Search

Several trials have evaluated the role of amiodarone in decreasing mortality in patients at high risk of developing sudden death. Current evidence does not support the prophylactic use of amiodarone in myocardial infarction (MI) survivors with a depressed left ventricular function and/or frequent or complex ventricular ectopy. Some postinfarction trials (e.g., the Spanish Study of Sudden Death [SSSD]) found mortality rates in controls much lower than the expected figures. Other postinfarction trials--the European Amiodarone Myocardial Infarction Arrhythmia Trial (EMIAT) and the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT)--despite observing a 2-year mortality rate of about 15% as expected, could not demonstrate a significant reduction in mortality. Amiodarone decreases the risk of sudden death in postinfarction patients by about 35%. In patients with a history of heart failure and left ventricular dysfunction, evidence is not sufficiently strong to use amiodarone for prevention of sudden death. The 2 major trials on such patients, Group for the Study of Survival in Heart Failure in Argentina (Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina or GESICA) and the Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure (STAT-CHF), arrived at conflicting results. Meta-analyses have been performed to overcome the small sample size of these trials, with the aim of assessing the benefit of amiodarone on total mortality. Differences among the recruited populations make it difficult to extract clinically applicable conclusions from these overviews. Even accepting that amiodarone might decrease total mortality by 10%, it is difficult to identify the patients for whom such a beneficial effect applies. A practical consequence of amiodarone trials is that this drug can be used rather safely in patients with left ventricular dysfunction of any etiology as, in contrast to some class I agents, it does not increase mortality. Therefore, amiodarone is the drug of choice when antiarrhythmic drug treatment is indicated in patients with left ventricular dysfunction. [ABSTRACT FROM AUTHOR]

The most common substrate for ventricular tachycardia (VT) is a postmyocardial infarction (MI) scar. Radiofrequency catheter ablation (RFCA) in post-MI VT faces clinical, electrophysiologic, anatomic, and methodologic difficulties not found in many other human tachycardias. The pathophysiologic understanding of post-MI VT is incomplete; this influences the process of selecting RFCA target sites, which is time consuming, demands catheter stability, and has low sensitivity and predictive value for VT interruption by RF current. Improving and simplifying the methodology of RFCA in post-MI VT is badly needed. We review the pathophysiology of post-MI VT from the data reported on endocardial, epicardial, and intramural ventricular mapping obtained either intraoperatively or in a Langendorff perfused set-up in hearts from transplanted patients. From these studies we conclude that (1) some post-MI VT cases are not amenable to RFCA (reentry around the scar, VT having a subepicardial or deep intramural substrate, or a wide, extensive, subendocardial intrascar area of slow conduction); and (2) searching for the endocardial exit is advantageous for selecting the RFCA targets. We also comment on a new self-reference mapping catheter that allows the recording of high gain, noise-free, unfiltered and filtered unipolar signals as well as unipolar pacing. Among the unresolved issues in these patients is the meaning of fast nonclinical VT induced after successful RFCA of the clinical VT, which may explain why a substantial number of these patients still receive an implantable cardioverter-defibrillator. [ABSTRACT FROM AUTHOR]

Patients with coronary artery disease may develop not only ischemic events but also heart failure and death due to previous myocardial damage. The purpose of this study was to test the prognostic value of a panel of plasma biomarkers related to vascular (monocyte chemoattractant protein-1 [MCP-1] and soluble tumor necrosis factor-like weak inducer of apoptosis) and myocardial damage (galectin-3, N-terminal fragment of brain natriuretic peptide [NT-proBNP], and neutrophil gelatinase-associated lipocalin) in 706 patients with chronic coronary artery disease followed for 2.2 ± 0.99 years. Secondary outcomes were the incidence of acute ischemic events (ST elevation myocardial infarction, non-ST elevation acute coronary syndrome, stroke, or transient ischemic attack) and death or heart failure. The primary outcome was the combination of the secondary outcomes. Cox proportional hazards model was used for analysis. Fifty-three patients developed acute ischemic events. Increasing MCP-1 plasma levels (p = 0.002), age, and body mass index predicted this outcome independently. Thirty-three patients developed death and/or heart failure. Galectin-3 (p = 0.007), NT-proBNP plasma levels (p = 0.004), hypertension, glomerular filtration rate, and the use of nitrates and anticoagulants were associated with this outcome independently. The development of the primary outcome was predicted independently by MCP-1 (p <0.001), NT-proBNP (p = 0.005), and galectin-3 (p = 0.019); hypertension; atrial fibrillation; and treatment with nitrates. Every biomarker with a value above the median increased the risk of developing this outcome by 1.832 (95% confidence interval 1.356 to 2.474, p <0.001). High-sensitivity C-reactive protein and lipid levels were not associated with any outcome. In conclusion, increasing MCP-1, galectin-3, and NT-proBNP plasma levels are associated with a greater incidence of cardiovascular events., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Antiarrhythmic drugs, mainly amiodarone and sotalol, radiofrequency catheter ablation, and the implantable cardioverter defibrillator (ICD) are the 3 therapeutic options in patients with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Idiopathic VT, incessant VT, frequently recurring, hemodynamically stable VT, and VT based on bundle branch reentry, are candidates for radiofrequency catheter ablation. Patients with high-risk ventricular tachyarrhythmias should receive ICDs as initial therapy. Two studies, the Antiarrhythmics Versus Implantable Defibrillator trial (AVID) and the Canadian Implantable Defibrillator Study (CIDS) have tried to approach the problem of these high-risk ventricular tachyarrhythmias. Although at 3 years, the ICD in AVID demonstrated a significant relative risk reduction over amiodarone of 31.5%, CIDS could not duplicate this finding. At 3 years, the relative risk reduction conferred by the ICD over amiodarone in CIDS was only 13.7%. A careful analysis of both studies suggests that CIDS was insufficiently powered to demonstrate statistically significant benefits similar to those shown by AVID, and furthermore, seemed to include an undetermined number of low-risk VT patients. The problem in the CIDS trial in this regard was the recruitment of patients in whom the inclusion criteria were met by the arrhythmias induced during the electrophysiology stimulation study, but which did not exist in real life. In addition CIDS included 14% of patients with (1) undocumented syncope and inducible monomorphic sustained VT; or (2) long runs of spontaneous nonsustained VT. Under these circumstances, the therapeutic implications of AVID remain unchallenged.

