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Item does not contain fulltext Aims: To determine the diagnostic yield of tissue characterization by cardiovascular magnetic resonance (CMR) in a large clinical population of patients with suspected acute myocarditis (AM) and to establish its diagnostic value within the 2013 European Society of Cardiology position statement criteria (ESC-PSC) for clinically suspected myocarditis. Methods and results: In this retrospective study, CMR examinations of 303 hospitalized patients referred for work-up of suspected AM in two tertiary referral centres were analysed. CMR was performed at median 7 days (interquartile range 4-20 days) after clinical presentation and included cine imaging, T2-weighted imaging, and late gadolinium enhancement. CMR images were evaluated to assign each patient to a diagnosis. By using non-CMR criteria only, the 2013 ESC-PSC were positive for suspected myocarditis in 151 patients and negative in 30. In the remaining 122 patients, there was insufficient information available for ESC-PSC assessment, mostly due to lack of coronary angiography (CAG) before the CMR examination (n = 116, 95%). There were no in-hospital deaths. CMR provided a diagnosis in 158 patients (52%), including myocarditis in 104 (34%), myocardial infarction in 44 (15%), and other pathology in 10 patients (3%). Non-urgent CAG (>24 h after presentation) was performed before the CMR examination in 85 patients, of which 20 (24%) were done in patients with subsequently confirmed AM, which could potentially have been avoided if CMR was performed first. ESC-PSC was correct in diagnosing AM before the CMR in 50 of the 151 patients (33%) and was correct in ruling out AM in all the 30 patients (100%). However, ESC-PSC provided an incorrect diagnosis of AM in 27 of the 151 patients (18%), which was corrected by CMR through the identification of new cardiac disease that could explain the clinical syndrome. Patients with insufficient ESC-PSC information had a relatively low pre-test probability of coronary artery disease. In this group, CMR confirmed the diagnosis of AM in a relatively high percentage (44%) but still revealed myocardial infarction in 8% of them. Conclusion: Tissue characterization by CMR provided a good diagnostic yield in this large clinical population of patients with suspected AM. CMR provided incremental diagnostic value to the ESC-PSC by ruling out the diagnosis of AM on one hand and by potentially sparing AM patients from CAG on the other.

Background We compared three-dimensional speckle tracking echocardiography (3DSTE) and its strain to cardiac magnetic resonance (CMR) with delayed contrast enhancement for left ventricular (LV) chamber quantification and transmurality of myocardial scar. Furthermore, we examined the ability of 3DSTE strain to differentiate between ischaemic and non-ischaemic LV dysfunction. Methods In 80 consecutive patients with ischaemic and 40 patients with non-ischaemic LV dysfunction, the correlations between LV volumes and ejection fraction were measured using 3DSTE and CMR. Global and regional 3DSTE strains and total or percentage enhanced LV mass were evaluated. Results LV end-diastolic and end-systolic volumes and ejection fraction correlated well between 3DSTE and CMR (r: 0.83, 0.88 and 0.89, respectively). However, 3DSTE significantly underestimated volumes. Correlation for LV mass was modest (r = 0.59). All 3DSTE regional strain values except for radial strain were lower in segments with versus segments without transmural enhancement. However, strain parameters could not identify the transmurality of scar. No significant difference between ischaemic and non-ischaemic LV dysfunction was observed in either global or regional 3DSTE strain except for twist, which was lower in the non-ischaemic group (4.9 ± 3.3 vs. 6.4 ± 3.2°, p = 0.03). Conclusion 3DSTE LV volumes are underestimated compared with CMR, while LV ejection fraction revealed excellent accuracy. Functional impairment by 3DSTE strain does not correlate well with scar localisation or extent by CMR. 3DSTE strain could not differentiate between ischaemic and non-ischaemic LV dysfunction. Future studies will need to clarify if 3DSTE strain and CMR delayed contrast enhancement can provide incremental value to the prediction of future cardiovascular events.

Objectives The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries. Background An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters. Methods Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11). Results In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = −0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p Conclusions CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction.

Objectives Native T1 mapping and late gadolinium enhancement (LGE) imaging offer detailed characterisation of the myocardium after acute myocardial infarction (AMI). We evaluated the effects of microvascular injury (MVI) and intramyocardial haemorrhage on local T1 and T2* values in patients with a reperfused AMI. Methods Forty-three patients after reperfused AMI underwent cardiovascular magnetic resonance imaging (CMR) at 4 [3-5] days, including native MOLLI T1 and T2* mapping, STIR, cine imaging and LGE. T1 and T2* values were determined in LGE-defined regions of interest: the MI core incorporating MVI when present, the core-adjacent MI border zone (without any areas of MVI), and remote myocardium. Results Average T1 in the MI core was higher than in the MI border zone and remote myocardium. However, in the 20 (47%) patients with MVI, MI core T1 was lower than in patients without MVI (MVI 1048±78ms, no MVI 1111±89ms, p=0.02). MI core T2* was significantly lower in patients with MVI than in those without (MVI 20 [18-23]ms, no MVI 31 [26-39]ms, p

The main eligibility criterion for primary prevention implantable cardioverter defibrillator (ICD) therapy, that is, left ventricular ejection fraction (LVEF), is based on large clinical trials using primarily 2-dimensional echocardiography (2DE). Presently, cardiac magnetic resonance imaging (MRI) is considered the gold standard for LVEF assessment. It has been demonstrated that cardiac MRI assessment results in lower LVEFs compared with 2DE. Consequently, cardiac MRI-LVEF assessment may lead to more patients eligible for ICD implantation with potential clinical consequences. The aim of this study was to evaluate the clinical impact of cardiac MRI-LVEF versus 2DE-LVEF assessment for ICD eligibility. A total of 149 patients with cardiac MRI-LVEF ≤35% referred for primary prevention ICD implantation who underwent both 2DE and cardiac MRI-LVEF assessment were retrospectively included. 2DE-LVEF was computed by Simpson's biplane method. Cardiac MRI-LVEF was computed after outlining the endocardial contours in short-axis cine images. Appropriate device therapy (ADT) and all-cause mortality were evaluated during 2.9 ± 1.7 years of follow-up. The present study found that cardiac MRI-LVEF was significantly lower compared with 2DE-LVEF (23 ± 8% vs 30 ± 8%, respectively, p0.001), resulting in 29 (19%) more patients eligible for ICD implantation according to the current guidelines (LVEF ≤35%). Patients with 2DE-LVEF35% but cardiac MRI-LVEF ≤35% experienced a lower ADT rate compared with patients having 2DE-LVEF ≤35% (2.1% vs 10.4% per year, respectively, p = 0.02). Application of cardiac MRI-LVEF cutoff of 30% resulted in 119 eligible patients experiencing 9.9% per year ADT, comparable with 2DE-LVEF cut-off value of 35%. In conclusion, cardiac MRI-LVEF assessment resulted in more patients eligible for ICD implantation compared with 2DE who showed a relatively low event rate during follow-up. The event rate in patients with cardiac MRI-LVEF ≤30% was comparable with patients having a 2DE-LVEF ≤35%. This study suggests the need for re-evaluation of cardiac MRI-based LVEF cut-off values for ICD eligibility.

