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Biomedical subjects

P J Podrid

Publications and source records attributed to P J Podrid.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1991

Comparative cost-effectiveness analysis of quinidine, procainamide and mexiletine.

Quinidine and procainamide have the potential for major organ toxicity, whereas mexiletine has been reported to have little risk of organ toxicity, serious proarrhythmia or congestive heart failure, but a relatively high incidence of nuisance side effects. In light of the potential adverse effects of all antiarrhythmic agents as highlighted by the Cardiac Arrhythmia Suppression Trial, the relative cost-effectiveness of these 3 agents was assessed. Based on a review of greater than 1,000 published reports, studies included in the analysis examined greater than or equal to 1 of these agents in adults, with adequate efficacy or safety data, or both. The majority of studies assessed patients with symptomatic or malignant arrhythmias, or both. Data were analyzed using a decision analysis/cost-effectiveness model. Probabilities were averaged using techniques of meta-analysis. Costs were obtained from a university medical center cost-accounting system and from expected follow-up visits to university clinics. Thirty-seven separate side effects were included in the analysis. In terms of overall cost, 12 months of mexiletine would engender $875, quinidine $1,239 and procainamide $1,911 of expenses. Mexiletine dominates the older agents in terms of cost per successful drug response, a result that holds over a wide range of efficacy and safety data. Analyses demonstrated no increase in all-cause mortality for quinidine and mexiletine over placebo, but a trend toward higher mortality with procainamide. The results suggest that mexiletine is a cost-saving alternative therapy for ventricular arrhythmias when adverse reactions are considered in addition to pharmaceutical costs and treatment efficacy.

Ambulatory Care↗
PubMed1991

Side effects from amiodarone.

Amiodarone causes many side effects involving all organ systems. Although most of the side effects are mild and do not limit the use of the drug, there are several that are serious. Since many of these toxic reactions develop only after a prolonged period of therapy, careful follow-up on a regular basis is essential.

Age Factors↗
PubMed1991

Role of combination drug therapy with a class IC antiarrhythmic agent and mexiletine for ventricular tachycardia.

The combination of mexiletine and a class IC antiarrhythmic agent (encainide, propafenone or flecainide) was evaluated by electrophysiologic testing in 14 patients with a history of sustained ventricular tachycardia whose tachycardia remained inducible during therapy with the class IC drug alone. During the control drug-free state, all patients had inducible ventricular tachycardia, with a mean cycle length of 260 ms (range 190 to 400). During monotherapy with the IC agent the tachycardia remained inducible in each patient, but there was a significant increase in the cycle length to 340 ms (240 to 500) (p less than 0.001). The effective refractory period of the ventricle was not altered. Treatment with mexiletine (oral in 13 and intravenous in 1) was begun and electrophysiologic testing was repeated. Ventricular tachycardia in one patient was rendered noninducible and one patient had arrhythmia aggravation. The tachycardia in the remaining 12 patients remained inducible but its average cycle length increased further to 392 ms (340 to 460) (p = NS). Nine patients had rate slowing and the average cycle length of the ventricular tachycardia in this group was significantly increased (302 to 388 ms, p less than 0.05). The average effective refractory period was significantly increased during combination therapy (267 ms) compared with no drug therapy (235 ms) and therapy with the class IC drug alone (247 ms) (p less than 0.05). After a mean follow-up interval of 22 months, seven patients continue on the combined treatment and have no ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Safety and toxicity of antiarrhythmic drug therapy: benefit versus risk.

