The Role of Magnetic Resonance Imaging in Risk Stratification of Patients with Acute Myocarditis.

BACKGROUND: Cardiac magnetic resonance (cMRI) is often used to diagnose acute myocarditis (AM). It is also performed after 6 months to monitor myocardial involvement. However, the clinical and predictive relevance of the 6-month cMRI is uncertain. OBJECTIVE: We used cMRI to assess the morphology and heart function of patients with AM, the correlation between left ventricular remodeling and biomarkers of heart dysfunction and myocardial fibrosis, and the involvement of myocardial fibrosis initially and 6 months after the acute episode. MATERIALS AND METHODS: We conducted a prospective study of 90 patients with the clinical suspicion of AM, where cMRI was performed within the first week after symptom onset and repeated after 6 months. RESULTS: Non-ischemic late gadolinium enhancement (LGE) was present in 88 (97.7%) patients and mainly involved the septum and inferior wall. cMRI at 6 months was associated with significantly reduced abnormalities of segmental kinetics (p < 0.001), myocardial edema (p < 0.001), presence of LGE (p < 0.05) and LGE mass (p < 0.01), native T1 mapping (p < 0.001), and presence of pericardial collection (p ≤ 0.001). At 6 months, signs of myocardial edema appeared in 34.4% of patients, and a complete cure (absence of edema and LGE) was found in 8.8% of patients. LGE disappeared in 15.2% of patients, and the mean number of myocardial segments involved decreased from 46% to 30%, remaining unchanged in 13% of patients. Patients with LGE without edema had a more severe prognostic condition than those with persistent edema. Patients with increased LGE extension on the control cMRI had a worse prognosis than those with modified or low LGE. The most significant independent predictive parameters for major cardiovascular events (MACEs) were LGE mass (adjusted OR = 1.27 [1.11-1.99], p < 0.001), myocardial edema (OR = 1.70 [1.14-209.3], p < 0.001), and prolonged native T1 (OR = 0.97 [0.88-3.06], p < 0.001). The mid-wall model of LGE and the presence of edema-free LGE were MACE-independent predictors. CONCLUSIONS: LGE, myocardial edema, and prolonged native T1 were predictors of MACEs. LGE does not necessarily mean constituted fibrosis in the presence of edema and may disappear over time. LGE without edema could represent fibrosis, whereas the persistence of edema represents active inflammation and could be associated with the residual chance of complete recovery. cMRI should be performed in all patients with AM at 6 months to evaluate progress and prognosis.

Left Ventricular Fibrosis by Cardiac Magnetic Resonance Tissue Characterization in Chronic Mitral Regurgitation Patients.

Background: Left ventricular remodeling in chronic mitral regurgitation (MR) encompasses two types of myocardial fibrosis: replacement fibrosis, identified by late gadolinium enhancement (LGE), and diffuse interstitial fibrosis, assessed by pre- and postcontrast T1 mapping techniques. These may explain irreversible LV dysfunction after MR correction. We aimed to assess the presence of myocardial fibrosis in patients with moderate and severe MR with no criteria for surgery versus mild MR controls. Methods: We enrolled 137 patients with chronic primary MR and 130 controls; all underwent cardiac magnetic resonance, and were followed up in a median of 2.9 years to assess mortality and the need for mitral valve replacement. Results: Patients in the study group displayed significantly higher degrees of LGE (28.4% vs 7.69%, p < 0.05), higher native T1 values (1167 ± 58.5 versus 971 ± 51.4 (p < 0.05)), and higher extracellular volumes compared to controls (32.3% ± 3.5 versus 23.9 ± 2.2, (p < 0.05)). The composite outcome occurred in 28 patients in the study group (20.4%), and significantly higher with LGE+ (78.5%). Replacement fibrosis (HR = 1.83, 95% CI, p < 0.01) and interstitial fibrosis (HR = 1.61, 95% CI, p < 0.01) were independent predictors for the composite outcome. Conclusions: Patients with moderate and severe MR with no criteria for surgery still exhibit a significant degree of both replacement and interstitial fibrosis, with prognostic implications.

Myocardial fibrosis in right heart dysfunction.

