[Incidence of bronchopneumopathies in patients with chronic ischemic heart disease].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Corea.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Arterial plasma noradrenaline and adrenaline concentrations before, during and after an attack of pain, induced first by constant supine exercise and then by multistep atrial pacing, were determined in four patients with coronary occlusion disease and stable angina pectoris. An identical protocol was applied to a patient with atypical precordial pain (anxiety state) and normal coronary arteriograms. When compared, the results led to the following conclusions: 1) during supine exercise arterial plasma catecholamine concentrations, particularly noradrenaline, progressively increase, reaching highest values in temporal coincidence with the onset or the peak of pain, 2) during multistep atrial pacing-induced angina no significant changes of arterial plasma catecholamine concentrations are seen. These data, obtained from the same patients, further emphasize that the application of atrial pacing to the study of pathophysiology of angina pectoris and for evaluating antianginal drugs, especially if interfering with adrenosympathetic system activity, must be considered with caution.
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.
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.
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.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We have investigated the antihypertensive activity of relatively low daily doses of captopril in patients with mild and moderate arterial hypertension. In a first trial, at the end of a 2-week placebo washout period, 18 patients with essential hypertension WHO Stage I or II were treated with captopril, 25 mg three times daily (t.i.d.), 25 mg twice daily (b.i.d.), 50 mg t.i.d., and 50 mg b.i.d., according to a randomized within-patient open design, with each regimen lasting for a 2-week period. In a second trial, 12 hypertensive patients not adequately controlled by chlorthalidone 25 mg daily as monotherapy (supine diastolic blood pressure at rest greater than 95 mm Hg), continued the diuretic treatment in combination with captopril, 25 mg t.i.d. and 25 mg b.i.d. according to a randomized within-patient open design. Analysis of variance did not reveal differences between the four captopril dosing schedules (1st trial), or between the two captopril dosing schedules (2nd trial). Both the patients on captopril monotherapy (1st trial) and those cotreated with chlorthalidone (2nd trial) showed lower systolic and diastolic blood pressure values on each captopril regimen compared to prerandomization values (all p less than 0.01). No relevant unwanted effects were noted. We conclude that in patients with mild or moderate essential hypertension, either untreated or resistant to chlorthalidone, captopril is effective in reducing blood pressure even at daily doses not exceeding 150 mg, without differences between a t.i.d. and a b.i.d. dosing schedule.
We tried to assess relationships between echocardiographic left ventricular hypertrophy (LVH), arterial pressure levels, and plasma norepinephrine concentration (NE) in 20 previously untreated stable hypertensive patients with LVH, and in 11 healthy normotensive control subjects. Interventricular septal (IVS) thickness, posterior wall (PW) thickness, and left ventricular mass index (LVMI) were related to arterial pressure levels and to NE by univariate and multivariate regression analyses. In addition, after 18 months of monotherapy with atenolol (carried out in nine of 20 patients), the relationship between echocardiographic changes and degree of pressure reduction was tested. Before treatment, PW thickness weakly correlated with systolic (r = 0.55; p less than 0.01) and mean (r = 0.50; p less than 0.05) arterial pressure. IVS thickness weakly correlated with NE (r = 0.53; p less than 0.05). On this relatively small sample, multivariate regression analysis showed an association of both IVS thickness (R = 0.57; p less than 0.05) and PW thickness (R = 0.58; p less than 0.05) with mean arterial pressure (MAP) and NE. After atenolol, there was a reduction in IVS thickness (1.15 to 1.02 cm; p less than 0.01), PW thickness (1.08 to 0.99 cm; p less than 0.01), and LVMI (136.3 to 113.8 g/m2; p less than 0.01), besides a significant reduction in blood pressure and heart rate. The degree of pressure reduction induced by treatment did not correlate the change in IVS or PW thickness. In contrast, the change in diastolic and mean arterial pressure positively correlated the change in LVMI (r = 0.72 and r = 0.75, respectively; both p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)