Ventricular longitudinal shortening is an independent predictor of death in heart failure patients with reduced ejection fraction

Reduced ventricular longitudinal shortening measured by atrioventricular plane displacement (AVPD) and global longitudinal strain (GLS) are prognostic markers in heart disease. This study aims to determine if AVPD and GLS with cardiovascular magnetic resonance (CMR) are independent predictors of cardiovascular (CV) and all-cause death also in heart failure with reduced ejection fraction (HFrEF). Patients (n = 287) were examined with CMR and AVPD, GLS, ventricular volumes, myocardial fibrosis/scar were measured. Follow-up was 5 years with cause of death retrieved from a national registry. Forty CV and 60 all-cause deaths occurred and CV non-survivors had a lower AVPD (6.4 ± 2.0 vs 8.0 ± 2.4 mm, p < 0.001) and worse GLS (− 6.1 ± 2.2 vs − 7.7 ± 3.1%, p = 0.001). Kaplan–Meier analyses displayed increased survival for patients in the highest AVPD- and GLS-tertiles vs. the lowest tertiles (AVPD: p = 0.001, GLS: p = 0.013). AVPD and GLS showed in univariate analysis a hazard ratio (HR) of 1.30 (per-mm-decrease) and 1.19 (per-%-decrease) for CV death. Mean AVPD and GLS were independent predictors of all-cause death (HR = 1.24 per-mm-decrease and 1.15 per-%-decrease), but only AVPD showed incremental value over age, sex, body-mass-index, EF, etiology and fibrosis/scar for CV death (HR = 1.33 per-mm-decrease, p < 0.001). Ventricular longitudinal shortening remains independently prognostic for death in HFrEF even after adjusting for well-known clinical risk factors.

An Intra-Cycle Optimal Control Framework for Ventricular Assist Devices Based on Atrioventricular Plane Displacement Modeling

A promising treatment for congestive heart failure is the implementation of a left ventricular assist device (LVAD) that works as a mechanical pump. Modern LVADs work with adjustable constant rotor speed and provide therefore continuous blood flow; however, recently undertaken efforts try to mimic pulsatile blood flow by oscillating the pump speed. This work proposes an algorithmic framework to construct and evaluate optimal pump speed policies with respect to generic objectives. We use a model that captures the atrioventricular plane displacement, which is a physiological indicator for heart failure. We employ mathematical optimization to adapt this model to patient specific data and to find optimal pump speed policies with respect to ventricular unloading and aortic valve opening. To this end, we reformulate the cardiovascular dynamics into a switched system and thereby reduce nonlinearities. We consider system switches that stem from varying the constant pump speed and that are state dependent such as valve opening or closing. As a proof of concept study, we personalize the model to a selected patient with respect to ventricular pressure. The model fitting results in a root-mean-square deviation of about 6 mmHg. The optimization that considers aortic valve opening and ventricular unloading results in speed modulation akin to counterpulsation. These in silico findings demonstrate the potential of personalized hemodynamical optimization for the LVAD therapy.

A Personalized Switched Systems Approach for the Optimal Control of Ventricular Assist Devices based on Atrioventricular Plane Displacement

ObjectiveA promising treatment for congestive heart failure is the implementation of a left ventricular assist device (LVAD) that works as a mechanical pump. Modern LVADs work with adjustable constant rotor speed and provide therefore continuous blood flow; however, recently undertaken efforts try to mimic pulsatile blood flow by oscillating the pump speed. This work proposes an algorithmic framework to construct and evaluate optimal pump speed policies.MethodsWe use a model that captures the atrioventricular plane displacement, which is a physiological indicator for heart failure. We employ mathematical optimization to adapt this model to patient specific data and to find optimal pump speed policies with respect to ventricular unloading and aortic valve opening. To this end, we reformulate the cardiovascular dynamics into a switched system and thereby reduce nonlinearities. We consider system switches that stem from varying the constant pump speed and that are state dependent such as valve opening or closing.ResultsAs a proof of concept study, we personalize the model to a selected patient with respect to ventricular pressure. The model fitting results in a root-mean-square deviation of about 6 mmHg. Optimized constant and piecewise constant rotor speed profiles improve the default initialized solution by 31% and 68% respectively.ConclusionThese in silico findings demon-strate the potential of personalized hemodynamical optimization for the LVAD therapy.SignificanceLVADs and their optimal configuration are active research fields. Mathematical optimization enhances our understanding of how LVADs should provide pulsatility.

Changes in left and right ventricular longitudinal function after pulmonary valve replacement in patients with Tetralogy of Fallot

Timing and indication for pulmonary valve replacement (PVR) in patients with repaired Tetralogy of Fallot (rToF) and pulmonary regurgitation (PR) are uncertain. To improve understanding of pumping mechanics, we investigated atrioventricular coupling before and after surgical PVR. Cardiovascular magnetic resonance was performed in patients ( n = 12) with rToF and PR > 35% before and after PVR and in healthy controls ( n = 15). Atrioventricular plane displacement (AVPD), global longitudinal peak systolic strain (GLS), atrial and ventricular volumes, and caval blood flows were analyzed. Right ventricular (RV) AVPD and RV free wall GLS were lower in patients before PVR compared with controls ( P < 0.0001; P < 0.01) and decreased after PVR ( P < 0.0001 for both). Left ventricular AVPD was lower in patients before PVR compared with controls ( P < 0.05) and decreased after PVR ( P < 0.01). Left ventricular GLS did not differ between patients and controls ( P > 0.05). Right atrial reservoir volume and RV stroke volume generated by AVPD correlated in controls ( r = 0.93; P < 0.0001) and patients before PVR ( r = 0.88; P < 0.001) but not after PVR. In conclusion, there is a clear atrioventricular coupling in patients before PVR that is lost after PVR, possibly because of loss of pericardial integrity. Impaired atrioventricular coupling complicates assessment of ventricular function after surgery using measurements of longitudinal function. Changes in atrioventricular coupling seen in patients with rToF may be energetically unfavorable, and long-term effects of surgery on atrioventricular coupling is therefore of interest. Also, AVPD and GLS cannot be used interchangeably to assess longitudinal function in rToF. NEW & NOTEWORTHY There is a clear atrioventricular coupling in patients with Tetralogy of Fallot (ToF) and pulmonary regurgitation before surgical pulmonary valve replacement (PVR) that is lost after operation, possibly because of loss of pericardial integrity. The impaired atrioventricular coupling complicates assessment of ventricular function after surgery when using measurements of longitudinal function. Left ventricular atrioventricular plane displacement (AVPD) found differences between patients and controls and changes after PVR that longitudinal strain could not detect. This indicates that AVPD and strain cannot be used interchangeably to assess longitudinal function in repaired ToF.

Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume

Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1–2 h after AMI in a microembolization model ( n = 12) and an ischemia-reperfusion model ( n = 14). A subset of pigs ( n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased ( P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease ( P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (−29 ± 14% vs. −15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas ( P < 0.001), and A-wave AVPD remained unchanged ( P = 0.93) whereas E-wave AVPD decreased ( P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction. NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI.