No abstract

In order to investigate nutritional status in relation to the metabolic state of skeletal muscle in patients with severe congestive heart failure, and to explore the influence of long-term dietary supplementation, 22 patients were randomized in a double-blind study to receive either a placebo (n = 13) or high caloric fluid (n = 9). Before treatment, the muscle content of adenosine triphosphate (ATP), creatine and glycogen was lower than in healthy individuals, and muscle biopsies revealed an excess of water. Two patients were found to be malnourished according to nutritional assessment criteria. Following study treatment, no significant changes occurred, either within or between the two subgroups. Thus, patients with severe congestive heart failure displayed metabolic derangement in skeletal muscle which did not seem to be explained by malnutrition.

Mitral and pulmonary venous flow velocity recordings are often used for the assessment of left ventricular diastolic function. These curves are, however, also influenced by other factors. To investigate whether mitral annulus motion carries additional information in this context, mitral annulus motion was compared to Doppler registrations of mitral and pulmonary flow velocities in 38 patients with heart failure (NYHA II-III) after myocardial infarction. Patients with an increased atrial contribution to mitral annulus motion (> 57%, n = 12) had a higher mitral late-to-early flow velocity ratio (A/E) and pulmonary systolic to diastolic filling ratio (< 0.01). Patients with atrial displacement above average for the group (> or = 5.1 mm, n = 19) had a higher mitral (A/E) ratio and pulmonary systolic to diastolic filling ratio than patients with a lower than average atrial component (P < 0.05). There was a significant correlation between a/T ratio and A/E ratio (r = 0.61, P < 0.001) and between pulmonary flow and transmitral flow (= 0.76, P < 0.001). We conclude that an increased atrial displacement of the mitral annulus is a frequent finding in patients with signs of left ventricular relaxation abnormality. There is a significant correlation between a/T ratio and A/E ratio but the information contained in the two indices are not identical.

Vasoactive humoral factors were measured in 27 patients before and during the first week of conventional treatment of acute heart failure. On admission, all patients were given frusemide intravenously, followed by oral digoxin and diuretic therapy. Before drug treatment, plasma renin activity and plasma angiotensin II concentrations were within normal ranges in the group of patients without previous diuretic treatment, but were significantly higher in those 16 patients already on diuretic drugs when admitted to hospital. After diuretic treatment, however, even the former group revealed activation of the renin-angiotensin system. Plasma concentrations of catecholamines were increased initially but normalized within 1 day. A majority of the patients initially had very high plasma concentrations of atrial natriuretic peptide (mean 276.9 +/- 39.0 pg ml-1) which decreased but did not normalize during the study period. High plasma levels of arginine vasopressin (mean 56.8 +/- 14.6 pg ml-1) were found, but tended to be reduced during treatment. Thus, patients with acute heart failure displayed increased plasma concentrations of atrial natriuretic peptide, arginine vasopressin and catecholamines, but these vasoactive hormones decreased in parallel to clinical improvement during diuretic therapy. In contrast, the renin-angiotensin system became clearly activated.

Background. Although our comprehension of nonrheumatic aortic stenosis (NRAS) has increased substantially during the last decade, less is known about the histopathology of rheumatic aortic stenosis (RAS). The aim of this study was to investigate rheumatic aortic stenosis by means of analyses previously used in nonrheumatic stenosis. Material and Methods. Valve specimens were obtained from 39 patients referred to hospital due to significant aortic stenosis. According to established macroscopic criteria the valves were divided into two groups consisting of 29 NRAS and 10 RAS valves. Mononuclear inflammatory cells and apolipoproteins were investigated using immunohistochemical analyses. Results. The localisation of calcification differed in tricuspid nonrheumatic valves when compared to bicuspid nonrheumatic and rheumatic valves. The RAS valves revealed a lower degree of T lymphocyte infiltration compared with the NRAS valves. Infiltration of macrophages was seen in all valves and there were no differences regarding deposition of apolipoprotein. Conclusion. Rheumatic and nonrheumatic aortic stenotic valves show a similar and significant chronic inflammation. The similarities regarding the localisation of calcification indicate that the valve anomaly/morphology can influence the pathogenesis of aortic stenosis. Finally, our findings highlight the question of a postinflammatory valvular disease of other causes than rheumatic fever.