Although antiarrhythmic drugs remain the first and most frequently used approach to therapy for arrhythmias, there is growing concern about their safety. It has long been recognized that this class of drug is associated with frequent side effects, especially in patients with extensive underlying heart disease. However, the recent report from the Cardiac Arrhythmia Suppression Trial (CAST) has pointed out that serious toxicity may occur even in patients with less serious heart disease. There are two major reasons for antiarrhythmic therapy. First is for relief of symptoms documented to be the result of arrhythmia. Although there are few studies showing that the antiarrhythmic drugs are effective for this indication, clinical experience does confirm that this is the case. The second indication is to prevent sudden cardiac death. Although antiarrhythmic drugs are of benefit for preventing recurrent arrhythmias in those patients who have already experienced a sustained ventricular tachyarrhythmia, there are, as yet, no data that they are effective for preventing such arrhythmias in patients thought to be at high risk; for example, postinfarction patients or those with a cardiomyopathy and who have nonsustained ventricular tachycardia. Unfortunately, therapy with antiarrhythmic drugs is associated with substantial risks. Although the majority of the side effects are not serious but only "nuisance" complaints, there are more serious toxic reactions that are often idiosyncratic. Organ toxicity may occur with some of these drugs. However, the most serious problems are cardiac side effects including conduction abnormalities, worsening of congestive heart failure, and aggravation of arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1990

Potassium and ventricular arrhythmias.

Potassium is a major determinant of the electrophysiologic properties of the myocardial membrane, and it plays an important role in the occurrence of arrhythmia. Hypokalemia has been associated with an increased frequency of ventricular premature complexes (VPCs) in some studies of hypertensive patients treated with diuretics, but other studies have failed to confirm any association. Studies involving patients with an acute myocardial infarction have also provided conflicting data about the association between hypokalemia and VPCs. Whereas the role of potassium in the genesis of simple VPCs remains uncertain, animal and clinical studies have demonstrated a strong relation between hypokalemia and the occurrence of sustained ventricular tachycardia and ventricular fibrillation during acute ischemic states. Hypokalemia may also affect the action of antiarrhythmic drugs by altering the electrophysiologic properties of the myocardium, potentially negating some of the antiarrhythmic activity of these agents. Although diuretic use is the most frequent cause of hypokalemia, epinephrine can also lower serum potassium as a result of stimulation of the beta 2 adrenoreceptor. This mechanism may, in part, explain the ability of beta blockers to prevent sudden death in patients with a recent myocardial infarction.

Arrhythmias, Cardiac↗
PubMed1990

Antiarrhythmic drug therapy for congestive heart failure with focus on moricizine.

Many patients who have serious ventricular arrhythmia requiring antiarrhythmic drug therapy have congestive heart failure (CHF). However, the pharmacokinetic and pharmacodynamic properties of the antiarrhythmic drugs are altered in the presence of CHF. It has been reported that some adverse effects, primarily aggravation of arrhythmia and CHF occur more frequently in patients with a history of left ventricular (LV) dysfunction. Moreover, antiarrhythmic drugs are less effective in patients with a history of CHF and a reduced LV ejection fraction (LVEF). Moricizine, a new antiarrhythmic drug, has been undergoing clinical trials for over 13 years in the United States. The data base involving 1,072 patients was analyzed to establish the effect of this agent in patients with CHF. The presence of CHF does not alter the absorption, half-life and clearance of moricizine. The incidence of CHF exacerbation definitely related to moricizine was low (2%) and occurred primarily in patients with a history of CHF. Aggravation of arrhythmia and conduction abnormalities also occurred more often in patients with prior CHF. However, the incidence of all other adverse effects involving other organ systems was the same in patients with and without CHF and was also unrelated to the baseline LVEF. The effect of moricizine for suppressing spontaneously occurring ventricular ectopy was also similar in patients with and without CHF and was independent of LVEF. However, the drug is less effective in preventing sustained ventricular arrhythmia in patients with CHF.

Anti-Arrhythmia Agents↗
PubMed1990

An analysis of the cost effectiveness of the implantable defibrillator.

