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113. Relationship between obstructive coronary artery disease and abnormal stress testing in patients with paroxysmal or persistent atrial fibrillation.

Author

Nucifora G, Schuijf JD, van Werkhoven JM, Trines SA, Kajander S, Tops LF, Turta O, Jukema JW, Schreur JH, Heijenbrok MW, Gaemperli O, Kaufmann PA, Knuuti J, van der Wall EE, Schalij MJ, Bax JJ, Nucifora, Gaetano, Schuijf, Joanne D, van Werkhoven, Jacob M, and Trines, Serge A

Abstract

Atrial fibrillation (AF) has been linked to the presence of underlying coronary artery disease (CAD). However, whether the higher burden of CAD observed in AF patients translates into higher burden of myocardial ischemia is unknown. In 87 patients (71% male, mean age 61 ± 10 years) with paroxysmal or persistent AF and without history of CAD, MSCT coronary angiography and stress testing (exercise ECG test or myocardial perfusion imaging) were performed. CAD was classified as obstructive (≥50% luminal narrowing) or not. Stress tests were classified as normal or abnormal. A population of 122 patients without history of AF, similar to the AF group as to age, gender, symptomatic status and pre-test likelihood, served as a control group. Based on MSCT, 17% of AF patients were classified as having no CAD, whereas 43% showed non-obstructive CAD and the remaining 40% had obstructive CAD. A positive stress test was observed in 49% of AF patients with obstructive CAD. Among non-AF patients, 34% were classified as having no CAD, while 41% showed non-obstructive CAD and 25% had obstructive CAD (P = 0.013 compared to AF patients). A positive stress test was observed in 48% of non-AF patients with obstructive CAD. In conclusion, the higher burden of CAD observed in AF patients is not associated to higher burden of myocardial ischemia. [ABSTRACT FROM AUTHOR]

Published
2011
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118. MDS1/EVI1 enhances TGF-beta1 signaling and strengthens its growth-inhibitory effect but the leukemia-associated fusion protein AML1/MDS1/EVI1, product of the t(3;21), abrogates growth-inhibition in response to TGF-beta1.

Author

Sood, R, Talwar-Trikha, A, Chakrabarti, S R, and Nucifora, G

Subjects
CELL differentiation, CELL division, CELLULAR signal transduction, CHROMOSOME abnormalities, CHROMOSOMES, COMPARATIVE studies, GENES, GRANULOCYTES, GROWTH factors, RESEARCH methodology, MEDICAL cooperation, PROTEINS, RECOMBINANT proteins, RESEARCH, TRANSCRIPTION factors, DNA-binding proteins, EVALUATION research
Abstract

MDS1/EVI1, located on chromosome 3 band q26, encodes a zinc-finger DNA-binding transcription activator not detected in normal hematopoietic cells but expressed in several normal tissues. MDS1/EVI1 is inappropriately activated in myeloid leukemias following chromosomal rearrangements involving band 3q26. The rearrangements lead either to gene truncation, and to expression of the transcription repressor EVI1, as seen in the t(3;3)(q21;q26) and inv(3)(q21q26), or to gene fusion, as seen in the t(3;21)(q26;q22) which results in the fusion protein AML1/MDS1/EVI1. This fusion protein contains the DNA-binding domain of the transcription factor AML1 fused in-frame to the entire MDS1/EVI1 with the exclusion of its first 12 amino acids. In this report, we have analyzed the response of the hematopoietic precursor cell line 32Dcl3, expressing either the normal protein MDS1/EVI1 or the fusion protein AML1/MDS1/EVI1, to factors that control cell differentiation or cell replication. The 32Dcl3 cells are IL-3-dependent for growth and they differentiate into granulocytes when exposed to G-CSF. They are growth-inhibited by TGF-beta1. We show that whereas the expression of MDS1/EVI1 has no effect on granulocytic differentiation induced by G-CSF, expression of AML1/MDS1/EVI1 blocks differentiation resulting in cell death. This effect is similar to that previously described by others for 32Dcl3 cells that express transgenic Evil. Furthermore, we show that whereas the expression of the fusion protein AML1/MDS1/EVI1 completely abrogates the growth-inhibitory effect of TGF-beta1 and allows 32Dcl3 cells to proliferate, expression of the normal protein MDS1/EVI1 has the opposite effect, and it strengthens the response of cells to the growth-inhibitory effect of TGF-beta1. By using the yeast two-hybrid system, we also show that EVI1 (contained in its entirety in MDS1/EVI1 and AML1/MDS1/EVI1) physically interacts with SMAD3, which is an intracellular mediator of TGF-beta1 signaling. Finally, we have correlated the response of the cells to G-CSF or TGF-beta1 with the ability of the normal and fusion proteins to activate or repress promoters which they can directly regulate by binding to the promoter site. We propose that mutations of MDS1/EVI1 either by gene truncation resulting in the transcription repressor EVI1 or by gene fusion to AML1 lead to an altered cellular response to growth and differentiation factors that could result in leukemic transformation. The different response of myeloid cells ectopically expressing the normal or the fusion protein to G-CSF and TGF-beta1 could depend on the different transactivation properties of these proteins resulting in divergent expression of downstream genes regulated by the two proteins. [ABSTRACT FROM AUTHOR]

Published
1999
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119. REARRANGEMENTS OF THE AML1ICBFA2 GENE IN MYELOID LEUKEMIA WITH THE 3;21 TRANSLOCATION: IN VITRO AND IN VIVO STUDIES.

Author

Zent, C., Rowley, J. D., and Nucifora, G.

Subjects
CHROMOSOMAL translocation, ONCOGENES, ACUTE myeloid leukemia, DNA-binding proteins, DNA topoisomerase II, RIBOSOMES, GENETICS
Abstract

A ML1 is involved at the breakpoint of chromosome 21 band q22 in several recurring chromosomal translocations associated with myeloid and lymphoid leukemias. AML1 corresponds to CBFA2, and encodes one of the DNA-binding subunits of the enhancer core binding factor CBF. Other members of this family of DNA-binding proteins are CBFA1 and CBFA3, also known as AML3 and AML2. The three proteins are characterized by a highly conserved domain (runt domain, >90% homology) at the amino end that is necessary for DNA-binding and protein dimerization, and by a unique domain at the carboxyl end that is necessary for transactivation. Two recurring chromosomal translocations involving AML1 associated with myeloid leukemias are the t(8;21)(q22;q22), seen in 20% of patients with acute myeloid leukemia (AML) M2, and the t(3;21)(q26; q22), that occurs in myeloid leukemias primarily following treatment with topoisomerase II inhibitors. In five patients with a t(3;21) whom we studied, AML1 is interrupted by the translocation breakpoint between the runt domain and the transactivation domain, and is fused to two genes on chromosome band 3q26: EAP, which encodes the ribosomal protein L22, and MDS1, which encodes a small polypeptide of unknown function. In one of the five patients we studied, a fusion with a third gene EVI1 also occurs. The fusion of EAP to AML1 is not in frame, and leads to a protein that is terminated shortly after the fusion junction by introduction of a stop codon. The fusion of AML1 to MDS1 is in frame, and adds 127 codons to the interrupted AML1. Thus, in the five cases that we studied, the 3;21 translocation results in expression of two coexisting chimeric mRNAs which contain the identical runt domain at the 5' region, but differ in the 3' region. In addition, the chimeric junction AML1/MDS1/EVI1 has been detected in ceils from one of our patients with the 3;21 translocation. Several genes necessary for myeloid lineage differentiation contain the target sequence for AMLI in their regulatory regions. We have compared the normal AML1 to AML1/MDS1 and AML1/EAP as transcriptional regulators of the CSF1 R promoter which contains the CBF target sequence. Our results indicate that whereas the normal AML1 can activate the promoter, the chimeric proteins compete with the normal AML1 and repress expression from the CSF1 R promoter. To determine the role of the chimeric proteins in cell growth, we expressed their cDNA in rat fibroblasts. When either fusion gene is expressed, the cells lose contact inhibition and form foci over the monolayer. However. only cells expressing AML1/MDS1 grow as large tumors in nude mice. Thus, although both chimeric genes have similar effects in transactivation of the CSF1 R promoter, they affect cell growth as tumor promoters differently in vivo. [ABSTRACT FROM AUTHOR]

Published
1997

120. Interaction of EVI1 with cAMP-responsive element-binding protein-binding protein (CBP) and p300/CBP-associated factor (P/CAF) results in reversible acetylation of EVI1 and in co-localization in nuclear speckles.

Author

Chakraborty, S, Senyuk, V, Sitailo, S, Chi, Y, and Nucifora, G

Abstract

EVI1 is a very complex protein with two domains of zinc fingers and is inappropriately expressed in many types of human myeloid leukemias. Using reporter gene assays, several investigators showed that EVI1 is a transcription repressor, and recently it was shown that EVI1 interacts with the co-repressor carboxyl-terminal binding protein 1 (CtBP1). Earlier, we showed that the inappropriate expression of EVI1 in murine hematopoietic precursor cells leads to their abnormal differentiation and to increased proliferation. Using biochemical assays, we have identified two groups of transcription co-regulators that associate with EVI1 presumably to regulate gene expression. One group of co-regulators includes the CtBP1 and histone deacetylase. The second group includes the two co-activators cAMP-responsive element-binding protein-binding protein (CBP) and p300/CBP-associated factor (P/CAF), both of which have histone acetyltransferase (HAT) activity. All of these proteins require separate regions of EVI1 for efficient interaction, and they divergently affect the ability of EVI1 to regulate gene transcription in reporter gene assays. Confocal microscopy analysis shows that in the majority of the cells, EVI1 is nuclear and diffused, whereas in about 10% of the cells EVI1 localizes in nuclear speckles. However, in the presence of the added exogenous co-repressors histone deacetylase or CtBP1, all of the nuclei have a diffuse EVI1 staining, and the proteins do not appear to reside together in obvious nuclear structures. In contrast, when CBP or P/CAF are added, defined speckled bodies appear in the nucleus. Analysis of the staining pattern indicates that EVI1 and CBP or EVI1 and P/CAF are contained within these structures. These nuclear structures are not observed when CBP is substituted with a point mutant HAT-inactive CBP with which EVI1 also physically interacts. Finally, we show that the interaction of EVI1 with either CBP or P/CAF leads to acetylation of EVI1. These results suggest that the assembly of EVI1 in nuclear speckles requires the intact HAT activity of the co-activators.

