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Feasibility of automated volume-derived cardiac functional evaluation has successfully been demonstrated using cardiovascular magnetic resonance (CMR) imaging. Notwithstanding, strain assessment has proven incremental value for cardiovascular risk stratification. Since introduction of deformation imaging to clinical practice has been complicated by time-consuming post-processing, we sought to investigate automation respectively. CMR data (n = 1095 patients) from two prospectively recruited acute myocardial infarction (AMI) populations with ST-elevation (STEMI) (AIDA STEMI n = 759) and non-STEMI (TATORT-NSTEMI n = 336) were analysed fully automated and manually on conventional cine sequences. LV function assessment included global longitudinal, circumferential, and radial strains (GLS/GCS/GRS). Agreements were assessed between automated and manual strain assessments. The former were assessed for major adverse cardiac event (MACE) prediction within 12 months following AMI. Manually and automated derived GLS showed the best and excellent agreement with an intraclass correlation coefficient (ICC) of 0.81. Agreement was good for GCS and poor for GRS. Amongst automated analyses, GLS (HR 1.12, 95% CI 1.08–1.16, p < 0.001) and GCS (HR 1.07, 95% CI 1.05–1.10, p < 0.001) best predicted MACE with similar diagnostic accuracy compared to manual analyses; area under the curve (AUC) for GLS (auto 0.691 vs. manual 0.693, p = 0.801) and GCS (auto 0.668 vs. manual 0.686, p = 0.425). Amongst automated functional analyses, GLS was the only independent predictor of MACE in multivariate analyses (HR 1.10, 95% CI 1.04–1.15, p < 0.001). Considering high agreement of automated GLS and equally high accuracy for risk prediction compared to the reference standard of manual analyses, automation may improve efficiency and aid in clinical routine implementation. Trial registration: ClinicalTrials.gov, NCT00712101 and NCT01612312. [ABSTRACT FROM AUTHOR]

MR imaging with an albumin-binding probe enables the visualization of endothelial permeability and damage in the arterial system. The goal of this study was to compare signal enhancement of lesions with different grades of stenosis segments on molecular CMR in combination with the albumin-binding probe gadofosveset. This prospective clinical study included patients with symptoms suggestive of coronary artery disease (CAD). Patients underwent gadofosveset-enhanced cardiovascular magnetic resonance (CMR) imaging and x-ray angiography (QCA) within 24 h. CMR imaging was performed prior to and 24 h following the administration of gadofosveset. Contrast-to-noise ratios (CNRs) between segments with different grades of stenosis were compared. Overall, n = 203 segments of 26 patients were included. Lesions with more than > 70% stenosis demonstrated significantly higher CNRs compared to lesions < 70% (7.6 ± 8.3 vs. 2.5 ± 4.9; p < 0.001). Post-stenotic segments of lesions > 70% stenosis showed significant higher signal enhancement compared to segments located upstream of these lesions (7.3 ± 8.8 vs. 2.8 ± 2.2; p = 0.02). No difference in signal enhancement between segments proximal and distal of lesions with stenosis greater than 50% was measured (3.3 ± 2.8 vs. 2.4 ± 2.7; p = 0.18). ROC analysis for the detection of lesions ≥ 70% revealed an area under the curve of 0.774 (95% CI 0.681-0.866). This study suggests that relevant coronary stenosis and their down-stream segments are associated with increased signal enhancement on Gadofosveset-enhanced CMR, suggesting a higher endothelial permeability in these lesions. An albumin-binding MR probe could represent a novel in vivo biomarker for the identification and characterization of these vulnerable coronary segments. [ABSTRACT FROM AUTHOR]

