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Hypertrophic cardiomyopathy (HCM) is the most common monogenic heart disease with a frequency as high as 1 in 200. In many cases, HCM is caused by mutations in genes encoding the different components of the sarcomere apparatus. Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy, myofibrillar disarray, and myocardial fibrosis. The phenotypic expression is quite variable. Although most patients with HCM are asymptomatic, serious consequences are experienced in a subset of affected individuals who present initially with sudden cardiac death or progress to refractory heart failure. The Hypertrophic Cardiomyopathy Registry study is a National Heart, Lung, and Blood Institute–sponsored 2,750-patient, 44-site, international registry and natural history study designed to address limitations in extant evidence to improve prognostication in HCM (NCT01915615). In addition to the collection of standard demographic, clinical, and echocardiographic variables, patients will undergo state-of-the-art cardiac magnetic resonance for assessment of left ventricular mass and volumes as well as replacement scarring and interstitial fibrosis. In addition, genetic and biomarker analyses will be performed. The Hypertrophic Cardiomyopathy Registry has the potential to change the paradigm of risk stratification in HCM, using novel markers to identify those at higher risk.

Cardiovascular magnetic resonance (CMR) has been established as a valuable tool in clinical and scientific cardiology. This study summarizes the current evidence and role of CMR in the guidelines of the European Society of Cardiology (ESC) and is an update of a former guideline analysis. Since the last guideline analysis performed in 2015, 28 new ESC guideline documents have been published. Twenty-seven ESC practice guidelines are currently in use. They were screened regarding CMR in the text, tables and figures. The main CMR-related sentences and recommendations were extracted. Nineteen of the 27 guidelines (70.4%) contain relevant text passages regarding CMR in the text and include 92 specific recommendations regarding the use of CMR. Seven guidelines (25.9%) mention CMR in the text, and 1 (3.7%, dyslipidemia) does not mention CMR. The 19 guidelines with recommendations regarding the use of CMR contain 40 class-I recommendations (43.5%), 28 class-IIa recommendations (30.4%), 19 class-IIb recommendations (20.7%) and 5 class-III recommendations (5.4%). Most of the recommendations have evidence level C (56/92; 60.9%), followed by level B (34/92; 37.0%) and level A (2/92; 2.2%). Twenty-one recommendations refer to the field of cardiomyopathies, 21 recommendations to stress perfusion imaging, 20 recommendations to vascular assessment, 12 to myocardial tissue characterization in general, 8 to left and right ventricular function assessment, 5 to the pericardium and 5 to myocarditis. CMR is integral part of the majority of the ESC guidelines. Its representation in the guidelines has increased since the last analysis from 2015, now comprising 92 instead of formerly 63 specific recommendations. To enable patient management in accordance to the ESC guidelines, CMR must become more widely available.

