Early prediction of final infarct volume with material decomposition images of dual-energy CT after mechanical thrombectomy.

PURPOSE: Evaluation of water material density images (wMDIm) of dual-energy CT (DECT) for earlier prediction of final infarct volume (fiV) in follow-up single-energy CT (SECT) and correlation with clinical outcome. METHODS: Fifty patients (69 years, ± 12.1, 40-90, 50% female) with middle cerebral artery (MCA) occlusions were included. Early infarct volumes were analyzed in monoenergetic images (MonoIm) and wMDIm at 60 keV and compared with the fiV in SECT 4.9 days (± 4) after thrombectomy. Association between infarct volume and functional outcome was tested by linear regression analysis. RESULTS: wMDIm shows a prior visible infarct demarcation (60.7 ml, ± 74.9 ml) compared with the MonoIm (37.57 ml, ± 76.7 ml). Linear regression analysis, Bland-Altman plots and Pearson correlation coefficients show a close correlation of infarct volume in wMDIm to the fiV in SECT (r = 0.86; 95% CI 0.76-0.92), compared with MonoIm and SECT (r = 0.81; 95% CI 0.69-0.89). The agreement with SECT is substantially higher in patients with infarct volumes < 70 ml (n = 33; 66%). Coefficients were smaller with r = 0.59 (95% CI 0.31; 0.78) for MonoIm and SECT compared with r = 0.77 (95% CI 0.57; 0.88) for wMDIm and SECT. At admission, the mean NIHSS score and mRS were 17.02 (± 4.7) and 4.9 (± 0.2). mRS ≤ 2 was achieved in 56% at 90 days with a mean mRS of 2.5 (± 0.8) at discharge. CONCLUSION: Material decomposition allows earlier visibility of the final infarct volume. This promises an earlier evaluation of the dimension and severity of infarction and may lead to faster initiation of secondary stroke prophylaxis.

Influence of vessel morphology and variations on technical and clinical success in mechanical thrombectomy: -In vivo and in vitro analyses.

PURPOSE: To determine the impact of vessel variation and anatomical features on technical and clinical success. MATERIALS AND METHODS: In vitro blood clots (n=100) were introduced into a silicon carotid-T flow model of 2, 3 or 4mm. The ICA/M1angle varied at 45°, 90°, 135° and 180°. Peripheral embolism was measured. In vivo 50 pat. (73.5 yrs.,±15) with MCA occlusion were examined for siphon variation, ICA morphology, vessel diameter and angles. The patients were divided according to the clinical success (mRS): group A: mRS≤2 after 90 day and group B: mRS≥3. Furthermore the technical success (TICI) and number of retrieval (n) were analysed. RESULTS: In vitro with larger vessel diameter the migrated thrombus load decreased (P=.001). The steeper the M1/ICA angles, the higher thrombus weighs (180°: 2.94mg; 135°: 6.32mg; 90°: 8.65mg, 45°: 10.69mg; P<.001). In vivo patients with mRS≤2 had significantly lower NIHSS (16.5 vs 20, P=.009) and higher ASPECTS (9 vs 6, P<.05). TICI≥2b was more often achieved (86.6 vs 40% P=.002). The procedure time was lower (45 vs. 80min, P<.05) with smaller number of retrieval (1.5 vs 4, P<05). Proximal ICA stenosis offers a trend to unfavourable outcome (P=.073). Siphon variation "D" is associated with less retrieval manoeuvre. CONCLUSION: While in vitro there is a close correlation between embolism and vascular anatomy, in vivo carotid artery stenosis and siphon variation influence clinical and technical success.

Assessment of disease severity and outcome in patients with systemic light-chain amyloidosis by the high-sensitivity troponin T assay.

Cardiac biomarkers provide prognostic information in light-chain amyloidosis (AL). Thus, a novel high-sensitivity cardiac troponin T (hs-TnT) assay may improve risk stratification. hs-TnT was assessed in 163 patients. Blood levels were higher with cardiac than renal or other organ involvement and were related to the severity of cardiac involvement. Increased sensitivity was not associated with survival benefit. Forty-seven patients died during follow-up (22.3 ± 1.0 months). Nonsurvivors had higher hs-TnT than survivors. Outcome was worse if hs-TnT more than or equal to 50 ng/L and best less than 3 ng/L. Survival of patients with hs-TnT 3 to 14 ng/L did not differ from patients with moderately increased hs-TnT (14-50 ng/L), but was worse if interventricular septum was more than or equal to 15 mm. Discrimination according to the Mayo staging system was only achieved by the use of the hs-TnT assay, but not by the fourth-generation troponin T assay. Multivariate analysis revealed hs-TnT, NT-proBNP, and left ventricular impairment as independent risk factors for survival. hs-TnT and NT-proBNP predicted survival, even after exclusion of patients with impaired renal function. Plasma levels of the hs-TnT assay are associated with the clinical, morphologic, and functional severity of cardiac AL amyloidosis and could provide useful information for clinicians on cardiac involvement and outcome.

Quantitative assessment of stenosis severity and atherosclerotic plaque composition using 256-slice computed tomography.

OBJECTIVE: To quantitatively estimate lumen narrowing and to assess the volume and composition of atherosclerotic plaque with 256-slice computed tomography angiography (CTA), using conventional quantitative coronary angiography (QCA) as the gold standard. METHODS: Twenty-seven consecutive patients with suspected coronary artery disease (CAD) underwent 256-slice CTA and subsequent coronary angiography within 4 weeks. Quantification of lumen narrowing was performed on curved multiplanar reformatted CTA images, in identical projections to those used for QCA. Atherosclerotic plaque volume and composition were assessed by using commercially available software. RESULTS: The overall correlation between the stenosis severity by QCA compared with CTA was high (r(2) = 0.79, p < 0.001). For the detection of >or=50% and >or=75% diameter lesions, CTA yielded high sensitivity, specificity and accuracy (86%, 95% and 90%; and 89%, 100% and 96%, respectively), using QCA as the standard reference. Furthermore, assessment of atherosclerotic plaque yielded highly reproducible results (inter-observer and intra-variability of 13% and 9%, respectively, for the assessment of plaque volume, and high agreement between observers (kappa = 0.86) for the differentiation between non-calcified, mixed and calcified plaque). CONCLUSIONS: Clinically indicated 256-slice CT angiography in symptomatic patients can aid both quantification of lumen narrowing and evaluation of atherosclerotic plaque, with high reproducibility.

Staged cardiovascular magnetic resonance for differential diagnosis of troponin T positive patients with low likelihood for acute coronary syndrome.

BACKGROUND: Cardiac troponin-T (cTnT) is a cardio-specific indicator of myocardial necrosis due to ischemic or non-ischemic events. Considering the multiple causes of myocardial injury and treatment consequences there is great clinical need to clarify the underlying reason for cTnT release. We sought to implement acute CMR as a non-invasive imaging method for differential diagnosis of elevated cTnT in chest-pain unit (CPU) patients with non-conclusive symptoms and ECG-changes and a low to intermediate probability for coronary artery disease (CAD). RESULTS: CPU patients (n = 29) who had positive cTnT were scanned at 1.5T with a new step-by-step CMR algorithm including cine-, perfusion-, T2-, angiography-and late gadolinium enhancement (LGE) imaging. For comparison patients also underwent echocardiography and coronary angiography if necessary. CMR was conducted successfully in all patients and detected 93% of cTnT releases of unknown cause, without adverse hemodynamic or arrhythmic events. Acute myocardial infarction was detected in 11, pulmonary embolism in 6, myocarditis in 5, renal disease and cardiomyopathy in 2, storage disorder in 1 patient. In 2 patients CMR was unable to reveal the cause of cTnT elevations. Mean CMR scan-time was 35 ± 8 min. In 4 patients, CMR led to immediate coronary angiography with correct prediction of the infarct related artery. CONCLUSIONS: We implemented a novel CMR algorithm to show the clinical value and practical feasibility of acute CMR in a non-conclusive patient cohort with unclear cTnT elevation. Since this pilot study has shown the feasibility of CMR in CPU patients, further prospective studies are warranted to compare CMR with other imaging modalities.

Myocardial late gadolinium enhancement cardiovascular magnetic resonance in patients with cirrhosis.

