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Reperfusion therapy for acute myocardial infarction (MI) is lifesaving. However, the benefit of reperfusion therapy can be paradoxically diminished by reperfusion injury, which can increase MI size.Hemorrhage is known to occur in reperfused MIs, but whether hemorrhage plays a role in reperfusion-mediated MI expansion is not known.We studied cardiac troponin kinetics (cTn) of ST-segment elevation MI patients (n = 70) classified by cardiovascular magnetic resonance to be hemorrhagic (70%) or nonhemorrhagic following primary percutaneous coronary intervention. To isolate the effects of hemorrhage from ischemic burden, we performed controlled canine studies (n = 25), and serially followed both cTn and MI size with time-lapse imaging.CTn was not different before reperfusion; however, an increase in cTn following primary percutaneous coronary intervention peaked earlier (12 hours vs 24 hours; P 0.05) and was significantly higher in patients with hemorrhage (P 0.01). In hemorrhagic animals, reperfusion led to rapid expansion of myocardial necrosis culminating in epicardial involvement, which was not present in nonhemorrhagic cases (P 0.001). MI size and salvage were not different at 1 hour postreperfusion in animals with and without hemorrhage (P = 0.65). However, within 72 hours of reperfusion, a 4-fold greater loss in salvageable myocardium was evident in hemorrhagic MIs (P 0.001). This paralleled observations in patients with larger MIs occurring in hemorrhagic cases (P 0.01).Myocardial hemorrhage is a determinant of MI size. It drives MI expansion after reperfusion and compromises myocardial salvage. This introduces a clinical role of hemorrhage in acute care management, risk assessment, and future therapeutics.

Sudden blockage of arteries supplying the heart muscle contributes to millions of heart attacks (myocardial infarction, MI) around the world. Although re-opening these arteries (reperfusion) saves MI patients from immediate death, approximately 50% of these patients go on to develop chronic heart failure (CHF) and die within a 5-year period; however, why some patients accelerate towards CHF while others do not remains unclear. Here we show, using large animal models of reperfused MI, that intramyocardial hemorrhage - the most damaging form of reperfusion injury (evident in nearly 40% of reperfused ST-elevation MI patients) - drives delayed infarct healing and is centrally responsible for continuous fatty degeneration of the infarcted myocardium contributing to adverse remodeling of the heart. Specifically, we show that the fatty degeneration of the hemorrhagic MI zone stems from iron-induced macrophage activation, lipid peroxidation, foam cell formation, ceroid production, foam cell apoptosis and iron recycling. We also demonstrate that timely reduction of iron within the hemorrhagic MI zone reduces fatty infiltration and directs the heart towards favorable remodeling. Collectively, our findings elucidate why some, but not all, MIs are destined to CHF and help define a potential therapeutic strategy to mitigate post-MI CHF independent of MI size.

We report a rare case of a 44-year-old male who underwent a diagnostic coronary angiogram following a non-ST elevation myocardial infarction complicated by an aortic valve leaflet tear requiring surgical intervention. Routine transthoracic echocardiogram demonstrated a mobile echogenic structure prolapsing into the left ventricular outflow tract. An intraoperative transesophageal echocardiogram confirmed that the structure originated from the ventricular side of left coronary cusp, causing malcoaptation between left and right coronary cusps, and subsequent moderate to severe aortic regurgitation.

Diaphragmatic eventration in old age is a rare phenomenon. Typically, it is thought to originate as a result of failure of development of the muscles of the diaphragm. Less commonly, it can occur secondary to acquired conditions resulting from spinal cord or phrenic nerve injury and is only detected incidentally when the patient presents with dyspnea, chest infection, or cardiac compression symptoms. Herein, we report a case of right diaphragmatic paralysis in a 58-year-old man with a presentation of marked elevation of the right hemidiaphragm and ascites causing a picture compatible with cardiac tamponade.

Cardiovascular magnetic resonance imaging has become the gold standard for evaluating myocardial function, volumes, and scarring. Additionally, cardiovascular magnetic resonance imaging is unique in its comprehensive tissue characterization, including assessment of myocardial edema, myocardial siderosis, myocardial perfusion, and diffuse myocardial fibrosis. Cardiovascular magnetic resonance imaging has become an indispensable tool in the evaluation of congenital heart disease, heart failure, cardiac masses, pericardial disease, and coronary artery disease. This review will highlight some recent novel cardiovascular magnetic resonance imaging techniques, concepts, and applications.

Background Heart transplant recipients (HTRs) experience multiple cardiac complications, many of which might produce myocardial fibrosis. Cardiovascular magnetic resonance imaging (CMR) can image myocardial fibrosis using late gadolinium enhancement (LGE) imaging. We hypothesized that the presence and volume of LGE in heart transplant recipients correlates with left ventricular (LV) functional parameters and clinical outcomes. Methods Thirty-eight stable HTRs underwent a CMR study and clinical follow-up. Results In 38 stable HTRs, LGE was seen in 19 patients (50%), of which 15 (79%) had a nonischemic pattern and 4 (21%) had an ischemic pattern. LGE volume was associated with reduced LV ejection fraction (EF) ( R 2 = 0.57; P = 0.001) and increased LV end-diastolic volume ( R 2 = 0.59; P = 0.001). The presence of LGE was associated with cardiovascular death or hospitalization within the next year ( P = 0.04), and patients who died or were hospitalized had more LGE than those that were not hospitalized (15 g vs 7 g; P = 0.03). Conclusions LGE is common in HTR and is associated with adverse ventricular remodelling and adverse clinical outcomes. LGE might be a useful noninvasive approach to monitor graft disease in asymptomatic patients after heart transplant.

