[An informal debate about nursing education].
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Biomedical subjects
Publications and source records attributed to K Thygesen.
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Long-term treatment of survivors of an acute myocardial infarction with angiotensin-converting enzyme inhibitors has a beneficial impact on their long-term outcome. We tested the hypothesis that captopril could reductively cleave the lipoprotein(a) molecule and in addition act as a scavenger of oxygen free radicals. In a double-blind trial, 20 patients were randomized to receive either captopril 50 mg daily or corresponding placebo. patients were followed for a period of 30 days. Blood samples were drawn prior to randomization and after 30 days of treatment. Plasma concentrations of lipoprotein(a) and malondialdehyde were evaluated. Captopril treatment produced a significant reduction in plasma content of lipoprotein(a) ( < 0.05) and at day 30 the plasma content of lipoprotein(a) was also significantly lower than that in the placebo group (p < 0.05). furthermore, on day 30 plasma concentrations of malondialdehyde, an indicator of oxidative damage, were significantly lower in the captopril group when compared to baseline values and corresponding placebo group values (p < 0.05). The observed effect of captopril treatment on lipoprotein(a) and malondialdehyde might be ascribed to the sulfhydryl group in the captopril molecule.
The study comprised 83 patients, mean (+/-SD) age 47 +/- 8 years, with essential hypertension. Systolic and diastolic blood pressure at inclusion were 171 +/- 16 and 110 +/- 7 mm Hg, respectively. Two small resistance arteries were dissected from a subcutaneous gluteal biopsy and mounted in an isometric small vessel myograph for measurement of the media:lumen ratio. Left ventricular mass (LVM) was estimated by echocardiography, and the occurrence of ventricular arrhythmias was assessed by ambulatory ECG for 48 h. Left ventricular hypertrophy (LVH) occurred in 67% of the patients. Systolic function was generally unimpaired. ST depression was found in 75%, and ventricular arrhythmias in 45%. Twenty-two patients had permanent ST depression, and they had also greater LVM and more frequent ventricular arrhythmias than those without permanent ST depression. The area under the ST trend curve of all significant ST depressions was correlated to the LVM (r = 0.42, p < 0.001). Patients with arrhythmias had significantly greater area under the ST trend curve of all significant ST depressions than patients without arrhythmias (p < 0.05). In patients with LVH and permanent ST depression, the media:lumen ratio of the peripheral vessels was greater than that of patients with LVH but without permanent ST depression (11.6 +/- 2.9 vs. 9.8 +/- 2.0, p < 0.01). This suggests that hypertensive structural changes similar to those observed in peripheral vessels might occur in the walls of myocardial resistance arteries.
The objective of this study was to evaluate the relationship between early hemodynamic instability and myocardial ischemia and the effect of early intravenous enalapril therapy on this relationship. In patients with myocardial infarction (MI), early treatment with angiotensin-converting enzyme inhibitors is controversial. In hypotensive patients, initiation of treatment may exacerbate myocardial ischemia and thereby affect the clinical outcome. Therefore, in the CONSENSUS II study, a total of 60 patients randomly allocated to either intravenous enalapril or placebo treatment commenced within 24 h after the onset of MI were evaluated by repeated blood pressure measurements, ambulatory ST-segment monitoring before discharge and exercise testing. Significant ST-depression was present in 34 patients. Patients with ST-depression before discharge (residual ischemia) during either exercise testing or ambulatory monitoring or both had a decrease in initial mean arterial blood pressure (MAP) of 20 vs. 9 mm Hg in those without ST-depression (n = 24), (p < 0.00001). However, patients (n = 13) with long-lasting ST-depression during Holter monitoring, (> 60 min of ST-depression) presented with the most severe fall in MAP of 29 mm Hg (p < 0.00001) and a lower systolic blood pressure at inclusion (p < 0.01) compared to the remainder of patients. Furthermore, the number of recurrent acute ischemic events during follow-up was higher in these patients (7 vs. 1; p < 0.01). Ten of the patients treated with enalapril showed a long-lasting ST-depression versus only 3 in the placebo group (p = 0.08), and the average duration of all significant ST-depressions during Holter monitoring was significantly longer in the enalapril group compared to the placebo group (p < 0.05). Finally, 7 enalapril patients (20%) suffered an acute ischemic event in contrast to 1 patient (4%) in the placebo group (p = 0.07). In conclusion, early administration of enalapril had a potential proischemic effect in hypotension-prone patients mediated through exacerbation of the hemodynamic response, inasmuch as initial blood pressure fall after MI is related to residual myocardial ischemia and recurrent acute ischemic syndromes.
Seventy-nine of 673 patients attending a hypertensive outpatient clinic were classified as diabetics at the first examination. These patients were age- and sex-matched to two control groups: nondiabetic hypertensives and the background population. Nondiabetic hypertensive patients had a significantly poorer survival than expected during a 10-year observation period; the survival of diabetic hypertensives was even poorer, although not significantly. No sex difference was observed in the survival rates of hypertensive diabetics, neither was a difference seen between insulin-dependent and non-insulin-dependent patients. Acute myocardial infarction was the most frequent cause of death in both diabetic (40%) and nondiabetic (42%) hypertensive persons.
The material consists of 404 hospitalized patients with their first AMI. After an observation time of 1 and 5 yr, respectively, the mortality was 27% and 45%, against an expected mortality of 3% and 17% in a corresponding normal population. The annual mortality rate was 5.5% from 1 to 3 yr after the acute infarction, against an expected 3.5%. 3-5 yr after occurrence of the infarction, both the observed and expected annual mortality rates were 3.5%. In patients alive 1 mth after the acute attack, congestive heart failure (CHF) or left bundle branch block (LBBB) or secondary ventricular fibrillation (VF) during the acute phase gave a lower long-term survival, as compared to patients without CHF, intraventricular block or VF, respectively. Left anterior hemiblock, complete atrioventricular block following inferior infarction, or primary VF had no influence on the long-term prognosis.