BACKGROUND: Portal hypertension and cardiac alterations previously described as "cirrhotic cardiomyopathy" are known complications of end stage liver disease (ELD). Cardiac failure contributes to morbidity and mortality, particularly after liver transplantation and transjugular intrahepatic portosystemic shunt (TIPS). We sought to identify myocardial tissue characterization and evaluate cardiovascular magnetic resonance (CMR) for diagnosis of cardiac impairment. RESULTS: Twenty ELD patients underwent CMR for morphological, functional and tissue characterization by late gadolinium enhancement (LGE). Based on extent of LGE, patients were dichotomized into high and low LGE groups and analyzed regarding liver, cardiocirculatory and renal functions. CMR demonstrated hyperdynamic left ventricular function and a patchy pattern of LGE of the myocardium to a variable extent (range 2-62%) in all patients. There were no significant differences in Model for End-Stage Liver Disease (MELD), Child-Pugh score or the left ventricular ejection fraction between high and low LGE groups. QTc-interval was prolonged in 25% of the patients. E/A ratio was at the upper limit of norm; no difference between groups. Patients showing high LGE had a higher CI (p < 0.05). Biomarkers of myocardial stress were elevated. While NT-proBNP and c-Troponin-T showed no differences, PLGF and sFLT1 were lower in the high LGE group. CONCLUSION: CMR shows myocardial involvement in patients with ELD resembling appearance of myocarditis. The hyperdynamic circulation in portal hypertension may be an important factor. Larger prospective trials are warranted to confirm the association with severity and outcome of liver disease and to test the predictive power of CMR for patients listed for liver transplantation.

Prediction of coronary artery disease by a systemic atherosclerosis score index derived from whole-body MR angiography.

BACKGROUND: Whole-body magnetic resonance angiography (WB-MRA) has shown its potential for the non-invasive assessment of nearly the entire arterial vasculature within one examination. Since the presence of extra-cardiac atherosclerosis is associated with an increased risk of coronary events, our goal was to establish the relationship between WB-MRA findings, including a systemic atherosclerosis score index, and the presence of significant coronary artery disease (CAD). METHODS: WB-MRA was performed on a 1.5T scanner in 50 patients scheduled to undergo elective cardiac catheterization for suspected CAD. In each patient, 40 extra-cardiac vessel segments were evaluated and assigned scores according to their luminal narrowing. The atherosclerosis score index (ASI) was generated as the ratio of summed scores to analyzable segments. RESULTS: ASI was higher in patients with significant (> 50% stenosis) CAD (n = 27) vs. patients without CAD (n = 22; 1.56 vs. 1.28, p = 0.004). ASI correlated with PROCAM (R = 0.57, p < 0.001) and Framingham (R = 0.36, p = 0.01) risk scores as estimates of the 10-year risk of coronary events. A ROC derived ASI of > 1.54 predicted significant CAD with a sensitivity of 59%, specificity of 86% and a positive predictive value of 84%. Logistic regression revealed ASI > 1.54 as the strongest independent predictor for CAD with a 11-fold increase in likelihood to suffer from significant coronary disease. On the contrary, while 15/27 (55%) of patients with CAD exhibited at least one extra-cardiac stenosis > 50%, only 3/22 (14%) of those patients without CAD did (p = 0.003). The likelihood for an extra-cardiac stenosis when CAD is present differed between vascular territories and ranged from 15% for a carotid stenosis to 44% for a stenosis in the lower extremities. CONCLUSION: This study provides important new evidence for the close association of extra-cardiac and coronary atherosclerosis. The novel findings that a WB-MRA derived systemic atherosclerosis score index is not only associated with established cardiovascular risk scores but is also predictive of significant CAD suggest its potential prognostic implications and underline the importance to screen for coronary disease in patients with extra-cardiac manifestations of atherosclerosis.

Tirofiban optimizes platelet inhibition for immediate percutaneous coronary intervention in high-risk acute coronary syndromes.

It was the aim of this study to compare the efficacy of early platelet inhibition by 600 mg clopidogrel and acetylsalicylic acid (ASA) to a triple therapy including a glycoprotein IIb-IIIa receptor blocker. Immediate percutaneous coronary intervention (PCI) is recommended for high-risk acute coronary syndromes. In this setting the efficacy of platelet inhibition is unknown. One hundred patients were randomized to receive ASA and 600 mg clopidogrel, or additional open-label tirofiban (bolus of 10 microg/kg body weight followed by continued infusion of 0.15 microg/kg body weight per minute) as soon as non-ST-segment elevation myocardial infarction was diagnosed. The primary endpoint was the reduction of infarct size determined by post-interventional increases of cardiac troponin T (cTnT). Secondary endpoints included platelet function measured by optical and impedance aggregometry using ADP (5 and 20 microM) and collagen (1 microg/ml) as platelet agonists. Tirofiban maximized platelet inhibition (p < 0.0001) immediately and was associated with significantly lower post-interventional cTnT concentrations (p = 0.0352). In the dual platelet inhibition arm, clopidogrel was not effective in 69% of patients at the time of coronary intervention, and still in 47%, if pre-treatment time was >120 minutes. The frequency of cardiovascular (death, myocardial infarction, revascularization) and bleeding events was comparable. Platelet aggregation is not adequately inhibited in cTnT-positive patients in the setting of immediate PCI with very short pre-treatment times. Only tirofiban provided consistent and effective inhibition of platelet aggregation at the time of immediate or very early invasive therapy.

