Myopericarditis following Campylobacter infection.

BACKGROUND: Myopericarditis can be caused by a wide range of infectious agents. There are a few reported cases implicating Campylobacter in the pathogenesis of myopericarditis. CONCLUSIONS: We believe that this case report represents the first documented case in Ireland of myopericarditis associated with Campylobacter enteritis.

Infection by Panton-Valentine leukocidin-producing Staphylococcus aureus clinically mimicking Lemierre's syndrome.

Lemierre's syndrome is an oropharyngeal infection which leads to severe septic thrombophlebitis of the internal jugular vein and metastatic abscesses of the lungs and other organs. It is usually caused by Fusobacterium necrophorum, a Gram-negative obligate anaerobe. An unusual case of Panton-Valentine leukocidin (PVL)-producing Staphylococcus aureus infection masquerading as Lemierre's syndrome is reported here. A 32-year-old fit and otherwise healthy male presented on Christmas morning with a boil on his left cheek for 2 days and generalized rash for 3 h. His general condition began to worsen, he developed facial swelling and loss of vision in the left eye and was transferred to the intensive care unit. His treatment was taken over by team of specialists and further investigations revealed thrombophlebitis of the left internal jugular vein and cavernous sinus thrombosis with multiple brain infarcts and lung abscesses. His condition remained critical with multiple cranial nerve involvement despite being on broad-spectrum antibiotics. Blood cultures grew S. aureus which was producing PVL toxin. He improved gradually over several weeks. He underwent intensive physiotherapy and made a good recovery. Although a rare entity, it is important to consider Lemierre's syndrome in septic patients who present with rapidly worsening symptoms.

Feasibility and long term outcome of home vs hospital initiated thrombolysis.

BACKGROUND: Thrombolytic therapy improves mortality in acute myocardial infarction especially in those who receive treatment early. Pre-hospital therapy can reduce the time to treatment. METHODS: Open, randomized study of patients with acute myocardial infarction of less than six hours duration in a rural community. Pre-hospital thrombolysis was administered using a mobile coronary care unit (MCCU) and all patients received IV streptokinase. RESULTS: Two-hundred and forty-eight patients were studied, 82 in the MCCU and 166 in the hospital group. The mean delay time to treatment was 136 minutes (MCCU group) and 196 minutes (hospital group) (p < 0.001). Reperfusion time was 116 minutes for the MCCU group and 118 minutes for the hospital group. Mortality at 30 days was 4.9% for the MCCU group and 15.7% for the hospital group (p = 0.014). Mortality at one year was 9.8% for the MCCU group and 23.5% for the hospital group (p = 0.009). Mortality for patients followed up to five years was 17.7% for the MCCU group and 35.2% for the hospital group (p = 0.005). There were no significant adverse events in either treatment group. CONCLUSION: Pre-hospital thrombolysis by MCCU is feasible and allows significant reduction in the delay time to treatment initiation. There are encouraging improvements in short- and long-term survival with no apparent reduction in safety profile.

Prehospital thrombolysis in a rural community: short- and long-term survival.

In order to assess the feasibility and outcome of using prehospital thrombolysis in acute myocardial infarction in a rural community, we performed an open randomized study of patients with symptoms of acute myocardial infarction of less than 6 hours. One hundred and forty-five patients with acute myocardial infarction were allocated to receive IV streptokinase prehospital by means of a mobile coronary care unit (MCCU) (n = 43) or to receive IV streptokinase in hospital (n = 102). The mean delay time to treatment was 138 minutes (MCCU group) and 172 minutes (hospital group) (p less than 0.02). Reperfusion time was 88 minutes for the MCCU group and 92 minutes for the hospital group. Mortality at 14 days was 2.3% for the MCCU group and 11.7% for the hospital group (p less than 0.05). Six month mortality was 4.9% for the MCCU group and 17.3% for the hospital group (p = 0.03). Mortality at 1 year was 6.1% for the MCCU group and 20.0% for the hospital group (p = 0.04). There were no significant adverse events in either treatment group. Thus, prehospital thrombolysis by streptokinase is feasible and allows significant reduction in the delay time to treatment initiation. There are encouraging improvements in both short- and long-term survival with no apparent reduction in safety profile.

Efficacy and tolerability of atenolol, nifedipine and their combination in the management of hypertension.

