SOSTIENICI
Dott.ssa Alberti Antonia
Pubblicazioni su PubMed
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Heart Rate in Patients with SARS-CoV-2 Infection: Prevalence of High Values at Discharge and Relationship with Disease Severity.
J Clin Med2021 Nov;10(23):. doi: 5590.
Maloberti Alessandro, Ughi Nicola, Bernasconi Davide Paolo, Rebora Paola, Cartella Iside, Grasso Enzo, Lenoci Deborah, Del Gaudio Francesca, Algeri Michela, Scarpellini Sara, Perna Enrico, Verde Alessandro, Santolamazza Caterina, Vicari Francesco, Frigerio Maria, Alberti Antonia, Valsecchi Maria Grazia, Rossetti Claudio, Epis Oscar Massimiliano, Giannattasio Cristina, On The Behalf Of The Niguarda Covid-Working Group
Abstract
The most common arrhythmia associated with COronaVIrus-related Disease (COVID) infection is sinus tachycardia. It is not known if high Heart Rate (HR) in COVID is simply a marker of higher systemic response to sepsis or if its persistence could be related to a long-term autonomic dysfunction. The aim of our work is to assess the prevalence of elevated HR at discharge in patients hospitalized for COVID-19 and to evaluate the variables associated with it. We enrolled 697 cases of SARS-CoV2 infection admitted in our hospital after February 21 and discharged within 23 July 2020. We collected data on clinical history, vital signs, laboratory tests and pharmacological treatment. Severe disease was defined as the need for Intensive Care Unit (ICU) admission and/or mechanical ventilation. Median age was 59 years (first-third quartile 49, 74), and male was the prevalent gender (60.1%). 84.6% of the subjects showed a SARS-CoV-2 related pneumonia, and 13.2% resulted in a severe disease. Mean HR at admission was 90 ± 18 bpm with a mean decrease of 10 bpm to discharge. Only 5.5% of subjects presented HR > 100 bpm at discharge. Significant predictors of discharge HR at multiple linear model were admission HR (mean increase = ? = 0.17 per bpm, 95% CI 0.11; 0.22,
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Eculizumab as a promising treatment in thymoma-associated myasthenia gravis.
Ther Adv Neurol Disord2020 ;13():1756286420932035. doi: 1756286420932035.
Vélez-Santamaría Valentina, Nedkova Velina, Díez Laura, Homedes Christian, Alberti M Antonia, Casasnovas Carlos
Abstract
Myasthenia gravis is a chronic autoimmune disorder caused by antibodies directed against the neuromuscular junction. Some patients may have an associated thymoma, which confers a worse prognosis. Eculizumab, a monoclonal antibody that inhibits the activation of terminal complement, has recently been approved for the treatment of refractory generalized myasthenia gravis. This is an early case report of thymoma-associated refractory myasthenia gravis successfully treated with eculizumab in a real-world setting.
© The Author(s), 2020.
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Analysis of HDL-microRNA panel in heterozygous familial hypercholesterolemia subjects with LDL receptor null or defective mutation.
Sci Rep2019 Dec;9(1):20354. doi: 20354.
Scicali Roberto, Di Pino Antonino, Pavanello Chiara, Ossoli Alice, Strazzella Arianna, Alberti Antonia, Di Mauro Stefania, Scamporrino Alessandra, Urbano Francesca, Filippello Agnese, Piro Salvatore, Rabuazzo Agata Maria, Calabresi Laura, Purrello Francesco
Abstract
In the last years increasing attention has been given to the connection between genotype/phenotype and cardiovascular events in subjects with familial hypercholesterolemia (FH). MicroRNAs (miRs) bound to high-density lipoprotein (HDL) may contribute to better discriminate the cardiovascular risk of FH subjects. Our aim was to evaluate the HDL-miR panel in heterozygous FH (HeFH) patients with an LDLR null or defective mutation and its association with pulse wave velocity (PWV). We evaluated lipid panel, HDL-miR panel and PWV in 32 LDLR null mutation (LDLR-null group) and 35 LDLR defective variant (LDLR-defective group) HeFH patients. HDL-miR-486 and HDL-miR-92a levels were more expressed in the LDLR-null group than the LDLR-defective group. When we further stratified the study population into three groups according to both the LDLR genotype and history of ASCVD (LDLR-null/not-ASCVD, LDLR-defective/not-ASCVD and LDLR/ASCVD groups), both the LDLR/ASCVD and the LDLR-null/not-ASCVD groups had a higher expression of HDL-miR-486 and HDL-miR-92a than the LDLR-defective/not-ASCVD group. Finally, HDL-miR-486 and HDL-miR-92a were independently associated with PWV. In conclusion, the LDLR-null group exhibited HDL-miR-486 and HDL-miR-92a levels more expressed than the LDLR-defective group. Further studies are needed to evaluate these HDL-miRs as predictive biomarkers of cardiovascular events in FH.
