Search PubMed⌕ Search

Biomedical subjects

J B Johansen

Publications and source records attributed to J B Johansen.

13 recordsLinked to original sources
PubMed2000

Clinical experience of a new rate drop response algorithm in the treatment of vasovagal and carotid sinus syncope.

Dual chamber pacing has proven beneficial in patients with sudden drops in heart rate as seen in vasovagal syncope and carotid sinus syndrome. Newer algorithms for faster detection of an insidious drop in heart rate and short lasting intervention pacing at a high rate, as in the rate drop response algorithm in the Medtronic Kappa series of pacemakers, might improve the effect of pacing. Two case reports, that demonstrate the use of these rate drop response algorithms, are presented. A 24-year-old woman with recurrent episodes of syncope and repeated tilt-table tests with vasovagal cardioinhibitory outcomes had a Medtronic Kappa 400 pacemaker implanted. Syncope was abolished during repeat tilt-table testing following pacemaker implantation and proper functioning of the rate drop response algorithm. The patient has been free of syncope during follow-up apart from a single episode that occurred due to neglect of vasovagal warning symptoms. A 52-year-old man with coronary artery disease developed recurrent blackouts. Carotid sinus massage resulted in 5.5 s of asystole and presyncope. A Medtronic Kappa 700 pacemaker with a rate drop response algorithm was implanted and the patient became asymptomatic. The rate drop response algorithm is discussed in detail based upon the case reports, and recommendations are given for the use of this algorithm in patients with vasovagal syncope and carotid sinus syndrome.

Adult↗
PubMed1999

Efficacy and safety of intravenously administered dofetilide in acute termination of atrial fibrillation and flutter: a multicenter, randomized, double-blind, placebo-controlled trial. Danish Dofetilide in Atrial Fibrillation and Flutter Study Group.

BACKGROUND: This study was designed to assess the efficacy and safety of intravenous dofetilide in acute termination of atrial fibrillation (AF) and flutter (AFL). Dofetilide, an investigational class III antiarrhythmic agent, selectively inhibits the rapid component of the delayed rectifier potassium current, thus prolonging the effective refractory period and duration of the action potential. Dofetilide can be administered intravenously and has a rapid onset of electrophysiologic action. METHODS AND RESULTS: Ninety-six patients with AF (n = 79) or AFL (n = 17) with a median arrhythmia duration of 62 days (range 1 to 180) were randomized to placebo (n = 30) or 8 micrograms/kg IV dofetilide (n = 66) over 30 minutes. Conversion was defined as termination of the atrial arrhythmia within 3 hours from the start of infusion. The conversion rate was 30.3% after dofetilide and 3.3% after placebo (P <.006). Conversion rate was higher in AFL than in AF: 64% versus 24% (P =. 012). In nonconverters, there was no statistically significant difference between the change in heart rate among the dofetilide-treated compared with the placebo-treated patients (P =. 42). Torsade de pointes ventricular tachycardia developed in 2 patients (3%). In both patients, drug infusion was discontinued before the event because of prolongation of the QT interval. CONCLUSIONS: Intravenous dofetilide is effective in acute termination of AF and AFL of medium duration, with a particularly high efficacy rate in AFL. A small but serious risk of proarrhythmia must be anticipated.

Aged↗
PubMed1999

Correlation between serial changes in left-sided heart chambers and atrial natriuretic peptide and N-terminal pro atrial natriuretic peptide after a first myocardial infarction. An echocardiographic study.