Cardiac fibrosis, associated with right heart dysfunction, results in significant morbidity and mortality. Stimulated by various cellular and humoral stimuli, cardiac fibroblasts, macrophages, CD4+ and CD8+ T cells, mast and endothelial cells promote fibrogenesis directly and indirectly by synthesizing numerous profibrotic factors. Several systems, including the transforming growth factor-beta and the renin-angiotensin system, produce type I and III collagen, fibronectin and α-smooth muscle actin, thus modifying the extracellular matrix. Although magnetic resonance imaging with gadolinium enhancement remains the gold standard, the use of circulating biomarkers represents an inexpensive and attractive means to facilitate detection and monitor cardiovascular fibrosis. This review explores the use of protein and nucleic acid (miRNAs) markers to better understand underlying pathophysiology as well as their role in the development of therapeutics to inhibit and potentially reverse cardiac fibrosis.

Metabolic Dysfunction Associated Liver Disease in Patients Undergoing Coronary Computed Tomography Angiography.

In this single-center cross-sectional study on patients undergoing coronary computed tomography angiography (CCTA), we assessed the prognostic significance of metabolic dysfunction associated steatotic liver disease (MASLD), metabolic syndrome (MetS), and CCTA-derived parameters for predicting major adverse cardiovascular events (MACE). Over a mean follow-up of 26.9 months, 2038 patients were analyzed, with 361 (17.7%) experiencing MACE. MASLD was associated with a higher MACE incidence (25.90% vs. 14.71% without MASLD, p < 0.001). Cox regression revealed significant associations between MASLD, coronary calcium score (CCS), number of plaques (NoP), epicardial fat volume (EFV), and MACE, with hazard ratios of 1.843, 1.001, 1.097, and 1.035, respectively (p < 0.001 for all). A composite risk score integrating CCS, NoP, EFV, and MASLD demonstrated superior predictive value for MACE (AUC = 0.948) compared to individual variables (p < 0.0001 for all). In conclusion, MASLD is linked to an elevated risk of MACE, and a comprehensive risk-scoring system incorporating imaging and clinical factors enhances MACE prediction accuracy.

Cardiac Magnetic Resonance Imaging in Appraising Myocardial Strain and Biomechanics: A Current Overview.

Subclinical alterations in myocardial structure and function occur early during the natural disease course. In contrast, clinically overt signs and symptoms occur during late phases, being associated with worse outcomes. Identification of such subclinical changes is critical for timely diagnosis and accurate management. Hence, implementing cost-effective imaging techniques with accuracy and reproducibility may improve long-term prognosis. A growing body of evidence supports using cardiac magnetic resonance (CMR) to quantify deformation parameters. Tissue-tagging (TT-CMR) and feature-tracking CMR (FT-CMR) can measure longitudinal, circumferential, and radial strains and recent research emphasize their diagnostic and prognostic roles in ischemic heart disease and primary myocardial illnesses. Additionally, these methods can accurately determine LV wringing and functional dynamic geometry parameters, such as LV torsion, twist/untwist, LV sphericity index, and long-axis strain, and several studies have proved their utility in prognostic prediction in various cardiovascular patients. More recently, few yet important studies have suggested the superiority of fast strain-encoded imaging CMR-derived myocardial strain in terms of accuracy and significantly reduced acquisition time, however, more studies need to be carried out to establish its clinical impact. Herein, the current review aims to provide an overview of currently available data regarding the role of CMR in evaluating myocardial strain and biomechanics.

Left atrial geometric and functional remodeling parameters measured by cardiac magnetic resonance imaging and outcome prediction in patients with severe aortic stenosis.

