Episodes Of Polymorphic Ventricular Tachycardia Research Articles

In-vivo mapping of human polymorphic ventricular tachycardia in Brugada syndrome

Abstract Background/introduction Brugada syndrome (BrS) is associated with ventricular fibrillation (VF) and polymorphic ventricular tachycardia (PMVT). Different mechanisms have been described for human PMVT, including epicardial drifting of rotational activity before stabilization on the apex. Purpose The aim of this study is mapping human PMVT mechanisms in BrS with ECG imaging (ECGI) in-vivo. Methods All BrS patients, were prospectively enrolled between 1992 and 2022. Inclusion criteria for the study were: 1) BrS diagnosis; 2) PMVT mapped with ECGI during thoracoscopic epicardial right ventricle outflow tract ablation. PMVT was adjudicated if a changing QRS pattern was present. Phase mapping was performed for each PMVT. All maps were imported on a dedicated software and analyzed offline. Left anterior descending coronary artery was added, based on CT scan reconstruction as a reference for the interventricular septum (in grey in Figure 1). Phase maps were performed using the Hilbert transform on detrended signals and the phases of wavefront propagation were color-coded. Rotational activity was defined as a continuous progression of phase from -π to +π around a phase singularity point. Focal activity was defined as a wavefront that appears de novo, without arising from another wavefront and spreading from its origin. Results A total of 21 BrS patients with VF were analyzed and 2 patients (9.5%) were found with PMVT. A total of 2 episodes of PMVT were mapped (one for each BrS patient) with a duration of 2.9 s and 1.3 s, respectively. Both PMVT had spontaneous initiation and termination. The mean number of rotational activities was 2.45 ± 0.07, with a mean of 2.9 ± 0.71 rotations on the apex and 0.8 ± 1.13 rotations on the septum. No other rotational activity was observed. There were 2 and 1 focal activities on the septum, respectively. No other focal activity was observed. The phase mapping of both PMVT episodes was consistent with the mechanism shown in Figure 1. In the first phase of PMVT (negative QRS) a stable rotor (white arrow) is found over ventricular apex (Figure 1, Panels A-D). In Figure 1, Panel E a septal activity appears (yellow arrow). The reduction of QRS voltage is secondary to a fusion between septal (yellow arrow) and apical (white arrow) rotational activities (Figure 1, Panels F-G). In the second phase of PMVT (positive QRS) a stable focal activity (yellow arrow) is found over the ventricular septum (Figure 1, Panels H-J). Conclusion In patients with BrS, change in the QRS pattern during PMVT is secondary to a fusion between rotational septal and apical activities.Figure 1

Takotsubo cardiomyopathy following pacemaker insertion complicated with polymorphic ventricular tachycardia: a case report

BackgroundTakotsubo cardiomyopathy is a novel form of rapidly reversible heart failure occurring secondary to a stressor that mimics an acute coronary event. The underlying etiology of the stressor is highly variable and can include medical procedures. Pacemaker insertion is an infrequent cause of Takotsubo cardiomyopathy.Case presentationAn 86-year-old Caucasian woman underwent an uncomplicated pacemaker insertion for symptomatic complete heart block in the background of slow atrial fibrillation. A transient episode of polymorphic ventricular tachycardia was noted on day 1 following the procedure; however, her pacemaker was checked and, as she remained stable, she was discharged home. She presented again 5 days later with symptomatic heart failure. Chest X-ray confirmed pulmonary edema. Echocardiography confirmed new onset severe left ventricle dysfunction. Pacemaker checks were normal and lead placement was confirmed. Though her troponin I was elevated, her coronary angiogram was normal. Contrast enhanced echocardiography suggested apical ballooning favoring Takotsubo cardiomyopathy. She was treated for heart failure and made a good recovery. Her follow-up echocardiography a month later showed significant improvement in left ventricle function.ConclusionsTakotsubo cardiomyopathy is mediated by a neuro-cardiogenic mechanism due to hypothalamic–pituitary–adrenal axis activation. It generally has a good prognosis. Complications though uncommon, can occur and include arrhythmias. Pacemaker insertion as a precipitant stressor is an infrequent cause of Takotsubo cardiomyopathy. As pacemaker insertions are more frequent in the elderly age group, this phenomenon should be recognized as a potential complication.