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Biomarker Identification, Safety, and Efficacy of High-Dose Antioxidants for Adrenomyeloneuropathy: a Phase II Pilot Study.
Neurotherapeutics2019 Oct;16(4):1167-1182. doi: 10.1007/s13311-019-00735-2.
Casasnovas Carlos, Ruiz Montserrat, Schlüter Agatha, Naudí Alba, Fourcade Stéphane, Veciana Misericordia, Castañer Sara, Albertí Antonia, Bargalló Nuria, Johnson Maria, Raymond Gerald V, Fatemi Ali, Moser Ann B, Villarroya Francesc, Portero-Otín Manuel, Artuch Rafael, Pamplona Reinald, Pujol Aurora
Abstract
X-Adrenoleukodystrophy (X-ALD) and its adult-onset, most prevalent variant adrenomyeloneuropathy (AMN) are caused by mutations in the peroxisomal transporter of the very long-chain fatty acid ABCD1. AMN patients classically present spastic paraparesis that can progress over decades, and a satisfactory treatment is currently lacking. Oxidative stress is an early culprit in X-ALD pathogenesis. A combination of antioxidants halts the clinical progression and axonal damage in a murine model of AMN, providing a strong rationale for clinical translation. In this phase II pilot, open-label study, 13 subjects with AMN were administered a high dose of ?-tocopherol, N-acetylcysteine, and ?-lipoic acid in combination. The primary outcome was the validation of a set of biomarkers for monitoring the biological effects of this and future treatments. Functional clinical scales, the 6-minute walk test (6MWT), electrophysiological studies, and cerebral MRI served as secondary outcomes. Most biomarkers of oxidative damage and inflammation were normalized upon treatment, indicating an interlinked redox and inflammatory homeostasis. Two of the inflammatory markers, MCP1 and 15-HETE, were predictive of the response to treatment. We also observed a significant decrease in central motor conduction time, together with an improvement or stabilization of the 6MWT in 8/10 subjects. This study provides a series of biomarkers that are useful to monitor redox and pro-inflammatory target engagement in future trials, together with candidate biomarkers that may serve for patient stratification and disease progression, which merit replication in future clinical trials. Moreover, the clinical results suggest a positive signal for extending these studies to phase III randomized, placebo-controlled, longer-term trials with the actual identified dose. ClinicalTrials.gov Identifier: NCT01495260.
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Systematic Lab Knowledge Integration for Management of Lipid Excess in High-Risk Patients: Rationale and Design of the SKIM LEAN Project.
Front Big Data2018 ;1():4. doi: 4.
Pavanello Chiara, Parolini Marina, Alberti Antonia, Carenini Michele, Maino Paolo, Mombelli Giuliana, Pazzucconi Franco, Origgi Gianni, Orsi Federica, Trivella Maria Giovanna, Calabresi Laura, De Maria Renata
Abstract
SKIM LEAN aims at exploiting Electronic Health Records (EHRs) to integrate knowledge derived from routine laboratory tests with background analysis of clinical databases, for the identification and early referral to specialist care, where appropriate, of patients with hypercholesterolemia, who may be inadequately controlled according to their cardiovascular (CV) risk level. SKIM LEAN addresses gaps in care that may occur through the lack of coordination between primary and specialist care, incomplete adherence to clinical guidelines, or poor patient's compliance to the physician's prescriptions because of comorbidities or drug side effects. Key project objectives include: (1) improved health professionals' competence and patient empowerment through a two-tiered educational website for general practitioners (GPs) and patients, and (2) implementation of a hospital-community shared care pathway to increase the proportion of patients at high/very-high CV risk (Familial Hypercholesterolemia, previous CV events) who achieve target LDL cholesterol (LDL-C) levels. Thanks to a close collaboration between clinical and information technology partners, SKIM LEAN will fully exploit the value of big data deriving from EHRs, and filter such knowledge using clinically-derived algorithms to risk-stratify patients. Alerts for GPs will be generated with interpreted test results. GPs will be able to refer patients with uncontrolled LDL-C within the shared pathway to the lipid or secondary prevention outpatient clinics of NIG hospital. Metrics to verify the project achievements include web-site visits, the number of alerts generated, numbers of patients referred by GPs, the proportion of secondary prevention patients who achieve LDL-C 50% decrease from baseline.