Background— Intramyocardial hemorrhage frequently accompanies large reperfused myocardial infarctions. However, its influence on the makeup and the ensuing effect on the infarcted tissue during the chronic phase remain unexplored. Methods and Results— Patients (n=15; 3 women), recruited after successful percutaneous coronary intervention for first segment–elevation myocardial infarction, underwent cardiovascular magnetic resonance imaging on day 3 and month 6 after percutaneous coronary intervention. Patients with hemorrhagic (Hemo+) infarctions, as determined by T2* cardiovascular magnetic resonance on day 3 (n=11), showed persistent T2* losses colocalized with scar tissue on the follow-up scans, suggesting chronic iron deposition. T2* values of Hemo+ territories were significantly higher than nonhemorrhagic (Hemo−) and remote territories ( P P =0.51). Canines (n=20) subjected to ischemia-reperfusion injury (n=14) underwent cardiovascular magnetic resonance on days 3 and 56 after ischemia-reperfusion injury. Similarly, sham-operated animals (Shams; n=3) were imaged using cardiovascular magnetic resonance at similar time points. Subsequently, hearts were explanted and imaged ex vivo, and samples of Hemo+, Hemo−, remote, and Sham myocardium were isolated and stained. The extent of iron deposition ([Fe]) within each sample was measured using mass spectrometry. Hemo+ infarcts showed significant T2* losses compared with the other (control) groups ( P P R 2 =0.7 and P Conclusions— Hemorrhagic myocardial infarction can lead to iron depositions within the infarct zones, which can be a source of prolonged inflammatory burden in the chronic phase of myocardial infarction.

Background— Emerging evidence indicates that persistent microvascular obstruction (PMO) is more predictive of major adverse cardiovascular events than myocardial infarct (MI) size. But it remains unclear how PMO, a phenomenon limited to the acute/subacute period of MI, drives adverse remodeling in chronic MI setting. We hypothesized that PMO resolves into chronic iron crystals within MI territories, which in turn are proinflammatory and favor adverse remodeling post-MI. Methods and Results— Canines (n=40) were studied with cardiac magnetic resonance imaging to characterize the spatiotemporal relationships among PMO, iron deposition, infarct resorption, and left ventricular remodeling between day 7 (acute) and week 8 (chronic) post-MI. Histology was used to assess iron deposition and to examine relationships between iron content with macrophage infiltration, proinflammatory cytokine synthesis, and matrix metalloproteinase activation. Atomic resolution transmission electron microscopy was used to determine iron crystallinity, and energy-dispersive X-ray spectroscopy was used to identify the chemical composition of the iron composite. PMO with or without reperfusion hemorrhage led to chronic iron deposition, and the extent of this deposition was strongly related to PMO volume ( r >0.8). Iron deposits were found within macrophages as aggregates of nanocrystals (≈2.5 nm diameter) in the ferric state. Extent of iron deposits was strongly correlated with proinflammatory burden, collagen-degrading enzyme activity, infarct resorption, and adverse structural remodeling ( r >0.5). Conclusions— Crystallized iron deposition from PMO is directly related to proinflammatory burden, infarct resorption, and adverse left ventricular remodeling in the chronic phase of MI in canines. Therapeutic strategies to combat adverse remodeling could potentially benefit from taking into account the chronic iron-driven inflammatory process.

Congenital absence of the pericardium is a very rare cardiac malformation, usually diagnosed fortuitously on autopsy or surgery. Symptoms related to these abnormalities are usually benign, and fatalities reported in the literature are almost exclusively secondary to herniation of the heart through a partial defect. We present the unusual case of a 44-year-old woman admitted for sudden cardiac arrest. Initial evaluation suggested acute anterior myocardial infarction, but further investigation ruled out coronary heart disease. No arrhythmia could be initiated on electrophysiological study, and absence of most of the left pericardium was confirmed by cardiac magnetic resonance imaging. After the exclusion of common etiologies such as idiopathic ventricular fibrillation, transient great vessel torsion due to hypermobility of the heart with secondary malignant arrhythmia was considered to be the most likely mechanism for the sudden cardiac arrest. A review of the available literature on clinical presentation, diagnostic tools, and therapeutic options is also presented.

