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.

Serum Biomarkers of Myocardial Remodeling and Coronary Dysfunction in Early Stages of Hypertrophic Cardiomyopathy in the Young.

Hypertrophic cardiomyopathy (HCM) remains the leading cause of sudden cardiac death in the young. Early markers for HCM are important to identify individuals at risk. The aim of this study was to investigate novel serum biomarkers reflecting myocardial remodeling, microfibrosis, and vascular endotheliopathy in the early stages of familial HCM in young patients. Twenty-three HCM patients, 16 HCM-risk individuals, and 66 controls (median 15 years) underwent echocardiography and serum analysis for cathepsin S, endostatin, myostatin, type I collagen degradation marker (ICTP), matrix metalloproteinase (MMP)-9, vascular endothelial growth factor receptor (VEGFR)-1, and vascular and intercellular adhesion molecules (VCAM, ICAM). In a subset of the population, global myocardial perfusion was performed by magnetic resonance imaging. Cathepsin S (p = 0.0009), endostatin (p < 0.0001), MMP-9 (p = 0.008), and VCAM (p = 0.04) were increased in the HCM group and correlated to left ventricular mass index and mitral E/e' (p < 0.01). In the HCM-risk group, myostatin was decreased (p = 0.004), whereas ICAM was increased (p = 0.002). Global perfusion was decreased in the HCM group (p < 0.05) versus controls. Endostatin and mitral E/e' correlated inversely to myocardial perfusion (p ≤ 0.05). This is the first study demonstrating adverse changes in biomarkers reflecting myocardial matrix remodeling, microfibrosis, and vascular endotheliopathy in early stage of hypertrophic cardiomyopathy in the young.