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Abstract Background Three-dimensional time-resolved (4D) phase-contrast (PC) CMR can visualize and quantify cardiovascular flow but is hampered by long acquisition times. Acceleration with SENSE or k-t BLAST are two possibilities but results on validation are lacking, especially at 3 T. The aim of this study was therefore to validate quantitative in vivo cardiac 4D-acquisitions accelerated with parallel imaging and k-t BLAST at 1.5 T and 3 T with 2D-flow as the reference and to investigate if field strengths and type of acceleration have major effects on intracardiac flow visualization. Methods The local ethical committee approved the study. 13 healthy volunteers were scanned at both 1.5 T and 3 T in random order with 2D-flow of the aorta and main pulmonary artery and two 4D-flow sequences of the heart accelerated with SENSE and k-t BLAST respectively. 2D-image planes were reconstructed at the aortic and pulmonary outflow. Flow curves were calculated and peak flows and stroke volumes (SV) compared to the results from 2D-flow acquisitions. Intra-cardiac flow was visualized using particle tracing and image quality based on the flow patterns of the particles was graded using a four-point scale. Results Good accuracy of SV quantification was found using 3 T 4D-SENSE (r2 = 0.86, -0.7 ± 7.6%) and although a larger bias was found on 1.5 T (r2 = 0.71, -3.6 ± 14.8%), the difference was not significant (p = 0.46). Accuracy of 4D k-t BLAST for SV was lower (p < 0.01) on 1.5 T (r2 = 0.65, -15.6 ± 13.7%) compared to 3 T (r2 = 0.64, -4.6 ± 10.0%). Peak flow was lower with 4D-SENSE at both 3 T and 1.5 T compared to 2D-flow (p < 0.01) and even lower with 4D k-t BLAST at both scanners (p < 0.01). Intracardiac flow visualization did not differ between 1.5 T and 3 T (p = 0.09) or between 4D-SENSE or 4D k-t BLAST (p = 0.85). Conclusions The present study showed that quantitative 4D flow accelerated with SENSE has good accuracy at 3 T and compares favourably to 1.5 T. 4D flow accelerated with k-t BLAST underestimate flow velocities and thereby yield too high bias for intra-cardiac quantitative in vivo use at the present time. For intra-cardiac 4D-flow visualization, however, 1.5 T and 3 T as well as SENSE or k-t BLAST can be used with similar quality.

Abstract Background Polymorphonuclear neutrophils, stimulated by the activated complement factor C5a, have been implicated in cardiac ischemia/reperfusion injury. ADC-1004 is a competitive C5a receptor antagonist that has been shown to inhibit complement related neutrophil activation. ADC-1004 shields the neutrophils from C5a activation before they enter the reperfused area, which could be a mechanistic advantage compared to previous C5a directed reperfusion therapies. We investigated if treatment with ADC-1004, according to a clinically applicable protocol, would reduce infarct size and microvascular obstruction in a large animal myocardial infarct model. Methods In anesthetized pigs (42-53 kg), a percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 minutes, followed by 4 hours of reperfusion. Twenty minutes after balloon inflation the pigs were randomized to an intravenous bolus administration of ADC-1004 (175 mg, n = 8) or saline (9 mg/ml, n = 8). Area at risk (AAR) was evaluated by ex vivo SPECT. Infarct size and microvascular obstruction were evaluated by ex vivo MRI. The observers were blinded to the treatment at randomization and analysis. Results ADC-1004 treatment reduced infarct size by 21% (ADC-1004: 58.3 ± 3.4 vs control: 74.1 ± 2.9%AAR, p = 0.007). Microvascular obstruction was similar between the groups (ADC-1004: 2.2 ± 1.2 vs control: 5.3 ± 2.5%AAR, p = 0.23). The mean plasma concentration of ADC-1004 was 83 ± 8 nM at sacrifice. There were no significant differences between the groups with respect to heart rate, mean arterial pressure, cardiac output and blood-gas data. Conclusions ADC-1004 treatment reduces myocardial ischemia-reperfusion injury and represents a novel treatment strategy of myocardial infarct with potential clinical applicability.

Abstract Background Ectonucleotidase dependent adenosine generation has been implicated in preconditioning related cardioprotection against ischemia-reperfusion injury, and treatment with a soluble ectonucleotidase has been shown to reduce myocardial infarct size (IS) when applied prior to induction of ischemia. However, ectonucleotidase treatment according to a clinically applicable protocol, with administration only after induction of ischemia, has not previously been evaluated. We therefore investigated if treatment with the ectonucleotidase apyrase, according to a clinically applicable protocol, would reduce IS and microvascular obstruction (MO) in a large animal model. Methods A percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 min, in 16 anesthetized pigs (40-50 kg). The pigs were randomized to 40 min of 1 ml/min intracoronary infusion of apyrase (10 U/ml, n = 8) or saline (0.9 mg/ml, n = 8), twenty minutes after balloon inflation. Area at risk (AAR) was evaluated by ex vivo SPECT. IS and MO were evaluated by ex vivo MRI. Results No differences were observed between the apyrase group and saline group with respect to IS/AAR (75.7 ± 4.2% vs 69.4 ± 5.0%, p = NS) or MO (10.7 ± 4.8% vs 11.4 ± 4.8%, p = NS), but apyrase prolonged the post-ischemic reactive hyperemia. Conclusion Apyrase treatment according to a clinically applicable protocol, with administration of apyrase after induction of ischemia, does not reduce myocardial infarct size or microvascular obstruction.

