Visualising myocardial injury after noncardiac surgery: a case series using postoperative cardiovascular MRI.

Myocardial injury after noncardiac surgery (MINS) and perioperative myocardial injury are associated with increased morbidity and mortality. Both are diagnosed by a perioperative increase in troponin, yet there is controversy if MINS is a genuine myocardial insult. We applied postoperative cardiovascular magnetic resonance T2 mapping techniques to visualise acute myocardial injury (i.e. oedema) in six patients with multiple cardiovascular risk factors who underwent aortic surgery. The burden of myocardial oedema was substantially higher in four patients with elevated troponin qualifying for MINS, compared with patients without MINS. The data and images suggest that MINS represents genuine myocardial injury.

Myocardial Oedema as a Consequence of Viral Infection and Persistence-A Narrative Review with Focus on COVID-19 and Post COVID Sequelae.

Microvascular integrity is a critical factor in myocardial fluid homeostasis. The subtle equilibrium between capillary filtration and lymphatic fluid removal is disturbed during pathological processes leading to inflammation, but also in hypoxia or due to alterations in vascular perfusion and coagulability. The degradation of the glycocalyx as the main component of the endothelial filtration barrier as well as pericyte disintegration results in the accumulation of interstitial and intracellular water. Moreover, lymphatic dysfunction evokes an increase in metabolic waste products, cytokines and inflammatory cells in the interstitial space contributing to myocardial oedema formation. This leads to myocardial stiffness and impaired contractility, eventually resulting in cardiomyocyte apoptosis, myocardial remodelling and fibrosis. The following article reviews pathophysiological inflammatory processes leading to myocardial oedema including myocarditis, ischaemia-reperfusion injury and viral infections with a special focus on the pathomechanisms evoked by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In addition, clinical implications including potential long-term effects due to viral persistence (long COVID), as well as treatment options, are discussed.

Serial echocardiographic evaluation of COVID-19 patients without prior history of structural heart disease: a 1-year follow-up CRACoV-HHS study.

Background: It is a well-known fact that COVID-19 affects the cardiovascular system by exacerbating heart failure in patients with preexisting conditions. However, there is a poor insight into the cardiovascular involvement and sequelae in patients without preexisting conditions. The aim of the study is to analyse the influence of COVID-19 on cardiac performance in patients without prior history of structural heart disease. The study is part of the CRACoV project, which includes a prospective design and a 12-month follow-up period. Material and methods: The study included 229 patients hospitalised with a diagnosis of COVID-19 (median age of 59 years, 81 were women). A standard clinical assessment and laboratory tests were performed in all participants. An extended echocardiographic image acquisition was performed at baseline and at a 3-, 6-, and 12-month follow-up. All analyses were performed off-line. A series of echocardiographic parameters was compared using repeated measures or Friedman analysis of variance. Results: In all subjects, the left ventricular (LV) ejection fraction at baseline was preserved [63.0%; Q1:Q3 (60.0-66.0)]. Elevated levels of high-sensitivity cardiac troponin T were detected in 21.3% of the patients, and elevated NT-proBNP levels were detected in 55.8%. At the 1-year follow-up, no significant changes were observed in the LV diameter and volume (LV 48.0 ± 5.2 vs. 47.8 ± 4.8 mm, p = 0.08), while a significant improvement of the parameters in the biventricular strain was observed (LV -19.1 ± 3.3% vs. -19.7 ± 2.5%, p = 0.01, and right ventricular -19.9 ± 4.5% vs. -23.2 ± 4.9%, p = 0.002). In addition, a decrease in the LV wall thickness was also observed (interventricular septum 10.4 ± 1.6 vs. 9.7 ± 2.0 mm, p < 0.001; LV posterior wall 9.8 ± 1.4 vs. 9.1 ± 1.5 mm, p < 0.001). Conclusions: In an acute phase of COVID-19, the elevation of cardiac biomarkers in patients with normal left ventricular ejection fraction is a frequent occurrence; however, it does not translate into clinically significant cardiac dysfunction after 1 year. The serial echocardiographic evaluations conducted in patients without preexisting structural heart disease demonstrate an overall trend towards an improved cardiac function and a reduced myocardial thickening at 1-year follow-up. This suggests that the acute cardiac consequences of COVID-19 are associated with systemic inflammation and haemodynamic stress in patients without preexisting conditions.