ObjectivesThe aim of this study was to investigate the capabilities of balanced steady-state free precession (bSSFP) cardiac magnetic resonance imaging as a novel cine imaging approach for characterizing myocardial edema in animals and patients after reperfused myocardial infarction.BackgroundCurrent cardiac magnetic resonance methods require 2 separate scans for assessment of myocardial edema and cardiac function.MethodsMini-pigs (n = 13) with experimentally induced reperfused myocardial infarction and patients with reperfused ST-segment elevation myocardial infarction (n = 26) underwent cardiac magnetic resonance scans on days 2 to 4 post-reperfusion. Cine bSSFP, T2-weighted short TI inversion recovery (T2-STIR), and late gadolinium enhancement were performed at 1.5-T. Cine bSSFP and T2-STIR images were acquired with a body coil to mitigate surface coil bias. Signal, contrast, and the area of edema were compared. Additional patients (n = 10) were analyzed for the effect of microvascular obstruction on bSSFP. A receiver-operator characteristic analysis was performed to assess the accuracy of edema detection.ResultsAn area of hyperintense bSSFP signal consistent with edema was observed in the infarction zone (contrast-to-noise ratio: 37 ± 13) in all animals and correlated well with the area of late gadolinium enhancement (R = 0.83, p < 0.01). In all patients, T2-STIR and bSSFP images showed regional hyperintensity in the infarction zone. Normalized contrast-to-noise ratios were not different between T2-STIR and bSSFP. On a slice basis, the volumes of hyperintensity on T2-STIR and bSSFP images correlated well (R = 0.86, p < 0.001), and their means were not different. When compared with T2-STIR, bSSFP was positive for edema in 25 of 26 patients (96% sensitivity) and was negative in all controls (100% specificity). All patients with microvascular obstruction showed a significant reduction of signal in the subendocardial infarction zone compared with infarcted epicardial tissue without microvascular obstruction (p < 0.05).ConclusionsMyocardial edema from ST-segment elevation myocardial infarction can be detected using cine bSSFP imaging with image contrast similar to T2-STIR. This new imaging approach allows evaluation of cardiac function and edema simultaneously, thereby reducing patient scan time and increasing efficiency. Further work is necessary to optimize edema contrast in bSSFP images.

ObjectivesThe purpose of this study was to validate T2*-weighted cardiac magnetic resonance (T2*-CMR) for the detection and quantification of reperfusion hemorrhage in vivo against an ex vivo gold standard, and to investigate the relationship of hemorrhage to microvascular obstruction, infarct size, and left ventricular (LV) functional parameters.BackgroundHemorrhage can contribute to reperfusion injury in myocardial infarction and may have significant implications for patient management. There is currently no validated imaging method to assess reperfusion hemorrhage in vivo. T2*-CMR appears suitable because it can create image contrast on the basis of magnetic field effects of hemoglobin degradation products.MethodsIn 14 mongrel dogs, myocardial infarction was experimentally induced. On day 3 post-reperfusion, an in vivo CMR study was performed including a T2*-weighted gradient-echo imaging sequence for hemorrhage, standard sequences for LV function, and post-contrast sequences for microvascular obstruction and myocardial necrosis. Ex vivo, thioflavin S imaging and triphenyl-tetrazoliumchloride (TTC) staining were performed to assess microvascular obstruction, hemorrhage, and myocardial necrosis. Images were analyzed by blinded observers, and comparative statistics were performed.ResultsHemorrhage occurred only in the dogs with the largest infarctions and the greatest extent of microvascular obstruction, and it was associated with more compromised LV functional parameters. Of 40 hemorrhagic segments on TTC staining, 37 (92.5%) were positive for hemorrhage on T2*-CMR (kappa = 0.96, p < 0.01 for in vivo/ex vivo segmental agreement). The amount of hemorrhage in 13 affected tissue slices as determined by T2*-CMR in vivo correlated strongly with ex vivo results (20.3 ± 2.3% vs. 17.9 ± 1.6% per slice; Pearson r = 0.91; r2 = 0.83, p < 0.01 for both). Hemorrhage size was not different between in vivo T2*-CMR and ex vivo TTC (mean difference 2.39 ± 1.43%; p = 0.19).ConclusionsT2*-CMR accurately quantified myocardial reperfusion hemorrhage in vivo. Hemorrhage was associated with more severe infarct-related injury.

Starting as a research method little more than a decade ago, cardiovascular magnetic resonance (CMR) imaging has rapidly evolved to become a powerful diagnostic tool used in routine clinical cardiology. The contrast in CMR images is generated from protons in different chemical environments and, therefore, enables high-resolution imaging and specific tissue characterization in vivo, without the use of potentially harmful ionizing radiation. CMR imaging is used for the assessment of regional and global ventricular function, and to answer questions regarding anatomy. State-of-the-art CMR sequences allow for a wide range of tissue characterization approaches, including the identification and quantification of nonviable, edematous, inflamed, infiltrated or hypoperfused myocardium. These tissue changes are not only used to help identify the etiology of cardiomyopathies, but also allow for a better understanding of tissue pathology in vivo. CMR tissue characterization may also be used to stage a disease process; for example, elevated T2 signal is consistent with edema and helps differentiate acute from chronic myocardial injury, and the extent of myocardial fibrosis as imaged by contrast-enhanced CMR correlates with adverse patient outcome in ischemic and nonischemic cardiomyopathies. The current role of CMR imaging in clinical cardiology is reviewed, including coronary artery disease, congenital heart disease, nonischemic cardiomyopathies and valvular disease.

