value varied inversely with weight (r = ?0.27, p < 0.002). The maximum T height in any lead had a mean of 8.6 ± 3 mm, with 22% (64 players) having a T height ≥11 mm. U waves were universally present. ST-T changes mimicking ischemia were noted in 39 of 289 players (13%), 22 (58%) of whom were black (p < 0.001). The maximal J-point elevation in any lead averaged 1.9 ± 0.9 mm. These findings confirm that the ECGs of power-trained athletes show changes similar to those of endurance-trained athletes. These changes most likely reflect the increased vagal tone and ventricular mass observed in conditioned athletes. Large body size masks the voltage changes expected with increased left ventricular mass. Ischemic-like ST-T-wave deviations were found predominantly in black athletes.     

Importance of the Conal Branch of the Right Coronary Artery in Patients With Acute Anterior Wall Myocardial Infarction: Electrocardiographic and Angiographic Correlation

Objectives. This study assessed prospectively the correlation between the conal branch of the right coronary artery and the pattern of ST segment elevation in leads V₁and V₃R during anterior wall acute myocardial infarction (AMI).Background. The traditional electrocardiographic (ECG) definition of anteroseptal AMI—ST segment elevation in leads V₁to V₃—has recently been challenged. The significance of ST segment elevation in lead V₁during anterior wall AMI is unclear.Methods. The admission 12-lead ECG with additional lead V₃R and the coronary angiograms performed within 10 days of hospital admission were evaluated in 28 consecutive patients (mean age ± SD 62 ± 9 years) admitted to the coronary care unit with anterior wall AMI. Patients were classified into two groups according to the magnitude of ST segment elevation in lead V₁: group A (elevation ≥1.5 mm, n = 12) and group B (elevation <1.5 mm, n = 16). Two types of conal branch were identified: small (not reaching the interventricular septum [IVS]) and large (reaching the IVS).Results. ST segment elevation in lead V₃R was found in 11 (92%) and 6 (37%) patients from group A and group B, respectively (p < 0.001); a small conal branch was seen in 10 (83%) and 3 (19%) patients, respectively (p < 0.001). Ten patients (all from group B) had a large conal branch.Conclusions. ST segment elevation in lead V₁in the admission ECG of patients with anterior wall AMI is strongly related to ST segment elevation in lead V₃R and is associated with a small conal branch. Our findings suggest that lead V₁reflects the right paraseptal area supplied by the septal branches of the left anterior descending coronary artery (LAD), alone or together with the conal branch. The absence of ST segment elevation in lead V₁during anterior AMI suggests that the IVS is protected by a large conal branch in addition to the septal branches of the LAD (double circulation).(J Am Coll Cardiol 1997;29:506–11)     

Radiofrequency Catheter Ablation of the Left Bundle Branch in a Canine Model

Left Bundle Branch Ablation. Introduction: Transcatheter ablation of the left bundle branch may be considered for management of selected macroreentrant ventricular tachycardias. Left bundle ablation can also change the sequence of left ventricular contraction and may simulate pacing in hypertrophic obstructive cardiomyopathy. The purpose of this study was to determine electrophysiologic and anatomic parameters for successful selective transcatheter left bundle ablation in a canine model. Methods and Results: A catheter was advanced to the left ventricular apex and the tip deflected toward the septum, until a discrete left bundle potential (LBP) was found. Radiofrequency (RF) energy was then applied until left bundle branch block or complete AV block occurred. In 29 (85%) dogs, an LBP (mean LBP-V 16 ± 3 msec; range 10 to 20 msec) was identified resulting in successful left bundle ablation. In 5 (15%) dogs, a similar potential (mean potential-V 28 ± 4 msec; P = 0.001 vs LBP-V) was identified, but RF energy application produced complete AV block. The A:V electrogram ratio at the successful LBP ablation site was < 1:10 in all 29 dogs successfully ablated, but only 2 (40%) of 5 dogs in the unsuccessful group (P = 0.0017). In 4 successfully ablated dogs, the right bundle potential was mapped and complete AV block was created by RF energy application, confirming that the left bundle was completely ablated. In 9 dogs, the left bundle and AV junction were sequentially ablated with 1 lesion at each site. Postmortem examination showed 2 discrete lesions 1.2 ± 0.7 cm apart. Conclusions: Selective transcatheter left bundle ablation was successfully guided by the LBP. The distance between the AV junction and the main left bundle was 1.2 cm in this canine model. An A:V ratio < 1:10 and an LBP-V time < 20 msec appear to minimize the risk of AV block. Prudent use of similar techniques may cure macroreentrant ventricular tachycardias and reduce the need for permanent pacing in hypertrophic obstructive cardiomyopathy.     

Longitudinal monitoring of cardiac siderosis using cardiovascular magnetic resonance T2* in patients with thalassemia major on various chelation regimens: A 6‐year study

Cardiovascular magnetic resonance (CMR) and hepatic magnetic resonance imaging (MRI) have become reliable noninvasive tools to monitor iron excess in thalassemia major (TM) patients. However, long‐term studies are lacking. We reviewed CMR and hepatic MRI T2* imaging on 54 TM patients who had three or more annual measurements. They were managed on various chelation regimens. Patients were grouped according to their degree of cardiac siderosis: severe (T2*, <10 msec), mild to moderate (T2* = 10–20 msec), and no cardiac siderosis (T2*, >20 msec). We looked at the change in cardiac T2*, liver iron concentration (LIC) and left ventricular ejection fraction (LVEF) at years 3 and 5. In patients with severe cardiac siderosis, cardiac T2* (mean ± SD) improved from 6.9 ± 1.6 at baseline to 13.6 ± 10.0 by year 5, mean ΔT2* = 6.7 (P = 0.04). Change in cardiac T2* at year 3 was not significant in the severe group. Patients with mild to moderate cardiac siderosis had mean cardiac T2* of 14.6 ± 2.9 at baseline which improved to 26.3 ± 9.5 by year 3, mean ΔT2* = 11.7 (P = 0.01). At baseline, median LICs (mg/g dry weight) in patients with severe, mild–moderate, and no cardiac siderosis were 3.6, 2.8, and 3.3, whereas LVEFs (mean ± SD) (%) were 56.3 ± 10.1, 60 ± 5, and 66 ± 7.6, respectively. No significant correlation was noted between Δ cardiac T2* and Δ LIC, Δ cardiac T2*, and Δ LVEF at years 3 and 5. Throughout the observation period, patients with no cardiac siderosis maintained their cardiac T2* above 20 msec. The majority of patients with cardiac siderosis improve cardiac T2* over time with optimal chelation. Am. J. Hematol. 88:652–656, 2013. © 2013 Wiley Periodicals, Inc.