Clinical Characteristics and Prognostic Factors of Myocarditis in New Zealand Patients.

BACKGROUND: Myocarditis is an inflammation of the heart muscle and an important cause of dilated cardiomyopathy. Its presentation is heterogeneous, and there are limited studies describing the clinical characteristics of these patients, or which factors predict adverse clinical outcomes. We performed a single-centre retrospective study to explore the clinical characteristics of patients with myocarditis. METHOD: Patients >15 years of age admitted to our centre with an ICD-10 diagnosis of myocarditis on their electronic discharge record between 2007 and 2016 were included. Clinical, biochemical and imaging factors were collected. The primary endpoint was combined major adverse cardiac events (MACE) consisting of all-cause mortality, decompensated heart failure leading to hospital admission, documented ventricular arrhythmia, recurrent myocarditis and heart transplantation. RESULTS: During this period, 178 patients were found to have a diagnosis of myocarditis (71% men, median age 39 years). Men were significantly younger than women (36 vs 53 years, U=4,543, p<0.001). ST-elevation on electrocardiogram was recorded in 59% of patients, and these patients were more likely to be male (85% vs 66%, p=0.012), younger (median age 32 vs 44 years, U=4,129, p=0.001) and to have chest pain (94% vs 65%, p<0.001). At a maximal follow-up of 8 years (mean 4.5 years), MACE occurred in 26 patients. MACE was associated with the presence of dyspnoea (26% vs 9%; hazard ratio [HR] 3.33, 95% confidence interval [CI] 1.53-7.28; p=0.003), pulmonary congestion on chest X-ray (54% vs 11%; HR 5.51; 95% CI 2.3-13.23; p<0.001), and left ventricular ejection fraction <50% on transthoracic echocardiography (24% vs 8%; HR 3.22; 95% CI 1.28-8.12; p=0.013). CONCLUSIONS: Myocarditis was more common in young men in our study. Factors associated with adverse outcomes in acute coronary syndromes were not seen in our younger population. Left ventricular dysfunction appears to be more important in predicting adverse outcomes in myocarditis.

ICare-ACS (Improving Care Processes for Patients With Suspected Acute Coronary Syndrome): A Study of Cross-System Implementation of a National Clinical Pathway.

BACKGROUND: Efforts to safely reduce length of stay for emergency department patients with symptoms suggestive of acute coronary syndrome (ACS) have had mixed success. Few system-wide efforts affecting multiple hospital emergency departments have ever been evaluated. We evaluated the effectiveness of a nationwide implementation of clinical pathways for potential ACS in disparate hospitals. METHODS: This was a multicenter pragmatic stepped-wedge before-and-after trial in 7 New Zealand acute care hospitals with 31 332 patients investigated for suspected ACS with serial troponin measurements. The implementation was a clinical pathway for the assessment of patients with suspected ACS that included a clinical pathway document in paper or electronic format, structured risk stratification, specified time points for electrocardiographic and serial troponin testing within 3 hours of arrival, and directions for combining risk stratification and electrocardiographic and troponin testing in an accelerated diagnostic protocol. Implementation was monitored for >4 months and compared with usual care over the preceding 6 months. The main outcome measure was the odds of discharge within 6 hours of presentation RESULTS: There were 11 529 participants in the preimplementation phase (range, 284-3465) and 19 803 in the postimplementation phase (range, 395-5039). Overall, the mean 6-hour discharge rate increased from 8.3% (range, 2.7%-37.7%) to 18.4% (6.8%-43.8%). The odds of being discharged within 6 hours increased after clinical pathway implementation. The odds ratio was 2.4 (95% confidence interval, 2.3-2.6). In patients without ACS, the median length of hospital stays decreased by 2.9 hours (95% confidence interval, 2.4-3.4). For patients discharged within 6 hours, there was no change in 30-day major adverse cardiac event rates (0.52% versus 0.44%; P=0.96). In these patients, no adverse event occurred when clinical pathways were correctly followed. CONCLUSIONS: Implementation of clinical pathways for suspected ACS reduced the length of stay and increased the proportions of patients safely discharged within 6 hours. CLINICAL TRIAL REGISTRATION: URL: https://www.anzctr.org.au/ (Australian and New Zealand Clinical Trials Registry). Unique identifier: ACTRN12617000381381.

