Response to nor-epinephrine, isoprenaline and spironolactone derivatives in normal and hypertensive rats.
One-thousand four hundred and thirty-five acute medical admissions, of whom 40 patients (2.8%) had AF.
Bradycardic (heart rate<50/min) and tachycardic heart rhythm disturbances (100/min) require rapid therapeutic strategies. Supraventricular tachycardias (SVT) are sinus tachycardia, atrial tachycardia, AV-nodal reentrant tachycardia and tachycardia due to accessory pathways. Mostly SVT are characterized by small QRS complexes (QRS width<0.12 ms). It is essential to evaluate the arrhythmia history, to perform a good physical examination and to exactly analyze the 12-lead electrocardiogram. An exact diagnosis is then possible in >90% of SVT patients. Ventricular tachycardias have a broad QRS complex (>or=0.12 s), ventricular flutter and ventricular fibrillation are associated with chaotic electrophysiologic findings. For acute therapy, we will present the new concept of the "5A" that includes adenosine, adrenaline, ajmaline, amiodarone and atropine. Additional "B, C and D strategies" include betablocking agents, cardioversion as well as defibrillation. The "5A" concept allows a safe and effective antiarrhythmic treatment of all bradycardic and tachycardic arrhythmias as well as asystolia.
The management of cardiac arrhythmias has changed dramatically over the past several years. New drugs and devices are now available to treat various arrhythmias. Many new agents have been developed that rely on different electrophysiologic mechanisms to elicit their effect on the heart rhythm. Though often effective, these drugs also pose a risk because all of them have a variety of potential adverse effects associated with their use. Many of these adverse reactions are common to all antiarrhythmic drugs, whereas others are unique to particular agents. This review discusses the notable adverse effects of selected antiarrhythmic drugs.
The principal aim of ALPS is to determine if survival is improved by amiodarone compared with placebo; secondary aim is to determine if survival is improved by lidocaine vs placebo and/or by amiodarone vs lidocaine. Prioritizing comparisons in this manner acknowledges where differences in outcome are most expected based on existing knowledge. Each aim also represents a clinically relevant comparison between treatments that is worth investigating.
The relation of electrophysiologic effects of amiodarone to long-term outcome was studied in 35 patients with hypertrophic cardiomyopathy (HC). Indications for electrophysiologic studies were: cardiac arrest (n = 3), syncope/presyncope (n = 27) and asymptomatic ventricular tachycardia (VT) (n = 5). Twenty-eight patients (80%) had VT, 3 (9%) atrial tachycardia and 3 (9%) paroxysmal atrial fibrillation during 24-hour Holter monitoring. The studies were repeated after a total amiodarone dose of 58 +/- 122 g and during a maintenance median daily dose of 400 mg. Amiodarone abolished paroxysmal atrial arrhythmias in all 6 patients. However, it caused marked atrioventricular nodal conduction abnormality in 3 patients and heart block or marked HV interval prolongation (to greater than or equal to 100 ms) in 4 patients. Sustained VT was induced in 26 patients (74%) at baseline study and in 23 patients (66%) taking amiodarone therapy. With amiodarone, VT was no longer inducible or was more difficult to induce in 11 patients (31%), and the drug abolished VT during Holter monitoring in all patients. However, VT was easier to induce with amiodarone or was induced only with amiodarone in 18 (51%) patients. Amiodarone significantly slowed the rate of induced VT (from 248 +/- 29 to 214 +/- 37 beats/min, p less than 0.001). This was associated with a change in its morphology from polymorphic to monomorphic VT in 7 patients. During a follow up of 18 +/- 14 months (range 2 to 56), amiodarone was discontinued because of adverse effects in 8 patients (23%).(ABSTRACT TRUNCATED AT 250 WORDS)
Newer studies compared the outcome of patients with atrial fibrillation and rhythm- or rate-control. Data from these studies (AFFIRM, RACE) clearly showed that rhythm control is not superior to rate control for the prevention of death and morbidity from cardiovascular causes. Therefore, rate-control may be an appropriate therapy in patients with recurrent atrial fibrillation after DC-cardioversion. Acute therapy of atrial flutter in intensive care patients depends on the clinical presentation. Atrial flutter can most often be successfully cardioverted to sinus rhythm with energies less than 50 joules. Ibutilide trials showed efficacy rates of 38-76% for conversion of atrial flutter to sinus rhythm compared with conversion rates of 5-13% when intravenous flecainide, propafenone, or verapamil was administered. In addition, a high dose (2 mg) of ibutilide was more effective than sotalol (1.5 mg/kg) in conversion of atrial flutter to sinus rhythm (70% versus 19%).
Our data show a superiority of DDD(R) mode versus VVI(R) mode regarding subjective and objective parameters as NYHA-classification, BNP, 6 minute walk test, left ventricular ejection fraction and left ventricular endsystolic volume after 12 months. The improvements seem to depend on the reduction of ventricular pacing with advanced atrial contraction. But only a small number of patients needed the upgradation.