No abstract

No abstract

These results suggest that plasma level of adrenomedullin are elevated in heart failure and that an increased plasma volume and an activated sympathetic nervous system in this condition may be related to its synthesis or secretion. Given that adrenomedullin exerts potent cardiovascular effects, increased adrenomedullin may be involved in the defense mechanism against further peripheral vascular resistance elevation in heart failure.

Previous studies have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are increased in essential hypertension. However, whether left ventricular geometry affects plasma ANP and BNP levels remains unknown. To investigate the effect of left ventricular geometry on plasma ANP and BNP levels in essential hypertension, we measured plasma ANP and BNP levels in 90 patients with essential hypertension. All patients were hospitalized, and fasting blood samples were obtained in the early morning after 30 minutes of bed rest. Plasma ANP and BNP levels were measured by immunoradiometric assay. Hypertensive patients were classified into four groups according to echocardiographic findings that showed normal geometry, concentric remodeling, eccentric hypertrophy, or concentric hypertrophy. Mean plasma ANP and BNP levels in all essential hypertensive patients were higher than those in age-matched normotensive control subjects. Plasma ANP levels in hypertensive patients with concentric remodeling, eccentric hypertrophy, and concentric hypertrophy were higher than in normotensive control subjects, although there were no differences between normotensive subjects and hypertensive patients with normal geometry. Plasma BNP levels tended to be higher in hypertensive patients with normal geometry, concentric remodeling, and eccentric hypertrophy than in normotensive control subjects; however, the differences were not significant. Plasma BNP levels and BNP/ANP ratio were specifically higher in concentric hypertrophy. There were significant correlations between ANP and left ventricular mass index, relative wall thickness, interventricular septal thickness, posterior wall thickness, and mean arterial pressure. Plasma BNP levels significantly correlated with relative wall thickness, interventricular septal thickness, posterior wall thickness, and left ventricular mass index but not with mean arterial pressure. In addition, plasma BNP levels were well correlated with ANP levels, and the slope for the linear regression model was steeper in concentric hypertrophy than in the other four groups. These results show that plasma ANP and BNP levels are increased in essential hypertensive patients with left ventricular hypertrophy. Furthermore, BNP secretion is augmented to a greater extent in concentric hypertrophy. Thus, measurement of plasma ANP and BNP levels may be useful for the detection of concentric left ventricular hypertrophy in patients with essential hypertension.

To establish guidelines for the surgical treatment of patients with infective endocarditis who have cerebrovascular complications, we conducted a detailed retrospective study of 181 of 244 patients with cerebral complications among 2523 surgical cases of infective endocarditis of the Japanese Association of Thoracic Surgery. The results showed that 9.7% of all patients with infective endocarditis had associated cerebral complications: 108 (44.3%) had active native valve endocarditis, 96 (39.3%) had healed native valve endocarditis, and 40 (16.4%) had prosthetic valve endocarditis. The hospital mortality of the patients with cerebral complications was 11.0% in the group as a whole: 13.9% in active native valve endocarditis, 3.1% in healed native valve endocarditis, and 37.5% in prosthetic valve endocarditis. Diseased valves included the following aortic valve in 55.5%, mitral valve 49.8%, tricuspid valve in 1.3%, and pulmonary valve in 1.3%. In 181 patients with cerebral complications, organisms were detected as follows: gram-positive cocci in 133 (73.5% [Streptococcus in 85, Staphylococcus in 32]), gram-negative in 18 (9.9%), fungus in 11 (6.1%), and unknown in 64.6%, cerebral bleeding in 31.5%, cerebral abscess in 2.8%, and meningitis in 1.1%. Hospital mortality rate and an exacerbation rate of cerebral complications, including related death, according to the interval from onset of cerebral infarction to cardiac surgery, were as follows: 66.3% and 45.5% within 24 hours, 31.3% and 43.8% between 2 and 7 days, 16.7% and 16.7% between 8 and 14 days, 10.0% and 10.0% between 15 and 21 days, 26.3% and 10.5% between 22 and 28 days, and 7.0% and 2.3% over 4 weeks later, respectively. A significant correlation existed between the interval and the exacerbation of cerebral complications (tied p = 0.008). Preoperative risk factors affecting exacerbation of cerebral complications were as follows: (1) severity of cerebral complications (p = 0.006), (2) intervals (p = 0.012), and (3) uncontrolled congestive heart failure as indications for cardiac surgery (p = 0.014). One patient underwent a cardiac operation within 24 hours of the onset of cerebral hemorrhage and died of cerebral damage. No exacerbations occurred in 10 patients who underwent their operation between 2 and 28 days. Nevertheless, exacerbations occurred in 19.0% of patients whose operation was done more than 4 weeks later. These data suggest that cardiac operations can be done safely 4 weeks after cerebral infarction, and if the delay is more than 2 weeks, the exacerbation rate will be around 10%. The risk of progression of cerebral damage is still significant 15 days and even 4 weeks after cerebral hemorrhage.