History Of Structural Heart Disease Research Articles

High-resolution three-dimensional late gadolinium-enhanced cardiac magnetic resonance imaging to identify the underlying substrate of ventricular arrhythmia.

AimsCardiac magnetic resonance (CMR) is recommended as a second-line method to diagnose ventricular arrhythmia (VA) substrate. We assessed the diagnostic yield of CMR including high-resolution late gadolinium-enhanced (LGE) imaging.Methods and resultsConsecutive patients with sustained ventricular tachycardia (VT), non-sustained VT (NSVT), or ventricular fibrillation/aborted sudden death (VF/SCD) underwent a non-CMR diagnostic workup according to current guidelines, and CMR including LGE imaging with both a conventional breath-held and a free-breathing method enabling higher spatial resolution (HR-LGE). The diagnostic yield of CMR was compared with the non-CMR workup, including the incremental value of HR-LGE. A total of 157 patients were enrolled [age 54 ± 17 years; 75% males; 88 (56%) sustained VT, 52 (33%) NSVT, 17 (11%) VF/SCD]. Of these, 112 (71%) patients had no history of structural heart disease (SHD). All patients underwent electrocardiography and echocardiography, 72% coronary angiography, and 51% exercise testing. Pre-CMR diagnoses were 84 (54%) no SHD, 39 (25%) ischaemic cardiomyopathy (ICM), 11 (7%) non-ischaemic cardiomyopathy (NICM), 3 (2%) arrhythmogenic right ventricular cardiomyopathy (ARVC), 2 (1%) hypertrophic cardiomyopathy (HCM), and 18 (11%) other. CMR modified these diagnoses in 48 patients (31% of all and 43% of those with no SHD history). New diagnoses were 9 ICM, 28 NICM, 8 ARVC, 1 HCM, and 2 other. CMR modified therapy in 19 (12%) patients. In patients with no SHD after non-CMR tests, SHD was found in 32 of 84 (38%) patients. Eighteen of these patients showed positive HR-LGE and negative conventional LGE. Thus, HR-LGE significantly increased the CMR detection of SHD (17–38%, P < 0.001).ConclusionCMR including HR-LGE imaging has high diagnostic value in patients with VAs. This has major prognostic and therapeutic implications, particularly in patients with negative pre-CMR workup.

New onset atrial fibrillation after initiating amphetamine-dextroamphetamine therapy for ADHD: A case report

Atrial fibrillation is a common arrhythmia in the general population, and is expected to significantly increase in prevalencein the near future. This case illustrates a 50-year-old male who developed atrial fibrillation after starting amphetaminedextroamphetaminefor attention deficit hyperactivity disorder (ADHD), with no previous history of structural heart disease. Central nervous system stimulant medications have significant cardiovascular implications and at risk patients should be monitoredclosely. Additionally, identifying causative agents for atrial fibrillation and other arrhythmias is imperative, as there is a significantassociation with morbidity and mortality.

Management of an asymptomatic patient with dynamically changing J wave from inferior early repolarization to Brugada pattern

Case report A 33-year-old man was referred to our institution for investigation of type 1 Brugada syndrome (BS) fortuitously discovered on a routine electrocardiogram (ECG) recorded at an occupational medicine clinic. The patient had no family history of structural heart disease or sudden death and no personal medical history. He was completely asymptomatic at the time of the initial examination. The 12-lead ECG at admission (Figure 1) reveals a normal sinus rhythm with a significant ST-segment elevation of more than 2 mm in leads V1 and V2 diagnostic of a type 1 BS. We also noted the presence of a significant slurred J wave in the inferior leads diagnostic of early repolarization (ER) pattern. At baseline, the maximal amplitude of the J wave was 5 mm (0.5 mV) in lead V1 and 4 mm (0.4 mV) in lead III. As we performed routine Valsava maneuvers, we observed significant change in the J wave in amplitude and distribution (Figure 2). Immediately after the end of maneuvers the J wave became maximal in the inferior leads and extended all the way to the T wave (amplitude of 5 mm in lead III) while J wave decreased in the anterior leads (disappeared in lead V1 and maximal amplitude of 4 mm in lead V2). Rapidly after the end of the Valsalva maneuver, a gradual transition of the ECG back to its initial form was subsequently observed. The same phenomenon was obtained reproducibly with Valsalva maneuvers. Multiple ECG recordings and continuous heart rhythm telemetry also demonstrated extreme fluctuation of the J wave in amplitude and distribution from predominant Brugada pattern to predominant ER pattern to normal ECG (Figure 3). During hospitalization, the patient underwent an extensive cardiac

