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Biomedical subjects

D Bonhorst

Publications and source records attributed to D Bonhorst.

45 records · Page 3Linked to original sources
PubMed1990

[Amiodarone and propafenone: evaluation using serial Holter recordings in patients with ventricular arrhythmia].

OBJECTIVE: To review the experience of the Arrhythmology Department in evaluating antiarrhythmic therapy for ventricular arrhythmias with serial Holter electrocardiographic recordings (ECG-H). To compare the results obtained with the most used drugs in this Department: amiodarone and propafenone (groups AMIO and PROP). DESIGN: Retrospective study. No statistically significant differences between the two groups were found in respect to age, sex, underlying disease, functional class, left ventricular function and associated therapy. SETTING: Arrythmology Department at a Cardiology Service. PATIENTS: 105 sequential patients with ventricular arrhythmias in a basal ECG-H recording, that were evaluated within 1 year with a new recording on amiodarone or propafenone, without major clinical events or therapeutic changes between the two recordings. INTERVENTIONS (daily oral doses): Amiodarone 200-600 (mean 270) mg or propafenone 300-900 (mean 602) mg. RESULTS: No statistically significant differences were found between the two groups, in either the basal ECG-H or that recorded on therapy. The two drugs were similar in the degree of suppression of ventricular premature complexes per hour (VPCH): equal or superior to 75% in 64.3% of the patients on amiodarone and in 63.9% of those on propafenone. The following reductions on therapy were statistically significant (p less than 0.001 if not specified): VPCH, from 346 +/- 480 to 86 +/- 158 on amiodarone and from 418 +/- 524 to 110 +/- 215 on propafenone; most complex arrhythmia recorded, on both drugs; number of patients with pairs, from 72.1 to 34.9% on amiodarone and from 69.4 to 33.9% on propafenone; number of patients with runs of nonsustained ventricular tachycardia (VT), from 27.9 to 2.3% on amiodarone (p less than 0.01); number of runs of VT per recording, from 3 +/- 5 to 1 on amiodarone (p less than 0.06); and maximum number of complexes per run of VT, from 8 +/- 8 to 4 on amiodarone and from 7 +/- 4 to 5 +/- 1 on propafenone (both with p less than 0.06). CONCLUSIONS: Holter recordings were useful in evaluating antiarrhythmic therapy. The effectiveness of amiodarone and propafenone in treating ventricular arrhythmias was not significantly different. The choice between one of these drugs must rely on their collateral effects profile.

Adult↗
PubMed1990

[Effects of coronary surgery on silent ischemia].

In order to assess the effects of coronary artery bypass surgery on silent myocardial ischemia, we studied a group of 39 consecutive patients, 38 male and 1 female with a mean age of 56 + 7 years, with stable chronic angina pectoris, by 48 hours-Holter monitoring and maximal treadmill exercise test before and after operation. The reduction of angina was 92% (p less than 0.0001) and of ischemia 57% (p less than 0.0001) after operation. Silent myocardial ischemia was detected in 21 patients (54%) before operation, 13 by Holter, 4 by exercise test and 4 by the two methods. After operation 13 patients (36%) continue to have silent ischemia depicted in 7 by Holter and in 7 by exercise test. No new patient developed silent ischemia after operation. The group of patients with silent ischemia preoperatively was not significantly different from the group without silent ischemia based on clinical and angiographic characteristics, results of surgery and exercise test parameters with exception of ST segment depression. In conclusion, silent myocardial ischemia may persist after successful coronary artery bypass surgery for the relief of angina pectoris, and should be monitored by serial Holter recordings and treated medically, if its prognosis and consequences proved to be similar to manifest symptomatic ischemia.

Adult↗
PubMed1989

[Role of antiplatelet agents in the treatment of ischemic cardiopathy].

In spite of the important role played by platelets in the thrombotic complications of coronary heart disease, it has been difficult to prove the preventive efficacy of antiplatelet therapy. Nevertheless, the overview of the results of several randomized trials together with the conclusions of some recent studies are strongly suggestive of the usefulness of those drugs, at least in some subsets of ischemic cardiopathy. So, drugs that affect platelets have been shown to reduce mortality and the risk of infarction in patients with unstable angina and probably also after myocardial infarction, and to preserve the patency of aortocoronary grafts. Their role in preventing thrombotic complications following coronary angioplasty is still uncertain. In spite of the results of recent publications it is still premature to recommend antiplatelet therapy in the primary prevention of ischemic heart disease. It is not yet established the more effective agent inside the group and also the more suitable doses.

Angina, Unstable↗
PubMed1975

Mechanism of action of antidysrhythmic drugs on ventricular conduction as studied with intramural electrodes.

