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Cardiovascular AND Tachycardia, ventricular, [keywords]
- Congenital and hereditary causes of sudden cardiac death in young adults: diagnosis, differential diagnosis, and risk stratification. [Journal Article]
- Radiographics 2013 Nov-Dec; 33(7):1977-2001.
Sudden cardiac death is defined as death from unexpected circulatory arrest-usually a result of cardiac arrhythmia-that occurs within 1 hour of the onset of symptoms. Proper and timely identification of individuals at risk for sudden cardiac death and the diagnosis of its predisposing conditions are vital. A careful history and physical examination, in addition to electrocardiography and cardiac imaging, are essential to identify conditions associated with sudden cardiac death. Among young adults (18-35 years), sudden cardiac death most commonly results from a previously undiagnosed congenital or hereditary condition, such as coronary artery anomalies and inherited cardiomyopathies (eg, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy [ARVC], dilated cardiomyopathy, and noncompaction cardiomyopathy). Overall, the most common causes of sudden cardiac death in young adults are, in descending order of frequency, hypertrophic cardiomyopathy, coronary artery anomalies with an interarterial or intramural course, and ARVC. Often, sudden cardiac death is precipitated by ventricular tachycardia or fibrillation and may be prevented with an implantable cardioverter defibrillator (ICD). Risk stratification to determine the need for an ICD is challenging and involves imaging, particularly echocardiography and cardiac magnetic resonance (MR) imaging. Coronary artery anomalies, a diverse group of congenital disorders with a variable manifestation, may be depicted at coronary computed tomographic angiography or MR angiography. A thorough understanding of clinical risk stratification, imaging features, and complementary diagnostic tools for the evaluation of cardiac disorders that may lead to sudden cardiac death is essential to effectively use imaging to guide diagnosis and therapy.
- Genome wide analysis of drug-induced torsades de pointes: lack of common variants with large effect sizes. [Journal Article]
- PLoS One 2013; 8(11):e78511.
Marked prolongation of the QT interval on the electrocardiogram associated with the polymorphic ventricular tachycardia Torsades de Pointes is a serious adverse event during treatment with antiarrhythmic drugs and other culprit medications, and is a common cause for drug relabeling and withdrawal. Although clinical risk factors have been identified, the syndrome remains unpredictable in an individual patient. Here we used genome-wide association analysis to search for common predisposing genetic variants. Cases of drug-induced Torsades de Pointes (diTdP), treatment tolerant controls, and general population controls were ascertained across multiple sites using common definitions, and genotyped on the Illumina 610k or 1M-Duo BeadChips. Principal Components Analysis was used to select 216 Northwestern European diTdP cases and 771 ancestry-matched controls, including treatment-tolerant and general population subjects. With these sample sizes, there is 80% power to detect a variant at genome-wide significance with minor allele frequency of 10% and conferring an odds ratio of ≥2.7. Tests of association were carried out for each single nucleotide polymorphism (SNP) by logistic regression adjusting for gender and population structure. No SNP reached genome wide-significance; the variant with the lowest P value was rs2276314, a non-synonymous coding variant in C18orf21 (p = 3×10(-7), odds ratio = 2, 95% confidence intervals: 1.5-2.6). The haplotype formed by rs2276314 and a second SNP, rs767531, was significantly more frequent in controls than cases (p = 3×10(-9)). Expanding the number of controls and a gene-based analysis did not yield significant associations. This study argues that common genomic variants do not contribute importantly to risk for drug-induced Torsades de Pointes across multiple drugs.
- Successful Ablation of a Narrow Complex Tachycardia arising from a Left Ventricular False Tendon: Mapping and Optimizing Energy Delivery. [JOURNAL ARTICLE]
- Heart Rhythm 2013 Nov 8.
Ventricular tachycardia arising in the His-Purkinje system is an important cause of narrow complex tachycardia that is often amenable to catheter ablation. Ventricular arrhythmias may require targeted mapping and ablation of endocavitary structures, such as papillary muscles or false tendons to eliminate symptomatic arrhythmia. We describe a patient with narrow QRS tachycardia who required mapping and ablation of a left ventricular false tendon. Intracardiac echocardiography was used to identify the target and optimize contact to successfully ablate this unique focus for arrhythmia.