Purpose: To verify MR measurements of myocardial extracellular volume fraction (ECV) based on clinically applicable T1‐mapping sequences against ECV measurements by radioisotope tracer in pigs and to relate the results to those obtained in volunteers. Methods: Between May 2016 and March 2017, 8 volunteers (25 ± 4 years, 3 female) and 8 pigs (4 female) underwent ECV assessment with SASHA, MOLLI5(3b)3, MOLLI5(3s)3, and MOLLI5s(3s)3s. Myocardial ECV was measured independently in pigs using a radioisotope tracer method. Results: In pigs, ECV in normal myocardium was not different between radioisotope (average ± standard deviation; 19 ± 2%) and SASHA (21 ± 2%; P = 0.086). ECV was higher by MOLLI5(3b)3 (26 ± 2%), MOLLI5(3s)3 (25 ± 2%), and MOLLI5s(3s)3s (25 ± 2%) compared with SASHA or radioisotope (P ≤ 0.001 for all). ECV in volunteers was higher by MOLLI5(3b)3 (26 ± 3%) and MOLLI5(3s)3 (26 ± 3%) than by SASHA (22 ± 3%; P = 0.022 and P = 0.033). No difference was found between MOLLI5s(3s)3s (25 ± 3%) and SASHA (P = 0.225). Native T1 of blood and myocardium as well as postcontrast T1 of myocardium was consistently lower using MOLLI compared with SASHA. ECV increased over time as measured by MOLLI5(3b)3 and MOLLI5(3s)3 for pigs (0.08% and 0.07%/min; P = 0.004 and P = 0.013) and by MOLLI5s(3s)3s for volunteers (0.07%/min; P = 0.032) but did not increase as measured by SASHA. Conclusion: Clinically available MOLLI and SASHA techniques can be used to accurately estimate ECV in normal myocardium where MOLLI‐sequences show minor overestimation driven by underestimation of postcontrast T1 when compared with SASHA. The timing of imaging after contrast administration affected the measurement of ECV using some variants of the MOLLI sequence. [ABSTRACT FROM AUTHOR]

Summary: Background: Total heart volume (THV) within the pericardium is not constant throughout the cardiac cycle and THV would intuitively be lowest at end systole. We have, however, observed a phase shift between ventricular outflow and atrial inflow which causes the minimum THV to occur before end systole. The aims were to explain the mechanism of the late‐systolic net inflow to the heart and determine whether this net inflow is affected by increased cardiac output or systolic heart failure. Methods and Results: Healthy controls (n = 21) and patients with EF<35% (n = 14) underwent magnetic resonance imaging with flow measurements in vessels to and from the heart, and this was repeated in nine controls during 140 μgram kg−1 min−1 adenosine infusion. Minimum THV occurred 78 ± 6 ms before end of systolic ejection (8 ± 1% of the cardiac cycle) in controls. The late‐systolic net inflow was 12·3 ± 1·1 ml or 6·0 ± 0·5% of total stroke volume (TSV). Cardiac output increased 66 ± 8% during adenosine but late‐systolic net inflow to the heart did not change (P = 0·73). In patients with heart failure, late‐systolic net inflow of the heart′s left side was lower (3·4 ± 0·5%) compared to healthy subjects (5·3 ± 0·6%, P = 0·03). Conclusions: Heart size increases before end systole due to a late‐systolic net inflow which is unaffected by increased cardiac output. This may be explained by inertia of blood that flows into the atria generated by ventricular systole. The lower late‐systolic net inflow in patients with systolic heart failure may be a measure of decreased ventricular filling due to decreased systolic function, thus linking systolic to diastolic dysfunction. [ABSTRACT FROM AUTHOR]

Background: 4D-flow magnetic resonance imaging (MRI) is increasingly used.Purpose: To validate 4D-flow sequences in phantom and in vivo, comparing volume flow and kinetic energy (KE) head-to-head, with and without respiratory gating.Material and Methods: Achieva dStream (Philips Healthcare) and MAGNETOM Aera (Siemens Healthcare) 1.5-T scanners were used. Phantom validation measured pulsatile, three-dimensional flow with 4D-flow MRI and laser particle imaging velocimetry (PIV) as reference standard. Ten healthy participants underwent three cardiac MRI examinations each, consisting of cine-imaging, 2D-flow (aorta, pulmonary artery), and 2 × 2 accelerated 4D-flow with (Resp+) and without (Resp-) respiratory gating. Examinations were acquired consecutively on both scanners and one examination repeated within two weeks. Volume flow in the great vessels was compared between 2D- and 4D-flow. KE were calculated for all time phases and voxels in the left ventricle.Results: Phantom results showed high accuracy and precision for both scanners. In vivo, higher accuracy and precision ( P < 0.001) was found for volume flow for the Aera prototype with Resp+ (-3.7 ± 10.4 mL, r = 0.89) compared to the Achieva product sequence (-17.8 ± 18.6 mL, r = 0.56). 4D-flow Resp- on Aera had somewhat larger bias (-9.3 ± 9.6 mL, r = 0.90) compared to Resp+ ( P = 0.005). KE measurements showed larger differences between scanners on the same day compared to the same scanner at different days.Conclusion: Sequence-specific in vivo validation of 4D-flow is needed before clinical use. 4D-flow with the Aera prototype sequence with a clinically acceptable acquisition time (<10 min) showed acceptable bias in healthy controls to be considered for clinical use. Intra-individual KE comparisons should use the same sequence. [ABSTRACT FROM AUTHOR]