To evaluate the association between impaired left ventricular (LV) longitudinal function and LV underfilling in patients with pulmonary arterial hypertension (PAH). Thirty-nine patients with PAH and 18 age and sex-matched healthy controls were included. LV volume and left atrial volume (LAV) were delineated in short-axis cardiac magnetic resonance (CMR) cine images. LV longitudinal function was assessed from atrio-ventricular plane displacement (AVPD) and global longitudinal strain (GLS) was assessed using feature tracking in three long-axis views. LV filling was assessed by LAV and by pulmonary artery wedge pressure (PAWP) using right heart catheterisation. Patients had a smaller LAV, LV volume and stroke volume as well as a lower LV-AVPD and LV-GLS than controls. PAWP was 6 [IQR 5––9] mmHg in patients. LV ejection fraction did not differ between groups. LV stroke volume correlated with LV-AVPD (r = 0.445, p = .001), LV-GLS (r = − 0.549, p < 0.0001) and LAVmax (r = .585, p < 0.0001). Furthermore, LV-AVPD (r = .598) and LV-GLS (r = − 0.675) correlated with LAVmax (p < 0.0001 for both). Neither LV-AVPD, LV-GLS, LAVmax nor stroke volume correlated with PAWP. Impaired LV longitudinal function was associated with low stroke volume, low PAWP and a small LAV in PAH. Small stroke volumes and LAV, together with normal LA pressure, implies that the mechanism causing reduced LV longitudinal function is underfilling rather than an intrinsic LV dysfunction in PAH.

To assess (1) global longitudinal strain (GLS) by feature tracking cardiac magnetic resonance (CMR) in the sub-acute and chronic phases after ST-elevation infarction (STEMI) and compare to GLS in healthy controls, and (2) the evolution of GLS and regional longitudinal strain (RLS) over time, and their relationship to infarct location and size. Seventy-seven patients from the CHILL-MI-trial (NCT01379261) who underwent CMR 2–6 days and 6 months after STEMI and 27 healthy controls were included for comparison. Steady state free precession (SSFP) long-axis cine images were obtained for GLS and RLS, and late gadolinium enhancement (LGE) images were obtained for infarct size quantifications. GLS was impaired in the sub-acute (− 11.8 ± 3.0%) and chronic phases (− 14.3 ± 2.9%) compared to normal GLS in controls (− 18.4 ± 2.4%; p < 0.001 for both). GLS improved from sub-acute to chronic phase (p < 0.001). GLS was to some extent determined by infarct size (sub-acute: r2 = 0.2; chronic: r2 = 0.2, p < 0.001). RLS was impaired in all 6 wall-regions in LAD infarctions in both the sub-acute and chronic phase, while LCx and RCA infarctions had preserved RLS in remote myocardium at both time points. Global longitudinal strain is impaired sub-acutely after STEMI and improvement is seen in the chronic phase, although not reaching normal levels. Global longitudinal strain is only moderately determined by infarct size. Regional longitudinal strain is most impaired in the infarcted region, and LAD infarctions have effects on the whole heart. This could explain why LAD infarcts are more serious than the other culprit vessel infarctions and more often cause heart failure.

Background Left ventricular (LV) functional assessment is of imminent value after ST-elevation infarction (STEMI). LV longitudinal strain (LS) evaluates ventricular function on a myocardial level. Feature Tracking (FT) assesses strain from cine cardiac magnetic resonance (CMR) images. It is unknown how LV FT Regional LS (RLS) and Global LS (GLS) changes between the sub-acute and chronic phase after STEMI compared to controls and how GLS and RLS are related to culprit vessel (LAD, LCX or RCA) and infarction size (IS). Aims To assess 1) GLS with FT after 2–6 days (sub-acute) and 6 months (chronic phase) after STEMI compared with controls, 2) if GLS changes between sub-acute and chronic phase, and 3) the relationship between GLS and RLS to IS and infarct location. Methods and results Seventy-seven patients underwent CMR 2–6 days and 6 months after STEMI as well as 27 healthy controls. GLS was impaired at the sub-acute (−8.9±2.3%) and chronic phase (−14.3±2.9%) compared to controls (−18.4±2.4%; p<0.001 for both). GLS improved between the sub-acute and chronic phase (p<0.001). GLS correlated to IS (R=0.47 sub-acute; 0.49 chronic, p<0.001). LAD infarctions had lowest GLS and largest IS. RLS was more impaired in the culprit vessel territory compared to remote. RLS in the RCA region was lower for LAD than RCA infarctions. RLS was impaired in all 6 wall-regions in LAD infarctions, while LCX and RCA infarctions had preserved RLS in remote myocardium. Global Longitudinal Strain (GLS) Conclusion GLS is impaired after STEMI and improves, but do not normalize, to the chronic phase. GLS is only moderately correlated to IS, indicating that other factors and co-morbidities are important to determine ventricular function. Even though RLS is most impaired in the affected region, remote regions can be substantially impaired in LAD-infarctions, why it would be difficult to pinpoint the culprit vessel based on RLS.