BACKGROUND: Emerging studies are beginning to describe the role of afflicted left atrium (LA) function and strain in cardiovascular diseases including aortic stenosis (AS), especially for risk stratification and outcome prediction. Cardiac magnetic resonance imaging (CMR) is becoming increasingly useful in determining LA parameters; however, in patients with AS, this approach has not been applied yet. AIMS: This study sought to evaluate the role of CMR in characterizing LA geometry and function in patients with severe AS. METHODS: We prospectively evaluated 70 patients with symptomatic severe AS and 70 controls. LA volumes, function, and strain were determined using CMR. A composite outcome (cardiac death, ventricular tachyarrhythmias, and heart failure hospitalization) was evaluated over a median of 13 months. Time-to-event outcomes were analyzed accordingly. RESULTS: Besides increased LA volumes (LAVs) and LA sphericity index (LASI) (P <0.001), LA phasic functions and strain were considerably defective in patients with AS (all P <0.001). LV mass (LVM), end-diastolic and end-systolic volumes were also significantly associated withal LA strain parameters (P <0.001). Regarding outcome prediction, decreased total (LA-εt), active (LA-εa), and passive strain (LA-εp), along with enhanced LASI were independently associated with outcome (P <0.001). Time-to-event analysis showed a significantly higher risk to reach the composite outcome for LA-εt <31.1% (hazard ratio [HR], 6.981; 95% confidence interval [CI], 2.74-17.77; P <0.001), LA-εp <14.5% (HR, 2.68; 95% CI, 1.00-7.18; P <0.01), and LA-εa <21.2% (HR, 2.02; 95% CI, 1.07-3.83, P <0.03). CONCLUSION: Patients with severe AS have a significantly remodeled LA, with impaired phasic function and strain. Amongst all CMR parameters, LAVmin, LASI, LAPF, and LA-εp appear to be independent predictors for outcomes.

The Role of Circulating Collagen Turnover Biomarkers and Late Gadolinium Enhancement in Patients with Non-Ischemic Dilated Cardiomyopathy.

Background: Myocardial scarring is a primary pathogenetic process in nonischemic dilated cardiomyopathy (NIDCM) that is responsible for progressive cardiac remodeling and heart failure, severely impacting the survival of these patients. Although several collagen turnover biomarkers have been associated with myocardial fibrosis, their clinical utility is still limited. Late gadolinium enhancement (LGE) determined by cardiac magnetic resonance imaging (CMR) has become a feasible method to detect myocardial replacement fibrosis. We sought to evaluate the association between collagen turnover biomarkers and replacement myocardial scarring by CMR and, also, to test their ability to predict outcome in conjunction with LGE in patients with NIDCM. Method: We conducted a prospective study on 194 patients (48.7 ± 14.3 years of age; 74% male gender) with NIDCM. The inclusion criteria were similar to those for the definition of NIDCM, performed exclusively by CMR: (1) LV dilation with an LV end-diastolic volume (LVEDV) of over 97 mL/m2; (2) global LV dysfunction, expressed as a decreased LVEF of under 45%. CMR was used to determine the presence and extent of LGE. Several collagen turnover biomarkers were determined at diagnosis, comprising galectin-3 (Gal3), procollagen type I carboxy-terminal pro-peptide (PICP) and N-terminal pro-peptide of procollagen type III (PIIINP). A composite outcome (all-cause mortality, ventricular tachyarrhythmias, heart failure hospitalization) was ascertained over a median of 26 months. Results: Gal3, PICP and PIIINP were considerably increased in those with LGE+ (p < 0.001), also being directly correlated with LGE mass (r2 = 0.42; r2 = 0.44; r2 = 0.31; all p < 0.001). Receiver operating characteristic (ROC) analysis revealed a significant ability to diagnose LGE, with an area under the ROC of 0.816 for Gal3, 0.705 for PICP, and 0.757 for PIIINP (all p < 0.0001). Kaplan−Meier analysis showed that at a threshold of >13.8 ng/dL for Gal3 and >97 ng/dL for PICP, they were able to significantly predict outcome (HR = 2.66, p < 0.001; HR = 1.93, p < 0.002). Of all patients, 17% (n = 33) reached the outcome. In multivariate analysis, after adjustment for covariates, only LGE+ and Gal3+ remained independent predictors for outcome (p = 0.008; p = 0.04). Nonetheless, collagen turnover biomarkers were closely related to HF severity, providing incremental predictive value for severely decreased LVEF of under 30% in patients with NIDCM, beyond that with LGE alone. Conclusions: In patients with NIDCM, circulating collagen turnover biomarkers such as Gal3, PICP and PIIINP are closely related to the presence and extent of LGE and can significantly predict cardiovascular outcome. The joint use of LGE with Gal3 and PICP significantly improved outcome prediction.

Nanoparticles Targeting the Molecular Pathways of Heart Remodeling and Regeneration.