Adverse events in families with hypertrophic or dilated cardiomyopathy and mutations in the MYBPC3 gene.

BACKGROUND: Mutations in MYBPC3 encoding myosin binding protein C belong to the most frequent causes of hypertrophic cardiomyopathy (HCM) and may also lead to dilated cardiomyopathy (DCM). MYBPC3 mutations initially were considered to cause a benign form of HCM. The aim of this study was to examine the clinical outcome of patients and their relatives with 18 different MYBPC3 mutations. METHODS: 87 patients with HCM and 71 patients with DCM were screened for MYBPC3 mutations by denaturing gradient gel electrophoresis and sequencing. Close relatives of mutation carriers were genotyped for the respective mutation. Relatives with mutation were then evaluated by echocardiography and magnetic resonance imaging. A detailed family history regarding adverse clinical events was recorded. RESULTS: In 16 HCM (18.4%) and two DCM (2.8%) index patients a mutation was detected. Seven mutations were novel. Mutation carriers exhibited no additional mutations in genes MYH7, TNNT2, TNNI3, ACTC and TPM1. Including relatives of twelve families, a total number of 42 mutation carriers was identified of which eleven (26.2%) had at least one adverse event. Considering the twelve families and six single patients with mutations, 45 individuals with cardiomyopathy and nine with borderline phenotype were identified. Among the 45 patients, 23 (51.1%) suffered from an adverse event. In eleven patients of seven families an unexplained sudden death was reported at the age between 13 and 67 years. Stroke or a transient ischemic attack occurred in six patients of five families. At least one adverse event occurred in eleven of twelve families. CONCLUSION: MYBPC3 mutations can be associated with cardiac events such as progressive heart failure, stroke and sudden death even at younger age. Therefore, patients with MYBPC3 mutations require thorough clinical risk assessment.

Xanthine oxidoreductase inhibition causes reverse remodeling in rats with dilated cardiomyopathy.

Increased reactive oxygen species (ROS) generation is implicated in cardiac remodeling in heart failure (HF). As xanthine oxidoreductase (XOR) is 1 of the major sources of ROS, we tested whether XOR inhibition could improve cardiac performance and induce reverse remodeling in a model of established HF, the spontaneously hypertensive/HF (SHHF) rat. We randomized Wistar Kyoto (WKY, controls, 18 to 21 months) and SHHF (19 to 21 months) rats to oxypurinol (1 mmol/L; n=4 and n=15, respectively) or placebo (n=3 and n=10, respectively) orally for 4 weeks. At baseline, SHHF rats had decreased fractional shortening (FS) (31+/-3% versus 67+/-3% in WKY, P<0.0001) and increased left-ventricular (LV) end-diastolic dimension (9.7+/-0.2 mm versus 7.0+/-0.4 mm in WKY, P<0.0001). Whereas placebo and oxypurinol did not change cardiac architecture in WKY, oxypurinol attenuated decreased FS and elevated LV end-diastolic dimension, LV end-systolic dimension, and LV mass in SHHF. Increased myocyte width in SHHF was reduced by oxypurinol. Additionally, fetal gene activation, altered calcium cycling proteins, and upregulated phospho-extracellular signal-regulated kinase were restored toward normal by oxypurinol (P<0.05 versus placebo-SHHF). Importantly, SHHF rats exhibited increased XOR mRNA expression and activity, and oxypurinol treatment reduced XOR activity and superoxide production toward normal, but not expression. On the other hand, NADPH oxidase activity remained unchanged, despite elevated subunit protein abundance in treated and untreated SHHF rats. Together these data demonstrate that chronic XOR inhibition restores cardiac structure and function and offsets alterations in fetal gene expression/Ca2+ handling pathways, supporting the idea that inhibiting XOR-derived oxidative stress substantially improves the HF phenotype.

Aging impairs the beneficial effect of granulocyte colony-stimulating factor and stem cell factor on post-myocardial infarction remodeling.

Granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) are potential new therapies to ameliorate post-myocardial infarction (post-MI) remodeling, as they enhance endogenous cardiac repair mechanisms and decrease cardiomyocyte apoptosis. Because both of these pathways undergo alterations with increasing age, we hypothesized that therapeutic efficacy of G-CSF and SCF is impaired in old versus young adult rats. MI was induced in 6- and 20-month-old rats by permanent ligation of the left coronary artery. In young animals, G-CSF/SCF therapy stabilized and reversed a decline in cardiac function, attenuated left ventricular dilation, decreased infarct size, and reduced cardiomyocyte hypertrophy. Remarkably, these effects on cardiac structure and function were absent in aged rodents. This could not be attributed to ineffective mobilization of bone marrow cells or decreased quantity of c-Kit(+) cells within the myocardium with aging. However, whereas the G-CSF/SCF cocktail reduced cardiac myocyte apoptosis in old as well as in young hearts, the degree of reduction was substantially less with age and the rate of cardiomyocyte apoptosis in old animals remained high despite cytokine treatment. These findings demonstrate that G-CSF/SCF lacks therapeutic efficacy in old animals by failing to offset periinfarct apoptosis and therefore raise important concerns regarding the efficacy of novel cytokine therapies in elderly individuals at greatest risk for adverse consequences of MI.

Very early cardiac magnetic resonance imaging for quantification of myocardial tissue perfusion in patients receiving tirofiban before percutaneous coronary intervention for ST-elevation myocardial infarction.

BACKGROUND: Assessment of myocardial blood flow is important for identification and monitoring of microvascular effects of glycoprotein IIb/IIIa inhibitors. Magnetic resonance imaging is a novel noninvasive method providing complementary information on myocardial blood flow and cardiac function. METHODS AND RESULTS: Patients (n = 53) admitted within 12 (mean, 5.8) hours after onset of symptoms were randomized to tirofiban or standard therapy before primary percutaneous coronary intervention (PCI) with stenting. Myocardial blood flow was graded by measurement of corrected Thrombolysis in Myocardial Infarction frame counts and by semiquantitative analysis of signal intensity curves from first-pass contrast-enhanced magnetic resonance perfusion. Pretreatment with tirofiban proved safe and resulted in a significantly lower corrected Thrombolysis in Myocardial Infarction frame counts (21 vs 34, P = .008) indicating improved myocardial blood flow. Magnetic resonance imaging revealed higher normalized peak signal intensities (2.19 vs 1.63, P = .046) and a trend to steeper upslopes (0.79 vs 0.48, P = .1). Cardiac left ventricular wall motion analysis resulted in a significantly lower number of myocardial segments with abnormal wall thickening (6.4 vs 8.5, P = .025). CONCLUSIONS: Pretreatment with tirofiban appears safe and improves myocardial flow after primary PCI with stenting. Magnetic resonance imaging proved useful as a complementary method for noninvasive assessment of myocardial blood flow and cardiac function in patients with ST-segment elevation myocardial infarction undergoing primary PCI.

Assessment of myocardial deformation with cardiac magnetic resonance strain imaging improves risk stratification in patients with dilated cardiomyopathy.

AIMS: To investigate the prognostic impact of left-ventricular (LV) cardiac magnetic resonance (CMR) deformation imaging in patients with non-ischaemic dilated cardiomyopathy (DCM) compared with late-gadolinium enhancement (LGE) quantification and LV ejection fraction (EF). METHODS AND RESULTS: A total of 210 subjects with DCM were examined prospectively with standard CMR including measurement of LGE for quantification of myocardial fibrosis and feature tracking strain imaging for assessment of LV deformation. The predefined primary endpoint, a combination of cardiac death, heart transplantation, and aborted sudden cardiac death, occurred in 26 subjects during the median follow-up period of 5.3 years. LV radial, circumferential, and longitudinal strains were significantly associated with outcome. Using separate multivariate analysis models, global longitudinal strain (average of peak negative strain values) and mean longitudinal strain (negative peak of the mean curve of all segments) were independent prognostic parameters surpassing the value of global and mean LV radial and circumferential strain, as well as NT-proBNP, EF, and LGE mass. A global longitudinal strain greater than -12.5% predicted outcome even in patients with EF < 35% (P < 0.01) and in those with presence of LGE (P < 0.001). Mean longitudinal strain was further investigated using a clinical model with predefined cut-offs (EF < 35%, presence of LGE, NYHA class, mean longitudinal strain greater than -10%). Mean longitudinal strain exhibited an independent prognostic value surpassing that provided by NYHA, EF, and LGE (HR = 5.4, P < 0.01). CONCLUSION: LV longitudinal strain assessed with CMR is an independent predictor of survival in DCM and offers incremental information for risk stratification beyond clinical parameters, biomarker, and standard CMR.

