CardioNerds (Drs. Apoorva Gangavelli, Cory Sejo, and Joseph Kassab) discuss the hemodynamics of valvular heart disease with Dr. Michael Brener. Using pressure-volume loops and clinical cases, they explain ventricular loading, myocardial energetics, and ventricular-arterial coupling, then apply these concepts to aortic stenosis, mitral regurgitation, and tricuspid regurgitation. Audio editing by CardioNerds Academy intern, Joshua Khorsandi.
This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli, and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds.
A normal PV loop describes one cardiac cycle. With pressure on the y-axis and volume on the x-axis, the loop moves counterclockwise through isovolumic contraction, ejection, isovolumic relaxation, and filling. The slope of the end-systolic pressure-volume relationship reflects contractility. The end-diastolic relationship describes diastolic properties, and the loop’s position along it reflects preload. Effective arterial elastance estimates afterload; the enclosed area represents stroke work. 1,2
Coupling relates contractility to afterload, while PV area reflects energy demand. Ventricular-arterial coupling is expressed as the ratio of end-systolic elastance to effective arterial elastance. Stroke work plus potential energy gives pressure-volume area, which correlates with myocardial oxygen consumption. A greater proportion of this area devoted to stroke work reflects greater mechanical efficiency.1,3
The normal RV loop operates at lower pressures and is more triangular than the LV loop. The RV has a shallower end-systolic pressure-volume relationship and a flatter ejection phase. Ejection can continue beyond peak elastance, making isovolumic relaxation less pronounced. Normal RV and LV diastolic properties are relatively similar.3,4
AS produces a taller, narrower LV loop. Increased afterload raises LV systolic pressure and limits stroke volume. After aortic valve replacement, expect lower LV pressure and wall stress with increased stroke volume. Interpret immediate post-TAVR measurements cautiously because rapid ventricular pacing and other procedural effects can alter hemodynamics.5
MR widens the LV loop and blunts its isovolumic phases. Primary MR can initially occur with preserved ventricular function. In ventricular secondary MR, the loop shifts rightward and the end-systolic relationship becomes shallower because the ventricle is already remodeled and dysfunctional. MR reduction is expected to narrow the loop, restore isovolumic contraction and relaxation, and increase systolic pressure as more ventricular force is directed into forward flow. 6
Correcting TR increases effective RV afterload. TR produces a wider loop with blunted isovolumic phases because blood can escape into the low-pressure right atrium. Eliminating this regurgitant pathway increases afterload. Valve replacement generally leaves less residual TR than edge-to-edge repair and therefore produces a greater afterload increase, which may be poorly tolerated when RV systolic reserve is limited. 7
Lower TAPSE/PASP suggests poorer RV-pulmonary artery coupling and less RV reserve. TAPSE reflects RV systolic function, while PASP captures one component of afterload. Ratios below 0.406 mm/mm Hg were associated with worse outcomes after transcatheter tricuspid intervention in the TriValve registry. It is important to interpret the ratio alongside invasive hemodynamics and RV imaging; it should not determine procedural selection by itself. 7
Imaging and AI may enable more accessible hemodynamic phenotyping. Noninvasive and minimally invasive approaches may reconstruct key features of pressure-volume physiology without routine conductance-catheter studies. These tools could help identify ventricular deterioration earlier and guide the timing and choice of valve intervention.
References
Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of Mechanical Circulatory Support. J Am Coll Cardiol. 2015;66:2663–2674.
Sarraf M, Chehab O, Nagaraja V. Understanding the Pressure-Volume Loop in Valvular Heart Disease. Heart Lung Circ. 2026;35:31–44.
Houston BA, Brittain EL, Tedford RJ. Right Ventricular Failure. N Engl J Med. 2023;388:1111–1125.
Brener MI, Masoumi A, Ng VG, et al. Invasive Right Ventricular Pressure-Volume Analysis: Basic Principles, Clinical Applications, and Practical Recommendations. Circ Heart Fail. 2022;15:e009101.
van den Enden AJM, van den Dorpel MMP, Mondellini GM, et al. Immediate changes in left ventricular cardiac mechanics following transcatheter aortic valve replacement for severe aortic stenosis – an in-vivo pressure-volume analysis study. Am Heart J. 2026;293:107302.
Gaemperli O, Biaggi P, Gugelmann R, et al. Real-time left ventricular pressure-volume loops during percutaneous mitral valve repair with the MitraClip system. Circulation. 2013;127:1018–1027.
Brener MI, Lurz P, Hausleiter J, et al. Right Ventricular-Pulmonary Arterial Coupling and Afterload Reserve in Patients Undergoing Transcatheter Tricuspid Valve Repair. J Am Coll Cardiol. 2022;79:448–461.