Aims Sympathetic denervation typically occurs in the infarcted myocardium and is associated with sudden cardiac death. Impaired innervation was also demonstrated in non-infarcted myocardium in ischaemic and dilated cardiomyopathy (ICMP and DCMP). Factors affecting sympathetic nerve integrity in remote myocardium are unknown. Perfusion abnormalities, even in the absence of epicardial coronary artery disease, may relate to sympathetic dysfunction. This study was aimed to assess the interrelations of myocardial blood flow (MBF), contractile function, and sympathetic innervation in non-infarcted remote myocardium. Methods and results Seventy patients with ICMP or DCMP and LVEF ≤35% were included. [15O]H2O- and [11C]hydroxyephedrine (HED) PET was performed to quantify resting MBF, hyperaemic MBF, and sympathetic innervation. Cardiovascular magnetic resonance (CMR) imaging was performed to assess left ventricular function, mass, wall thickening, and scar size. Wall thickening, [11C]HED retention index (RI), and MBF were assessed in remote segments without scar, selected on CMR. [11C]HED RI was correlated with resting MBF ( r = 0.41, P < 0.001) and hyperaemic MBF ( r = 0.55, P < 0.001) in remote myocardium in both ICMP and DCMP. In addition, LV volumes ( r = −0.40, P = 0.001), LV mass ( r = −0.31, P = 0.008), and wall thickening ( r = 0.45, P < 0.001) correlated with remote [11C]HED RI. Multivariable analysis revealed that hyperaemic MBF ( B = 0.79, P < 0.001), wall thickening ( B = 0.01, P = 0.03), and LVEDV ( B = −0.03, P = 0.02) were independent predictors for remote [11C]HED RI. Conclusion Hyperaemic MBF is independently associated with sympathetic innervation in non-infarcted remote myocardium in patients with ICMP and DCMP. This suggests that microvascular dysfunction might be an important factor related to sympathetic nerve integrity. Whether impaired hyperaemic MBF is the primary cause of this relation remains unclear.

Objectives Although myocardial strain analysis is a potential tool to improve patient selection for cardiac resynchronization therapy (CRT), there is currently no validated clinical approach to derive segmental strains. We evaluated the novel segment length in cine (SLICE) technique to derive segmental strains from standard cardiovascular MR (CMR) cine images in CRT candidates. Methods Twenty-seven patients with left bundle branch block underwent CMR examination including cine imaging and myocardial tagging (CMR-TAG). SLICE was performed by measuring segment length between anatomical landmarks throughout all phases on short-axis cines. This measure of frame-to-frame segment length change was compared to CMR-TAG circumferential strain measurements. Subsequently, conventional markers of CRT response were calculated. Results Segmental strains showed good to excellent agreement between SLICE and CMR-TAG (septum strain, intraclass correlation coefficient (ICC) 0.76; lateral wall strain, ICC 0.66). Conventional markers of CRT response also showed close agreement between both methods (ICC 0.61–0.78). Reproducibility of SLICE was excellent for intra-observer testing (all ICC ≥0.76) and good for interobserver testing (all ICC ≥0.61). Conclusions The novel SLICE post-processing technique on standard CMR cine images offers both accurate and robust segmental strain measures compared to the ‘gold standard’ CMR-TAG technique, and has the advantage of being widely available. Key Points • Myocardial strain analysis could potentially improve patient selection for CRT. • Currently a well validated clinical approach to derive segmental strains is lacking. • The novel SLICE technique derives segmental strains from standard CMR cine images. • SLICE-derived strain markers of CRT response showed close agreement with CMR-TAG. • Future studies will focus on the prognostic value of SLICE in CRT candidates. Electronic supplementary material The online version of this article (doi:10.1007/s00330-017-4890-0) contains supplementary material, which is available to authorized users.

Background Findings from recent studies show that microvascular injury consists of microvascular destruction and intramyocardial hemorrhage ( IMH ). Patients with ST‐segment elevation myocardial infarction ( STEMI ) with IMH show poorer prognoses than patients without IMH . Knowledge on predictors for the occurrence of IMH after STEMI is lacking. The current study aimed to investigate the prevalence and extent of IMH in patients with STEMI and its relation with periprocedural and clinical variables. Methods and Results A multicenter observational cohort study was performed in patients with successfully reperfused STEMI with cardiovascular magnetic resonance examination 5.5±1.8 days after percutaneous coronary intervention. Microvascular injury was visualized using late gadolinium enhancement and T2‐weighted cardiovascular magnetic resonance imaging for microvascular obstruction and IMH , respectively. The median was used as the cutoff value to divide the study population with presence of IMH into mild or extensive IMH . Clinical and periprocedural parameters were studied in relation to occurrence of IMH and extensive IMH , respectively. Of the 410 patients, 54% had IMH . The presence of IMH was independently associated with anterior infarction (odds ratio, 2.96; 95% CI , 1.73–5.06 [ P II b/ III a inhibitor treatment (odds ratio, 2.67; 95% CI , 1.49–4.80 [ P IMH was independently associated with anterior infarction (odds ratio, 3.76; 95% CI , 1.91–7.43 [ P IMH was associated with larger infarct size, greater extent of microvascular obstruction, larger left ventricular dimensions, and lower left ventricular ejection fraction (all P Conclusions Occurrence of IMH was associated with anterior infarction and glycoprotein II b/ III a inhibitor treatment. Extensive IMH was associated with anterior infarction. IMH was associated with more severe infarction and worse short‐term left ventricular function in patients with STEMI.

Contains fulltext : 176975.pdf (Publisher’s version ) (Open Access) OBJECTIVES: To characterize the temporal alterations in native T1 and extracellular volume (ECV) of remote myocardium after acute myocardial infarction (AMI), and to explore their relation to left ventricular (LV) remodeling. METHODS: Forty-two patients with AMI successfully treated with primary PCI underwent cardiovascular magnetic resonance after 4-6 days and 3 months. Cine imaging, late gadolinium enhancement, and T1-mapping (MOLLI) was performed at 1.5T. T1 values were measured in the myocardial tissue opposite of the infarct area. Myocardial ECV was calculated from native- and post-contrast T1 values in 35 patients, using a correction for synthetic hematocrit. RESULTS: Native T1 of remote myocardium significantly decreased between baseline and follow-up (1002 +/- 39 to 985 +/- 30ms, p

Acute myocardial infarction (AMI) is accompanied by increased expression of Toll like receptors (TLR)-2 and TLR4 on circulating monocytes. In animal models, blocking TLR2/4 signaling reduces inflammatory cell influx and infarct size. The clinical consequences of TLR activation during AMI in humans are unknown, including its role in long-term cardiac functional outcome Therefore, we analyzed gene expression in whole blood samples from 28 patients with an acute ST elevation myocardial infarction (STEMI), enrolled in the EXenatide trial for AMI patients (EXAMI), both at admission and after 4-month follow-up, by whole genome expression profiling and real-time PCR. Cardiac function was determined by cardiac magnetic resonance (CMR) imaging at baseline and after 4-month follow-up. TLR pathway activation was shown by increased expression of TLR4 and its downstream genes, including IL-18R1, IL-18R2, IL-8, MMP9, HIF1A, and NFKBIA. In contrast, expression of the classical TLR-induced genes, TNF, was reduced. Bioinformatics analysis and in vitro experiments explained this noncanonical TLR response by identification of a pivotal role for HIF-1α. The extent of TLR activation and IL-18R1/2 expression in circulating cells preceded massive troponin-T release and correlated with the CMR-measured ischemic area (R=0.48, p=0.01). In conclusion, we identified a novel HIF-1-dependent noncanonical TLR activation pathway in circulating leukocytes leading to enhanced IL-18R expression which correlated with the magnitude of the ischemic area. This knowledge may contribute to our mechanistic understanding of the involvement of the innate immune system during STEMI and may yield diagnostic and prognostic value for patients with myocardial infarction.

Background— Risk stratification for ventricular arrhythmias (VAs) is important to refine selection criteria for primary prevention implantable cardioverter defibrillator therapy. Impaired hyperemic myocardial blood flow (MBF) is associated with increased mortality rate in ischemic and nonischemic cardiomyopathy, which may be attributed to electric instability inducing VAs. The aim of this pilot study was to assess whether hyperemic MBF impairment may be related with VA inducibility in patients with ischemic cardiomyopathy. Methods and Results— Thirty patients with ischemic cardiomyopathy referred for primary prevention implantable cardioverter defibrillator implantation were prospectively included (26 men; 65±8 years old; left ventricular ejection fraction, 29±6%). [ 15 O]H 2 O positron-emission tomography was performed to quantify resting MBF, hyperemic MBF, and coronary flow reserve. Left ventricular dimensions, function, and scar burden were assessed with cardiovascular magnetic resonance imaging. An electrophysiological study was performed to test VA inducibility. Positive electrophysiological study patients (n=12) showed reduced hyperemic MBF (1.25±0.30 versus 1.66±0.38 mL·min −1 ·g −1 ; P P 75% transmurality was higher ( P Conclusions— In this pilot study, impaired hyperemic MBF and coronary flow reserve were associated with VA inducibility in patients with ischemic cardiomyopathy. These results are hypothesis generating for a potential role of quantitative positron-emission tomography perfusion imaging in risk stratification for VAs.

