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Latent pulmonary vascular disease is a distinct feature already in the early pathophysiology of masked heart failure with preserved ejection fraction (HFpEF) and associated with reduced right ventricular (RV) functional reserve. We hypothesized that serial real-time cardiovascular magnetic resonance (CMR) imaging at rest and during exercise-stress may detect early progress in pathophysiological alterations in HFpEF. Patients presenting with exertional dyspnoea and signs of diastolic dysfunction (E/e’>8, left ventricular (LV) ejection fraction > 50%) were prospectively enrolled in the HFpEF Stress Trial (NCT03260621). Rest and exercise-stress echocardiography, CMR and right heart catheterisation were performed at baseline. Pulmonary capillary wedge pressure (PCWP) was used for classification of HFpEF (≥ 15/25mmHg at rest/during exercise-stress) and non-cardiac dyspnoea (NCD). Repeat rest and exercise-stress CMR was performed in median 2.94 years after recruitment during which timeframe some HFpEF patients had undergone interatrial shunt device (IASD) implantation. Cardiovascular events were assessed after 4 years.Serial CMR scans were available for NCD n  = 10, HFpEF n  = 10 and HFpEF with IASD implantation following baseline diagnosis n  = 6. RV long axis strain at rest and during exercise-stress decreased in HFpEF ( p  = 0.007 for both) but neither in NCD nor HFpEF with IASD. In contrast, in NCD, an improvement in LA LAS during exercise-stress ( p  = 0.028) was noted. There were no functional alterations in HFpEF patients who had undergone IASD implantation. RV functional deterioration may be a pathophysiological feature during early-stage disease progress in HFpEF. In this observational study RV functional deterioration was detected in HFpEF patients only but not patients with NCD and patients with HFpEF that were treated with IASD placement. These findings should next be explored in adequately powered future research trials. Clinicaltrials.gov : NCT03260621 (First posted date 24/08/2017).

Brief interventions based on personalized feedback have shown promising results in reducing risky alcohol use among university students. We investigated the effects of activating deliberative (predecisional) or implemental (postdecisional) mindsets on the effectiveness of a standardized brief intervention, the ASSIST-linked Brief Intervention. This intervention comprises a personalized feedback and a decisional balance exercise. We hypothesized that participants in a deliberative mindset should show better outcomes related to risk perception and behavior than participants in an implemental mindset. A sample of 257 students provided baseline measures on risk perception, readiness to change, and alcohol use. Of those, 64 students with risky alcohol use were randomly allocated to one of two mindset induction conditions-deliberative or implemental mindset. Thereafter, they received the ASSIST-linked Brief Intervention and completed self-report questionnaires on changes in risk perception, alcohol use, and readiness to change at post-intervention and four-week follow-up. In contrast to our hypotheses, the four-weeks follow-up revealed that participants in the implemental mindset consumed significantly less alcohol than participants in a deliberative mindset did. The former decreased and the latter increased their alcohol intake; resistance to the brief intervention was stronger in the latter condition. However, neither deliberative nor implemental mindset participants showed any changes in risk perceptions or in their readiness to change alcohol consumption. These findings suggest that mindset induction is a powerful moderator of the effects of the ASSIST-linked Brief Intervention. We argue that systematic research on mindset effects on brief intervention techniques aimed to reduce risky alcohol use is highly needed in order to identify the processes involved with commitment and resistance being the main candidates.

