The effects of acute dynamic exercise on haemostasis in fi rst class Scottish football referees.

PURPOSE: Physical fitness may confer protection from thrombosis; however, exercise-induced platelet activation may be involved in the triggering of acute vascular events. This study aimed to assess haemostatic responses to acute exercise in trained and sedentary middle-aged subjects. METHODS: 21 first class Scottish football referees and 15 sedentary controls performed a treadmill exercise test. Blood sampling was performed before, immediately after and 30 minutes post-exercise. Samples were analysed for platelet count, prothrombin time, activated partial thromboplastin time (APTT) and serum fibrinogen. Platelet activation was assessed using flow cytometry with CD62 (P-selectin) and antifibrinogen antibodies at rest and in response to ADP and epinephrine. RESULTS: Mean maximal oxygen consumption (Vo2) (ml/kg per minute) achieved was 47.23 (5.02) in the referees and 30.1 (5.2) in sedentary controls. Total platelet count (x10(-9)/l) increased immediately post-exercise (228.2 (40.5), 278.6 (48.9) p=0.001) remaining elevated at 30 minutes in both groups. APTT (s) was reduced immediately post-exercise (32.15 (3.1), 29.7 (3.94) p=0.001) with a further reduction seen at 30 minutes (32.15 (3.1), 28.4 (3.31) p=0.001). In the referees, percentage CD62 expression increased immediately post-exercise (0.688 (0.52), 1.42 (1.3) p=0.008). Percentage antifibrinogen expression increased post-exercise (5.19 (4.31), 13.01 (14.24) p=0.017), with a further increase at 30 minutes (5.19 (4.31), 20.47 (26.8) p=0.02). Similar trends were seen in sedentary controls. CONCLUSION: This study suggests that in an older athletic population, physical fitness does not protect against the prothrombotic effects of exercise. These data suggest that during a football match when referees achieve approximately 80% of peak VO2 (23) they may be at risk of significant platelet activation. Prophylactic platelet inhibition should be considered in this group after appropriate screening and risk stratification.

Infective endocarditis in a racially mixed community: a 10 year review of 78 cases.

Over a 10 year period, 78 cases of infective endocarditis were seen at a general hospital serving a multiracial community. There was a bimodal distribution by age and by race. Rheumatic heart disease was a predisposing factor in 45% of cases and was particularly common in young Polynesians. Only eight patients had undergone procedures which might have caused bacteraemia. Most cases were due to streptococci (67%) or staphylococci (27%). Eighteen of 78 patients (23%) died in hospital, usually as a result of overwhelming sepsis or neurological complications. The 60 discharged have been followed for an average of almost three years. There have been 11 deaths but only two related to the previous endocarditis. Three of 41 patients infected with viridans streptococci died. There were no relapses and only one microbiological failure due to these organisms. All 14 patients with viridans streptococcal endocarditis treated with combined therapy for two weeks were cured. Ten of 16 cases of Staph aureus endocarditis were fatal. All but one involved the left side of the heart. The series included no intravenous drug abusers. Sixteen cases of endocarditis involved prosthetic valves and in this group the mortality, frequency of complications and need for surgery were significantly more frequent than in those with native valve infection.

Effects of fibronectin and group B streptococci on tumour necrosis factor-alpha production by human culture-derived macrophages.

Group B streptococci (GBS) are an important cause of sepsis and shock in the new-born. We have previously reported that GBS induce the production of tumour necrosis factor-alpha (TNF-alpha) by human monocytes and culture-derived macrophages. We have also shown that fibronectin (FN) promotes interaction between GBS and human phagocytes. In the present study, we investigated the effect of FN and GBS on the production of TNF-alpha by adult and neonatal culture-derived macrophages. We report that soluble FN alone was a strong stimulus for the production of TNF-alpha by culture-derived macrophages (FN 50 micrograms/ml = 623.33 +/- 47 pg/ml TNF, versus media alone 3 +/- 1.5 pg/ml; P < 0.0001). While GBS also induce the production of TNF-alpha by macrophages, the addition of FN to GBS had more than an additive effect on TNF-alpha levels. FN-mediated TNF-alpha production by macrophages was inhibited by both soluble arginine-glycine-aspartic acid (RGD) peptide (71%; P < 0.0001) and anti-beta 3-integrin monoclonal antibody 7G2 (54%; P < 0.0001). Neonatal culture-derived macrophages produced significantly more TNF-alpha in response to GBS (356.4 pg/ml +/- 27.7) than adult cells did (222.0 pg/ml +/- 21.0; P = 0.037), and dramatically more in response to FN alone (neonatal 1931.0 pg/ml +/- 23.0 versus adult 463.5 43.5 pg/ml; P < 0.0001). FN may contribute to the high levels of TNF-alpha production implicated in the pathophysiology of GBS sepsis and shock.