Cardiac Mechanoenergetics in Patients With Acute Myocardial Infarction
Highlights
- End-systolic pressure-volume relationship (ESPVR) is defined by the line connecting the left upper corner of multiple pressure-volume (PV) loops under different LV loading conditions (preload and afterload). It provides the maximal LV pressure at any given LV volume, that is, ESPVR represents the LV systolic property (View Highlight)
- The X-intercept of ESPVR is V0, that is, unstressed LV volume (View Highlight)
- The slope of ESPVR, end-systolic elastance (Ees), which has been also referred to as Emax based on the time-varying elastance model,27,29 load-independently represents LV contractility (View Highlight)
(View Highlight)- As the LV volume increases to a higher range, the LV pressure also rises more steeply. The elastin fibers, myocytes, and titin molecules in a sarcomere play a role in the process of forming LV stiffness.38, 39, 40 At higher LV pressure and volume ranges, the collagen fibers and titin are overstretched, resulting in further resistance (View Highlight)
- Effective arterial elastance (Ea) is a conceptual framework of total afterload imposed on LV, which integrates arterial stiffness and peripheral arterial resistance, and is calculated by measuring the ratio of ventricular end-systolic pressure to stroke volume (Ea = ESP/SV) (View Highlight)
- The interaction between the LV and aorta known as ventricular-arterial coupling is essential in cardiovascular function, and therefore, the ratio of Ea to ESPVR (Ea/Ees) obtained from the PV diagram is often used to elucidate mechanical efficiency and performance of the ventricular-arterial system (View Highlight)
(View Highlight)- PE is residual mechanical energy stored in myocardium at end-systole, which is not released as external work, and is believed to be dissipated as heat during relaxation15 (View Highlight)
- There is a linear correlation between PVA and myocardial oxygen consumption (Vo2) per beat.14,22,26,51, 52, 53, 54, 55 Because PVA has the dimensions of energy (1 mm Hg·mL = 1.33 × 10−4 J), the concept of PVA can provide a valuable framework to elucidate the LV mechanical efficiency (View Highlight)
- The ratio of SW to PVA is known as LV EET.57 EET represents the efficiency of mechanical energy transfer from the LV to the arterial system (EET = SW/PVA)49 (View Highlight)
- In AMI, LV contractility is decreased, leading to a reduction in stroke volume and blood pressure. The PV loop shifts rightward (initially along the original EDPVR) due to increases in both LV end-diastolic and end-systolic volumes. The global ischemia caused by severe hypoxemia or multivessel coronary artery disease results in generalized hypokinesis of myocardium. This is depicted in the PV diagram as a decrease in Ees with unchanged V0, resulting in a smaller stroke volume.59 It is of note that ESPVR may fail to reflect LV systolic dysfunction when LV diastolic pressure is markedly elevated,60 because ESP is composed of resting diastolic pressure and developed pressure (View Highlight)
- in regional ischemia, ESPVR shifts rightward parallel with similar or slightly decreased Ees when compared at a comparable systolic pressure range (View Highlight)
- Qload can become maximum when Ea equals Ees (Ea/Ees = 1) (View Highlight)
- mechanical efficiency per beat is also maximized when Ea/Ees is close to 0.5 (View Highlight)
- both Qload and Qheart become close to being most efficient when Ea/Ees is between 0.5 and 1.0, which enables the heart to maximize EW for a given LV preload and minimize the cardiac oxygen consumption, simultaneously. (View Highlight)
- Changes in LV EDPVR during myocardial ischemia/infarction are not uniform, depending on the state of coronary flow (maintained or discontinued) and the extent of ischemia (global or regional), and therefore result in multiple forms of pathophysiology and hemodynamic consequences in association with changes in ESPVR (View Highlight)
- The current understandings of changes in EDPVR in an acute or subacute phase are that (1) EDPVR shifts to the upper-left during hypoxemia (ie, global ischemia/hypoxemia with maintained coronary flow), (2) EDPVR shifts upward during effort angina or pacing-induced ischemia (ie, regional demand ischemia with coronary artery stenosis), and (3) EDPVR is unchanged or may shift to the lower-right when coronary blood flow is reduced (ie, regional supply ischemia with coronary artery occlusion) (View Highlight)
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