Dilatation of the left ventricle predicts morbidity and mortality after acute myocardial infarction. We compared serial echocardiographic examinations of the left atrium and ventricle with measurements of plasma atrial natriuretic peptide (ANP) and plasma N-terminal pro atrial natriuretic peptide (NT-proANP) in 22 patients during the first 6 months following a first myocardial infarction. ANP, but not NT-proANP, was found to be significantly correlated to the diastolic/systolic size of the left atrium (r = 0.58/0.60) and the systolic size of the left ventricle (r = 0.43) in the acute phase 2-4 days after infarction. At 10-12 days after the infarction, we found a significant correlation between all sizes of the left-sided chambers and ANP, whereas NT-proANP only correlated with the left atrial sizes. Three months after the infarction, all sizes of the left-sided chambers correlated with both ANP and NT-proANP, with the exception of a non-significant correlation between NT-proANP and the left atrial diastolic size. After 6 months only the area of the diastolic and systolic left atrium correlated with plasma ANP and only the systolic size of the left atrium correlated with NT-proANP. The percentage change in the size of the left atrium, but not the left ventricle, correlated significantly with the percentage change in both ANP (r = 0.57) and NT-proANP (r = 0.70). We conclude that the distension of the left atrium rather than the dilatation of the left ventricle is related to the concentration of ANP and NT-proANP after an acute myocardial infarction.

Adult↗
PubMed1996

[Acute arsenic poisoning].

We report three cases of arsenic poisoning in a chemical factory. Three workers were exposed to vinyzene 10,10'-oxydephenarsine and developed mild symptoms of acute poisoning. All patients were treated with dimercaprol, and recovered after a few days. Urine analysis did not show increased arsenic excretion, but this could be due to the large urine samples taken. It is recommended that a urine sample is taken right after admission to hospital and new samples after eight and 16 hours.

Accidents, Occupational↗
PubMed1996

[Angioneurotic edema in relation to therapeutic use of angiotensin-converting enzyme inhibitor].

Angioneurotic oedema secondary to angiotensin-converting enzyme (ACE) inhibitors is a rare condition, but it is a side effect which is likely to be seen more frequently because of the increased use of these drugs in the treatment of heart failure and hypertension. We report two cases which illustrate problems in the diagnosis and management of this life-threatening condition, and also demonstrate that angioedema re-occurs if the ACE inhibitor is not discontinued. If angioedema is suspected, therapy with any angiotensin converting-enzyme inhibitor should be discontinued promptly, respiratory distress should be treated appropriately, and subsequent therapy should be initiated with an agent from an alternative class of drugs.

Aged↗
PubMed1993

[Neurohormonal activity in heart insufficiency].

The maintenance of cardiac pumping ability in the presence of a primary disturbance of myocardial contractility and/or an excessive haemodynamic strain on the heart is dependent on several compensatory mechanisms. Particular attention has formerly been paid to the importance of the Frank-Starling mechanism and cardiac hypertrophy and dilatation in maintaining a blood supply sufficient to cover the metabolic needs of various tissues in heart failure. In recent years, however, it has been found that certain neurohormonal systems (the sympathetic nervous system, the renin-angiotensin-aldosterone system, atrial natriuretic peptide and several locally acting vaso-active substances) undergo considerable changes according to the degree of heart failure. These compensatory mechanisms support the circulation wholly or partially in acute heart failure, however sustained neurohormonal activation may be harmful in chronic heart failure, where several neurohormonal factors may be activated to ill-effect. The most significant neurohormonal systems and their importance in heart failure are reviewed on the basis of the available literature.

Atrial Natriuretic Factor↗
PubMed1993

Neurohormonal systems during progression of heart failure: a review.

In the presence of a primary disorder in myocardial contractility and/or extraordinary hemodynamic pressure on the heart, ventricular performance depends on several compensating mechanisms. In the past, studies were mostly focused on the importance of the Frank-Starling mechanism and the hypertrophy and dilation of the heart in maintaining a circulation sufficient for metabolic intake during heart failure. Recently, however, the existence of neurohormonal systems has been demonstrated (the sympathetic nervous system, the renin-angiotensin system, atrial natriuretic peptide and several locally produced vasoactive substances), which change considerably according to the severity of the heart failure. While these compensatory mechanisms support the circulation in patients with acute heart failure, in whole or in part, neurohormonal activation over an extended period of time might be harmful to patients with chronic congestive heart failure since several neurohormonal factors might be inappropriately activated. This article will review the key neurohormonal systems and their importance in heart failure on the basis of the current literature.

Atrial Natriuretic Factor↗