P03 : Structural heart disease predicts success rates of pulmonary vein isolation with the cryoballoon catheter

Aim To retrospectively evaluate clinical predictors of successful ablation of atrial fibrillation following pulmonary vein isolation using the Medtronic Arctic Front Cryoballoon catheter. Background Cryoablation is an effective technique for the treatment of AF. Long-term data measuring the rates of recurrence and symptom reduction is lacking. Methods 73 patients undergoing cryoablation for symptomatic paroxysmal or persistent AF using the Arctic Front Cardiac CryoAblation balloon catheter (Medtronic, Inc.) were retrospectively examined. One patient had a repeat procedure for a total of 74. Patient characteristics, AF type, recurrence of AF, symptomatic reduction, and the presence of structural heart disease was recorded. Recurrence of AF was measured at 6 and 12 months. Methods of monitoring included EKG, mobile cardiac telemetry (MCT), holter monitor, and implantable devices such as internal loop recorders, pacemakers, and implantable cardioverter–defibrillators. The presence of structural heart disease was defined as a left atrial diameter >4.0 cm and/or ejection fraction (EF) Results A total of 74 procedures were performed from October 2011 through April 2013. Diaphragmatic palsy occurred in 1 patient, leading to an incomplete ablation procedure with immediate failure. At 6 months 84.2% of patients were free of recurrent atrial fibrillation. At 12 months, 65.2% of patients were free of recurrent atrial fibrillation. There was no difference in success rates between men and women. The presence of structural heart disease was a significant predictor of long-term success. In patients with structurally normal hearts, success rates were 93.3% and 77.8% at 6 and 12 months. In patients with structural heart disease, success rates at 6 and 12 months were 70.6% and 45.5%, respectively. Patients with structural heart disease had a mean left atrial diameter of 4.79 cm with an EF of 38.8%. Patients without structural heart disease had a mean left atrial diameter of 3.36 cm with an EF of 57.2%. The type of AF also influenced outcomes at the 6-month follow-up, with procedural success in 90% of those with paroxysmal AF and 62.5% of those with persistent AF. This pattern was not seen at 12-month follow-up, with success rates of 64.7% and 66.7% in those with paroxysmal and persistent AF, respectively. Conclusion Cryoablation serves as an alternative approach for the treatment of drug-refractory atrial fibrillation with high rates of immediate success and low rates of recurrence. Success rates are highest in those with paroxysmal AF without a history of structural heart disease.

Free Floating Left Atrial Ball Thrombus: A Rare Cause of Stroke

In the setting of mitral valve stenosis and atrial fibrillation, left atrial ball thrombus is a rare but recognized cause of stroke and can occur even in the presence of therapeutic anticoagulation. This case report highlights the need for echocardiography to rule out treatable cardioembolic substrates for stroke. We report a case of cardioembolic stroke as a result of free floating left atrial ball thrombus presenting as a complication of rheumatic mitral valve disease. This case highlights that, in all patients with a history of structural heart disease, atrial fibrillation, or rheumatic fever, prompt cardiac ultrasound to exclude free floating atrial thrombus is essential.