Cardiovascular diseases are the main cause of death worldwide, a trend that will continue to grow over the next decade. The heart consists of a complex cellular network based mainly on cardiomyocytes, but also on endothelial cells, smooth muscle cells, fibroblasts, and pericytes, which closely communicate through paracrine factors and direct contact. These interactions serve as valuable targets in understanding the phenomenon of heart remodeling and regeneration. The advances in nanomedicine in the controlled delivery of active pharmacological agents are remarkable and may provide substantial contribution to the treatment of heart diseases. This review aims to summarize the main mechanisms involved in cardiac remodeling and regeneration and how they have been applied in nanomedicine.

Diastolic Function Assessment of Left and Right Ventricles by MRI in Systemic Sclerosis Patients.

BACKGROUND: Heart involvement is frequent although often clinically silent in systemic sclerosis (SSc) patients. Early identification of cardiac involvement can be improved by noninvasive methods such as MRI, in addition to transthoracic echocardiography (TTE). PURPOSE: To assess the ability of phase-contrast (PC)-MRI to detect subclinical left (LV) and right (RV) ventricular diastolic dysfunction in SSc patients. STUDY TYPE: Prospective. POPULATION: Thirty-five consecutive SSc patients (49 ± 14 years) and 35 sex- and age-matched healthy controls (48.6 ± 13.5 years) who underwent TTE and MRI in the same week. FIELD STRENGTH/SEQUENCE: 5 T/PC-MRI using a breath-hold velocity-encoded gradient echo sequence. ASSESSMENT: LV TTE (E/E') and LV and RV PC-MRI indices of diastolic function (LV early and late transmitral [EM , EfM , AM , AfM ] and RV transtricuspid [ET , EfT , AT , AfT ] peak filling flow velocities and flow rates, as well as LV [ E M ' ] and RV [ E T ' ] peak longitudinal myocardial velocities during diastole) were measured. STATISTICAL TESTS: Two-tailed t-test, Wilcoxon test, or Fischer test for comparison of variables between SSc and healthy control groups; sensitivity, specificity, receiver-operating-characteristic (ROC) area under the curve (AUC) to assess discriminative ability of variables. A P-value <0.05 was considered statistically significant. RESULTS: TTE LV E/E' and MRI EM / E M ' and ET / E T ' were significantly higher in SSc patients than in controls (8.27 ± 1.25 vs. 6.70 ± 1.66; 9.43 ± 2.7 vs. 6.51 ± 1.50; 6.51 [4.70-10.40] vs. 4.13 [3.22-5.75], respectively) and separated SSc patients and healthy controls with good sensitivity (68%, 71%, and 80%), specificity (85%, 94%, and 62%), and AUC (0.787, 0.807, and 0.765). LV EfM was significantly higher in SSc patients than in controls (347.1 ± 113.7 vs. 284.7 ± 94.6) as RVAfT (277 [231-355] vs. 220 [154-253] mL/sec) with impaired relaxation pattern (EfT /AfT , 0.95 [0.87-1.21] vs. 1.12 [0.93-1.47]). DATA CONCLUSION: MRI was able to detect LV and RV diastolic dysfunction in SSc patients with good accuracy in the absence of LV systolic dysfunction at echocardiography. Use of MRI can allow to better assess the early impact of myocardial fibrosis related to SSc. LEVEL OF EVIDENCE: 1 TECHNICAL EFFICACY STAGE: 2.

Advanced cardiovascular multimodal imaging and aortic stenosis.

Aortic valve stenosis has become the most common valvular heart disease on account of aging population and increasing life expectancy. Echocardiography is the primary diagnosis tool for this, but it still has many flaws. Therefore, advanced cardiovascular multimodal imaging techniques are continuously being developed in order to overcome these limitations. Cardiac magnetic resonance imaging (CMR) allows a comprehensive morphological and functional evaluation of the aortic valve and provides important data for the diagnosis and risk stratification in patients with aortic stenosis. CMR can functionally assess the aortic flow using two-dimensional and time-resolved three-dimensional velocity-encoded phase-contrast techniques. Furthermore, by late gadolinium enhancement and T1-mapping, CMR can reveal the presence of both irreversible replacement and diffuse interstitial myocardial fibrosis. Moreover, its role in guiding aortic valve replacement procedures is beginning to take shape. Recent studies have rendered the importance of active and passive biomechanics in risk stratification and prognosis prediction in patients with aortic stenosis, but more work is required is just in its infancy, but data are promising. In addition, cardiac computed tomography is particularly useful for the diagnosis of aortic valve stenosis, and in preprocedural evaluation of the aorta, while positron emission tomography can be also used to assess valvular inflammation and active calcification. The purpose of this review is to provide a comprehensive overview of current available data regarding advanced cardiovascular multimodal imaging in aortic stenosis.