Background: Cardiac PET has recently found novel applications in coronary atherosclerosis imaging using [18F]NaF as a radiotracer, highlighting vulnerable plaques. However, the resulting uptakes are relatively small, and cardiac motion and respiration-induced movement of the heart can impair the reconstructed images due to motion blurring and attenuation correction mismatches. This study aimed to apply an MR-based motion compensation framework to [18F]NaF data yielding high-resolution motion-compensated PET and MR images. Methods: Free-breathing 3-dimensional Dixon MR data were acquired, retrospectively binned into multiple respiratory and cardiac motion states, and split into fat and water fraction using a model-based reconstruction framework. From the dynamic MR reconstructions, both a non-rigid cardiorespiratory motion model and a motion-resolved attenuation map were generated and applied to the PET data to improve image quality. The approach was tested in 10 patients and focal tracer hotspots were evaluated concerning their target-to-background ratio, contrast-to-background ratio, and their diameter. Results: MR-based motion models were successfully applied to compensate for physiological motion in both PET and MR. Target-to-background ratios of identified plaques improved by 7 ± 7%, contrast-to-background ratios by 26 ± 38%, and the plaque diameter decreased by −22 ± 18%. MR-based dynamic attenuation correction strongly reduced attenuation correction artefacts and was not affected by stent-related signal voids in the underlying MR reconstructions. Conclusions: The MR-based motion correction framework presented here can improve the target-to-background, contrast-to-background, and width of focal tracer hotspots in the coronary system. The dynamic attenuation correction could effectively mitigate the risk of attenuation correction artefacts in the coronaries at the lung-soft tissue boundary. In combination, this could enable a more reproducible and reliable plaque localisation. [ABSTRACT FROM AUTHOR]

Background: Cardiac magnetic resonance myocardial feature tracking (CMR-FT)-derived global strain assessments provide incremental prognostic information in patients following acute myocardial infarction (AMI). Functional analyses of the remote myocardium (RM) are scarce and whether they provide an additional prognostic value in these patients is unknown. Methods: 1034 patients following acute myocardial infarction were included. CMR imaging and strain analyses as well as infarct size quantification were performed after reperfusion by primary percutaneous coronary intervention. The occurrence of major adverse cardiac events (MACE) within 12 months after the index event was defined as primary clinical endpoint. Results: Patients with MACE had significantly lower RM circumferential strain (CS) compared to those without MACE. A cutoff value for RM CS of − 25.8% best identified high-risk patients (p < 0.001 on log-rank testing) and impaired RM CS was a strong predictor of MACE (HR 1.05, 95% CI 1.07–1.14, p = 0.003). RM CS provided further risk stratification among patients considered at risk according to established CMR parameters for (1) patients with reduced left ventricular ejection fraction (LVEF) ≤ 35% (p = 0.038 on log-rank testing), (2) patients with reduced global circumferential strain (GCS) > − 18.3% (p = 0.015 on log-rank testing), and (3) patients with large microvascular obstruction ≥ 1.46% (p = 0.002 on log-rank testing). Conclusion: CMR-FT-derived RM CS is a useful parameter to characterize the response of the remote myocardium and allows improved stratification following AMI beyond commonly used parameters, especially of high-risk patients. Trial registration: ClinicalTrials.gov, NCT00712101 and NCT01612312 Defining remote segments (R) in the presence of infarct areas (I) for the analysis of remote circumferential strain (CS). Remote CS was significantly lower in patients who suffered major adverse cardiac events (MACE) and a cutoff value for remote CS of − 25.8% best identified high-risk patients. In addition, impaired remote CS ≥ − 25.8 % (Remote −) and preserved remote CS < − 25.8 % (Remote +) enabled further risk stratification when added to established parameters like left ventricular ejection fraction (LVEF), global circumferential strain (GCS) or microvascular obstruction (MVO). [ABSTRACT FROM AUTHOR]