Copyright © 2018 Pavanello, Parolini, Alberti, Carenini, Maino, Mombelli, Pazzucconi, Origgi, Orsi, Trivella, Calabresi and De Maria.
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Substrate interaction defects in histidyl-tRNA synthetase linked to dominant axonal peripheral neuropathy.
Hum Mutat2018 Mar;39(3):415-432. doi: 10.1002/humu.23380.
Abbott Jamie A, Meyer-Schuman Rebecca, Lupo Vincenzo, Feely Shawna, Mademan Inès, Oprescu Stephanie N, Griffin Laurie B, Alberti M Antonia, Casasnovas Carlos, Aharoni Sharon, Basel-Vanagaite Lina, Züchner Stephan, De Jonghe Peter, Baets Jonathan, Shy Michael E, Espinós Carmen, Demeler Borries, Antonellis Anthony, Francklyn Christopher
Abstract
Histidyl-tRNA synthetase (HARS) ligates histidine to cognate tRNA molecules, which is required for protein translation. Mutations in HARS cause the dominant axonal peripheral neuropathy Charcot-Marie-Tooth disease type 2W (CMT2W); however, the precise molecular mechanism remains undefined. Here, we investigated three HARS missense mutations associated with CMT2W (p.Tyr330Cys, p.Ser356Asn, and p.Val155Gly). The three mutations localize to the HARS catalytic domain and failed to complement deletion of the yeast ortholog (HTS1). Enzyme kinetics, differential scanning fluorimetry (DSF), and analytical ultracentrifugation (AUC) were employed to assess the effect of these substitutions on primary aminoacylation function and overall dimeric structure. Notably, the p.Tyr330Cys, p.Ser356Asn, and p.Val155Gly HARS substitutions all led to reduced aminoacylation, providing a direct connection between CMT2W-linked HARS mutations and loss of canonical ARS function. While DSF assays revealed that only one of the variants (p.Val155Gly) was less thermally stable relative to wild-type, all three HARS mutants formed stable dimers, as measured by AUC. Our work represents the first biochemical analysis of CMT-associated HARS mutations and underscores how loss of the primary aminoacylation function can contribute to disease pathology.
© 2017 Wiley Periodicals, Inc.
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Assessment of Targeted Next-Generation Sequencing as a Tool for the Diagnosis of Charcot-Marie-Tooth Disease and Hereditary Motor Neuropathy.
J Mol Diagn2016 Mar;18(2):225-34. doi: 10.1016/j.jmoldx.2015.10.005.
Lupo Vincenzo, García-García Francisco, Sancho Paula, Tello Cristina, García-Romero Mar, Villarreal Liliana, Alberti Antonia, Sivera Rafael, Dopazo Joaquín, Pascual-Pascual Samuel I, Márquez-Infante Celedonio, Casasnovas Carlos, Sevilla Teresa, Espinós Carmen
Abstract
Charcot-Marie-Tooth disease is characterized by broad genetic heterogeneity with >50 known disease-associated genes. Mutations in some of these genes can cause a pure motor form of hereditary motor neuropathy, the genetics of which are poorly characterized. We designed a panel comprising 56 genes associated with Charcot-Marie-Tooth disease/hereditary motor neuropathy. We validated this diagnostic tool by first testing 11 patients with pathological mutations. A cohort of 33 affected subjects was selected for this study. The DNAJB2 c.352+1G>A mutation was detected in two cases; novel changes and/or variants with low frequency (A mutation was also detected in three additional families. On haplotype analysis, all of the patients from these five families shared the same haplotype; therefore, the DNAJB2 c.352+1G>A mutation may be a founder event. Our gene panel allowed us to perform a very rapid and cost-effective screening of genes involved in Charcot-Marie-Tooth disease/hereditary motor neuropathy. Our diagnostic strategy was robust in terms of both coverage and read depth for all of the genes and patient samples. These findings demonstrate the difficulty in achieving a definitive molecular diagnosis because of the complexity of interpreting new variants and the genetic heterogeneity that is associated with these neuropathies.
Copyright © 2016 American Society for Investigative Pathology and the Association for Molecular Pathology. Published by Elsevier Inc. All rights reserved.
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Sural nerve biopsy and functional studies support the pathogenic role of a novel MPZ mutation.
Neuropathology2015 Jun;35(3):254-9. doi: 10.1111/neup.12179.