Determination of Clinical Outcome in Mitral Regurgitation With Cardiovascular Magnetic Resonance Quantification.

BACKGROUND: Surgery for severe mitral regurgitation is indicated if symptoms or left ventricular dilation or dysfunction occur. However, prognosis is already reduced by this stage, and earlier surgery on asymptomatic patients has been advocated if valve repair is likely, but identifying suitable patients for early surgery is difficult. Quantifying the regurgitation may help, but evidence for its link with outcome is limited. Cardiovascular magnetic resonance (CMR) can accurately quantify mitral regurgitation, and we examined whether this was associated with the future need for surgery. METHODS AND RESULTS: One hundred nine asymptomatic patients with echocardiographic moderate or severe mitral regurgitation had baseline CMR scans and were followed up for up to 8 years (mean, 2.5±1.9 years). CMR quantification accurately identified patients who progressed to symptoms or other indications for surgery: 91% of subjects with regurgitant volume ≤55 mL survived to 5 years without surgery compared with only 21% with regurgitant volume >55 mL (P<0.0001). A similar separation was observed for regurgitant fraction ≤40% and >40%. CMR-derived end-diastolic volume index showed a weaker association with outcome (proportions surviving without surgery at 5 years, 90% for left ventricular end-diastolic volume index <100 mL/m(2) versus 48% for ≥100 mL/m(2)) and added little to the discriminatory power of regurgitant fraction/volume alone. CONCLUSIONS: CMR quantification of mitral regurgitation was associated with the development of symptoms or other indications for surgery and showed better discriminatory ability than the reference-standard CMR-derived ventricular volumes. CMR may be able to identify appropriate patients for early surgery, with the potential to change clinical practice, although the clinical benefits of early surgery require confirmation in a clinical trial.

Aortic regurgitation quantification using cardiovascular magnetic resonance: association with clinical outcome.

BACKGROUND: Current indications for surgery in patients with significant aortic regurgitation (AR) focus on symptoms and left ventricular dilation/dysfunction. However, prognosis is already reduced by this stage, and earlier identification of patients for surgery could be beneficial. Quantifying the regurgitation may help, but there are limited data on its link with outcome. Cardiovascular magnetic resonance (CMR) can accurately quantify AR, and we examined whether this was associated with the future need for surgery. METHODS AND RESULTS: One hundred thirteen patients with echocardiographic moderate or severe AR were monitored for up to 9 years (mean 2.6 ± 2.1 years) following a CMR scan, and the progression to symptoms or other indications for surgery was monitored. AR quantification identified outcome with high accuracy: 85% of the 39 subjects with regurgitant fraction >33% progressed to surgery (mostly within 3 years) in comparison with 8% of 74 subjects with regurgitant fraction ≤ 33% (P<0.0001); the area under the curve on receiver operating characteristic analysis was 0.93 (P<0.0001). This ability remained strong on time-dependent Kaplan-Meier survival curves. CMR-derived left ventricular end-diastolic volume >246 mL had good, although lower, discriminatory ability (area under the curve 0.88), but the combination of this measure with regurgitant fraction provided the best discriminatory power. CONCLUSIONS: High degrees of CMR-quantified AR were associated with the development of symptoms or other indications for surgery. Quantifying AR showed slightly better discriminatory ability than "gold standard" CMR ventricular volume assessment. This could provide a new paradigm for the timing of surgical intervention but requires confirmation in a clinical trial.

Assessment of valvular heart disease by cardiovascular magnetic resonance imaging: a review.