Using the Dürrer electrode needle to record the intramural electrogram and a standard peripheral electrocardiogram (ECG) lead as reference, the authors studied the action of 9 different drugs in the conduction system of dogs. The authors concluded that diphenylhydantoin and lignocaine would be useful in dysrhythmias related to increased excitability and perhaps increased automatism. Ajmaline and quinidine may be some of some interest in dysrhythmias due to conduction disturbances; and, finally, ajmaline, diphenylhydantoin, di-isopyramide and quinidine may be useful in dysrhythmias due to focal re-entry.

Ajmaline↗
PubMedDate not supplied

[Unsustained ventricular tachycardia and accelerated idioventricular rhythm--clinical and electrocardiographic features].

OBJECTIVE: To compare clinical and electrocardiographic characteristics of Nonsustained Ventricular Tachycardia (NSVT) and Idioventricular Accelerated Rhythm (IVAR). MATERIAL AND METHODS: We studied 155 patients, 113 men and 42 women, with mean age 54 +/- 14 retrospectively, of these, 108 had NSVT and 47 IVAR. The arrhythmias were defined as follows: NSVT-more than 3 ventricular consecutive beats with an heart rate superior to 110 b/m and lasting less than 30 s.; IVAR-3 or more ventricular consecutive beats with an heart rate equal or superior to 50 and lower than 110 b/m, lasting less than 30 s. We evaluated clinical data (symptoms, functional class and anti-arrhythmic therapy), electrocardiographic data (rhythm, changes in conduction and repolarization) and ventricular function (with ECO, Radionuclide Angiography or Ventriculography). In the Holter recording (ECG-H), we analysed the presence of associated ventricular arrhythmias, their electrocardiographic characteristics (number of episodes, number of beats per episode, previous arrhythmia rate, morfology, regularity) and the relations of the arrhythmia with symptoms. RESULTS: Analysis of underlying pathology showed in both groups, the importance of coronary artery disease (44.5% vs 40%) followed by valvular heart disease (24% vs 27.6%) and cardiomyopathy (22.2% vs 17%) respectively to NSVT and IVAR. Only in the NSVT group there were patients without cardiac pathology (3.6%). Comparing with one control group of our department, this distribution was substantially different (p less than 0.0001). All IVAR episodes were assympthomatic compared with 90% of NSVT. Ventricular premature beats were found in all NSVT patients and in 90% of IVAR patients, and were frequent (greater than 10/h) in 79% and 60%, couplets in 84% and 53% respectively (ns). The previous rate of the arrhythmia was 85.3 +/- 20 b/m in NSVT against 68.7 +/- 14 in IVAR (p less than 0.0001). We found left ventricular disfunction in 60% of NSVT patients and in 63.7% in IVAR patients, being serious in 35% and 39% respectively. The follow-up was of 18.5 months (1-72) and posterior evolution showed 14.8% and 17% of deaths with no relation to the arrhythmia, although in NSVT the number of complexes and episodes were related with the ventricular disfunction (p = 0.02 and p = 0.05). CONCLUSION: Both arrhythmias appeared in patients with similar clinical and arrhythmic setting and identified a population with structural cardiopathy, bad function and poor outcome.

Adult↗
PubMedDate not supplied

[Sudden cardiac death: its definition and mechanisms].

Sudden cardiac death (SD) is reviewed concerning its definition and mechanisms. About the syndrome definition, one concludes that the most suitable way to discriminate arrhythmic death, is to consider both the time since the beginning of the symptoms and the clinical condition before circulatory arrest. During several years the "arrhythmic hypothesis" prevailed to explain SD mechanism. It postulates that, by a fortuitous association, a ventricular ectopic beat activated a re-entry circuit, unchaining the lethal tachycardia. From that hypothesis, a lot of antiarrhythmic clinical trials were conducted in myocardial infarction survivors, recepting that the ventricular ectopic beats suppression would reduce the probability of lethal arrhythmias. Nevertheless no trial confirmed that hypothesis and CAST showed an increase in mortality in patients treated with antiarrhythmic drugs able to suppress ventricular premature beats. From that observation resulted a reinforcement of the "ischemic hypothesis", supported by several arguments. Today we believe that both factors (ischemic and arrhythmic) are important in SD. It was proposed a SD description as a disfunction of a biological system resulting from the interaction between a "pathological structure" and "functional events". The electrogenic component remains central in that model, but is integrated into a structure/function scheme. Under most conditions, the system requires both abnormal structural components (usually chronic) and functional factors (often transient). The structural pathology is most related to old myocardial infarction scars, and the functional factors are ischemia/reperfusion, metabolic alterations (electrolyte imbalance, hypoxemia, acidosis), hemodynamic failure, neurophysiological fluctuations and toxic effects (like proarrhythmia).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