What Is Acute Cardiac Unloading?
Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the power expenditure of the ventricle and limits the hemodynamic forces that lead to ventricular remodeling after insult or injury to the heart.
Cardiac Unloading Achieves Four Primary Endpoints:
Cardiac output is supplanted (either fully or partially) by the mechanical circulatory device, thereby decreasing the myocardial oxygen consumption (MVO2) associated with the mechanical work of pumping blood
Arterial perfusion pressure is increased and maintained independent of ventricular function
Ventricular preload is reduced leading to decreased ventricular wall stress
Coronary blood flow and myocardial oxygen delivery is increased
How it works
Acute cardiac unloading produces a state in which the myocardium is able to more fully rest and recover. The heart actively pumps blood through the cardiovascular system. This process consumes energy. Pumping blood is considered the workload of the heart. Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the workload and oxygen demand of the heart. The clinical, preclinical, and basic research of the A-CURE Working Group focuses primarily on the use of mechanical circulatory support devices as the means to unload the heart.
The Science Behind Acute Unloading
The ultimate goal of acute cardiac unloading is to minimize cardiac workload and allow the heart to more fully rest and recover from damage. To achieve this goal, cardiac unloading must limit myocardial oxygen demand.
Myocardial oxygen consumption, MVO2, is a measure of the total energy requirements of the heart, including the energy used to conduct the mechanical work of pumping blood 1, 2. An increase in MVO2 compared to resting conditions is indicative that the heart is working harder and is under stress. 2 Conversely, a decrease in MVO2 indicates that the heart is under a lesser amount of stress, and less energy is required to maintain proper blood flow. Therefore, decreased power expenditure directly correlates with a diminished MVO2. 2-5
Cardiac pressure-volume (PV) loop analysis provides a framework for understanding cardiac unloading and power expenditure. Click here to watch Dr. Dan Burkhoff explain acute cardiac unloading in the context of the cardiac PV loop. The size of the pressure-volume area (PVA) on the PV loop directly correlates with MVO2. As cardiac workload goes down, so does the size of the PVA. Therefore, acute unloading can be visualized as an overall decrease in the pressure-volume area on the PV loop.
Work by members of the A-CURE® Faculty and other independent labs have demonstrated that using a percutaneous support device to mechanically unload the heart decreases MVO2 in two ways. First, a device can continuously aspirate blood directly from the ventricle into the aorta. This decreases cardiac preload, left-shifts the PV loop, and decreases the PVA. A direct consequence of aspirating blood from the ventricle into the ascending aorta is an increase in mean aortic pressure. This perfusion pressure is maintained by the pump. Second, as the level of mechanical circulatory support increases to higher flow rates and ventricular volume is proportionally decreased, the ventricle no longer develops sufficient pressure necessary to open the aortic valve. When the maximum developed LV pressure falls below the mean arterial pressure the heart no longer ejects blood, and cardiac output is maintained by the device. Therefore, in the unloaded heart:
When the maximum developed LV pressure falls below the mean arterial pressure the heart no longer ejects blood, and cardiac output is maintained by the device. Therefore, in the unloaded heart:
- Cardiac output is uncoupled from ventricular function 6, 7
- Perfusion pressure is uncoupled from ventricular function 7-9
- MVO2 is spared 9, 10
Unloading the ventricle of blood volume also decreases ventricular wall stress. 9, 11, 12 When wall stress is high, as is the case during myocardial infarction or pathological remodeling, the coronary vasculature is compressed. This increases the resistance to blood flow and exacerbates ischemia. 13 Moreover, increased ventricular wall stress itself is a known stimulus for apoptosis in the heart. 14 By alleviating wall stress and simultaneously increasing mean arterial pressure, mechanical unloading increases blood flow through the coronary vasculature and may also limit apoptotic signaling.
In addition to these hemodynamic benefits, preclinical data also indicates that acute unloading activates cardioprotective molecular signaling in the heart (see video). These pleiotropic effects of acute unloading have been demonstrated to limit myocardial infarct scar size in several animal studies when unloading was applied prior to reperfusion .
- Burkhoff D and Naidu SS. The science behind percutaneous hemodynamic support: a review and comparison of support strategies. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2012;80:816-29.
- Suga H. Total mechanical energy of a ventricle model and cardiac oxygen consumption. The American journal of physiology. 1979;236:H498-505.
- Khalafbeigui F, Suga H and Sagawa K. Left ventricular systolic pressure-volume area correlates with oxygen consumption. The American journal of physiology. 1979;237:H566-9.
- Nozawa T, Cheng CP, Noda T and Little WC. Relation between left ventricular oxygen consumption and pressure-volume area in conscious dogs. Circulation. 1994;89:810-7.
- Kelly RP, Tunin R and Kass DA. Effect of reduced aortic compliance on cardiac efficiency and contractile function of in situ canine left ventricle. Circulation research. 1992;71:490-502.
- Saku K, Kakino T, Arimura T, Sakamoto T, Nishikawa T, Sakamoto K, Ikeda M, Kishi T, Ide T and Sunagawa K. Total Mechanical Unloading Minimizes Metabolic Demand of Left Ventricle and Dramatically Reduces Infarct Size in Myocardial Infarction. PLoS One. 2016;11:e0152911.
- Burkhoff DS, G.; Doshi, D., Uriel, N. Hemodynamics of Mechanical Circulatory Support. Journal of the American College of Cardiology. 2015;66:2663-74.
- Verma S, Burkhoff D and O’Neill WW. Avoiding hemodynamic collapse during high-risk percutaneous coronary intervention: Advanced hemodynamics of impella support. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2016.
- Kapur NK, Paruchuri V, Urbano-Morales JA, Mackey EE, Daly GH, Qiao X, Pandian N, Perides G and Karas RH. Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial infarct size. Circulation. 2013;128:328-36.
- Meyns B, Stolinski J, Leunens V, Verbeken E and Flameng W. Left ventricular support by catheter-mounted axial flow pump reduces infarct size. Journal of the American College of Cardiology. 2003;41:1087-95.
- Kapur NK, Qiao X, Paruchuri V, Morine KJ, Syed W, Dow S, Shah N, Pandian N and Karas RH. Mechanical Pre-Conditioning With Acute Circulatory Support Before Reperfusion Limits Infarct Size in Acute Myocardial Infarction. JACC Heart failure. 2015;3:873-82.
- Remmelink M, Sjauw KD, Henriques JP, de Winter RJ, Vis MM, Koch KT, Paulus WJ, de Mol BA, Tijssen JG, Piek JJ and Baan J, Jr. Effects of mechanical left ventricular unloading by Impella on left ventricular dynamics in high-risk and primary percutaneous coronary intervention patients. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2010;75:187-94.
- Delepine S, Furber AP, Beygui F, Prunier F, Balzer P, Le Jeune JJ and Geslin P. 3-D MRI assessment of regional left ventricular systolic wall stress in patients with reperfused MI. American journal of physiology Heart and circulatory physiology. 2003;284:H1190-7.
- Di Napoli P, Taccardi AA, Grilli A, Felaco M, Balbone A, Angelucci D, Gallina S, Calafiore AM, De Caterina R and Barsotti A. Left ventricular wall stress as a direct correlate of cardiomyocyte apoptosis in patients with severe dilated cardiomyopathy. American heart journal. 2003;146:1105-11.