Left Atrial Geometry and Phasic Function Determined by Cardiac Magnetic Resonance Are Independent Predictors for Outcome in Non-Ischaemic Dilated Cardiomyopathy.

Left atrial (LA) geometry and phasic functions are frequently impaired in non-ischaemic dilated cardiomyopathy (NIDCM). Cardiac magnetic resonance (CMR) can accurately measure LA function and geometry parameters. We sought to investigate their prognostic role in patients with NIDCM. We prospectively examined 212 patients with NIDCM (49 ± 14.2-year-old; 73.5% males) and 106 healthy controls. LA volumes, phasic functions, geometry, and fibrosis were determined using CMR. A composite outcome (cardiac death, ventricular tachyarrhythmias, heart failure hospitalization) was ascertained over a median of 26 months. LA phasic functions, sphericity index (LASI) and late gadolinium enhancement (LA-LGE) were considerably impaired in the diseased group (p < 0.001) and significantly correlated with impaired LV function parameters (p < 0.0001). After multivariate analysis, LA volumes, LASI, LA total strain (LA-εt) and LA-LGE were associated with increased risk of composite outcome (p < 0.001). Kaplan-Meier analysis showed significantly higher risk of composite endpoint for LA volumes (all p < 0.01), LASI > 0.725 (p < 0.003), and LA-εt < 30% (p < 0.0001). Stepwise Cox proportional-hazards models demonstrated a considerable incremental predictive value which resulted by adding LASI to LA-εt (Chi-square = 10.2, p < 0.001), and afterwards LA-LGE (Chi-Square = 15.8; p < 0.0001). NIDCM patients with defective LA volumes, LASI, LA-LGE and LA-εt had a higher risk for an outcome. LA-εt, LASI and LA-LGE provided independent incremental predictive value for outcome.

Cardiotoxicity in HER2-positive breast cancer patients.

Due to the recent advances in diagnosis and management of patients with HER2-positive breast cancer, especially through novel HER2-targeted agents, cardiotoxicity becomes an emerging problem. Although chemotherapy significantly increases survival, the risk of cardiovascular disease development is high and still underestimated and could imply treatment discontinuation. Frequently, due to lack of rigorous diagnosis strategies, cardiotoxicity assessment is delayed, and, moreover, the efficacy of current therapy options in restoring heart function is questionable. For a comprehensive risk assessment, it is vital to characterize the clinical spectrum of HER2-targeted agents and anthracyclines, as well as their pathogenic pathways involved in cardiotoxicity. Advanced cardiovascular multimodal imaging and circulating biomarkers plays primary roles in early assessing cardiotoxicity and also in guiding specific preventive measures. Even though the knowledge in this field is rapidly expanding, there are still questions that arise regarding the optimal approach in terms of timing and methods. The aim of the current review aims to providean overview of currently available data.

Phenotypes of hypertrophic cardiomyopathy: genetics, clinics, and modular imaging.

Hypertrophic cardiomyopathy (HCM) is the most common cardiovascular disease with genetic transmission, characterized by the hypertrophy of any segment of the left ventricle (LV), not totally explained by improper loading conditions, with LV systolic function preserved, increased, or reduced. The histopathological mechanism involved in HCM refers to the primary injury of the myocardium, as follows: disorganized array of myocytes, extracellular matrix modification, microvascular dysfunction, with subsequent appearance of myocardial fibrosis. Multiple sarcomere proteins mutations are responsible for HCM, but two of them are involved in 70% of the cases of HCM: ß-myosin heavy chain (MYH7) and myosin-binding protein C (MYBPC3). The development of new genetic techniques involving genome editing is promising to discover a gene therapy for patients with HCM. Clinical presentation may differ from asymptomatic to sudden cardiac death (SCD), the last one targeting younger adults. In this case, the diagnosis and evaluation of SCD risk factors is extremely important. The common method of diagnosis is transthoracic echocardiography, but cardiac magnetic resonance (CMR) imaging represents "gold standard" in the evaluation of HCM patients. Treatment includes pharmacological therapy, surgery, alcohol ablation, and not least SCD prevention.

