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The effects of propofol on cardiovascular dynamics were studied, by means of SO2 Swan-Ganz catheter, in 12 patients scheduled for elective pulmonary resection and in 10 patients undergoing closed heart mitral valve commissurotomy. Myocardial contractility was also investigated in 10 patients (5 pulmonary and 5 mitral valve patients) by means of transthoracic echocardiography. The patients were premedicated with morphine (0.1 mg/kg i.m.), scopolamine (0.005 mg/kg i.m.) and diazepam (0.1 mg/kg p.o.). Anaesthesia was induced with propofol (2 mg/kg i.v.) and fentanyl (0.005 mg/kg i.v.) and maintained with propofol (6 mg/kg/h) plus fentanyl (0.005 mg/kg/h) infusion. Muscle relaxation was assured by pancuronium bromide (0.1 mg/kg). Ventilation (O2-N2O 50%) was controlled to maintain ETCO2 between 30 and 40 mmHg. All the patients undergoing pulmonary resection were intubated with double lumen endotracheal tube. Measurements were performed with the patients awake, after induction, during steady state anaesthesia, before and after thoracotomy. Propofol together with fentanyl significantly decreased arterial pressure (more than 35%) and cardiac index (more than 40%) in both groups of patients; heart rate showed no significant changes even after intubation. Right atrial pressure didn't change meanwhile wedge pressure showed a reduction, with statistical significance only in pulmonary patients. Total systemic resistances didn't show any variation in both groups of patients. The echocardiographic data revealed an important impairment of myocardial contractility after bolus of propofol, mainly in cardiac patients, as evidenced by decrease of ejection fraction values (20%) and by increase of left ventricle end systolic volume index (10%) from baseline. SVO2 and DO2/VO2 ratio values were stable, according with deep anaesthesia level and adequate metabolic balance. In pulmonary patients, during one lung ventilation, the intrapulmonary shunt values did not differed either during or without propofol infusion, thus suggesting that propofol doesn't interfere with pulmonary hypoxic vasoconstrictor response. In conclusion an aware use of propofol and a careful haemodynamic monitoring would be advisable primarily in patients with a well known or supposed cardiovascular disease.

The in-hospital mortality, the causes of death, the actuarial survival curves were compared in two subsequent groups of patients admitted to our CCU for acute myocardial infarction: the first (group A) includes 791 pts, admitted from september '67 to december '72, the second (group B) includes 542 pts admitted from january '78 to june '80. The in-hospital mortality was significantly reduced in group B (A: 186/791, 23.5%; B: 72/542, 13,3%, p less than 0.01). This could be due to a reduction of the number of deaths for cardiogenic shock (A: 71/791, 9%; B: 30/542, 5.6%; p less than 0.01) and to reduction in the mortality rate for pulmonary oedema (from 6% to 1.5%, p less than 0.01), although the frequency of pulmonary oedema was the same during the two periods (A: 205 pts, 26%; B/156 pts 29%). We did not observe any significant difference in the long-term prognosis (54 months: A 79.3%, B 71.5%). The actuarial survival curves overlapped after the 1st semester after discharge. The most frequent cause of death during follow-up was a new myocardial infarction. None in the group A and only 3% in the group B were referred to the surgeon for coronary artery bypass grafting. We conclude that, in spite of a significant reduction of the in-hospital mortality, possibly related to the evolution in diagnosis and management of the disease, the long-term survival was not improved in a non-surgically treated population with myocardial infarction.

Eight patients with NYHA Class II congestive heart failure were studied before and after captopril with right heart catheterization, cycloergometric stress tests and radionuclide 99Tc cineventriculography. Acute administration of captopril increased stroke volume and cardiac index and reduced left ventricular filling pressure. Similar changes though less marked were seen after 30 days of captopril therapy. Functional aerobic capacity and left ventricular performance improved over 15 and 30 days of captopril respectively. We therefore suggest that captopril can be effective also in patients with moderate congestive heart failure.

Forty-four consecutive patients with acute myocardial infarction were studied with equilibrium radionuclide angiography (RNA) within 24 hours from the onset of symptoms, three days after admission and three days before hospital discharge (14 +/- 3 days). To assess the prognostic value of RNA derived parameters we assessed: the ejection fraction (EF), the left ventricular end-systolic volume index (ESVI), the left ventricular end-diastolic volume index (EDVI), the cardiac index (CI), the stroke volume index (SVI) and the peak systolic pressure/end-systolic volume index ratio (PSP/ESVI); we also determined Peel's prognostic index (PI) on admission and measured systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and cardiac frequency (CF) as the same time as the radioisotopic parameters were taken. Thirty-nine patients were discharged without signs of ventricular failure with and without medical treatment (group A), 5 died during hospitalization (group B). Using EF alone, we obtained a very clear distinction between the two groups (Group A 43 +/- 12%; Group B 22 +/- 3%; p less than 0.005). Stepwise, multivariate analysis showed that, by linking PSP/ESVI to EF, we can even obtain a function that correlate better with hospital survival (F = 0.09832 X EF - 0.32035 X PSP/ESVI - 3.12981; p less than 0.002). There was good exponential correlation between EF and PSP/ESVI (r = 0.781) and this would seem to confirm that PSP/ESVI is a more sensitive contractility index for patients with a not very depressed EF.