Prada Valeria, Capponi Simona, Ursino Giulia, Alberti Antonia, Callegari Ilaria, Passalacqua Mario, Marotta Roberto, Mandich Paola, Bellone Emilia, Schenone Angelo, Grandis Marina
Abstract
Our patient is a 65-year-old woman presenting with bilateral pes cavus, pronounced distal muscle wasting, weakness and areflexia. Electrophysiological findings included diffuse unrecordable motor and sensory responses. While the CMT phenotype was evident, the lack of family history and the severe, but unspecific electrophysiological impairment, was a challenge for genetic diagnosis. A sural nerve biopsy was performed, showing a severe loss of myelinated fibers with residual axons surrounded by myelin outfoldings. Whereas myelin outfoldings are a pathological hallmark of autosomal recessive CMT4B1 and CMT4B2, due to mutations in myotubularin-related 2 (MTMR2) and 13 (MTMR13) genes respectively, they may also occur in nerve biopsies from CMT1B patients. By direct sequencing, a novel heterozygous transversion c.410G>T in MPZ gene was demonstrated, producing an amino acid change from glycine to valine in position 108 (p.G108V). In HeLa cells the fusion P0G108V-EGFP was normally trafficked to the cell membrane, but with decreased P0 adhesion function, compared with wild-type P0, thus supporting a pathogenic role of the new variant. In conclusion this case highlights the relevance, in selected cases, of sural nerve biopsy to orient the genetic/molecular tests, while in vitro analyses may strengthen the pathogenic role of novel mutations.
© 2014 Japanese Society of Neuropathology.
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[Ross syndrome: an infrequent neurological cause of sweating disorders].
Rev Neurol2014 Oct;59(7):334-5.
Balcells Anna, Sanahuja Jordi, Guitard Luisa, Albertí Antonia, Ortiz Ariadna, Barcenilla Fernando
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Influence of comorbidities on the phenotype of patients affected by Charcot-Marie-Tooth neuropathy type 1A.
Neuromuscul Disord2013 Nov;23(11):902-6. doi: 10.1016/j.nmd.2013.07.002.
Ursino Giulia, Alberti M Antonia, Grandis Marina, Reni Lizia, Pareyson Davide, Bellone Emilia, Gemelli Chiara, Sabatelli Mario, Pisciotta Chiara, Luigetti Marco, Santoro Lucio, Massollo Laura, Schenone Angelo
Abstract
Charcot-Marie-Tooth type 1A (CMT1A) is the most common inherited neuropathy. The phenotype of patients affected by CMT1A is highly variable and may be influenced by several conditions. We evaluated how comorbidities such as diabetes, hypothyroidism, exposure to toxins and obesity can modify or exacerbate the clinical and neurophysiological phenotype of CMT1A patients. Disability was measured using the classic CMT neuropathy score. Compared to controls, all groups of CMT1A patients with comorbidities had higher CMT neuropathy score. In particular, patients with CMT1A and diabetes mellitus show motor subscores which are significantly higher than in control CMT1A. Amplitudes of ulnar CMAP are lower in patients with CMT1A and diabetes mellitus, but not at a significant level. As expected, motor nerve conduction velocity is not influenced by any of the comorbidities. The presence of concomitant diseases shows a tendency to worsen the clinical and neurophysiological CMT1A phenotype, especially in patients with CMT1A and diabetes mellitus, where higher values in the CMT neuropathy score and clinical motor subscore have been observed.
Copyright © 2013 Elsevier B.V. All rights reserved.
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Unusual insertion of a mitral chord causing severe valve regurgitation.
Eur J Cardiothorac Surg2010 Sep;38(3):387. doi: 10.1016/j.ejcts.2010.02.036.
Taglieri Corrado, Botta Luca, Roghi Alberto, Alberti Antonia
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Diagnosis of Charcot-Marie-Tooth disease.
J Biomed Biotechnol2009 ;2009():985415. doi: 985415.
Banchs Isabel, Casasnovas Carlos, Albertí Antonia, De Jorge Laura, Povedano Mónica, Montero Jordi, Martínez-Matos Juan Antonio, Volpini Victor
Abstract
Charcot-Marie-Tooth (CMT) disease or hereditary motor and sensory neuropathy (HMSN) is a genetically heterogeneous group of conditions that affect the peripheral nervous system. The disease is characterized by degeneration or abnormal development of peripheral nerves and exhibits a range of patterns of genetic transmission. In the majority of cases, CMT first appears in infancy, and its manifestations include clumsiness of gait, predominantly distal muscular atrophy of the limbs, and deformity of the feet in the form of foot drop. It can be classified according to the pattern of transmission (autosomal dominant, autosomal recessive, or X linked), according to electrophysiological findings (demyelinating or axonal), or according to the causative mutant gene. The classification of CMT is complex and undergoes constant revision as new genes and mutations are discovered. In this paper, we review the most efficient diagnostic algorithms for the molecular diagnosis of CMT, which are based on clinical and electrophysiological data.