Published
2001
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121. Feasibility of Diastolic Function Assessment With Cardiac CT Feasibility Study in Comparison With Tissue Doppler Imaging

Author

Boogers, M.J., Werkhoven, J.M. van, Schuijf, J.D., Delgado, V., El-Naggar, H.M., Boersma, E., Nucifora, G., Geest, R.J. van der, Paelinck, B.P., Kroft, L.J., Reiber, J.H.C., Roos, A. de, Bax, J.J., Lamb, H.J., Cardiology, and Cardiothoracic Surgery

Subjects
compute tomography diastole echocardiography imaging ventricular filling pressures spiral computed-tomography myocardial-infarction coronary-angiography ejection fraction flow velocities pulmonary vein echocardiography disease catheterization, diastole, SDG 3 - Good Health and Well-being, cardiovascular system, echocardiography, imaging, computed tomography
Abstract

OBJECTIVES This study aimed to demonstrate the feasibility of multidetector row computed tomography (CT) for assessment of diastolic function in comparison with 2-dimensional (2D) echocardiography using tissue Doppler imaging (TDI). BACKGROUND Diastolic left ventricular (LV) function plays an important role in patients with cardiovascular disease. 2D echocardiography using TDI has been used most commonly to evaluate diastolic LV function. Although the role of cardiac CT imaging for evaluation of coronary atherosclerosis has been explored extensively, its feasibility to evaluate diastolic function has not been studied. METHODS Patients who had undergone 64-multidetector row CT and 2D echocardiography with TDI were enrolled. Diastolic function was evaluated using early (E) and late (A) transmitral peak velocity (cm/s) and peak mitral septal tissue velocity (Ea; cm/s). Peak transmitral velocity (cm/s) was calculated by dividing peak diastolic transmitral flow (ml/s) by the corresponding mitral valve area (cm(2)). Mitral septal tissue velocity was calculated from changes in LV length per cardiac phase. Subsequently, the estimation of LV filling pressures (E/Ea) was determined. RESULTS Seventy patients (46 men; mean age 55 +/- 11 years) who had undergone cardiac CT and 2D echocardiography with TDI were included. Good correlations were observed between cardiac CT and 2D echocardiography for assessment of E (r = 0.73; p < 0.01), E/A (r = 0.87; p < 0.01), Ea (r = 0.82; p < 0.01), and E/Ea (r = 0.81; p < 0.01). Moreover, a good diagnostic accuracy (79%) was found for detection of diastolic dysfunction using cardiac CT. Finally, the study showed a low intraobserver and interobserver variability for assessment of diastolic function on cardiac CT. CONCLUSIONS Cardiac CT imaging showed good correlations for transmitral velocity, mitral septal tissue velocity, and estimation of LV filling pressures when compared with 2D echocardiography. Additionally, cardiac CT and 2D echocardiography were comparable for assessment of diastolic dysfunction. Accordingly, cardiac CT may provide information on diastolic dysfunction. (J Am Coll Cardiol Img 2011;4:246-56) (C) 2011 by the American College of Cardiology Foundation

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122. Blunt traumatic abdominal aortic rupture: CT imaging.

Author

Nucifora G, Hysko F, Vasciaveo A, Nucifora, Gaetano, Hysko, Fjoralba, and Vasciaveo, Annarosa

Abstract

Blunt abdominal aortic trauma is a rare but potentially lethal event. It is commonly associated with high-speed motor vehicle accidents. Intimal flap, thrombosis, and pseudoaneurysm of the abdominal aorta are the more common findings. We present a case of blunt abdominal aortic trauma in which CT disclosed free aortic rupture with intraabdominal bleeding and a huge retroperitoneal hematoma, an extremely rare finding among patients reaching the hospital alive, due to its high and immediate mortality rate. [ABSTRACT FROM AUTHOR]

Published
2008
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123. Involvement of the AML1 gene in the t(3;21) in therapy-related leukemia and in chronic myeloid leukemia in blast crisis

Author

Nucifora, G, Birn, DJ, Espinosa, R 3d, Erickson, P, LeBeau, MM, Roulston, D, McKeithan, TW, Drabkin, H, and Rowley, JD

Abstract

A nonrandom translocation between chromosomes 3 and 21, t(3;21)(q26.2;q22) has been detected in patients with a myelodysplastic syndrome or acute myeloid leukemia after treatment (t-MDS/t-AML) for a primary malignant disease and in chronic myelogenous leukemia in blast crisis (CML-BC). In these patients, the breakpoint on chromosome 21 is at band 21q22. This band is also involved in the t(8;21)(q22;q22) detected in 40% of the patients with acute myeloid leukemia subtype M2 (AML-M2) de novo who have an abnormal karyotype. In the t(8;21), the AML1 gene is the site of the breakpoint on chromosome 21. The AML1 gene is transcribed from telomere to centromere, and in the t(8;21) the 5' part of AML1 is fused to the ETO gene on chromosome 8 to produce the chimeric AML1/ETO on the der(8) chromosome. We found that AML1 is also rearranged in two t-AML patients and in one CML-BC patient with the t(3;21), but the breakpoints are approximately 40 to 60 kb downstream to those of AML-M2 patients. This region contains at least one additional exon of AML1, as determined by using an AML1 cDNA as a probe in Southern blot analysis. The t(3;21) breakpoints for the remaining patients could not be determined because, by fluorescence in situ hybridization analysis, the breaks are outside of the region covered by the available probes.

Published
1993
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124. Cadmium resistance from Staphylococcus aureus plasmid pI258 cadA gene results from a cadmium-efflux ATPase.

Author

Nucifora, G, Chu, L, Misra, T K, and Silver, S

Abstract

Cadmium resistance specified by the cadA determinant of Staphylococcus aureus plasmid pI258 results from the functioning of a cadmium-efflux system. In the nucleotide sequence of the DNA fragment containing the cadA determinant, two open reading frames were identified. The larger one, corresponding to a predicted polypeptide of 727 amino acid residues, is necessary and sufficient for expression of cadmium resistance. Comparison of the CadA amino acid sequence with known protein sequences suggested that CadA is a member of the E1E2 cation-translocating ATPases, similar to the K+-uptake ATPases of Gram-positive and Gram-negative bacteria. The sequence homology is lower but significant with other E1E2-type ATPases, including the H+-efflux ATPases of eukaryotic microbes and the Ca2+- and Na+/K+-ATPases of animals. A frame-shift mutation in the middle of the gene destroys the Cd2+-resistance phenotype. A detailed model for the putative CadA ATPase based on homologies to other E1E2 ATPases is presented and discussed.

Published
1989
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125. Mercury operon regulation by the merR gene of the organomercurial resistance system of plasmid pDU1358

Author

Nucifora, G, Chu, L, Silver, S, and Misra, T K

Abstract

The structural basis for induction of the mercury resistance operon with inorganic mercury and with the organomercurial compound phenylmercuric acetate was addressed by DNA sequencing analysis and by lac fusion transcription experiments regulated by merR in trans from broad-spectrum-resistance plasmid pDU1358 (Hg2+ and phenylmercury responding). The lac fusion results were compared with those from a narrow-spectrum-resistance (Hg2+ responding but not phenylmercuric responding) operon and the pDU1358 merR deleted at the 3' end. The nucleotide sequence of the beginning region of the broad-spectrum mer operon of plasmid pDU1358 was determined, including that of the merR gene, the operator-promoter region, the merT and merP genes, and the first 60% of the merA gene. Comparison of this sequence with DNA sequences of narrow-spectrum mer operons from transposon Tn501 and plasmid R100 showed that a major difference occurred in the 3' 29 base pairs of the merR gene, resulting in unrelated C-terminal 10 amino acids. A hybrid mer operon consisting of the merR gene from pDU1358, a hybrid merA gene (determining mercuric reductase enzyme), and lacking the merB gene (determining phenylmercury lyase activity) was inducible by both phenylmercury and inorganic Hg2+. This shows that organomercurial lyase is not needed for induction by organomercurial compounds. A mutant form of pDU1358 merR missing the C-terminal 17 amino acids responded to inorganic Hg2+ but not to phenylmercury. Thus, the C-terminal region of the MerR protein of the pDU1358 mer operon is involved in the recognition of phenylmercury.

Published
1989
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127. 553 Prognostic value of non-ischemic ring-like left ventricular scar pattern in patients with apparently idiopathic ventricular arrhythmias: a CMR imaging study.

Author

Muser, D, Santangeli, P, Castro, S, Arroyo, R Casado, Maeda, S, Benhayon, D, Liuba, I, Liang, J, Sadek, M, Chahal, A, Magnani, S, Garcia, F, Marchlinski, F, Selvanayagam, J, and Nucifora, G

Subjects
LEFT heart ventricle, HEART ventricle diseases, CONFERENCES & conventions, DIAGNOSTIC imaging, MAGNETIC resonance imaging, FIBROSIS, VENTRICULAR arrhythmia, DIAGNOSIS
Published
2019
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134. Involvement of the AML1 gene in the t(3;21) in therapy-related leukemia and in chronic myeloid leukemia in blast crisis

Author

Nucifora G, Dj, Birn, Rd, Espinosa R., Erickson P, Mm, Lebeau, Roulston D, Timothy McKeithan, Drabkin H, and Jd, Rowley

Subjects
Adult, Male, Leukemia, Base Sequence, Chromosomes, Human, Pair 21, Molecular Sequence Data, Restriction Mapping, Chromosome Mapping, DNA, Neoplasm, Middle Aged, Polymerase Chain Reaction, Translocation, Genetic, Chromosome Banding, Blotting, Southern, Chromosome Walking, Oligodeoxyribonucleotides, Karyotyping, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Myelodysplastic Syndromes, Humans, Female, Chromosomes, Human, Pair 3, Blast Crisis, Aged
Abstract

A nonrandom translocation between chromosomes 3 and 21, t(3;21)(q26.2;q22) has been detected in patients with a myelodysplastic syndrome or acute myeloid leukemia after treatment (t-MDS/t-AML) for a primary malignant disease and in chronic myelogenous leukemia in blast crisis (CML-BC). In these patients, the breakpoint on chromosome 21 is at band 21q22. This band is also involved in the t(8;21)(q22;q22) detected in 40% of the patients with acute myeloid leukemia subtype M2 (AML-M2) de novo who have an abnormal karyotype. In the t(8;21), the AML1 gene is the site of the breakpoint on chromosome 21. The AML1 gene is transcribed from telomere to centromere, and in the t(8;21) the 5' part of AML1 is fused to the ETO gene on chromosome 8 to produce the chimeric AML1/ETO on the der(8) chromosome. We found that AML1 is also rearranged in two t-AML patients and in one CML-BC patient with the t(3;21), but the breakpoints are approximately 40 to 60 kb downstream to those of AML-M2 patients. This region contains at least one additional exon of AML1, as determined by using an AML1 cDNA as a probe in Southern blot analysis. The t(3;21) breakpoints for the remaining patients could not be determined because, by fluorescence in situ hybridization analysis, the breaks are outside of the region covered by the available probes.

