Magnetic Resonance Imaging Characterization and Clinical Outcomes of Dilated and Arrhythmogenic Left Ventricular Cardiomyopathies.

BACKGROUND: Nondilated left ventricular cardiomyopathy (NDLVC) has been recently differentiated from dilated cardiomyopathy (DCM). A comprehensive characterization of these 2 entities using cardiac magnetic resonance (CMR) and genetic testing has never been performed. OBJECTIVES: This study sought to provide a thorough characterization and assess clinical outcomes in a large multicenter cohort of patients with DCM and NDLVC. METHODS: A total of 462 patients with DCM (227) or NDLVC (235) with CMR data from 4 different referral centers were retrospectively analyzed. The study endpoint was a composite of sudden cardiac death or major ventricular arrhythmias. RESULTS: In comparison to DCM, NDLVC had a higher prevalence of pathogenic or likely pathogenic variants of arrhythmogenic genes (40% vs 23%; P < 0.001), higher left ventricular (LV) systolic function (LV ejection fraction: 51% ± 12% vs 36% ± 15%; P < 0.001) and higher prevalence of free-wall late gadolinium enhancement (LGE) (27% vs 14%; P < 0.001). Conversely, DCM showed higher prevalence of pathogenic or likely pathogenic variants of nonarrhythmogenic genes (23% vs 12%; P = 0.002) and septal LGE (45% vs 32%; P = 0.004). Over a median follow-up of 81 months (Q1-Q3: 40-132 months), the study outcome occurred in 98 (21%) patients. LGE with septal location (HR: 1.929; 95% CI: 1.033-3.601; P = 0.039) was independently associated with the risk of sudden cardiac death or major ventricular arrhythmias together with LV dilatation, older age, advanced NYHA functional class, frequent ventricular ectopic activity, and nonsustained ventricular tachycardia. CONCLUSIONS: In a multicenter cohort of patients with DCM and NDLVC, septal LGE together with LV dilatation, age, advanced disease, and frequent and repetitive ventricular arrhythmias were powerful predictors of major arrhythmic events.

The additive prognostic value of end-systolic pressure-volume relation by stress CMR in patients with known or suspected coronary artery disease.

PURPOSE: The difference between rest and peak stress end-systolic pressure-volume relation (ΔESPVR) is an afterload-independent index of left ventricular (LV) contractility. We assessed the independent prognostic value of ΔESPVR index by dipyridamole stress-cardiovascular magnetic resonance (CMR) in patients with known/suspected coronary artery disease (CAD). METHODS: We considered 196 consecutive patients (62.74 ± 10.66 years, 49 females). Wall motion and perfusion abnormalities at rest and peak stress were analysed. Replacement myocardial fibrosis was detected by late gadolinium enhancement (LGE) technique. The ESPVR was evaluated at rest and peak stress from raw measurement of systolic arterial pressure and end-systolic volume by biplane Simpson's method. RESULTS: A reduced ΔESPVR index (≤ 0.02 mmHg/mL/m2) was found in 88 (44.9%) patients and it was associated with a lower LV ejection fraction (EF) and with a higher frequency of abnormal stress CMR and myocardial fibrosis. During a mean follow-up of 53.17 ± 28.21 months, 50 (25.5%) cardiac events were recorded: 5 cardiac deaths, 17 revascularizations, one myocardial infarction, 23 hospitalisations for heart failure or unstable angina, and 4 ventricular arrhythmias. According to Cox regression analysis, diabetes, family history, LVEF, abnormal stress CMR, myocardial fibrosis, and reduced ΔESPVR were significant univariate prognosticators. In the multivariate analysis the independent predictors were ΔESPVR index ≤ 0.02 mmHg/mL/m2 (hazard ratio-HR = 2.58, P = 0.007), myocardial fibrosis (HR = 2.13, P = 0.036), and diabetes (HR = 2.33, P = 0.012). CONCLUSION: ΔESPVR index by stress-CMR was independently associated with cardiac outcomes in patients with known/suspected CAD, in addition to replacement myocardial fibrosis and diabetes. Thus, the assessment of ΔESPVR index may be included into the standard stress-CMR exam to further stratify the patients.

