Riyaz Somani

Procainamide infusion in the evaluation of unexplained cardiac arrest: From the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER)

BACKGROUND Provocative testing with sodium channel blockers is advocated for the evaluation of unexplained cardiac arrest (UCA) with the primary purpose of unmasking the typical ECG features of Brugada syndrome. The Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER) systematically assesses subjects with UCA or a family history of sudden death (FHSD). OBJECTIVE The purpose of this study was to determine the clinical yield of procainamide infusion in a national registry of subjects with either UCA or a FHSD. METHODS Subjects with either UCA or a FHSD without evidence of a Brugada pattern at baseline underwent procainamide testing (15 mg/kg to a maximum of 1 g at 50 mg/min). A test was considered positive for Brugada pattern if there was an increase in ST elevation >1 mm or if there was >1 mm of new ST elevation in leads V1 and/or V2. Genetic testing was performed on the basis of phenotype detection. RESULTS Procainamide testing was performed in 174 subjects (age 46.8 ± 15.4 years, 47% female). Testing provoked a Brugada pattern in 12 subjects (6.9%), 5 of whom had no ST abnormalities at baseline. No subjects with a negative procainamide challenge were subsequently diagnosed with Brugada syndrome. Genetic testing was conducted in 10 of the 12 subjects with a provoked Brugada pattern and was positive for a mutation in the SCN5A gene in 1. CONCLUSION Irrespective of the baseline ECG, procainamide testing provoked a Brugada pattern in a significant proportion of subjects with UCA or a FHSD, thereby facilitating a diagnosis of Brugada syndrome, and is recommended in the workup of UCA.

Long QT syndrome complicating atrioventricular block: arrhythmogenic effects of cardiac memory.

Background— The magnitude of QT prolongation in response to bradycardia, rather than the bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB). However, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. We hypothesized that in patients who develop significant QRS vector changes during AVB, the effects of cardiac memory lead to excessive QT prolongation. Methods and Results— We studied 91 patients who presented with AVB and who also had an ECG predating the bradyarrhythmia for comparison. We correlated changes in QRS morphology and axis taking place during AVB with the bradycardia-induced QT prolongation. Patients with and without QRS morphology changes at the time of AVB were of similar age and sex. Moreover, despite similar R-R interval during AVB, cases with a QRS morphology change had significantly longer QT (648±84 versus 561±84; P <0.001) than those without. Patients who developed a change in QRS morphology at the time of AVB had a 7-fold higher risk of developing long QT. This risk nearly doubled when the change in QRS morphology was accompanied by a change in QRS axis. Conclusions— Cardiac memory resulting from a change in QRS morphology during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.Background—The magnitude of QT prolongation in response to bradycardia, rather than the bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB). However, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. We hypothesized that in patients who develop significant QRS vector changes during AVB, the effects of cardiac memory lead to excessive QT prolongation. Methods and Results—We studied 91 patients who presented with AVB and who also had an ECG predating the bradyarrhythmia for comparison. We correlated changes in QRS morphology and axis taking place during AVB with the bradycardia-induced QT prolongation. Patients with and without QRS morphology changes at the time of AVB were of similar age and sex. Moreover, despite similar R-R interval during AVB, cases with a QRS morphology change had significantly longer QT (648±84 versus 561±84; P<0.001) than those without. Patients who developed a change in QRS morphology at the time of AVB had a 7-fold higher risk of developing long QT. This risk nearly doubled when the change in QRS morphology was accompanied by a change in QRS axis. Conclusions—Cardiac memory resulting from a change in QRS morphology during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.

Ablation of a left lateral accessory pathway in a patient with dextroposition of the heart.

Figure 1. A. 12-lead ECG depicts ventricular pre-excitation through a left lateral accessory pathway (short PR interval + delta waves) in a patient with dextroposition of the heart (negative P-waves in leads I and aVL, reversed R-wave progression from V1 to V6); B. Chest X-ray in the antero-posterior view. The heart is on the right side of the chest. A ventriculo-peritoneal shunt can be seen. A 21 year-old male presented with palpitations and syncope. His comorbid pathology included congenital hypoplasia of the right lung, esophageal atresia and Budd-Chiari syndrome ameliorated with a ventriculo-peritoneal shunt. A Wolff-Parkinson-White pattern was identified on a 12-lead electrocardiogram (Fig. 1A) and the patient was referred for an electrophysiological study. A chest X-ray revealed cardiac dextroposition with situs solitus (Fig. 1B) and a subsequent computed tomography scan confirmed atrio-ventricular and ventriculo-arterial concordance (Fig. 1C). During the electrophysiological study, the fluoroscopic antero-posterior projection was equivalent to what would normally be expected in the left anterior oblique view (Fig. 1D). A retrograde trans-aortic approach was used to ablate the accessory pathway which was localized on the left lateral aspect of the mitral annular ring. Three dimensional mapping was also employed (Ensite, St Jude Medical, St Paul, MN, USA) which highlighted the anterior position of the left ventricle (Fig. 1E). The post ablation ECG, with the precordial leads on the right side of the chest, showed resolution of pre-excitation with T wave memory phenomenon (Fig. 1F). The patient remained asymptomatic after a follow-up period of 36 months.