Purpose: To investigate the effects of cell therapy on myocardial perfusion recovery after treatment of acute myocardial infarction (MI) with primary percutaneous coronary intervention (PCI).Materials and Methods: In this HEBE trial substudy, which was approved by the institutional review board (trial registry number IS-RCTN95796863), the authors assessed the effects of intra-coronary infusion with bone marrow-derived mononuclear cells (BMMCs) or peripheral blood-derived mononuclear cells (PBMCs) on myocardial perfusion recovery by using cardiac magnetic resonance (MR) imaging after revascularization. In 152 patients with acute MI treated with PCI, cardiac MR imaging was performed after obtaining informed consent-before randomization to BMMC, PBMC, or standard therapy (control group)-and repeated at 4-month follow-up. Cardiac MR imaging consisted of cine, rest first-pass perfusion, and late gadolinium enhancement imaging. Perfusion was evaluated semiquantitatively with signal intensity-time curves by calculating the relative upslope (percentage signal intensity change). The relative upslope was calculated for the MI core, adjacent border zone, and remote myocardium. Perfusion differences among treatment groups or between baseline and follow-up were assessed with the Wilcoxon signed rank or Mann-Whitney U test.Results: At baseline, myocardial perfusion differed between the MI core (median, 6.0%; interquartile range [IQR], 4.1%-8.0%), border zone (median, 8.4%; IQR, 6.4%-10.2%), and remote myocardium (median, 12.2%; IQR, 10.5%-15.9%) (P

Patients with chest pain and a prehospital ST-segment elevation myocardial infarction (STEMI) are preferably treated with immediate percutaneous coronary intervention (PCI). However, patients with normalization of symptoms and ST-segment elevation upon hospital arrival (transient STEMI) received inconsistent therapy due to logistic reasons and the absence of evidence or explicit guidelines. In this trial, the optimal timing of coronary angiography and subsequent revascularisation is investigated in patients presenting with transient STEMI. In this prospective, multicentre, randomized controlled clinical trial, 142 consecutive patients with initially acute chest pain and STEMI, whose symptoms and ST-segment elevation resolve upon admission, are randomized to immediate intervention or a delayed intervention. Primary outcome is infarct size measured at 4 days determined by cardiovascular magnetic resonance. Secondary outcomes are left ventricular function and volumes, myocardial salvage and microvascular injury at baseline; the change in left ventricular function, volumes and infarct size at 4 months; and major adverse cardiac events at 4 and 12 months. The TRANSIENT Trial evaluates whether a delayed invasive strategy (according to NSTEMI-guidelines) is superior to an immediate invasive strategy (according to STEMI-guidelines) in patients with a transient STEMI.

Myocardial perfusion imaging using positron emission tomography (PET) is a valuable tool in the diagnosis of coronary artery disease. And although PET using [15O]H2O has a high diagnostic accuracy for predicting coronary artery disease in routine clinical practices [(1)][1], left ventricular (LV)

BACKGROUND: Most patients with noncardiac chest pain experience anxiety and depressive symptoms. Commonly they are reassured and referred back to primary care, leaving them undiagnosed and untreated. Some small studies have suggested efficacy of 12 cognitive behavioral therapy (CBT) sessions. Our aim was to examine efficacy of brief CBT in reducing anxiety and depressive symptoms in patients with noncardiac chest pain and comorbid panic and/or depressive disorders. METHODS: In this 24-week randomized controlled trial comparing CBT (n = 60) versus treatment as usual (TAU, n = 53), we included all adults who presented at the cardiac emergency unit of a university hospital with noncardiac chest pain, scored >/=8 on the hospital anxiety and depression scale (HADS) and were diagnosed with a comorbid panic and/or depressive disorder with the Mini International Neuropsychiatric Interview. CBT consisted of six individual sessions. Main outcome was disease severity assessed with the clinical global inventory (CGI) by a blinded independent rater. RESULTS: ANCOVA in the intention-to-treat and completer sample showed that CBT was superior to TAU after 24 weeks in reducing disease severity assessed with CGI (P < .001). Secondary outcomes on anxiety (HADS-anxiety, state trait anxiety inventory (STAI)-trait) and depressive symptoms (Hamilton depression rating scale) were in line with these results except for HADS-depression (P = .10), fear questionnaire (P = .13), and STAI-state (P = .11). CONCLUSIONS: Brief CBT significantly reduces anxiety and depressive symptoms in patients with noncardiac chest pain who are diagnosed with panic and/or depressive disorders. Patients presenting with noncardiac chest pain should be screened for psychopathology and if positive, CBT should be considered.

Objective Non-invasive imaging of myocardial perfusion, sympathetic denervation and scar size contribute to enhanced risk prediction of ventricular arrhythmias (VA). Some of these imaging parameters, however, may be intertwined as they are based on similar pathophysiology. The aim of this study was to assess the predictive role of myocardial perfusion, sympathetic denervation and scar size on the inducibility of VA in patients with ischaemic cardiomyopathy in a head-to-head fashion. Methods 52 patients with ischaemic heart disease and left ventricular ejection fraction (LVEF) ≤35%, referred for primary prevention implantable cardioverter-defibrillator (ICD) implantation, were included. Late gadolinium-enhanced cardiovascular MRI was performed to assess LV volumes, function and scar size. Using [ 15 O]H 2 O and [ 11 C]hydroxyephedrine positron emission tomography, both resting and hyperaemic myocardial blood flow (MBF), and sympathetic innervation were assessed. After ICD implantation, an electrophysiological study (EPS) was performed and was considered positive in case of sustained VA. Results Patients with a positive EPS (n=25) showed more severely impaired global hyperaemic MBF (p=0.003), larger sympathetic denervation size (p=0.048) and tended to have larger scar size (p=0.07) and perfusion defect size (p=0.06) compared with EPS-negative patients (n=27). No differences were observed in LV volumes, LVEF and innervation-perfusion mismatch size. Multivariable analysis revealed that impaired hyperaemic MBF was the single best independent predictor for VA inducibility (OR 0.78, 95% CI 0.65 to 0.94, p=0.007). A combination of risk markers did not yield incremental predictive value over hyperaemic MBF alone. Conclusions Of all previously validated approaches to evaluate the arrhythmic substrate, global impaired hyperaemic MBF was the only independent predictor of VA inducibility. Moreover, a combined approach of different imaging variables did not have incremental value.

To reduce long-term morbidity after revascularised acute myocardial infarction, different therapeutic strategies have been investigated. Cell therapy with mononuclear cells from bone marrow (BMMC) or peripheral blood (PBMC) has been proposed to attenuate the adverse processes of remodelling and subsequent heart failure. Previous trials have suggested that cell therapy may facilitate arrhythmogenesis. In the present substudy of the HEBE cell therapy trial, we investigated whether intracoronary cell therapy alters the prevalence of ventricular arrhythmias after 1 month or the rate of severe arrhythmogenic events (SAE) in the first year. In 164 patients of the trial we measured function and infarct size with cardiovascular magnetic resonance (CMR) imaging. Holter registration was performed after 1 month from which the number of triplets (3 successive PVCs) and ventricular tachycardias (VT, a parts per thousand yen4 successive PVCs) was assessed. Thirty-three patients (20%) showed triplets and/or VTs, with similar distribution amongst the groups (triplets: control n = 8 vs. BMMC n = 9, p = 1.00; vs. PBMC n = 10, p = 0.67. VT: control n = 9 vs. BMMC n = 9, p = 0.80; vs. PBMC n = 11, p = 0.69). SAE occurred in 2 patients in the PBMC group and 1 patient in the control group. In conclusion, intracoronary cell therapy is not associated with an increase in ventricular arrhythmias or SAE.