136. Leiomyosarcoma of the spermatic cord. Case report and review of the literature

Author

Racalbuto, A., Puleo, S., Di Cataldo, A., Scilletta, B., Giovanni Li Destri, Succi, L., Nucifora, G., Latteri, F., and Rodolico, G.

Subjects
Leiomyosarcoma, Male, Spermatic Cord, Antineoplastic Combined Chemotherapy Protocols, Genital Neoplasms, Male, Humans, Middle Aged
Abstract

An additional case of leiomyosarcoma of spermatic cord which brings the total reported number to 49, is described. The case is compared with the others and further data on histogenesis and histological behaviour of the tumor, are given. Surgical treatment and role of radiotherapy and chemotherapy, are discussed.

138. Development and validation of automated endocardial and epicardial contour detection for MRI volumetric and wall motion analysis

Author

Caiani, E. G., Redaelli, A., Parodi, O., Votta, E., Francesco Maffessanti, Tripoliti, E., Nucifora, G., Marchi, D., Tarroni, G., Lombardi, M., Corsi, C., E.G. Caiani, A. Redaelli, O. Parodi, E. Votta, F. Maffessanti, E. Tripoliti, G. Nucifora, D. De Marchi, G. Tarroni, M. Lombardi, and C. Corsi

Subjects
contour detection, LV mass, cardiac magnetic resonance
Abstract

Dynamic, ECG-gated, steady-state free precession short-axis images were obtained (GE Healthcare, 1.5T) in 8-12 slices in 15 patients with previous myocardial infarction. An expert cardiologist provided the reference values for: 1) left ventricular (LV) volumes and mass, by manually tracing endo and epicardial contours; 2) regional wall motion (WM) interpretation, by grading (normal, abnormal) three slices selected at apical, mid and basal level. Custom software based on image noise distribution and on image gradient was applied, from which end-diastolic (ED) and end-systolic (ES) volumes and mass were computed, as well as regional fractional area change (RFAC), from which automated classification of regional WM abnormality was defined. Comparison with reference values was performed by: 1) linear regression and Bland-Altman analyses for LV volumes and mass; 2) levels of agreement between the cardiologist WM grades and the automated classification. Optimal correlations (r2>;.97) and no bias were found for ED and ES volumes, while LV mass resulted in a good correlation (ED: r2 = .81; ES: r2 = .74) with a minimal overestimation (ED: 15.2g; ES: 8.7g) and narrow 95% limits of agreement (ED: ±30g; ES: ±33g). The automated interpretation resulted in high sensitivity, specificity, and accuracy (78%, 85%, 82%, respectively) of WM abnormalities. Combined automated endo and epicardial border detection from MRI images provides reliable measurements of LV dimensions and regional WM classification.

139. Poster session 3

Author

Winter, R, Lindqvist, P, Sheehan, F, Fazlinezhad, A, Vojdanparast, M, Nezafati, P, Martins Fernandes, S, Teixeira, R, Pellegrino, M, Generati, G, Bandera, F, Labate, V, Alfonzetti, E, Guazzi, M, Iriart, X, Dinet, ML, Jalal, Z, Cochet, H, Thambo, JB, Moustafa, S, Ho, TH, Shah, P, Murphy, K, Nelluri, BK, Lee, H, Wilansky, S, Mookadam, F, Stolfo, D, Tonet, E, Merlo, M, Barbati, G, Gigli, M, Pinamonti, B, Ramani, F, Zecchin, M, Sinagra, G, Bieseviciene, M, Vaskelyte, JJ, Mizariene, V, Lesauskaite, V, Verseckaite, R, Karaliute, R, Jonkaitiene, R, Patel, S, Li, L, Craft, M, Danford, D, Kutty, S, Vriz, O, Pellegrinet, M, Zito, C, Carerj, S, Di Bello, V, Cittadini, A, Bossone, E, Antonini-Canterin, F, Sarvari, S I, Rodriguez, M, Sitges, M, Sepulveda-Martinez, A, Gratacos, E, Bijnens, B, Crispi, F, Santos, M, Leite, L, Martins, R, Baptista, R, Barbosa, A, Ribeiro, N, Oliveira, A, Castro, G, Pego, M, Berezin, A, Samura, T, Kremzer, A, Stoebe, S, Tarr, A, Pfeiffer, D, Hagendorff, A, Benyounes Iglesias, N, Van Der Vynckt, C, Gout, O, Devys, JM, Cohen, A, De Chiara, B, Musca, F, D'angelo, L, Cipriani, MG, Parolini, M, Rossi, A, Santambrogio, GM, Russo, C, Giannattasio, C, Moreo, A, Soliman, A, Moharram, M, Gamal, A, Reda, A, Oni, O, Adebiyi, A, Aje, A, Ricci, F, Aquilani, R, Dipace, G, Bucciarelli, V, Bianco, F, Miniero, E, Scipioni, G, De Caterina, R, Gallina, S, Tumasyan, LR, Adamyan, KG, Chilingaryan, AL, Tunyan, LG, Kim, KH, Cho, JY, Yoon, HJ, Ahn, Y, Jeong, MH, Cho, JG, Park, JC, Popa, B A, Popa, A, Cerin, G, Ecocardiografico, Campagna Provinciale di Screening, Yiangou, K, Azina, CH, Yiangou, A, Georgiou, C, Zitti, M, Ioannides, M, Chimonides, S, Olsen, R H, Pedersen, LR, Snoer, M, Christensen, TE, Ghotbi, AA, Hasbak, P, Kjaer, A, Haugaard, SB, Prescott, E, Cacicedo, A, Velasco Del Castillo, S, Gomez Sanchez, V, Anton Ladislao, A, Onaindia Gandarias, J, Rodriguez Sanchez, I, Jimenez Melo, O, Garcia Cuenca, E, Zugazabeitia Irazabal, G, Romero Pereiro, A, Monti, L, Nardi, B, Di Giovine, G, Malanchini, G, Scardino, C, Balzarini, L, Presbitero, P, Gasparini, GL, Holte, E, Orlic, D, Tesic, M, Zamaklar-Trifunovic, D, Vujisic-Tesic, B, Borovic, M, Milasinovic, D, Zivkovic, M, Kostic, J, Belelsin, B, Ostojic, M, investigators, PATA STEMI, Trifunovic, D, Krljanac, G, Savic, L, Asanin, M, Aleksandric, S, Petrovic, M, Zlatic, N, Lasica, R, Mrdovic, I, Nucifora, G, Muser, D, Zanuttini, D, Tioni, C, Bernardi, G, Spedicato, L, Proclemer, A, Casalta, AC, Galli, E, Szymanski, C, Salaun, E, Lavoute, C, Haentjens, J, Tribouilloy, C, Mancini, J, Donal, E, Habib, G, Cavalcante, JL, Delgado-Montero, A, Dahou, A, Caballero, L, Rijal, S, Gorcsan, J, Monin, JL, Pibarot, P, Lancellotti, P, Keramida, K, Kouris, N, Kostopoulos, V, Giannaris, V, Trifou, E, Markos, L, Mihalopoulos, A, Mprempos, G, Olympios, CD, Calin, A, Mateescu, AD, Rosca, M, Beladan, CC, Enache, R, Gurzun, MM, Varga, P, Calin, C, Ginghina, C, Popescu, BA, Almeida Morais, L, Galrinho, A, Branco, L, Gomes, V, Timoteo, A T, Daniel, P, Rodrigues, I, Rosa, S, Fragata, J, Ferreira, R, Bandera, F, Generati, G, Pellegrino, M, Carbone, F, Labate, V, Alfonzetti, E, Guazzi, M, Galli, E, Leclercq, C, Samset, E, Donal, E, Kamal, H M, Oraby, MA, Eleraky, A Z, Yossuef, M A, Leite, L, Baptista, R, Teixeira, R, Ribeiro, N, Oliveira, AP, Barbosa, A, Castro, G, Martins, R, Elvas, L, Pego, M, Polte, CL, Gao, SA, Lagerstrand, KM, Johnsson, AA, Bech-Hanssen, O, Martinez Santos, P, Vilacosta, I, Batlle Lopez, E, Sanchez Sauce, B, Jimenez Valtierra, J, Espana Barrio, E, Campuzano Ruiz, R, De La Rosa Riestra, A, Alonso Bello, J, Perez Gonzalez, F, Jin, CN, Wan, S, Sun, JP, Lee, AP, Generati, G, Bandera, F, Pellegrino, M, Carbone, F, Labate, V, Alfonzetti, E, Guazzi, M, Reali, M, Cimino, S, Salatino, T, Silvetti, E, Mancone, M, Pennacchi, M, Giordano, A, Sardella, G, Agati, L, Kalcik, M, Yesin, M, Gunduz, S, Gursoy, MO, Astarcioglu, MA, Karakoyun, S, Bayam, E, Cersit, S, Ozkan, M, Cacicedo, A, Velasco Del 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Abstract

Purpose: We developed a transthoracic echo simulator that can measure psychomotor skill in echo to assist in training as well as for certification of competence. The simulator displays cine loops on a computer in response to the user scanning a mannequin with a mock transducer. The skill metric is the deviation angle between the image acquired by the user and the anatomically correct plane for the specified view. We sought to determine whether the simulator-based test could distinguish levels of expertise. Methods: Attendees at an echo course or at the annual meeting of the Swedish Heart Association were invited to take a 15 min test on the simulator. On the test, the user scanned the mannequin and acquired 4 views: parasternal long axis (pLAX) in patient 1, apical 4 chamber (a4c) and aLAX in patient 2, and pLAX in patient 3. Scan time was limited to 15 min. Attendees were asked regarding current work status, position, and experience with echo assessed from duration in years and procedure volume in the past 12 months. Results: Of the 61 participants there were 22 sonographers, 2 nurses, and 37 doctors who were all in practice except 1 doctor who was a resident. The data of nurses was combined with that of sonographers because their procedure volume was nearer to that of sonographers (850 ± 599 tests/yr) than doctors (312 ± 393, p < 0.001). Doctors and non-doctors had similar duration of experience (9 ± 8 vs. 12 ± 11 yrs, p=NS). The test was not completed by 12 participants (18%) but unfamiliarity with the simulator may have contributed because the deviation angle for pLAX dropped between the first and third patients (23 ± 11 to 18 ± 10 degrees, p<0.020). The average deviation angle over the 4 views was slightly lower for sonographers than for doctors (26 ± 11 vs. 30 ± 14 degrees, p=NS). The deviation angle for pLAX (55 ± 37 degrees) was higher than for a4C (17 ± 22 degrees) or either pLAX view (p<0.00001). pLAX was the only view whose deviation angle correlated significantly with experience and only with procedure volume (r=-0.302, p=0.025). Conclusions: The results of this study demonstrate that the skill metric employed, angle of deviation between the plane of an acquired view and the plane of the anatomically correct image for that view, can distinguish the relative experience of sonographers and doctors in practice. Simulation-based testing provides objective and quantitative assessment of the psychomotor skill of image acquisition and may be of value in certification of trainees and in maintenance of certification examination of practicing sonographers and doctors.