Unnecessary shock from an implantable cardioverter-defibrillator following transcutaneous pacing.

As the population ages and cardiovascular disease becomes more prevalent, an increasing number of patients are receiving implantable cardioverter-defibrillators (ICDs). When these patients present to the emergency department, it is imperative that physicians are not only aware of the possible underlying medical issues that may have precipitated their admission but should also have a good understanding of the potential interactions that any medical intervention may have on the patients device. We discuss a case in which a patient known to have an ICD in situ was transcutaneously paced for the management of bradycardia, leading to an unnecessary shock.

Alternating atrial pacing cycle length during ventricular tachycardia: what is the mechanism?

Case summary A 62-year-old man with a background of ischemic cardiomyopathy and sick sinus syndrome underwent implantation of a cardiac resynchronization therapy defibrillator (CRTD) device (Medtronic Concerto, Minneapolis, MN). Table 1 lists the basic pacing programming of the device. At routine follow-up, a ventricular event was detected that was terminated successfully following 3 antitachycardia pacing therapies. The dot-plot relating to the ventricular event initially demonstrated some variation in the cycle length of the ventricular tachycardia (VT), resulting in V-V intervals drifting above and below the ventricular tachycardia detection interval (VTDI) set at 400 ms (Figure 1). Simultaneous critically short coupled ventricular tracked events during this period of VT were seen in association with those V-V intervals that were just above the VTDI. Careful analysis of the corresponding electrograms also revealed an interesting pattern of atrial pacing with alternating cycle lengths of 680 and 490 ms occurring concurrently in the presence of VT (Figure 2). Further inspection of the episode revealed that once acceleration of the VT occurred with V-V intervals falling consistently below the VTDI, cessation of atrial pacing was seen, followed by the successful detection and subsequent termination of the VT episode with antitachycardia pacing. The questions that arise are as follows. (1) Which algorithm was responsible for the simultaneous critically short coupled ventricular tracked events observed following initiation of VT? (2) Why, despite ongoing VT,

The role of Emergency Medical Services in the assessment and management of syncope

Syncope is defined as a transient loss of consciousness and postural tone followed by prompt spontaneous recovery and is caused by a transient reduction in blood flow to the reticular activating system of the brain. Syncope is a common reason for calling the Emergency Medical Services (EMS) and accounts for 1–1.5% of emergency department (ED) visits with 13–83% of these resulting in hospital admission [1,2]. The identification of patients at high risk and differentiating these from thosewhomay have amore benign etiology remain a challenge for physicians assessing syncopal patients in the ED [2]. The EMS are often the first to arrive at the scene of a syncopal patient and are involved in the preliminary assessment of these patients and offer initial medical assistance. The EMS are therefore oftenwell placed to gain valuable clinical informationwhichmay aid in determining the cause of syncope. However, the assessment findings of the EMS may not always be taken into account in determining the potential cause of syncope. The value of this initial first response assessment, and the impact it has on decisionmaking in the EDhave not been previously evaluated. This retrospective study was aimed to analyze the findings of the EMS and to determine their contribution in the management of syncopal patients. Three blinded investigators reviewed the electronic charts of all consecutive patients presenting with syncope to the ED at three academic hospitals from the Hamilton Health Sciences Corporation, Ontario, Canada, over a three month period. The time of arrival of the EMS, their initial assessment findings and their relationship with the final diagnosis were evaluated. A total of 23,701 patients were seen in the ED during the screening period. Syncope was the reason for presentation in 343 patients (1.44%). Of these, 226 patients (66%) were assessed by the EMS with an arrival time of (mean±SD) 7±5.8 min. The mean age was 69±22 years with 65% being female. The EMS recorded abnormal findings in 56/226 patients (25%) with bradycardia (b50 bpm) reported in 6 patients (11%), tachycardia (N100 bpm) in 18 patients (32%), hypotension (b90/50 mm Hg) in 18 patients (32%), hypertension (N150/90 mm Hg) in 21 patients (37%) and loss of consciousness in 4 patients (7%). The proportion of patients in whom a discharge diagnosis was achieved in the ED and the proportion of patients subsequently diagnosed with vasovagal syncope following review of their electronic charts are summarized in Table 1. There was no significant difference in the number of patients in whom a discharge diagnosis was reached by ED physicians, irrespective of whether they had been assessed by the EMS or not. All patients who had been assessed by the EMS with a tentative diagnosis of vasovagal syncope were discharged home avoiding hospital admission. Following review of the electronic charts by the study investigators, the number of patients diagnosed with vasovagal syncope was 67% higher in those patients assessed by the EMS. Despite the limitations inherent to a retrospective analysis, the results from the present study were striking and strongly suggest that the EMS assessment of syncopal patients failed to have any impact on the number of patients in whom a discharge diagnosis was reached and implies that this assessment may often be overlooked by busy ED physicians. Our chart review indicates that the proportion of patients diagnosed with vasovagal syncope was 1.7 fold higher in those assessed by the EMS compared to those patients not assessed. This finding suggests that the EMS assessment may provide invaluable clinical information which if taken into consideration may have aided ED physicians in reaching a diagnosis of vasovagal syncope, thus potentially avoiding unnecessary hospital admissions and their associated costs [3]. We postulate that this is likely to be related to the rapid assessment by the EMS of syncopal patients in close proximity to the episode where hemodynamic and rhythm disturbances are most likely to be apparent. Given the transient episodic nature of syncope it is not surprising that relevant clinical findings at the time of an event may have resolved by the time patients are evaluated in the ED. The findings of this brief report highlight the importance of early assessment by the EMS, and suggest that if their findings are taken into account as part of the overall assessment of syncopal patients presenting to the ED, a significant proportion may be easily stratified as low risk with vasovagal syncope, potentially reducing unnecessary hospital admissions and costs. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology (Shewan and Coats, 2010; 144:1–2).