Multiple Implantable Cardioverter-Defibrillator Shocks in Ischemic Cardiomyopathy Compels Coronary Vascularization Reassessment

Abstract The increasing number of patients with heart failure and implantable cardioverter-defibrillators (ICD) has led to a growing of the emergency presentations for ICD internal shocks. Appropriate shocks are sometimes caused by acute events in the course of disease and could be one of the earliest symptoms contributing to the diagnosis and timely treatment of these acute conditions. We present the case of a 64-year-old male patient with ischemic cardiomyopathy, ICD carrier, who presented to the emergency department for recurrent appropriate ICD shocks caused by episodes of polymorphic ventricular tachycardia and ventricular fibrillation. Even if he did not have chest pain, he was referred to cath lab, where the coronary angiography has shown a severe stenosis at the origin of the left anterior descending artery and a moderate stenosis at the proximal left circumflex artery. The percutaneous revascularization of both lesions resulted in the eradication of the sustained ventricular arrhythmias and the improvement of the clinical status. The case argues for the need for coronary vascularization assessment in ICD carrier patients with ischemic heart failure and adequate recurrent shocks, also emphasizing the importance of remote monitoring in early diagnosis of acute conditions in these patients.

Pharmacological treatment of short-coupled idiopathic ventricular fibrillation: A review

Short-coupled idiopathic ventricular fibrillation (IVF) is a subtype of IVF in which episodes of polymorphic ventricular tachycardia or ventricular fibrillation are initiated by short-coupled premature ventricular contractions (PVCs). Our understanding of the pathophysiology is evolving, with evidence suggesting that these malignant PVCs originate from the Purkinje system. In most cases, the genetic underpinning has not been identified. Whereas the implantation of an implantable cardioverter-defibrillator is uncontroversial, the choice of pharmacological treatment is the subject of discussion. In this review, we summarize the available knowledge on pharmacological therapy in short-coupled IVF and provide our recommendations for management of patients with this syndrome.

CARDIAC SARCOIDOSIS: WHEN THE RIGHT VENTRICLE ISN’T RIGHT

CARDIAC SARCOIDOSIS: WHEN THE RIGHT VENTRICLE ISN’T RIGHT

Short-coupled ventricular ectopics leading to cardiac arrest in a young woman

BackgroundThis case report highlights the importance of recognizing that ventricular ectopy may be a cause for syncope and sudden cardiac death, through triggered disorganized arrhythmia. In the context of syncope, ventricular ectopy should be carefully assessed for coupling interval and morphology.Case presentationA 39-year-old woman, who had presented with recurrent syncope, had a cardiac arrest shortly after admission that required emergency defibrillation. Review of her cardiac monitoring revealed an episode of polymorphic ventricular tachycardia which had degenerated into ventricular fibrillation. The dysrhythmia had been initiated by a short-coupled (R-on-T) ventricular ectopic (VE) beat. Anti-arrhythmic therapy was initiated in the form of hydroquinidine, but the patient continued to have frequent VEs of right bundle branch block (RBBB) morphology with a relatively narrow QRS complex and a variation in frontal axis. A cardiac MRI revealed late gadolinium enhancement of the posterior papillary muscle (indicative of focal scarring). The patient underwent electrophysiological mapping and catheter ablation of her ectopy. The patient made a good recovery and was discharged from hospital with a secondary prevention implantable cardioverter-defibrillator (ICD) in situ.ConclusionsShort-couped VEs that are superimposed onto the preceding T wave (R-on-T) are indicative of electrical instability of the heart and should prompt urgent investigation. By studying the morphologies and axes of the QRS complexes produced by VEs, we can identify their likely origins and ascertain their clinical significance.