Comparison of different types of cardiac amyloidosis by cardiac magnetic resonance imaging.

OBJECTIVES: We sought to determine cardiac morphological and functional differences between light-chain (AL), mutant-type transthyretin (ATTRmt) and wild-type TTR (ATTRwt) amyloidosis using contrast-enhancement cardiac magnetic resonance imaging (CE-CMR). Finally, we attempted to establish the diagnostic and prognostic impact of these findings. INTRODUCTION: The most common forms of cardiac amyloid are AL and ATTR amyloidosis, but the clinical courses of these variants are quite heterogeneous. While CE-CMR is used to evaluate patients with cardiac amyloidosis, its ability to predict prognosis in these patients is debatable. METHODS: About 130 patients with cardiac amyloidosis (AL, n = 62; ATTRmt, n = 30, ATTRwt, n = 33) were assessed by CE-CMR (cardiac morphology, cardiac function, late gadolinium enhancement). RESULTS: Left ventricular (LV) mass, basal and mid-ventricular maximal wall thickness, and thickness of the inter-atrial septum were higher in ATTRwt when compared to AL and ATTRmt amyloidosis. Tricuspid annular excursion was lower in ATTRwt amyloidosis than in AL amyloidosis. CE was observed in 94.6% of the patients (AL 80.6%; ATTRmt 90%; ATTRwt 87.9%) with significant differences in quality and intensity between the groups. Differentiation of amyloid types was achieved by combination of age, number of organs, the presence of inferolateral CE-CMR, thickness of inter-atrial septum and troponin T. Overall 1-year-survival rates were 93.3, 93.9 and 70.5% in ATTRwt, ATTRmt and AL amyloidosis, respectively. LV mass, mitral annular excursion and NT-proBNP in AL amyloidosis, LV mass maximal apical wall thickness and troponin T in ATTRwt amyloidosis, and finally NT-proBNP and renal function in ATTRmt amyloidosis were independent predictors of outcome. CONCLUSIONS: This study demonstrates that CE-CMR can highlight morphological and functional differences between different types of cardiac amyloidosis. In addition, CE-CMR and cardiac biomarkers provide useful prognostic information in patients with cardiac amyloidosis.

Admission troponin T, advanced age and male gender identify patients with improved myocardial tissue perfusion after abciximab administration for ST-segment elevation myocardial infarction.

The aim was to investigate the effect of abciximab on microvascular perfusion in different subgroups of patients undergoing direct PCI for acute STEMI. We enrolled 145 consecutive patients with TIMI grade 3 flow after direct PCI for acute STEMI. The GPIIb/IIIa inhibitor abciximab was administered in 57 patients (39.3%). Myocardial perfusion was the primary outcome measure and was assessed by analysis of cardiac troponin T wash-out. Treatment effects on myocardial perfusion and clinical outcome were tested for predefined subgroups including patients with an admission cTnT > or = 0.1 microg/L, diabetes mellitus, male gender, age > 70 years, and time from symptom onset to reperfusion > 6 hours. A significant improvement of cTnT wash-out was seen in patients with an admission cTnT > or = 0.1 microg/L, in males and in older patients. Improved tissue level reperfusion did not translate into a significant reduction of cardiac mortality or the incidence of the combined endpoint consisting of cardiac death, nonfatal reinfarction and need for target vessel revascularisation during 30 day- and long-term follow-up (mean 274 days). In conclusion, adjunctive administration of abciximab improves myocardial perfusion in patients with normal epicardial flow after direct PCI, particularly in patients with an cTnT > or = 0.1 microg/L on admission, age over 70 years and male gender.

Late gadolinium enhancement assessed by cardiac magnetic resonance imaging in heart transplant recipients with different stages of cardiac allograft vasculopathy.

