T-wave alternans (TWA) has been linked to increased vulnerability to ventricular fibrillation in different settings including myocardial ischemia. In this study, we propose a methodology for the characterization of TWA induced by transient, regional ischemia. We studied the prevalence, magnitude and spatio-temporal relationship between TWA and ischemia in 95 patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Two electrocardiogram records of each patient, a control recording before PTCA and the PTCA record, were analyzed using a robust, recently proposed method for TWA analysis. The detected episodes were characterized in terms of their time-course, lead distribution and alternans waveform. One third of the patients (33.7%) showed TWA episodes during PTCA. The highest prevalence (51.7%) and amplitude were found in patients with left anterior descendent artery occlusion. The onset of TWA was detected after the first 1-2 min of occlusion, suggesting that some level of ischemia must be attained before TWA arises, while disappearance of TWA following reperfusion was much more rapid. The TWA lead distributions and waveforms showed distinct distributions according to the occluded artery reflecting the regional nature of the TWA phenomenon.

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Percutaneous transluminal coronary angioplasty provides an excellent opportunity to investigate the location and quantity of hypoperfusion during sudden complete occlusion of one of the major coronary arteries. Thirty-five patients referred for elective percutaneous transluminal coronary angioplasty were injected intravenously with 99mTc-sestamibi during balloon inflation. To visualize and quantify the hypoperfused region, a map of perfusion was constructed from that occlusion study and from the control study performed on the following day. Patients were divided into groups according to proximal or distal occlusion within each of the three coronary arteries. The region of myocardium supplied by each coronary artery varied in location and extended outside the typical borders for all arteries, but most prominently for the left circumflex coronary artery. The quantities of hypoperfusion varied within each artery group, but the average hypoperfusion was greater for the left anterior descending coronary artery than for either the right coronary artery or the left circumflex coronary artery. It is concluded that the quantities of hypoperfusion were highly variable within each artery group. Occlusion of the left anterior descending coronary artery was associated with the largest ischaemic region. The area of hypoperfusion extended outside the typical borders, most prominently for the left circumflex coronary artery.

1 Blood plasma and free lignocaine concentrations have been measured 12 h after beginning a constant infusion of 2 mg/min and again at the end of the infusion (36‐72 h) in five patients with myocardial infarction (MI) and compared with five control patients who did not develop objective evidence of MI. 2 In MI patients, total plasma concentration rose significantly between 12 h and the end of infusion. Because of an increase in alpha 1 acid glycoprotein (AAG) plasma binding increased, so that free drug concentration did not change. The rise in whole blood concentration was less than that in plasma as a result of drug redistribution out of red cells due to enhanced binding. 3 In control patients, neither blood nor plasma concentrations changed with time and plasma binding remained constant. Free drug concentrations, however, rose slightly. 4 The concentrations of GX and MEGX remained unchanged in all patients, but the ratio of lignocaine/MEGX concentrations fell in controls but rose in MI patients. 5 Pharmacokinetic modelling suggested that at least some of the rise in blood lignocaine concentration was due to reduced clearance resulting from enhanced plasma binding. 6 We conclude that the rise in AAG following MI is responsible for increased plasma binding and drug redistribution within blood. These changes, together with a reduction in lignocaine clearance, can explain much of the phenomenon of lignocaine accumulation in MI.

The incidence and prognosis of myocardial infarct extension were studied prospectively among patients presenting without symptomatic heart failure (Killip class I or II). Infarct extension was defined as a new clinical event (recurrent pain, arrhythmias or worsening hemodynamic status) that occurred at least 24 hours after a documented myocardial infarction and accompanied by at least two of the following: 1) new