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Objective: Endoscopic trans-thoracic sympathectomy is a well documented, safe and successful treatment for palmar and axillary hyperhidrosis. This may also be helpful in the management of patients with intractable angina and advanced coronary disease unsuitable for coronary artery bypass graft (CABG) or percutaneous transluminal coronary angioplasty (PTCA). We evaluated video assisted thoracoscopic sympathectomy (VATS) in such patients with the aim of improving symptoms and quality of life., Methods: Video assisted thoracoscopic sympathectomy, a minimally invasive procedure, was performed under general anaesthesia with alternating single lung ventilation. Three stab incisions were made at the level of the fourth intercostal space in the anterior and posterior axillary lines, and at the fifth intercostal space in the mid-axillary line through which an extensive thoracic sympathectomy was performed to include second to the fourth ganglia, bilaterally., Results: A total of 16 patients aged 46-76 (mean 61) years were assessed for VATS. Of these 10 patients had the procedure performed; nine with previous CABG and one with diffuse coronary disease. Six patients were excluded because of an evolving MI (n = 1), left ventricular ejection fraction (LVEF) < 30% (n = 2), and chronic stable angina with no objective evidence of ischaemia (n = 3). All 10 patients had marked symptomatic improvement with reduction of both angina frequency and intensity of attacks. Mean follow-up period 11.5 months. Exercise tolerance and time to onset of angina measured on exercise treadmill was significantly increased post-VATS (P = 0.028) and maintained 1 year post-operative., Conclusion: VATS was associated with both reduction in angina symptoms and an increase in exercise time to onset of angina. An improved quality of life was evident.

We describe a patient with post-infarction left ventricular rupture exhibiting several atypical features. A successful outcome was achieved after serendipitous surgery.

A 45-year-old female presented with typical recent-onset exertional angina pectoris. Subsequent investigation showed that the likely cause was an aberrant origin of the right coronary artery arising from the left coronary sinus. This anomaly is uncommon and is not usually associated with angina pectoris. Surgical rerouting of the origin of the right coronary artery produced complete resolution of ischaemia.

Elevated oestradiol (E2) levels may be a risk factor for ischaemic heart disease in men, although the mechanisms for the elevation of oestrogen and for its adverse effects remain unclear. We have studied 100 Caucasian males undergoing elective coronary angiography for ischaemic chest pain and measured serum oestradiol, a profile of haemostatic tests, extent of coronary artery disease and evidence of previous myocardial infarction in order to assess any relationships which could explain the effect of elevated serum oestradiol levels. Levels were significantly higher in men with a history of myocardial infarction compared to those without (p less than 0.01), but were unrelated to the extent of coronary disease or to the haemostatic tests. These results suggest that the association of oestradiol with coronary events relates to myocardial infarction, not to atherogenesis, and is not due to any currently measurable alterations of haemostasis. Current beta-adrenoceptor blocker treatment was associated with lower oestradiol and thromboxane B2 concentrations (both, p = 0.06). These incidental findings suggest that further studies of the effects of beta-blockade on oestradiol and thromboxane metabolism are indicated.

Pre-discharge exercise tests were performed in 359 survivors of an acute myocardial infarction to determine the frequency, characteristics and prognostic implications of silent ischaemia. Tests were negative in 152 patients (42%), silent ischaemia was observed in 103 (29%) and painful ischaemia in 82 (23%). Heart rates at the development of ischaemia and the final double products were similar in both ischaemic groups but patients with silent ischaemia were able to exercise for longer (13.1 +/- 0.5 min) than those with painful ischaemia (9.3 +/- 0.5 min; P less than 0.0001). The 12 month mortality rose from 2% in patients with a negative test, to 4% in those with silent ischaemia and to 8% in those with painful ischaemia. Re-infarction rates increased similarly across the groups (3%, 8% and 18% respectively). Patients with silent ischaemia subsequently developed angina more frequently (47%) than those with negative tests (16%; P less than 0.001). These results suggest that exercise-induced silent ischaemia following myocardial infarction was common, occurring in 29% of patients. Although the final myocardial oxygen consumption was similar in both ischaemic groups those with silent ischaemia were able to exercise for longer. Finally silent ischaemia conferred an intermediate risk of death or re-infarction and was a strong predictor of subsequent angina pectoris.