Hidden Whirlpools Inside the Heart Reveal Why Failing Ventricles Waste Energy

Every heartbeat hides a choreography of swirling blood that most of us never think about, yet those invisible vortices may hold the key to understanding one of the most common forms of heart failure. In a new study published in the Annals of Biomedical Engineering, researchers at the University of Southern California have built a transparent, beating model of the human left ventricle and used high-speed laser imaging to watch, frame by frame, how blood spirals into the chamber under healthy and diseased filling conditions. Their findings show that when the heart’s filling pattern goes wrong, the ventricle literally begins to waste energy, and the way it wastes it depends on the specific stage of disease.

The team, led by Kagan Ucak, Coskun Bilgi, and Niema M. Pahlevan, focused on diastole, the relaxation phase of the cardiac cycle when the left ventricle fills with blood returning from the lungs. Filling happens in two waves: an early passive rush of blood called the E-wave, driven by the ventricle’s own relaxation, and a later surge called the A-wave, produced when the atrium contracts. Between the two lies diastasis, a quiet interval in which little blood moves at all. Cardiologists have long used the ratio of the peak velocities of these two waves, the E/A ratio, to classify diastolic function into normal filling, impaired relaxation, and restrictive filling, the latter marking the most severe stage of dysfunction. What has remained murky is precisely how these different inflow patterns reshape the fluid dynamics inside the chamber and what that reshaping costs the heart in mechanical efficiency.

To find out, the researchers constructed a physiologically accurate left ventricle simulator: a compliant, transparent silicone sac submerged in a pressurized acrylic tank and driven by a programmable piston pump. The sac was fitted with artificial mitral and aortic valves and connected to a hydraulic circuit with adjustable resistance and compliance, allowing the team to tune afterload and preload independently. A blood-analog fluid, mixed from water, glycerol, and urea to match the viscosity and density of real blood, was seeded with tiny fluorescent microspheres. By illuminating a thin laser sheet through the ventricle’s mid-plane and capturing images with a 12.6-megapixel high-speed camera, the researchers performed phase-locked particle image velocimetry, or PIV, resolving velocity fields with a spatial resolution of roughly 0.4 millimeters across 29 repeated cardiac cycles for each experimental condition.

The elegance of the setup lies in its control. In patients, it is nearly impossible to isolate the effect of a single parameter, because heart rate, stroke volume, filling pressure, and ventricular geometry all change together as disease progresses. In the simulator, the team could dial in an E/A ratio below 0.8 to mimic impaired relaxation, above 2.0 to mimic restrictive filling, or an intermediate value for normal filling, while independently varying the duration of diastasis from zero to twenty percent of the cardiac cycle, the heart rate from 60 to 90 beats per minute, and the cardiac output from 2.0 to 3.3 liters per minute. Crucially, the resulting inflow velocities of 0.5 to 0.9 meters per second fell squarely within the range measured clinically by Doppler echocardiography, and the calculated vortex formation times matched values previously reported in patients.

What the camera revealed was striking. Under normal filling, the E-wave generates a pair of counter-rotating vortices that sweep toward the ventricular apex, settle near the walls, and gently fade as the A-wave delivers its own vortex pair into the center of the chamber. The two vortex systems coexist in an orderly, energy-efficient sequence. Under restrictive filling, by contrast, the E-wave arrives with far greater force, producing larger, more intense vortices that dominate the chamber, while the weakened A-wave enters without forming any coherent vortex structure at all. The result is a burst of intense dissipation early in diastole followed by an almost stagnant ventricle, with the velocity field nearly motionless by the time systole begins.

The quantitative consequences were dramatic. Restrictive filling patterns produced a peak viscous energy dissipation fifty percent higher than normal filling, along with a 38 percent increase in peak turbulent kinetic energy and a 21 percent higher peak shear rate. Impaired relaxation patterns told a different story: because the weak E-wave vortices linger in the chamber, the arriving A-wave vortices catch up and merge with them, creating a single, larger, tilted vortex structure that persists into early systole. This merging event drove the highest peak turbulent kinetic energy of all, 57 percent above normal, and pushed peak energy dissipation 46 percent above the healthy baseline. Elevated shear rates and turbulent kinetic energy are clinically meaningful because both have been linked to damage of blood cells and platelets, suggesting that severely diseased filling patterns may impose additional hemodynamic stress on the blood itself.

