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Biomedical subjects

S Effert

Publications and source records attributed to S Effert.

At least 109 records · Page 6Linked to original sources
PubMed1980

[Mexiletin for treatment of ventricular ectopic rhythm in patients with acute myocardial infarction (author's transl)].

In a controlled investigation on 84 patients with acute myocardial infarction, the effect of mexiletine on ectopic ventricular rhythms was tested with respect to mexiletine serum concentration. Malignant ventricular arrhythmias were observed 10 times in the control group and 5 times in the treated group. In the latter patients, mexiletine serum concentrations were below or at the lower therapeutical range (0.5 microgram/ml). During the second day of treatment, ventricular ectopic beats were significantly suppressed in the treated group with effective mexiletine serum concentration between 0.5 and 2.0 microgram/ml. As a side effect, vomiting was noticed in some patients in coincidence with an initial intravenous dosis of 2 mg per kg bodyweight; however, in no case it was necessary to interrupt treatment. There were no significant alterations in hemodynamical data, derived from Swan-Ganz catheter measurements, with mean maximal serum concentrations, on the second day, of approximately 1.15 microgram/ml.

Acute Disease↗
PubMed1979

[Ventricular arrhythmias in mitral valve prolapse syndrome (author's transl)].

Long-term ECG monitoring over 22 hours and exercise ECGs were performed in 72 patients with mitral valve prolapse syndrome. 70% of the patients had ventricular arrhythmias. In 28% severe arrhythmias in the form of multifocal atopic beats and ventricular runs were demonstrated. Long-term ECG monitoring was a suitable method for detection of these arrhythmias and superior to exercise ECG. Clinical, electrocardiographic and echocardiographic findings could not be correlated to the severity of ventricular arrhythmias.

Adolescent↗
PubMed1979

[A new method of pericardiocentesis and quantification of pericardial effusions by echocardiography (author's transl)].

With a new method for safe and complete evacuation of pericardial effusions it was possible to check the quantification of pericardial fluid is was possible to check the quantification of pericardial fluid by echocardiography. Using a formula based on the assumption that in systole the pericardial fluid is distributed equally around the contracting heart (like a coat enveloping a sphere), it was demonstrated that pericardial effusions ranging from 250 to 600 ml could be fairly accurately measured. Smaller effusions were not so readily determined. Effusions over 600 ml could be only roughly measured, usually being underestimated.

Echocardiography↗
PubMed1979

The vulnerability of the right atrium. III. Electrophysiologic correlates of atrial vulnerability.

70 patients were investigated by means of the atrial extrastimulus method at three different driving rates: 80, 100 and 120/min. At each rate the effective, the relative, the total and the functional refractory periods were measured. 30 patients who showed signs of atrial vulnerability at least one of the tested rates were included in the so called vulnerability group. The remaining 40 patients, who did not fulfill the criteria for atrial vulnerability, were included in the nonvulnerability group. When the two groups were compared to each other there were significant larger P waves (p less than 0.005), shorter effective refractory periods (p less than 0.001) and longer relative refractory periods (p less than 0.001) in the vulnerability group. With increasing driving rate there was an increased tendency to repletitive firing in the vulnerability group. The phenomenon of vulnerability correlated well with the rate-induced shortening of the effective and the lengthening of the relative refractory period. The above described phenomena are compatible with the concept of re-entry as the electrophysiologic mechanism of atrial vulnerability in man.

Atrial Fibrillation↗
PubMed1979

Left ventricular ejection power in coronary artery disease during atrial pacing.

Peak and mean left ventricular ejection power were measured during atrial pacing in 6 normal subjects (group I), 6 patients with coronary artery disease without myocardial infarction (group IIa), and 10 patients with coronary artery disease after myocardial infarction (group IIb). Pacing rates were 80 and 120/min. Power was determined by computer analysis of pressure, volume, and time. Data were normalised by end-diastolic volume and left ventricular muscle mass. Peak left ventricular ejection power normalised by end-diastolic volume values at a pacing rate of 120 min were significantly lower in group IIa and IIb than in normal subjects. Mean muscle mass in normal subjects was 179 g and in group IIa 216 g (P smaller than 0.05). Peak power normalised by muscle mass in normal subjects tended to increase at 120/min whereas in group IIa it declined by 26 per cent (P less than 0.001). These data indicate that the energy output of the left ventricle at rest may be the same in patients with significant coronary artery disease as in normal subjects. Increasing the heart rate from 80 to 120/min in a normal myocardium augments power but in coronary artery disease it remains static or falls.

Adult↗
PubMed1979

Spontaneous course of ST-segment elevation in acute anterior myocardial infarction.

The spontaneous course of ST-segment elevation (sigmaST) in 24 patients with acute anterior myocardial infarction (AMI) was studied by precordial ST-segment mapping, which was recorded at 2-hour intervals during the first 48 hours after admission. Change of sigmaST between two registrations was expressed as mV/hr, and was compared with clinical and hemodynamic parameters, course of MB-CK curve, calculated infarct mass and arrhythmias. After an initial rapid increase, there was a decrease of sigmaST, which reaches a plateau-like curve approximately 12 hours after the onset of chest pain. A second new increase of sigmaST exceeding a value of 0.6 mV/hr correlates well with extension of necrosis, verified by re-elevation of MB-CK. During the first 2 days, extension of necrosis could be detected in 50% of our patients. As new ischemic episodes and extension of necrosis in AMI occur frequently and are promptly indicated by an increase of sigmaST, the physician should, while monitoring therapeutic interventions, concentrate on such a second increase rather than on a decrease of sigmaST (which may occur spontaneously), as has been suggested in most previous reports.