Abnormal release of cardiac biomarkers in the presence of myocardial oedema evaluated by cardiac magnetic resonance after uncomplicated revascularization procedures.

AIMS: To analyse the association of myocardial oedema (ME), observed as high T2 signal intensity (HT2) in cardiac magnetic resonance imaging, with the release of cardiac biomarkers, ventricular ejection, and clinical outcomes after revascularization. METHODS AND RESULTS: Patients with stable coronary artery disease with the indication for revascularization were included. Biomarker levels [troponin I (cTnI) and creatine kinase MB (CK-MB)] and T2-weighted and late gadolinium enhancement (LGE) images were obtained before and after the percutaneous or surgical revascularization procedures. The association of HT2 with the levels of biomarkers, with and without LGE, evolution of left ventricular ejection fraction (LVEF), and 5-year clinical outcomes were assessed. A total of 196 patients were divided into 2 groups: Group 1 (HT2, 40) and Group 2 (no HT2, 156). Both peak cTnI (8.9 and 1.6 ng/mL) and peak CK-MB values (44.7 and 12.1 ng/mL) were significantly higher in Group 1. Based on the presence of new LGE, patients were stratified into Groups A (no HT2/LGE, 149), B (HT2, 9), C (LGE, 7), and D (both HT2/LGE, 31). The peak cTnI and CK-MB values were 1.5 and 12.0, 5.4 and 44.7, 5.0 and 18.3, and 9.8 and 42.8 ng/mL in Groups A, B, C, and D, respectively, and were significantly different. The average LVEF decreased by 4.4% in Group 1 and increased by 2.2% in Group 2 (P = 0.057). CONCLUSION: ME after revascularization procedures was associated with increased release of cardiac necrosis biomarkers, and a trend towards a difference in LVEF, indicating a role of ME in cardiac injury after interventions.

Incremental significance of myocardial oedema for prognosis in hypertrophic cardiomyopathy.

AIMS: To explore the prognosis of myocardial oedema measured by T2 mapping in hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: A total of 674 patients with HCM (age: 50 ± 15 years, 60.5% males) who underwent cardiovascular magnetic resonance were prospectively enrolled from 2011 to 2020. One hundred healthy controls (age: 48 ± 19 years, 58.0% males) were included for comparison. Myocardial oedema was quantitatively measured by T2 mapping in both global and segmental myocardium. The endpoints were defined as a combination of cardiovascular death and appropriate implantable cardioverter defibrillator discharge. During a median follow-up of 36 months (interquartile range: 24-60 months), 55 patients (8.2%) had cardiovascular events. Patients with cardiovascular events had a higher T2 max, T2 min, and T2 global values (all P < 0.001) than patients who remained event free. Survival analysis demonstrated that patients with HCM with late gadolinium enhancement [LGE(+)] and T2 max ≥44.9 ms had a higher risk of developing cardiovascular events (P < 0.001). A multivariate Cox regression analysis showed that T2 max, T2 min, and T2 global provided significant prognostic value to predict cardiovascular events (all P < 0.001). According to the C-index (0.825, 0.814), net reclassification index (0.612, 0.536, both P < 0.001), and integrative discrimination index (0.029, 0.029, both P < 0.05), T2 max or T2 min significantly increased the predictive performance of established risk factors, including extensive LGE. CONCLUSION: Patients with HCM with LGE(+) and higher T2 had worse prognosis than those with LGE(+) and lower T2.

Myocardial oedema contributes to interstitial expansion and associates with mechanical and electrocardiographic changes in takotsubo syndrome: a CMR T1 and T2 mapping study.