CMR is a comprehensive non-invasive tool capable of evaluating all aspects of valvular heart disease. It has advantages over echo including direct quantification of regurgitant lesions, highly accurate assessment of ventricular size and function, visualisation myocardial scar, and interrogation of extracardiac abnormalities. Although these gains can be realised with current scanning techniques, CMR's full potential has yet to be realised, and further studies of clinical outcomes are needed before CMR data can be integrated into the management algorithms for patients with significant valvular lesions.

An uncommon cause of myocardial infarction.

A 73 year-old lady with hypertension and chronic atrial fibrillation (AF) developed chest pain followed by ventricular fibrillation (VF) cardiac arrest. Her electrocardiogram post-cardioversion revealed inferior ST-elevation myocardial infarction (MI). Her coronary arteries were angiographically normal. Contrast-enhanced cardiac magnetic resonance(CE-CMR) demonstrated both an inferior subendocardial infarction and left atrial (LA) appendage thrombus suggesting cardioembolism as the most likely cause of her presentation.

Stress perfusion imaging using cardiovascular magnetic resonance: a review.

Stress perfusion CMR can provide both excellent diagnostic and important prognostic information in the context of a comprehensive assessment of cardiac anatomy and function. This coupled with the high spatial resolution, and the lack of both attenuation artefacts and ionising radiation, make CMR stress perfusion imaging a highly attractive stress imaging modality. It is now in routine use in many centres, and shows promise in evaluating patients with clinical problems beyond those of epicardial coronary disease.

Causal Link between Ventricular Ectopy and Concussion.

We present a unique case study report of a male individual with a history of mild nonischaemic cardiomyopathy, with no ventricular ectopy, that at the age of 76 years sustained multiple concussions (i.e., mild traumatic brain injury) within a week of each other. Concussion symptoms included cognitive difficulties, "not feeling well," lethargy, fatigue, and signs of depression. He was later medically diagnosed with postconcussion syndrome. The patient, WJT, was referred for cardiac and neurological assessment. Structural neuroimaging of the brain (MRI) was unremarkable, but electrocardiography (ECG) assessments using a 24-hour Holter monitor revealed significant incidence of ventricular ectopy (9.4%; 9,350/99,836 beats) over a period of 5-6 months after injury and then a further increase in ventricular ectopy to 18% (15,968/88,189 beats) during the subsequent 3 months. The patient was then prescribed Amiodarone 200 mg, and his ventricular ectopy and concussion symptoms completely resolved simultaneously within days. To the authors' knowledge, our study is the first to show a direct link between observable and documented cardiac dysregulation and concussion symptomology. Our study has important implications for both cardiac patients and the patients that sustain a concussion, and if medically managed with appropriate pharmacological intervention, it can reverse ventricular ectopy and concussion symptomology. More research is warranted to investigate the mechanisms for this dramatic and remarkable change in cardiac and cerebral functions and to further explore the brain-heart interaction and the intricate autonomic interaction that exists between the extrinsic and intracardiac nervous systems.

Myocardial scar detected by contrast-enhanced cardiac magnetic resonance imaging is associated with ventricular tachycardia in hypertrophic cardiomyopathy patients.

INTRODUCTION: Hypertrophic cardiomyopathy (HCM) is associated with myocardial scarring and ventricular tachycardia (VT). Contrast-enhanced cardiac magnetic resonance imaging (CE-CMR) can quantify myocardial scar, and scar imaging has been documented in patients with HCM. We investigated the assessment of myocardial scar in HCM patients using CE-CMR, and its correlation with proven VT. METHODS: Twenty-five patients (mean age 54 +/- 8) with HCM who underwent CE-CMR were identified, and clinical data obtained from chart review. Parameters of LV function were calculated from cine imaging, and myocardial scar was assessed using delayed enhancement imaging following gadolinium administration. RESULTS: Myocardial scar was detected in 16 (64%) patients with a mean mass 9 +/- 15 g. Scar was patchy, mid-myocardial and located in the basal anteroseptum, and RV insertion sites. Scar was seen in septal, apical and concentric variants of HCM. Scar mass correlated with both LV Mass (r2 = 0.74) and maximal LV wall thickness (r2 = 0.42). VT occurred in 32% of patients, and was associated with both increased scar mass and wall thickness compared to non-VT patients (21 +/- 22 g vs. 4 +/- 6 g, and 2.4 +/- 0.5 cm vs. 1.8 +/- 0.5 cm, p < 0.05). LV size and function were similar in patients with and without VT. A scar mass of >7 g predicted the presence of VT with a sensitivity of 75% and specificity 82%. CONCLUSIONS: Myocardial scar imaged by CE-CMR is common in patients with HCM, and is predictive of VT. Scar is seen in all HCM variants, and is associated with maximal wall thickness. There may be a role for CE-CMR in improved risk stratification for individual patients with HCM.