Aims We evaluated the accuracy of three-dimensional speckle-tracking echocardiography (3DSTE) to evaluate left ventricular (LV) volumes, ejection fraction (EF), and global circumferential strain (CS) in comparison with cardiac magnetic resonance imaging (MRI) in a healthy population. Methods and results A total of 45 out of 50 consecutive healthy subjects (38 males, age 45 ± 15 years) successfully underwent both 3DSTE and MRI on the same day. Three-dimensional echocardiography data sets were analysed using speckle tracking to measure LV end-diastolic and end-systolic volumes, EF, and global CS. With MRI, the method of discs approximation was used to obtain volumes and the EF, whereas CS was acquired using myocardial tissue tagging. Inter-technique comparisons included regression and the Bland–Altman analysis. For quantification of LV volumes, 3DSTE correlated well with MRI ( r : 0.75–0.81), but volumes were significantly underestimated with relatively large biases (13–34 mL) and wide limits of agreement (SD: 11–25 mL). However, excellent accuracy was revealed for measurement of EF by 3DSTE with a good correlation ( r : 0.91), minimal bias, and narrow limits of agreement (0.6 ± 1.7%) compared with MRI. For measurement of CS, a large mean bias was found between techniques (10.0%), despite narrow limits of agreement (SD: 1.7%) and a good correlation between techniques ( r : 0.80). Conclusion Although 3DSTE-derived LV volumes are underestimated in most patients compared with MRI, measurement of the LVEF revealed excellent accuracy. Measurements of CS were systematically greater (i.e. more negative) with 3DSTE than MRI, which likely reflects various inter-technique differences that preclude direct comparability of their measurements.

Sudden cardiac death is a major cause of mortality in patients with ischaemic cardiomyopathy. Risk stratification remains challenging. Currently, there is growing interest in scar characteristic assessment as a predictor of sudden cardiac death using cardiac magnetic resonance imaging (CMR). Standard analysis methods are lacking. The present study evaluated previously validated methods of scar assessment by CMR with late gadolinium enhancement (LGE) in their ability to predict ventricular tachyarrhythmias.Patients with ischaemic cardiomyopathy who received an implantable cardioverter defibrillator for primary prevention and in whom a LGE-CMR was performed, were included. Scar core size, peri-infarct zone and total scar size, which is defined as the sum of the core size and peri-infarct zone, were assessed using three previously validated models, and their ability to predict ventricular tachyarrhythmias was evaluated.Fifty-five patients were included (mean age 64.6 ± 10.8 years, 43 men). During a median follow-up of 2.0 years (IQR 1.0-3.0 years) 26% of patients reached the endpoint of ventricular tachyarrhythmia. All scar characteristics (ie, total scar size, scar core size and peri-infarct zone) of the three methods were predictors of the endpoint (p0.01). Total scar size was comparable, whereas scar core size and peri-infarct zone varied significantly between the tested models. Receiver operating characteristic curves of the different scar characteristics showed comparable areas under the curve varying from 0.721 to 0.812.LGE-CMR-derived scar tissue characteristics are of predictive value for the occurrence of ventricular tachyarrhythmias in patients with ischaemic cardiomyopathy. Additional estimation of scar core size and/or peri-infarct zone does not appear to increase the diagnostic accuracy over total scar size alone.

UNLABELLED: We report a term neonate presenting after birth with shock and cyanosis for which he was intubated. Echocardiography showed no contractions of the left ventricle. Systemic circulation was provided by the right ventricle via shunting through the arterial duct. Left ventricular dysfunction was confirmed by electrocardiography and increased troponin T levels. Hemodynamics quickly improved, and the child could be weaned of the ventilator without residual problems. We concluded that the patient suffered from transient myocardial ischaemia. At 3 weeks of life, we performed delayed-enhancement magnetic resonance imaging (DE-MRI) of the heart which did not show signs of permanent macroscopic damage of the myocardium. CONCLUSION: This is the first reported case report on the use of DE-MRI in a neonate with transient myocardial ischaemia. DE-MRI may provide information that helps to predict recovery in the acute stage of left ventricular dysfunction or at a later stage when absence of recovery of left ventricular function needs to be explained.

Purpose: To test whether image normalization using either a separate 3D proton-density (PD)-weighted prescan, or 2D PD-weighted images prior to the perfusion series, improves correction of differences in spatial sensitivity induced by radiofrequency (RF) surface receiver coils. Originally, this correction was applied using the baseline signal in the myocardium before arrival of the contrast agent. This is of importance, as quantitative analysis of magnetic resonance (MR) myocardial perfusion using deconvolution with the arterial input assumes equal signal sensitivity over the heart. Materials and Methods: First-pass myocardial perfusion measurements were obtained in 13 patients without known coronary artery disease. Absolute perfusion values were assessed for 18 myocardial segments without any normalization and using the three different normalization methods. Results: Using 2D or 3D PD-weighted normalization, similar mean perfusion values were found, but with reduced spatial variance over the 18 segments. The relative dispersion of perfusion at rest was 23% and 35% for the 3D prescan normalization and the baseline normalization, respectively. With 2D and 3D PD-weighted prescan normalization the relative dispersion was closer to the expected physiological heterogeneity. Conclusion: PD-weighted prescan normalization proved to be a valuable addition to quantitative analysis of myocardial perfusion, and better than baseline-based normalization. J. Magn. Reson. Imaging 2010;31:227–233. © 2009 Wiley-Liss, Inc.

OBJECTIVES This study investigated early electrocardiographic findings in relation to left ventricular (LV) function, extent and size of infarction, and microvascular injury in patients with acute myocardial infarction (MI) treated with percutaneous coronary intervention (PCI).BACKGROUND The electrocardiogram (ECG) is the most used and simplest clinical method to evaluate the risk for patients immediately after reperfusion therapy for acute MI. ST-segment resolution and residual ST-segment elevation have been used for prognosis in acute MI, whereas Q waves are related to outcome in chronic MI. We hypothesized that the combination of these electrocardiographic measures early after primary PCI would enhance risk stratification.METHODS We prospectively included 180 patients with a first acute ST-segment elevation MI to assess ST-segment resolution, residual ST-segment elevation, and number of Q waves using the 12-lead ECG acquired on admission and 1 h after successful PCI. The ECG findings were related to LV function, infarction size and transmurality, and microvascular injury as assessed with cine and gadolinium-enhanced cardiac magnetic resonance 4 +/- 2 days after reperfusion therapy.RESULTS Residual ST-segment elevation (beta = -2.00, p = 0.004) and the number of Q waves (beta = -1.66, p = 0.005) were independent ECG predictors of LV ejection fraction. Although the number of Q waves was the only independent predictor of infarct size (beta = 2.01, p CONCLUSIONS In patients after successful coronary intervention for acute MI, residual ST-segment elevation and the number of Q waves on the post-procedural ECG offer valuable complementary information on prediction of myocardial function and necrosis and its microvascular status. (J Am Coll Cardiol Img 2009; 2: 1187-94) (C) 2009 by the American College of Cardiology Foundation

Background: In cardiac syndrome X, which is a syndrome defined as chest pain, positive exercise stress testing and/or reversible myocardial perfusion defects during myocardial scintigraphy and normal coronary angiograms, the ischemic origin is still debated. No previous study compared the myocardial perfusion in stress first-pass cardiac magnetic resonance (CMR) versus stress single-photon emission computed tomography (SPECT) in cardiac syndrome X. Methods: We performed stress SPECT and CMR imaging for 20 syndrome X patients. Perfusion analysis of the CMR was done by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion index (MPI) and the myocardial perfusion reserve index (MPRI). The SPECT images were visually scored by 3 observers using a seg- mental model. Results: An MPRI of  1.2 was found for 31 (9%) of the 335 segments, indicating local ischemia. SPECT indicated re- versible perfusion defects for 39 (12%) of the 335 segments. However, the combination of both an MPRI  1.2 and a re- versible perfusion defect was detected in only 3 segments. Conclusions: Our data show about 10% stress-induced myocardial perfusion abnormalities on CMR and SPECT, suggest- ing local ischemia. However, only in 1% of the segments there was concordance for the presence of myocardial ischemia with both exams. This result may be evidence for the variability over time of the mechanisms responsible for coronary microvascular dysfunction.