Published
2015
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140. Abstracts

Author

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A, Barone-Rochette, G, Pierard, S, Seldrum, S, De Meester de Ravensteen, C, Melchior, J, Maes, F, Pouleur, A-C, Vancraeynest, D, Pasquet, A, Vanoverschelde, J-L, L Gerber, B, Bekele, S, Singh, A, Khan, JN, Nazir, SA, Kanagala, P, McCann, GP, Singh, A, Steadman, CD, Bekele, S, Khan, JN, Nazir, SA, Kanagala, P, McCann, GP, Paelinck, BP, Vandendriessche, T, De Bock, D, De Maeyer, C, Parizel, PM, Christiaan, J, Trauzeddel, RF, Gelsinger, C, Butter, C, Barker, A, Markl, M, Schulz-Menger, J, von Knobelsdorff, F, Florian, A, Schäufele, T, Ludwig, A, Rösch, S, Wenzelburger, I, Yilmaz, A, Sechtem, U, López-Lereu, M.P, Bonanad, C, Monmeneu, J.V, Sanchís, J, Estornell, J, Igual, B, Maceira, A, Chorro, F.J, Focardi, M, Cameli, M, Bennati, E, Massoni, A, Solari, M, Carbone, F, Banchi, B, Mondillo, S, Miia, H, Kirsi, L, Helena, H, Tiina, H, Jyri, L, Pauli, P, Sari, K, Schumm, J, Greulich, S, Grün, S, Ong, P, Klingel, K, Kandolf, R, Sechtem, U, Mahrholdt, H, Raimondi, F, Ou, P, Boudjemline, Y, Bajolle, F, Iserin, F, Bonnet, D, Collins, J, Kalisz, K, Benefield, B, Sarnari, R, Katz, D, Bi, X, Cordts, M, Guetter, C, Jolly, M-P, Freed, B, Flukiger, J, Kansal, P, Lee, D, Shah, S, Markl, M, Carr, J, Sokolowska, B, Miszalski-Jamka, T, Szczeklik, W, Karwat, K, Miszalski-Jamka, K, Belzak, K, Mazur, W, Kereiakes, DJ, Jazwiec, P, Musial, J, Silva, G, Almeida, AG, Resende, C, Marques, JS, Silva, D, David, C, Amaro, C, Costa, P, Silva, JAP, Diogo, AN, Tsokolov, AV, Senchilo, VG, Vertelkin, AV, Hoffmann, P, Mykjåland, G, Wangberg, H, Tønnessen, T, Sjaastad, I, Nordsletten, L, Hjørnholm, U, Løset, A, Rostrup, M, Meloni, A, Gulino, L, Keilberg, P, Palazzi, G, Maddaloni, D, Ascioti, C, Missere, M, Salvatori, C, Positano, V, Lombardi, M, Pepe, A, Meloni, A, Filosa, A, Gulino, L, Pulini, S, Salvatori, C, Chiodi, E, Ascioti, C, Keilberg, P, Positano, V, Lombardi, M, Pepe, A, Meloni, A, Gulino, L, Pietrapertosa, A, Izzi, G, De Marchi, D, Valeri, G, Preziosi, P, Positano, V, Lombardi, M, Pepe, A, Meloni, A, Ruffo, GB, Keilberg, P, Gulino, L, Gerardi, C, Sallustio, G, Tudisca, C, Positano, V, Lombardi, M, Pepe, A, Greulich, S, Backes, M, Schumm, J, Grün, S, Sechtem, U, Mahrholdt, H, Dorniak, K, MSc, AS, Szurowska, E, Fijalkowski, M, Rawicz-Zegrzda, D, Dudziak, M, Raczak, G, Hamdan, A, Baker, FA, Klein, M, Di Segni, E, Goitein, O, Fibisch, G, Konen, E, Müller-Bierl, B, Tanaka, K, Buls, N, Fierens, Y, van Cauteren, T, Willekens, I, van Laere, S, Luypaert, R, de Mey, J, Muzzarelli, S, Faragasso, E, Pedrazzini, G, Sürder, D, Pasotti, E, Moccetti, T, Faletra, F, Qayyum, AA, Hasbak, P, Larsson, HB, Mathiasen, AB, Vejlstrup, NG, Kjaer, A, Kastrup, J, Moschetti, K, Favre, D, Pinget, C, Pilz, G, Petersen, S, Wagner, A, Wasserfallen, JB, Schwitter, J, Ghosh Dastidar, A, Cengarle, M, McAlindon, E, Augustine, D, Nightingale, AK, Bucciarelli-Ducci, C, Dandekar, VK, Ertel, AW, Dickens, C, Gonzalez, RC, Farzaneh-Far, A, Ripley, DP, Higgins, D, McDiarmid, AK, Bainbridge, GJ, Uddin, A, Kidambi, A, Herzog, B, Greenwood, JP, Plein, S, Khanji, M, Newton, T, Westwood, M, Sekhri, N, and Petersen, SE

Abstract

Background-Aims: Early post-infarction pericardial injury is a common finding but its diagnosis remains elusive. Though C-reactive protein (CRP) is considered a marker of myocardial damage, reflecting myocardial inflammation at the infarcted area, we sought to assess the relationship between CRP and pericardial injury depicted by cardiovascular magnetic resonance (CMR) imaging in patients with ST elevation myocardial infarction (MI). Methods and results: 181 MI patients (84% male) were studied with CMR in the first week and at 4 months post-infarction to assess infarct characteristics, left ventricular volumes/function and pericardial injury. The latter was defined as pericardial fluid >4mm and/or enhancement on late gadolinium enhancement CMR. The CRP-value at day 2 (according to previous literature) was used for correlation with CMR and clinical parameters. Pericardial injury was noted in 87 patients, i.e. effusion (n = 30), inflammation (n = 46), both (n = 11). Patients with pericardial injury had significantly higher peak values of cardiac biomarkers (p<0.001) and higher peak CRP-values than patients with normal pericardium (median 13 vs 43 mg/dl, p<0.001). A strong correlation was found between peak CRP-values and a) left venticular ejection fraction and infarct size both at 1 week and 4 months, b) myocardial hemorrhage, microvascular obstruction (MVO) and pericardial injury at 1 week, c) cardiac biomarkers values and time to PCI. However in a multiple regression model only pericardial injury (p = 0.003) and less importantly time to PCI (p = 0.022) were the independent predictors of CRP values. Conclusion: Pericardial damage described by cardiac MRI occurs often after acute ST elevation MI. CRP-values at the acute phase of MI reflect not only inflammation at the infarcted area but even more the inflammation of the surrounding pericardial tissue. Table 1 Comparison of baseline clinical and biochemical parameters of patients with or without evidence of early post-infarct pericardial damage on CMR Normal Group (n = 94)Pericardial injury group (n = 87)p-valueAgem, years59±1160±120.48Male, n(%)83 (88)69 (79)0.10Diabets, n(%)12 (13)9 (10)0.61Smoker, n(%)52 (55)44 (51)0.52Hyperlipidemia, n(%)56 (60)55 (63)0.62BSA m22.0 ± 0.22.0 ± 0.20.20Time to PCI, min195 (155 − 274)223 (160 − 335)0.20Troponin I, μ/l44 (19 − 92)90 (44 − 149)>0.001CK-MB, U/L128 (77 − 216)250 (143 − 443)>0.001CRP, mg/dL13 (7 − 28)43 (16 − 96)>0.001Day of peak CRP2 (1 − 3)2 (1 − 3)0.39 Table 2 Significant correlations between CRP Values and corresponding CMR measurements, cardic biomarkers and clinical related parameters VariblesSpearmanscorrelations rp-valueCMR parameters 1 weekLV EF−0.28>0,001Infractsize(%ofLV)0.40>0,001Microvasular obstruction0.27>0,001Hemorrhage0.33>0,001Size of area atrisk0.31>0,001Transmurality0.30>0,001Pericaldial damage0.43>0,001CMR parameters 4 monthsLVEF−0.43>0,001Infarctsize(%ofLV)0.46>0,001Cardiac BiomarkersPeak TnI0.34>0,001Peak CK-MB0.32>0,001OtherTime to PCI0,1820,007

Published
2013
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141. Poster session 5

