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Indium-111 antimyosin scintigraphy was performed in 24 consecutive patients after percutaneous transluminal coronary angioplasty to assess whether repeated periods of ischaemia during balloon inflation results in myocardial cell damage even after a successful procedure. Patients with unstable angina, prior myocardial infarction and whose procedure was complicated were excluded. Indium-111 monoclonal antimyosin antibodies (80 MBq) were injected 24 h after coronary angioplasty and planar images were collected 24 h later. The relative antimyosin uptake was assessed subjectively and by a heartllung count density ratio. In addition, the intracardiac gradient of activity was assessed by a count density profile analysis of the cardiac region of interest to distinguish better the focal as opposed to the diffuse antimyosin uptake. The antimyosin uptake index was calculated by multiplying the heartllung ratio to the intracardiac gradient of activity. After coronary angioplasty, nine patients had minor ST-T wave changes on the surface ECG, but no patient demonstrated a new Q wave. Only three patients showed a mild rise in cardiac enzyme (CK-MB) serum levels. Indium-Ill antimyosin uptake (heartllung>1.55) was present in eight patients (33%) and was intense (heartllung>1.9) in five (21%). Antimyosin uptake was always seen in myocardial segments corresponding to the treated coronary artery. Patients with a positive antimyosin scan had a longer duration of balloon-induced ischaemia compared with patients with no evidence of antimyosin uptake (541 ± 211 vs 331 ± 137 s , P 500 s. There was a significant correlation between the antimyosin index and the total duration of ischaemia during the procedure ( r =0.76, P

We describe a case of fatal myocardial rupture and tamponade following a successful transcoronary chemical ablation of incessant ventricular tachycardia. Pathological examination showed a subepicardial dissection of the heart at the ablation site with fibrous and fatty degeneration of the myocardium. The present report calls for caution, underlying a possible lethal complication of ethanol ablation which has not been described before.

Background: Application of the traditional diagnostic criteria validated for exercise testing may be inappropriate when dobutamine infusion is associated with radionuclide ventriculography (RNV). The objective of this study was to establish appropriate diagnostic criteria for evaluation of dobutamine stress testing with RNV for the detection of early postinfarction ischemia. Methods: RNV was performed at baseline and during dobutamine infusion in 10 control subjects and in 30 patients who were studied within 1 week after uncomplicated myocardial infarction. Several quantitative parameters including left ventricular ejection fraction (EF), regional EF, and absolute change in global and regional EF were tested. In addition, regional wall-motion changes were scored by visual analysis. The limit of normal response for each quantitative parameter was defined as the 95th percentile of the distribution observed in control subjects. On the basis of predischarge clinical evaluation and exercise stress testing, patients were grouped as having evidence of residual ischemia (group 1, 15 patients) or no evidence of ischemia (group 2, 15 patients). Sensitivity, specificity, and accuracy in the detection of postinfarction ischemia were calculated for each parameter, and empiric receiver-operating characteristic curves were generated. Results: The limits of the normal response to dobutamine infusion in the control subjects were found to be a 7.5% and a 12.5% increase in global EF at low and high dose, respectively. Median baseline EF was significantly lower in patients than in control subjects (Mann-Whitney U test: P < .001). There were no differences in resting EF between group 1 and group 2 patients. However, median high-dose EF and increase in EF were significantly lower in group 1 as compared with group 2 patients (56% vs 72% and 5% vs 17%, respectively; Mann-Whitney U test: P < .0001 for both). A biphasic (up-and-down) response with initial increase at low dose followed by decrease or no change in EF at high dose was observed in 66% of group 1 patients and only in 13% of group 2 subjects. The best criterion for detection of postinfarction ischemia was a change of

Emergency percutaneous transluminal coronary angioplasty (PTCA) was performed during an acute myocardial infarction (AMI) after either systemic or intracoronary thrombolytic therapy in six patients with severe ischaemic left ventricular dysfunction or cardiogenic shock, among 37 patients (17%) who were treated with PTCA during AMI over a 13-month period. Thrombolytic therapy with streptokinase (1.5×10 Units) was initiated after a mean (± SD) time delay of 55±1.3 h from the onset of symptoms. The infarct-related artery was found to be occluded (TIMI grade 0–1) in three patients and partially reperfused (TIMI grade 2) in the remaining patients at baseline coronary angiography. Intracoronary administration of urokinase (100–200 000 Units) was ineffective in those patients failing systemic thrombolysis and resulted in only a slight increase of residual lumen in three patients. The coronary artery could be opened by a guidewire mechanical technique in patients with persistent coronary artery occlusion and coronary dilation could be done in all patients. The mean percentage diameter stenosis of the infarct-related vessel was reduced from 98.8 ± 2% to 27±11% ( P < 0.005). After the procedure, left ventricular ejection fraction increased from 27±8% to 41±7% ( P

SummaryPlatelet count, and plasma thromboxane B2 (TXB2) and circulating platelet aggregates (CPA) were determined in the coronary sinus (CS), aortic bulb (AO) and cubital vein (V) in 21 patients with stable angina and in 6 control subjects before and after atrial pacing (AP). TXB2 measurements were repeated before and after AP in 6 of the 21 angina patients after 15 days’ sulphinpyrazone treatment. Platelet count and CPA ratio were similar in angina patients and controls at all three sampling sites and were unchanged at AP peak. In the controls, basal TXB2 values in CS, AO and V were not significantly different and were unchanged at AP peak. In the angina patients compared with the controls, basal TXB2 values in the AO, CS and V were not significantly different whereas the CS/AO TBX2 ratio was significantly higher; at AP-induced ischaemia, CS TXB2 was significantly increased and the CS/AO TXB2 ratio was increased. A weak but significant direct correlation was found between CS/ AO TXB2 ratio and coronary score. Sulphinpyrazone treatment reduced CSTXB2 levels at rest and after AP, but not the ischaemic threshold at AP.