Liver T1 and T2 mapping in a large cohort of healthy subjects: normal ranges and correlation with age and sex.

OBJECTIVE: We established normal ranges for native T1 and T2 values in the human liver using a 1.5 T whole-body imager (General Electric) and we evaluated their variation across hepatic segments and their association with age and sex. MATERIALS AND METHODS: One-hundred healthy volunteers aged 20-70 years (50% females) underwent MRI. Modified Look-Locker inversion recovery and multi-echo fast-spin-echo sequences were used to measure hepatic native global and segmental T1 and T2 values, respectively. RESULTS: T1 and T2 values exhibited good intra- and inter-observer reproducibility (coefficient of variation < 5%). T1 value over segment 4 was significantly lower than the T1 values over segments 2 and 3 (p < 0.0001). No significant regional T2 variability was detected. Segmental and global T1 values were not associated with age or sex. Global T2 values were independent from age but were significantly lower in males than in females. The lower and upper limits of normal for global T1 values were, respectively, 442 ms and 705 ms. The normal range for global T2 values was 35 ms-54 ms in males and 39 ms-54 ms in females. DISCUSSION: Liver T1 and T2 mapping is feasible and reproducible and the provided normal ranges may help to establish diagnosis and progression of various liver diseases.

Epidemiology and geographic clustering of Erdheim-Chester disease in Italy and France.

This geoepidemiological study, performed in Italy and France, shows that Erdheim-Chester disease is increasingly diagnosed and cases cluster in specific geographic areas, namely southern Italy and central France. Disease frequency inversely correlates with the Human Development Index.

Biventricular Tissue Tracking with Cardiovascular Magnetic Resonance: Reference Values of Left- and Right-Ventricular Strain.

We derived reference values of left-ventricular (LV) and right-ventricular (RV) strain parameters in a cohort of 100 healthy subjects by feature tracking cardiac magnetic resonance (FT-CMR). Global and regional strain values were calculated for the LV; circumferential and radialSAX strain parameters were derived from the short-axis (SAX) stack, while longitudinal and radialLAX strain parameters were assessed in three long-axis (LAX) views. Only global longitudinal strain (GLS) was calculated for the RV. Peak global LV circumferential strain was -16.7% ± 2.1%, LV radialSAX strain was 26.4% ± 5.1%, LV radialLAX strain was 31.1% ± 5.2%, LV GLS was -17.7% ± 1.9%, and RV GLS was -23.9% ± 4.1%. Women presented higher global LV and RV strain values than men; all strain values presented a weak relationship with body surface area, while there was no association with age or heart rate. A significant association was detected between all LV global strain measures and LV ejection fraction, while RV GLS was correlated to RV end-diastolic volume. The intra- and inter-operator reproducibility was good for all global strain measures. In the regional analysis, circumferential and radial strain values resulted higher at the apical level, while longitudinal strain values were higher at the basal level. The assessment of cardiac deformation by FT-CMR is feasible and reproducible and gender-specific reference values should be used.

Cardiac magnetic resonance findings and prognosis in type 1 myotonic dystrophy.

