Abstract 4368095: A New Analytical Approach for Noninvasive Reconstruction of the Entire Left Ventricular Pressure Waveform in Myocardial Ischemia and Infarction

Introduction: Left ventricular pressure (LVP) waveforms offer critical insight into cardiac function after myocardial infarction. LVP is typically assessed via invasive catheterization, limiting routine use and longitudinal monitoring. We propose a novel analytical approach to reconstruct the entire LVP waveform using only carotid pressure waveforms (now measurable noninvasively with a phone camera) and standard echocardiography. We validated the method under normal and acute physiological conditions in an experimental model of myocardial ischemia and myocardial infarction (MI). Methods: Thirty-nine Sprague Dawley rats (28% female) were anesthetized and underwent coronary artery occlusion/reperfusion (30 min occlusion, 3 h reperfusion). Simultaneous LV and carotid pressures (via Millar Mikro-Tip catheters) and echocardiograms were recorded. LVP waveforms were reconstructed using a novel five-step analytical method at baseline, 15 min post-occlusion (ischemia), and 3 h post-reperfusion (acute MI, confirmed by TTC staining) for total of 71 cases. The reconstruction approach incorporated models of ventricular relaxation, diastolic filling, and systolic ejection governed by arterial-ventricular coupling, with constraints on temporal and morphological continuity of the waveform. Reconstructed waveforms were compared to invasive LVP recordings. Evaluation focused on accuracy in key clinical ischemia/MI metrics, including LV end-diastolic pressure (LVEDP) and subendocardial viability ratio (SEVR). SEVR is calculated as the ratio of myocardial oxygen supply to demand, serving as a surrogate for myocardial perfusion and correlates with cardiovascular risk. Results: Reconstructed LVP waveforms from carotid pressure closely matched invasive measurements during control, ischemia, and infarction (Figure 1). Reconstructed LVEDP strongly correlated with catheter measurements (Figure 2; r = 0.91), capturing its elevation during ischemia and partial recovery post-reperfusion. SEVR derived from reconstructions also closely matched invasive values (Figure 3; r = 0.96). Conclusions: Our findings show that the algorithm accurately reconstructs LVP waveforms and predicts clinically relevant metrics across physiological states. It captured elevated LVEDP and reduced SEVR during ischemia, with partial recovery after reperfusion. These results support its potential for noninvasive, longitudinal monitoring of left ventricular pressure in managing heart failure and myocardial infarction.