T lymphocyte infiltration in non-rheumatic aortic stenosis: a comparative descriptive study between tricuspid and bicuspid aortic valves.

BACKGROUND: The two most common causes of aortic stenosis are primary "degenerative" calcification of tricuspid aortic valves and secondary calcification of congenital bicuspid valves. T lymphocyte infiltration occurs in stenotic tricuspid aortic valves, indicating an inflammatory component, but it has not been shown whether it also occurs in stenotic bicuspid valves. OBJECTIVE: To compare non-rheumatic tricuspid and bicuspid stenotic aortic valves for the presence and distribution of T lymphocytes. SETTING: University hospital. PATIENTS AND DESIGN: Valve specimens were obtained from 29 patients (15 women, 14 men, mean age 69 years (range 52-81 years)), referred to the hospital for aortic valve replacement because of symptomatic aortic valve stenosis. There were 17 tricuspid valves (from 10 women and seven men, mean age 71 years) and 12 bicuspid valves (from five women and seven men, mean age 67 years). To identify mononuclear inflammatory cells, sections were stained with antibodies for CD3 (pan-T cell antigen, Dako 1:400) and then graded histologically according to the degree of T cell infiltrate. RESULTS: T lymphocyte infiltration was present in both tricuspid and bicuspid stenotic aortic valves, without any significant differences in extent or localisation. CONCLUSIONS: Stenotic bicuspid aortic valves show the same degree of T lymphocyte infiltration as degenerative tricuspid aortic valves. Inflammation needs to be considered in the pathogenesis of acquired aortic stenosis, irrespective of the primary valve anomaly.

Femoral artery haemostasis with a pneumatic compression device versus a clamp after coronary angiography.

To evaluate the safety and efficacy of a new pneumatic compression device for achieving haemostasis after femoral artery catheterization, 1,017 patients undergoing selective coronary angiography by a 5F unilateral femoral route were prospectively randomised to pneumatic or the routinely used clamp compression technique. All initial bleedings could be controlled in the pneumatic group, whereas in 38 patients (8%) of the clamp group the initial positioning of the clamp was unsuccessful or was not tolerated by the patient (p < 0.05). Ultrasound Doppler study of the puncture site because of suspected postcatheterization vascular complication revealed two haematomas which needed no further measure and two pseudoaneurysms which were successfully treated with ultrasound-guided compression or surgical repair. The rate of complications requiring treatment (pseudoaneurysms) was 0.2% overall, 0.5% in the clamp group and nil in the pneumatic compression group (NS). We conclude that the pneumatic compression device is effective, convenient and at least as safe as the clamp and, by shortening the time in the catheterization laboratory, offers time for further angiograms.

Treatment with ramipril improves systolic function even in patients with mild systolic dysfunction and symptoms of heart failure after acute myocardial infarction.

BACKGROUND: Clinical signs of heart failure such as pulmonary rales and dyspnea, ventricular dysfunction, and ventricular arrhythmia are independent predictors of a poor prognosis after acute myocardial infarction (AMI). HYPOTHESIS: The study aimed to assess the effect of ramipril treatment on mildly depressed left ventricular (LV) systolic function, assessed by atrioventricular (AV) plane displacement in patients with congestive heart failure after AMI. METHODS: The study was a substudy in the Acute Infarction Ramipril Efficacy Study, a double-blind, randomized, place-bo-controlled trial of ramipril versus placebo in patients with symptoms of heart failure after AMI. In all, 56 patients were included in the main study, 4 refused to participate in the substudy, and 4 were excluded for logistical reasons. Echocardiography was performed at entry and after 6 months. Patients who underwent coronary artery bypass grafting during the follow-up period were excluded. RESULTS: At baseline, the patients had modest LV dysfunction, and mean AV plane displacement of 9.7 mm. During follow-up, AV plane displacement increased in ramipril-treated patients from 9.5 to 10.9 mm (p < 0.01). No statistically significant changes were seen in the placebo group. CONCLUSIONS: Ramipril improves LV systolic function in patients with clinical signs of heart failure and only modest systolic dysfunction after AMI. Measurement of AV plane displacement is a simple and reproducible method for detection of small changes in systolic function and may be used instead of ejection fraction in patients with poor image quality.

Assessment of left ventricular diastolic function from mitral annulus motion, a comparison with pulsed Doppler measurements in patients with heart failure.

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.

Nutritional assessment and muscle energy metabolism in severe chronic congestive heart failure--effects of long-term dietary supplementation.

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.

Muscle energy metabolism in severe chronic congestive heart failure--effect of treatment with enalapril.

By using biopsies, skeletal muscle metabolism was investigated in 22 patients with severe chronic heart failure. All the patients were in New York Heart Association functional class IV and constituted a subgroup of the previously published CONSENSUS trial. After this initial investigation of muscle metabolism in patients with chronic heart failure, the influence of the angiotensin converting enzyme inhibitor, enalapril, on skeletal muscle metabolism was studied by randomizing the patients in a double-blind manner to receive either placebo (n = 11) or enalapril (n = 11) in addition to conventional treatment. At the time of inclusion, the muscle content of energy-rich compounds, i.e. glycogen and the high energy phosphates, adenosine triphosphate (ATP) and phosphocreatine, was reduced as compared with healthy subjects and muscle lactate content tended to be higher than normal. Following study treatment, no significant changes occurred, neither within nor between the two subgroups. Thus, patients with severe chronic congestive heart failure display metabolic derangement in muscle, which, in this study, was not corrected by treatment with enalapril.

Muscle water and electrolytes in severe chronic congestive heart failure before and after treatment with enalapril.

To investigate the electrolyte and water content in peripheral skeletal muscle in patients suffering from severe chronic congestive heart failure, New York Heart Association functional class IV, and to study the influence of the angiotensin-converting enzyme inhibitor, enalapril, 22 patients were randomized in a double-blind study to receive either placebo (n = 11) or enalapril (n = 11) in addition to their conventional treatment. The patients included a subgroup in the previously published CONSENSUS study. At the beginning of the study, the content of potassium and magnesium was significantly reduced in muscle as compared with healthy subjects while sodium and water were increased. The muscle content was not predictable from the serum concentrations of the electrolytes. Following study treatment no significant changes occurred, neither within nor between the two subgroups. Thus, patients with severe chronic congestive heart failure, New York Heart Association functional class IV, displayed disturbed electrolyte and water content in muscle, which, in this study, was not corrected by treatment with enalapril.

Neuroendocrine response in acute heart failure and the influence of treatment.

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.