BACKGROUND: Cardiac involvement is a major determinant of prognosis in type 1 myotonic dystrophy (DM1), but limited information is available about myocardial remodeling and tissue changes. The aim of the study was to investigate cardiac magnetic resonance (CMR) findings and their prognostic significance in DM1. METHODS: We retrospectively identified all DM1 patients referred from a neurology unit to our CMR laboratory from 2009 to 2020. RESULTS: Thirty-four patients were included (aged 45 ±â€Š12, 62% male individuals) and compared with 68 age-matched and gender-matched healthy volunteers (43 male individuals, age 48 ±â€Š15 years). At CMR, biventricular and biatrial volumes were significantly smaller (all P < 0.05), as was left ventricular mass (P < 0.001); left ventricular ejection fraction (LVEF) and right ventricular ejection fraction (RVEF) were significantly lower (all P < 0.01). Five (15%) patients had a LVEF less than 50% and four (12%) a RVEF less than 50%. Nine patients (26%) showed mid-wall late gadolinium enhancement (LGE; 5 ±â€Š2% of LVM), and 14 (41%) fatty infiltration. Native T1 in the interventricular septum (1041 ±â€Š53 ms) was higher than for healthy controls (1017 ±â€Š28 ms) and approached the upper reference limit (1089 ms); the extracellular volume was slightly increased (33 ±â€Š2%, reference <30%). Over 3.7 years (2.0-5.0), 6 (18%) patients died of extracardiac causes, 5 (15%) underwent device implantation; 5 of 21 (24%) developed repetitive ventricular ectopic beats (VEBs) on Holter monitoring. LGE mass was associated with the occurrence of repetitive VEBs (P = 0.002). Lower LV stroke volume (P = 0.017), lower RVEF (P = 0.016), a higher LVMi/LVEDVI ratio (P = 0.016), fatty infiltration (P = 0.04), and LGE extent (P < 0.001) were associated with death. CONCLUSION: DM1 patients display structural and functional cardiac abnormalities, with variable degrees of cardiac muscle hypotrophy, fibrosis, and fatty infiltration. Such changes, as evaluated by CMR, seem to be associated with the development of ventricular arrhythmias and a worse outcome.

Management and treatment of cardiotoxicity due to anticancer drugs: 10 questions and answers.

Since the introduction of anthracyclines into clinical practice in the 1960s, chemotherapy has always been associated with cardiotoxicity. Patients on cardiotoxic drugs can develop a wide range of cardiovascular diseases, including left ventricular (LV) systolic dysfunction and heart failure (HF), arrhythmias, hypertension, and coronary artery disease (CAD). The rising number of cancer patients, population ageing, and the frequent overlap of cardiovascular and oncological diseases have highlighted the importance of close collaboration between cardiologists and oncologists. As a result, in 1995, cardiologists at the IEO (European Institute of Oncology) coined the term cardioncology, a new discipline focused on the dynamics of cardiovascular disease in cancer patients. Given the complex scenario characterized by a constant dialogue between the oncological condition and cardiovascular comorbidity, it is essential for the clinician to get the knowledge to properly fulfill the needs of the oncological patient under cardiotoxic treatment. Through the answer to 10 questions, we aim to describe the complex issue of cardiotoxicity by addressing the main critical points and current evidence related to the assessment, management, treatment, and surveillance of cancer patients under chemotherapy.

Bidirectional Relationship Between Cancer and Heart Failure: Insights on Circulating Biomarkers.

Cancer and heart failure are the two leading causes of death in developed countries. These two apparently distinct clinical entities share similar risk factors, symptoms, and pathophysiological mechanisms (inflammation, metabolic disturbances, neuro-hormonal and immune system activation, and endothelial dysfunction). Beyond the well-known cardiotoxic effects of oncological therapies, cancer and heart failure are thought to be tied by a bidirectional relationship, where one disease favors the other and vice versa. In this context, biomarkers represent a simple, reproducible, sensitive and cost-effective method to explore such relationship. In this review, we recapitulate the evidence on cardiovascular and oncological biomarkers in the field of cardioncology, focusing on their role in treatment-naïve cancer patients. Cardioncological biomarkers are useful tools in risk stratification, early detection of cardiotoxicity, follow-up, and prognostic assessment. Intriguingly, these biomarkers might contribute to better understand the common pathophysiology of cancer and heart failure, thus allowing the implementation of preventive and treatment strategies in cardioncological patients.

In Vivo Murine Models of Cardiotoxicity Due to Anticancer Drugs: Challenges and Opportunities for Clinical Translation.

Modern therapeutic approaches have led to an improvement in the chances of surviving a diagnosis of cancer. However, this may come with side effects, with patients experiencing adverse cardiovascular events or exacerbation of underlying cardiovascular disease related to their cancer treatment. Rodent models of chemotherapy-induced cardiotoxicity are useful to define pathophysiological mechanisms of cardiac damage and to identify potential therapeutic targets. The key mechanisms involved in cardiotoxicity induced by specific different antineoplastic agents are summarized in this state-of-the-art review, as well as the rodent models of cardiotoxicity by different classes of anticancer drugs, along with the strategies tested for primary and secondary cardioprotection. Current approaches for early detection of cardiotoxicity in preclinical studies with a focus on the application of advanced imaging modalities and biomarker strategies are also discussed. Potential applications of cardiotoxicity modelling in rodents are illustrated in relation to the advancements of promising research topics of cardiotoxicity. Created with BioRender.com.