Author

Colunga Blanco, S, Garcia Campos, A, Capin Sampedro, E, Corros Vicente, C, Martin Fernandez, M, Leon Arguero, V, Fidalgo Arguelles, A, Velasco Alonso, E, Lopez Iglesias, F, De La Hera Galarza, JM, Gonzalez Matos, C, Chaparro-Munoz, M, Recio-Mayoral, A, Angelis, A, Vlachopoulos, C, Ioakeimidis, N, Felekos, I, Abdelrasoul, M, Aznaouridis, K, Chrysohoou, C, Rousakis, G, Aggeli, K, Tousoulis, D, Dinis, P G, Faustino, AC, Paiva, L, Fernandes, A, Costa, M, Cachulo, MC, Goncalves, L, Chinali, M, Emma, F, Rinelli, G, Esposito, C, Franceschini, A, Doyon, A, Raimondi, F, Schaefer, F, Pongiglione, G, Mateucci, MC, Toth, A, Vago, H, Juhasz, C, Janosa, C, Oprea, V, Balint, OH, Temesvari, A, Simor, T, Kadar, K, Merkely, B, Andreassi, M G, Bruno, R M, Borghini, A, Stea, F, Gargani, L, Mercuri, A, Sicari, R, Picano, E, Rodriguez Munoz, D, Lozano Granero, C, Carbonell San Roman, A, Moya Mur, JL, Fernandez-Golfin, C, Moreno Planas, J, Fernandez Santos, S, Casas Rojo, E, Hernandez-Madrid, A, Zamorano Gomez, JL, Reid, A B, Pearce, K, Gamlin, W, Miller, C, Schmitt, M, Park, JH, Seong, IW, Kim, KH, Kim, MJ, Jung, HO, Sohn, IS, Park, SM, Cho, GY, Choi, JO, Park, SW, study, NORMAL, Shetye, A, Nazir, SA, Khan, JN, Singh, A, Kanagala, P, Squire, I, Mccann, GP, Novo, G, Di Lisi, D, Meschisi, MC, Brunco, V, Badalamenti, G, Bronte, E, Russo, A, Novo, S, De Marchi, S F, Von Tscharner, M, Urheim, S, Aakhus, S, Seiler, C, Schmalholz, S, Cikes, M, Biering-Sorensen, T, Cheng, S, Oparil, S, Izzo, J, Pitt, B, Solomon, SD, Smarz, K, Zaborska, B, Jaxa-Chamiec, T, Tysarowski, M, Budaj, A, Illatopa, V, Cordova, F, Aguirre, O, Sanabria, S, Ortega, J, Peluso, D, Romeo, G, Perazzolo Marra, M, Tona, F, Famoso, G, Pigatto, E, Cozzi, F, Iliceto, S, Badano, LP, Wellnhofer, E, Kriatselis, C, Gerds-Li, JH, Kropf, M, Pieske, B, Graefe, M, De La Rosa Riestra, A, Martinez Santos, P, Batlle Lopez, E, Vilacosta, I, Sanchez Sauce, B, Espana Barrio, E, Jimenez Valtierra, J, Campuzano Ruiz, R, Alonso Bello, J, Martin 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S, Pergolini, M, Vitarelli, A, Caravaca, P, Lujan Valencia, JE, Chaparro, M, Garcia-Guerrero, A, Cristo Ropero, MJ, Izquierdo Bajo, A, Madrona, L, Recio-Mayoral, A, Maceira Gonzalez, A M, Monmeneu, JV, Igual, B, Lopez Lereu, P, Garcia, MP, Iriart, X, Selmi, W, Jalal, Z, Thambo, JB, Jug, B, Kosuta, D, and Fras, Z

Abstract

Background: Handheld ultrasound devices allow for a bedside screening although quantitative parameters are not easily obtained. We aim to assess the reliability of visual qualitative evaluation of left ventricle (LV) compared with standard quantitative evaluation with 2D transthoracic echocardiography (TTE). Methods: Two cardiologists have reviewed 135 consecutive standard TTE examinations. Both observers visually assessed LV size, hypertrophy (LVH) and ejection fraction (EF). LV diameter, volume, wall thickness and EF (Teichholz and Simpson) were also measured by both observers. Visual and quantitative agreement and inter and intraobserver variability were calculated. Results: Image quality allowed for evaluation of 130 examinations. Visually assessed EF compared with Simpson had better consistency (Intraclass correlation coefficient [ICC] 0,91 IC95% 0,88-0,94) than with Teichholz (ICC 0,75 IC95% 0,66-0,82). We have also observed good interobserver agreement regarding visually assessed EF (ICC 0,81 IC95% 0,71-0,87) and Simpson EF (ICC 0,80 IC95% 0,70-0,89) as well as good intraobserver agreement (visual EF: ICC 0,81 IC95% 0,74-0,86; Simpson: ICC 0,89 IC95% 0,84-0,93). Regarding LVH we found moderate agreement between visual and quantitative assessment (weighted Kappa [wK] 0,44 (IC95% 0,32-0,56)), moderate interobserver agreement for quantitative assessment (ICC 0,59 IC95% 0,44-0,71) and poor interobserver agreement for visual assessment (wK 0,19 IC95% 0,08-0,30). Intraobserver variability regarding LVH visual estimation was moderate (wK 0,40 IC95% 0,29-0,52) and regarding LVH quantification was good (ICC 0,78 IC95% 0,70-0,84). LVH was visually overestimated in 25% of examinations. Regarding LV size, we found poor agreement between visual assessment and its quantification with end-diastolic diameter (wK 0,22 IC95% 0,06-0,39) and moderate agreement between visual assessment and end-systolic LV volume (wK 0,62 IC95% 0,47-0,77). Interobserver agreement regarding quantitative volume assessment was good (ICC 0,90 IC95% 0,85-0,94) and regarding visual assessment was moderate (wK 0,43 IC95% 0,26-0,70). We found good intraobserver variability of volume measurement (wK 0,64 IC95% 0,50-0,78) and of visual size assessment (ICC 0,96 IC95% 0,94-0,97). Conclusions: Visual LVEF assessment is consistent with quantitative assessment and should be regarded as a reliable parameter that can be obtained from bedside examination with a handheld device. Visual assessment of LV size and wall thickness is less reliable than its quantification and should be confirmed with standard measurements.

Published
2015
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142. Poster session 1