Objectives The aim of this research was to identify the diagnostic performance of gadolinium-enhanced and T2-weighted cardiovascular magnetic resonance (CMR) in suspected acute myocarditis. Background Acute myocarditis is difficult to diagnose; CMR provides various means to visualize myocardial inflammatory changes. A CMR approach with clear-cut diagnostic criteria would be desirable. Methods We investigated 25 patients with suspected acute myocarditis (18 males, 44 +/- 17 years) and 23 healthy controls (13 males, 29 +/- 10 years). Cardiovascular magnetic resonance studies included the following sequences: 1) T2-weighted triple inversion recovery; 2) T1-weighted spin echo before and over 4 min after gadolinium injection; and 3) inversion recovery-gradient echo 10 min after gadolinium injection. Qualitative and quantitative image analysis was performed for: 1) focal and global T2 signal intensity (SI); 2) myocardial global relative enhancement (gRE); and 3) areas of late gadolinium enhancement (LGE). Results Both global T2 SI and gRE were higher in patients than in controls (T2: 2.3 +/- 0.4 vs. 1.7 +/- 0.4; p Conclusions A combined CMR approach using T2-weighted imaging, early and late gadolinium enhancement, provides a high diagnostic accuracy and is a useful tool in the diagnosis and assessment of patients with suspected acute myocarditis.

Background: Reperfusion hemorrhage following acute myocardial infarction (AMI) leads to abnormal accumulation of iron deposits (IDs) within the infarcted territory. Given that these IDs drive a prolonged recruitment of macrophages into scar tissue, we investigated the physicochemical characteristics

Churg-Strauss syndrome (CSS) is a rare entity that is characterized by widespread vasculitis, which affects both small and medium-sized blood vessels of nearly all organs. More than 50% of these cases have cardiac involvement, which is the major cause of morbidity and mortality. We describe a case of a patient with cardiac biopsy proven CSS, and we discuss the usefulness of cardiovascular MRI for its diagnosis.

‘From a research tool used by mainly radiologists as little as 10 years ago, increased involvement of cardiologists into CMR research, the advent of improved hardware and development of highly sophisticated imaging sequences have turned CMR into what can be regarded today as the single most comprehensive imaging method in clinical cardiology.’

We encountered a 65-year-old woman with typical electrocardiogram (ECG) changes and new-onset left ventricular dysfunction with apical ballooning that exhibited typical changes of tako-tsubo-like cardiomyopathy. We used cardiac magnetic resonance (CMR) and cardiac magnetic field mapping (CMFM) to detect changes in structural, mechanical, and electrophysiological myocardial properties during follow-up. CMR displayed an acute myocardial injury, but neither fibrosis nor necrosis. CMFM exhibited severely disturbed repolarization with an inhomogeneous magnetic field. These pathological findings persisted much longer than the abnormalities detected by CMR and the ECG.

Congenital absence of the pericardium is a very rare cardiac malformation, usually diagnosed fortuitously on autopsy or surgery. Symptoms related to these abnormalities are usually benign, and fatalities reported in the literature are almost exclusively secondary to herniation of the heart through a partial defect. We present the unusual case of a 44-year-old woman admitted for sudden cardiac arrest. Initial evaluation suggested acute anterior myocardial infarction, but further investigation ruled out coronary heart disease. No arrhythmia could be initiated on electrophysiological study, and absence of most of the left pericardium was confirmed by cardiac magnetic resonance imaging. After the exclusion of common etiologies such as idiopathic ventricular fibrillation, transient great vessel torsion due to hypermobility of the heart with secondary malignant arrhythmia was considered to be the most likely mechanism for the sudden cardiac arrest. A review of the available literature on clinical presentation, diagnostic tools, and therapeutic options is also presented.

This chapter describes the utility of cardiovascular magnetic resonance (CMR) imaging in patients with acute myocardial infarction.

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Background The presence and absolute amount of microvascular obstruction (MO) are associated with adverse left ventricular remodelling and prognosis in patients with acute myocardial infarction. MO can be detected with cardiovascular magnetic resonance imaging (CMR) using the technique of first pass perfusion imaging, late contrast enhanced CMR or early contrast enhanced CMR. It has not been shown which standardized definition of hypoenhancement related to the signal of remote myocardium is appropriate to evaluate the presence and the extent of MO on first pass perfusion images. Methods We studied 52 patients with reperfused acute myocardial infarction which showed MO defined as persistent subendocardial hypoenhancement on rest perfusion images. We analyzed rest first-pass perfusion images, early contrast enhanced images and late contrast enhanced images scanned in a 1.5-T magnetic resonance imaging system. The size of MO was measured on rest perfusion images visually and quantitatively using signal intensity (SI) below 2SD and 3SD of remote myocardium as a threshold. The size of MO was also measured visually on early contrast enhanced images and quantitatively on late contrast enhanced images quantitatively defined as the area which did not show SI more than 5 SD above the remote myocardium surrounded by abnormal enhancement. Results On rest perfusion images, standardized analysis using the threshold of �2SD of remote myocardium showed good agreement with visual analysis (ICC= 0.793). Mean MO size using threshold of �2SD of remote myocardium was not significantly different from those by visual assessment (2.22±1.25 cm 2 and 2.40±1.25 cm 2 , p=N.S.), whereas those using threshold of �3SD of remote myocardium was significantly smaller (1.00±0.85 cm 2 , p

Background Microvascular obstruction (MO) is one of the most important predictors of adverse outcome after reperfusion therapy in acute myocardial infarction (MI). Myocardial hemorrhage has been described as a contributor to reperfusion injury. Due to a lack of appropriate imaging techniques, the consequences of reperfusion hemorrhage have not been studied. The purpose of this study is to investigate the relationship between myocardial hemorrhage and regional left ventricular functional recovery using T2*-weighted cardiovascular magnetic resonance (CMR) imaging.