Lebensbedrohliche Herzrhythmusstörungen

Life-threatening arrhythmias are a frequent indication for mobile intensive care unit (MICU) missions. In part these are for patients requiring cardiopulmonary resuscitation but other patients are still conscious and need careful evaluation before treatment. Symptoms such as severe angina pectoris and clinical signs such as low blood pressure <90 mmHg, dizziness and left ventricular failure as well as a history of structural heart disease are valuable criteria for distinguishing stable from unstable patients. Generally an unstable patient with bradycardia needs immediate pacing or pharmacological support. An unstable patient with tachycardia needs immediate electrical cardioversion, whereas stable patients require targeted out-of-hospital treatment or in many cases, while being monitored, may be transported to a nearby qualified hospital for definitive evaluation and treatment. A 12-lead ECG should be registered at the scene wherever possible: this is the mainstay for targeted treatment and also after hospital admission helps the specialist in the diagnostic process. If a pharmacological strategy is chosen, treatment with multiple anti-arrhythmic agents should be avoided because of potentially uncontrollable reactions.

Successful Catheter Ablation of Focal Automatic Left Ventricular Tachycardia Presented with Tachycardia-Mediated Cardiomyopathy

Non-reentrant focal tachycardias occur spontaneously, facilitated by catecholamine infusion, but they cannot be initiated or terminated with programmed stimulation. These tachycardias exhibit early activation before the QRS, however, do not typically show the mid-diastolic potential that is crucial for reentrant tachycardia maintenance. Electrophysiological studies are useful for distinguishing focal from macro-reentrant ventricular tachycardia. We report herein a case of patient without a history of structural heart disease who presented with a focal Purkinje ventricular tachycardia and heart failure. The focal Purkinje ventricular tachycardia was eliminated by radiofrequency catheter ablation. All of the patien's symptoms were improved after ablation.

Outcome of anatomic ganglionated plexi ablation to treat paroxysmal atrial fibrillation: a 3-year follow-up study

A new strategy for anatomically based ganglionated plexi (GP) ablation for the treatment of paroxysmal atrial fibrillation (AF) has been proposed recently. We aimed to assess the long-term outcome of patients undergoing anatomic GP ablation for paroxysmal AF, in comparison with circumferential pulmonary vein (PV) isolation. The study population consisted of 70 patients (mean age 56.6 ± 10.9 years; 41 males) with paroxysmal AF and no history of structural heart disease: 35 subjects underwent anatomic GP ablation, while 35 consecutive patients had circumferential PV isolation (CPVI) (control group). The groups were not different in demographic and clinical parameters. Anatomic GP ablation required more ablation points (85.6 ± 5.5 vs. 74.4 ± 6.2, P < 0.05) and equal duration of total procedure and fluoroscopy times. During a mean follow-up period of 36.3 ± 2.3 months, freedom from any atrial tachyarrhythmia without antiarrhythmics was achieved in 34.3% patients after anatomic GP ablation and 65.7% patients after CPVI (log-rank test P = 0.008). Early arrhythmia recurrences and anatomic GP ablation were independent predictors of late recurrence [HR 6.44 (CI 95%; 3.14-13.18; P < 0.001) and HR 2.08 (CI 95%; 1.03-4.22; P = 0.04), respectively]. Six patients in the group of GP ablation underwent subsequent CPVI, plus peri-mitral flutter ablation in two of them, with no further arrhythmia episodes in five patients. Anatomic GP ablation yields a significantly lower success rate over the long-term follow-up period, when compared with CPVI. Recurrences include AF and macro re-entrant atrial tachycardias.

NT-pro-BNP for diagnostic and prognostic evaluation in patients hospitalized for syncope

