Biomedical subjects
Publications and source records attributed to S Effert.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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Of 80 patients with acute myocardial infarction who had a cardiac arrest without shock 42 (52.5%) were resuscitated in a cardiological intensive care unit. Twenty-six were finally discharged from hospital. After an average of four years, 21 patients were still alive. Prognosis of primary ventricular fibrillation, the most frequent cause of circulatory arrest (51) was more favourable than that of primary asystole (23 patients). The younger the patient the better the prognosis: the average age of the 21 who survived for several years was 12 years less than those who had died. Follow-up examination indicated that 13 had signs of heart failure. Ventricular extrasystoles were demonstrated by ECG in 11. Eight had depressive episodes. It is likely that a further decrease in death-rate can be achieved only if the interval between onset of infarction and admission to an intensive care unit can be shortened.
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Obstructive and non-obstructive asymmetrical septal hypertrophy (ASH) is a relatively common disease which has no characteristic clinical symptoms. In only 14 of 71 patients in whom the diagnosis had been confirmed echocardiographically had it been possible to make the diagnosis by clinical means alone. Most of the patients had no specific clinical symptoms (angina, dyspnoea, systolic murmur, non-specific ECG changes) indicating a cardiomyopathy. Every patient with such uncharacteristic signs should therefore be studied by echocardiography in order to exclude ASH. In 17 patients there were no clinical symptoms at all, the diagnosis being made entirely by echocardiography.
27 patients (8 women, 19 men) aged 39-79 (mean 61) years with acute transmural mycoardial infarction and limitation of left ventricular function were treated in the acute stage for 24-72 (mean 55) hours with intravenous infusions of sodium nitroprusside in concentrations of 10-200 microng/min. Haemodynamic measurements before and 12 hours after onset of treatment showed a significant reduction in mean arterial pressure by 19%, in end-diastolic pressure in the pulmonary artery by 33% and in the total peripheral resistance by 32%, whereas stroke volume and cardiac index rose by 12% and 17%, respectively. The percentage improvement was most marked in those patients most severely affected. The mortality rate of cardiogenic shock was reduced to 25%. In a control group with haemodynamically similar left ventricular failure the mortality rate was 55%. However, the total mortality was nearly unchanged as the number of sudden unexpected deaths after the fourth day rose from 23 to 50%. Further investigations will show how these sudden deaths, mainly due to arrhythmias, can be prevented.
The vulnerability of the right atrium to single electrical stimuli was investigated in 100 non-selected patients. According to the response pattern to extrasystolic stimulation of the right atrium during the relative refractory period, the patients could be divided in 3 groups: Group A: no signs of vulnerability. Group B: 1 to 5 additional atrial extrasystoles after the premature atrial stimulus. Group C: runs of atrial flutter or fibrillation for at least 8 s. The 3 groups were compared with respect to the duration of the effective and relative refractory period of the right atrium. From group A to group C the effective refractory period showed a tendency to shorten, while the relative refractory period showed a tendency to prolong. These results are interpreted as supporting a reentry as the underlying mechanism of the here described atrial vulnerability.
The left ventricular hemodynamics of 70 patients with acute myocardial infarction were determined from measurements of pulmonary arterial end-diastolic pressure, cardiac index, mean arterial pressure and heart rate during the acute phase(first study, 5 hours after admission), 4 to 6 weeks later (second study, during convalescence) and in 35 percent of all subjects 6 to 12 months after the acute infarction (third study). Serial analysis of serum creatine kinase was carried out during the acute phase. The peak CK value normalized for body surface area was used as a rough index of the extent of the acute myocardial necrosis. The condition of all survivors of the acute stage improved. Patients with only slightly reduced left ventricular performance during the acute stage recovered to nearly normal during convalescence. The condition of patients with greatly reduced left ventricular function also improved but remained impaired during convalescence. In all patients the main changes in left ventricular hemodynamics occurred within the first 4 to 6 weeks; there was almost no further alteration during the following 9 months.
The on-line computer-system for the analysis of cathlab data developed by us allows the immediate evaluation of the conventional pressure- and valve-opening as well as a new hemodynamic parameters. In addition the volume-analysis is performed by the videometry-program. In simultaneous pressure-volume-registrations the complementary calculation of important energetic items is possible. This expanded analysis by the aid of the computer-system enables a detailed pre- and postoperative study of great clinical-practical and scientific importance.
In 50 patients with proven acute myocardial infarction (AMI), left ventricular hemodynamics (pulmonary end-diastolic pressure [PAEDP]; cardiac index [CI]; stroke volume index [SVI]; and SVI/PAEDP were related to the size of the acute infarct. Acute infarct mass was calculated from serial determinations of serum creatine phosphokinase (CPK) every two hours, using a computer program. In 15 cases postmortem measurement of acute infarct size after staining with Nitro-BT was made and correlated with calculated infarct size. Correlation in this limited number of cases was good with a mean difference of 7 g. Acute infarct mass in 38 survivors was 46 +/- 5 g and was significantly smaller (P less than 0.05) than in the 12 nonsurvivors (76 +/- 12 g.) PAEDP in surviving patients was significantly lower (17 +/- 1 mm Hg) and SVI (36 ml/m2) and SVI/PAEDP (2.4 ml/m2/mm Hg) significantly higher than in the nonsurvivors (PAEDP: 24 mm Hg; SVI: 23 ml/m2; SVI/PAEDP: 0.86 ml/m2/mm Hg) (P less than 0.001 for all differences). Similar significant differences were observed between patients not in shock and those in cardiogenic shock. Although in 39 patients, in whom the infarction was their first, infarct mass was larger (58 +/- 6 g) than in 11 patients with repeat infarctions (37 +/- 8 g), left ventricular hemodynamics were slightly more impaired in reinfarctions (PAEDP: 21 +/- 3 mm Hg; CI:2.60 L/min/m2) than in first infarctions (PAEDP: 18 +/- 1 mm Hg; CI:2.82 L/min/m2). The occurrence of cardiogenic shock was a strong predictor of death; however, the wide scatter of the data for the parameters cardiac index, PAEDP, and acute acute infarct mass precluded their usefulness, when taken individually, in predicting survival. When a relationship between hemodynamics and infarct size was looked for, four constellations of individual patients were identified. These groups were defined by PAEDPs of above or below 18 mm Hg and infarct sizes above or below 65 g. Class A patients (N = 22) had a small infarct (29 +/- 4 g) and good pump function (PAEDP: 13 mm Hg; SVI: 40 ml/m2; SVI/PAEDP: 3.27 ml/m2/mm Hg); prognosis was good for these patients. In class B (N = 13) the infarct was large (96 +/- 8 g) and pump function markedly impaired (PAEDP: 26 mm Hg; SVI: 24 ml/m2; SVI/PAEDP: 0.98 ml/m2/mm Hg); 54% of these patients died. Five patients in class C had, in the presence of a large infarct (84 g), only a slightly elevated PAEDP of 17 mm Hg and an almost normal SVI of 37 ml/m2. In contrast, the ten class D patients had an infarct size (34 g) similar to that in class A, but high PAEDP (23 mm Hg) and moderately reduced SVI (31 ml/m2). In this group a high incidence of reinfarctions (six out of ten) occurred. It is concluded that infarct mass calculated from serial CPK analysis, as a single parameter, cannot be used to predict mortality or development of cardiogenic shock in an individual patient.
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