Aims Sepsis‐induced cardiomyopathy is a major complication of septic shock and contributes to its high mortality. This pilot study investigated myocardial tissue differentiation in critically ill, sedated, and ventilated patients with septic shock using cardiovascular magnetic resonance (MR). Methods and results Fifteen patients with septic shock were prospectively recruited from the intensive care unit. Individuals received a cardiac MR scan (1.5 T) within 48 h after initial catecholamine peak and a transthoracic echocardiography at 48 and 96 h after cardiac MR. Left ventricular ejection fraction was assessed using both imaging modalities. During cardiac MR imaging, balanced steady‐state free precession imaging was performed for evaluation of cardiac anatomy and function in long‐axis and short‐axis views. Native T1 maps (modified Look–Locker inversion recovery 5 s(3 s)3 s), T2 maps, and extracellular volume maps were acquired in mid‐ventricular short axis and assessed for average plane values. Patients were given 0.2 mmol/kg of gadoteridol for extracellular volume quantification and late gadolinium enhancement imaging. Critical care physicians monitored sedated and ventilated patients during the scan with continuous invasive monitoring and realized breathholds through manual ventilation breaks. Laboratory analysis included high‐sensitive troponine T and N terminal pro brain natriuretic peptide levels. Twelve individuals with complete datasets were available for analysis (age 59.5 ± 16.9 years; 6 female). Nine patients had impaired systolic function with left ventricular ejection fraction (LVEF) < 50% (39.8 ± 5.7%), and three individuals had preserved LVEF (66.9 ± 6.7%). Global longitudinal strain was impaired in both subgroups (LVEF impaired: 11.0 ± 1.8%; LVEF preserved: 16.0 ± 5.8%; P = 0.1). All patients with initially preserved LVEF died during hospital stay; in‐hospital mortality with initially impaired LVEF was 11%. Upon echocardiographic follow‐up, LVEF improved in all previously impaired patients at 48 (52.3 ± 9.0%, P = 0.06) and 96 h (54.9 ± 7.0%, P = 0.02). Patients with impaired systolic function had increased T2 times as compared with patients with preserved LVEF (60.8 ± 5.6 ms vs. 52.2 ± 2.8 ms; P = 0.02). Left ventricular GLS was decreased in all study individuals with impaired LVEF (11.0 ± 1.8%) and less impaired with preserved LVEF (16.0 ± 5.8%; P = 0.01). T1 mapping showed increased T1 times in patients with LVEF impairment as compared with patients with preserved LVEF (1093.9 ± 86.6 ms vs. 987.7 ± 69.3 ms; P = 0.03). Extracellular volume values were elevated in patients with LVEF impairment (27.9 ± 2.1%) as compared with patients with preserved LVEF (22.7 ± 1.9%; P < 0.01). Conclusions Septic cardiomyopathy with impaired LVEF reflects inflammatory cardiomyopathy. Takotsubo‐like contractility patterns occur in some cases. Cardiac MR is safely feasible in critically ill, sedated, and ventilated patients using extensive monitoring and experienced staff. Trial Registration: retrospectively registered (ISRCTN85297773)

Background To demonstrate the applicability of acoustic cardiac triggering (ACT) for imaging of the heart at ultrahigh magnetic fields (7.0 T) by comparing phonocardiogram, conventional vector electrocardiogram (ECG) and traditional pulse oximetry (POX) triggered 2D CINE acquisitions together with (i) a qualitative image quality analysis, (ii) an assessment of the left ventricular function parameter and (iii) an examination of trigger reliability and trigger detection variance derived from the signal waveforms. Results ECG was susceptible to severe distortions at 7.0 T. POX and ACT provided waveforms free of interferences from electromagnetic fields or from magneto-hydrodynamic effects. Frequent R-wave mis-registration occurred in ECG-triggered acquisitions with a failure rate of up to 30% resulting in cardiac motion induced artifacts. ACT and POX triggering produced images free of cardiac motion artefacts. ECG showed a severe jitter in the R-wave detection. POX also showed a trigger jitter of approximately Δt = 72 ms which is equivalent to two cardiac phases. ACT showed a jitter of approximately Δt = 5 ms only. ECG waveforms revealed a standard deviation for the cardiac trigger offset larger than that observed for ACT or POX waveforms. Image quality assessment showed that ACT substantially improved image quality as compared to ECG (image quality score at end-diastole: ECG = 1.7 ± 0.5, ACT = 2.4 ± 0.5, p = 0.04) while the comparison between ECG vs. POX gated acquisitions showed no significant differences in image quality (image quality score: ECG = 1.7 ± 0.5, POX = 2.0 ± 0.5, p = 0.34). Conclusions The applicability of acoustic triggering for cardiac CINE imaging at 7.0 T was demonstrated. ACT's trigger reliability and fidelity are superior to that of ECG and POX. ACT promises to be beneficial for cardiovascular magnetic resonance at ultra-high field strengths including 7.0 T.