Myocardial T2 values at 1.5 T by a segmental approach with healthy aging and gender.

OBJECTIVES: Our aims were to obtain myocardial regional and global T2 values as a reference for normality for the first time using a GE scanner and to assess their association with physiological variables. METHODS: One hundred healthy volunteers aged 20-70 years (50% females) underwent cardiovascular magnetic resonance. Basal, mid-ventricular, and apical short-axis slices of the left ventricle were acquired by a multi-echo fast-spin-echo (MEFSE) sequence. Image analysis was performed with a commercially available software package. The T2 value was assessed in all 16 myocardial segments and the global value was the mean. RESULTS: The global T2 value averaged across all subjects was 52.2 ± 2.5 ms (range: 47.0-59.9 ms). Inter-study, intra-observer, and inter-observer reproducibility was good (coefficient of variation < 5%). 3.6% of the segments was excluded because of artifacts and/or partial-volume effects. Segmental T2 values differed significantly (p < 0.0001), with the lowest value in the basal anterolateral segment (50.0 ± 3.5 ms) and the highest in the apical lateral segment (54.9 ± 5.1 ms). Mean T2 was significantly lower in the basal slice compared to both mid-ventricular and apical slices and in the mid-ventricular slice than in the apical slice. Aging was associated with increased segmental and global T2 values. Females showed higher T2 values than males. T2 values were not correlated to heart rate. A significant inverse correlation was detected between global T2 values and mean wall thickness. CONCLUSIONS: The optimized MEFSE sequence allows for robust and reproducible quantification of segmental T2 values. Gender- and age-specific segmental reference values must be defined for distinguishing healthy and diseased myocardium. KEY POINTS: • In healthy subjects, T2 values differ among myocardial segments and are influenced by age and gender. • Normal T2 values in the myocardium, usable as a benchmark by other GE sites, were established.

Arrhythmic risk stratification by cardiac magnetic resonance tissue characterization: disclosing the arrhythmic substrate within the heart muscle.

Sudden cardiac death (SCD) is a pivotal health problem worldwide. The identification of subjects at increased risk of SCD is crucial for the accurate selection of candidates for implantable cardioverter defibrillator (ICD) therapy. Current strategies for arrhythmic stratification largely rely on left ventricular (LV) ejection fraction (EF), mostly measured by echocardiography, and New York Heart Association functional status for heart failure with reduced EF. For specific diseases, such as hypertrophic and arrhythmogenic cardiomyopathy, some risk scores have been proposed; however, these scores take into account some parameters that are a partial reflection of the global arrhythmic risk and show a suboptimal accuracy. Thanks to a more comprehensive evaluation, cardiac magnetic resonance (CMR) provides insights into the heart muscle (the so-called tissue characterization) identifying cardiac fibrosis as an arrhythmic substrate. Combining sequences before and after administration of contrast media and mapping techniques, CMR is able to characterize the myocardial tissue composition, shedding light on both intracellular and extracellular alterations. Over time, late gadolinium enhancement (LGE) emerged as solid prognostic marker, strongly associated with major arrhythmic events regardless of LVEF, adding incremental value over current strategy in ischemic heart disease and non-ischemic cardiomyopathies. The evidence on a potential prognostic role of mapping imaging is promising. However, mapping techniques require further investigation and standardization. Disclosing the arrhythmic substrate within the myocardium, CMR should be considered as part of a multiparametric approach to personalized arrhythmic stratification.

Cardiovascular magnetic resonance for the diagnosis and management of heart failure with preserved ejection fraction.

