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Modifiable risk factor management is becoming one of the 3 treatment pillars in atrial fibrillation management along with anticoagulation as well as conventional rate and rhythm control strategies. Preventive therapies, such as reducing blood pressure and treating obstructive sleep apnea, are paramount in the strategy of preventing atrial fibrillation. Identification of new modifiable risk factors and triggers also could help in the global strategy to reduce atrial fibrillation. This article covers alcohol intake, tobacco smoking, caffeine, chocolate, cannabis use, and air pollution as social risk factors related to lifestyle habits that potentially could contribute to atrial fibrillation development.

Cardiac fibrosis is a significant increase in collagen volume fraction of myocardial tissue. It plays an important role in the pathophysiology of many cardiovascular abnormalities. Electrophysiologically, myocardial fibrosis produces anisotropic conduction, inhomogeneity, and conduction delay. Several markers are available to detect myocardial fibrosis. CMRI is the most common imaging technique; late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) provides markers for tissue characterization, disease progression and arrhythmic events. LGE-CMR can be used as risk marker of occurrence of pathologic conditions. LGE-CMR demonstrates specific patterns related to different pathologic substrates. We discuss the role of CMRI in ventricular arrhythmogenesis.

The electrocardiogram and various echocardiography modalities are important risk markers for atrial fibrillation (AF). Electrocardiographic criteria of left atrial enlargement, advanced interatrial block, and PR-interval prolongation are atrial risk markers for AF. Transthoracic echocardiography is elementary for risk stratification of AF. Transesophageal echocardiography is a valuable tool to detect cardiac sources of embolism if early cardioversion is necessary. Intracardiac echocardiography is a real-time tool for guidance of percutaneous interventions, including radiofrequency ablation and left atrial appendage closure in patients with AF.

Class I antiarrhythmic agents or Na+ channel blockers are among the first drugs that have been used for several decades, and are divided into three groups, according to their cellular electrophysiologic effects. The sodium ion currents or INa enter the cell very fast during phase-0 of action potential and is responsible for depolarization.

Fascicular ventricular tachycardia (FVT) usually involves the left fascicular system; namely the left posterior fascicle, anterior fascicle, and rarely the upper septal fascicle. It may also involve the right Purkinje arborization. This tachycardia can be seen in normal heart or in the setting of structural heart diseases. Monomorphic FVT can be reentrant or nonreentrant and verapamil-sensitive left FVT is the second most common type of idiopathic ventricular tachycardia (VT) after right ventricular outflow tract VT. This article focuses on the practical approach for both reentrant and nonreentrant FVT, explaining the mechanism, electrocardiographic features, and electrophysiologic features of FVT.

Cardiac mapping has witnessed significant and unprecedented progress over more than a century. At present, several mapping/imaging technologies are commercially available, alone or in combination. This article briefly discusses the advantages and limitations (disadvantages) of each technique.

BACKGROUND Paroxysmal atrioventricular (A-V) block is relatively rare, and due to its transient nature, it is often under recognized. It is often triggered by atrial, junctional, or ventricular premature beats, and occurs in the presence of a diseased His-Purkinje system (HPS). Here, we present a 45-year-old white male who was admitted for observation due to recurrent syncope and near-syncope, who had paroxysmal A-V block. The likely cellular electrophysiological mechanisms(s) of paroxysmal A-V block and its differential diagnosis and management are discussed. METHODS Continuous electrocardiographic monitoring was done while the patient was in the cardiac unit. RESULTS Multiple episodes of paroxysmal A-V block were documented in this case. All episodes were initiated and terminated with atrial/junctional premature beats. The patient underwent permanent pacemaker implantation and has remained asymptomatic since then. CONCLUSIONS Paroxysmal A-V block is rare and often causes syncope or near-syncope. Permanent pacemaker implantation is indicated according to the current guidelines. Paroxysmal A-V block occurs in the setting of diseased HPS and is bradycardia-dependent. The detailed electrophysiological mechanisms, which involve phase 4 diastolic depolarization, and differential diagnosis are discussed.