- Prevalence, Correlates, and Temporal Trends in Antiarrhythmic Drug Use at Discharge After Implantable Cardioverter Defibrillator Placement (from the National Cardiovascular Data Registry [NCDR]). [JOURNAL ARTICLE]
- Am J Cardiol 2013 Oct 4.
Patients with implantable cardioverter defibrillators (ICDs) can require antiarrhythmic drugs to manage arrhythmias and prevent device shocks. We sought to determine the prevalence, clinical correlates, and institutional variation in the use of antiarrhythmic drugs over time after ICD implantation. From the ICD Registry (2006 to 2011), we analyzed the trends in the use of antiarrhythmic agents prescribed at hospital discharge for patients undergoing first-time ICD placement. The patient, provider, and facility level variables associated with antiarrhythmic use were determined using multivariate logistic regression models. A median odds ratio was calculated to assess the hospital-level variation in the use of antiarrhythmic drugs. Of the cohort (n = 500,995), 15% had received an antiarrhythmic drug at discharge. The use of class III agents increased modestly (13.9% to 14.9%, p <0.01). Amiodarone was the most commonly prescribed drug (82%) followed by sotalol (10%). Among the subgroups, the greatest increase in prescribing was for patients who had received a secondary prevention ICD (26% in 2006% and 30% in 2011, p <0.01) or with a history of ventricular tachycardia (23% to 27%, p <0.01). The median odds ratio for antiarrhythmic prescription was 1.45, indicating that 2 randomly selected hospitals would have had a 45% difference in the odds of treating identical patients with an antiarrhythmic drug. In conclusion, antiarrhythmic drug use, particularly class III antiarrhythmic drugs, is common among ICD recipients at hospital discharge and varies by hospital, suggesting an influence from local treatment patterns. The observed hospital variation suggests a role for augmentation of clinical guidelines regarding the use of antiarrhythmic drugs for patients undergoing implantation of an ICD.
- Ambulatory ECG-Based T-Wave Alternans Monitoring for Risk Assessment and Guiding Medical Therapy: Mechanisms and Clinical Applications. [Journal Article]
- Prog Cardiovasc Dis 2013 Sep-Oct; 56(2):172-85.
Identification of individuals at risk for sudden cardiac death (SCD), the main cause of adult mortality in developed countries, remains a major challenge. The main contemporary noninvasive marker, left ventricular ejection fraction (LVEF), has not proved adequately reliable, as the majority of individuals who die suddenly have relatively preserved cardiac mechanical function. Monitoring of T-wave alternans (TWA), a beat-to-beat fluctuation in ST-segment or T-wave morphology, on ambulatory electrocardiogram (AECG) is an attractive approach on both scientific and clinical grounds. Specifically, TWA's capacity to assess risk for malignant arrhythmias has been shown to rest on sound electrophysiologic principles and AECG-based TWA monitoring can be performed in the flow of routine clinical evaluation. This review addresses: (1) electrophysiologic and ionic mechanisms underlying TWA's predictivity, (2) principles and practical aspects of AECG-based TWA monitoring, (3) clinical evidence supporting this approach to SCD risk stratification, and (4) current and potential applications in guiding medical therapy.
- Prognostic Significance of Ambulatory ECG Monitoring for Ventricular Arrhythmias. [Journal Article]
- Prog Cardiovasc Dis 2013 Sep-Oct; 56(2):133-42.
Ventricular arrhythmia can be detected in ambulatory ECG monitoring in individuals with or without cardiac disease, and its prognostic value varies, depending on the underlying condition. The use of continuous or intermittent ambulatory ECG monitoring can be helpful for diagnosis when there is a high pre-test probability of identifying a transient arrhythmia. In addition, Holter monitoring can be used for risk stratification of patients, in the context of the prognostic value of non-sustained ventricular arrhythmias in various clinical settings, as discussed in detail.
- Bidirectional Ventricular Tachycardia? [JOURNAL ARTICLE]
- Ann Noninvasive Electrocardiol 2013 Nov 5.
A 65-year-old woman was admitted to the hospital because of a syncopal episode with documented transient complete atrioventricular block. A DDD pacemaker was implanted. Post implantation, the patient was diagnosed with bidirectional ventricular tachycardia. Analysis of the arrhythmia and differential diagnosis is performed.
- Maximal heart rate does not limit cardiovascular capacity in healthy humans: insight from right atrial pacing during maximal exercise. [JOURNAL ARTICLE]
- J Physiol 2013 Dec 2.