Takotsubo syndrome (TTS) is an acute and mostly reversible cardiomyopathy that mimics an acute coronary syndrome with left ventricular (LV) systolic dysfunction without relevant obstructive coronary artery disease. Its prevalence is probably underestimated and reaches 1.2-2% in patients with acute coronary syndrome undergoing coronary catheterization. Although supraphysiological epinephrine levels have been associated with TTS, the detailed pathophysiology is incompletely understood. Chest pain is the most common clinical presentation; however, cardiac decompensation, cardiogenic shock, and sudden cardiac death due to ventricular fibrillation may also be the first clinical manifestations. Patients are mostly postmenopausal women, in whom the condition is commonly associated with emotional triggers; however, men have a higher prevalence of TTS being associated with physical triggers, which has a worse prognosis compared with TTS associated with emotional triggers. As a diagnosis of exclusion, TTS has no single definitive diagnostic test. According to the distribution of LV wall motion abnormalities, various morphological subtypes have been identified. The final diagnosis depends on cardiac imaging with left ventricular angiography during acute heart catheterization, as well as on echocardiography and cardiac magnetic resonance. Most patients recover completely, albeit several factors have been associated with worse prognosis. Management is based on observational data, while randomized multicenter studies are still lacking. This review provides a general overview of TTS and focuses on the hypothesized pathophysiology, and especially on current practices in diagnosis, prognosis, and treatment. [ABSTRACT FROM AUTHOR]

Meta-analysis on immunohistological (IHC) concepts for the detection of inflammatory cardiomyopathy (InfCM) in endomyocardial biopsies (EMB). We included 61 publications, with 10,491 patients (mean age 47.1 years; men 66%) who underwent EMB and IHC evaluation. The 460 control patients were devoid of IHC proof of InfCM. The mean IHC detection rate of InfCM was 50.8% (95% CI 47.7-53.8%; range 18.4-91.7%). A publication bias was excluded (Funnel Plot p = 0.4264). This IHC detection rate was significantly (p < 0.0001) higher compared to the histological detection of myocarditis according to the Dallas criteria (mean 8.04%; 95% CI 5.08-12.5%; subset of 3274 patients in 30 publications). However, 13 different diagnostic IHC criteria were described in the publications, with various thresholds of diverse phenotypes of quantified infiltrates, and endothelial expression of diverse cell adhesion molecules (CAM), quantified either visually or by digital image analysis (DIA). The comparison of IHC with cardiac magnetic resonance (CMR) data available in a subset of 13 publications with 1185 patients revealed a sensitivity for CMR of 69% (95% CI 58-79%), a specificity of 73% (95% CI 59-84%), and a ROC-AUC of 0.77 (95% CI 0.73-0.81). This meta-analysis encompassing 10,491 patients confirms a mean detection rate of InfCM in 50.8% of EMB, being significantly more sensitive compared to the histological Dallas criteria. IHC cannot be fully substituted by CMR. However, standardization of the diverse IHC markers and protocols seems pertinent, especially considering the published adverse prognostic impact of IHC-confirmed InfCM and its published suitability for the selection of candidates responding favorably to immunosuppression. [ABSTRACT FROM AUTHOR]

Background: Prognosis in acute myocardial infarction (AMI) depends on the amount of infarct-related artery (IRA)-subtended myocardium and associated damage but has not been described in great detail. Consequently, we sought to describe IRA-associated pathophysiological consequences using cardiac magnetic resonance (CMR). Methods: 1235 AMI patients (n = 795 ST-elevation (STEMI) and 440 non-STEMI) underwent CMR following percutaneous coronary intervention. Blinded core-laboratory data were compared according to left anterior descending (LAD), left circumflex (LCx) and right coronary artery (RCA) regarding major adverse clinical events (MACE) within 12 months. Left ventricular (LV) global longitudinal/circumferential/radial (GLS/GCS/GRS) as well as left atrial (LA) total (εs), passive (εe) and active (εa) strains were determined using CMR-feature tracking. Tissue characterisation included infarct size (IS) and microvascular obstruction. Results: LAD and LCx were associated with higher mortality compared to RCA lesions (4.6% and 4.4% vs 1.6%). LAD lesions showed largest IS (16.8%), largest ventricular [LV ejection fraction (EF) 47.4%, GLS − 13.2%, GCS − 20.8%] and atrial (εs 20.2%) impairment. There was less impairment in LCx (IS 11.8%, LVEF 50.8%, GLS − 17.4%, GCS − 25.0%, εs 20.7%) followed by RCA lesions (IS 11.3%, LVEF 50.8%, GLS − 19.1%, GCS − 26.6%, εs 21.7%). In AUC analyses, εs (LAD, RCA) and GLS (LCx) best predicted MACE (AUC > 0.69). Multivariate analyses identified εs (p = 0.017) in LAD and GLS (p = 0.034) in LCx infarcts as independent predictors of MACE. Conclusions: CMR allows IRA-specific phenotyping and characterisation of morphologic and functional changes. These alterations carry infarct-specific prognostic implications, and may represent novel diagnostic and therapeutic targets following AMI. Trial registration: ClinicalTrials.gov: NCT00712101 and NCT01612312 [ABSTRACT FROM AUTHOR]