Methods In 19 patients (age 57 ± 11), a CMR study was performed 6 ± 1 days after reperfusion therapy for acute ST-elevation myocardial infarction. In a short axis orientation, covering the entire left ventricle (slice thickness 10 mm/0 mm), the following sequences were obtained: cine SSFP images for functional and volumetric analyses, T2*-weighted GE-EPI for hemorrhage; after injection of 0.1 mmol/kgBW early post-conrast IR-GE images were obtained for MO, and after 10 min, late gadolinium enhancement images were obtained for infarct size. Images were analyzed semiquantitatively using a threshold-based signal detection.

Methods We studied nineteen patients with reperfused acute MI without microvascular obstruction (LAD: n = 7; LCX: n = 1; RCA: n = 11). We also studied six healthy subjects. Patients underwent cine CMR imaging, T2-weighted CMR (STIR), and late gadolinium enhancement (LGE) CMR 2.5 +/1.2 days after acute MI. Each short axis was divided into 12-equi-angular segments. The presence of edema and infarction was verified and evaluated semi-quantitatively for each segment, using 2SD above the mean of normal myocardium as a threshold on T2-weighted CMR and 5SD above the mean on LGE images. Wall thickness was measured in the salvaged area at risk, the infarction and in region without evidence for edema using a centerline method with 48 chords (Figure 1). We used the mean of 4 chords as EDWT, resulting in a total of 12 segments. from 13th Annual SCMR Scientific Sessions Phoenix, AZ, USA. 21-24 January 2010

hemorrhage in the myocardium following myocardial infarction, especially larger amounts, leads to severe regional inflammation and affects the healing process as well as local physiology. Thus, detection of myocardial hemorrhage by noninvasive techniques such as cardiac magnetic resonance could add

Cardiovascular magnetic resonance (CMR) has become the primary tool for noninvasive assessment of myocardial inflammation in patients with suspected myocarditis. The International Consensus Group on CMR Diagnosis of Myocarditis was founded in 2006 to achieve consensus among CMR experts and develop recommendations on the current state-of-the-art use of CMR for myocarditis. The recommendations include indications for CMR in patients with suspected myocarditis, CMR protocol standards, terminology for reporting CMR findings, and diagnostic CMR criteria for myocarditis (i.e., “Lake Louise Criteria”).

Introduction: Reperfusion injury in myocardial infarction leads to microvascular obstruction, which can occur with or without gross reperfusion hemorrhage. The incidence and implications of reperfusion hemorrhage are not well investigated. A recently described in vivo imaging approach using T2*-weighted cardiovascular magnetic resonance can help investigate the pathophysiology of reperfusion hemorrhage in vivo. Hypothesis: We hypothesized that hemorrhage reflects a severer from of reperfusion injury and therefore occurs with larger infarct size and worse LV function as compared to reperfusion injury without hemorrhage. Methods: In 14 female mongrel dogs, myocardial infarction was induced by ligation of the left anterior descending coronary artery for 2–4 hours, followed by reperfusion. On day 3 ± 1, a cardiovascular magnetic resonance study was performed in vivo to (1) assess presence of microvascular obstruction, defining reperfusion injury (2) assess presence of reperfusion hemorrhage (3) quantify left ventricular end-diastolic volume, ejection fraction and cardiac output and (4) quantify infarct size with late enhancement. An independent-samples t-test was performed to compare these parameters in dogs with and without hemorrhage in reperfusion injury. Results: From 14 dogs, 9 had microvascular obstruction, and 4/9 had reperfusion hemorrhage in addition to microvascular obstruction. Dogs with hemorrhagic infarcts had significantly larger infarct size (26.1 ± 6.6 g vs. 5.5 ± 3.9 g, p < 0.05), lower LV ejection fraction (28 ± 7% vs. 53 ± 12%, p < 0.05), and lower cardiac output (1.9 ± 0.2 l/min vs. 2.8 ± 0.5 l/min, p < 0.05). There were no differences in LV end-diastolic volume and LV mass. Discussion and conclusion: In this dog model of ischemia/reperfusion injury, gross hemorrhage was associated with significantly larger infarct size and worse LV functional parameters. This supports the hypothesis that hemorrhage may occur with advanced, severe ischemic tissue injury only.