The automatic implantable defibrillator has been shown to decrease the mortality of patients who have survived cardiac arrest due to ventricular tachycardia or fibrillation and are at high risk for recurrence. We performed a cost-effectiveness analysis of this seemingly expensive new technology with data obtained from the 1984 Medicare data base, the medical literature, Medicare carriers, individual pharmacies and hospitals, and expert opinion. Analyzing combinations of principal and secondary discharge diagnoses across 18 diagnosis-related groups, we estimated the cost of hospitalization for a comparison group of patients. Hospitalization costs for the defibrillator group were obtained from reported empirical data. Rehospitalization rates and other health-care use estimates were solicited from an expert panel of physicians, and mortality rates for both groups were obtained from the literature. Using a decision-analytic model, we estimated that the net cost effectiveness of the defibrillator, when used in the high-risk patient, is approximately $17,100 per life-year saved, with sensitivity analyses suggesting that the true value lies between $15,000 and $25,000. This estimate is well within the range that is currently accepted by the US medical care system for other life-saving interventions. We also estimated the cost effectiveness of the defibrillator in a 1991 scenario to be $7,400 per life-year saved, when the device would have greater longevity, would be programmable, and would not require a thoracotomy. Sensitivity analyses suggest that the true value lies between a value that is cost saving (less expensive than pharmacologic therapy) and $19,600 per life-year saved.

Arrhythmias, Cardiac↗
PubMed1990

Evaluation of cardiac arrhythmias by exercise testing.

Exercise testing is an important noninvasive method for the exposure of arrhythmias. It provides complementary information to that obtained from ambulatory monitoring or electrophysiologic testing. By producing a number of important physiologic changes, especially activation of the sympathetic nervous system and an increase in circulating catecholamines, exercise testing provides a more complete assessment. On continuous monitoring, exercise-induced ventricular premature beats may be found in up to 34% of healthy subjects, in 60 to 70% of those with heart disease and in all patients who have experienced sustained ventricular tachycardia. Couplets or nonsustained ventricular tachycardia can be found during exercise in 0 to 6% of healthy subjects, in 15 to 31% of patients with heart disease and in 75% of those with sustained ventricular tachycardia. Even in patients with heart disease, there is only a small risk of inducing sustained ventricular tachycardia or ventricular fibrillation during exercise. The prognostic relevance of exercise-induced ventricular arrhythmias in patients with coronary artery disease or cardiomyopathy has not been clearly established. There appears to be an increased risk, however, in patients with ventricular premature beats as well as ST-segment depression or in patients with repetitive forms of ventricular arrhythmias during exercise which cannot be medically controlled. In healthy subjects, exercise-induced ventricular premature beats are of no prognostic relevance. In particular, for patients in whom arrhythmias are induced by exercise, exercise testing should be used to assess the effectiveness of antiarrhythmic drug treatment. Importantly, serious cardiac toxicity, often not observed at rest or during routine activities, may become apparent during exercise testing. It should be a standard part of arrhythmia assessment and management.

Cardiac Complexes, Premature↗
PubMed1990

Role of the sympathetic nervous system in the genesis of ventricular arrhythmia.

Activation of the sympathetic nervous system is an important factor in the genesis of ventricular arrhythmias in patients with impaired ventricular function. Such patients have an appropriate substrate that is capable of generating rhythm abnormalities, which may be related to enhanced automaticity, triggered automaticity, and reentrant mechanisms; all three mechanisms are markedly potentiated by the action of catecholamines. Additionally, the sympathetic nervous system can provoke the development of hypokalemia and ischemia (which can independently lead to the occurrence of rhythm disturbances), and catecholamines may negate the beneficial electrophysiological actions of antiarrhythmic drugs. A substantial amount of experimental data implicates the sympathetic nervous system as a potent stimulus for ventricular tachyarrhythmias and sudden cardiac death, especially in the setting of myocardial ischemia. Two important mechanisms that have been identified include 1) enhanced sympathetic outflow from the central nervous system and 2) nonuniform myocardial denervation resulting in beta-receptor up-regulation and catecholamine hypersensitivity in the infarct zone. Disruption of sympathetic neural innervation of the heart and the use of beta-blocking agents may reduce the occurrence of sudden death and improve survival in animal models of arrhythmias and in some subsets of patients, including those with the long QT syndrome, a recent myocardial infarction, and perhaps those with a cardiomyopathy. The mechanism of this beneficial effect remains to be defined.

Adrenergic beta-Antagonists↗