Heart failure with preserved ejection fraction (HFpEF) is characterized by an impaired ventricular filling resulting in the development of dyspnea and other HF symptoms. Even though echocardiography is the cornerstone to demonstrate structural and/or functional alterations of the heart as the underlying cause for the clinical presentation, cardiovascular magnetic resonance (CMR) represents the noninvasive gold standard to assess cardiac morphology, function, and tissue changes. Indeed, CMR allows quantification of biventricular volumes, mass, wall thickness, systolic function, and intra- and extracardiac flows; diastolic functional indices include transmitral and pulmonary venous velocities, left ventricular and left atrial filling velocities from volumetric changes, strain analysis from myocardial tagging, tissue phase contrast, and feature tracking. Moreover, CMR allows superior tissue characterization of the myocardium and the pericardium, which are crucial for a noninvasive etiological and histopathological assessment of HFpEF: conventional T1-weighted, T2-weighted, and post-contrast sequences are now complemented by quantitative mapping sequences, including T1 and T2 mapping as well as extracellular volume quantification. Further experimental sequences comprise diffusion tensor analysis, blood oxygenation-dependent sequences, hyperpolarized contrast agents, spectroscopy, and elastography. Finally, artificial intelligence is beginning to help clinicians deal with an increasing amount of information from CMR exams.

Subclinical cardiac damage in cancer patients before chemotherapy.

Cancer and cardiovascular diseases, including heart failure (HF), are the main causes of death in Western countries. Several anticancer drugs and radiotherapy have adverse effects on the cardiovascular system, promoting left ventricular dysfunction and ultimately HF. Nonetheless, the relationship between cancer and HF is likely not unidirectional. Indeed, cancer and HF share common risk factors, and both have a bidirectional relationship with systemic inflammation, metabolic disturbances, and neurohormonal and immune activation. Few studies have assessed the impact of untreated cancer on the heart. The presence of an active cancer has been associated with elevated cardiac biomarkers, an initial impairment of left ventricular structure and function, autonomic dysfunction, and reduced exercise tolerance. In turn, these conditions might increase the risk of cardiac damage from chemotherapy and radiotherapy. HF drugs such as beta-blockers or inhibitors of the renin-angiotensin-aldosterone system might exert a protective effect on the heart even before the start of cancer therapies. In this review, we recapitulate the evidence of cardiac involvement in cancer patients naïve from chemotherapy and radiotherapy and no history of cardiac disease. We also focus on the perspectives for an early diagnosis and treatment to prevent the progression to cardiac dysfunction and clinical HF, and the potential benefits of cardioactive drugs on cancer progression.

Pressure-volume relationship by pharmacological stress cardiovascular magnetic resonance.

The variation between rest and peak stress end-systolic pressure-volume relation (ΔESPVR) is an index of myocardial contractility, easily obtained during routine stress echocardiography and never tested during dipyridamole stress-cardiac magnetic resonance (CMR). We assessed the ΔESPVR index in patients with known/suspected coronary artery disease (CAD) who underwent dipyridamole stress-CMR. One-hundred consecutive patients (24 females, 63.76 ± 10.17 years) were considered. ESPVR index was evaluated at rest and stress from raw measurement of systolic arterial pressure and end-systolic volume by biplane Simpson's method. The ΔESPVR index showed a good inter-operator reproducibility. Mean ΔESPVR index was 0.48 ± 1.45 mmHg/mL/m2. ΔESPVR index was significantly lower in males than in females. ΔESPVR index was not correlated to rest left ventricular end-diastolic volume index or ejection fraction. Forty-six of 85 patients had myocardial fibrosis detected by the late gadolinium enhancement technique and they showed significantly lower ΔESPVR values. An abnormal stress CMR was found in 25 patients and they showed significantly lower ΔESPVR values. During a mean follow-up of 56.34 ± 30.04 months, 24 cardiovascular events occurred. At receiver-operating characteristic curve analysis, a ΔESPVR < 0.02 mmHg/mL/m2 predicted the presence of future cardiac events with a sensitivity of 0.79 and a specificity of 0.68. The noninvasive assessment of the ΔESPVR index during a dipyridamole stress-CMR exam is feasible and reproducible. The ΔESPVR index was independent from rest LV dimensions and function and can be used for a comparative assessment of patients with different diseases. ΔESPVR index by CMR can be a useful and simple marker for additional prognostic stratification.