Today, cardiology seems to be driven by mega-trials and meta-analyses. Guidelines published by scientific and professional cardiovascular societies, such as the American Heart Association, the American College of Cardiology, and the European Society of Cardiology, follow the rules of evidence-based medicine. Such evidence is not always sufficiently conclusive to practice clinically helpful medicine. Sometimes, relatively small trials, such as the Multicenter Automatic Defibrillator Implantation Trial and the Antiarrhythmics Versus Implantable Defibrillators study, may be taken as guides for current clinical decisions and as inspiration for future investigations. Large mega-trials with a great lack of homogeneity among the recruited patients are less important for clinically helpful medicine than studies enrolling well-defined, high-risk patients. It is probably important to acknowledge that the best possible treatment for many patients with ventricular tachyarrhythmias remains obscure. Among these situations are the following: (1) sustained ventricular tachycardia (VT) in patients without coronary artery disease; (2) sustained, nonsyncopal VT in patients with coronary artery disease and left ventricular dysfunction; (3) post myocardial infarction survivors with an ejection fraction < or = 35%, frequent/complex ventricular arrhythmias, depressed heart rate variability, and inducible sustained ventricular tachyarrhythmias during electrophysiologic study. Many studies are being conducted to add light where uncertainty exists, but probably only a few will contribute to the practice of clinically helpful medicine, although some will be used to produce meta-analysis to sustain evidence-based medicine.

The effect of procainamide, quinidine, ajmaline and amiodarone on the effective refractory period of the accessory pathway in the (A-V) anterograde and retrograde directions was studied in relation to the length of this period before drug administration. All patients had the Wolff-Parkinson-White syndrome and were studied with intracavitary recordings and programmed electrical stimulation of the heart using identical basic cycle lengths and test stimulus intervals before and after drug administration. The patients were separated into two groups, those in whom the effective refractory period of the accessory pathway was 270 ms or greater (Group 1) and those in whom it was less than 270 (Group 2). In the anterograde direction the magnitude of increase in the length of the effective refractory period of the accessory pathway after drug administration was related to its initial length. Only modest lengthening of this period could be accomplished in patients with an initially short period. In evaluating the effect of drugs in patients with the Wolff-Parkinson-White syndrome, the role of the initial length of the effective refractory period of the accessory pathway should be considered.

In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longst ventricular premature stimulus interval resulting in tachycardia and th duration of the basic cycle length of the paced ventricular rhythm) above 54 percent. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54 percent or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

Three patients with reentrant tachycardia are described who had an accessory pathway with a very long conduction time that was incorporated in the tachycardia circuit. The accessory pathway was able to conduct in one direction only, in retrograde manner in two patients and in anteriograde manner in the remaining patient. Evidence is presented that reveals that in the first two patients the accessory pathway was septally located, had completely bypassed the normal atrioventricular (A-V) conduction system, had properties of decremental conduction, and had an atrial exit close to the coronary sinus and a ventricular exit relatively far from the atrioventricular A-V ring. In the third patient, who manifested wide QRS complex during tachycardia, the ventricular end of the accessory pathway seemed to be located close to the right ventricular apex. The atrial end of the pathway could not be localized exactly.