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Biomedical subjects

F Nager

Publications and source records attributed to F Nager.

At least 55 records · Page 3Linked to original sources

[Interaction of amiodarone and digoxin].

A clinical investigation was carried out in 13 patients in order to answer the question of a possible interaction between amiodarone (A) and digoxin (D) and to study the extent to which plasma digoxin levels (PDL) may be influenced by A. Combined therapy with A + D was instituted in patients with supraventricular tachyarrhythmia where treatment with D alone was insufficient. All patients had normal renal function. Amiodarone was added to the treatment regimen of patients receiving D at doses ranging from 0.125 to 0.5 mg daily on a long term basis. The initial dosage of A was 1200 mg daily for 5 days to achieve saturation, followed by a maintenance dose of 200-400 mg daily. 3 PDL were measured before therapy with A was added and during combined A and D treatment at weeks 1, 2 and 3 and 3 months after the addition of A. In 11 patients a significant increase in PDL occurred as early as the 1st and 2nd weeks following the addition of A. In one patient PDL was elevated only after 3 months and in one other patient it remained unchanged. In 4 patients the PDL increase was associated with nausea. No other subjective or objective symptoms of digitalis intoxication were observed. This investigation has demonstrated a clinically relevant interaction between A and D. Regular monitoring of PDL is recommended during the first 3 weeks of combined treatment with A + D, and the D doses should be adjusted accordingly.

Adult↗

The antiarrhythmic effects of controlled release disopyramide phosphate and long acting propranolol in patients with ventricular arrhythmias.

The antiarrhythmic effect of slow-release disopyramide phosphate (DR) 300 mg twice daily and of long-acting propranolol (PR) 1 X 160 mg daily was compared in a randomized cross-over study in patients with premature ventricular beats (PVB). 12 patients with PVB (Lown Classes II-V) were given: placebo I for 3 days, DR or PR for 7 days, placebo II for 5 days and PR or DR for 7 days. During each study phase Holter-ECG recordings were taken over a period of 24 h. With DR 6 patients showed a positive qualitative effect, improving by at least one Lown class, whereas only 2 patients did so with PR. With DR reduction of PVB greater than 80% occurred in 7 patients, and with PR in 2 patients. In all patients with any reduction in PVB, the median decrease was 85% with DR and 59% with PR. The overall results suggest that the antiarrhythmic effect of disopyramide phosphate in the slow-release preparation is at least satisfactory and comparable to that of disopyramide phosphate in the standard capsule formulation given in the usual and more complicated regime of four divided doses. The antiarrhythmic effect of PR in the recommended dose as given was not convincing.

Adolescent↗

[Antiarrhythmic effect of disopyramid retard versus propranolol retard in ventricular extrasystole].

The antiarrhythmic effect of disopyramide retard (DR) in a dose of 2 X 300 mg/day, propranolol retard (PR) in one of 1 X 160 mg/day and placebo was compared in a randomized crossover study in patients with ventricular premature beats (VPB). 10 patients with VPB (Lown classes II-V) were given the drugs as follows: placebo I for 3 days. DR or PR for 7 days, placebo II for 5 days and PR or DR for 7 days. During every phase Holter ECG was registered over a period of 24 hours. Under DR 6 patients showed a favourable qualitative effect improving by at least one Lown class, while under PR only one patient did so. Under DR an over 80% reduction of VPB occurred in 6 patients and under PR in one patient. In all patients with any reduction of VPB this reduction was 79% under DR and 57% under PR. These results suggest that the antiarrhythmic effect of disopyramide in slow release preparations is comparable with that of disopyramide in standard capsule formulation given in the usual and more complicated regime with four divided doses. In the above mentioned (and still recommended) dose PR has no antiarrhythmic effect.

Adult↗

[Changes in infectious endocarditis in 3 decades].