Non-ischemic dilated cardiomyopathy and cardiac fibrosis.

Cardiac fibrosis is associated with non-ischemic dilated cardiomyopathy, increasing its morbidity and mortality. Cardiac fibroblast is the keystone of fibrogenesis, being activated by numerous cellular and humoral factors. Macrophages, CD4+ and CD8+ T cells, mast cells, and endothelial cells stimulate fibrogenesis directly by activating cardiac fibroblasts and indirectly by synthetizing various profibrotic molecules. The synthesis of type 1 and type 3 collagen, fibronectin, and α-smooth muscle actin is rendered by various mechanisms like transforming growth factor-beta/small mothers against decapentaplegic pathway, renin angiotensin system, and estrogens, which in turn alter the extracellular matrix. Investigating the underlying mechanisms will allow the development of diagnostic and prognostic tools and discover novel specific therapies. Serum biomarkers aid in the diagnosis and tracking of cardiac fibrosis progression. The diagnostic gold standard is cardiac magnetic resonance with gadolinium administration that allows quantification of cardiac fibrosis either by late gadolinium enhancement assessment or by T1 mapping. Therefore, the goal is to stop and even reverse cardiac fibrosis by developing specific therapies that directly target fibrogenesis, in addition to the drugs used to treat heart failure. Cardiac resynchronization therapy had shown to revert myocardial remodeling and to reduce cardiac fibrosis. The purpose of this review is to provide an overview of currently available data.

Left Ventricular Geometry and Replacement Fibrosis Detected by cMRI Are Associated with Major Adverse Cardiovascular Events in Nonischemic Dilated Cardiomyopathy.

To investigate the relationship between left ventricular (LV) long-axis strain (LAS) and LV sphericity index (LVSI) and outcomes in patients with nonischemic dilated cardiomyopathy (NIDCM) and myocardial replacement fibrosis confirmed by late gadolinium enhancement (LGE) using cardiac magnetic resonance imaging (cMRI), we conducted a prospective study on 178 patients (48 ± 14.4 years; 25.2% women) with first NIDCM diagnosis. The evaluation protocol included ECG monitoring, echocardiography and cMRI. LAS and LVSI were cMRI-determined. Major adverse cardiovascular events (MACEs) were defined as a composite outcome including heart failure (HF), ventricular arrhythmias (VAs) and sudden cardiac death (SCD). After a median follow-up of 17 months, patients with LGE+ had increased risk of MACEs. Kaplan-Meier curves showed significantly higher rate of MACEs in patients with LGE+ (p < 0.001), increased LVSI (p < 0.01) and decreased LAS (p < 0.001). In Cox analysis, LAS (HR = 1.32, 95%CI (1.54-9.14), p = 0.001), LVSI [HR = 1.17, 95%CI (1.45-7.19), p < 0.01] and LGE+ (HR = 1.77, 95%CI (2.79-12.51), p < 0.0001) were independent predictors for MACEs. In a 4-point risk scoring system based on LV ejection fraction (LVEF) < 30%, LGE+, LAS > -7.8% and LVSI > 0.48%, patients with 3 and 4 points had a significantly higher risk for MACEs. LAS and LVSI are independent predictors of MACEs and provide incremental value beyond LVEF and LGE+ in patients with NIDCM and myocardial fibrosis.

A 63-year-old woman with multiple secondary tumours.