Aims This study aims to assess subclinical changes in functional and morphological myocardial magnetic resonance parameters very early into an anthracycline treatment, which may predict subsequent development of anthracycline‐induced cardiomyopathy (aCMP). Methods and results Thirty sarcoma patients with planned anthracycline‐based chemotherapy (360–400 mg/m2 doxorubicin‐equivalent) were recruited. Median treatment time was 19.1 ± 2.1 weeks. Enrolled individuals received three cardiovascular magnetic resonance studies (before treatment, 48 h after first anthracycline treatment, and upon completion of treatment). Native T1 mapping (modified Look–Locker inversion recovery 5s(3s)3s), T2 mapping, and extracellular volume maps were acquired in addition to a conventional cardiovascular magnetic resonance with steady‐state free precession cine imaging at 1.5 T. Patients were given 0.2 mmol/kg gadoteridol for extracellular volume quantification and late gadolinium enhancement imaging. Development of relevant aCMP was defined as drop of left ventricular ejection fraction (LVEF) by >10%. For analysis, 23 complete data sets were available. Nine patients developed aCMP with LVEF reduction >10% until end of chemotherapy. Baseline LVEF was not different between patients with and without subsequent aCMP. When assessed 48 h after first dose of antracyclines, patients with subsequent aCMP had significantly lower native myocardial T1 times compared with before therapy (1002.0 ± 37.9 vs. 956.5 ± 29.2 ms, P < 0.01) than patients who did not develop aCMP (990.9 ± 56.4 vs. 978.4 ± 57.4 ms, P > 0.05). Patients with aCMP had decreased left ventricular mass upon completion of therapy (86.9 ± 24.5 vs. 81.1 ± 22.3 g; P = 0.02), while patients without aCMP did not show a change in left ventricular mass (81.8 ± 21.0 vs. 79.2 ± 18.1 g; P > 0.05). No patient developed new myocardial scars or compact myocardial fibrosis under chemotherapy. Conclusions Early decrease of T1 times 48 h after first treatment with anthracyclines can predict the development of subsequent aCMP after completion of chemotherapy.

The evidence that physical exercise lowers metabolic and cardiovascular risk is undisputed. Normobaric hypoxia training has been introduced to facilitate the effects of exercise. We tested the hypothesis that hypoxia training augments exercise‐related effects. We randomized 23 men with metabolic‐syndrome to single‐blinded exercise at normoxia (FiO2 21%) or hypoxia (FiO2 15%). Six weeks endurance training on a treadmill, 3 days per week, over 60 min at 60% VO2max was required. The study included the following: (1) metabolic phenotyping by indirect calorimetry and adipose and muscle tissue microdialysis to gain insight into effects on resting, postprandial, and exercise metabolism, (2) cardiac imaging, and (3) biopsies. Primary endpoint was the change in cardiorespiratory fitness; secondary endpoints were as follows: changes in body weight, waist circumference, blood pressure, cardiac dimensions, and adipose and muscle tissue metabolism and gene expression. Our subjects reduced waist circumference and improved several cardiovascular risk markers including blood pressure. However, these effects were similar in both training groups. Cardiac dimensions were not influenced. We focused on glucose metabolism. After an oral glucose load, adipose tissue metabolism was significantly shifted to a more lipolytic state under hypoxia, whereas muscle metabolism was similar under both conditions. Postprandial energy expenditure was significantly increased under hypoxia, whereas activity energy expenditure was improved under normoxia. Gene expression was not consistently influenced by FiO2. Adipose tissue triglyceride lipase, leptin, and hypoxia‐inducible factor‐alpha expression were increased by normoxia but not hypoxia. We had reported earlier that altitude (normobaric hypoxia) training at FIO2 15% might facilitate the effects of exercise training in normal people. We now tested this hypothesis in men with the metabolic syndrome. Exercise lowered blood pressure, reduced waist circumference, and improved metabolism. Adding hypoxia during training, however, caused no further improvement.