S3534 FOLFOX Causing Fatal Cardiac Adverse Event While Managing Colorectal Cancer

Introduction: Colorectal cancer (CRC) is the 3rd most common cancer worldwide and the 3rd leading cause of cancer death in women and the 4th in men. 5-fluorouracil (5-FU)–based regimens remain a cornerstone in managing CRC. Given the high incidence of CRC and ultimately the high rate of utilization of 5-FU, the adverse events of 5-FU must be well addressed – including the rare ones. We present a 36-year-old man with no prior cardiac history who had nearly fatal cardiac complications after receiving 5-FU. Case Description/Methods: A 36-year-old man with type 1 Diabetes Mellitus, end-stage renal disease (secondary to hemolytic uremic syndrome) status-post (s/p) transplant, and stage III mucinous adenocarcinoma of the ascending colon s/p partial colectomy presented with chest pain while receiving 5-FU bolus as part of his first FOLFOX cycle. Initial troponin I was elevated at 0.14 and kept up trending. EKG was suggestive of myopericarditis (Fig. 1A). Transthoracic echocardiogram showed reduced ejection fraction of 25-30% and global hypokinesis. 24 hours later, the patient had pulseless electrical activity and was resuscitated followed by another 2 episodes of polymorphic ventricular tachycardia (pVT) arrest. Cardiac catheterization was done subsequently and a 5 cm clot was removed from the left circumflex artery (LCX) (Fig. 1B). Post-clot removal, he suffered 3 more pVT arrests. Repeat coronary angiogram revealed small clot had embolized to the distal first obtuse marginal vessel which was not able to be retrieved. An implantable cardioverter-defibrillator was discussed for secondary prevention but ultimately the patient decided against it given his immunosuppressive state and the high likelihood of infections. He had no further cardiac events and was discharged. His upcoming oncologic management of CRC will not involve 5-FU based regimens. Discussion: We presented a young patient with no prior cardiac history who had 6 cardiac arrests, secondary to myopericarditis, within 48 hours of receiving 5-FU. It is highly unlikely that the patient had ischemic cardiomyopathy given his age and the lack of other risk factors. The clot in the LCX is mostly secondary to coronary vasospasms due to 5-FU. This case aims to highlight an extreme – yet possible – complication of 5-FU in CRC patients. More research is needed to help risk stratify patients with CRC before receiving 5-FU.Figure 1.: (A) Diffuse ST Elevations with Diffuse PR Depressions That are Most Consistent with Pericarditis (B) 5 cm Clot in Left Circumflex Artery.