Objectives We examined the relation between angiographic, electrocardiographic, and gadolinium-enhanced cardiovascular magnetic resonance (CMR) characteristics of microvascular obstruction (MVO), and their predictive value on functional recovery after acute myocardial infarction (AMI). Background Microvascular obstruction on CMR has been shown to predict left ventricular (LV) remodeling, but it is not well known how it compares with commonly used criteria of microvascular injury, and earlier reports have produced conflicting results on the significance and extent of MVO. Methods Thrombolysis In Myocardial Infarction (TIMI) flow grade, myocardial blush grade (MBG), and ST-segment resolution were assessed in 60 patients with AMI treated with primary stenting. Cardiovascular magnetic resonance was performed between 2 and 9 days after revascularization to determine early MVO on first-pass perfusion imaging, late MVO on late gadolinium-enhanced imaging, and infarct size and transmural extent. Cine imaging was used to determine LV volumes and global and regional function at baseline and 4-month follow-up. Results Early and late MVO were both related to incomplete ST-segment resolution (p = 0.002 and p = 0.01, respectively), but not to TIMI flow grade and MBG. Of all angiographic, electrocardiographic, and CMR variables, late MVO was the strongest parameter to predict changes in end-diastolic volume (β = 0.53; p = 0.001), end-systolic volume (β = 8.67; p = 0.001), and ejection fraction (β = 3.94; p = 0.006) at follow-up. Regional analysis showed that late MVO had incremental diagnostic value to transmural extent of infarction (odds ratio: 0.18; p Conclusions In patients after revascularized AMI, late MVO proved a more powerful predictor of global and regional functional recovery than all of the other characteristics, including transmural extent of infarction.

Purpose: Cardiovascular magnetic resonance (CMR) is considered the standard imaging modality in clinical trials to monitor patients after acute myocardial infarction (AMI). However, limited data is available with respect to infarct size, presence, and extent of microvascular injury (MVO), and changes over time, in relation to cardiac function in these optimally treated patients. In this study, we prospectively investigate the change of infarct size over time, and the incidence and significance of MVO in a uniform, optimally treated patient group after AMI. Methods: Forty patients underwent cine and late gadolinium-enhanced CMR within 9 days and at 4 months after primary stenting. Left ventricular ejection fraction (LVEF), infarct size (IS) and MVO size were calculated. Results: IS decreased with 19.0% at follow-up (p < 0.01). The 23 (57.5%) patients with MVO had larger infarct size, higher left ventricular volumes and lower LVEF and more involution of IS at follow-up. Overall, LVEF improved from 42.3 ± 9.8% to 44.0 ± 9.8% (p = 0.06), irrespective of presence or size of MVO. Conclusion: Infarct size reduces over time by 19.0% in optimally treated patients after AMI. Despite optimal reperfusion, MVO was found in the majority of patients. Although patients with MVO had larger infarcts and worse indices of left ventricular remodelling, functional change at follow-up was comparable to patients without MVO.

Aims: On the basis of an MRI study it has been suggested that subendocardial hypoperfusion is present in patients with cardiac syndrome X. However, further work is required to test whether these findings can be generalized. Methods and results: MRI was used to visually and semi-quantitatively assess subendocardial and subepicardial perfusion, at rest and during an infusion of adenosine, in 20 patients with angina pectoris and normal coronary angiograms. A myocardial perfusion index (MPI) was calculated using the normalized upslope of myocardial signal enhancement. An index for myocardial perfusion reserve (MPRI) was calculated by dividing the MPI values at maximal vasodilatation by the values at rest. The MPI in our study population increased significantly during adenosine infusion in both the subendocardium (from 0.091 ± 0.020 to 0.143 ± 0.030; P < 0.001) and the subepicardium (from 0.074 ± 0.017 to 0.135 ± 0.03; P < 0.001). The overall MPRI was 1.83 ± 0.50. Conclusion: The results show that patients with chest pain and normal coronary angiograms had significant perfusion responses to adenosine in both the subendocardium and subepicardium. In the present study we found no evidence for subendocardial hypoperfusion in these patients. © The European Society of Cardiology 2007. All rights reserved.

OBJECTIVE: The purpose of our study was to assess the presence and extent of delayed contrast enhancement of ventricular myocardium in pulmonary artery hypertension.SUBJECTS AND METHODS: Fifteen patients (age, 45.6 +/- 13 years; 13 New York Heart Association class III) with pulmonary artery hypertension (11 idiopathic, four systemic sclerosis) were studied. All patients had undergone a comprehensive diagnostic workup, and pulmonary artery hypertension (mean pulmonary artery pressure, 54 +/- 16 mm Hg) was confirmed by cardiac catheterization. Cardiac MRI was performed on a 1.5-T scanner to determine ventricular volumes and mass. Delayed contrast enhancement of a mass was seen 10-20 minutes after the i.v. injection of 0.2 mmol/kg of gadopentetate dimeglumine using an inversion recovery gradient-echo sequence.RESULTS: All patients showed delayed contrast enhancement at the insertion points of the right ventricular free wall to the interventricular septum (15 inferior, 13 anterior). The mean weight of the delayed contrast-enhanced myocardial mass was 3.1 +/- 1.9 g (size range, 0.3-3.9% of the total myocardial mass). The extent of the delayed contrast-enhancing myocardium was inversely related to the right ventricular ejection fraction (r = -0.63, p = 0.001), right ventricular stroke volume (r = -0.67, p = 0.006), and right ventricular end-systolic volume index (r = -0.51, p = 0.05) but not to any invasively measured hemodynamic index or N-terminal pro brain natriuretic peptide.CONCLUSION: Myocardial delayed contrast enhancement occurs frequently in patients with severe symptomatic pulmonary artery hypertension and is inversely related to measures of right ventricular systolic function.

The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries.An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters.Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11).In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = -0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p0.001) with consistent observations in swine (Δ = -0.9; 1.5 ± 0.4 vs. 2.4 ± 0.9 for after and before AMI, respectively; p = 0.04). An increased baseline and a decreased hyperemic flow contributed to the reduction in CFR in both patients (baseline flow: Δ = +5 and hyperemic flow: Δ = -7 cm/s) and swine (baseline flow: Δ = +8 and hyperemic flow: Δ = -6 cm/s). Similar changes were observed in nonculprit arteries (CFR: 2.8 ± 0.7 vs. 2.0 ± 0.7 for STEMI patients and control subjects; p0.001). CFR significantly correlated with infarct size as a percentage of the left ventricle in both patients (r = -0.48; p = 0.001) and swine (r = -0.61; p = 0.047).CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction.