AIMS: myocardial oedema is largely represented in takotsubo syndrome (TTS) and may contribute to alter the myocardium morphology and function. The aim of the study is to describe relationships between oedema, mechanical, and electrical abnormalities in TTS. METHODS AND RESULTS: the study included n = 32 hospitalized TTS patients and n = 23 controls. Cardiac magnetic resonance (CMR) with tissue mapping and feature tracking was performed with concomitant 12-lead electrocardiogram (ECG) recording. Mean age of TTS was 72 ± 12 years old, 94% women. Compared with controls, patients had higher left ventricular (LV) mass, worse systolic function, higher septal native T1 (1116 ± 73 msec vs. 970 ± 23 msec, P < 0.001), T2 (56 ± 5 msec vs. 46 ± 2 msec, P < 0.001), and extracellular volume (ECV) fraction (32 ± 5% vs. 24 ± 1%, P < 0.001). TTS patients had higher apicobasal gradient of T2 values (12 ± 6 msec vs. 2 ± 6 msec, P < 0.001); basal LV wall displayed higher native T1, T2, and ECV (all P < 0.002) but similar circumferential strain against controls (-23 ± 3% vs. -24 ± 4%, P = 0.351). In the TTS cohort, septal T2 values showed significant correlations with native T1 (r = 0.609, P < 0.001), ECV (r = 0.689, P < 0.001), left ventricular ejection fraction (r = -0.459, P = 0.008) and aVR voltage (r = -0.478, P = 0.009). Negative T-wave voltage and QTc length correlated with apicobasal T2 mapping gradient (r = 0.499, P = 0.007 and r = 0.372, P = 0.047, respectively) but not with other tissue mapping measurements. CONCLUSIONS: CMR T1 and T2 mapping demonstrated increased myocardial water content conditioning interstitial expansion in acute TTS, detected even outside areas of abnormal wall motion. Oedema burden and distribution associated with mechanical and electrocardiographic changes, making it a potential prognostic marker and therapeutic target in TTS.

Global myocardial oedema in resuscitated out-of-hospital cardiac arrest patients assessed by cardiac magnetic resonance: a pilot study.

AIMS: Myocardial dysfunction is well described after out-of-hospital cardiac arrest (OHCA); however, the underlying mechanisms are not yet understood. We hypothesized that this dysfunction is associated to a global myocardial oedema. Using cardiac magnetic resonance (CMR), we assessed the presence of such oedema early after successful resuscitation from OHCA. METHODS AND RESULTS: Comatose patients resuscitated from OHCA and admitted to the cardiac intensive care unit were consecutively included and underwent CMR in general anaesthesia within 36 h after cardiac arrest with anaesthetic support. To assess global myocardial oedema, T1 and T2 segmented maps were generated from three representative short-axis slices, and values from each segment were then used to determine a mean global T1 and T2 time for each patient. Healthy subjects were used as controls. CMR was obtained in 16 patients and compared with nine controls. The OHCA patients were 60 ± 9 years old, and acute myocardial infarction (MI) was diagnosed in six cases. On admission, left ventricular ejection fraction assessed by transthoracic echocardiography was 35 ± 15%, and this improved significantly to 43 ± 14% during hospitalization (P < 0.05). Mean global T1 and T2 time was significantly higher in OHCA patients compared with the control group (1071 ms vs. 999 ms, P = 0.002, and 52 ms vs. 46 ms, P < 0.001, respectively), and this difference remained significant when segments involved in the MI were excluded. CONCLUSION: Assessed with CMR, we for the first time document an early global myocardial oedema in patients successfully resuscitated from OHCA.

A 17-year-old boy with chest pain and transient ventricular wall thickening.

We describe the case of a 17-year-old boy who developed acute myopericarditis associated with transient ventricular wall thickening. This is a unique teaching case illustrating that acute myocarditis can be associated with significant oedema, secondary to inflammation, causing marked wall thickening that is apparent on echocardiography. This oedema resolves completely with anti-inflammatory drug treatment.

Myocardial oedema: pathophysiological basis and implications for the failing heart.