SEVERE CORONARY ARTERY SPASM WITH CARDIAC ARREST IN A PATIENT WITH COVID-19

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: SARS-CoV-2 has been associated with cardiac complications, especially in patients with pre-existing cardiovascular disease. We present a case of a patient without any history of coronary artery disease (CAD), who contracted COVID-19 and developed severe coronary artery spasms resulting in cardiac arrest. CASE PRESENTATION: A 55-year-old man with past medical history of tobacco use of 30 years was admitted with severe COVID-19 pneumonitis with acute hypercapnic and hypoxemic respiratory failure, requiring invasive mechanical ventilation. On hospital day 9, he had intermittent episodes of polymorphic ventricular tachycardia. An EKG showed acute ST elevations in leads II, III, aVF and V1-V3 with troponin T rise to 0.83 ng/mL. He developed cardiac arrest due to polymorphic ventricular tachycardia. Successful resuscitation was achieved after 5 minutes including defibrillation and 2 cycles of CPR. An emergent left heart catheterization revealed insignificant CAD, normal left ventricular systolic function and no wall motion abnormalities with a presumptive diagnosis of coronary artery spasm (CAS) as the most likely cause for his cardiac arrest. He was started on a nitroglycerin patch, and his vasopressor support was switched from norepinephrine to epinephrine. The previously observed EKG changes resolved within five hours and troponin levels started to decline. A head CT showed diffuse cerebral edema with early uncal herniation and following goals of care discussion, the patient was transitioned to comfort with terminal extubation. DISCUSSION: Rarely does CAS result in polymorphic ventricular tachycardia with cardiac arrest, in patients without CAD. Initial reports showed that patients with COVID-19 and ST segment elevations are found to have myocardial injury with non-obstructive coronary arteries (MINOCA), however there are no reports of COVID-19 patients with CAS resulting in cardiac arrest. The pathophysiology of CAS is not completely understood however, the current literature has described multiple mechanisms including endothelial dysfunction, systemic inflammation, oxidative stress and smooth muscle hyperreactivity, amongst others. CONCLUSIONS: More studies are required to elucidate the mechanism of myocardial injury associated with COVID-19 infection in order to risk stratify those patients at increased risk of CAS and arrthymias and possibly tailor their management;including choice of vasopressor support and use of nitrates to lower the risk of life-threatening complications. REFERENCE #1: Bangalore S, Sharma A, Slotwiner A, et al. ST-Segment Elevation in Patients with Covid-19 — A Case Series. N Engl J Med. 2020;382(25):2478-2480. doi:10.1056/NEJMc2009020 REFERENCE #2: Matta A, Bouisset F, Lhermusier T, et al. Coronary Artery Spasm: New Insights. J Intervent Cardiol. 2020;2020:1-10. doi:10.1155/2020/5894586 REFERENCE #3: Rivero F, Antuna P, Cuesta J, Alfonso F. Severe coronary spasm in a COVID -19 patient. Catheter Cardiovasc Interv. Published online August 2020:ccd.29056. doi:10.1002/ccd.29056 DISCLOSURES: No relevant relationships by Andres Cordova Sanchez, source=Web Response No relevant relationships by Markus Gutsche, source=Web Response No relevant relationships by Matthew Kovach, source=Web Response No relevant relationships by Jasmine Sandhu, source=Web Response

Polymorphic Ventricular Tachycardia with a Normal QTc Interval in a Patient with COVID-19 and Fever: Case Report

Arrhythmias or conduction system disease are not the most common manifestation of COVID-19 infection in patients requiring hospital admission. Torsade de pointes typically occurs in bursts of self-limiting episodes with symptoms of dizziness and syncope. However, it may occasionally progress to ventricular fibrillation and sudden death. In this article, we report a case of COVID-19 patient who developed polymorphic ventricular tachycardia with torsade de pointes morphology with normal QTc interval in the setting of fever. An 81-year-old woman was admitted with symptoms of COVID-19. She was treated with hydroxychloroquine, azithromycin, and doxycycline at an outside facility and finished the treatment 5 days prior to admission to our facility. Her course was complicated by atrial fibrillation with rapid ventricular response requiring cardioversion. Later, she developed two episodes of polymorphic ventricular tachycardia with TdP morphology with normal QTc. There was a correlation with fever triggering the ventricular tachycardia. We advocated aggressive fever control given the QTc was normal and stable. Following fever control, the patient remained stable and had no abnormal rhythm. COVID-19 patients are prone to different arrhythmias including life-threatening ventricular arrhythmias with normal left ventricular systolic function and normal QTc, and they should be monitored for fever and electrolyte abnormality during their hospital stay.