Prognostic role of global longitudinal strain by feature tracking in patients with hypertrophic cardiomyopathy: The STRAIN-HCM study.

BACKGROUND: The assessment of myocardial fiber deformation with cardiac magnetic resonance feature tracking (CMR-FT) has shown to be promising in terms of prognostic information in several structural heart diseases. However, little is known about its role in hypertrophic cardiomyopathy (HCM). Aims of the present study were: 1) to assess the prognostic role of CMR-FT derived strain parameters in patients with HCM. METHODS: CMR was performed in 130 consecutive HCM patients (93 males, mean age (54 ± 17 years) with an estimated 5-year risk of sudden cardiac death (SCD) <6% according to the HCM Risk-SCD calculator. 2D- and 3D-Global Radial (GRS), Longitudinal (GLS) and Circumferential (GCS) Strain was evaluated by FT analysis. The primary outcome of the study was a composite of major adverse cardiac events (MACE) including SCD, resuscitated cardiac arrest due to ventricular fibrillation (VF) or hemodynamically unstable ventricular tachycardia (VT), and hospitalization for heart failure. RESULTS: After a median follow-up of 51.7 (37.1-68.8) months, 4 (3%) patients died (all of them suffered from SCD) and 36 (28%) were hospitalized for heart failure. After multivariable adjustment for clinical and imaging covariates, among all strain parameters, only GLS remained a significant independent predictor of outcome events in both the model including 2D strain (HR 1.12, 95% CI 1.03-1.23, p = 0.01) and the model including 3D strain (HR 1.14, 95% CI 1.01-1.30, p = 0.04). The addition of 2D-GLS into the model with clinical and imaging predictors resulted in a significant increase in the C-statistic (from 0.48 to 0.65, p = 0.03). CONCLUSION: CMR-FT derived GLS is a powerful independent predictor of MACE in patients with HCM, incremental to common clinical and CMR risk factors including left ventricular ejection fraction and late gadolinium enhancement.

The Role of Cardiovascular Magnetic Resonance in ARVC.

PURPOSE OF REVIEW: Aim of the paper was to address all strengths and weakness of cardiac magnetic resonance (CMR) in arrhythmogenic cardiomyopathy, trying to highlight areas where further research and investigations should be carried out to fill current gaps in scientific knowledge. RECENT FINDINGS: Arrhythmogenic cardiomyopathy represents a multifaceted clinical entity associated with arrhythmias and sudden death. Even though different diagnostic tools are available for appropriate identification and risk stratification, over the last few years cardiac magnetic resonance (CMR) has surfaced as an unmatched non-invasive imaging tool. CMR is mandatory in the evaluation of arrhythmogenic cardiomyopathy. It is the only imaging technique providing the identification of myocardial fibrosis, particularly for left ventricular myocardium, as recent evidences demonstrated that left ventricular involvement in arrhythmogenic cardiomyopathy is associated with greater risk of sudden death than lone right ventricular involvement.

Myocardial T1 Values at 1.5 T: Normal Values for General Electric Scanners and Sex-Related Differences.