Introduction Hemorrhage can complicate reperfusion injury in myocardial infarction, but no in vivo imaging method exists. We hypothesized that a T2*-weighted cardiovascular magnetic resonance imaging (CMR) sequence accurately detects myocardial hemorrhage in vivo. Methods Reperfused myocardial infarcts were generated in 14 dogs by ligation of the LAD for 3– 6 hours. At day 3, a CMR study was performed using established sequences for quantification of function, microvascular obstruction and myocardial infarction in short axis slices covering the entire myocardium. For hemorrhage, a T2*-weighted multi-echo gradient-echo sequence was applied (TE=35msec, TR=1 RR, FOV 380x280mm, matrix 256 x 192). A segmental analysis was performed using 6 segments per slice: T2*-segments were considered hemorrhagic when signal intensity was >2 standard deviations below the mean of remote myocardium. The contrast-to-noise ratio of hemorrhagic segments over normal segments was assessed. Post-mortem TTC staining was performed with infarcted and hemorrhagic areas analyzed with the same segmental approach. In vivo/ ex vivo correlation statistics were performed. Results In 14 dogs, 378 segments were assessed. Of the T2* CMR segments, 10.2% were excluded due to artifacts; 27 segments yielded a signal drop consistent with hemorrhage (see figure ). The correlation with ex vivo TTC staining was R=0.79 and contrast-to-noise ratio was 9.2±3.4. Sensitivity to detect a hemorrhagic segment was 77%, specificity 99%. Conclusion T2*-weighted CMR accurately detects reperfusion hemorrhage in vivo. The method may be applied in patients to study hemorrhage as a complication of reperfusion injury.

We report the CMR findings of a patient with stenotic biological mitral valve prosthesis that was complicated by thrombus formation in the left atrium. The case illustrates the ability of CMR to assess biological prosthetic valves and to provide a comprehensive diagnostic approach in this clinical scenario.

The aim of this research was to identify the diagnostic performance of gadolinium-enhanced and T2-weighted cardiovascular magnetic resonance (CMR) in suspected acute myocarditis.Acute myocarditis is difficult to diagnose; CMR provides various means to visualize myocardial inflammatory changes. A CMR approach with clear-cut diagnostic criteria would be desirable.We investigated 25 patients with suspected acute myocarditis (18 males, 44 +/- 17 years) and 23 healthy controls (13 males, 29 +/- 10 years). Cardiovascular magnetic resonance studies included the following sequences: 1) T2-weighted triple inversion recovery; 2) T1-weighted spin echo before and over 4 min after gadolinium injection; and 3) inversion recovery-gradient echo 10 min after gadolinium injection. Qualitative and quantitative image analysis was performed for: 1) focal and global T2 signal intensity (SI); 2) myocardial global relative enhancement (gRE); and 3) areas of late gadolinium enhancement (LGE).Both global T2 SI and gRE were higher in patients than in controls (T2: 2.3 +/- 0.4 vs. 1.7 +/- 0.4; p0.0001, gRE: 6.8 +/- 4.0 vs. 3.7 +/- 2.3; p0.001). The sensitivity, specificity, and diagnostic accuracy for T2 (cutoff value of 1.9) were 84%, 74%, and 79%, respectively; gRE: (cutoff value of 4.0) 80%, 68%, and 74.5% respectively; LGE: 44%, 100%, and 71%, respectively. The best diagnostic performance was obtained when "any-two" of the three sequences were positive in the same patient yielding a 76% sensitivity, 95.5% specificity, and 85% diagnostic accuracy.A combined CMR approach using T2-weighted imaging, early and late gadolinium enhancement, provides a high diagnostic accuracy and is a useful tool in the diagnosis and assessment of patients with suspected acute myocarditis.

Background— Delayed enhancement (DE) cardiovascular magnetic resonance (CMR) detects acute and chronic myocardial infarction (MI) by visualizing contrast media accumulation in infarcted segments. T2-weighted CMR depicts infarct-related myocardial edema as a marker of acute but not chronic myocardial injury. We investigated the clinical utility of an approach combining both techniques to differentiate acute from chronic MI. Methods and Results— Seventy-three MI patients were studied in 2 groups. Group A consisted of 15 acute MI patients who were studied twice, on day 1 and 3 months after MI. In group B, 58 patients with acute or chronic MI underwent 1 CMR scan. T2-weighted and DE images of matched slices were acquired on a 1.5-T system. In group A, quantitative segmental and region of interest-based analyses were performed to observe signal changes between the acute and chronic phases. In group B, T2-weighted and DE images were examined visually by 2 blinded observers for the presence or absence of hyperintense areas in corresponding segments. For infarct localization, coronary angiography and/or ECG changes served as the reference standard. In group A, the contrast-to-noise ratio on T2-weighted images dropped in the infarcted segments from 2.7±1.1 on day 1 to 0.1±1.2 after 3 months ( P P =NS). The qualitative assessment of T2-weighted and DE images in group B yielded a specificity of 96% to differentiate acute from chronic lesions. Conclusions— An imaging approach combining DE and T2-weighted CMR accurately differentiates acute from chronic MI.

Over the last decades, cardiac magnetic resonance (CMR) has transformed from a research tool to a widely used diagnostic method in clinical cardiology. This method can now make useful, unique contributions to the work-up of patients with ischemic and non-ischemic heart disease. Advantages of CMR, compared to other imaging methods, include very high resolution imaging with a spatial resolution up to 0.5 mm × 0.5 mm in plane, a large array of different imaging sequences to provide in vivo tissue characterization, and radiation-free imaging. The present manuscript highlights the relevance of CMR in the current clinical practice and new perspectives in cardiology.