Amyloidosis is caused by extracellular deposition of insoluble abnormal fibrils constituted by misfolded proteins, which can modify tissue anatomy and hinder the function of multiple organs including the heart. Amyloidosis that can affect the heart includes mostly systemic amyloidosis (amyloid light chain, AL) and transthyretin amyloidosis (ATTR). The latter can be acquired in elderly patients (ATTRwt), or be inherited in younger individuals (ATTRm). The diagnosis is demanding given the high phenotypic heterogeneity of the disease. Therefore, "red flags," which are suggestive features giving support to diagnostic suspicion, are extremely valuable. However, the lack of broad awareness among clinicians represents a major obstacle for early diagnosis and treatment of ATTR. Furthermore, recent implementation of noninvasive diagnostic techniques has revisited the need for endomyocardial biopsy (EMB). In fact, unlike AL amyloidosis, which requires tissue confirmation and typing for diagnosis, ATTR can now be diagnosed noninvasively with the combination of bone scintigraphy and the absence of a monoclonal protein. Securing the correct diagnosis is pivotal for the newly available therapeutic options targeting both ATTRm and ATTRwt, and are directed to either stabilization of the abnormal protein or the reduction of the production of transthyretin. The purpose of this article is to review the contemporary aspects of diagnosis and management of transthyretin amyloidosis with cardiac involvement, summarizing also the recent therapeutic advances with tafamidis, patisiran, and inotersen. [ABSTRACT FROM AUTHOR]

Treatment of left ventricular outflow tract (LVOT) obstruction in hypertrophic obstructive cardiomyopathy (HOCM) with septal reduction, either with myectomy or alcohol septal ablation, is aiming to reduce the LVOT gradient and improve symptoms in patients who are refractory to or do not tolerate medical treatment. Apart from contributing to the evolution to heart failure, LVOT obstruction is considered a risk factor for sudden cardiac death (SCD). Both septal reduction treatments have been proven effective in reducing symptoms and seem to improve survival, which has been shown equal to the expected in the normal population. SCD is probably reduced after septal reduction, implying that LVOT obstruction is a major factor predisposing to ventricular tachyarrhythmias. Although available algorithms for SCD stratification have not been tested in patients after septal reduction treatments, effective treatment improves SCD risk profile substantially. Furthermore, high-risk patients with already implanted implantable cardioverter defibrillators (ICDs) before septal reduction show very low appropriate ICD shock rate after effective treatment. It should be noted, however, that the best outcomes for septal myectomy or ablation have been reported in HOCM patients treated in high-volume centres, which substantiates the need to refer patients to centres with high procedural expertise. [ABSTRACT FROM AUTHOR]

In iron overload diseases (thalassemia, sickle cell, and myelodysplastic syndrome), iron is deposited in all internal organs, leading to functional abnormalities. Hematopoietic stem cell transplantation (HSCT) is the only treatment offering a potential cure in these diseases. Our aim was to describe the experience in the field and the role of magnetic resonance imaging in the evaluation of iron overload before and after HSCT. Magnetic resonance imaging (MRI), using T2*, is the most commonly used tool to diagnose myocardial-liver iron overload and guide tailored treatment. Currently, HSCT offers complete cure in thalassemia major, after overcoming the immunologic barrier, and should be considered for all patients who have a suitable donor. The overall thalassemia-free survival of low-risk, HLA-matched sibling stem cell transplantation patients is 85-90%, with a 95% overall survival. The problems of rejection and engraftment are improving with the use of adequate immunosuppression. However, a detailed iron assessment of both heart and liver is necessary for pre- and post-transplant evaluation. In iron overload diseases, heart and liver iron evaluation is indispensable not only for the patients' survival, but also for evaluation before and after HSCT. [ABSTRACT FROM AUTHOR]