Detection of myocardial scar by contrast-enhanced cardiac magnetic resonance imaging in patients with troponin-positive chest pain and minimal angiographic coronary artery disease.

Patients who present with chest pain and elevated serum troponin levels may have minimal angiographic coronary artery disease, leading to diagnostic confusion. We investigated patients with troponin-positive acute coronary syndromes and minimal coronary artery disease (CAD) using contrast-enhanced cardiac magnetic resonance imaging to assess for myocardial scar. Twenty-three patients (54 +/- 8 years of age) who presented with chest pain, high troponin I level, and minimal angiographic CAD were included. Patients with a clinical pericarditis/myocarditis, tachyarrhythmia at presentation, previous myocardial infarction, or an alternative explanation for increased troponin I level were excluded. Myocardial scar was assessed with delayed-enhancement inversion-recovery imaging after administration of gadolinium. Hyperenhancement consistent with myocardial scar was seen in 7 of 23 patients (30%) and was located primarily in the right coronary artery distribution. Peak troponin level, clinical characteristics, and volumetric parameters were similar in patients with or without hyperenhancement. One patient had mid-myocardial enhancement that suggested undiagnosed myocarditis. There was a linear relation between the mass of myocardial scar and peak serum troponin level. In follow-up, subsequent cardiac events were more frequent in patients with hyperenhancement (43% vs 12.5%). In conclusion, patients with troponin-positive acute coronary syndromes may have significant myocardial scar even when minimal CAD is found on angiography.

Bias associated with left ventricular quantification by multimodality imaging: a systematic review and meta-analysis.

PURPOSE: Cardiac MR (CMR) is the gold standard for left ventricular (LV) quantification. However, two-dimensional echocardiography (2DE) is the most common approach, and both three-dimensional echocardiography (3DE) and multidetector CT (MDCT) are increasingly available. The clinical significance and interchangeability of these modalities remains under-investigated. Therefore, we undertook a systemic review to evaluate the accuracy and absolute bias in LV quantification of all the commonly available non-invasive imaging modalities (2DE, CE-2DE, 3DE, MDCT) compared to cardiac MR (CMR). METHODS: Studies were included that reported LV echocardiographic (2DE, CE-2DE, 3DE) and/or MDCT measurements compared to CMR. Only modern CMR (SSFP sequences) was considered. Studies involving small sample size (<10 patients) and unusual cardiac geometry (ie, congenital heart diseases) were excluded. We evaluated LV end-diastolic volume (LVEDV), end-systolic volume (LVESV) and ejection fraction (LVEF). RESULTS: 1604 articles were initially considered: 65 studies were included (total of 4032 scans (echo, CT, MRI) performed in 2888 patients). Compared to CMR, significant biased underestimation of LV volumes with 2DE was seen (LVEDV-33.30 mL, LVESV -16.20 mL, p<0.0001). This difference was reduced but remained significant with CE-2DE (LVEDV -18.05, p<0.0001) and 3DE (LVEDV -14.41, p<0.001), while MDCT values were similar to CMR (LVEDV -1.20, p=0.43; LVESV -0.13, p=0.91). However, excellent agreement for echocardiographic LVEF evaluation (2DE LVEF 0.78-1.01%, p=0.37) was observed, especially with 3DE (LVEF 0.14%, p=0.88). CONCLUSIONS: Comparing imaging modalities to CMR as reference standard, 3DE had the highest accuracy in LVEF estimation: 2DE and 3DE-derived LV volumes were significantly underestimated. Newer generation CT showed excellent accuracy for LV volumes.