Aims The pathophysiology of heart failure with preserved ejection fraction (HFpEF) includes pulmonary vascular remodelling and right ventricular (RV) involvement. We sought to investigate the significance of non‐invasive cardiovascular magnetic resonance (CMR)‐derived RV loading conditions. Methods Patients with exertional dyspnoea and diastolic dysfunction [E/e′ > 8, left ventricular ejection fraction (LVEF) >50%] underwent rest and exercise‐stress echocardiography, right heart catheterization and CMR. HFpEF was defined by pulmonary capillary wedge pressure [rest ≥15 mmHg (overt) or stress ≥25 mmHg (masked)]; otherwise, patients were classified as non‐cardiac dyspnoea (NCD). CMR‐derived RV haemodynamic indices were defined as follows: afterload Ea = end‐systolic pressure (ESP)/stroke volume (SV), contractility Ees = ESP/left ventricular end‐systolic volume and RV/pulmonary artery coupling as Ea/Ees. Results HFpEF (n = 34; female 73.5%; median age 69 years) patients showed increased afterload and contractility at rest (Ea 1.20 vs. 0.85, P = 0.001, Ees 0.61 vs. 0.37, P < 0.001) and during exercise (Ea 2.48 vs. 1.53, Ees 1.00 vs. 0.74, P < 0.001) compared with NCD (n = 34; female 55.9%; median age 66 years). The relative increase of contractility from rest to stress was smallest in overt HFpEF (overt 1.40 vs. masked 1.86, P = 0.001) and highest in NCD (HFpEF 1.56 vs. NCD 1.97, P = 0.022). The out‐of‐proportion increase in afterload over contractility in HFpEF was reflected in a statistical trend towards increased Ea/Ees from rest to stress in HFpEF (P = 0.078) while Ea/Ees decreased in NCD (P = 0.002). Patients with resting Ea or Ees above the median showed lower exercise‐induced increases in cardiac index (Ea: below: 2.8 vs. above: 2.2, P = 0.031; Ees: below: 2.9, above: 2.1, P < 0.001). Conclusions Resting RV afterload elevation in HFpEF results in a compensatory increase in contractility. Out‐of‐proportion increase of afterload paralleled by inadequate increase in contractility results in failure to increase the cardiac index in HFpEF, potentially associated with exertional functional failure. Non‐cardiac dyspnoea (n = 34, NCD) and heart failure with preserved ejection fraction (n = 34, HFpEF) patients were classified according to right heart catheterisation. Cardiovascular magnetic resonance derived right ventricular (RV) haemodynamic indices for afterload (Ea), contractility (Ees) and RV/pulmonary artery coupling (Ea/Ees) were evaluated. At rest, RV afterload elevation in HFpEF results in a compensatory increase in contractility. During exercise‐stress an out‐of‐proportion increase of afterload paralleled by inadequate increase in contractility results in failure to increase the cardiac index in HFpEF but not in NCD.

BackgroundCardiovascular magnetic resonance (CMR) plays a pivotal role in diagnosing myocardial inflammation. In addition to late gadolinium enhancement (LGE), native T1 and T2 mapping as well as extracellular volume (ECV) are essential tools for tissue characterization. However, the differentiation of cardiac sarcoidosis (CS) from myocarditis of other etiology can be challenging. Positron-emission tomography-computed tomography (PET-CT) regularly shows the highest Fluordesoxyglucose (FDG) uptake in LGE positive regions. It was therefore the aim of this study to investigate, whether native T1, T2, and ECV measurements within LGE regions can improve the differentiation of CS and myocarditis compared with using global native T1, T2, and ECV values alone.MethodsPET/CT confirmed CS patients and myocarditis patients (both acute and chronic) from a prospective registry were compared with respect to regional native T1, T2, and ECV. Acute and chronic myocarditis were defined based on the 2013 European Society of Cardiology position paper on myocarditis. All parametric measures and ECV were acquired in standard fashion on three short-axis slices according to the ConSept study for global values and within PET-CT positive regions of LGE.ResultsBetween 2017 and 2020, 33 patients with CS and 73 chronic and 35 acute myocarditis patients were identified. The mean ECV (± SD) in LGE regions of CS patients was higher than in myocarditis patients (CS vs. acute and chronic, respectively: 0.65 ± 0.12 vs. 0.45 ± 0.13 and 0.47 ± 0.1; p < 0.001). Acute and chronic myocarditis patients had higher global native T1 values (1157 ± 54 ms vs. 1196 ± 63 ms vs. 1215 ± 74 ms; p = 0.001). There was no difference in global T2 and ECV values between CS and acute or chronic myocarditis patients.ConclusionThis is the first study to show that the calculation of regional ECV within LGE-positive regions may help to differentiate CS from myocarditis. Further studies are warranted to corroborate these findings.