Cardiomyopathies are complex diseases of multifactorial pathogenesis and have a high morbidity and mortality. Over the past decades, several revisions of classifications and definitions of cardiomyopathies have been proposed, primarily focusing on the phenotypic characterization of cardiomyopathies. The MOGE(S) classification system published in 2013 encompasses the classification of rapidly growing knowledge on genetic mutations, acquired causes (i.e., intramyocardial inflammation, viral infections), and further conditions involved in the induction of cardiomyopathies (e.g., storage diseases, toxicity). It is based on five attributes, including morphofunctional characteristics (M), organ involvement (O), genetic or familial inheritance pattern (G), etiological annotation (E), and optional information about the heart failure functional status (S). This review summarizes the development, the cornerstones of the MOGE(S) classification, and the published data on the clinical relevance of the MOGE(S) classification. We furthermore discuss new issues which might be considered for future updates of the MOGE(S) classification of cardiomyopathies. [ABSTRACT FROM AUTHOR]

A 74-year-old female patient was referred to our department in 2015 with dyspnea, cough and dysphagia. She had been diagnosed with adenocarcinoma of the right breast in 1986 and underwent mastectomy. When she presented with a local recurrence in 1988, she was receiving high-voltage radiation therapy. Transthoracic echocardiography and magnetic resonance imaging revealed tricuspid regurgitation grade III and unclear right heart failure with a massively dilated right atrium. Coronary heart disease could be ruled out. In summary, the patient's findings represented right ventricular myocardial restriction which we attributed to irradiation of the right anterior chest 17 years previously. [ABSTRACT FROM AUTHOR]

Late gadolinium enhancement (LGE) is widely used to precisely localize and determine the extent and transmurality of myocardial scarring. Performing LGE imaging at end-systole may reduce motion artefacts. It is therefore important to know whether end-systolic imaging influences infarct transmurality in patients with ischemic scar. 107 dysfunctional segments were studied in 20 consecutive patients with established coronary artery disease. Patient specific trigger delays were used to obtain end-diastolic and end-systolic LGE images (LGE, LGE). Wall thickness (WT, WT), thickness of the remaining viable rim (RIM, RIM) and end-diastolic scar thickness were measured manually. There was LGE in 84% of all dysfunctional segments with a mean scar of 3.4 ± 2.5 mm. Total wall thickness and the thickness of the remaining viable rim increased from diastole to systole (WT 7.8 ± 1.9 vs. WT 8.4 ± 2.2; P < 0.001; RIM 4.4 ± 3.1 vs. RIM 5 ± 3.4; P < 0.001). Transmurality of scar decreased from end-diastole to end-systole (LGE 46 ± 33% vs. LGE 44 ± 33%; P < 0.001). This was most pronounced in a subgroup of segments ( n = 15) with visual scar transmurality between 50 and 75% (LGE 75 ± 15% vs. LGE 70 ± 16%; P < 0.001). The change in transmurality was inversely correlated with the change of the thickness of the remaining viable rim between diastole and systole ( r = −0.7; P < 0.001). Scar transmurality was reduced by up to 12% in the individual patient. Scar transmurality changes due to thickening of the remaining viable rim. Whereas these differences might not impact on clinical decision-making in most patients, there will be an occasional misclassification if cut-off values are used (e.g. scar <50 or >50%) or if exact data is required for research studies. [ABSTRACT FROM AUTHOR]

Platelets have been regarded as static cells that do not move once they adhere to a matrix. The present study explored, whether platelets are able to migrate. In contrast to the current opinion, we found that platelets were mobile, able to migrate over a surface, and transmigrate through a transwell membrane and endothelium toward a source of stromal cell-derived factor 1 (SDF-1). Platelet migration was stimulated by SDF-1, which led to the downstream activation and phosphorylation of Wiskott-Aldrich syndrome protein. SDF-1 signaling and subsequent platelet migration could be inhibited by CXCR4-receptor blocker AMD3100, pertussis toxin, inhibition of phosphoinositol 3-kinase (PI3 kinase) with LY294002 or wortmannin, and disruption of actin polymerization with cytochalasin B. The potential of platelets to migrate in an SDF-1-mediated fashion may redefine the role of platelets in the pathophysiology of vascular inflammation, subsequent atherosclerotic degeneration, and vascular regeneration. [ABSTRACT FROM AUTHOR]