The course, clinical picture and outcome were compared in 101 patients with infective endocarditis (1975-79, phase III) with our earlier investigations 1947-57 (phase I) and 1961-74 (phase II). An impressive change in this disease was found: - The average age of the patients is higher. - Acute cases and postoperative courses (after valve replacement) are more common and the outcome in these cases is better. Subacute courses are on the decrease. The clinical picture often is oligosymptomatic: - Fever is absent in a quarter, cardiac murmur in nearly a fifth and splenomegaly in four fifths of the patients. - For the first time 5 patients with right-heart endocarditis were observed in phase III. Three of these patients were intravenous drug abusers. The initial clinical picture was misinterpreted as pneumonia or pulmonary embolism. - The most common infective agents were streptococci, followed by staphylococci. The portion of negative blood cultures was strikingly high (35%). - Despite the higher frequency of acute courses, mortality has decreased. Urgent cardiac valve replacement, which has been performed in a fifth of our patients, can prevent irreversible congestive heart failure.

Adult↗

[Physical symptoms in heart failure].

Certain physical signs of heart failure found on examination of the neck veins, the arteries and the heart itself often are ignored. These neglected though important signs are abnormalities of the jugular venous pulse, arterial pulsus alternans, alterations of the apical impulse and, on auscultation, the third heart sound. Certain clinical conditions cause specific signs of heart failure, i.e. acute myocardial infarction, pulmonary hypertension, cardiac constriction and tamponade as well as acute rupture of the aortic valve. These general and specific signs of heart failure are discussed.

Blood Pressure↗

[Atenolol in the treatment of angina pectoris].

18 patients with angina pectoris participated in a double blind trial with atenolol (100 mg and 200 mg once daily, or 100 mg twice daily) and propranolol (80 mg twice daily). The number of anginal attacks (NAP), the number of days free of pain (NAFT), consumption of sublingual nitroglycerin (NNT) and bicycle ergometry data (EFE) were recorded. Atenolol given in a dose of 100 g twice daily significantly reduced NAP and NNT as compared with the other dose schedules for atenolol and propranolol. There was, however, no difference between NAFT and EFE under any of the treatment schedules mentioned above. Only with 100 mg atenolol twice daily was it possible to reduce heart rate at rest and immediately after exercise testing, and also diastolic blood pressure (at rest, upright and after stress testing). In spite of the long plasma T 1/2 (= 24 hours) reported by others, atenolol given twice daily seems to be the most effective schedule. It is concluded that atenolol (100 mg twice daily) has a more potent anti-anginal effect than propranolol (80 mg twice daily). In addition, atenolol has the advantage of being cardioselective.

Aged↗

[Atenelol and bendrofluazide in the treatment of medium and severe hypertension (preliminary report)].

In 15 patients with moderate to severe hypertension (WHO II--III) atenolol was evaluated against a thiazide diuretic (bendrofluazide) in a single blind crossover study. Systolic blood pressure values were lowered more efficiently by the diuretic, while diastolic pressure values were significantly better controlled by atenolol. Atenolol and bendrofluazide, by mere addition of the pressure effects of the single components, clearly afforded the best pressure control. Side effects of atenolol were frequent but mild, never causing major concern with the patients or a dropout from the study. Although the pressure response to atenolol was significantly better in the normal and high renin group of patients, there was no statistically significant correlation between the reduction in plasma renin and blood pressure induced by atenolol. In turn, the pressure response to the diuretic was significantly better in low renin than in normal and high renin patients.

Atenolol↗

[The diagnosis of the sinus node syndrome].

The "specific" investigations for sinus node syndrome (SNS) in 22 patients are analyzed. SNS was defined as sinusbradycardia below 40/min and sinus-standstill over 2 sec. Atropin (1 mg i.v.), exercise test and carotid pressure were of little help in establishing the diagnosis, while Holter monitoring and sinus-node recovery time were significantly abnormal in all patients investigated.

Aged↗

[Cardiac syncope].

Clinical cases are presented on the general theme of cardiovascular syncope. A case is cited to illustrate the clinical picture of idiopathic hypertrophic obstructive cardiomyopathy, a frequently disguised and misinterpreted cause of syncope. Chief attention is focused on the concept of fascicular heart block causing syncope. In the light of 3 patients, the various possibilities with respect to etiology, evolution, clinical picture and prognosis of fascicular heart block are outlined. In this context the diagnostic, prognostic and therapeutic significance of His bundle electrocardiography is discussed. Finally, 2 cases are cited to illustrate the sick sinus syndrome as a major cause of syncope. The diagnostic procedure in patients with suspected lazy sinus node is discussed and the results are presented of 16 personally observed cases with this disorder.

Adult↗