Aims This study aims to assess subclinical changes in functional and morphologic myocardial MR parameters very early into a repetitive high‐dose anthracycline treatment (planned cumulative dose >650 mg/m2), which may predict subsequent development of anthracycline‐induced cardiomyopathy (aCMP). Methods Thirty sarcoma patients with previous exposition of 300‐360 mg/m2 doxorubicin‐equivalent chemotherapy who were planned for a second treatment of anthracycline‐based chemotherapy (360 mg/m2 doxorubicin‐equivalent) were recruited. Enrolled individuals received three CMR studies (before treatment, 48 h after first anthracycline treatment and upon completion of treatment). Native T1 mapping (MOLLI 5s(3s)3s), T2 mapping, and extracellular volume (ECV) maps were acquired in addition to a conventional CMR with SSFP‐cine imaging at 1.5 T. Patients were given 0.2 mmol/kg gadoteridol for ECV quantification and LGE imaging. Blood samples for cardiac biomarkers were obtained before each scan. Development of relevant aCMP was defined as drop of left ventricular ejection fraction (LVEF) by >10% compared with baseline. Results Twenty‐three complete datasets were available for analysis. Median treatment time was 20.7 ± 3.0 weeks. Eight patients developed aCMP with LVEF reduction >10% until end of chemotherapy. Baseline LVEF was not different between patients with and without subsequent aCMP. Patients with aCMP had decreased LV mass upon completion of therapy (99.4 ± 26.5 g vs. 90.3 ± 24.8 g; P = 0.02), whereas patients without aCMP did not show a change in LV mass (91.5 ± 20.0 g vs. 89.0 ± 23.6 g; P > 0.05). On strain analysis, GLS (−15.3 ± 1.3 vs. ‐13.4 ± 1.6; P = 0.02) and GCS (−16.7 ± 2.1 vs. ‐14.9 ± 2.6; P = 0.04) were decreased in aCMP patients upon completion of therapy, whereas non‐aCMP individuals showed no change in GLS (−15.4 ± 3.3 vs. −15.4 ± 3.4; P = 0.97). When assessed 48 h after first dose of anthracyclines, patients with subsequent aCMP had significantly elevated myocardial T2 times compared with before therapy (53.0 ± 2.8 ms vs. 49.3 ± 5.2 ms, P = 0.02) than patients who did not develop aCMP (50.7 ± 5.1 ms vs. 51.1 ± 3.9 ms, P > 0.05). Native T1 times decreased at 48 h after first dose irrespective of development of subsequent aCMP (1020.2 ± 28.4 ms vs. 973.5 ± 40.3 ms). Upon completion of therapy, patients with aCMP had increased native T1 compared with baseline (1050.8 ± 17.9 ms vs. 1022.4 ± 22.0 ms; P = 0.01), whereas non‐aCMP patients did not (1034.5 ± 46.6 ms vs. 1018.4 ± 29.7 ms; P = 0.15). No patient developed new myocardial scars or compact myocardial fibrosis under chemotherapy. Cardiac biomarkers were elevated independent of development of aCMP. Conclusions With high cumulative anthracycline doses, early increase of T2 times 48 h after first treatment with anthracyclines can predict the development of subsequent aCMP after completion of chemotherapy. Early drop of native T1 times occurs irrespective of development of aCMP in high‐dose anthracycline therapy.

Whereas evidence supporting the diagnostic value of cardiovascular magnetic resonance (CMR) has increased, there exists significant worldwide variability in the clinical utilization of CMR. A recent study demonstrated that CMR is represented in the majority of European Society for Cardiology (ESC) guidelines, with a large number of specific recommendations in particular regarding coronary artery disease. To further investigate the gap between the evidence and clinical use of CMR, this study analyzed the role of CMR in the guidelines of the American College of Cardiology (ACC) and American Heart Association (AHA). Twenty-four AHA/ACC original guidelines, updates and new editions, published between 2006 and 2017, were screened for the terms “magnetic”, “MRI”, “CMR”, “MR” and “imaging”. Non-cardiovascular MR examinations were excluded. All CMR-related paragraphs and specific recommendations for CMR including the level of evidence (A, B, C) and the class of recommendation (I, IIa, IIb, III) were extracted. Twelve of the 24 guidelines (50.0%) contain specific recommendations regarding CMR. Four guidelines (16.7%) mention CMR in the text only, and 8 (33.3%) do not mention CMR. The 12 guidelines with recommendations for CMR contain in total 65 specific recommendations (31 class-I, 23 class-IIa, 6 class-IIb, 5 class-III). Most recommendations have evidence level C (44/65; 67.7%), followed by level B (21/65; 32.3%). There are no level A recommendations. 22/65 recommendations refer to vascular imaging, 17 to congenital heart disease, 8 to cardiomyopathies, 8 to myocardial stress testing, 5 to left and right ventricular function, 3 to viability, and 2 to valvular heart disease. CMR is represented in two thirds of the AHA/ACC guidelines, which contain a number of specific recommendations for the use of CMR. In a simplified comparison with the ESC guidelines, CMR is less represented in the AHA/ACC guidelines in particular in the field of coronary artery disease.