Purpose: We sought to assess the relationship between left ventricular regional end-diastolic myocardial wall thickness (EDWT) and myocardial edema defined using T2-weighted Cardiovascular Magnetic Resonance (CMR) after acute myocardial ischemia and reperfusion. Methods: T2-weighted and cine CMR images for 7 dogs at baseline, during coronary occlusion (mean 33 ± 4 minutes) and after reperfusion were studied. The EDWT was measured in segments with high signal intensity (SI) on T2-weighted images, adjacent segments and remote segments according to a 16-segment model. Results: The EDWT after reperfusion in segments with high SI on T2-weighted images was significantly increased compared to baseline (6.28 ± 1.06 mm and 5.51 ± 1.40 mm, p < 0.05), whereas EDWT after the reperfusion in adjacent and remote segments did not show significant difference compared to baseline (adjacent: 6.48 ± 1.55 mm and 6.38 ± 1.26 mm, p = N.S., remote: 6.41 ± 1.11mm and 6.42 ± 1.27mm, p = N.S.). The % increase in EDWT after reperfusion from baseline in segments with high SI on T2-weighted images was higher than those in adjacent and remote segments (19 ± 30%, 1.3 ± 15% and 1.5 ± 16%, respectively, p < 0.05). Conclusions: After a brief period of ischemia and reperfusion, edema as defined by high SI on T2-weighted CMR is related to an increase in EDWT. This increase however is too small to be clinically relevant to be used for the detection of acute myocardial injury. Edema imaging is more sensitive and is an essential part of the reliable assessment of acute ischemic myocardial injury.

A 24-year-old healthy man consulted to our center because of typical on-and-off chest-pain and an electrocardiogram showing ST-segment elevation in inferior leads. An urgent coronary angiography showed angiographically normal coronary arteries. Cardiovascular magnetic resonance imaging confirmed acute myocarditis. Although acute myocarditis triggering coronary spasm is an uncommon association, it is important to recognize it, particularly for the management for those patients presenting with ST-segment elevation and suspect myocardial infarction and angiographically normal coronary arteries. The present report highlights the role of cardiovascular magnetic resonance imaging to identify acute myocarditis as the underlying cause.

Background Late reperfusion of acutely ischemic myocardium may result in intramyocardial hemorrhage that has been described as a contributor t or eperfusion injury. In patients with reperfused acute myocardial infarction (MI), the presence of myocardial hemorrhage can be detected by T2*-weighted cardiovascular magnetic resonance (CMR). This study aimed to identify clinical parameters associated with myocardial hemorrhage. Methods Thirty patients underwent CMR three days after acute reperfused MI including cine, hemorrhage-sensitive T2*weighted imaging, early (2-5 minutes post contrast) and late gadolinium enhancement (LGE) imaging for microvascular obstruction (MO) and necrosis, respectively. The extent of MO was measured on both early and late post-contrast images. Stepwise logistic regression analysis was performed to identify associations of clinical parameters with the presence of hemorrhage. The parameters tested were age, gender, risk factors, left ventricular (LV) volume and function, the extent of MO on early post-contrast images, the extent of MO on LGE images, the extent of infarc tion, time from the onset of pain to reperfusion, culprit artery, blood pressure, heart rate, TIMI flow, use of a thrombolytic agent, use of thrombo-aspiration devices, maximum value of troponin T and creatine kinase (CK), LDL, and HbA1c. LV volume was indexed by body surface area and infarct mass and MO mass were indexed by LV myocardial mass. Results Out of 30 patients, 19 patients showed MO and 18 of this group also showed hemorrhage. Indexed LV enddiastolic volume, the indexed MO mass on LGE images, the indexed infarction mass, maximum CK and troponin T were related to the presence of hemorrhage. The indexed infarct mass was the strongest predictor of the presence of hemorrhage (estimated regression coefficient 0.241(SE .095), p=0.011). Conclusions The presence of hemorrhage is associated with larger LV end-diastolic volume, larger infarct size, greater MO on LGE images, higher CK and troponin T value with infarct mass being the strongest predictor. These findings indicate that myocardial hemorrhage is strongly associated with the extent of myocardial damage in reperfused acut eM I. However, this study was limited by the small sample size. Future studies with larger sample size could provide more definitive conclusions.

Methods Cardiac MR was used to investigate the development and persistence of edema volume increases in the acute postinfarct period using both T2-weighted STIR imaging and T2 maps. LAD instrumented canines (n=9) underwent three hours of no-flow ischemia followed by reperfusion and were studied [using Siemens 1.5 T Espree scanner] at five time points (before and during ischemia and 2, 5, 7 and 56 days post-reperfusion). Scan parameters for T2-STIR acquisitions were: TE=64ms, TR=2-3 R-R intervals, resolution=0.9x0.9x8.0mm 3 .T 2 maps were computed from multiple T2-prepared acquisitions with different preparation times (0, 24, and 55 ms) with spatial-resolution of 1.0x1.0x8.0mm 3 . Late-enhancement imaging confirmed LAD infarction. Areas of interest were determined as follows: For T2 maps - region with T2 values greater than 2SD from remote territories; and for T2-STIR images- regions exceeding 2SD of the signal intensity of the remote regions. Edema volume was computed as highlighted areas multiplied by imaging slice thickness. Percent volume of edema was computed relative to total myocardial volume. Results are reported as mean ± SEM for each time point. Results Percent volume of edema (Area-At-Risk) - T2 Maps: Pre-ischemia: 0.8±0.4%; Ischemia: 2.5±1.4%; Day 2: 18.3

