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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., (Copyright © 2019 Elsevier Inc. All rights reserved.)

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., (Copyright © 2019 Elsevier Inc. All rights reserved.)

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., (Copyright © 2017 Elsevier Inc. All rights reserved.)

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., (Copyright © 2016 Elsevier Inc. All rights reserved.)

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., (Copyright © 2016 Elsevier Inc. All rights reserved.)

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., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Ventricular late potentials detected at the end of the QRS complex by the signal-averaged ECG have been shown to predict arrhythmic events after acute myocardial infarction. Spectral turbulence analysis is a novel technique for detecting abnormalities of cardiac electric activation inside the QRS complex. The purpose of this study was to combine these two analysis methods in order to increase the predictive power of the signal-averaged ECG in post-infarction patients. The study comprised a prospective series of 778 males under 66 years of age who survived the acute phase of myocardial infarction. Signal-averaged ECG recordings were performed before hospital discharge 2 to 3 weeks after infarction. The original Simson method was used for recording and analysing the time-domain signal-averaged ECG. Spectral turbulence analysis was performed using the same averaged vector magnitude QRS complexes (Del Mar Avionics). During the follow-up period of 6 months, 33 patients (4.2%) had an arrhythmic event (sustained monomorphic ventricular tachycardia in 13 cases, ventricular fibrillation in eight cases and sudden cardiac death in 12 cases). The predictive power of late potentials in the time domain, spectral turbulence analysis and their combinations were tested together with clinical variables using the Cox regression method.(ABSTRACT TRUNCATED AT 250 WORDS)

Low-amplitude, high frequency components in the terminal QRS-complex (so-called late potentials) are thought to arise from diseased myocardial tissue that forms the "electrophysiologic substrate" for ventricular tachyarrhythmias. Recording of late potentials is now commercially available in several systems and may possibly become clinically routine in the near future. Increased attention has been given recently to heart rate variability as an indicator of conditions of the autonomic nervous system that might trigger ventricular tachyarrhythmias. The value of late potentials and heart rate variability for identification of patients at risk for developing life-threatening ventricular tachyarrhythmias is discussed, as are the other applications and limitations of both methods.

Holter monitoring, electrocardiographic (ECG) signal-averaging, body surface potential mapping (BSPM) for PQRST isoarea maps, and electrophysiologic study (EPS) were performed in 100 patients with syncope. Coronary artery disease (CAD) was found in 46 patients and other heart disease was found in 19. EPS was diagnostic in 44 patients, while Holter monitoring suggested a diagnosis in only 21 patients. Abnormal BSPM was frequently seen (56%), especially in CAD (70%), or with inducible ventricular tachycardia (VT) (87%). Late potentials were recorded in 13 patients with CAD; five had inducible VT. In seven other patients with VT, they were either absent or bundle branch block (BBB) was found. Thirteen deaths (three sudden) occurred in our series. EPS-guided therapy resulted in a low rate of total cardiac death. In conclusion, EPS had a higher diagnostic yield than Holter monitoring regardless of cardiac pathology. ECG signal-averaging was useful in predicting VT only in patients with CAD without BBB. BSPM was abnormal in most patients with cardiac disease, but poorly predicted VT.

Catheter ablation is gaining increasing interest for the therapy of symptomatic, sustained arrhythmias of various origins. The scope of this review is to give an overview of the biophysical aspects and major characteristics of some of the most widely used energy sources in catheter ablation, e.g., the discharge of conventional defibrillators, modified defibrillators, laser light, and radiofrequency current application. Results from animal studies are considered to explain the basic mechanisms of catheter ablation. The recent achievements with the use of radiofrequency current to modify or ablate cardiac conduction properties are outlined in more detail.