Author

Haberka, M, Banska, K, Gasior, Z, Garcia Martin, A, Moya-Mur, JL, Carbonell-San Roman, S-A, Rodriguez-Munoz, D, Garcia-Lledo, A, Casas-Rojo, E, Hinojar, R, Jimenez-Nacher, JJ, Fernandez-Golfin, C, Zamorano-Gomez, JL, Barbier, P, Ravani, A, Cefalu, C, Maltagliati, A, Frigerio, B, Sansaro, D, Amato, M, Baldassarre, D, Pellegrino, M, Bandera, F, Generati, G, Labate, V, Alfonzetti, E, Guazzi, M, Angelis, A, Aggeli, K, Ioakeimidis, N, Abdelrasoul, M, Felekos, I, Gourgouli, I, Aznaouridis, K, Rousakis, G, Vlachopoulos, C, Tousoulis, D, Howlett, PJ, Darasz, K, Mahmoudi, M, Shah, N, Jabr, RI, Hickman, M, Leatham, EW, Fry, CH, PREDICT-PAF, Madeira, M, Teixeira, R, Almeida, I, Caetano, F, Fernandes, A, Cassandra, M, Reis, L, Costa, M, Goncalves, L, Carrero, PJ, Nielsen, AJ, Carrero, MC, Saubidet, GL, Peralta, SP, Argentina, Aorta Abdominal, Hansen, KL, Moeller-Soerensen, H, Kjaergaard, J, Jensen, MB, Lund, JT, Pedersen, MM, Olesen, JB, Jensen, JA, Nielsen, MB, Trunina, I, Sharykin, AS, Karelina, EV, Telezhnikova, ND, Basar, C, Ozhan, H, Kayapinar, O, Albayrak, ES, Lie, OH, Saberniak, J, Dejgaard, L, Nestaas, E, Edvardsen, T, Haugaa, KH, Sade, LE, Bal, U, Eroglu, S, Pirat, B, Muderrisoglu, H, Gopal, A S, Muthukumar, L, Saha, SK, Toole, RS, Klug, G, Reinstadler, S, Feistritzer, HJ, Pernter, B, Mayr, A, Franz, WM, Mueller, S, Metzler, B, Rodriguez Gonzalez, E, Mingo Santos, S, Palomero Monivas, V, Gonzalez Mirelis, J, Goirigolzarri Artaza, J, Zorita Gil, B, Fernandez Diaz, JA, Goicolea Ruigomez, J, Restrepo Cordoba, MA, Alonso Pulpon, L, Ferrara, F, Gargani, L, D'alto, M, Ghio, S, Acri, E, Carannante, L, Argiento, P, D'andrea, A, Vriz, O, Bossone, E, Moustafa, S, Ho, TH, Shah, P, Murphy, K, Nelluri, BK, Lee, H, Wilansky, S, Mookadam, F, Naksuk, N, Peeraphatdit, T, Chaiteerakij, R, Klarich, KW, Cantinotti, M, Scalese, M, Melo, M, Assanta, N, Marotta, M, Crocetti, M, Spadoni, I, Giordano, R, Kutty, S, Iervasi, I, Michelsen, MM, Mygind, ND, Pena, A, Frestad, D, Hoest, N, Prescott, E, Fernandes, JMG, Romao, BO, Rivera, IR, Mendonca, MA, Carvalho, AC, Campos, O, Amato, A, Moises, VA, Demir, OM, Bashir, A, Marshall, K, Douglas, M, Wasan, B, Plein, S, Alfakih, K, Cano Carrizal, R, Casanova Rodriguez, C, Cadenas Chamorro, R, Iglesias Del Valle, D, Martin-Penato Molina, A, De Juan Baguda, J, Prieto Moriche, E, Garcia Garcia, A, De La Cruz Berlanga, E, Plaza Perez, I, Bouzas-Mosquera, A, Peteiro, J, Broullon, FJ, Alvarez-Garcia, N, Barbeito-Caamano, C, Larranaga-Moreira, JM, Maneiro-Melon, N, Martinez-Ruiz, D, Yanez, JC, Vazquez-Rodriguez, JM, Leao, S, Cordeiro, F, Magalhaes, P, Moz, M, Trigo, J, Mateus, P, Fontes, P, Moreira, I, Kuznetsov, VA, Krinochkin, DV, Plusnin, AV, Soldatova, AM, Nazir, S A, Shetye, A, Khan, JN, Singh, A, Kanagala, P, Swarbrick, DJ, Graham-Brown, M, Mccann, GP, Trifunovic, D, Krljanac, G, Savic, L, Asanin, M, Aleksandric, S, Lasica, R, Srdic, M, Zlatic, N, Petrovic, M, Mrdovic, I, Rodriguez Gonzalez, E, Mingo Santos, S, Monivas Palomero, V, Gonzalez Mirelis, J, Zorita Gil, B, Fernandez Diaz, JA, Restrepo Cordoba, MA, Goirigolzarri Artaza, J, Rivero Arribas, B, Goicolea Ruigomez, J, Spampinato, RA, Dobrovie, M, Da Rocha E Silva, JG, Bonamigo Thome, F, Kluttig, R, Schloma, V, Dmitrieva, Y, Strotdrees, E, Mohr, FW, Antonini-Canterin, F, Luzza, G, Caruso, R, Belfiore, R, Della Mattia, A, Poli, S, Vriz, O, Zito, C, La Carrubba, S, Carerj, S, Ribeiro, JM, Teixeira, R, Goncalves, L, Morgado, GJ, Carvalho, JF, Gomes, AC, Caldeira, D, Cruz, IR, Stuart, B, Maia, R, Fazendas, P, Pereira, H, Trifunovic, D, Rakocevic, I, Tutos, V, Petrovic, O, Petrovic, M, Boricic-Kostic, M, Stepanovic, J, Jovanovic, I, Banovic, M, Vujisic-Tesic, B, Reis, L, Teixeira, R, Leite, L, Fernandes, A, Cassandra, M, Madeira, M, Botelho, A, Santos, M, Nascimento, J, Goncalves, L, Naratrekoon, B, Yingchoncharoen, T, Vathesatogkit, P, Yamwong, S, Sritara, P, Soto-Ruiz, RM, Bonaque Gonzalez, J C, Abellan-Huerta, J, Rubio-Paton, R, Soria, F, Ramos, JL, Egea, S, Garcia-Gomez, J, Martinez Diaz, JJ, Castillo, JA, Penicka, M, Vecera, J, Mirica, C, Kotrc, M, Kockova, R, Zilberszac, R, Gabriel, H, Maurer, G, Rosenhek, R, De Chiara, B, Botta, L, Musca, F, Belli, O, Costetti, A, Trolese, I, Spano, F, Russo, C, Giannattasio, C, Moreo, A, Rifai, R, Berthelot, E, Le, MT, Hilpert, L, Montani, D, Sitbon, O, Jais, X, Humbert, M, Assayag, P, Gunduz, S, Yesin, M, Kalcik, M, Gursoy, MO, Cersit, S, Astarcioglu, MA, Karakoyun, S, Aykan, AC, Ozkan, M, Cersit, S, Gunduz, S, Tabakci, M, Kalcik, M, Yesin, M, Bayam, E, Ozkan, M, Devecchi, C, Degiovanni, A, Di Ruocco, MV, Marino, P, Ancona, F, Rosa, I, Stella, S, Barletta, M, Marini, C, Latib, A, Montorfano, M, Colombo, A, Margonato, A, Agricola, E, Smith, D, Ray, R, Gallagher, M, Nazir, M, Perreso, V, Sharma, R, Gargani, L, Pang, PS, Miglioranza, M, Landi, P, Dini, FL, Picano, E, Asmarats Serra, L, Pons Llinares, J, Macaya Ten, F, Pericas Ramis, P, Caldes Llull, O, Grau Sepulveda, A, Frontera, G, Bethencourt, A, Abreu, A, Santa Clara, H, Santos, V, Oliveira, M, Cunha, P, Portugal, G, Rio, P, Branco, L, Ferreira, R, Mota Carmo, M, Ikonomidis, I, Paraskevaidis, I, Papadopoulos, C, Stasinos, V, Parissis, J, Lekakis, J, Biernacka, B, Rubis, P, Gackowski, A, Wisniowska-Smialek, S, Lesniak-Sobelga, A, Kostkiewicz, M, Gomes, AC, Bento, D, Correia, E, Teles, L, Picarra, B, Lourenco, C, Faria, R, Magalhaes, P, Domingues, K, Azevedo, O, Caballero, L, Climent Paya, V, Martinez Moreno, M, Gimeno, JR, Oliva, MJ, Saura, D, Sanchez Quinones, J, Garcia Honrubia, A, Valdes, M, De La Morena, G, Mansencal, N, Richard, P, Guerard, S, Brion, R, Paul, P, Dubourg, O, Komajda, M, Isnard, R, Arslan, M, Charron, P, Venturini, C, Avegliano, G, Andres, S, Costabel, JP, Kuschnir, P, Sciancalepore, A, Mendoza, O, Perea, G, Ronderos, R, Zaroui, A, Ben Said, RYM, EL Chalbia, TEJ, Wali, SANA, Mourali, MS, Mechmeche, RACHID, Leren, I S, Saberniak, J, Haland, TF, Edvardsen, T, Haugaa, KH, Astrom Aneq, M, Svetlichnaya, J S, Shikha, SS, Scheinmann, MS, Klein, LK, Nucifora, G, Prati, G, Vitrella, G, Allocca, G, Cukon Buttignoni, S, Muser, D, Morocutti, G, Pinamonti, B, Sinagra, G, Proclemer, A, Rocon, CRLA, Melo, MDTM, Bocchi, EAB, Araujo, JABAF, Demarchi, LMMFD, Mady, CM, Biselli, BB, Kalil, RKF, Salemi, VMCS, Tuma, RT, Cho, J Y, Kim, K H, Yoon, H J, Lee, K J, Park, H, Kim, J H, Ahn, Y, Jeong, M H, Cho, J G, Park, J C, Cho, J Y, Kim, K H, Yoon, H J, Park, H J, Kim, J H, Ahn, Y, Jeong, M H, Cho, J G, Park, J C, Sade, LE, Kozan, H, Eroglu, S, Pirat, B, Sezgin, A, Aydinalp, A, Muderrisoglu, H, Stampfli, S F, Oezkartal, T, Bernhart, S, Flammer, AJ, Vecchiati, A, Froehlich, GM, Ruschitzka, F, Tanner, FC, Cho, EJ, Choi, KY, Kim, DB, Jang, SW, Cho, JS, Park, CS, Jung, HO, Jeon, HK, Youn, HJ, Stevanovic, A, Dekleva, M, Pena, J L, Fortes, PRL, Passos, BR, Rodrigues, AB, Sampaio, IH, Oliveira, MCN, Silva, MG, Cardoso, RAF, Tofani, FA, Moreira, MCV, Ognibeni, F, Cioffi, G, Viapiana, O, Dalbeni, A, Fracassi, E, Di Nora, C, Cherubini, A, Mazzone, C, Di Lenarda, A, Rossini, M, Colunga, S, Corros, C, Garcia-Campos, A, Martin, M, Rodriguez-Suarez, M, Leon, V, Fidalgo, A, Lopez-Iglesias, F, Moris, C, De La Hera, JM, Borowiec, A, Dabrowski, R, Wozniak, J, Jasek, S, Chwyczko, T, Kowalik, I, Musiej-Nowakowska, E, Szwed, H, Hristova, K, Marinov, R, Stamenov, G, Mihova, M, Chacheva, K, Persenska, S, Racheva, A, Kosmala, W, Przewlocka-Kosmala, M, Rojek, A, Karolko, B, Mysiak, A, Marwick, TH, Lesniak-Sobelga, A M, Kostkiewicz, M, Wisniowska-Smialek, S, Biernacka, B, Rubis, P, Kaldararova, M, Tittel, P, Kardos, M, Vrsanska, V, Ondriska, M, Hraska, V, Nosal, M, Masura, J, Simkova, I, Stanojevic, D, Apostolovic, S, Salinger-Martinovic, S, Jankovic-Tomasevic, R, Djordjevic-Radojkovic, D, Stanojlovic, T, Atanaskovic, V, Pavlovic, M, Tahirovic, E, Dungen, HD, Carbonell San Roman, A, Moya Mur, JL, Rodriguez-Munoz, D, Lozano Granero, C, Jimenez Nacher, JJ, Gonzalez Gomez, A, Fraile Sanz, C, Segura De La Cal, T, Fernandez-Golfin, C, Zamorano Gomez, JL, Hoetink, A, Jansen Klomp, WW, Van 'T Hof, AWJ, Brandon Bravo Bruinsma, GJ, Spanjersberg, AJ, Grandjean, J, Nierich, AP, Ferreira, R, Ferreira, J, Lazaro Mendes, S, Martins, R, Monteiro, S, Pego, M, Rohani, A, Khamene Bagheri, R, Wierzbowska-Drabik, K, Peruga, JZ, Sobczak, M, Plewka, M, Wcislo, T, Krecki, R, Kasprzak, JD, Carvalho, J F, Morgado, G, Cruz, I, Caldeira, D, Almeida, AR, Joao, I, Lopes, L, Fazendas, P, Cotrim, C, Pereira, H, Cherubini, A, Cioffi, G, Mazzone, C, Faganello, G, Pandullo, C, Russo, G, Stefenelli, C, Furlanello, F, Tarantini, L, Di Lenarda, A, Teramoto, K, Suzuki, K, Satoh, Y, Minami, K, Mizukoshi, K, Kamijima, R, Kou, S, Takai, M, Izumo, M, Akashi, YJ, May, CJH, Ayuk, J, Geh, I, Shah, T, Edwards, NC, Steeds, RP, Wejner-Mik, P, Sobczak, M, Miskowiec, D, Wdowiak-Okrojek, K, Kasprzak, JD, Lipiec, P, Gurzun, M M, Rosca, M, Calin, A, Beladan, C, Serban, M, Ginghina, C, Popescu, BA, Perea, GO, Lombardero, M, Henquin, R, Corneli, M, Tinetti, M, Laveau, F, Hekimian, G, Achkar, M, Isnard, R, Combes, A, Hammoudi, N, Mahmoud, HM, Al-Ghamdi, M, Ghabashi, A, Ezzat, M H, Al-Amin, A, Sanz, M, Giraldeau, G, Sarvari, SI, Marin, J, Brambila, C, Gabrielli, L, Bijnens, B, Sitges, M, Sanchez-Martinez, S, Duchateau, N, Erdei, T, Fraser, A, Bijnens, B H, Piella, G, Montserrat, S, Sanchis, L, Borras, R, Vidal, B, Prat, S, Azqueta, M, Pare, C, Grazioli, G, Sanz, M, Sitges, M, Kowalczyk, E, Kasprzak, JD, Wejner-Mik, P, Wdowiak-Okrojek, K, Lipiec, P, Park, CS, Jung, MH, Ahn, HS, Kim, JH, Cho, JS, Jeon, HK, Youn, HJ, Hinojar, R, Fernandez-Golfin, C, Megias, A, Alonso, GL, Gonzalez-Gomez, A, Rincon, LM, Esteban, A, Fernandez Mendez, MA, Barrios, V, Zamorano, JL, Van Berendoncks, A M, Van Gaal, L, De Block, C, Salgado, R, Vrints, C, Shivalkar, B, Guedes, H, Pereira, A, Santos, R, Marques, L, Moreno, N, Carvalho, R, Pires, M, Sousa, R, Andrade, A, Pinto, P, Nestaas, E, Stoylen, A, Fugelseth, D, Onut, R, Tautu, O, Onciul, S, Marinescu, C, Zamfir, D, Dorobantu, M, Moran, L, Sanchez Sanchez, V, Navas, P, Garcia-Cosio, D, Diaz, B, Carballo-Alzola, L, Lombera, F, Delgado, J, Kisko, A, Babcak, M, Kishko, N, Agmon, Y, Eitan, A, Mutlak, D, Kehat, I, Corneli, M, Meretta, AH, Perea, GO, Belcastro, F, Aguirre, E, Rosa, D, Zaefferer, P, Masoli, O, Peovska Mitevska, IPM, Srbinovska, ES, Bosevski, MB, Antova, EA, Pop Gorceva, DPG, Barreiro Perez, M, Martin Fernandez, M, Costilla Garcia, SM, Diaz Pelaez, E, and Moris De La Tassa, C