Clinical introductionA 63-year-old woman recently diagnosed with lung metastasis, after routine chest radiography, was admitted to our hospital for unspecified symptoms, such as dyspnoea on minimal exertion and dry cough. Physical examination showed uncommon signs. The electrocardiogram showed sinus rhythm and incomplete left bundle branch block. Thoracic CT scan revealed bilateral lung and pleural metastases and pelvic CT showed a right femoral bone mass. Transthoracic echocardiography revealed a heterogeneous mass, lateral to the right ventricle, with pericardial effusion. Further, cardiac MRI (cMRI) was performed (figure 1A,B). Diagnosis was completed with an ultrasound-guided biopsy and histopathological examination (figure 1C,D).heartjnl;106/3/202/F1F1F1Figure 1(A,B) Cardiac MRI: asterisk is suggestive of fluid and the white arrow indicates fibrous encapsulation by LGE, (C) H&E stain:white arrow indicating a tumoral cell with atypical mitosis and (D) immunohistochemical staining for smooth muscle actin antibody. QUESTION: Which of the following is the most likely diagnosis?Pericardial lymphoma.Pericardial leiomyosarcoma.Pericardial cyst.Secondary malignant cardiac tumour.Pericardial teratoma.

The role of advanced multimodality imaging in chronic mitral regurgitation.

Mitral regurgitation (MR), the second most common valvular heart disease, still constitutes a major diagnostic and thera-peutic challenge, due to its complex nature and to its consequences on cardiac remodelling. Life quality and expectancy are determined by the irreversibility of the left ventricular systolic dysfunction, which, despite current guidelines, remains a major drawback. In order to accurately establish "the point of no return" for left ventricular systolic function, the embedment of clinical, biological and imaging data is a requirement. The purpose of this review is to provide an overview of the current multimodal imaging techniques that are useful in correctly assessing patients with MR. Cardiac magnetic resonance strain imaging techniques and 3D echocardiography, in addition to current echocardiographic criteria may help identify the patients who will benefit from early surgery. The technical development of new transcatheter techniques in mitral valve repair could lead to the extension of current guidelines.

Pentraxin-3 and endothelial dysfunction.

Pentraxin 3 (PTX3) is involved in vascular inflammation and endothelial dysfunction through various mechanisms. Until now, most studies confirmed an important link between PTX3 and endothelial dysfunction and identified several pathogenetic pathways. PTX3 modulates inflammatory cells, thus stimulating vascular inflammation. Within endothelial cells, it decreases nitric oxide (NO) synthesis, inhibits cell proliferation and alters their functions. PTX3 blocks the effect of fibroblast growth factor 2 (FGF2) by making a molecular complex with these molecules inactivating them. However, there are substances like the tumor necrosis factor-inducible gene 6 protein (TSG-6) that block the PTX3-FGF2 interaction. Interacting with P-selectin, it promotes vascular inflammatory response and endothelial dysfunction. PTX3 also increases the matrix metalloproteinases synthesis directly or by blocking NO synthesis. From a clinical point of view, PTX3 positively correlates with arterial hypertension, flow mediated dilation and, with intima media thickness. Therefore, the involvement of PTX3 in the pathogenesis and evaluation of endothelial dysfunction is clear, and it may become a biomarker in this direction, but further studies are needed to determine its reliability in this direction. Last but not least, PTX3 could become an effective therapeutic target for preventing this dysfunction, but further research needs to be conducted.

Catheter ablation of a right posterior accessory pathway in a patient with left ventricular noncompaction: A case report.

RTIONALE: Left ventricular noncompaction (LVNC) is a genetic cardiomyopathy characterized by the presence of a thin compacted layer of myocardium and a spongy subendocardial layer with trabeculations and recesses. LVNC associated Wolf-Parkinson-White syndrome is very rare. PATIENT CONCERNS: A 32-year-old male presented with short episodes of palpitations and a syncope 6 months before his hospitalization. DIAGNOSIS: His ECG revealed the presence of a right posterior accessory pathway. Echocardiography identified trabeculations of the septal, apical, and lateral wall of the left ventricle, consistent with left ventricular noncompaction. Cardiac MRI confirmed the diagnosis, as the ratio between the noncompacted and compacted myocardial layer was 2.3. INTERVENTIONS: The electrophysiological study revealed a malignant right posterior accessory pathway. Catheter ablation was successfully performed at the level of posterior tricuspid annulus. Programmed ventricular stimulation could not induce any arrhythmia at the end of the procedure. OUTCOMES: During 15 months of follow-up, the patient presented no more episodes of palpitations or syncope. LESSONS: Left ventricular noncompaction with right accessory pathway is a rare association with genetic basis and gives a higher risk of sudden cardiac death. Catheter ablation of the accessory pathway is a valuable way of treatment in this category of patients, lowering the risk of sudden cardiac death.