Background Primary coronary slow flow (CSF) is defined as delayed opacification of the distal epicardial vasculature during coronary angiography in the absence of relevant coronary artery stenoses. Microvascular disease is thought to be the underlying cause of this pathology. Epicardial fat tissue (EFT) is an active endocrine organ directly surrounding the coronary arteries that provides pro-inflammatory factors to the adjacent tissue by paracrine and vasocrine mechanisms. The aim of the present study was to investigate a potential association between EFT and primary CSF and whether EFT can predict the presence of primary CSF. Methods Between 2016 and 2017, n  = 88 patients with high-grade aortic stenosis who were planned for transcatheter aortic valve implantation (TAVI) were included in this retrospective study. EFT volume was measured by pre-TAVI computed tomography (CT) using dedicated software. The presence of primary CSF was defined based on the TIMI frame count from the pre-TAVI coronary angiograms. Results Thirty-nine of 88 TAVI patients had CSF (44.3%). EFT volume was markedly higher in patients with CSF (142 ml [IQR 107–180] vs. 113 ml [IQR 89–147]; p  = 0.009) and was strongly associated with the presence of CSF (OR 1.012 [95%CI 1.002–1.021]; p  = 0.014). After adjustment, EFT volume was still an independent predictor of CSF (OR 1.016 [95%CI 1.004–1.026]; p  = 0.009). Conclusion Primary CSF was independently associated with increased EFT volume. Further studies are needed to validate this finding and elucidate whether a causal relationship exists.

The impact of former COVID-19 infection on the performance of athletes is not fully understood. We aimed to identify differences in athletes with and without former COVID-19 infections. Competitive athletes who presented for preparticipation screening between April 2020 and October 2021 were included in this study, stratified for former COVID-19 infection, and compared. Overall, 1200 athletes (mean age 21.9 ± 11.6 years; 34.3% females) were included in this study from April 2020 to October 2021. Among these, 158 (13.1%) athletes previously had COVID-19 infection. Athletes with COVID-19 infection were older (23.4 ± 7.1 vs. 21.7 ± 12.1 years, p < 0.001) and more often of male sex (87.7% vs. 64.0%, p < 0.001). While systolic/diastolic blood pressure at rest was comparable between both groups, maximum systolic (190.0 [170.0/210.0] vs. 180.0 [160.0/205.0] mmHg, p = 0.007) and diastolic blood pressure (70.0 [65.0/75.0] vs. 70.0 [60.0/75.0] mmHg, p = 0.012) during the exercise test and frequency of exercise hypertension (54.2% vs. 37.8%, p < 0.001) were higher in athletes with COVID-19 infection. While former COVID-19 infection was not independently associated with higher blood pressure at rest and maximum blood pressure during exercise, former COVID-19 infection was related to exercise hypertension (OR 2.13 [95%CI 1.39–3.28], p < 0.001). VO2 peak was lower in athletes with compared to those without COVID-19 infection (43.4 [38.3/48.0] vs. 45.3 [39.1/50.6] mL/min/kg, p = 0.010). SARS-CoV-2 infection affected VO2 peak negatively (OR 0.94 [95%CI 0.91–0.97], p < 0.0019). In conclusion, former COVID-19 infection in athletes was accompanied by a higher frequency of exercise hypertension and reduced VO2 peak.

Myocardial inflammation and edema are major pathological features in myocarditis. Myocardial tissue water content and myocardial edema can be quantified via T2 mapping. Thus, cardiac magnetic resonance (CMR) is the noninvasive gold standard for diagnosing myocarditis. Several studies showed an impact of short-term volume changes on T2 relaxation time. Plasma volume status (PVS) is a good surrogate parameter to quantify a patient’s volume status, and it is simple to use. The aim of this study was to determine the effect of PVS on the diagnostic value of T2 relaxation time in myocardial inflammation. Between April 2017 and December 2022, patients who were indicated for cardiac CMR were included in our prospective clinical registry. Patients with myocardial inflammation and those with unremarkable findings were analyzed in the present study. A blood sample was drawn, and PVS was calculated. Patients were separated into PVS tertiles to explore a possible nonlinear dose–response relationship. Logistic regression analysis was used to determine whether T2 is an independent predictor of myocardial inflammation. A total of 700 patients (47.43% female) were eligible for analysis. Of these, 551 patients were healthy (78.7%), while 149 (21.3%) showed signs of myocardial inflammation. The T2 relaxation time was elevated in patients with myocardial inflammation (40 ms [IQR 37–42 ms] vs. 38.0 ms [IQR 36–39 ms], p < 0.001). PVS showed no difference between the groups (−12.94 [IQR −18.4–−7.28] vs.−12.19 [IQR −18.93–−5.87], p = 0.384). T2 showed a clear dose–response relationship with PVS, with increasing T2 values along the PVS tertiles. In spite of this, T2 was found to be an independent marker of myocardial inflammation in logistic regression (OR T2 1.3 [95% CI 1.21–1.39], p < 0.001), even after adjusting for PVS (OR T2 [adj. PVS] 1.31 [95% CI 1.22–1.40], p < 0.001). Despite a dose–response relationship between T2 and the volume status, T2 was found to be an independent indicator of myocardial inflammation.