Abstract

Background: The attainment of the primary (low density lipoprotein cholesterol; LDL-C) and the secondary (non-high density lipoprotein cholesterol; non-HDL) lipid therapeutic targets may depend on several potential factors. Our aim was assess the associations between ultrasound fat indexes, lipid levels and the lipid goals attainment in high and very high cardiovascular (CV) risk patients. Methods: Four hundred twenty (n=420) patients (F/M=146/274; age=61 ± 7 y.o.) with high (43%) or very high (57%) cardiovascular risk and chronic statin treatment (³12 months) were enrolled into the study. Obesity measures (body-mass index, BMI; bioelectrical impedance body fat; BF, waist circumference, WC, body adiposity index; BAI), serum levels of lipids (total cholesterol–TC, LDL-C, HDL-C and triglycerides–TG) and goal lipid levels (LDL-C and non-HDL-C) according to the CV risk were determined in all patients. The following ultrasound fat parameters were used in the study: intraabdominal fat (IAT), preperitoneal fat thickness (PreFT), epicardial (EFT) and pericardial (PFT) fat thickness and were indexed to BMI. Results: Our study patients had 5.2 ± 1.7 CV risk factors (80% hypertension, 32% diabetes, 59% metabolic syndrome), 49% were obese, 63% had high BF% and 85% had increased waist circumference (F>80 or M>94cm). All the patients were on a long-term statin treatment (rosuvastatin, atorvastatin or simvastatin). The attainment of the target lipid levels in the study group was as follows: LDL-C–34%, non-HDL-C–39%, both LDL-C and non-HDL-C 31%. Mean fat parameters in the study group were as follows: IAT–76.4 ± 26mm, PreFT–23.3 ± 6.5mm, EFT–3.5 ± 1.5mm and PFT–8.6 ± 3.8mm. Patients with LDL-C goal attainment had significantly higher BAI (34.6 ± 33 vs 30.5 ± 7, p=0.04), but significantly lower IAT/BMI (2.35 ± 0.7 vs 2.51 ± 0.7, p<0.05) with no differences in other clinical (BMI, BF%, WC) and ultrasound (PreFT/BMI, EFT/BMI, PFT/BMI) indexes. The LDL-C goal achievement revealed inverse association with IAT/BMI (r=-0.15, p<0.05) and no associations with PreFT/BMI, EFT/BMI or PFT/BMI. Multivariable regression analysis revealed independent association between IAT/BMI and the LDL-C goal achievement. Conclusions: Intraabdominal fat thickness representing visceral adipose tissue is inversely associated with the LDL-C goal attainment independently from general obesity. It may help to identify individuals requiring more aggressive management of dylipidaemia.

Published
2015
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144. 284 The incremental prognostic significance of restrictive filling pattern in hypertrophic cardiomyopathy: a Doppler echocardiographic study

Author

Di Lenarda, A., Pinamonti, B., Gregori, D., Nucifora, G., Perkan, A., Aleksova, A., Merlo, M., and Sinagra, G.F.

Subjects
CARDIOMYOPATHIES, HYPERTROPHIC cardiomyopathy
Abstract

An abstract of the study "The Incremental Pognostic Significance of Restrictive Filling Pattern in Hypertrophic Cardiomyopathy: A Doppler Echocardiographic Study," by A. Di Lenarda and colleagues, is presented.

Published
2006

145. Post-discharge arrhythmic risk stratification of patients with acute myocarditis and life-threatening ventricular tachyarrhythmias

Author

Enrico Ammirati, Tatsuo Aoki, Maria Frigerio, Manlio Cipriani, Jeness Campodonico, Anne G. Raafs, Aldostefano Porcari, Emeline M. Van Craenenbroeck, Andrea Perkan, Mark Hazebroek, Eric D. Adler, Daniele Muser, Matthieu Schmidt, Andreja Cerne Cercek, Marzia Colopi, Caroline M. Van De Heyning, Piergiuseppe Agostoni, Andrea Garascia, Florent Huang, Rossana Bussani, Luciano Potena, Koichiro Sugimura, Piero Gentile, Alberto Foà, Gaetano Nucifora, Giulia Barbati, Marco Merlo, Naveen L. Pereira, Paolo G. Camici, Sanskriti Shrivastava, Antonio Cannatà, Stephane Heymans, Hiroaki Shimokawa, Gianfranco Sinagra, Giovanni Donato Aquaro, Michela Brambatti, Simone Sala, Paolo Della Bella, Massimo Imazio, Giovanni Peretto, Jessica Artico, Gentile P., Merlo M., Peretto G., Ammirati E., Sala S., Della Bella P., Aquaro G.D., Imazio M., Potena L., Campodonico J., Foa A., Raafs A., Hazebroek M., Brambatti M., Cercek A.C., Nucifora G., Shrivastava S., Huang F., Schmidt M., Muser D., Van de Heyning C.M., Van Craenenbroeck E., Aoki T., Sugimura K., Shimokawa H., Cannata A., Artico J., Porcari A., Colopi M., Perkan A., Bussani R., Barbati G., Garascia A., Cipriani M., Agostoni P., Pereira N., Heymans S., Adler E.D., Camici P.G., Frigerio M., Sinagra G., Cardiologie, RS: Carim - H02 Cardiomyopathy, Gentile, P., Merlo, M., Peretto, G., Ammirati, E., Sala, S., Della Bella, P., Aquaro, G. D., Imazio, M., Potena, L., Campodonico, J., Foa, A., Raafs, A., Hazebroek, M., Brambatti, M., Cercek, A. C., Nucifora, G., Shrivastava, S., Huang, F., Schmidt, M., Muser, D., Van de Heyning, C. M., Van Craenenbroeck, E., Aoki, T., Sugimura, K., Shimokawa, H., Cannata, A., Artico, J., Porcari, A., Colopi, M., Perkan, A., Bussani, R., Barbati, G., Garascia, A., Cipriani, M., Agostoni, P., Pereira, N., Heymans, S., Adler, E. D., Camici, P. G., Frigerio, M., and Sinagra, G.

Subjects
Adult, Male, medicine.medical_specialty, Myocarditis, Cardiac magnetic resonance, Arrhythmic risk stratification, medicine.medical_treatment, Fulminant, Aftercare, Contrast Media, Gadolinium, Risk Assessment, Implantable cardioverter-defibrillator, Sudden cardiac death, Ventricular arrhythmias, INFLAMMATION, Internal medicine, Acute myocarditi, medicine, MANAGEMENT, Humans, FULMINANT, PREDICTORS, Retrospective Studies, Heart Failure, business.industry, Incidence (epidemiology), Acute myocarditis, Hazard ratio, LATE GADOLINIUM ENHANCEMENT, ASSOCIATION, medicine.disease, Patient Discharge, EUROPEAN-SOCIETY, Heart failure, CARDIOVASCULAR MAGNETIC-RESONANCE, Ventricular fibrillation, Tachycardia, Ventricular, Cardiology, cardiovascular system, Female, Human medicine, Cardiology and Cardiovascular Medicine, business, SUDDEN CARDIAC DEATH
Abstract

Background The outcomes of patients presenting with acute myocarditis and life-threatening ventricular tachyarrhythmias (LT-VA) are unclear. The aim of this study was to assess incidence and predictors of recurrence of major arrhythmic events (MAEs) after hospital discharge in such patients. Methods and results We retrospectively analysed 156 patients (median age 44 years; 77% males) discharged with a diagnosis of acute myocarditis and LT-VA from 16 hospitals worldwide. Diagnosis of myocarditis was based on histology or on the combination of increased markers of cardiac injury and cardiac magnetic resonance (CMR) Lake Louise criteria. MAEs were defined as the relapse, after discharge, of sudden cardiac death (SCD) or ventricular fibrillation defibrillated successfully or sustained ventricular tachycardia (sVT) requiring implantable cardioverter-defibrillator therapy or synchronized external cardioversion. Median follow-up period was 23 months (first to third quartile [Q1-Q3] 7-60). Fifty-eight (37.2%) patients experienced MAEs after discharge, at a median time of 8 months (Q1-Q3 2.5-24.0 months; 60.3% of MAEs within the first year). At multivariable Cox analysis, variables independently associated to MAEs were presentation with sVT (hazard ratio [HR] 2.90, 95% confidence interval [CI] 1.38-6.11); late gadolinium enhancement (LGE) involving ≥2 myocardial segments (HR 4.51, 95% CI 2.39-8.53); and absence of positive short-tau inversion recovery (STIR) (HR 2.59, 95% CI 1.40-4.79) at first CMR. Conclusions Among patients discharged with the diagnosis of myocarditis and LT-VA, 37.2% had recurrences of MAEs during follow-up. Initial CMR pattern and sVT at presentation stratify the risk of arrhythmic recurrence.

Published
2021

147. Survivin modulates genes with divergent molecular functions and regulates proliferation of hematopoietic stem cells through Evi-1.