BackgroundSingle clinical parameters are inaccurate for diagnostic and prognostic estimation in patients with syncope. The cardiac marker NT-pro-BNP has not thoroughly been evaluated for this application. MethodsNT-pro-BNP was assessed in 161 consecutive patients (median age 69years, 58% male) hospitalized for syncope in a cardiological university department and association (odds ratio: OR, 95% confidence interval: CI) with diagnosis of cardiac cause and 6-months outcome was analyzed. ResultsNT-pro-BNP levels were significantly higher in patients with cardiac (n=78) compared to non-cardiac syncope (n=83). At a cutoff of 156pg/ml, NT-pro-BNP showed a sensitivity of 89.7%, a specificity of 51.8% and a negative predictive value of 84.3% for the diagnosis of cardiac syncope. Increasing NT-pro-BNP was a significant predictor of cardiac syncope (OR 3.7, 95% CI 2.3–5.8 per standard deviation of Log NT-pro-BNP, p<0.001) and addition of NT-pro-BNP significantly improved a predictive model including heart rate, history of structural heart disease and abnormal ECG. Adding left-ventricular ejection fraction to the model did not change results. Sixty-three patients had an adverse event during hospitalization or 6-months follow-up. NT-pro-BNP>156pg/ml significantly predicted an adverse outcome (OR 2.7, 95% CI 1.04–6.9, p=0.04) after multivariate adjustment. ConclusionsIn patients hospitalized for syncope, NT-pro-BNP was a strong and independent diagnostic and prognostic marker and addition to conventional criteria of history and examination improved the discriminatory performance. Randomized trials must clarify the benefit and position of NT-pro-BNP in the management algorithm of patients with syncope.

First Do No Harm … Reduction?

An expert panel convened to discuss how to incorporate methadone's possible effect on the QT interval into clinical practice. The findings and recommendations of some of the panel members appear in...

QTc Interval Screening in Methadone Treatment

An independent panel developed cardiac safety recommendations for physicians prescribing methadone. Expert panel members reviewed and discussed the following sources regarding methadone: pertinent English-language literature identified from MEDLINE and EMBASE searches (1966 to June 2008), national substance abuse guidelines from the United States and other countries, information from regulatory authorities, and physician awareness of adverse cardiac effects. RECOMMENDATION 1 (DISCLOSURE): Clinicians should inform patients of arrhythmia risk when they prescribe methadone. RECOMMENDATION 2 (CLINICAL HISTORY): Clinicians should ask patients about any history of structural heart disease, arrhythmia, and syncope. RECOMMENDATION 3 (SCREENING): Obtain a pretreatment electrocardiogram for all patients to measure the QTc interval and a follow-up electrocardiogram within 30 days and annually. Additional electrocardiography is recommended if the methadone dosage exceeds 100 mg/d or if patients have unexplained syncope or seizures. RECOMMENDATION 4 (RISK STRATIFICATION): If the QTc interval is greater than 450 ms but less than 500 ms, discuss the potential risks and benefits with patients and monitor them more frequently. If the QTc interval exceeds 500 ms, consider discontinuing or reducing the methadone dose; eliminating contributing factors, such as drugs that promote hypokalemia; or using an alternative therapy. RECOMMENDATION 5 (DRUG INTERACTIONS): Clinicians should be aware of interactions between methadone and other drugs that possess QT interval-prolonging properties or slow the elimination of methadone.

The Significance of Cardiac Sympathetic Nervous System Abnormality in the Long-Term Prognosis of Patients with a History of Ventricular Tachyarrhythmia

Severe left ventricular dysfunction or cardiac sympathetic nervous system (SNS) abnormality predicts cardiac death in various heart diseases, including arrhythmogenic disorders. However, it is not clear whether SNS abnormality predicts sudden cardiac death during long-term follow-up in patients with a history of ventricular tachyarrhythmia. We hypothesized that SNS abnormality would be associated with recurrent ventricular arrhythmic events. 123I-metaiodobenzylguanidine (MIBG) scintigraphy was performed on 86 patients (mean age+/-SD, 46+/-19 y, 65.1% men) with a history of ventricular tachycardia or fibrillation. 123I-MIBG (111 MBq) was intravenously administered under resting conditions, and planar images were obtained 15 min and 4 h later (anterior view for 6 min; 512x512 matrices; zoom ratio, 1.0). SNS activity was assessed using the heart-to-mediastinum ratio on delayed imaging. During about 11 y of follow-up (mean+/-SD, 5.2+/-3.7 y), 3 patients (3.5%) had sudden cardiac death and 21 patients (24.4%) had sustained ventricular tachyarrhythmic events. SNS abnormality, defined as a heart-to-mediastinum ratio of less than 2.8, and left ventricular dysfunction, defined as a left ventricular ejection fraction of less than 50%, were associated with sudden cardiac death or recurrent ventricular tachyarrhythmic events (18/40 patients [45%] with SNS abnormality, vs. 6/46 patients [13%] without, P=0.004; 9/15 patients [60%] with left ventricular dysfunction, vs. 15/71 patients [21.1%] without, P=0.008). After adjustment for potential confounding variables such as age, sex, coronary risk factors, medication use, history of structural heart disease, and left ventricular function, SNS abnormality was a powerful predictor of recurrent arrhythmic events, with a hazard ratio of 3.6 [95% confidence interval, 1.4-9.2, P=0.007]). Further, SNS abnormality had incremental and additive prognostic power in combination with left ventricular dysfunction, with an adjusted hazard ratio of 4.4 [95% confidence interval, 1.9-9.9, P<0.0001]). SNS abnormality predicted recurrent ventricular tachyarrhythmic events during long-term follow-up. 123I-MIBG scintigraphic evaluations for SNS abnormality may be an option for screening patients at high risk for sudden cardiac death.