Aims Neprilysin (NEP), a zinc metallopeptidase, degrades a variety of bioactive peptides including natriuretic peptides terminating their biological action on arterial blood pressure and natriuresis. Pharmacological inhibition of NEP reduces mortality in patients with heart failure with reduced ejection fraction. Physiological interventions reducing NEP levels are unknown in humans. Because obesity leads to increased NEP levels and increases the risk for heart failure, we hypothesized that weight loss reduces NEP concentrations in plasma and tissue. Methods and results We randomized overweight to obese human subjects to a low‐fat or low‐carbohydrate hypocaloric 6 month weight loss intervention. Soluble NEP was determined in plasma, and NEP mRNA was analysed from subcutaneous adipose tissue before and after diet. Low‐fat diet‐induced weight loss reduced soluble NEP levels from 0.83 ± 0.18 to 0.72 ± 0.18 μg/L (P = 0.038), while subcutaneous adipose tissue NEP mRNA expression was reduced by both dietary interventions [21% (P = 0.0057) by low‐fat diet and 16% (P = 0.048) by low‐carbohydrate diet]. We also analysed the polymorphisms of the gene coding for NEP, rs9827586 and rs701109, known to be associated with plasma NEP levels. For both single‐nucleotide polymorphisms, minor allele carriers (A/A) had higher baseline plasma NEP levels (rs9827586: β = 0.53 ± 0.23, P < 0.0001; rs701109: β = 0.43 ± 0.22, P = 0.0016), and minor allele carriers of rs9827586 responded to weight loss with a larger NEP reduction (rs9827586: P = 0.0048). Conclusions Our study identifies weight loss via a hypocaloric low‐fat diet as the first physiological intervention in humans to reduce NEP in plasma and adipose tissue. Specific single‐nucleotide polymorphisms further contribute to the decrease. Our findings may help to explain the beneficial effect of weight loss on cardiac function in patients with heart failure.

Aims Heart failure with preserved ejection fraction is still a diagnostic and therapeutic challenge, and accurate non‐invasive diagnosis of left ventricular (LV) diastolic dysfunction (DD) remains difficult. The current study aimed at identifying the most informative cardiovascular magnetic resonance (CMR) parameters for the assessment of LVDD. Methods and results We prospectively included 50 patients and classified them into three groups: with DD (DD+, n = 15), without (DD−, n = 26), and uncertain (DD±, n = 9). Diagnosis of DD was based on echocardiographic E/E′, invasive LV end‐diastolic pressure, and N‐terminal pro‐brain natriuretic peptide. CMR was performed at 1.5 T to assess LV and left atrial (LA) morphology, LV diastolic strain rate (SR) by tissue tracking and tagging, myocardial peak velocities by tissue phase mapping, and transmitral inflow profile using phase contrast techniques. Statistics were performed only on definitive DD+ and DD− (total number 41). DD+ showed enlarged LA with LA end‐diastolic volume/height performing best to identify DD+ with a cut‐off value of ≥0.52 mL/cm (sensitivity = 0.71, specificity = 0.84, and area under the receiver operating characteristic curve = 0.75). DD+ showed significantly reduced radial (inferolateral E peak: DD−: −14.5 ± 6.5%/s vs. DD+: −10.9 ± 5.9%/s, P = 0.04; anterolateral A peak: DD−: −4.2 ± 1.6%/s vs. DD+: −3.1 ± 1.4%/s, P = 0.04) and circumferential (inferolateral A peak: DD−: 3.8 ± 1.2%/s vs. DD+: 2.8 ± 0.8%/s, P = 0.007; anterolateral A peak: DD−: 3.5 ± 1.2%/s vs. DD+: 2.5 ± 0.8%/s, P = 0.048) SR in the basal lateral wall assessed by tissue tracking. In the same segments, DD+ showed lower peak myocardial velocity by tissue phase mapping (inferolateral radial peak: DD−: −3.6 ± 0.7 ms vs. DD+: −2.8 ± 1.0 ms, P = 0.017; anterolateral longitudinal peak: DD−: −5.0 ± 1.8 ms vs. DD+: −3.4 ± 1.4 ms, P = 0.006). Tagging revealed reduced global longitudinal SR in DD+ (DD−: 45.8 ± 12.0%/s vs. DD+: 34.8 ± 9.2%/s, P = 0.022). Global circumferential and radial SR by tissue tracking and tagging, LV morphology, and transmitral flow did not differ between DD+ and DD−. Conclusions Left atrial size and regional quantitative myocardial deformation applying CMR identified best patients with DD.