Cardiac angiography was reviewed in 91 patients with post-infarction ventricular septal rupture. The results were compared with those of 123 stable survivors who had a positive submaximal exercise test early after infarction. Anterior infarction and occlusion of the infarct vessel were more common in those with ventricular septal rupture than in the comparison group. In the group with ventricular septal rupture there was more left ventricular damage, with aneurysm formation in two thirds, and coronary angiography showed more single than triple vessel disease. In the comparison group there was more triple vessel disease than single vessel disease. Angiographically demonstrable collaterals to the infarct territory were not seen or only very faintly seen in 82% of those with septal rupture. Well developed collaterals were seen in two thirds of the comparison group. These patterns of coronary disease suggest that ventricular septal rupture is more likely in patients with coronary occlusion and little or no collateral support to the infarct territory.

Objective-To determine whether diabetic patients with coronary artery disease are more likely to experience silent myocardial ischaemia than subjects without diabetes. Subjects-Patients undergoing coronary angiography at a regional cardiothoracic unit, identified as having diabetes from the local district diabetic register/ database. Design-The coronary angiograms and exercise treadmill tests of 100 diabetic and 100 non-diabetic patients who all had significant coronary artery disease and maximal eVort exercise tests were reviewed.Patients were individually matched for age group, gender, severity of coronary artery disease, and indication for treadmill test. Outcome measures-Significant coronary artery disease was defined as a stenosis of greater than 50% diameter in at least one of the major coronary artery segments. Exercise tests were graded as positive if the electrocardiographic (ECG) recording showed planar or downsloping ST segment depression of >1 mm in more than two leads at 80 ms post J-point or if there was a blood pressure fall >10 mm Hg after an initial rise. A negative exercise test was defined as one in which the subject experienced no pain, had no ECG changes after maximal eVort and had a normal blood pressure response. Subjects who did not experience any form of typical angina-type pain during a positive exercise test were defined as having an episode of silent ischaemia. Patients with symptomatic ischaemia were those who experienced typical angina-type pain with accompanying ST segment changes. Patients with a negative exercise test were defined as having "undetermined ischaemia". This category included all those without ECG evidence of myocardial ischaemia during the exercise test (with or without accompanying chest pain). Results-In the diabetic patients, 34% had ECG evidence of silent ischaemia on treadmill testing compared with only 19% of the non-diabetic controls (p<0.02). Conclusions-This study shows that diabetic patients with proved coronary artery disease have a higher risk of developing silent myocardial ischaemia during exercise than non-diabetic patients. (Postgrad Med J 2001;77:395-398)

Asymptomatic ("silent") ischaemia has been shown to be of prognostic significance in patients with stable and unstable angina and more recently in patients recovering after myocardial infarction. No therapeutic regimen has yet been shown to improve the prognosis of patients with silent ischaemia after infarction, which can be found in as many as a third of these patients. Attempts to achieve therapeutic revascularisation in all these patients may be undesirable, but early revascularisation could be especially beneficial in some selected high risk patients. Two hundred and fifty consecutive clinically stable survivors of myocardial infarction who had predischarge submaximal exercise tests were followed up for a year. Silent ischaemia was found in 27% of these patients; 15% had symptomatic ischaemia. Patients with a positive exercise test were prescribed a beta blocker before discharge. Mortality in patients with silent (9.4%) and symptomatic (5.4%) ischaemia in the first year after infarction was not significantly different. Patients with symptomatic ischaemia were more likely to have undergone coronary artery bypass grafting in the first year. Patients with silent ischaemia were, however, significantly more likely to die than patients with a negative exercise test (relative odds 12:1). Patients with silent ischaemia and an abnormal blood pressure response or who could not complete a submaximal exercise protocol were at particularly high risk, being 32 times more likely to die than those with a negative test (95% confidence interval from 3.3 to 307 times more likely). First year mortality in this group was 22%. The benefits of therapeutic revascularisation in this high risk group need to be studied.

Acute coronary syndromes are responsible for the deaths of tens of thousands of patients every year. Rupture of coronary atheromatous plaques with resultant luminal thrombosis is the cause in most cases. Although great steps forward have been taken in the management of acute myocardial infarction (MI) and unstable angina (UA), new therapeutic strategies are required to reduce further the incidence and risk of these events. At present, aspirin, nitrates and heparin are the conventional treatments for unstable angina. Aspirin, in combination with a thrombolytic agent or with percutaneous transluminal coronary angioplasty (PTCA), has been shown to be effective in reducing mortality in acute MI. Heparin is conventionally used in all PTCA procedures, whereas its efficacy in enhancing the therapeutic role of thrombolytic agents remains uncertain and may depend on the thrombolytic agent used. PTCA, which is also an effective therapy for stable angina, can be complicated by intimal dissection and thrombosis in a minority of cases, with vessel restenosis leading to recurrent symptoms in approximately 30% of cases. A number of new agents are being evaluated in both acute coronary syndromes and PTCA. These can be classified as adenosine diphosphate (ADP) receptor antagonists, Factor Xa inhibitors (low-molecular weight heparin [LMWH], direct thrombin inhibitors, new thrombolytic agents and glycoprotein IIb/IIIa receptor blockers. Of the latter, the most studied is abciximab, the Fab fragment of the chimeric monoclonal antibody, 7E3. This is a potent inhibitor of platelet aggregation. Four major clinical studies of PTCA in high-risk patients have demonstrated clear efficacy of abciximab in reducing acute ischaemic complications, mainly by reducing the frequency of MI and the need for repeat revascularisation. Unlike other glycoprotein IIb/IIIa receptor blockers, both short- and long-term efficacy have been demonstrated. Its impact on the rate of restenosis after PTCA is unclear. Abciximab's role in an era of intracoronary stent implantation is undergoing further study (with encouraging early results). Its role in other situations, such as the early (non-angioplasty) management of unstable angina and its ability to enhance the efficacy of thrombolytic agents, is under active investigation.

Conclusion Cardiac readmission's continue to occur after 10% of percutaneous coronary intervention procedures. Whilst the prognosis is good, measures to reduce these rates are required.