BACKGROUND: No data are available about normal ranges for native T1 in human myocardium using General Electric (GE) scanners. PURPOSE: To establish normal ranges for myocardial T1 values and evaluate regional variability and the influence of physiological factors. STUDY TYPE: Prospective. SUBJECTS: One hundred healthy volunteers with normal electrocardiogram, no cardiovascular/systemic diseases, or risk factors (age range: 20-70 years; 50 females). FIELD STRENGTH/SEQUENCE: 1.5 T/Steady-state free precession cine and a modified Look-Locker inversion recovery sequence in diastole (also in systole for 61 volunteers). ASSESSMENT: Image analysis was performed by operators with >10 years experience in cardiac MR using commercially available software. T1 values were calculated for 16 myocardial segments, and the global value was the mean. Segments were grouped according to circumferential region (anterior, septal, inferior, and lateral) and to level (basal, medial, apical). Twenty images were analyzed twice by the same operator and by a different operator to assess reproducibility. STATISTICAL TESTS: Independent-samples t-test or Mann-Whitney test; paired sample t-test or Wilcoxon signed-rank test; one-way repeated measures ANOVA or Friedman tests; Pearson's or Spearman's correlation. Reproducibility evaluated using coefficient of variability (CoV). RESULTS: Due to artifacts and/or partial-volume effects, 45/1600 (2.8%) segments were excluded. A good intra- and inter-operator reproducibility was detected (CoV < 5%). There were significant differences in segmental T1 values (P < 0.05). A significant circumferential variability was present (P < 0.05): the mean native T1 value over the lateral region was significantly lower than in the other three regions. An increasing gradient from basal to apical slices was detected (P < 0.05). Segmental and global T1 values were not associated with age (range P = 0.052-0.911) but were significantly lower in males than in females (global: 993 ± 32 vs. 1037 ± 27 ms; P < 0.05) and significantly correlated with heart rate (range R for segmental values = 0.247-0.920; P < 0.05). Almost all segmental T1 values were inversely correlated with wall thickness (R from -0.233 to -0.514; P < 0.05). Systolic T1 values were significantly lower than diastolic values in basal anteroseptal segment, in all medial segments except the inferior one, and in all apical segments (P < 0.05). DATA CONCLUSION: Myocardial T1 values differ among myocardial regions, are influenced by sex, heart rate, and wall thickness and vary according to the cardiac cycle in healthy adults. LEVEL OF EVIDENCE: 2 TECHNICAL EFFICACY: Stage 2.

Cardiac magnetic resonance in patients with muscular dystrophies.

Muscular dystrophies are inherited disorders sharing similar clinical features and dystrophic changes on muscle biopsy. Duchenne muscular dystrophy is the most common inherited muscle disease of childhood, and Becker muscular dystrophy is a milder allelic variant with a slightly lower prevalence. Myotonic dystrophy is the most frequent form in adults. Cardiac magnetic resonance is the gold standard technique for the quantification of cardiac chamber volumes and function, and also enables a characterisation of myocardial tissue. Most cardiac magnetic resonance studies in the setting of muscular dystrophy were carried out at single centres, evaluated small numbers of patients and used widely heterogeneous protocols. Even more importantly, those studies analysed more or less extensively the patterns of cardiac involvement, but usually did not try to establish the added value of cardiac magnetic resonance to standard echocardiography, the evolution of cardiac disease over time and the prognostic significance of cardiac magnetic resonance findings. As a result, the large and heterogeneous amount of information on cardiac involvement in muscular dystrophies cannot easily be translated into recommendations on the optimal use of cardiac magnetic resonance. In this review, whose targets are cardiologists and neurologists who manage patients with muscular dystrophy, we try to summarise cardiac magnetic resonance findings in patients with muscular dystrophy, and the results of studies evaluating the role of cardiac magnetic resonance as a tool for diagnosis, risk stratification and follow-up. Finally, we provide some practical recommendations about the need and timing of cardiac magnetic resonance examination for the management of patients with muscular dystrophy.

Oxidative stress and inflammation: determinants of anthracycline cardiotoxicity and possible therapeutic targets.

Chemotherapy with anthracycline-based regimens remains a cornerstone of treatment of many solid and blood tumors but is associated with a significant risk of cardiotoxicity, which can manifest as asymptomatic left ventricular dysfunction or overt heart failure. These effects are typically dose-dependent and cumulative and may require appropriate screening strategies and cardioprotective therapies in order to minimize changes to anticancer regimens or even their discontinuation. Our current understanding of cardiac damage by anthracyclines includes a central role of oxidative stress and inflammation. The identification of these processes through circulating biomarkers or imaging techniques might then be helpful for early diagnosis and risk stratification. Furthermore, therapeutic strategies relieving oxidative stress and inflammation hold promise to prevent heart failure development or at least to mitigate cardiac damage, although further evidence is needed on their efficacy, either alone or as part of combination therapies with neurohormonal antagonists, which are the current adopted standard.