582 Clinical and Genetic Characterisation of Long QT Syndrome in Indigenous Australians

There is little data on the clinical and genetic characteristics of long QT syndrome (LQTS) in Indigenous Australians. Here, three Indigenous Australian patients from Central Australia with LQTS are described. Patient 1 is a 38-year-old female who presented feeling generally unwell, with a background of alcohol abuse. No electrolyte abnormalities were detected. Her QTc measurements were 580–625ms. Genetic testing subsequently revealed heterogenicity for a likely pathogenetic variant in KCNQ1, c.1018T>C p.Phe340Leu. Patient 2 is a 21-year-old female who presented with loss of consciousness following seizure-like activity, with a background of suspected seizures and alcohol abuse. QTc remained intermittently above 500ms despite electrolyte correction. On monitoring, she developed torsades de pointes. Echocardiogram showed a mild dilated cardiomyopathy thought to be alcoholic in aetiology. Genetic testing revealed a variant of uncertain significance in ANK2. Patient 3 is a 39-year-old female who presented with a second episode of polymorphic ventricular tachycardia following excess alcohol consumption, with a background of mild rheumatic valvular disease and alcohol abuse. No family history was suggestive of LQTS. QTc remained elevated above 500ms despite electrolyte correction. Genetic testing is pending. All 3 patients received an implantable cardioverter-defibrillator without complications. This series on LQTS adds significantly to the paucity of data on arrhythmic disorders in Indigenous Australians and highlights the potential importance of exacerbating factors in this population.

Catecholaminergic Polymorphic Ventricular Tachycardia: An Unusual Case of Fright-Induced Prehospital Cardiac Arrest in a Healthy 6-Year-Old Child

Catecholaminergic Polymorphic Ventricular Tachycardia is a rare but often lethal genetic disorder that affects approximately 1 in 10,000 people. It often first manifests as stress or exercise-related syncope or sudden unexplained cardiac death, primarily in the pediatric and young adult population. We present a case of a 6-year-old male who had a sudden unexplained prehospital cardiac arrest after being scared by a domestic animal and who presented in ventricular fibrillation. The patient was subsequently defibrillated with a return of spontaneous circulation. During the course of care, medications with beta-1 and -2 agonist properties were administered, followed by multiple further episodes of polymorphic ventricular tachycardia (PVT)/ventricular fibrillation (VF). Once these medications were discontinued and beta blockers were administered, the patient had no further episodes of PVT/VF and was subsequently discharged from hospital 7 days later, completely neurologically intact. This case suggests the need for caution when considering administering beta agonists in a pediatric cardiac arrest patient with no known history of heart disease who presents in VF or PVT after an incident of extreme stress or strenuous physical activity.

Primary hyperaldosteronism presenting as recurrent polymorphic ventricular tachycardia (RCDD code: VI-2)

Primary hyperaldosteronism (PH) is a frequently overlooked cause of secondary hypertension mostly due to an aldosterone-producing adrenal adenoma. We report the case of a 48-year-old female who presented with recurrent episodes of polymorphic ventricular tachycardia before an aldosterone-producing adrenal adenoma was diagnosed. Although her past medical history was remarkable for poorly-controlled hypertension since age 30, she had never been examined for secondary causes. The patient underwent adrenalectomy resulting in stabilisation of her clinical condition, although residual hypertension remained. Causes of atypical presentation and diagnostic pitfalls are discussed. JRCD 2018; 4 (1): 26-30.

Eliminating the trigger for polymorphic ventricular tachycardia

A 60-year-old female patient was referred to our hospital because of recurrent syncope. The resting 12-lead ECG showed sinus rhythm with left bundle branch block and a high burden of monomorphic single premature ventricular beats (PVCs). Imaging studies confirmed a structurally normal heart and ischaemic heart disease was ruled out by coronary angiography. Telemetry revealed repeated episodes of polymorphic ventricular tachycardia (VT) triggered by monomorphic PVCs causing syncope. Therefore, an ICD was implanted and the patient was discharged on bisoprolol 10 mg/day. A few weeks later, she was referred to our hospital owing to repeated ICD shocks triggered by monomorphic PVCs with long-short sequences. Radio­frequency catheter ablation targeting the monomorphic PVC causing polymorphic VT was performed. With an almost perfect pace map within the distal coronary sinus, ablation in this region did not abolish the PVC. Therefore, we antegradely mapped the LV via transseptal access. Endocardial mapping at the anterior mitral anulus using the reverse S-curve technique revealed the earliest bipolar activation in close proximity to the ablated region within the coronary sinus. Ablation at this site abolished the clinical PVC. ECG monitoring at 3, 6 and 12 months did not reveal any PVC, and no ICD discharges have occurred since ablation.

