Campylobacter myocarditis; loose bowels and a baggy heart.

We report an unusual case of acute myocarditis associated with Campylobacter jejuni enterocolitis leading to severe impairment of left ventricular systolic function. Contrast-enhanced cardiac magnetic resonance imaging was used to confirm the presence of acute myocardial inflammation and its resolution.

Health service costs of coronary angioplasty and coronary artery bypass surgery: the Randomised Intervention Treatment of Angina (RITA) trial.

For some patients with coronary artery disease, percutaneous transluminal coronary angioplasty (PTCA) is an alternative to coronary artery bypass grafting (CABG). We report comparative health service costs of these interventions within the Randomised Intervention Treatment of Angina (RITA) trial. Medications were costed at published UK prices; other resource use was costed with a set of unit costs estimated at two recruiting centres to the RITA trial, one in London and one outside. Over 2-year follow-up of 1011 patients, the estimated mean additional cost for those randomised to CABG compared with PTCA was 1050 pounds (95% CI 621 pounds-1479 pounds), with unit costs from the non-London centre, and 1823 pounds (1202 pounds-2444 pounds), with unit costs from the London centre. The initial average cost of treating a patient randomised to PTCA is about 52% of that of CABG, but after 2 years this increased to about 80% because of the greater need for subsequent interventions. The balance of advantage between PTCA and CABG may change after several years: funding has been obtained to continue RITA follow-up for 10 years. However, on the basis of patients' status at 2 years, the cost advantages of PTCA cannot be ignored. Further research is necessary to assess whether the advantage of PTCA in terms of cost is translated into one of cost-effectiveness.

Influence of angiotensin converting enzyme inhibition on exercise performance and clinical symptoms in chronic heart failure: a multicentre, double-blind, placebo-controlled trial.

One hundred and seven patients with chronic heart failure (NYHA class II to IV) stabilized on digitalis and/or diuretics, recruited from 11 centres were randomized into a double-blind, placebo-controlled study to assess the effect of 12 weeks of cilazapril therapy on exercise tolerance and clinical status. Thirty-five patients were randomized to placebo and 72 to cilazapril at a starting dose of 1 mg daily; titration to cilazapril 2.5 mg at week 4 and 5 mg at week 8 (or matching placebo) was carried out in patients who did not improve clinically. Demographic characteristics, including exercise test duration increased from 402 s (+/- 17 SEM) at baseline to 462 s (+/- 19 SEM) at week 12 for the cilazapril group (+15%) and from 405 s (+/- 23 SEM) at baseline to 408 s (+/- 30 SEM) at week 12 in patients on placebo (+1%) (P < 0.001). In the placebo group, patients able to exercise for more than 6 min at baseline showed an increase in exercise duration at week 12 while those able to exercise for up to 6 min at baseline showed a decrease (P = ns). In contrast, cilazapril-treated patients showed an increase in exercise tolerance regardless of baseline exercise test duration; patients with the most impaired exercise tolerance at baseline showed a greater improvement than patients with mildly impaired baseline exercise tolerance (P < 0.05 vs placebo). NYHA class improved by at least one grade in 51% of the cilazapril group vs 32% in the placebo group (P = ns). At the end of the trial, 15% of the patients were non-responders on cilazapril vs 41% on placebo (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of enalapril and bendrofluazide for treatment of systemic hypertension.

The antihypertensive and biochemical effects of the angiotensin-converting enzyme inhibitor enalapril were compared with those of the thiazide diuretic bendrofluazide. Patients with untreated mild to moderate essential hypertension were entered into a randomized, double-blind, double-dummy, parallel-group study. Blood pressure (BP) decreased significantly (p less than 0.001) with either drug therapy: from 172/103 to 147/87 mm Hg (n = 18) with enalapril and from 179/104 to 165/95 mm Hg (n = 22) with bendrofluazide; thus, enalapril produced a greater reduction (p less than 0.05) than bendrofluazide. The median dose of enalapril was 20 mg/day (range 10 to 40) and that of bendrofluazide was 5 mg/day (range 2.5 to 10). Both drugs reduced serum sodium levels by small amounts. This was significant only for enalapril (decrease of 1.3 mmol/liter, p less than 0.05). Hyponatremia was not seen in any patient. Three patients were withdrawn from each treatment group due to adverse effects, although both drugs were generally well tolerated.

Trial of early nifedipine in acute myocardial infarction: the Trent study.

Over 30 months 9292 consecutive patients admitted to nine coronary care units with suspected myocardial infarction were considered for admission to a randomised double blind study comparing the effect on mortality of nifedipine 10 mg four times a day with that of placebo. Among the 4801 patients excluded from the study the overall one month fatality rate was 18.2% and the one month fatality rate in those with definite myocardial infarction 26.8%. A total of 4491 patients fulfilled the entry criteria and were randomly allocated to nifedipine or placebo immediately after assessment in the coronary care unit. Roughly 64% of patients in both treatment groups sustained an acute myocardial infarction. The overall one month fatality rates were 6.3% in the placebo treated group and 6.7% in the nifedipine treated group. Most of the deaths occurred in patients with an in hospital diagnosis of myocardial infarction, and their one month fatality rates were 9.3% for the placebo group and 10.2% for the nifedipine group. These differences were not statistically significant. Subgroup analysis also did not suggest any particular group of patients with suspected acute myocardial infarction who might benefit from early nifedipine treatment in the dose studied.

The vasomotor centre and its afferent pathways.

1. Experiments were carried out on two groups of anaesthetized greyhounds. The response of the first group to infusions of angiotensin II into a vertebral artery for 5 min and to bilateral occlusion of the common carotid arteries for 2 min was studied before and after bilateral ablation of the areas postrema. The response of the second group to infusions of angiotensin and to carotid occlusion was studied before and after mid-collicular transection of the midbrain. 2. Bilateral ablation of the areas postrema abolished the response to angiotensin infused into a vertebral artery at the dose used but did not significantly alter the response to carotid occlusion. Transection of the midbrain did not abolish the response to either procedure. 3. It is concluded that the structures involved in the cardiovascular response to carotid occlusion are anatomically distinct from the area postrema and that neither response requires the integrity of connections above the pons. 4. An attempt has been made to construct a schematic diagram of the vasomotor centre.

Importance of central vasomotor effects in angiotensin-induced hypertension.

Ablation of the areas postrema in 10 dogs caused a highly significant reduction in the pressor response to intravenous infusions of angiotensin yet was without significant effect on the pressor response to intravenous infusions of noradrenaline. The reduction in the pressor response to angiotensin is almost certainly due to abolition of the specific central autonomic effects of the hormone which are dependent on the integrity of the areas postrema. It is suggested that this central effect also contributes to the cardiovascular response to endogenous angiotensin.