Noninvasive imaging of myocardial reperfusion injury using leukocyte-targeted contrast echocardiography.

BACKGROUND: We hypothesized that myocardial contrast echocardiography (MCE) with leukocyte-targeted microbubbles could temporally and spatially characterize the severity of postischemic myocardial inflammation. METHODS AND RESULTS: In 9 open-chest dogs, either the left anterior descending or left circumflex coronary artery was occluded for 90 minutes (n=6), while the remaining dogs served as non-ischemic controls. During occlusion, MCE was performed to determine the risk area (RA) and regions supplied by collateral flow. Myocardial inflammation was assessed 5, 60, and 120 minutes after reflow by MCE imaging of leukocyte-targeted (phosphatidylserine-containing) lipid microbubbles. The spatial extent and severity of inflammation were also assessed by radionuclide imaging of the neutrophil-avid tracer 99mTcRP517 and tissue myeloperoxidase activity. Early after reflow, MCE detected inflammation throughout the entire risk area, the extent of which decreased over time due to reduced signal in collateral-supplied regions. The spatial extent of inflammation late after reflow was similar for MCE and radionuclide imaging. The severity of inflammation in the infarct zone, the noninfarcted risk area, and collateral-supplied territories determined by quantitative MCE correlated well with myeloperoxidase activity (r=0.81). CONCLUSIONS: MCE with leukocyte-targeted microbubbles can temporally assess the severity and extent of postischemic myocardial inflammation and could be used to evaluate new treatment strategies designed to limit inflammation in acute coronary syndromes.

Myocardial and microcirculatory kinetics of BR14, a novel third-generation intravenous ultrasound contrast agent.

OBJECTIVES: This study sought to investigate the myocardial and microvascular kinetics of BR14, a novel third-generation ultrasound contrast agent. BACKGROUND: BR14 produces persistent myocardial opacification after the administration of a single intravenous bolus when the left ventricular cavity contrast has considerably diminished. The mechanism of this finding is unknown. METHODS: Nine open-chest dogs with non-critical stenosis of a single coronary artery were given intravenous bolus injections of BR14 during coronary hyperemia. Time versus acoustic intensity (AI) plots were generated from the normal and stenosed beds and myocardial blood flow (MBF) was measured with radiolabeled microspheres. Intravital microscopy was performed on an exteriorized cremaster muscle in 11 wild-type mice to study the microvascular kinetics of the agent. RESULTS: At peak contrast enhancement, the ratio between AI in the stenosed and normal bed was 0.44+/-0.23, which was similar to the radiolabeled microsphere-derived MBF ratio between the two beds (0.45 +/-0.20). At 400 s after injection, the AI ratio between the two beds approximated unity (0.99+/-0.07) despite no changes in MBF, indicating redistribution of the agent. The myocardial kinetics of BR14 was best characterized by a modified lagged normal density function. Only about 3% of administered microbubbles were estimated to be retained in the myocardium. Intravital microscopy showed that most of these bubbles were retained only transiently (2 to 3 s) within capillaries. CONCLUSIONS: BR14 demonstrates redistribution because of transient retention within capillaries. Therefore, similar to (201)Tl, it could potentially be used to detect both coronary stenosis and myocardial viability after a single injection during stress.

Influence of microbubble surface charge on capillary transit and myocardial contrast enhancement.