Abstract 726: Cardiac Sympathetic Nerve System Abnormality Predicts Long-Term Outcome in Patients with Paroxysmal Atrial Fibrillation who did not have Conventional Risk Factors

Backgrounds: A history of structural heart disease, heart failure, or stroke increases mortality in patients with atrial fibrillation (AF). However, a useful marker for predicting mortality is not clarified in AF patients without those conventional risks. We recently reported cardiac sympathetic nerve system (SNS) abnormality as a predictor of arrhythmogenic mortality. We hypothesized that SNS abnormality would be associated with increased mortality in patients with paroxysmal AF who didn’t have conventional risk factors. Methods and Results: Iodine-123 metaiodobenzylguanidine scintigraphy was performed to measure Heart/Mediastinum (H/M) ratio as SNS activity in 48 patients (mean ± standard deviation, age: 65 ± 14 years, 65% males) with paroxysmal AF who didn’t have structural heart disease, heart failure, or stroke. P wave dispersion on 12-lead ECG and left atrial dimension on echocardiography were also measured to evaluate structural and electrical properties. Over 11 years follow up, 15 patients (31.3%) transited to permanent AF, and 12 (25%) had cardio/cerebrovascular events. SNS abnormality (defines as H/M ratio &lt;2.7) was a powerful predictor of vascular events (50% in 9 of 18 patients with SNS abnormality vs 10% in 3 of 30 patients without those, p=0.0008). After adjustment for potential confounding variables such as age, gender, P wave dispersion, left atrial dimension, transit to permanent AF, and medications, SNS abnormality remained predictive of vascular events with hazard ratio of 6.9 [95% confidence interval, 1.9 to 25.7 (p=0.004)]. Conclusion: SNS abnormality is predictive of mortality in patients with paroxysmal AF who did not have conventional risk.

Electrocardiographic Artifact Mimicking Ventricular Tachycardia During High-Frequency Oscillatory Ventilation: A Case Report

One cause of ECG artifacts is simultaneous use of other equipment while the ECG is being monitored or recorded. ECG artifacts mimicking either atrial or ventricular arrhythmia have been reported with the use of a variety of equipment (see Table). Muscle contractions (eg, tremors, shivering, convulsions) and body motion (eg, changing body position, brushing the teeth, combing the hair, physiotherapy, coughing, hiccoughing) can also cause ECG disturbances that simulate arrhythmias. To my knowledge, the following is the first report of an ECG artifact due to high-frequency oscillatory ventilation. A 54-year-old woman with no history of structural heart disease or arrhythmia was admitted to the intensive care unit (ICU) with a diagnosis of acute respiratory distress syndrome complicating acute pancreatitis. She was sedated, and mechanical ventilation was started. Her hypoxemia persisted despite maximal respiratory support with high positive end-expiratory pressure and a fraction of inspired oxygen of 1.00. She was given a paralytic agent, and high-frequency oscillatory ventilation was started at 5 Hz. After a few hours, ICU staff noted a change in heart rhythm from sinus tachycardia to apparent ventricular tachycardia. A defibrillator was placed near the patient’s bed, and the physician on duty was summoned. The patient had no marked changes in blood pressure, central venous pressure, or oxygen saturation as measured by pulse oximetry. Arterial blood gas analysis and measurements of serum levels of electrolytes also did not reveal any marked changes. Findings on direct monitoring of arterial pressure, central venous pressure waveforms, and plethysmographic results were not changed. An ECG artifact was suspected.