Introduction ST-elevated myocardial infarction (STEMI) is most frequently caused by coronary occlusion due to formation of an intracoronary thrombus in reaction to rupture of atherosclerotic plaques. Little is known about kinetics of coagulation markers after STEMI in patients treated according to current guidelines. We aimed to investigate kinetics of important coagulation markers in percutaneous coronary intervention (PCI)-treated STEMI patients. Materials and methods 60 consecutive PCI-treated STEMI patients were prospectively included. Blood samples were collected immediately after as well as 1, 4 and 7 days following PCI. Samples collected 90 days after PCI served as baseline values. ADAMTS13 activity, VWF (von Willebrand factor) activity, VWF antigen, VWF propeptide, fibrinogen antigen, D-dimer, alpha2-antiplasmin (α2AP), plasmin-alpha2-antiplasmin complex (PAP), prothrombin fragment F1 + 2 (F1 + 2), prothrombin time (PT), activated partial thromboplastin time (aPTT), and anti-factor Xa (anti-Xa) were measured. Cardiac magnetic resonance (CMR) was performed at 4–6 and 90 days after PCI in 49 patients and left ventricular ejection fraction (LVEF), infarct size and microvascular injury (MVI) were determined. Results Immediately after PCI, ADAMTS13 activity, fibrinogen antigen and α2AP levels were significantly decreased and VWF activity, VWF antigen and VWF propeptide levels were significantly elevated, compared to baseline. Individual coagulation markers and different combinations thereof were not related to LVEF or infarct size at 90 days, or the occurrence of MVI at 4–6 days after PCI. Conclusion Coagulation parameters show a very dynamic profile in the early days after STEMI. However, individual coagulation parameters or combinations thereof do not predict CMR-defined LVEF, infarct size or MVI.

A 51-year-old male presented with acute chest pain several days after an episode of acute tonsillitis. Physical examination revealed hypotension (95/60 mmHg) but no fever. The electrocardiogram showed sinus tachycardia (110 bpm) with regional ST-segment elevation in inferolateral ECG leads (see Supplementary material online, Figure S1 ). Troponin-T (0.735 μg/L) and CK-MB (25.7 μg/L) levels were elevated. Furthermore, CRP (277 mg/L) and leukocyte count (16.1 × 109/L) were raised. Invasive coronary angiography showed normal coronary arteries. Transthoracic echocardiogram displayed severely impaired left ventricular function (LVF) with global wall motion abnormalities (see Supplementary material online, Video S1 ). Myocarditis was suspected and the patient was …

Background— A total of 40% to 50% of patients with ST-segment–elevation myocardial infarction develop microvascular injury (MVI) despite angiographically successful primary percutaneous coronary intervention (PCI). We investigated whether hyperemic microvascular resistance (HMR) immediately after angiographically successful PCI predicts MVI at cardiovascular magnetic resonance and reduced myocardial blood flow at positron emission tomography (PET). Methods and Results— Sixty patients with ST-segment–elevation myocardial infarction were included in this prospective study. Immediately after successful PCI, intracoronary pressure–flow measurements were performed and analyzed off-line to calculate HMR and indices derived from the pressure–velocity loops, including pressure at zero flow. Cardiovascular magnetic resonance and H 2 15 O PET imaging were performed 4 to 6 days after PCI. Using cardiovascular magnetic resonance, MVI was defined as a subendocardial recess of myocardium with low signal intensity within a gadolinium-enhanced area. Myocardial perfusion was quantified using H 2 15 O PET. Reference HMR values were obtained in 16 stable patients undergoing coronary angiography. Complete data sets were available in 48 patients of which 24 developed MVI. Adequate pressure–velocity loops were obtained in 29 patients. HMR in the culprit artery in patients with MVI was significantly higher than in patients without MVI (MVI, 3.33±1.50 mm Hg/cm per second versus no MVI, 2.41±1.26 mm Hg/cm per second; P =0.03). MVI was associated with higher pressure at zero flow (45.68±13.16 versus 32.01±14.98 mm Hg; P =0.015). Multivariable analysis showed HMR to independently predict MVI ( P =0.04). The optimal cutoff value for HMR was 2.5 mm Hg/cm per second. High HMR was associated with decreased myocardial blood flow on PET (myocardial perfusion reserve P =0.04). Conclusions— Doppler-flow–derived physiological indices of coronary resistance (HMR) and extravascular compression (pressure at zero flow) obtained immediately after successful primary PCI predict MVI and decreased PET myocardial blood flow. Clinical Trial Registration— URL: http://www.trialregister.nl . Unique identifier: NTR3164.

Objective This study assesses the feasibility and outcome of the implementation of a screening program for classifying panic disorder (PD) in patients presenting with noncardiac chest pain (NCCP 1 1Noncardiac chest pain.), when integrated in routine cardiac emergency department (CED 2 2Cardiac emergency department.) care. Methods Barrier analyses were made during the pilot phase and implementation period. NCCP patients aged 18–70 years presenting at the CED ( n =252) were eligible for screening with the Hospital Anxiety and Depression Scale (HADS). Those scoring above cutoff on the HADS were referred to the psychiatric department and received the Composite International Diagnostic Interview. Results Screening was initiated in 60 patients (23.8%), of whom nine refused participation. Staff adherence remained low despite implementing several improvements in the screening procedure. In total, 39 patients completed the program; 8 were diagnosed with a psychiatric disorder, including 2 patients with PD. Conclusion Feasibility of implementation of this screening program for PD in NCCP patients in routine CED care was limited because offering screening frequently conflicted with provision of acute care and because patients showed relatively high refusal rates. Contrasting our assumption, various other psychiatric disorders besides PD were classified.

Methods All patients admitted with an acute coronary syndrome (ACS)-like presentation of myocarditis, with confirmed diagnosis at baseline according to standard CMR criteria and follow-up examination available, were retrospectively identified in our database. CMR images were analyzed to determine left ventricular (LV) dimensions, LV mass and total amount of late gadolinium enhancement. LGE was quantified using signal intensity >5 SD above normal myocardium and was expressed as percentage of LV mass. Improvement of LV function (LVF) was defined as in increase in ejection fraction (EF) of ≥5%. Results Fifteen consecutive patients were included in the present study. Follow-up CMR was performed at a mean of 282 ± 187 days after admission. At baseline, mean EF was 51 ± 7% and was impaired in 11 patients (47 ± 4 %). EF improved in 8 of these 11 patients (73%). Total indexed myocardial mass (TMM) and the extent of LGE at baseline did not differ between patients that improved and those that did not (52.9 ± 12.4 vs. 56.9 ± 21.2, p = 0.697; 8.2 ± 6.3 vs. 9.2 ± 6.8, p = 0.821). At follow-up, the extent of LGE decreased in patients with and patients without LV improvement (-3.0±5.0 vs. -5.0±4.9, p=0.570). However, TMM decreased in patients that showed EF improvement, and not in patients without improvement (-10.8±7.9 vs. 1.9±4.1, p=0.029). Conclusions The majority of patients with an ACS-like presentation of myocarditis have a good prognosis. The improvement of LVF was accompanied by a decrease in myocardial mass. This decrease in myocardial mass likely reflects the resolution of acute inflammatory changes in acute myocarditis.

Myocarditis, i.e. inflammation of the myocardium, is one of the leading causes of sudden cardiac death (SCD) and dilated cardiomyopathy (DCM) in young adults, and is an important cause of symptoms such as chest pain, dyspnea and palpitations. The pathophysiological process of disease progression leading to DCM involves an ongoing inflammation as a result of a viral-induced auto-immune response or a persisting viral infection. It is therefore crucial to detect the disease early in its course and prevent persisting inflammation that may lead to DCM and end-stage heart failure. Because of the highly variable clinical presentation, ranging from mild symptoms to severe heart failure, and the limited available diagnostic tools, the evaluation of patients with suspected myocarditis represents an important clinical dilemma in cardiology. New approaches for the diagnosis of myocarditis are needed in order to improve recognition, to help unravel its pathophysiology, and to develop new therapeutic strategies to treat the disease. In this review, we give a comprehensive overview of the current diagnostic strategies for patients with suspected myocarditis, and demonstrate several new techniques that may help to improve the diagnostic work-up.