Although the antiarrhythmic aspect of amiodarone has been extensively studied, its effects on His-Purkinje system conduction and refractoriness have not been systematically investigated in human beings. In 24 patients, anterograde His-Purkinje system conduction (HV intervals) and variables of His-Purkinje system refractoriness using the ventricular extrastimulus (V2) technique were analyzed before and after long-term therapy with amiodarone. The mean duration of amiodarone therapy at the time of repeat study was 16.2 +/- 7.7 weeks (range 11 to 42). The anterograde His-Purkinje system conduction time (HV interval) measured 49.6 +/- 9.5 ms (range 40 to 80) before and 60.6 +/- 10.7 ms (range 45 to 90) after amiodarone (p less than 0.005). During retrograde refractory period studies, the longest V1V2 interval at which a retrograde His bundle potential (H2) emerged from the V2 electrogram (relative refractory period of the His-Purkinje system) was consistently longer after amiodarone as compared with the control period (376.4 +/- 46.6 versus 318.8 +/- 33.1 ms, p less than 0.005). Similarly, the shortest and longest His-Purkinje system conduction times ( V2H2 interval) at comparable V1V2 intervals were uniformly and significantly prolonged after administration of the drug. Amiodarone also abolished macroreentry in the His-Purkinje system in six of the nine patients who showed such reentry during the control period. The effective refractory period of the ventricular myocardium was also increased from a mean of 227.1 +/- 13.9 to 259.2 +/- 20.2 ms (p less than 0.005) in this series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone has remarkable efficacy, but it also has a high incidence of severe side effects. Nevertheless, it is extensively used. The findings of an amiodarone treatment follow-up period of one to 72 months (mean 19 +/- 17) in 95 patients with recurrent life threatening arrhythmias resistant to other antiarrhythmic drugs are described. The mean loading dose of 800 mg/day for one week was followed by an average dose of 600 mg/day for two weeks. The long term daily dose was 400 mg in 80 patients and 200 mg in the remaining 15 patients. Amiodarone was particularly effective in suppressing complex ventricular arrhythmias. It also decreased premature ventricular beats by 83% and atrial premature beats by 41%. Supraventricular tachycardias were completely controlled and the ventricular response to atrial fibrillation was slowed. Twelve of the 95 patients (12.6%) died while taking amiodarone, two of sudden death and 10 of heart failure. Side effects were recorded in 77 (81%) patients. They were generally dose related and subsided with a decrease in dose or discontinuation of the medication. There was a correlation between the concentration of rT3 and the significance of the side effects. Thirty-nine patients stopped taking amiodarone, however, only 14 of these stopped because of toxicity: five developed pulmonary fibrosis; three had neurological toxicity; two had bradyarrhythmias; two developed hepatic dysfunction; one had hypothyroidism; and one patient suffered an aggravation of a pre-existent heart failure. It was concluded that amiodarone is a very effective treatment for supraventricular and ventricular arrhythmias. However, it does have numerous and severe side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone, a potent antiarrhythmic agent, has been shown to depress sinus node function. Therefore, this study was undertaken to assess the effect of chronic amiodarone therapy on heart rate during graded exercise testing. 13 patients treated with amiodarone for ventricular arrhythmias were administered symptom-limited graded exercise testing before and 12 weeks after drug therapy. None of the patients had prior evidence of sinus node dysfunction. The mean resting heart rate (beats per minute; bpm) before and after amiodarone therapy was 75 +/- (SD) 13 versus 60 +/- 7 bpm, respectively (p less than 0.005), and the maximal heart rate was 135 +/- 30 versus 109 +/- 24 bpm (p less than 0.005). However, the change in heart rate from rest to maximum exercise (heart rate reserve) was not affected by the drug. Heart rate measured at comparable exercise levels before and during amiodarone therapy was 124 +/- 25 versus 104 +/- 31 (p less than 0.025). There was no change in the systolic blood pressure readings at these respective measured heart rates. Estimated maximal functional capacity before and after drug therapy was 4.9 +/- 1.8 versus 4.7 +/- 2.2 METs (p = NS). In conclusion, chronic amiodarone therapy significantly decreases heart rate at rest and during exercise without altering systolic blood pressure and functional capacity.