Myocardial fluid homeostasis relies on a complex interplay between microvascular filtration, interstitial hydration, cardiomyocyte water uptake and lymphatic removal. Dysregulation of one or more of these mechanisms may result in myocardial oedema. Interstitial and intracellular fluid accumulation disrupts myocardial architecture, intercellular communication, and metabolic pathways, decreasing contractility and increasing myocardial stiffness. The widespread use of cardiac magnetic resonance enabled the identification of myocardial oedema as a clinically relevant imaging finding with prognostic implications in several types of heart failure. Furthermore, growing experimental evidence has contributed to a better understanding of the physical and molecular interactions in the microvascular barrier, myocardial interstitium and lymphatics and how they might be disrupted in heart failure. In this review, we summarize current knowledge on the factors controlling myocardial water balance in the healthy and failing heart and pinpoint the new potential therapeutic avenues.

Early Myocardial Changes in Patients with Rheumatoid Arthritis without Known Cardiovascular Diseases-A Comprehensive Cardiac Magnetic Resonance Study.

Clinically silent cardiac disease is frequently observed in rheumatoid arthritis (RA), and cardiovascular complications are the leading cause of mortality in RA. We sought to evaluate the myocardium of young RA patients without known cardiac disease using cardiac magnetic resonance (CMR), including T1/T2 mapping sequences. Eighteen RA patients (median age 41 years, 83% females) mainly with low disease activity or in remission and without any known cardiovascular disease were prospectively included to undergo CMR. A control group consisted of 10 sex- and age-matched patients without RA or any known structural cardiovascular disease. Heart chambers size and left/right ventricular systolic function were similar in patients with RA and controls. Signs of myocardial oedema were present in up to 39% of RA patients, including T2 time above cut-off value in 7 patients (39%) in comparison to none of the controls (p = 0.003) and T2 signal intensity ratio above the cut-off value in 6 patients (33%) and in none of the controls (p = 0.06). Extracellular volume was similar in both groups signifying a lack of diffuse fibrosis in studied group of RA patients. There were also no signs of late gadolinium enhancement (LGE) in either group except for one patient with RA who was found to have prior silent myocardial infarction. No correlation was found between markers of disease severity and markers of oedema observed on CMR in patients with RA. Nevertheless, patients with increased T2 time (≥50 ms) were more likely to have X-ray erosions (p = 0.02) and a longer duration between symptom onset and diagnosis (p = 0.02). Finally, there were no significant arrhythmias on 24-h ECG Holter monitoring in RA patients. CMR features of myocardial oedema without signs of myocardial fibrosis were found in 39% of young RA patients without known heart disease or cardiac symptoms. Presence of myocardial oedema was associated with X-ray erosions and a longer duration between symptom onset and diagnosis. The clinical significance of the observed early myocardial changes accompanying RA requires additional studies.

Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance.

BACKGROUND: Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients. METHODS AND RESULTS: One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms). CONCLUSIONS: During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.

Clinical features, cardiac magnetic resonance imaging findings and outcome of patients with suspected myocarditis.

Myocarditis is largely underdiagnosed due to subclinical symptoms and non-availability of diagnostic techniques necessitating high index of suspicion and early disease identification. This study aimed to assess the clinical presentation, cardiac magnetic resonance (CMR) imaging findings and prognosis of these patients. After reviewing the CMR data of Aga Khan University Hospital from January 2011 to December 2019, a total of 24 patients were included in the study with the confirmed diagnosis of myocarditis on CMR. Mean age was 33.4±15 years with the majority (58%) being male. Dyspnoea was the commonest symptom seen in 15(62%) cases followed by chest pain in 13 (54%). On echocardiogram, 15 (62.5%) cases showed LV dysfunction. Common CMR findings were late gadolinium enhancement in 18 (75%) and bright T2 signals in 11 (45%) patients. With a mean follow-up of 3.6±2 years, one patient died of non-cardiac cause. Nine out of 14 patients (for whom repeat echocardiogram was done) had resolution of LV dysfunction suggesting favourable prognosis.

R2 prime (R2') magnetic resonance imaging for post-myocardial infarction intramyocardial haemorrhage quantification.