In patients with acute myocardial infarction (AMI), the guideline-recommended treatment is mechanical revascularization by percutaneous coronary intervention (PCI), which is effective at reducing mortality. However, a substantial proportion of patients with AMI develop chronic cardiac failure owing to poor restoration of microvascular function and myocardial perfusion, despite restoration of epicardial vessel patency. This occurrence is called the 'no-reflow' phenomenon. Although pathological and clinical observations initially seemed to support the hypothesis that no-reflow was the result of microvascular obstruction, irreversible microvascular injury and subsequent intramyocardial haemorrhage are now also thought to be important factors in this process. Intramyocardial haemorrhage shares several pathophysiological features with the haemorrhagic transformation that occurs after ischaemic stroke. Understanding of the role of intramyocardial haemorrhage in the no-reflow phenomenon and myocardial injury is crucial to the development of new therapeutic strategies to treat AMI. In this Review, we provide a comprehensive overview of the pathogenesis and clinical relevance of intramyocardial haemorrhage, and discuss diagnostic options and future therapeutic strategies.

In most patients with heart disease left ventricular dysfunction is the principle physiologic disorder leading to heart failure and is an important prognostic factor. Various imaging methods have been developed for the evaluation of left ventricular function and a substantial body of literature is available describing these methods. The right ventricle (RV) may be predominantly involved in certain cardiac or pulmonary pathological conditions such as arrhythmogenic right ventricular cardiomyopathy or pulmonary hypertension. Also in many congenital or acquired cardiac diseases primarily affecting the left ventricle (LV), right heart involvement has an important role in disease prognosis. The RV is difficult to evaluate using two-dimensional (2D) cross-sectional imaging modalities due to its complex shape and orientation. Cardiovascular magnetic resonance imaging (CMR) is a virtually three-dimensional (3D) tomographic technique which has entered the mainstream of clinical cardiovascular imaging over the last decade. Compared to other imaging methods CMR allows the accurate quantification of RV volumes, myocardial mass, and transvalvular flow with the added benefit of tissue characterisation and without the use of ionising radiation. The manuscript presents a review of the contemporary use of CMR for the evaluation of right heart involvement in various cardio-pulmonary diseases.

Cardiovascular magnetic resonance imaging (MRI) has evolved from an effective research tool into a clinically proven, safe and comprehensive imaging modality. It provides anatomic and functional information in acquired and congenital heart disease and is the most precise technique for quantification of ventricular volumes, function and mass. Owing to its excellent interstudy reproducibility, cardiovascular MRI is the optimal method for assessment of changes in ventricular parameters after therapeutic intervention. Delayed contrast enhancement is an accurate and robust method used in the diagnosis of ischemic and nonischemic cardiomyopathies and less common diseases, such as cardiac sarcoidosis and myocarditis. First-pass magnetic contrast myocardial perfusion is becoming an alternative to radionuclide techniques for the detection of coronary atherosclerotic disease. In this review we outline the techniques used in cardiovascular MRI and discuss the most common clinical applications.

Background: The water-perfusable tissue index (PTI) is assumed to differentiate viable myocardium from scar tissue, but histological comparisons in humans are lacking. The present study compares PTI with delayed contrast-enhanced magnetic resonance imaging (DCE-MRI), a validated marker of fibrotic tissue, in patients with ischemic left ventricular (LV) dysfunction. In addition, the optimal PTI threshold for detection of myocardial viability was defined when DCE-MRI was taken as a reference.Materials: Twenty patients with ischemic LV dysfunction were studied with positron emission tomography, using oxygen-15-labeled water and carbon monoxide as tracers, and DCE-MRI.Results: Of the 200 analyzed segments, 112 demonstrated DCE and were subsequently divided in three subgroups according to the severity of enhancement. PTI was 1.04 +/- 0.21 in control segments and gradually decreased with increasing extent of DCE to 0.77 +/- 0.31 for segments with transmural enhancement (p Conclusions: PTI is inversely related to the extent of scar tissue estimated by DCE-MRI in patients with chronic ischemic heart disease and LV dysfunction. However, with increasing quantities of scar tissue, PTI overestimates the extent of residual viable tissue. A PTI threshold of 0.89 yields the best diagnostic accuracy for viability detection.

PURPOSE: To prospectively assess the effect of including or excluding endocardial trabeculae in left ventricular (LV) measurements and the reproducibility of these measurements at cine cardiovascular magnetic resonance (MR) imaging with true fast imaging with steady-state precession (FISP). MATERIALS AND METHODS: The study was approved by the local ethics committee, and each subject gave informed consent before participating. Twenty healthy subjects and 20 consecutive patients underwent 1.5-T cardiovascular MR imaging. Seven to 12 short-axis views encompassing the entire LV were acquired by using true FISP. Endocardial and epicardial contours were traced manually. The data sets in each patient were analyzed twice: with inclusion of endocardial trabeculae in the LV cavity volume and with exclusion of endocardial trabeculae from the cavity volume. On the basis of these two contour sets, the end-diastolic (ED) and end-systolic (ES) LV volumes, ejection fraction (EF), and LV mass were calculated. Additionally, interobserver and interexamination reproducibility was assessed by using Bland-Altman analysis. RESULTS: Compared with exclusion of trabeculae, inclusion of trabeculae in the LV cavity volume resulted in significantly larger ED and ES LV volumes (mean differences, 21 mL ± 11 [standard deviation] and 19 mL ± 33, respectively; P < .001) and lower EFs (mean difference, -2% ± 2; P < .001). The calculated LV mass was significantly smaller with inclusion than with exclusion of trabeculae (mean difference, -21 g ± 12; P < .001). All interobserver and interexamination limits of agreement based on inclusion of trabeculae, except those for EF measurements, were superior to those based on exclusion of trabeculae. At measurement reproducibility comparisons, differences in interobserver ED LV volume, and LV mass and interexamination LV mass were statistically significant, favoring the inclusion of trabeculae in the LV cavity volume. CONCLUSION: Trabeculae significantly affect quantifications of LV volume and mass. The superior reproducibility of LV measurements with the inclusion of endocardial trabeculae in the cavity volume favors this tracing algorithm for clinical use. © RSNA, 2005.

Purpose. To evaluate a standardized definition of delayed hyperenhancement in the analysis of contrast-enhanced cardiac magnetic resonance (ceCMR) imaging. Patients and Methods. CeCMR was performed in 15 patients with chronic ischemic heart disease. Delayed hyperenhancement was analyzed both by visual analysis by an experienced team of observers, and after thresholding the window setting of the images at 2, 3, 4, 5, and 6 SD above the mean signal intensity of remote, normal myocardium in the same slice. In each patient, total infarct size (TIS) and segmental infarct extent (SIE) were calculated. Results. TIS and SIE were 22.9 ± 12.2 mL and 32 ± 28% after visual analysis. Thresholding the window setting at 2, 3, 4, and 6 SD above signal intensity of remote caused a 40%, 31%, and 17% increase (p < 0.007) and a 7% decrease (p = NS) in TIS, and a 75%, 41%, and 16% increase and 22% decrease in SIE (p < 0.001), respectively. There was no difference between visual analysis and analysis after thresholding at 5 SD. Conclusion. Analyzing ceCMR with a standardized definition of hyperenhancement related to the signal of remote, nonenhanced myocardium may result in considerable overestimation of infarct size at the usual cut-off of 2 SD.

We present a coincidental finding of quadricuspid pulmonary valve and left pulmonary artery aneurysm. As both the pulmonary valve and the pulmonary trunk with its main branches are hard to visualise with cardiac ultrasound, most abnormalities described so far are from autopsy series. With the increasing use of CMR and its excellent potential for visualising both pulmonary valve and pulmonary arteries, we believe more cases will be discovered in the near future. Although pulmonary artery aneurysm are rare, timely detection may prevent lethal bleeding. Electronic supplementary material The online version of this article (doi:10.1007/s12471-011-0115-3) contains supplementary material, which is available to authorized users.