This randomised, double-blind, crossover study investigated the haemodynamic effects of a beta-blocker (atenolol 50mg) and a calcium antagonist (sustained release nifedipine 20mg) given either separately or in combination in 3 groups of patients with mild to moderate essential hypertension. Each treatment was administered twice daily. The fixed combination given twice daily for 4 weeks produced reductions in blood pressure which lasted for at least 12 hours after administration of the final dose. The control of blood pressure by the combination was superior to that achieved by its individual components. Side effects normally associated with nifedipine therapy were less frequent when it was administered with atenolol. Compliance with treatment was good, but it was best when the drugs were given together rather than separately. A fixed combination of atenolol and nifedipine may prove useful in treating hypertensive patients inadequately controlled on beta-blocker therapy alone.

The efficacy and tolerability of atenolol, nifedipine, and their combination in the management of hypertension.

In this randomized, double-blind, cross-over study we investigated the haemodynamic effects of a beta-blocker (atenolol 50 mg) and a calcium antagonist (nifedipine SR 20 mg) given either separately or in combination in three groups of hypertensive patients. Each treatment was administered twice daily. The fixed combination given twice daily for four weeks produced reductions in blood pressure which lasted for at least 12 h after administration of the last dose. The control of blood pressure by the combination was superior to that achieved by its individual components. Adverse effects normally associated with nifedipine were less frequent when it was given with atenolol. Compliance with treatment was good, but best when the drugs were given together rather than separately. A fixed combination of atenolol and nifedipine may prove useful in treating hypertensive patients inadequately controlled on beta-blocker therapy alone.

Heart failure associated with infective endocarditis. A review of 40 cases.

Thirty one (78%) of 40 consecutive patients (aged 13-79, mean 44 years) with infective endocarditis had congestive heart failure at presentation. Twenty six (65%) had had rheumatic heart disease and 17 (43%) patients had prosthetic valves. Eight (20%) patients had undergone dental procedures within three months of presentation. Blood cultures were positive in only 22 (55%) of the patients. In nine (41%) of them streptococci of the viridans group were isolated and in seven (32%) patients endocarditis was due to Staphylococcus aureus. Eight patients had Q fever endocarditis. Sixteen patients required operation because of haemodynamic deterioration while they were in hospital; 11 patients had native valves and five had prosthetic valves. Seven had emergency operations and were pyrexial at that time. Four of the seven died in hospital. Of the 12 who were alive and well after surgery only two required further surgery two and three years after the initial operation. Twelve (30%) of the 40 patients died in hospital; in 10 death was mainly due to left ventricular failure or congestive heart failure. All patients died who had renal failure (four cases), myocardial infarction (two cases), complete heart block (one case), or ventricular fibrillation (two cases) before operation. Six (33%) of the 18 patients with culture negative endocarditis died. Two of the four patients seen and treated more than 12 weeks after the onset of symptoms died, as did three of the five patients with prosthetic valves who required surgery while in hospital. Three patients with neurological complications survived and only two (29%) of the seven patients with blood cultures that were positive for Staphylococcus aureus died. Of these 40 high risk patients optimal antibiotic treatment and early surgery for haemodynamic difficulty ensured that 28 (70%) were discharged from hospital alive and well.

Discrete subaortic stenosis.

Data concerning 17 consecutive patients with discrete subaortic stenosis are recorded. Twelve patients underwent operative resection of the obstructing lesion. Of these all except one were symptomatic and all had electrocardiographic evidence of left ventricular hypertrophy or left ventricular hypertrophy with strain. They had a peak resting systolic left ventricular outflow tract gradient of greater than 50 mmHg as predicted from the combined cuff measurement of systolic blood pressure and the echocardiographically estimated left ventricular systolic pressure and/or as determined by cardiac catheterisation. The outflow tract gradient as predicted from M-mode echocardiography and peak systolic pressure showed close correlation with that measured at cardiac catheterisation or operation. During the postoperative follow-up from one month to 11 years, of 11 patients, one patient required a further operation for recurrence of the obstruction four years after the initial operation. All patients are now asymptomatic. Five patients have not had an operation. The left ventricular outflow tract gradient as assessed at the time of cardiac catheterisation was greater than 50 mmHg. One patient has been lost to follow-up. The remaining four have been followed from four to eight years and have remained asymptomatic and the electrocardiograms have remained unchanged. Careful follow-up of all patients is essential with continuing clinical assessment, electrocardiograms, M-mode and two-dimensional echocardiograms, and if necessary cardiac catheterisation. Prophylaxis against bacterial endocarditis is also essential.