OBJECTIVE: The goal of the study was to determine whether microbubble charge influences the microvascular retention of microbubble contrast agents. BACKGROUND: Interactions between serum proteins and lipid membranes are greater with anionic compared with neutral membranes. These interactions may influence the microvascular behavior of anionic lipid microbubbles. METHODS: Intravital microscopy of the cremaster muscle was performed in six wild-type mice and three C3-deficient mice during intravenous injection of lipid-shelled microbubbles with either a neutral or a negative charge. Both agents were prepared with and without a protective surface layer of polyethyleneglycol (PEG). Complement attachment to microbubbles was assessed by flow cytometry with flourescein isothiocyanate-conjugated anti-C3b monoclonal antibody. Myocardial contrast echocardiography was performed in six dogs to assess pulmonary and myocardial retention of microbubbles. RESULTS: Size-independent capillary retention of microbubbles, occurring for a few seconds to >10 min, was frequently observed with anionic, but rarely with neutral, microbubbles (4.3 +/- 0.3 vs. 0.4 +/- 0.1 mm(-3), p < 0.01). Anionic microbubble retention was reduced by 70% by surface PEG and was also markedly reduced in C3-deficient mice (1.4 +/- 0.1 mm(-3), p < 0.05 vs. wild-type). Flow cytometry demonstrated complement attachment to only anionic microbubbles. Contrast echocardiography indicated both pulmonary and myocardial retention of only anionic microbubbles, the latter evidenced by persistent opacification >10 min after bolus intravenous injection. CONCLUSIONS: Lipid microbubbles with a net negative charge can be retained within capillaries via complement-mediated attachment to endothelium. This property may be useful for the development of ultrasound contrast agents that can be imaged late after venous injection.

Evaluation of a New Zealand program to improve transition of care for older high risk adults.

Transition interventions aim to improve care and reduce hospital readmissions but evaluations of these interventions have reported inconsistent results. We report on the evaluation of an intervention implemented in Auckland, New Zealand. Participants were people over the age of 65 who had an acute medical admission and were at high risk of readmission. The intervention included an improved discharge process and nurse telephone follow-up soon after discharge. Outcomes were 28 day readmission rates and emergency attendances. The study is observational, using both interrupted times series and regression discontinuity designs. 5239 patients were treated over a one year period. There was no change in readmission rates or ED attendances or secondary outcomes. Not all patients received all components of the intervention. This transition intervention was not successful. Possible reasons for this and implications are discussed. Although non-experimental methods were used, we believe the results are robust.

Targeted-microbubble binding selectively to GPIIb IIIa receptors of platelet thrombi.

RATIONALE AND OBJECTIVES: New targeted microbubbles directed to the GPIIb IIIa receptor have been developed. The objective was to determine whether targeting microbubbles to clots would enhance ultrasound imaging. Systematic studies were designed to determine whether in vitro methodology is an acceptable predictor of in vivo efficacy. MATERIALS AND METHODS: Bioconjugate ligands were inserted into lipid-coated membranes of perfluorocarbon gas microbubbles and binding studies performed on activated platelets immobilized on cell culture plates. Targeted microbubble binding to clots in a flow through chamber was also assessed. Finally, microbubble binding studies on arteriolar and venular clots in a mouse cremasteric muscle model were conducted. RESULTS: Binding studies on platelet-immobilized plates demonstrated an affinity for targeted microbubbles versus untargeted microbubbles. Semiquantitative light obscuration techniques helped to measure extent of targeted microbubble binding. Targeted microbubbles similarly bound to platelet clots in the flow model. Finally, studies in the mouse model confirmed binding of targeted microbubbles in both venules and arterioles. CONCLUSION: The use of receptor selective targeted microbubbles improved binding to vascular thrombi in both in vitro and in vivo settings.

Targeted tissue transfection with ultrasound destruction of plasmid-bearing cationic microbubbles.

