Key result
Perfusion defects provoked by transient coronary occlusion during PTCA showed similar size and severity to myocardial damage after infarction (e.g., LAD defect index 28.4% vs 27.1%).
Why the study?
Does 99Tcm-sestamibi injection during transient coronary occlusion delineate the myocardial area at risk similarly to myocardial damage observed after infarction?
Observational (n=72)
Does 99Tcm-sestamibi injection during transient coronary occlusion delineate the myocardial area at risk similarly to myocardial damage observed after infarction?
Perfusion defects provoked by transient coronary occlusion during PTCA closely match the topography and extent of myocardial damage observed after infarction in the same vascular territories.
99Tcm-sestamibi during PTCA may delineate area at risk; supports similarity in this cohort but leaves prospective validation open.
A peripheral perfusion tracer injection at the time of coronary occlusion during percutaneous transluminal coronary angioplasty (PTCA) may delineate the myocardial ‘area at risk’ related to a given artery. To evaluate the location, size and severity of the corresponding scintigraphic defects, we conducted a prospective study of 36 patients who received a 99Tcm-sestamibi injection during single-vessel coronary angioplasty (PTCA=18 LAD, 16 RCA and 2 LCX) followed by SPET. For comparison, a reference group of 36 successive patients examined during the early phase of myocardial infarction (MI), matched for the same vascular territories (18 anterior, 16 inferior and 2 lateral), were analysed in the same way after standard stress/reinjection 201Tl SPET. The imaging characteristics of both groups showed excellent agreement as well degree of uptake defects, in terms of topography and extent. A defect index, taking into account both size and severity, was in the same range for PTCA and MI patients (mean±standard deviation): for LAD vs anterior = 28.4±13.5% (PTCA), 27.1±12.2% (MI-stress) and 24.2±10.0% (MI-reinjection); for RCA vs inferior = 15.5±10.2% (PTCA), 14.7±9.7% (MI-stress) and 13.2±8.2% (MI-reinjection). Sectoral correlations between PTCA and MI groups were also highly significant.
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Bontemps et al. (2000) conducted an observational in Coronary artery disease and myocardial infarction (n=72). 99Tcm-sestamibi SPET during PTCA vs. 201Tl SPET during early phase of MI was evaluated on Defect index (size and severity). Perfusion defects provoked by transient coronary occlusion during PTCA showed similar size and severity to myocardial damage after infarction (e.g., LAD defect index 28.4% vs 27.1%).
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