Adenosine-induced chest pain: is it due to myocardial ischaemia? Clinical, electrocardiographic, haemodynamic and metabolic study.

Adenosine has recently been demonstrated to be a mediator of angina in human beings. The present study was undertaken to document the presence or absence of myocardial ischaemia on clinical, haemodynamic, electrocardiographic and metabolic evidences after intracoronary administration of adenosine. Fifteen patients with chronic stable angina (12 males and 3 females), positive exercise stress test and documented significant stenosis of the left anterior descending coronary artery (LAD) were included in the study. The surface and intracoronary electrocardiograms (ECGs), pulmonary artery diastolic pressure and coronary sinus lactate levels were monitored at baseline and after intracoronary administration of adenosine in all patients. Adenosine was administered intracoronary in doses of 1000-8000 microgram depending on the provocation of chest pain. Typical angina was observed in all patients. There were no signs of ischaemia on surface or intracoronary ECG. There was no statistically significant difference between the pulmonary artery diastolic pressure and coronary sins lactate levels at baseline and post-adenosine administration (p > 0.05). It is concluded that intracoronary administration of adenosine produces chest pain in patients with chronic stable angina by mechanism other than myocardial ischaemia.

Coronary artery stenting in acute myocardial infarction.

Little information is available on the use of coronary stents to treat suboptimal results during direct angioplasty in acute myocardial infarction (AMI). In this study, we report 16 cases of AMI who underwent stent implantation in infarct-related artery for suboptimal results and their 6 months angiographic follow-up. Immediate angiographic success was achieved in all patients. The minimal luminal diameter increased from 0.06 +/- 0.12 mm to 2.89 +/- 0.12 mm (p < 0.001). One patient died in the hospital on day 8 due to subacute stent thrombosis. No patient required emergency bypass surgery. Two patients required blood transfusion for groin haematoma and one required intracoronary thrombolysis. All patients underwent exercise stress test at 1 month and at 3 months and coronary angiography at 4 months or earlier it indicated. At the end of 6 months follow-up, 4 patients had a positive exercise test and coronary angiography revealed angiographic restenosis in 3 and progression of disease in other vessels in 1 patient. We conclude that stent deployment is a viable option to treat suboptimal results after direct angioplasty in AMI.