In humans, maximal aerobic power (VO2max) is associated with a plateau in cardiac output (Q), but the mechanisms regulating the interplay between maximal heart rate (HRmax) and stroke volume (SV) are unclear. To evaluate the effect of tachycardia and elevations in HRmax on cardiovascular function and capacity during maximal exercise in healthy humans, twelve young male cyclists performed incremental cycling and one-legged knee-extensor exercise (KEE) to exhaustion with and without right atrial pacing to increase HR. During control cycling, Q and leg blood flow increased up to 85% of maximal workload (WLmax) and remained unchanged until exhaustion. SV initially increased, plateaued and then decreased before exhaustion (P<0.05) despite an increase in right atrial pressure (RAP) and a tendency (P=0.056) for a reduction in left ventricular transmural filling pressure (LVFP). Atrial pacing increased HRmax from 184±2 to 206±3 beats min(-1) (P<0.05), but Q remained similar to the control condition at all intensities because of a lower SV and LVTP (P<0.05). No differences in arterial pressure, peripheral haemodynamics, catecholamines or VO2 were observed, but pacing increased the rate pressure product and RAP (P<0.05). Atrial pacing had a similar effect on haemodynamics during KEE, except that pacing decreased RAP. In conclusion, the human heart can be paced to a higher HR than observed during maximal exercise, suggesting that HRmax and myocardial work capacity do not limit VO2max in healthy individuals. A limited left ventricular filling and possibly altered contractility reduces SV during atrial pacing, whereas a plateau in LVFP appears to restrict Q close to VO2max.
- Antagonistic Effects of Tetrodotoxin on Aconitine-induced Cardiac Toxicity. [Journal Article]
- J Nippon Med Sch 2013; 80(5):350-61.
Aconitine, well-known for its high cardiotoxicity, causes severe arrhythmias, such as ventricular tachycardia and ventricular fibrillation, by opening membrane sodium channels. Tetrodotoxin, a membrane sodium-channel blocker, is thought to antagonize aconitine activity. Tetrodotoxin is a potent blocker of the skeletal muscle sodium-channel isoform Nav1.4 (IC50 10 nM), but micromolar concentrations of tetrodotoxin are required to inhibit the primary cardiac isoform Nav1.5. This suggests that substantial concentrations of tetrodotoxin are required to alleviate the cardiac toxicity caused by aconitine. To elucidate the interaction between aconitine and tetrodotoxin in the cardiovascular and respiratory systems, mixtures of aconitine and tetrodotoxin were simultaneously administered to mice, and the effects on electrocardiograms, breathing rates, and arterial oxygen saturation were examined. Compared with mice treated with aconitine alone, some mice treated with aconitine-tetrodotoxin mixtures showed lower mortality rates and delayed appearance of arrhythmia. The decreased breathing rates and arterial oxygen saturation observed in mice receiving aconitine alone were alleviated in mice that survived after receiving the aconitine-tetrodotoxin mixture; this result suggests that tetrodotoxin is antagonistic to aconitine. When the tetrodotoxin dose is greater than the dose that can block tetrodotoxin-sensitive sodium channels, which are excessively activated by aconitine, tetrodotoxin toxicity becomes prominent, and the mortality rate increases because of the respiratory effects of tetrodotoxin. In terms of cardiotoxicity, mice receiving the aconitine-tetrodotoxin mixture showed minor and shorter periods of change on electrocardiography. This finding can be explained by the recent discovery of tetrodotoxin-sensitive sodium-channel cardiac isoforms (Nav1.1, 1.2, 1.3, 1.4 and 1.6).
- Ventricular arrhythmias: state of the art. [Journal Article]
- Cardiol Clin 2013 Nov; 31(4):595-605.
The management of ventricular tachycardia and ventricular fibrillation in the cardiac intensive care unit can be complex. These arrhythmias have many triggers, including ischemia, sympathetic stimulation, and medication toxicities, as well as many different substrates, ranging from ischemic and nonischemic cardiomyopathies to rare genetic conditions such as Brugada syndrome and long QT syndrome. Different settings, such as congenital heart disease, postoperative ventricular arrhythmias, and ventricular assist devices, increase the complexity of management. This article reviews the variety of situations and cardiac conditions that give rise to ventricular arrhythmias, focusing on inpatient management strategies.