Quantification of Cardiac Kinetic Energy and Its Changes During Transmural Myocardial Infarction Assessed by Multi-Dimensional Seismocardiography

Abstract

Introduction: Seismocardiography (SCG) records cardiac and blood-induced motions transmitted to the chest surface as vibratory phenomena. Evidences demonstrate that acute myocardial ischemia (AMI) profoundly affects the SCG signals. Multidimensional SCG records cardiac vibrations in linear and rotational dimensions, and scalar parameters of kinetic energy can be computed. We speculate that AMI and revascularization profoundly modify cardiac kinetic energy as recorded by SCG. Methods: Under general anesthesia, 21 swine underwent 90 min of myocardial ischemia induced by percutaneous sub-occlusion of the proximal left anterior descending (LAD) coronary artery and subsequent revascularization. Invasive hemodynamic parameters were continuously recorded. SCG was recorded during baseline, immediately and 80 min after LAD sub-occlusion, and immediately and 60 min after LAD reperfusion. iK was automatically computed for each cardiac cycle (iK ^CC ) in linear (iK _Lin ) and rotational (iK _Rot ) dimensions. iK was calculated as well during systole and diastole (iK ^Sys and iK ^Dia , respectively). Echocardiography was performed at baseline and after revascularization, and the left ventricle ejection fraction (LVEF) along with regional left ventricle (LV) wall abnormalities were evaluated. Results: Upon LAD sub-occlusion, 77% of STEMI and 24% of NSTEMI were observed. Compared to baseline, troponins increased from 13.0 (6.5; 21.3) ng/dl to 170.5 (102.5; 475.0) ng/dl, and LVEF dropped from 65.0 ± 0.0 to 30.6 ± 5.7% at the end of revascularization (both p < 0.0001). Regional LV wall abnormalities were observed as follows: anterior MI, 17.6% (three out of 17); septal MI, 5.8% (one out of 17); antero-septal MI, 47.1% (eight out of 17); and infero-septal MI, 29.4% (five out of 17). In the linear dimension, ${iK}_{Lin}^{CC}$ , ${iK}_{Lin}^{Sys}$ , and ${iK}_{Lin}^{Dia}$ dropped by 43, 52, and 53%, respectively (p < 0.0001, p < 0.0001, and p = 0.03, respectively) from baseline to the end of reperfusion. In the rotational dimension, ${iK}_{Rot}^{CC}$ and ${iK}_{Rot}^{Sys}$ dropped by 30 and 36%, respectively (p = 0.0006 and p < 0.0001, respectively), but ${iK}_{Rot}^{Dia}$ did not change (p = 0.41). All the hemodynamic parameters, except the pulmonary artery pulse pressure, were significantly correlated with the parameters of iK, except for the diastolic component. Conclusions: In this very context of experimental AMI with acute LV regional dysfunction and no concomitant AMI-related heart valve disease, linear and rotational iK parameters, in particular, systolic ones, provide reliable information on LV contractile dysfunction and its effects on the downstream circulation. Multidimensional SCG may provide information on the cardiac contractile status expressed in terms of iK during AMI and reperfusion. This automatic system may empower health care providers and patients to remotely monitor cardiovascular status in the near future.

Keywords: acute myocardial infarction; animal model for acute coronary syndrome; cardiac monitoring; kinetic energy; seismocardiography.

Figure 1

Modifications of HR, CO, and pulse pressure parameters during coronary sub-occlusion and reperfusion. HR, heart rate; CO, cardiac output; LV PP, pulse pressure of LV pressure; Ao PP, pulse aortic pressure; Fem PP, femoral pulse pressure; PA PP, pulse pressure of pulmonary artery pressure; BSL, baseline; AMI_t0−t80, acute myocardial infarction at t0 and t80, respectively; RE_t0−t60, reperfusion at t0 and t60, respectively. A generalized mixed model was used, with time as the fixed factor. The level of significance was set at 0.05. *p < 0.05; **p < 0.01; ***p < 0.0001. Data are presented as mean ± SEM for each variable (N = 17).

Figure 2

Modifications of parameters of iK during coronary sub-occlusion and reperfusion. ${iK}_{Lin}^{CC}$, ${iK}_{Lin}^{Sys}$, ${iK}_{Lin}^{Dia}$, iK of seismocardiography (SCG) in the linear dimension computed over the whole cardiac cycle (CC), the systolic phase (Sys), and the diastolic phase (Dia), respectively; ${iK}_{Rot}^{CC}$, ${iK}_{Rot}^{Sys}$, ${iK}_{Rot}^{Dia}$, iK of SCG in the rotational dimension computed over the whole CC, Sys, and Dia, respectively; BSL, baseline; AMI_t0−t80, acute myocardial infarction at t0 and t80, respectively; RE_t0−t60, reperfusion at t0 and t60, respectively. A generalized mixed model was used, with time as the fixed factor. The level of significance was set at 0.05. *p < 0.05; **p < 0.01; ***p < 0.0001. Data are presented as mean ± SEM for each variable (N = 17).

Figure 3

Representative figure showing the evolution of waveforms of iK computed from the seismocardiography (SCG) signals during the experimental procedure, specifically during baseline (BSL), AMI_t0, AMI_t80, RE_t0, RE_t60. The two solid lines [from the beginning of the P wave of beat n to the beginning of the P wave of beat n + 1 on the synchronous electrocardiogram (ECG)] denote the iK computed over the whole cardiac cycle (iK_CC). The waveforms between the solid line and the dotted line (from the beginning of the P wave to the end of the T wave of beat n on the synchronous ECG) represent the iK of the systolic wave (iK_Sys). The waveforms between the dotted line and the solid line (from the end of the T wave of beat n to the beginning of the P wave of beat n + 1 on the synchronous ECG) represent the iK of the diastolic phase (iK_Dia). (A) ECG. (B) iK in the linear dimension. (C) iK in the rotational dimension. Linear (B) and rotational (C) iK drop at the onset of coronary sub-occlusion (AMI_t0), compared to BSL, remains far below baseline values during the whole duration of AMI (AMI_t80) and returns to normal level during reperfusion (RE_t0−t60). BSL, baseline; AMI t0-t80, acute myocardial infarction at t0 and t80, respectively; RE t0-t60, reperfusion at t0 and t60, respectively; iK, integral of kinetic energy (J·s).