Long QT Syndrome Complicating Atrioventricular BlockCLINICAL PERSPECTIVE: Arrhythmogenic Effects of Cardiac Memory

Background— The magnitude of QT prolongation in response to bradycardia, rather than the bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB). However, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. We hypothesized that in patients who develop significant QRS vector changes during AVB, the effects of cardiac memory lead to excessive QT prolongation. Methods and Results— We studied 91 patients who presented with AVB and who also had an ECG predating the bradyarrhythmia for comparison. We correlated changes in QRS morphology and axis taking place during AVB with the bradycardia-induced QT prolongation. Patients with and without QRS morphology changes at the time of AVB were of similar age and sex. Moreover, despite similar R-R interval during AVB, cases with a QRS morphology change had significantly longer QT (648±84 versus 561±84; P <0.001) than those without. Patients who developed a change in QRS morphology at the time of AVB had a 7-fold higher risk of developing long QT. This risk nearly doubled when the change in QRS morphology was accompanied by a change in QRS axis. Conclusions— Cardiac memory resulting from a change in QRS morphology during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.Background—The magnitude of QT prolongation in response to bradycardia, rather than the bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB). However, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. We hypothesized that in patients who develop significant QRS vector changes during AVB, the effects of cardiac memory lead to excessive QT prolongation. Methods and Results—We studied 91 patients who presented with AVB and who also had an ECG predating the bradyarrhythmia for comparison. We correlated changes in QRS morphology and axis taking place during AVB with the bradycardia-induced QT prolongation. Patients with and without QRS morphology changes at the time of AVB were of similar age and sex. Moreover, despite similar R-R interval during AVB, cases with a QRS morphology change had significantly longer QT (648±84 versus 561±84; P<0.001) than those without. Patients who developed a change in QRS morphology at the time of AVB had a 7-fold higher risk of developing long QT. This risk nearly doubled when the change in QRS morphology was accompanied by a change in QRS axis. Conclusions—Cardiac memory resulting from a change in QRS morphology during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.

Long QT Syndrome Complicating Atrioventricular BlockCLINICAL PERSPECTIVE

Background— The magnitude of QT prolongation in response to bradycardia, rather than the bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB). However, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. We hypothesized that in patients who develop significant QRS vector changes during AVB, the effects of cardiac memory lead to excessive QT prolongation. Methods and Results— We studied 91 patients who presented with AVB and who also had an ECG predating the bradyarrhythmia for comparison. We correlated changes in QRS morphology and axis taking place during AVB with the bradycardia-induced QT prolongation. Patients with and without QRS morphology changes at the time of AVB were of similar age and sex. Moreover, despite similar R-R interval during AVB, cases with a QRS morphology change had significantly longer QT (648±84 versus 561±84; P <0.001) than those without. Patients who developed a change in QRS morphology at the time of AVB had a 7-fold higher risk of developing long QT. This risk nearly doubled when the change in QRS morphology was accompanied by a change in QRS axis. Conclusions— Cardiac memory resulting from a change in QRS morphology during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.Background—The magnitude of QT prolongation in response to bradycardia, rather than the bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB). However, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. We hypothesized that in patients who develop significant QRS vector changes during AVB, the effects of cardiac memory lead to excessive QT prolongation. Methods and Results—We studied 91 patients who presented with AVB and who also had an ECG predating the bradyarrhythmia for comparison. We correlated changes in QRS morphology and axis taking place during AVB with the bradycardia-induced QT prolongation. Patients with and without QRS morphology changes at the time of AVB were of similar age and sex. Moreover, despite similar R-R interval during AVB, cases with a QRS morphology change had significantly longer QT (648±84 versus 561±84; P<0.001) than those without. Patients who developed a change in QRS morphology at the time of AVB had a 7-fold higher risk of developing long QT. This risk nearly doubled when the change in QRS morphology was accompanied by a change in QRS axis. Conclusions—Cardiac memory resulting from a change in QRS morphology during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.