The aim of this study was to assess the relative efficacy and mechanism of gene transfection by ultrasound (US) destruction of plasmid-bearing microbubbles. Luciferase reporter plasmid was charge-coupled to cationic lipid microbubbles. Rat hindlimb skeletal muscle was exposed to intermittent high-power US during dose-adjusted intra-arterial (IA) or IV administration of plasmid-bearing microbubbles via the carotid artery or jugular vein, respectively. At 4 days, luciferase activity in US-exposed skeletal muscle was 200-fold greater with IA than with IV administration of plasmid-bearing microbubbles, and was similar to transfection achieved by IM injection of plasmid (positive control). No transfection occurred with US and IA injection of plasmid alone. Intravital microscopy of the cremaster muscle in mice following administration of microbubbles and US exposure demonstrated perivascular deposition of fluorescent plasmid, the extent of which was twofold greater for IA compared to IV injection. Electron microscopy demonstrated a greater extent of myocellular microporations in US-exposed muscle after IA injection of microbubbles. We conclude that muscle transfection by US destruction of plasmid-bearing cationic microbubbles is amplified by IA, rather than IV, injection of microbubbles due to greater extravascular deposition of plasmid and to greater extent of myocellular microporation.

Skin perfusion assessed by contrast ultrasound predicts tissue survival in a free flap model.

The purpose of this study was to assess perfusion in a free skin flap model using contrast-enhanced ultrasound (CEU), and to determine if the extent of perfusion early after venous occlusion predicted long-term flap survival. Perfusion was assessed in an autologous abdominal skin flap and adjacent healthy skin in rats using CEU imaging before venous occlusion and following reflow. Perfusion assessment was possible in all flaps and quantitative measurements of microvascular blood volume (BV) and blood velocity were expressed as a ratio to that in the healthy skin. Proximal flap BV 18 h after venous occlusion was significantly greater in those that survived (n = 4) vs. those that became necrotic (n = 6) (BV ratio 0.8 +/- 0.1 vs. 0.2 +/- 0.1, p = 0.0001). A BV ratio of 0.5 predicted graft viability with a sensitivity and specificity of 100%. Microvascular blood velocity at 18 h was similar in grafts that survived and those that became necrotic. Qualitative assessment of perfusion by a "blinded" observer correlated well with quantitative data and predicted flap outcome in all cases. We conclude that skin perfusion can be assessed with CEU. Perfusion 18 h following a secondary ischemic insult in a free flap accurately predicts subsequent tissue survival in this model.

Utility of cardiac magnetic resonance in the evaluation of unselected patients with possible arrhythmogenic right ventricular cardiomyopathy.

INTRODUCTION: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare but important cause of sudden cardiac death. We investigated the role of cardiac magnetic resonance imaging (CMR) in the evaluation of patients with suspected ARVC referred by a general cardiology service. METHODS: Ninety-two patients (mean age 48 ± 15, 49% female), referred for CMR assessment of possible ARVC, were reviewed. CMR included both functional and tissue characteristic imaging. RESULTS: No patients had ARVC based on the 1994 Task Force Criteria (TFC) prior to CMR, but 4 met proposed Modified TFC; 15% met one major (±1 minor) TFC, 71% 1 or 2 minor TFC, and 14% no TFC. Reasons for CMR referral included symptomatic arrhythmia of likely RV origin (28%), Electrocardiogram/Holter abnormalities (28%), echocardiographic features suspicious of ARVC (19%), and family history of ARVC (8%). CMR findings strongly suggestive of ARVC were found in nine patients (10%), although only three were considered typical. Of these patients two met 1 major TFC and seven met 1 or 2 minor TFC. CMR findings included RV thinning, aneurysm, and diastolic out-pouching, but only 1 patient had definite fatty infiltration of the RV. Incidentally, CMR detected important, previously undiagnosed pathology, including anomalous pulmonary venous drainage (2 patients) and non-ischaemic cardiomyopathy (6%). CMR was normal in 63%, with minor abnormalities in 29%. CONCLUSIONS: CMR may play an important diagnostic role in the evaluation of possible ARVC. Patients who do not meet TFC for diagnosis may have CMR features typical of ARVC. Additionally CMR may detect other hitherto undiagnosed structural or functional abnormalities that alter patient management. However the majority of patients referred have a low pretest probability of ARVC, and the rate of normal CMR scans is high.