Background: Type-2 diabetes is accompanied by a prothrombotic state influenced by endothelial dysfunction, inflammatory condition and platelet hyperreagibility. We aimed to characterize the relationship of inflammation and residual platelet aggregability (RPA) under antiplatelet therapy with regard to prognosis in an unselected PCI-cohort of diabetics. Methods: In a first step, a consecutive collective of 75 type 2 diabetics compared to 153 non-diabetic controls was evaluated at the time of PCI. Inflammatory markers, Interleukin 6 and C-reactive protein were measured by immunoassays. ADP and Aspirin assays were performed by multiple electrode aggregometry. Then, we consecutively evaluated ADP-induced RPA in 542 diabetics and 1,161 non-diabetics undergoing PCI and treated by standard antiplatelet therapy. Major CV-events were assessed at 30 days after PCI. Results: Inflammatory markers were significantly increased in diabetics with peri-interventional hyperglycemic state and inversely correlated with responsiveness to clopidogrel and aspirin. In a large scale cohort, diabetics showed a higher RPA compared to non-diabetics (median 38.1 vs. 28.8%; p < 0.001). After adjustment for relevant co-factors, diabetes remained a strong predictor for increased RPA (OR 4.39; 95% CI 1.95-6.83; p < 0.001). Furthermore, diabetics with high RPA had an increased risk for 30-day MI and CV-death than diabetics with low RPA (adjusted HR 1.05; 95% CI 1.02-1.07; p < 0.001). Conclusions: We demonstrate that peri-interventional inflammatory degree and glycaemic control correlate with decreased antiplatelet drug responsiveness in diabetics. In addition, we identified high RPA as strong predictor for short-term CV-events in this group. Therefore, approaches to treat these entities are needed to improve outcome in diabetics undergoing PCI. [ABSTRACT FROM AUTHOR]

Several lines of evidence suggest a viral infection as the initiating event for the development of myocarditis (MC). Especially enteroviruses like coxsackie B3 virus have been shown to induce MC in humans and strains of MC-prone mice after an infection. The further course of the disease is, however, determined not only by the viral infection but also by the host’s immune system. Both the humoral and the cellular immune system can modify the extent of the damage caused by the disease. The humoral immune system mounts an anti-viral immune response immediately after the infection; however, during the course of the disease, autoantibodies against a variety of different autoantigens emerge. The epitopes recognized by the anti-viral antibodies and those of several autoantibodies have been identified using synthetic peptides. The human disease could be transferred into SCID mice using peripheral blood leukocytes of patients, suggesting a pathophysiological significance of the autoimmune reaction. However, the significance of the humoral immune responses needs to be tested in randomized, prospective studies using immunoadsorption of autoantibodies in patients with inflammatory cardiomyopathy. [ABSTRACT FROM AUTHOR]

Purpose of Review: The purpose of this paper is to review the latest advancements and developments in non-invasive coronary magnetic resonance (MR) and hybrid positron emission tomography (PET)/MR imaging. Recent Findings: Coronary MRI has advanced in recent years in different aspects, especially regarding technical developments, scan protocols, and molecular probes. Recently introduced hybrid PET/MR scanners have already demonstrated great potential in improving cardiovascular imaging. Summary: Coronary atherosclerosis and acute myocardial infarction remain major threats to physical health worldwide. Several techniques, from invasive intravascular imaging to non-invasive imaging methods, are studied extensively to identify patients with vulnerable plaques at risk for adverse coronary events. While imaging of vulnerable plaques is getting more and more sophisticated, the clinical impact of molecular plaque imaging on prognosis and disease management still has to be fully defined. [ABSTRACT FROM AUTHOR]