AIMS: To assess whether R2* is more accurate than T2* for the detection of intramyocardial haemorrhage (IMH) and to evaluate whether T2' (or R2') is less affected by oedema than T2* (R2*), and thus more suitable for the accurate identification of post-myocardial infarction (MI) IMH. METHODS AND RESULTS: Reperfused anterior MI was performed in 20 pigs, which were sacrificed at 120 min, 24 h, 4 days, and 7 days. At each time point, cardiac magnetic resonance (CMR) T2- and T2*-mapping scans were recorded, and myocardial tissue samples were collected to quantify IMH and myocardial water content. After normalization by the number of red blood cells in remote tissue, histological IMH increased 5.2-fold, 10.7-fold, and 4.1-fold at Days 1, 4, and 7, respectively. The presence of IMH was correlated more strongly with R2* (r = 0.69; P = 0.013) than with T2* (r = -0.50; P = 0.085). The correlation with IMH was even stronger for R2' (r = 0.72; P = 0.008). For myocardial oedema, the correlation was stronger for R2* (r = -0.63; P = 0.029) than for R2' (r = -0.50; P = 0.100). Multivariate linear regressions confirmed that R2* values were significantly explained by both IMH and oedema, whereas R2' values were mostly explained by histological IMH (P = 0.024) and were little influenced by myocardial oedema (P = 0.262). CONCLUSION: Using CMR mapping with histological validation in a pig model of reperfused MI, R2'more accurately detected IMH and was less influenced by oedema than R2* (and T2*). Further studies are needed to elucidate whether R2' is also better suited for the characterization of post-MI IMH in the clinical setting.

Acute impact of an endurance race on cardiac function and biomarkers of myocardial injury in triathletes with and without myocardial fibrosis.

AIMS: The aim of this study was to investigate the occurrence of myocardial injury and cardiac dysfunction after an endurance race by biomarkers and cardiac magnetic resonance in triathletes with and without myocardial fibrosis. METHODS AND RESULTS: Thirty asymptomatic male triathletes (45 ± 10 years) with over 10 training hours per week and 55 ± 8 ml/kg per minute maximal oxygen uptake during exercise testing were studied before (baseline) and 2.4 ± 1.1 hours post-race. Baseline cardiac magnetic resonance included cine, T1/T2, late gadolinium enhancement (LGE) and extracellular volume imaging. Post-race non-contrast cardiac magnetic resonance included cine and T1/T2 mapping. Non-ischaemic myocardial fibrosis was present in 10 triathletes (LGE+) whereas 20 had no fibrosis (LGE-). At baseline, LGE + triathletes had higher peak exercise systolic blood pressure with 222 ± 21 mmHg compared to LGE- triathletes (192 ± 30 mmHg, P < 0.01). Post-race troponin T and creatine kinase MB were similarly increased in both groups, but there was no change in T2 and T1 from baseline to post-race with 54 ± 3 ms versus 53 ± 3 ms (P = 0.797) and 989 ± 21 ms versus 989 ± 28 ms (P = 0.926), respectively. However, post-race left atrial ejection fraction was significantly lower in LGE + triathletes compared to LGE- triathletes (53 ± 6% vs. 59 ± 6%, P < 0.05). Furthermore, baseline atrial peak filling rates were lower in LGE - triathletes (121 ± 30 ml/s/m2) compared to LGE + triathletes (161 ± 34 ml/s/m2, P < 0.01). Post-race atrial peak filling rates increased in LGE- triathletes to 163 ± 46 ml/s/m2, P < 0.001), but not in LGE + triathletes (169 ± 50ml/s/m2, P = 0.747). CONCLUSION: Despite post-race troponin T release, we did not find detectable myocardial oedema by cardiac magnetic resonance. However, the unfavourable blood pressure response during exercise testing seemed to be associated with post-race cardiac dysfunction, which could explain the occurrence of myocardial fibrosis in triathletes.

Myocardial oedema in an 8-year-old Chinese boy with Idiopathic systemic capillary leak syndrome.