Hypertension (HTN) is the most common cause of hypertensive heart disease, which comprises of left ventricular hypertrophy (LVH), left atrial enlargement, diastolic dysfunction, functional mitral regurgitation and neurohormonal changes. All of these lead to significant arrhythmias such as atrial fibrillation (AF) as well as ventricular arrhythmias, and are known risk factors for sudden cardiac death (SCD). The association between LVH and SCD is well established, especially in the presence of myocardial ischemia, fibrosis and scar tissue, and AF. Inflammation, fibrosis and oxidative stress, as well as ischemia play a significant role and are the leading pathways to remodeling, arrhythmias, and SCD. Aggressive HTN control may lead, at least in part, to regression of LVH and thus lower the risk of AF and SCD. Therefore, LVH is a powerful, independent predictor of AF, ventricular arrhythmias and SCD, and is significantly underrecognized. Further investigation of the relationship and management of diastolic dysfunction, LVH and genetic factors and their association with SCD is certainly warranted.

Cardiac mapping has evolved from single point-by-point registration of cardiac electrical activity to its utmost real-time multimodality of mapping and imaging for catheter ablation of arrhythmias. The technology began with electrocardiogram recordings and evolved to the simultaneous registration of depolarization and repolarization using optical mapping and real-time multimodality imaging. Zero to near-zero fluoroscopy is currently used in practice to avoid radiation exposure. Real-time noninvasive mapping, imaging, and ablation of arrhythmias are in use in practice. We present the contemporary up-to-date progress on the role of cardiac mapping and imaging in the diagnosis and management of cardiac arrhythmias.

Although the electrocardiograph (ECG) was invented more than 100 years ago, it remains the most commonly used test in clinical medicine. It is easy to perform, relatively cheap, and results are readily available. Interpretation, however, needs expertise and knowledge. New data, phenomenon, and syndromes are continually discovered by the ECG. It is important to differentiate between normal and abnormal ECGs first and then try to correlate the findings with clinical pathologies. Furthermore, the ECG is an integral part of the screening model for a variety of conditions such as channelopathies, athletes, preoperative risk profile, and remains the cardiologist's best friend.

Ventricular arrhythmias remain a significant cause of sudden cardiac death (SCD), and knowledge of their cause and high-risk features is important. SCD occurs when the interaction between vulnerable substrates and acute triggers results in sustained ventricular tachycardia progressing to ventricular fibrillation. Here, the authors aim to review the role of ventricular arrhythmias in SCD, first by approaching the substrates that support ventricular arrhythmias, and then by exploring features of these substrates and the acute triggers that may lead to SCD.

Left ventricular hypertrophy (LVH) poses an independent risk of increased morbidity and mortality, including atrial arrhythmias, ventricular arrhythmias, and sudden cardiac death. The most common causes of LVH are hypertension and valvular heart disease. Electrocardiography and echocardiography are the first steps in the diagnosis and evaluation of therapy in patients with LVH. Cardiac MRI is the gold standard in diagnosis and assessment of response to therapy. Management of LVH should be based on etiology, evidence, and guideline adherence. Timely and optimal management of the underlying cause of LVH results in improvement (regression) of LVH and its related complications.

Background A 72-year-old white male with a history of rapid nonsustained ventricular tachycardia, hypertrophic cardiomyopathy, and intermittent Brugada-type ECG had a single-lead implantable cardioverter-defibrillator (ICD) implantation and received a sudden ICD shock while in the hot tub. To the best of our knowledge this is the first case report of hot tub jet-induced inappropriate ICD shock. Methods ICD interrogation and analysis of intracardiac electrograms and event markers. Results ICD interrogation revealed inappropriate ICD shocks due to electrical interference of hot tub engine; 60-cycle electrical artifact mimicking fast ventricular fibrillation erroneously detected by the device. The device then delivered a 34.8 joules shock while the patient was actually in sinus rhythm. Conclusions Electrical interference due to external sources such as hot tub engines may occur and produce an inappropriate detection and ICD shock. Precaution and patient education is warranted.

Mohammad Shenasa, MD Cardiac mapping has always been an integral part of basic and clinical electrophysiology. Indeed, direct cardiac mapping with recording of local electrograms has been used since the early 19th century, well before intracardiac catheter mapping.1,2 Walter H. Gaskell measured cardiac contraction to investigate the sequence of cardiac activation.1 Thomas Lewis used direct electrogram mapping in a dog model with atrial and ventricular arrhythmias (Figure 1).2 Intraoperative direct epicardial and endocardial mapping was later reported in patients with preexcitation syndromes and conduction disturbances, initially by the Amsterdam group3; however, systematic use of endocardial and epicardial mapping for ventricular tachycardia (VT) was pioneered by Josephson and colleagues at the University of Pennsylvania, although epicardial mapping was reported earlier by Fontaine et al.4–8 These reports greatly improved our understanding of pathophysiology and mechanisms of VT initially in patients with coronary artery disease and previous myocardial infarction. Intraoperative endocardial mapping revealed that reentry circuits were often localized on the endocardial surface or subendocardially and that resection of those regions eliminated the substrate of VT.9,10 These intraoperative studies led directly to the techniques we use in catheter ablation of VT today and has been applied to other VT substrates. Figure 1. Thomas Lewis’s activation map for direct electrogram recording in a dog heart.2 DBL indicates descending branch of left (coronary artery); DBR, descending branch of right (coronary artery); IVC, inferior vena cava; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; and SVC, superior vena cava. In modern interventional electrophysiology, cardiac mapping and imaging are integrated, and this merging is critical for success in complex ablation procedures. However, electrogram mapping remains an essential part of physiological understanding of the mechanism(s) of VT. The Penn group has set standards for …

Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with significant morbidity and mortality, the so-called AF burden. Despite significant progress in the understanding, the mechanisms and pathophysiology of AF treatments are often unsatisfactory. This in part may be related to the complexity of this arrhythmia, as well as its evolution overtime. Atrial fibrillation has many aetiologies and underlying causes. The anti-arrhythmic drugs (AADs) and interventions aimed at controlling AF should therefore be based on aetiology and associated conditions, rather than electrophysiological mechanisms. The current guideline in the management of AF in most part is based on safety and outcome. This review will discuss the approach to management, based on primary prevention of AF with the aim to target at risk factors, triggers, specific substrates related to aetiology rather than mechanisms. The development of new pharmacological agents and therapeutic strategies should consider not only evidence based, but also include patient-specific personalized context system biology and pharmacology; otherwise, we will continue to see moderate drug efficacy at best and negative results and outcomes.

The last two decades have witnessed dramatic progress in our understanding of cardiac ion channels, and their structure, function, and regulation. We have learned about the role of various ion channels in cardiac physiology and their involvement in cardiac pathophysiology. We have also learned a great deal about the genetic control of channels, by both genes encoding the subunits that form channels and associated/regulatory subunits that are essential for normal ion channel properties. A great deal of information has been obtained by studying mutations in ion channel genes that cause cardiac disease. Sodium, potassium, and calcium ion channels are crucial for cardiac homeostasis and are implicated in physiologic regulation and pathologic conditions; potassium channels constitute the most diverse and complex cardiac ion channel family. In December 2014, Cardiac Electrophysiology Clinics published an issue dedicated to cardiac sodium channel disorders. We are delighted that the Consulting Editors invited us to be the Guest Editors of the current issue on “Cardiac Potassium Channel Disorders: From Basics to Clinics.” Despite the presence of much material in the literature about cardiac

Dofetilide is a class III antiarrhythmic agent with a selective blockade of rapid component of delayed rectifier potassium current (IKr). Dofetilide was found to be safe in patients after myocardial infarction and those with congestive heart failure and left ventricular systolic dysfunction (ejection fraction of less than 35%). An important adverse effect of dofetilide is its potential proarrhythmic risk of ventricular tachyarrhythmias, mostly torsades de pointes. Because dofetilide has about an 80% renal excretion, dose adjustment is required in patients with impaired renal function. Dofetilide should not be given or discontinued if the QTc is greater than 500 ms.

Ranolazine is currently approved as an antianginal agent in patients with chronic angina (class IIA). Ranolazine exhibits antiarrhythmic effects that are related to its multichannel blocking effect, predominantly inhibition of late sodium (late INa) current and the rapid potassium rectifier current (IKr), as well as ICa, late ICa, and INa-Ca. It also suppresses the early and delayed after depolarizations. Ranolazine is effective in the suppression of atrial and ventricular arrhythmias (off-label use) without significant proarrhythmic effect. Currently, ongoing trials are evaluating the efficacy and safety of ranolazine in patients with cardiac arrhythmias; preliminary results suggest that ranolazine, when used alone or in combination with dronedarone, is safe and effective in reducing atrial fibrillation. Ranolazine is not currently approved by the US Food and Drug Administration as an antiarrhythmic agent.

Hypertension (HTN) constitutes the most common chronic cardiovascular disease with an estimated 70 million Americans and over one billion individuals worldwide. HTN accounts as a risk factor for coronary artery disease, myocardial infarction, stroke, heart failure (both systolic and diastolic), atrial fibrillation, ventricular arrhythmias and sudden cardiac death (SCD) (Dellsperger et al. Circulation 82:941–950, 1990).