Cardiac magnetic resonance (CMR) is currently the gold standard for evaluating right ventricular (RV) function, which is critical in patients with pulmonary hypertension. CMR feature-tracking (FT) strain analysis has emerged as a technique to detect subtle changes. However, the dependence of RV strain on load is still a matter of debate. The aim of this study was to measure the afterload dependence of RV strain and to correlate it with surrogate markers of contractility in a cohort of patients with chronic thromboembolic pulmonary hypertension (CTEPH) under two different loading conditions before and after pulmonary endarterectomy (PEA). Between 2009 and 2022, 496 patients with 601 CMR examinations were retrospectively identified from our CTEPH cohort, and the results of 194 examinations with right heart catheterization within 24 h were available. The CMR FT strain (longitudinal (GLS) and circumferential (GCS)) was computed on steady-state free precession (SSFP) cine CMR sequences. The effective pulmonary arterial elastance (Ea) and RV chamber elastance (Ees) were approximated by dividing mean pulmonary arterial pressure by the indexed stroke volume or end-systolic volume, respectively. GLS and GCS correlated significantly with Ea and Ees/Ea in the overall cohort and individually before and after PEA. There was no general correlation with Ees; however, under high afterload, before PEA, Ees correlated significantly. The results show that RV GLS and GCS are highly afterload-dependent and reflect ventriculoarterial coupling. Ees was significantly correlated with strain only under high loading conditions, which probably reflects contractile adaptation to pulsatile load rather than contractility in general.

ObjectiveTo evaluate changes in cardiac magnetic resonance (CMR) tissue characteristics in patients with active cardiac sarcoidosis (CS) confirmed by positron emission tomography (PET)-CT undergoing immunomodulatory therapy (IMT), and to explore their potential use for inflammation monitoring.DesignRetrospective observational cohort study.SettingTertiary care referral centre in Germany.ParticipantsFrom a cohort of 47 patients with CS, 24 patients with PET-confirmed active myocardial inflammation and complete baseline and follow-up CMR imaging after ≥6 months of IMT were included.Primary and secondary endpointsPrimary outcome: Changes in CMR-derived tissue characteristics (T1, T2 mapping, late gadolinium enhancement (LGE) mass). Secondary outcomes: Changes in functional (ejection fraction (EF) and global longitudinal strain (GLS)) and morphological parameters (end-diastolic/systolic volume indices (EDVi/ESVi)).ResultsPatients with PET-confirmed active CS show increased global T1 and T2 compared with healthy volunteers. Over the course of IMT, significant reductions in global T2 (median (IQR): 39 (38–41) ms vs 37 (36–39) ms; p=0.002), LGE-region T2 (43 (40–46) ms vs 41 (38–42) ms; p=0.003), and relative LGE mass (23% (17–38) vs 15% (8–32); p=0.006) were observed. No significant differences were found in EF (p=0.78), GLS (p=0.49), EDVi (p=0.56), ESVi (p=0.28) or native T1 values (p=0.23).ConclusionIn patients with PET-confirmed active CS undergoing IMT, serial CMR demonstrated measurable changes in T2 mapping and LGE parameters, suggesting a potential role for CMR tissue characterisation in monitoring myocardial inflammation. However, due to the observational design and absence of a control group, causal treatment effects cannot be confirmed. Further prospective studies are needed to validate the utility of CMR for treatment monitoring in CS.