D.C. conversion in patients on amiodarone.

3 patients with atrial fibrillation, of varying origin, have been successfully converted to sinus rhythm by D.C. shock while on the antiarrhythmic drug amiodarone. D.C. shock did not cause rhythm disturbance. D.C. conversion may not be contraindicated in patients taking amiodarone.

Sotalol as a hypotensive agent in pregnancy.

Sotalol, a beta-adrenoceptor blocking drug, was administered to 12 hypertensive pregnant women. The concentration of the drug was assayed in samples of maternal plasma, amniotic fluid and mixed umbilical cord plasma at delivery and, in five mothers who elected to breast feed, in paired samples of maternal plasma and breast milk. Sotalol reduced blood pressure effectively at a mean daily dose of 433.1 +/- 54.1 mg but crossed the placental barrier. The mean maternal: fetal plasma concentration ratio was 1:1.05 and the mean amniotic fluid concentration was 7.0 +/- 2.7 microgram/ml. Delivery occurred at mean gestational age of 37.7 +/- 0.7 weeks; 12 infants were liveborn with a mean weight of 2.8 +/- 0.1 kg and eight of them had no significant neonatal problems. Of the other four, two died from severe congenital anomalies, one had perinatal asphyxia and one mild transient hypoglycaemia. High sotalol concentrations were found in breast milk (mean plasma: milk ratio was 1:5.4) raising the possibility of pharmacological effect in the newborn infant. The results suggest that sotalol adequately controls blood pressure in hypertension complicating pregnancy but because, unlike results from the pregnant ewe, it crosses the human placental barrier it offers no apparent advantages over other beta-adrenoceptor antagonists.

Comparison of the activity and plasma levels of oxprenolol, slow release oxprenolol, long acting propranolol and sotalol.

Observations were made in 5 healthy subjects who exercised before and 1, 3, 6, 8 and 24 h after the oral administration on separate occasions of 160 mg oxprenolol, 160 mg slow release oxprenolol, 160 mg long acting propranolol and 400 mg sotalol. Blood samples were obtained before and at 1, 2, 3, 6, 8, 10 and 24 h after drug administration and assayed for drug concentration. Although the plasma concentration of oxprenolol after S.R. oxprenolol was significantly less at 1 and 2 h and significantly greater at 24 h than after conventional oxprenolol, there was little difference between the effects of the two drugs on an exercise tachycardia. The plasma level of propranolol and the reduction in an exercise tachycardia after L.A. propranolol increased slowly to reach a peak at 6 h and then declined gradually to 24 h. The maximum plasma concentration and effect after sotalol occurred at 3 h and then declined with an elimination half-life of 12.1 h. At 24 h the percentage reduction in an exercise tachycardia was 8.3 +/- 2.5 after oxprenolol, 10.0 +/- 2.3 after S.R. oxprenolol, 18.0 +/- 3.2 after L.A. propranolol and 14.7 +/- 3.4% after sotalol.

Chronic Q fever endocarditis.

Eight patients with chronic Q fever endocarditis were treated with tetracycline for up to 40 months. In addition, five of these patients received co-trimoxazole. Six patients had prosthetic valves. Two patients who had Q fever endocarditis on their native valves required valve replacement because of haemodynamic difficulties: in only one did the Q fever endocarditis contribute to the haemodynamic difficulty. One patient died. It is suggested that medical treatment is continued until clinically and haematologically there is no evidence of endocarditis and the Q fever phase 1 antibody titre is less than 200. No recurrence of Q fever endocarditis has been detected in three of our patients who have now stopped treatment.

Observations on some properties of a long-acting preparation of propranolol.

1. The effects of 160 mg of propranolol and 160 mg of a long-acting (LA) formulation of propranolol were studied in healthy subjects. 2. Both drugs reduced an exercise tachycardia but the peak was less and the 24 h effect greater after long-acting propranolol than after propranolol. 3. These differences were maintained on repeated dosing for 8 days. 4. In contrast to single doses of 400 mg of sotalol, 160 mg of oxprenolol and 160 mg of slow-release oxprenolol, the peak effect of long-acting propranolol was less and that at 24 h was greater.