BACKGROUND: Idiopathic systemic capillary leak syndrome (ISCLS) is rare, and there has been about 32 cases reported in children worldwide since this disorder was first described in 1960. Clinical guidelines on the management approach stemming from robust scientific evidence are lacking. This case report presents the first reported paediatric case of severe ISCLS with significant myocardial oedema and emphasizes this disease's impact on a child's cardiac function. CASE PRESENTATION: A Chinese boy had his first attack of severe hypovolaemic shock that responded to fluid resuscitation when he was 6 years of age. His second attack developed at 8 years of age. He was then transferred to our cardiac unit for refractory hypotensive shock. The patient's echocardiogram revealed ventricular wall thickening with significant cardiac dysfunction requiring extracorporeal membrane oxygenation support. Subsequently, he made a full recovery, including his myocardial wall thickness and function. The echocardiographic findings suggested myocardial oedema that was transient in nature. Clinical and laboratory investigation from both episodes were compatible with ISCLS. CONCLUSION: ISCLS is rare, and therefore there is only a limited understanding on the pathophysiology of this disorder. The current treatment approach is based on a few case reports and series. During the acute phase, optimal supportive management is paramount. Our case highlights the importance of early recognition and consideration for extracorporeal membrane oxygenation support in patients with a life-threatening presentation, as it was lifesaving for this child who suffered myocardial oedema and ventricular dysfunction.

Cardiovascular magnetic resonance imaging pattern in patients with autoimmune rheumatic diseases and ventricular tachycardia with preserved ejection fraction.

BACKGROUND: Ventricular tachycardia/fibrillation (VT/VF) may occur in autoimmune rheumatic diseases (ARDs). We hypothesized that cardiovascular magnetic resonance (CMR) can identify arrhythmogenic substrates in ARD patients. PATIENTS - METHODS: Using a 1.5 T system, we evaluated 61 consecutive patients with various types of ARDs and normal left ventricular ejection fraction (LVEF) on echocardiography. A comparison of patients with recent VT/VF and those that never experienced VT/VF was performed. CMR parameters included left and right ventricular (LV and RV) end-systolic and end-diastolic volumes (ESV and EDV), T2 signal ratio of myocardium over skeletal muscle, early/late gadolinium enhancement (EGE and LGE), T1/T2-mapping and extracellular volume fraction (ECV). RESULTS: 21 (34%) patients had a history of recent, electrocardiographically identified, VT/VF. No demographic or functional CMR variables differed significantly between groups. The same was the case for T2 signal ratio and EGE/LGE. Median native T1 mapping values were significantly higher in patients with VT/VF compared to those without [1135.0 (1076.0, 1201.0) vs. 1050.0 (1025.0, 1078.0), p < 0.001], as was the case for mean T2 mapping [60.4 (6.6) vs. 55.0 (7.9), p = 0.009] and median ECV values [32.0 (30.0, 32.0) vs. 29.0 (28.0, 31.5), p = 0.001]. After multivariate corrections for age, LVEDV, LVEF, RVEDV, RVEF, T2 signal ratio, EGE and LGE, these remained significant predictors of having experienced VT/VF in the past. CONCLUSIONS: T1/T2-mapping and ECV offer incremental value as identifiers of arrhythmogenic substrates in ARD patients, beyond traditionally used indices. They can thus guide implantable cardiac defibrillator (ICD) implantation in ARD patients presenting with VT/VF and normal LVEF.

Diagnostic and prognostic role of cardiac magnetic resonance in acute myocarditis.

Acute myocarditis (AM) is commonly found in everyday clinical practice. Differential diagnosis between various causes of myocardial damage with non-obstructive coronary arteries can be cumbersome for clinician. Moreover, AM may be provoked by a number of different causes and clinical presentation can be heterogeneous with potential overlap going from asymptomatic or subclinical to severe heart failure, arrhythmias, and death. Cardiac magnetic resonance (CMR) over the last decades has proven to be the diagnostic technique of choice since it allows identifying AM with excellent diagnostic accuracy. Latest technological advancement with parametric imaging such as T1 and T2 mapping further increases sensitivity and provides additional help towards a correct diagnosis. CMR however is no longer to be considered as a mere diagnostic tool but also as a powerful source of prognostic information. Scientific evidence has corroborated CMR's role beyond diagnosis demonstrating how late gadolinium enhancement (LGE) presence is a powerful predictor of cardiac events and how the presence of septal LGE is to be considered of worst prognosis regardless of LGE extension even in patients with preserved global systolic function. CMR should be routinely performed in all patients with AM suspicion since its diagnostic and prognostic role is of paramount important and could modify therapeutic strategy and subsequent clinical decisions.