OBJECTIVES: The aim of this study was to evaluate myocardial infarction induced by percutaneous transluminal septal myocardial ablation (PTSMA) in symptomatic patients with hypertrophic obstructive cardiomyopathy using contrast-enhanced (CE) magnetic resonance imaging (MRI). BACKGROUND: Contrast-enhanced MRI delineates the extent of myocardial infarction in coronary artery disease, but its role in ethanol-induced infarction has not been established. METHODS: Cine and CE MRI were performed before and one month after PTSMA in 24 patients. Size and location of the induced infarction were related to left ventricular (LV) mass reduction, enzyme release, volume of ethanol administered, LV outflow tract gradient reduction, and coronary ablation site. RESULTS: One month after PTSMA, regional hyperenhancement was visualized in the basal interventricular septum in all patients. Mean infarction size was 20 ± 9 g, corresponding to 10 ± 5% and 31 ± 16% of total LV and septal mass, respectively. Total LV mass decreased from 219 ± 64 to 205 ± 64 g (p < 0.01), and septal mass from 76 ± 25 to 68 ± 22 g (p < 0.01). Total LV mass reduction exceeded septal mass reduction (p < 0.01). Infarction size correlated with peak creatine phosphokinase-MB (β = 0.67, p < 0.01), volume of ethanol administered (β = 0.47, p = 0.02), total LV and septal mass reduction (β = 0.50, p = 0.02; β = 0.73, p < 0.01), and gradient reduction (β = 0.63, p < 0.01). Seven patients with exclusively right-sided septal infarction had smaller infarction size and less gradient reduction than remaining patients with left-sided or transmural infarction (p < 0.01). In five of these, PTSMA was performed distal in the target artery. CONCLUSIONS: Contrast-enhanced MRI allowed detailed evaluation of size and location of septal myocardial infarction induced by PTSMA. Infarction size correlated well with clinical indexes of infarct size.

OBJECTIVES: We evaluated whether delayed contrast-enhanced magnetic resonance imaging (DCE-MRI) using an extracellular contrast agent could predict improvement of dysfunctional but viable myocardium after acute reperfused myocardial infarction (MI). BACKGROUND: The transmural extent of hyperenhancement at DCE-MRI has been related to improvement of function in reperfused MI. However, evidence is still limited, and earlier reports have produced conflicting results regarding the significance of contrast patterns after infarction. METHODS: Thirty patients (mean age 59 ± 11 years, 27 males) underwent cine MRI and DCE-MRI 7 ± 3 days after a first reperfused acute MI and follow-up cine MRI at 13 ± 3 weeks. Segmental wall thickening and segmental extent of hyperenhancement were scored in 1,689 segments. RESULTS: Of 500 dysfunctional segments, 273 (55%) improved at follow-up. There was no difference in likelihood of improvement or complete functional recovery between segments with 0% and 1% to 25% hyperenhancement. The likelihood of improvement of segments without hyperenhancement was 2.9, 14.3, and 20 times higher than that of segments with 26% to 50%, 51% to 75%, and >75% hyperenhancement, respectively (p < 0.001). The likelihood of complete functional recovery of segments without hyperenhancement was 3.8, 11.1, and 50 times higher than that of segments with 26% to 50%, 51% to 75%, and >75% hyperenhancement, respectively (p < 0.001). CONCLUSIONS: In patients with recent reperfused MI, functional improvement of stunned myocardium is predicted by DCE-MRI.

Objectives: We sought to compare contrast-enhanced magnetic resonance imaging (ceMRI) with nuclear metabolic imaging for the assessment of myocardial viability in patients with chronic isch...

Objectives: Our aim was to validate 3-dimensional echocardiography (3DE) for assessment of left ventricular (LV) end-diastolic volume, end-systolic volume (ESV), stroke volume, and ejection fraction (EF) using the freehand-acquisition method. Furthermore, LV volumes by breath hold—versus free breathing—3DE acquisition were assessed and compared with magnetic resonance imaging (MRI). Methods: From the apical position, a fan-like 3DE image was acquired during free breathing and another, thereafter, during breath hold. In 27 patients, 28 breath hold— and 24 free breathing—3DE images were acquired. A total of 17 patients underwent both MRI and 3DE. MRI contours were traced along the outer endocardial contour, including trabeculae, and along the inner endocardial contour, excluding trabeculae, from the LV volume. Results: All 28 (100%) breath hold— and 86% of free breathing—3DE acquisitions could be analyzed. Intraobserver variation (percentual bias ± 2 SD) of end-diastolic volume, ESV, stroke volume, and EF for breath-hold 3DE was, respectively, 0.3 ± 10.2%, 0.3 ± 14.6%, 0.1 ± 18.4%, and −0.1 ± 5.8%. For free-breathing 3DE, findings were similar. A significantly better interobserver variability, however, was observed for breath-hold 3DE for ESV and EF. Comparison of breath-hold 3DE with MRI inner contour showed for end-diastolic volume, ESV, stroke volume, and EF, a percentual bias (± 2 SD) of, respectively, −13.5 ± 26.9%, −17.7 ± 47.8%, −10.6 ± 43.6%, and −1.8 ± 11.6%. Compared with the MRI outer contour, a significantly greater difference was observed, except for EF. Conclusions: 3DE using the freehand method is fast and highly reproducible for (serial) LV volume and EF measurement, and, hence, ideally suited for clinical decision making and trials. Breath-hold 3DE is superior to free-breathing 3DE regarding image quality and reproducibility. Compared with MRI, 3DE underestimates LV volumes, but not EF, which is mainly explained by differences in endocardial contour tracing by MRI (outer contour) and 3DE (inner contour) of the trabecularized endocardium. Underestimation is reduced when breath-hold 3DE is compared with inner contour analysis of the MRI dataset. (J Am Soc Echocardiogr 2003;16:101-9.)

Introduction: Early recognition of viable myocardium is of great clinical importance after acute myocardial infarction (AMI). Delayed contrast-enhanced magnetic resonance imaging (DCE-CMR) has been validated extensively for the detection of viability. An alternative method for detecting viability is the perfusable tissue index (PTI), a positron emission tomography (PET) derived parameter, which is inversely related to the extent of myocardial scar (nonperfusable tissue). Aims: To investigate the predictive value of PTI on recovery of LV function after percutaneous coronary intervention (PCI) for AMI. Methods: Twenty-six patients with AMI successfully treated by PCI were included. Subjects were examined one week and three months after AMI with [15O]H2O PET and DCE-CMR to assess PTI, regional function and scar. Viability was defined as recovery of systolic wall thickening (SWT) ≥ 3.0 mm at follow-up. Results: A total of 396 segments were available for serial analysis. At baseline, 166 segments were dysfunctional, of which 125 (75%) exhibited significant DCE and were located in the myocardial territory supplied by the culprit-artery. Fourty-nine of these dysfunctional segments showed full recovery during follow-up (viable), whereas 76 segments remained dysfunctional (nonviable). Baseline PTI of viable segments was 0.94 ± 0.07 and was significantly higher compared to nonviable segments (0.80 ± 0.11, p = 0.01). The optimal cut-off value for the PTI was 0.85 with a sensitivity of 92% and specificity of 71%, and an area under the curve (AUC) of 0.88. In comparison, a cut-off value of 40% for the extent of DCE resulted in a sensitivity of 75% and a specificity of 65%, and an AUC of 0.75 (p = 0.02 vs PTI). Conclusions: This study shows that assessment of myocardial viability shortly after reperfused AMI is feasible with PET, and that the PTI is a good prognostic indicator for recovery of contractile function when compared to DCE-CMR.

Reperfusion by means of percutaneous coronary intervention or thrombolytic therapy is the most effective treatment for acute myocardial infarction, markedly reducing mortality and morbidity. Reperfusion however induces necrotic and apoptotic damages to cardiomyocytes, that were viable prior to reperfusion, a process called lethal reperfusion injury. This process, consisting of many single processes, may be responsible of up to half of the final infarct size. A myriad of therapies as an adjunct to reperfusion have been studied with the purpose to attenuate reperfusion injury. The majority of these studies have been disappointing or contradicting, but recent proof-of-concept trials show that reperfusion injury still is a legitimate target. This overview will discuss these trials, the progression in attenuating myocardial reperfusion injury, promising therapies, and future perspectives.