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H Kulbertus

Publications and source records attributed to H Kulbertus.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Clinical study of the month. The ATLAS study].

The Atlas Study was set up to compare the efficacy and safety of low doses and high doses of ACE inhibition by lisinopril on the risk of death and hospitalization in chronic heart failure. Three thousand one hundred sixty-four patients with class II to IV heart failure and an ejection fraction below 30% were randomly assigned to double blind treatment with either low doses (2.5-5 mg/daily, n = 1596) or high doses (32.5-35 mg/daily, n = 1568) of the ACE inhibitor lisinopril for 39 to 58 months while background therapy for heart failure was continued. Patients in the high dose group had a non significant 8% lower risk of death (p = 0.128), but a significant 12% lower risk of death or hospitalizations for any reason (p = 0.002) and 24% fewer hospitalizations for heart failure (p = 0.002). Side-effects such as dizziness and renal insufficiency were more frequently encountered in the high dose group, but there was no difference between the two groups in terms of number of patients requiring discontinuation of study medication. These findings indicate that patients with heart failure should not, as too frequently is, be maintained on very low dose of an ACE inhibitor unless this is the only dose that can be tolerated. The patients are expected to benefit more if they receive higher doses close to those used in the large clinical trials which have demonstrated a reduction by ACE inhibition in morbidity and mortality in heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

[How I study syncope].

The diagnosis of the cause of a syncope is based, above all, on the basis of a careful clinical history obtained from the patient or from persons who attended one of the episodes of loss of consciousness. It should also include a careful clinical examination comprising an electrocardiogram and, most often, an echocardiogram. The selection of further investigations should be guided by the existence or absence of an underlying cardiac disease. In the presence of a patent cardiac disease, one should first try to detect a disorder of cardiac rhythm (Holter, mini-Holter, possibly invasive electrophysiology); a dysfunction of the autonomic regulation of the cardiovascular system should only be considered in a second step (Tilt table test). The sequence of investigation should be reversed when syncope occurs in a patient without underlying cardiac disorder.

Arrhythmias, Cardiac↗
PubMed1998

[Long QT syndrome: from clinical discovery to molecular etiopathogenesis].

Before the era of Molecular Biology the etiopathogenic mechanism of the long QT Syndrome (LQTS) was hypothetized to be an inhomogeneity in the innervation of the myocardium by the sympathetic system resulting in abnormal myocardial repolarisation, prolongation of the QT interval and various rhythm disorders. The progress of Molecular Biology has led to abandon this hypothesis; it is now agreed that the etiopathology of the various forms of the LQTS and of the arrythmias which are associated with it lies in the presence of mutations localized on genes coding either for cardio-specific ionic channels or for proteins which modulate the activity of these ionic channels. Thus, the alterations, direct or indirect, of these cardio-specific ionic channels lead to a delayed repolarization of myocardial cells which manifest itself on the electrocardiogram by a prolongation of the QT interval. This delayed repolarization of myocardial cells would induce a reactivation of myocardial ionic channels of the L-Ca++ type which leads to the development of secondary late depolarization which represent the underlying cellular mechanisms for "torsade de pointes". This hypothesis is experimentally reinforced by the observation both in animals and in men of a prolongation of the QT interval as well as aspecific tachyarrythmias after pharmacologic blockade of myocardial potassium channels. Therefore the long QT syndromes probably find their origin in genetic abnormalities of the electro-ionic system of the heart whereas the mechanical function and the autonomic innervation appear to be entirely normal.

Animals↗
PubMed1998

[How I study the assessment of the risk of sudden death in Wolff-Parkinson-White syndrome].

The identification of a WPW impose to evaluate the potential risk of sudden cardiac death. The risk depends on the duration of the refractory period of the accessory pathway. If the preexcitation disappears when the patient is stressed on a treadmill, there is no risk of sudden death. If it does not, an electrophysiological study will have to be performed to measure the refractory period of the accessory pathway. If a risk of sudden death is present (refractory period < 220 ms), the accessory pathway has to be ablated using radiofrequency.

Catheter Ablation↗
PubMed1998

[The treatment of heart decompensation using angiotensin converting enzyme inhibitors. Pharmaco-economic aspects].

Heart failure is a challenge for modern cardiology, Common, disabling, lethal, this condition represents a major economic burden for Public Health. When patients with heart failure receive an ACE inhibitor in addition to diuretics and digoxin, they have fewer symptoms, are less frequently admitted to hospital and live longer. The currently available pharmaco-economic analyses support the use of ACE inhibitors in heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

[Follow-up of patients treated by amiodarone].

Amiodarone is a highly effective antiarrhythmic agent. Its iodine content and tissue accumulation are however responsible for various side effects. In this article, we review the various amiodarone related side effects and propose a monitoring chart for patients treated by this specific agent.

Amiodarone↗
PubMed1997

Atrial flutter: historical background.

For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiology in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified inferiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.

Animals↗
PubMed1997

[Vasovagal syncope].

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Adrenergic beta-Antagonists↗