Myocardial tissue characterisation and detection of myocardial oedema by cardiovascular magnetic resonance in women with pre-eclampsia: a pilot study.

BACKGROUND: Pre-eclampsia is characterised by increased left ventricular wall thickness on transthoracic echocardiography (TTE). This is assumed to be myocardial hypertrophy, however TTE cannot determine myocardial structure which may be muscle, oedema or fibrosis. Given the high incidence of peripheral oedema in pre-eclampsia, we hypothesised that increased thickness could represent oedema. Cardiovascular magnetic resonance (CMR) characterises myocardial tissue, differentiating between hypertrophy, oedema and fibrosis. This pilot study was designed to characterise myocardial composition using CMR in pregnant women (healthy or with pre-eclampsia) and to compare cardiac output and left ventricular mass using TTE and CMR. METHODS: Thirty-six women (31 healthy, five with pre-eclampsia) underwent TTE and CMR and left ventricular mass was assessed applying standard definitions. Myocardial signal intensities were measured from left ventricular segments and compared to serratus anterior muscle to determine global myocardial signal intensity. Myocardial oedema was defined as a myocardial:skeletal signal intensity ratio >1.9. Agreement between devices for cardiac output and left ventricular mass, and inter- and intra-observer measurements used Bland Altman methodology, calculating the agreement tolerable interval: >1.5 is unacceptable, 1.0-1.5 is marginal and <1.0 is acceptable agreement. RESULTS: Myocardial oedema was present in two (40%) pre-eclamptic women but no healthy women (P=0.017). Agreement for cardiac output was acceptable, for left ventricular mass marginal, and for inter- and intra-observer measurements acceptable. CONCLUSIONS: Cardiovascular magnetic resonance was used to characterise the myocardial tissue in women with pre-eclampsia. Data suggest that some women with pre-eclampsia have myocardial oedema rather than hypertrophy.

Effects of glycaemic variability on cardiac remodelling after reperfused myocardial infarction: Evaluation of streptozotocin-induced diabetic Wistar rats using cardiac magnetic resonance imaging.

AIMS: In addition to hyperglycaemia, glycaemic variability seems to be associated with poor outcomes after acute myocardial infarction. This study explored the impact of glycaemic variability in diabetic Wistar rats subjected to myocardial ischaemia/reperfusion. METHODS: Animals with streptozotocin-induced diabetes received insulin either to maintain stable hyperglycaemia (Dh group) or to generate glycaemic variability (Dv). After experimental myocardial ischaemia/reperfusion was surgically induced, 7T cardiac magnetic resonance imaging (CMR) was performed at weeks 1 (w1) and 3 (w3). RESULTS: Twenty-six rats were randomized [sham group (S): n=5; control group (C): n=7; Dh group: n=6; and Dv group: n=8]. The mean amplitude of glucose reflecting glycaemic variability was higher in the Dv than in the Dh group (9.1±2.7mmol/L vs 5.9±1.9mmol/L; P<0.05). CMR assessment at w3 revealed ventricular enlargement in both Dh and Dv groups compared with the C and S groups (end-diastolic volume: 1.60±0.22 and 1.36±0.30mL/kg compared with 1.11±0.13 and 0.87±0.11mL/kg, respectively; P<0.05). Circumferential strain was altered between w1 and w3 in the remote area only in the Dv group, resulting in a lower value in this group than in the S, C and Dh groups (-0.11±0.01 vs -0.17±0.05, -0.15±0.03 and -0.16±0.03, respectively; P<0.05). In addition, at w3, oedema was also higher in the remote area in the Dv than in the C group (18.3±4.9ms vs 14.5±1.7ms, respectively; P<0.05). CONCLUSION: In the context of experimental myocardial ischaemia/reperfusion, our results suggest that glycaemic variability might have a potentially deleterious impact on myocardial outcomes beyond the classical glucose metrics.