Prevalence and Clinical Course of the Juveniles with Brugada‐Type ECG in Japanese Population

Although many studies on Brugada syndrome have been done, with many reports of genetic findings and clinical features, little evidence exists to support the role of this syndrome in sudden cardiac death in a juvenile population. We sought to determine the prevalence and clinical course in children exhibiting Brugada-type ECG in a community-based population. Our study population comprised 21,944 subjects (11,282 boys and 10,662 girls) who underwent ECG during their first-year elementary school health examinations between 1992 and 2001 in Izumi City, Osaka. Brugada-type ECG was defined as demonstrating ST-segment elevation (coved or saddle-back type, J wave amplitude > or =0.2 mV) in the right precordial leads. We also divided Brugada-type ECGs into three types according to a consensus report. Type 1: coved ST-segment elevation displaying high J wave amplitude followed by a negative T wave; Type 2: high take-off and gradually descending ST-segment elevation (remaining > or =1 mm) followed by a positive or biphasic T wave; and Type 3: ST-segment elevation of <1 mm of both types. Four subjects showed Brugada-type ECG (0.02%) (2 boys and 2 girls). Only one subject, a girl, met Type 1 criteria (0.005%). No history of structural heart disease was documented in these four subjects. During 6.8 +/- 1.0 years of follow-up, no episode of unexpected sudden death, syncopal attack, and fatal arrhythmia occurred. The prevalence of Brugada-type ECG in a juvenile population was extremely low. To investigate when the typical Brugada-type ECG might be manifested, it could be necessary to check ECGs after adolescence.

Right Atrial Tachycardia in a Patient with Severe Atrial Conduction Disturbances and an Anatomically Normal Heart

We describe a case of abnormal right atrial (RA) conduction in a patient with atrial tachycardia (AT) but no history of structural heart disease or cardiac surgery. Following ablation of AT, the patient experienced typical atrial flutter (AFL) and a postcardioversion ECG suggestive of low atrial rhythm. Repeat EPS and three-dimensional electroanatomic activation mapping showed unusual RA activation during SR. This case illustrates the possibility that abnormal intraatrial conduction may lead to unusual patterns of activation in the RA which can serve as a necessary substrate for the initiation and maintenance of macro-reentry circuits.

719-1 Does Vasodepressor Syncope Require Normal Ventricular Function?

Vasodepressor syncope is believed to be preceded by hypercontractility which leads to mechanoreceptor stimulation. Therefore, a preserved left ventricular function is supposedly required to trigger the reflex. We analyzed our experience in patients with positive head-up tilt test. Out of 500 patients 32 had previous history of structural heart disease. Of them 8 patients had severe left ventricular dysfunction (EF &lt; 30%). The mean age was 52 ± 8 years, 5 were male and 3 female. Mean EF was 22 ± 5%. Six patients had dilated cardiomyopathy and 2 had myocardial infarction. Electrophysiologic study was negative in 6 patients while the remaining two had inducible sustained monomorphic ventricular tachycardia requiring defibrillator implant. Syncope was witnessed by physicians in 6 out of 8 patients and was associated with bradycardia and hypotension. In all 8 patients head-up tilt reproduced symptoms. Upright tilt was positive at baseline in 7 patients and during isoproterenol infusion in 1 patient. Five patients were treated with theophylline, 1 with ephedrine, and 2 with disopyramide. After a mean follow-up of 2.2 ± 1.3 years all 8 patients were free of vasodepressor-related syncope. We conclude that vasodepressor syncope is possible even in the presence of severely impaired ventricular function and should, therefore, be entertained in such cases. Alternative mechanisms may mediate the circulatory response in this population.