Adult↗
PubMed1979

Efficacy of propranolol versus placebo in long-term treatment in patients with mitral valve prolapse.

In 60 patients with mitral valve prolapse syndrome a randomized controlled interindividual double-blind study of propranolol (p) was performed. Patients received p 80 mg (A), 160 mg (B) and placebo (C) orally for 4 weeks. Prior to and after treatment, heart rate (HR) and blood pressure (RR) as well as systolic time intervals (STI) were measured and corrected for heart rate--electromechanical systole (QS2I), left ventricular ejection time (LVETI), and preejection period (PEPI). The ratio PEP/LVET was calculated. Plasma levels were measured by an optimized fluorimetric method. 1. STI lay in the upper part of the normal range, indicating that some patients had a hyperkinetic cardiac function. 2. P had no influence on QS2I and LVETI in A and B. PEPI was prolonged (A: +13.2 ms, B: +14.2 ms) and PEP/LVET was increased (A: +0.040, B: +0.050). 3. As indicated by the changes in HR, RR, PEPI, and PEP/LVET p showed in B compared to A only minor additional effects. 4. Plasma levels of p were in B three times higher than in A (A: 89.2 +/- 10.0 nmol/l B: 246.7 +/- 30.5 nmol/l). With a dose of 80 mg propranolol a point close to the plateau of maximum efficacy was reached, where a higher dose resulted only in small additional negative inotropic effects.

Clinical Trials as Topic↗
PubMed1979

[Pharmacodynamic studies in suicidal digoxin poisoning (author's transl)].

In two patients with suicidal digoxin poisoning the correlations between serum digoxin concentration and changes in the duration of QTc and the flattening of the T-waves were studied. The digoxin serum half-life following suicidal digoxin poisoning was in the first patient (10 mg beta-acetyl derivative of digoxin) 77 h, prolonged cause of renal insufficiency, and in the second patient 39.6 h. (20 mg beta-acetyl derivative of digoxin). In both patients the digoxin induced flattening of the T-wave reached a plateau of maximum efficacy at a serum level of 2-3 ng/ml with no further change up to a serum level of 13.2 ng/ml and 9.6 ng/ml respectively. A linear correlation, however, was found between the digoxin serum concentration and the digoxin induced shortening of QTc, r = 0.88 and r = 0.92 respectively. A plateau maximum efficacy was not found. The regression equations were y = -12.0 chi + 430.8 and y = -8.0 chi + 391.9 respectively. The shortening of QTc is therefore an important parameter for the diagnosis of digoxin poisoning. It can be determined very quick with no methodical problems.

Digoxin↗
PubMed1978

[Special diagnostic procedures in atrial tumours of the heart (author's transl)].

A vascular myxoma which prolapsed into the mitral valve was found in the left atrium of a 47-year old man. Two-dimensional ultrasonic tomography yielded relevant non-invasive diagnostic information on the pattern of movement of the pedunculated tumour. Highly accurate determination of the tumour volume was achieved via angiocardiography and videometry. Coronography of the tumour vessels allowed identification of an unusual point of insertion of the myxoma. The risk of obstruction of the mitral orifice was documented haemodynamically by a steep gradient above the mitral valve when holding breath during the expiratory phase.

Angiocardiography↗
PubMed1978

[Haemodynamic effects of nefopam (author's transl)].

The haemodynamic effects of nefopam (0.3 mg/kg i.v.) were measured for 45 minutes in ten patients with coronary heart disease. The drug is a new and highly potent analgesic without any respiratory depressant effect. Arterial blood pressure and cardiac output rose moderately, while left ventricular enddiastolic pressure remained unchanged. Heart rate did not exceed 91/min. Max dp/dt, min dp/dt, Vpm and V40 rose by a maximum of 16% above control. Thus nefopam differs from other potent analgesics in having a slight inotropic effect.

Adult↗
PubMed1978

[Evaluation of infarct size using serum concentration of the CK-MB isoenzyme (author's transl)].

The size of infarction was determined in 21 patients with acute myocardial infarction aged 42 to 76 years using serial analyses of the serum concentrations of the total creatine kinase (CK) and of the CK-MB isoenzyme. CK-MB isoenzyme concentrations reached their maximum in serum three hours earlier on average and returned to the initial value 10 to 12 hours before the total CK. CK-MB isoenzyme concentrations reached a maximum of 12.4% of maximum total CK activity. In 17 uncomplicated cases the infarct weight determined from total CK (40 +/- 23 g) and from CK-MB isoenzyme (35 +/- 23 g) was only different by 5 g (r = 0.92). In 4 patients with infarction and defibrillation or reanimation use of total CK led to an overestimation of the infarct size by more than double. The determination of the infarct size from CK-MB isoenzyme values proves that without extracardial CK release, estimation of the infarct size can also be done sufficiently exactly from the total CK concentrations. In complicated cases, however, the specific myocardial CK isoenzyme makes determination of the infarct size possible

Acute Disease↗