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.

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.

Cardiac signal estimation based on the arterial and venous pressure signals of a hemodialysis machine.

Continuous cardiac monitoring is usually not performed during hemodialysis treatment, although a majority of patients with kidney failure suffer from cardiovascular disease. In the present paper, a method is proposed for estimating a cardiac pressure signal by combining the arterial and the venous pressure sensor signals of the hemodialysis machine. The estimation is complicated by the periodic pressure disturbance caused by the peristaltic blood pump, with an amplitude much larger than that of the cardiac pressure signal. Using different techniques for combining the arterial and venous pressure signals, the performance is evaluated and compared to that of an earlier method which made use of the venous pressure only. The heart rate and the heartbeat occurrence times, determined from the estimated cardiac pressure signal, are compared to the corresponding quantities determined from a photoplethysmographic reference signal. Signals from 9 complete hemodialysis treatments were analyzed. For a heartbeat amplitude of 0.5 mmHg, the median absolute deviation between estimated and reference heart rate was 1.3 bpm when using the venous pressure signal only, but dropped to 0.6 bpm when combining the pressure signals. The results show that the proposed method offers superior estimation at low heartbeat amplitudes. Consequently, more patients can be successfully monitored during treatment without the need of extra sensors. The results are preliminary, and need to be verified on a separate dataset.