Celiac Disease: aA Rare Cardiac Sequel

We explore the case of a 52-year-old woman who was transferred to our facility with recurrent torsade de pointes requiring repeated defibrillations. She had no previous medical history nor did she report any clear emotional or stressful triggers. In transit there were 14 episodes of polymorphic ventricular tachycardia, 11 of which required defibrillation. Her presenting electrocardiogram showed sinus rhythm with wide spread T-wave inversions and a QTc of 544 ms. In transit she was treated with intravenous potassium and magnesium. On arrival an isoprenaline infusion was commenced, which stabilised the patient. Coronary angiography showed non–obstructive disease with the left ventricular (LV) gram showing mid-wall variant Takotsubo cardiomyopathy. Bedside echocardiography showed low–normal LV systolic function of 55%, with no significant valvulopathy. Cardiac magnetic resonance imaging showed the resolving Takotsubo cardiomyopathy with no evidence of infiltrative disease. Despite clinical improvement, she had persistent hypomagnesaemia. Cardiomyopathy screening and investigations for hypomagnesaemia returned unremarkable with the exception of a strongly positive coeliac serology. With beta blockade, aggressive magnesium replacement, and gluten avoidance her QTc shortened and episodes of polymorphic ventricular tachycardia also settled as a consequence. She was discharged when stable and at the 6-month follow-up she remained asymptomatic with a resolution of her prolonged QT interval. This case identifies coeliac disease as a cause of severe electrolyte disturbances that resulted in recurrent torsade de pointes and Takotsubo cardiomyopathy that was treated conservatively (Figure 1, Figure 2). Figure 2Takotsubo LV gram. View Large Image Figure Viewer Download Hi-res image

Conduction Disturbances and Ventricular Arrhythmias Associated with High- Dose Loperamide

Although loperamide has been widely used for the treatment of diarrhea, there is growing popularity over its abuse potential in alleviating opioid-withdrawal symptoms and achieving euphoria. Toxic levels of loperamide have been associated with life-threatening ventricular tachyarrhythmias and cardiac arrest. We report a case of high-dose loperamide ingestion in a patient presenting initially with unstable bradycardia followed by episodes of polymorphic ventricular tachycardia, and an unmasked Brugada ECG pattern. This is the first such report of the Brugada pattern being unmasked on ECG with loperamide ingestion. The patient stabilized with supportive care without the need for inotropic support. We discuss potential mechanisms of toxicity leading to conduction abnormalities and provide a literature review of all published cases of loperamide toxicity to describe proposed treatment options. Recognition of the abuse potential and hazards of this over-the-counter anti-diarrheal therapy will alert the clinician of associated toxidromes and management strategies.

Idiopathic Intractable Diarrhoea Leading to Torsade de Pointes.

An 81-year-old lady was admitted to our hospital with a 3-year history of noninfective diarrhoea and recurrent syncopal events over the last 3 months. Her initial electrocardiogram (ECG) revealed trigeminy and prolonged QTc interval. She had a structurally normal heart with no coronary artery disease. Investigations revealed low potassium at 3.0 mmol/L. Sigmoidoscopy and colonoscopy suggested a possible diagnosis of diverticulitis. Soon after admission she had an unresponsive episode with spontaneous recovery. Telemetry and Holter analysis confirmed multiple episodes of polymorphic ventricular tachycardia (Torsade de Pointes). Following electrolyte supplementation the episodes of polymorphic VT improved. Due to the protracted nature of the diarrhoea, the recurrent syncopal events, and recurrent hypokalaemia documented over recent years, an Implantable Cardioverter Defibrillator (ICD) was sanctioned by the multidisciplinary team (MDT). In summary, chronic diarrhoea may result in life threatening polymorphic VT due to hypokalaemia and QTc prolongation. In these patients an ICD may be considered.

Temporal distribution of arrhythmic events in chronic kidney disease: Highest incidence in the long interdialytic period

Chronic kidney disease (CKD) patients undergoing hemodialysis (HD) have a high risk of sudden cardiac death (SCD). A unique risk factor may be a longer interval between HD sessions (interdialytic period). Inherent in conventional HD (thrice-weekly) are two 48-hour short breaks (SIDP) and one 72-hour long break (LIDP) between HD sessions. We used an implantable cardiac monitor (ICM) to define the incidence and timing of significant arrhythmias in an HD population. Fifty CKD patients undergoing HD with left ventricular ejection fraction >35% had an ICM inserted, with intensive follow-up to record SCD events and predefined bradyarrhythmias and tachyarrhythmias. Mean age of the patients was 67 ± 11 years; 72% were male, and the mean follow-up was 18 ± 4 months. There were 8 unexpected SCDs (16%), all during the LIDP. The terminal event was severe bradycardia with asystole in each recorded case. No episodes of polymorphic ventricular tachycardia (VT) occurred. A total of 7686 arrhythmia events were recorded in 43 patients (86%), including bradycardia in 15 patients (30%), sinus arrest in 14 (28%), second-degree atrioventricular block in 4 (8%), nonsustained VT in 10 (20%), and new-onset paroxysmal atrial fibrillation in 14 (28%). The LIDP was the highest-risk period for all arrhythmias (P < .001). The arrhythmia event rate per hour was greatest during the first pre-HD period of the week compared with any other peri-HD period (P < .001). Risk of SCD and significant arrhythmias is greatest during the LIDP. SCD was attributable to severe bradycardia and asystole. Interventions to prevent this type of SCD or shorten the LIDP deserve further evaluation. URL: https://www.anzctr.org.au (Unique identifier: ACTRN12613001326785).

Quinine Syncope Diagnosed by Life Vest

We present the case of a patient with ischemic cardiomyopathy using quinine as a remedy for leg cramps. A wearable cardioverter defibrillator (WCD) (LifeVest, Zoll Medical Corporation) recorded a sustained episode of polymorphic ventricular tachycardia resulting in syncope. Electrolyte concentrations were normal while QT interval was prolonged which improved after cessation of quinine and grapefruit juice.

Inverted Takotsubo Cardiomyopathy—Clinicopathologic Correlation

We report the case of a 34-year-old woman who presented after a witnessed out-of-hospital arrest. Initial cardiac rhythm at the time of resuscitation was ventricular fibrillation. Subsequently in hospital, she developed further episodes of polymorphic ventricular tachycardia and ventricular fibrillation. Urgent echocardiography showed features suggestive of an inverted takotsubo cardiomyopathy. Twenty-four hours after admission, there was a further episode of polymorphic ventricular tachycardia from which the patient could not be resuscitated. An autopsy confirmed the cause of death as inverted takotsubo cardiomyopathy. We present the pathological findings from the postmortem autopsy.

Infant Ventricular Fibrillation After ST-Segment Changes and QRS Widening

Background— Ventricular arrhythmia–related sudden cardiac arrest in infants with structurally normal hearts is rare. There have been no previously published reports of infants &lt;3 months of age with ventricular fibrillation in which a primary diagnosis could not be defined. Methods and Results— Retrospective chart review of 3 unrelated infants &lt;2 months of age from 3 different tertiary care centers within the United States and Australia was conducted. All 3 infants survived sudden cardiac arrest secondary to multiple episodes of polymorphic ventricular tachycardia and ventricular fibrillation. Each infant demonstrated unique and transient ECG findings consisting of ST changes and QRS widening before arrhythmia onset, which have not been previously reported. Amiodarone, sedation, sodium channel–blocking agents, and ventricular pacing were effective in suppressing acute events. Despite thorough investigation, including genetic testing, the cause of ventricular arrhythmias in each of these infants remains unclear. Conclusions— This is the first report of idiopathic ventricular fibrillation in young infants preceded by stereotypical transient ECG changes. These findings may represent a new, potentially treatable cause of sudden infant death. Recognition of these prodromal changes may be important in future management and survival of these infants.