Perhaps the most surprising discovery concerned diastasis, the quiet pause between the filling waves, which had never been systematically studied before. The researchers found that a moderate diastasis duration, around ten percent of the cardiac cycle, minimized viscous energy dissipation across all E/A ratios, revealing a local energetic optimum that corresponds precisely to the normal filling pattern with an E/A ratio near 1.5. Too little diastasis forces the filling waves to collide and interact chaotically; too much allows the E-wave vortices to dissipate completely before the A-wave arrives, forfeiting any beneficial interaction. Intriguingly, this optimum vanished under low-cardiac-output conditions, hinting that the energetic landscape of the ventricle shifts with the heart’s overall workload.

The team also uncovered distinct scaling laws for the impaired relaxation pattern. When stroke volume was varied from 27 to 53 milliliters at a fixed heart rate, diastole-averaged energy dissipation rose nonlinearly, following a second-order polynomial trend. When heart rate was varied from 60 to 90 beats per minute at constant cardiac output, dissipation per cycle stayed essentially constant, meaning total wasted energy scaled linearly with heart rate. The authors note an intriguing parallel with exercise physiology: stroke volume and heart rate both rise linearly with exercise intensity up to a threshold, beyond which stroke volume plateaus and falls while heart rate keeps climbing. The nonlinear energy penalty associated with increasing stroke volume may help explain why the heart sheds stroke volume at high exertion, particularly in patients whose ventricles are already filling inefficiently.

More than 6.7 million adults in the United States live with heart failure, and elevated left ventricular filling pressure is a central driver of the disease. Current diagnosis of diastolic dysfunction relies on Doppler indices such as the E/A ratio, mitral annular velocities, and estimates of filling pressure, but these provide only indirect glimpses of what the blood is actually doing inside the chamber. The USC team’s results suggest that flow-based energetic metrics, such as viscous energy dissipation, turbulent kinetic energy, and the presence of vortex merging, could serve as complementary markers of disease severity, potentially measurable at the bedside with echocardiographic particle image velocimetry, a technique already being explored in clinical settings.

The researchers are careful to note the limitations of their model. The simulator cannot replicate the full complexity of living myocardium, including fiber architecture, ventricular twist, and aortic root recoil, and its two-dimensional imaging cannot capture out-of-plane velocities in an inherently three-dimensional flow. The reported turbulent kinetic energy values, computed from 29 phase-locked cycles, should be read as comparative measures of flow fluctuation rather than direct measurements of fully developed turbulence. Still, as a controlled mechanistic study, the work delivers something clinical imaging cannot: a clean, parameter-by-parameter demonstration that the balance between early and late filling is not merely a diagnostic curiosity but a genuine determinant of the heart’s hydraulic efficiency. If future clinical studies confirm that these vortex signatures track with disease progression, the humble whirlpool inside the beating heart could become a powerful new window into heart failure, one that physicians could watch swirl, merge, and dissipate in real time.

Subject of Research: In vitro analysis of left ventricular vortex dynamics and energy dissipation across diastolic function filling patterns

Article Title: Vortex Dynamics and Energy Dissipation in Left Ventricular Diastolic Filling Across Diastolic Function Inflow Patterns: An In Vitro Quantitative Flow Analysis

Article References: Ucak, K., Bilgi, C., & Pahlevan, N. M. (2026). Vortex Dynamics and Energy Dissipation in Left Ventricular Diastolic Filling Across Diastolic Function Inflow Patterns: An In Vitro Quantitative Flow Analysis. Annals of Biomedical Engineering. https://doi.org/10.1007/s10439-026-04369-2

Image Credits: AI Generated

DOI: 10.1007/s10439-026-04369-2

Keywords: diastolic dysfunction, left ventricle, vortex dynamics, particle image velocimetry, energy dissipation, turbulent kinetic energy, heart failure, E/A ratio, diastasis, hemodynamics, in vitro model, cardiac fluid mechanics