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Biomedical subjects

R I Fogel

Publications and source records attributed to R I Fogel.

7 recordsLinked to original sources
PubMed1997

Atrial fibrillation/flutter induced by implantable ventricular defibrillator shocks: difference between epicardial and endocardial energy delivery.

INTRODUCTION: We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory. METHODS AND RESULTS: Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 +/- 6 shocks (mean +/- SD) per patient compared with the endocardial group, which received 181 total shocks and 6 +/- 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41%) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 +/- 9 J, lower than the endocardial mean energy of 20 +/- 9 J (P < 0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 +/- 6 defibrillator shocks < 15 J and 4 +/- 2 shocks > or = 15 J, yet AF occurred in only 2.3% versus 9.6% (P < 0.05) of defibrillator shocks < 15 J and > or = 15 J, respectively. Of note, AF was not induced with energy < 4 J or > 31 J. CONCLUSIONS: In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.

Adult↗
PubMed1994

Flecainide.

Flecainide is a Class IC antiarrhythmic agent whose primary electrophysiologic effect is a slowing of conduction in a wide range of cardiac tissues. It is well absorbed and effective in suppressing isolated premature ventricular contractions (PVCs) or nonsustained ventricular arrhythmia but has only a modest efficacy when electrophysiologic testing is used as an endpoint. Its adverse effect on mortality in the CAST trial suggested a propensity to proarrhythmia--a phenomenon to which the Class IC agents appear particularly prone. Despite the applicability of the CAST study only to patients with a prior myocardial infarction, there has been a shift away from flecainide in ventricular arrhythmia, but the low noncardiac side effect profile of the agent allows for its continued use in a wide variety of supraventricular arrhythmias.

Atrial Fibrillation↗
PubMed1992

Ventricular arrhythmia in congestive heart failure.

The importance of ventricular arrhythmia is based on its association with sudden death. In certain groups of patients, ventricular arrhythmia--primarily runs of nonsustained ventricular tachycardia (NSVT)--is associated with an increased risk for sudden death. Although this relationship has been most often reported in patients with recent myocardial infarction, it has also been recognized in patients with dilated cardiomyopathy, regardless of etiology. Therefore, ventricular arrhythmia is common in patients with CHF due to cardiomyopathy. A number of studies have reported that 70-95% of patients with cardiomyopathy and congestive heart failure (CHF) have frequent ventricular premature beats, and 40-80% will manifest runs of NSVT. Many factors are responsible for ventricular arrhythmia in such patients, including structural abnormalities, electrolyte imbalance, hemodynamic impairment, activation of neurohormonal mechanisms, and pharmacologic therapy. Many studies have reported a high yearly mortality in patients with cardiomyopathy and CHF; greater than 40% of deaths are sudden, most often the result of sustained ventricular tachyarrhythmia. Most studies have noted an association between presence (and frequency) of NSVT and risk of sudden cardiac death in these patients. Unfortunately, other techniques--such as the signal-averaged electrocardiogram and electrophysiologic testing--are not helpful in identifying the individual at risk. Although several drug interventions will reduce mortality from progressive CHF, these drugs have not been shown to reduce sudden death and, indeed, have a variable effect on ventricular arrhythmia. Although NSVT is a marker for increased risk for sudden death, it is uncertain if antiarrhythmic drugs will prevent this outcome. Antiarrhythmic drugs have not been shown to be effective for preventing sudden death, although there are as yet no well-controlled randomized trials. Several studies suggest that amiodarone and beta blockers are beneficial, but this requires confirmation. For patients who have been resuscitated following an episode of sudden death due to a sustained ventricular tachyarrhythmia, antiarrhythmic therapy guided by invasive and noninvasive techniques appears to reduce risk of recurrent arrhythmia. However, the response rate to antiarrhythmic agents is low and side effects are common in patients with CHF. Especially important is the increased risk of precipitating CHF and aggravating the arrhythmia being treated. For many such patients who have had serious ventricular tachyarrhythmia, the automatic implantable cardioverter defibrillator may prove a better option. Other drugs used for management of CHF reduce overall mortality, but not risk of sudden death.

Electrodiagnosis↗
PubMed1992

Evaluating patients with ventricular arrhythmia. Role of the signal-averaged electrocardiogram, exercise test, ambulatory electrocardiogram, and electrophysiologic studies.

There are several methods available for the evaluation of patients with ventricular arrhythmia. The most effective approaches, however, involve the use of techniques that provide objective data. These include ambulatory monitoring and exercise testing (a noninvasive approach), and electrophysiologic testing (invasive). The information derived from these two approaches is complementary, and both are important for patient evaluation and management. These methods are useful for establishing the risk of arrhythmia occurrence in certain patient groups and for establishing the effect of antiarrhythmic agents. The signal-averaged ECG is of help in establishing risk in some patient groups, but it has no role for evaluating drug therapy.

Arrhythmias, Cardiac↗
PubMed1990

Metastatic renal cell carcinoma. An unusual cause of syncope.

A 77-year-old man with a history of renal cell carcinoma presented with orthostatic syncope. Investigation revealed metastatic carcinoma in the left lung extending through the pulmonary veins into the left atrium obstructing the mitral orifice. On review of the literature, this case appears to be the first to describe metastatic carcinoma to the left atrium presenting as a primary cause of syncope.

Aged↗