AIMS: Cardiac allograft vasculopathy (CAV), which limits long-term survival after heart transplantation (HTX), is usually evaluated by coronary angiography (CA). Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) is a non-invasive technique that can detect CAV-related myocardial infarctions. We aimed to investigate the presence of LGE infarct-typical patterns in a large sample of HTX recipients and to correlate these findings with the severity of CAV assessed by CA. METHODS AND RESULTS: LGE-CMR was performed in 132 HTX patients on a 1.5-T MRI scanner (Philips, Best, the Netherlands). Infarct-typical LGE areas were identified as bright lesions with subendocardial involvement. Infarct-atypical LGE was classified as follows: (i) right ventricle (RV) insertion, (ii) intramural, (iii) epicardial, and (iv) diffuse. CA was performed for the assessment of CAV (CAV0 = no lesion, CAV1 = mild lesions, CAV2 = moderate lesions, CAV3 = severe lesions, or mild/moderate lesions with allograft dysfunction). Infarct-typical LGE patterns were detected in 29 (22%) patients distributed in all groups and they were already present in nearly every fifth CAV0 patient, increasing significantly among CAV groups (CAV0 = 19%, CAV1 = 10%, CAV2 = 36%, and CAV3 = 71%; P < 0.01). CONCLUSION: LGE-CMR was useful to identify myocardial scar possibly related to early CAV in a significant proportion of HTX recipients, otherwise classified as low-risk patients based on CA. Therefore, LGE-CMR could be helpful to intensify CAV monitoring, medical therapy, and clinical risk stratification.

Clinical feasibility study for detection of myocardial oedema by a cine SSFP sequence in comparison to a conventional T2-weighted sequence.

BACKGROUND: Cardiovascular magnetic resonance (CMR) T2-imaging is oedema-sensitive and can detect increased myocardial water content to potentially distinguish acute from chronic myocardial infarction (AMI/CMI). Currently applied conventional black-blood T2-weighted-turbo-spin-echo (T2-BB-TSE)-sequences cause various artefacts which limit their image quality and possibly hamper their interpretation. Image contrast of conventional cine steady-state free precession (SSFP)-sequences partly consists of T2 oedema-sensitive information. We therefore sought to prospectively evaluate SSFP cine-imaging to detect myocardial oedema and differentiate AMI from CMI. METHODS: We examined 60 patients with AMI, 30 patients with CMI and 30 healthy volunteers using a 1.5 Tesla-MR whole body scanner. In a blinded fashion, myocardial oedema was assessed with T2-BB-TSE and SSFP-sequences, late gadolinium contrast-enhanced (LGE) CMR images being deemed as the standard reference for identification of infarcted myocardium. Assessment of presence of CMR detectable myocardial oedema was performed visually and quantitatively. P < 0.05 was considered statistically significant. RESULTS: The contrast-to-noise ratio (CNR) in AMI patients was significantly higher (SSFP-STEMI and SSFP-NSTEMI: 19 ± 12 and 20 ± 14; T2-BB-TSE STEMI and T2-BB-TSE-NSTEMI: 33 ± 16 and 31 ± 13) than in CMI for both MR-sequences (SSFP-STEMI and NSTEMI: 3.5 ± 1.5 and T2-BB-TSE:9.3 ± 9.6, p for all <0.001). By visual analysis, SSFP images achieved a sensitivity of 96%, a specificity of 87%, positive and negative predictive values of 95 and 92% when compared to the existence of gadolinium contrast-enhanced scar imaging. Similarly, for T2-BB-TSE, sensitivity and specificity were 93 and 83% with positive and negative predictive values of 92 and 90%. Inter-observer variability was 0.90 for SSFP and 0.83 for T2-BB-TSE images. CONCLUSION: A standard clinical SSFP sequence is not inferior to T2-BB-TSE for the detection of myocardial oedema and can be used to reliably distinguish AMI from CMI. Especially in patients with insufficient T2-BB-TSE image quality, the SSFP sequence may be an alternative for the detection of myocardial oedema.

Green tea halts progression of cardiac transthyretin amyloidosis: an observational report.

