Abstract 246: Dissociation Between Hemodynamic and Electrocardiographic Indices of Spontaneous Myocardial Ischemia in Telemetered Swine with Hibernating Myocardium and Sudden Death
Background: Swine with a chronic LAD stenosis develop hibernating myocardium without infarction as a consequence of repetitive episodes of reversible ischemia. This study was performed to identify the relation between hemodynamic and electrocardiographic indices of ischemia before sudden cardiac death (SCD) compared to spontaneous sympathetic activation in survivors and sham controls.
Methods: Swine (n=26) were chronically instrumented with a 1.5 mm proximal LAD stenosis and a 3 channel telemetry system (DSI) capable of continuously digitizing LV pressure, a subepicardial ECG, and surface ECG at 1000 Hz. Unrestrained animals were monitored for up to 5 months or until SCD. Hemodynamics and ECG changes at rest and during sympathetic activation were compared to sham controls (n=6).
Results: Microsphere flow measurements 3 months after a chronic LAD stenosis showed a critical reduction in LAD subendocardial flow reserve (Adenosine/ Rest flow, 1.1 ± 0.3 vs. 5.4 ± 0.5 in remote, p<0.001). The Table⇓ shows hemodynamic and ECG parameters 66 ± 3 days after instrumentation. All episodes of SCD occurred during sympathetic activation and were secondary to VT degenerating into VF, without pathological infarction. ST deviation from baseline was infrequent (5 of 26), and was no different between survivors with hibernating myocardium and those with SCD. In contrast, all animals with an LAD stenosis developed increases in LV end-diastolic pressure (EDP) during sympathetic activation. LV +dP/dt at a similar peak heart rate was lower in animals with SCD than those that survived.
Conclusion: These data indicate that 1) subendocardial ischemia that is sufficient to lead to apoptosis-induced myocyte loss from reversible ischemia in hibernating myocardium is frequently electrocardiographically silent but leads to transient increases in LVEDP, and 2) the extent to which LVEDP is increased or the frequency of ST changes are no different in animals that develop SCD than those that survive.