ContextMorbidity and mortality rates in hemodialysis patients remain excessive. Alterations in the delivery of dialysis may lead to improved patient outcomes.ObjectiveTo compare the effects of frequent nocturnal hemodialysis vs conventional hemodialysis on change in left ventricular mass and health-related quality of life over 6 months.Design, Setting, and ParticipantsA 2-group, parallel, randomized controlled trial conducted at 2 Canadian university centers between August 2004 and December 2006. A total of 52 patients undergoing hemodialysis were recruited.InterventionParticipants were randomly assigned in a 1:1 ratio to receive nocturnal hemodialysis 6 times weekly or conventional hemodialysis 3 times weekly.Main Outcome MeasuresThe primary outcome was change in left ventricular mass, as measured by cardiovascular magnetic resonance imaging. The secondary outcomes were patient-reported quality of life, blood pressure, mineral metabolism, and use of medications.ResultsFrequent nocturnal hemodialysis significantly improved the primary outcome (mean left ventricular mass difference between groups, 15.3 g, 95% confidence interval [CI], 1.0 to 29.6 g; P = .04). Frequent nocturnal hemodialysis did not significantly improve quality of life (difference of change in EuroQol 5-D index from baseline, 0.05; 95% CI, −0.07 to 0.17; P = .43). However, frequent nocturnal hemodialysis was associated with clinically and statistically significant improvements in selected kidney-specific domains of quality of life (P = .01 for effects of kidney disease and P = .02 for burden of kidney disease). Frequent nocturnal hemodialysis was also associated with improvements in systolic blood pressure (P = .01 after adjustment) and mineral metabolism, including a reduction in or discontinuation of antihypertensive medications (16/26 patients in the nocturnal hemodialysis group vs 3/25 patients in the conventional hemodialysis group; P

ObjectivesWe assessed the role of late enhancement cardiovascular magnetic resonance imaging (LE-CMR) for the diagnosis of right ventricular infarction (RVI).BackgroundRight ventricular infarction occurs in about one-half of patients with inferior myocardial infarction (MI). It is associated with an unfavorable prognosis, but established methods often lack the diagnostic accuracy to detect it. Late enhancement cardiovascular magnetic resonance imaging accurately detects left ventricular MI.MethodsThirty-seven patients with acute inferior MI were included. To test for RVI, they prospectively underwent a physical examination, an electrocardiogram (ECG) for ST-segment elevation in the V4r right precordial lead, and an echocardiogram. After coronary reperfusion, LE-CMR was performed for assessing presence and extent of late enhancement in the right ventricular (RV) wall. The LE-CMR data were compared with the other results; interobserver variability was assessed. The LE-CMR was repeated after 13 months.ResultsLate enhancement cardiovascular magnetic resonance imaging detected RVI in 21 of 37 (57%) patients with acute inferior MI. Interobserver variability was very good (kappa 0.83); physical exam was positive for RVI in 7 of 37 (19%) patients, V4r ECG in 13 of 37 (35%) patients, and echocardiogram in 6 of 37 (16%) patients. The LE-CMR findings for RVI showed only mild agreement with findings for RVI on physical exam (kappa 0.30), V4r ECG (kappa 0.38), and echocardiography (kappa 0.32). Irreversible injury of the RV persisted at 13 months (kappa 0.85).ConclusionsIn patients with acute inferior MI, RVI is more frequently detected by LE-CMR than by current standard diagnostic techniques. Further CMR studies might allow for analyzing its clinical and prognostic relevance.

Background Cardiovascular Magnetic Resonance (CMR) based assessments of area-at-risk and salvageable myocardium on the basis of myocardial edema in the setting of acute coronary syndrome is of significant clinical interest. However, their dependence on the choice of acquisition method and time to imaging has not been studied. In this study, we investigated the temporal evolution of myocardial edema during ischemia and reperfusion phases using both T2 maps and T2-STIR images. Methods Canines (n=10), subjected to I-R injury, underwent CMR (1.5T) before ischemia (baseline), during ischemia and on days 2, 5, and 7 post-reperfusion. T2-preapred SSFP (T2-preparation durations = 0, 24 and 55 ms; TR/TE =

All CMR images were obtained on a 1.5 T clinical system (Siemens, Germany), using the following sequences in a short axis orientation (slice thickness 10 mm, 0 gap): conventional cine SSFP, T2-STIR (patients only), late enhancement (10 min after injection of 0.2 mmol/kg GdDTPA), applying typical sequence parameters. Semiquantitative threshold-based image analysis of late enhancement images (LE) identified the infarct region and infarct area was calculated. In the infarction zone and remote myocardium, on corresponding T2-STIR and SSFP images, signal and contrast, as well as the area of edema were measured and compared using paired t-tests, correlation statistics.