BACKGROUND: Treatment options in patients with amyloidotic transthyretin (ATTR) cardiomyopathy are limited. Epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea (GT), inhibits fibril formation from several amyloidogenic proteins in vitro. Thus, it might also halt progression of TTR amyloidosis. This is a single-center observational report on the effects of GT consumption in patients with ATTR cardiomopathy. METHODS: 19 patients with ATTR cardiomyopathy were evaluated by standard blood tests, echocardiography, and cardiac MRI (n = 9) before and after consumption of GT and/or green tea extracts (GTE) for 12 months. RESULTS: Five patients were not followed up for reasons of death (n = 2), discontinuation of GT/GTE consumption (n = 2), and heart transplantation (n = 1). After 12 months no increase of left ventricular (LV) wall thickness and LV myocardial mass was observed by echocardiography. In the subgroup of patients evaluated by cardiac MRI a mean decrease of LV myocardial mass (-12.5 %) was detected in all patients. This was accompanied by an increase of mean mitral annular systolic velocity of 9 % in all 14 patients. Total cholesterol (191.9 ± 8.9 vs. 172.7 ± 9.4 mg/dL; p < 0.01) and LDL cholesterol (105.8 ± 7.6 vs. 89.5 ± 8.0 mg/dL; p < 0.01) decreased significantly during the observational period. No serious adverse effects were reported by any of the participants. CONCLUSIONS: Our observation suggests an inhibitory effect of GT and/or GTE on the progression of cardiac amyloidosis. We propose a randomized placebo-controlled investigation to confirm our observation.

Image quality and radiation dose in 256-slice cardiac computed tomography: comparison of prospective versus retrospective image acquisition protocols.

PURPOSE: To assess coronary artery image quality and patient radiation exposure in patients who underwent clinically indicated 256-slice CTA. METHODS: Consecutive patients (n=193) underwent 256-slice CTA, using (1) retrospective gating without radiation dose modulation, (2) retrospective gating with radiation dose modulation and (3) prospective gating. Image quality was determined by consensus of two experienced observers using a 5-grade scale. The effective dose was calculated. RESULTS: In all patients, CTA was performed without adverse events. Retrospective CTA was assessed in 39 patients with and 39 without dose modulation, while 115 patients underwent prospective CTA. Heart rate was related to image quality with all protocols (r=0.46, p<0.001). Up to a heart rate of 75 bpm no significant difference in overall image quality was observed for all three protocols, while no significant differences could be observed between retrospective CTA with and without dose modulation for any segments or heart rates. Prospective and retrospective CTA with dose modulation showed radiation savings of ∼75 % and ∼30 %, respectively compared to retrospective CTA without dose modulation (p<0.001). CONCLUSIONS: In patients with heart rates up to 75 bpm prospective CTA should be the first choice acquisition protocol. For heart rates >75 bpm, retrospective CTA with dose modulation should be considered.

Determinants of troponin release in patients with stable coronary artery disease: insights from CT angiography characteristics of atherosclerotic plaque.

OBJECTIVE: To understand the determinants of troponin release in patients with stable coronary artery disease (CAD) by comparing high sensitive troponin T (hsTnT) levels with computed tomography angiography (CTA) characteristics of atherosclerotic plaque. METHODS: hsTnT was determined in 124 consecutive patients with stable angina, who underwent clinically indicated 256-slice CTA for suspected CAD. CTA was used to assess (1) coronary calcification; (2) stenosis severity; (3) non-calcified plaque volume; (4) plaque composition (soft or mixed, described as 'non-calcified' versus calcified) and (5) the presence of vascular remodeling in areas of non-calcified plaque. RESULTS: All CT scans were performed without adverse events, and diagnostic image quality was achieved in 1830/1848 available coronary segments (99.0%). In 29/124 patients, hsTnT was ≥14 pg/ml (range 14.0-34.4). Weak, albeit significant, correlations were found between hsTnT and calcium scoring (r=0.45, p<0.001), while a stronger correlation was found between hsTnT and the total non-calcified plaque burden (r=0.79, p<0.001). Patients with non-calcified plaque (n=44) yielded significantly higher hsTnT values than those with normal vessels (n=46) or those with only calcified lesions (n=26), (12.6 ± 5.2 vs 8.3 ± 2.6 and 8.8 ± 3.0 pg/ml, respectively, p<0.001). Furthermore, those with remodeled non-calcified plaque (n=8) showed even higher hsTnT values of 26.3 ± 6.5 pg/ml than all other groups (p<0.001). This allowed the identification of patients with remodeled non-calcified plaque by hsTnT with high accuracy (area under the curve=0.90, SE=0.07, 95% CI 0.84 to 0.95). CONCLUSIONS: Chronic clinically silent rupture of non-calcified plaque with subsequent microembolisation may be a potential source of troponin elevation. In light of recent imaging studies, in which patients with positively remodeled non-calcified plaque were shown to be at high risk for developing acute coronary syndromes, hsTnT may serve as a biomarker for such 'vulnerable' coronary lesions even in presumably stable CAD.