Author

Fukuda, S, Hoggatt, J, Singh, P, Abe, M, Speth, J M, Hu, P, Conway, E M, Nucifora, G, Yamaguchi, S, and Pelus, L M

Subjects
*HEMATOPOIETIC stem cells, *APOPTOSIS, *SURVIVIN (Protein), *LABORATORY mice, *ONCOLOGY research, *BONE marrow
Abstract

The inhibitor of apoptosis protein Survivin regulates hematopoiesis, although its mechanisms of regulation of hematopoietic stem cells (HSCs) remain largely unknown. While investigating conditional Survivin deletion in mice, we found that Survivin was highly expressed in phenotypically defined HSCs, and Survivin deletion in mice resulted in significantly reduced total marrow HSCs and hematopoietic progenitor cells. Transcriptional analysis of Survivin−/− HSCs revealed altered expression of multiple genes not previously linked to Survivin activity. In particular, Survivin deletion significantly reduced expression of the Evi-1 transcription factor indispensable for HSC function, and the downstream Evi-1 target genes Gata2, Pbx1 and Sall2. The loss of HSCs following Survivin deletion and impaired long-term HSC repopulating function could be partially rescued by ectopic Evi-1 expression in Survivin −/− HSCs. These data demonstrate that Survivin partially regulates HSC function by modulating the Evi-1 transcription factor and its downstream targets and identify new genetic pathways in HSCs regulated by Survivin. [ABSTRACT FROM AUTHOR]

Published
2015
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148. Prevalence, Correlates, and Prognostic Relevance of Mid-Wall Late Gadolinium Enhancement in Patients With Ischemic Cardiomyopathy

Author

Thomas Caiffa, Joshua Bradley, Matthias Schmitt, Giulia De Angelis, Christopher A. Miller, Gianfranco Sinagra, Daniele Muser, Gaetano Nucifora, Zoi Tsoumani, Nucifora, G., Tsoumani, Z., De Angelis, G., Caiffa, T., Muser, D., Bradley, J., Sinagra, G., Miller, C., and Schmitt, M.

Subjects
medicine.medical_specialty, Contrast Media, Gadolinium, 030204 cardiovascular system & hematology, 030218 nuclear medicine & medical imaging, 03 medical and health sciences, 0302 clinical medicine, Predictive Value of Tests, Internal medicine, Prevalence, Late gadolinium enhancement, Medicine, Humans, Radiology, Nuclear Medicine and imaging, In patient, cardiovascular diseases, Ischemic cardiomyopathy, business.industry, Prognosis, Magnetic Resonance Imaging, Ischemic Cardiomyopathy, embryonic structures, Risk stratification, cardiovascular system, Cardiology, Myocardial fibrosis, Cardiology and Cardiovascular Medicine, business, Cardiac magnetic resonance, Cardiomyopathies
Abstract

Background. Late gadolinium enhancement (LGE) imaging is an established cardiac magnetic resonance (CMR) technique for the assessment of myocardial replacement fibrosis. The presence of mid-wall LGE has been described in ~30% of patients with non-ischemic dilated cardiomyopathy and is known to be associated with poor outcome. Conversely, little is known regarding the clinical significance of mid-wall LGE in patients with ischemic cardiomyopathy (ICM). Therefore, the aim of the present study was to investigate the prevalence, correlates and prognostic role of mid-wall LGE in a consecutive cohort of patients with ICM. Methods and Results. A total of 319 consecutive outpatients with ICM (mean age 64±11 years, 87% males) enrolled in the UHSM CMR Study (ClinicalTrials.gov NCT02326324) were included. All patients had CMR with LGE imaging and were followed for a median of 13 months (25th–75th percentiles, 6–28 months). The outcome end-point was a composite of cardiovascular death, aborted sudden cardiac death, appropriate implantable cardioverter-defibrillator therapy, heart failure hospitalisations, implantation of left ventricular (LV) assist device or occurrence of heart transplant. At CMR with LGE imaging, mean LV ejection was 37±9%, mean ischemic-type LGE expressed as % of LV mass was 16±9%, while mid-wall LGE was observed in 32 (10%) patients. LVEDV index (OR 1.02, 95% CI 1.01-1.03, p = 0.001) and LV sphericity index (OR 1.04, 95%CI 1.01-1.07, p = 0.024) were the only variables significantly and independently related to the presence of mid-wall LGE. The outcome end-point was documented in 37 (12%) patients. Ischemic-type LGE expressed as % of LV mass (HR 1.04, 95% CI 1.01-1.08; p = 0.015) and the presence of mid-wall LGE (HR 4.5, 95% CI 2.2-9.2; p < 0.001) were the only independent predictors of the composite outcome. Furthermore, mid-wall LGE had significant incremental predictive value compared to the extent of ischemic-type LGE (Dχ2 = 16.5, p

Published
2021

149. The alcohol-induced cardiomyopathy: A cardiovascular magnetic resonance characterization

Author

Gerry Carr-White, Pier Giorgio Masci, Giulia De Angelis, Gaetano Nucifora, Clint Asher, Jessica Artico, Martina Perazzolo Marra, Lorenzo Pagnan, Manuel Belgrano, Silvia Pica, Manuel De Lazzari, Marco Merlo, Aldostefano Porcari, Antonio Cannatà, Massimo Lombardi, Antonio De Luca, Amedeo Chiribiri, Gianfranco Sinagra, Giancarlo Vitrella, Artico, J., Merlo, M., Asher, C., Cannata, A., Masci, P. G., De Lazzari, M., Pica, S., De Angelis, G., Porcari, A., Vitrella, G., De Luca, A., Belgrano, M., Pagnan, L., Chiribiri, A., Marra, M. P., Sinagra, G., Nucifora, G., Lombardi, M., and Carr-White, G.

Subjects
Cardiomyopathy, Dilated, Male, medicine.medical_specialty, Magnetic Resonance Spectroscopy, Cardiac magnetic resonance, Cardiomyopathy, medicine.medical_treatment, Left, Dilated cardiomyopathy, Magnetic Resonance Imaging, Cine, Contrast Media, Predictive Value of Test, Gadolinium, Alcoholic cardiomyopathy, Late gadolinium enhancement, Ventricular Function, Left, Predictive Value of Tests, Internal medicine, Dilated, Medicine, Humans, Ventricular Function, cardiovascular diseases, Alcohol-induced, Stroke Volume, Cardiomyopathy, Alcoholic, Heart transplantation, Ejection fraction, medicine.diagnostic_test, business.industry, Magnetic resonance imaging, musculoskeletal system, medicine.disease, Alcoholic, Magnetic Resonance Imaging, Cine, cardiovascular system, Cardiology, Cardiology and Cardiovascular Medicine, business, Human
Abstract

Background: Alcoholic cardiomyopathy(ACM) is part of the non-ischaemic dilated cardiomyopathy(NI-DCM) spectrum. Little is known about cardiovascular magnetic resonance(CMR) features in ACM patients. The aim of this study is to describe CMR findings and their prognostic impact in ACM patients. Methods: Consecutive ACM patients evaluated in five referral CMR centres from January 2005 to December 2018 were enrolled. CMR findings and their prognostic value were compared to idiopathic NI-DCM(iNI-DCM) patients. The main outcome was a composite of death/heart transplantation/life-threatening arrhythmias. Results: Overall 114 patients (52 with ACM and 62 with iNI-DCM) were included. ACM patients were more often males compared to iNI-DCM (90% vs 64%, respectively, p ≤ 0.001) and were characterized by a more pronounced biventricular adverse remodelling than iNI-DCM, i.e. lower LVEF (31 ± 12% vs 38 ± 11% respectively, p = 0.001) and larger left ventricular end-diastolic volume (116 ± 40 ml/m2 vs 67 ± 20 ml/m2 respectively, p < 0.001). Similarly to iNI-DCM, late gadolinium enhancement (LGE), mainly midwall, was present in more than 40% of ACM patients but, conversely, it was not associated with adverse outcome(p = 0.15). LGE localization was prevalently septal (87%) in ACM vs lateral in iNI-DCM(p < 0.05). Over a median follow-up of 42 months [Interquartile Range 24–68], adverse outcomes were similar in both groups(p = 0.67). Conclusions: ACM represents a specific phenotype of NI-DCM, with severe morpho-functional features at the onset, but similar long-term outcomes compared to iNI-DCM. Despite the presence and pattern of distribution of LGE was comparable, ACM and iNI-DCM showed a different LGE localization, mostly septal in ACM and lateral in iNI-DCM, with different prognostic impact.

Published
2021

150. Prognostic Utility of Oxygen-Sensitive Cardiac Magnetic Resonance Imaging in Diabetic and Nondiabetic Chronic Kidney Disease Patients With No Known Coronary Artery Disease

Author

Zach Liang, Emma Smith, Jonathan M. Gleadle, Richard J. Woodman, Randall J. Faull, Craig Bradbrook, Joseph B. Selvanayagam, Gaetano Nucifora, Rebecca Perry, Ranjit Shah, S. Parnham, Shah, R, Parnham, S, Liang, Z, Perry, Rebecca, Bradbrook, C, Smith, E, Faull, R, Woodman, RJ, Nucifora, G, Gleadle, JM, and Slevanayagam, JB

Subjects
medicine.medical_specialty, Myocardial ischemia, Heart Diseases, Pilot Projects, 030204 cardiovascular system & hematology, urologic and male genital diseases, 030218 nuclear medicine & medical imaging, 03 medical and health sciences, Oxygen Consumption, 0302 clinical medicine, Predictive Value of Tests, Risk Factors, Cardiac magnetic resonance imaging, Cause of Death, Diabetes mellitus, Internal medicine, Diabetes Mellitus, medicine, Humans, Radiology, Nuclear Medicine and imaging, Prospective Studies, Renal Insufficiency, Chronic, Prospective cohort study, Cause of death, medicine.diagnostic_test, business.industry, Myocardium, Prognosis, medicine.disease, Magnetic Resonance Imaging, female genital diseases and pregnancy complications, Predictive value of tests, Disease Progression, Cardiology, Known Coronary Artery Disease, Cardiology and Cardiovascular Medicine, business, Kidney disease
Abstract

Diabetes mellitus (DM) and chronic kidney disease (CKD) often coexist, and both are recognized risk factors for future cardiovascular events. Painless myocardial ischemia occurs more commonly in CKD patients than in individuals with normal renal function and is associated with a higher mortality

Published
2019

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