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Charcot-Marie-tooth disease.
Foot Ankle Spec2008 Dec;1(6):350-4. doi: 10.1177/1938640008326247.
Casasnovas Carlos, Cano Luis Miguel, Albertí Antonia, Céspedes Maria, Rigo Gillem
Abstract
Charcot-Marie-Tooth disease (CMT) or hereditary motor and sensory neuropathy constitutes a genetically heterogeneous group of diseases that affect the peripheral nervous system. CMT is characterized by degeneration or abnormal development of the peripheral nerve and is transmitted with different genetic patterns. In most cases, the disease starts in infancy. Its symptoms, among others, are an awkward gait; muscular atrophy of the 4 extremities, particularly distally; and foot deformities, such as cavus foot. People with CMT have an altered gait; most have a high stepping gait and frequently trip or fall. CMT disease can be classified according to the pattern of inheritance (autosomal dominant, autosomal recessive, or X-linked), electrophysiological findings (evidence of demyelination or axonal degeneration), or the mutated gene that causes the disease. This classification of CMT is complex and continually updated as new genes and mutations are found. CMT should be suspected in any patient with cavus foot, particularly if other members of the family have been diagnosed with the disease. Treatment decisions must be individualized and based on a clear history, careful examination, and well-defined patient goals.
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[The "Appropriatezza ECO Milano" project. Assessment of appropriateness of indications, prescriptions and clinical utility of two-dimensional Doppler echocardiography among inpatients and outpatients of Milan, Italy].
G Ital Cardiol (Rome)2008 Dec;9(12):844-52.
Mantero Antonio, Gentile Francesco, Alberti Antonia, Bencini Chiara, Bongarzoni Amedeo, Bragato Renato, Branzi Giovanna, Casazza Franco, Cialfi Alessandro, Dihel Livia, Giagnoni Erminia, Heyman Joanna, Lombardi Leonida, Mattioli Roberto, Mazzola Anna Alice, Montericcio Vincenzo, Pepi Mauro, Tusa Maurizio, Morabito Alberto
Abstract
BACKGROUND:
The value of echocardiography in the diagnosis and follow-up of most cardiovascular diseases is well established, even though the ever-increasing demand for the use of this technique is not always justifiable. The "Appropriatezza ECO Milano" project was developed among hospitals in Milan (Italy) to foster a rational use of echocardiography. The aim of this study was to evaluate and improve appropriateness of requests for two-dimensional color Doppler echocardiography, considering indications, prescription behaviors and clinical utility in both the outpatient and inpatient settings.
METHODS:
Following several meetings, a consensus was reached whereby a multicenter, observational study would be undertaken. We assessed the value of each request in agreement with the 2003 American College of Cardiology/American Heart Association/American Society of Echocardiography guidelines. An ad hoc Microsoft Access database was developed to collect study data, which refer to May 2007. Eleven hospitals participated in the study.
RESULTS:
4130 echocardiographic examinations were considered (2300 performed in men and 1830 performed in women; mean age 64 +/- 16 years); 1701 examinations were performed in hospitalized patients and 2429 in outpatients. The incidence of pathological findings was higher in hospitalized patients (73%) than in outpatients (53%) (Pearson chi2 = 29, p
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Relation of terminal QRS distortion to left ventricular functional recovery and remodeling in acute myocardial infarction treated with primary angioplasty.
Am J Cardiol2005 Nov;96(9):1233-6.
Bigi Riccardo, Mafrici Antonio, Colombo Paola, Gregori Dario, Corrada Elena, Alberti Antonia, De Biase Annamaria, Orrego Pedro Silva, Fiorentini Cesare, Klugmann Silvio
Abstract
The association between admission electrocardiogram and 6-month change in left ventricular function and volume was assessed in 200 patients who had acute myocardial infarction that was treated with primary percutaneous coronary intervention. Logistic regression analysis indicated peak creatine phosphokinase-MB, number of Q-wave leads, QRS interval distortion, wall motion score index, and angiographic Thrombolysis In Myocardial Infarction flow grade as predictors of no functional recovery and QRS interval distortion and Thrombolysis In Myocardial Infarction flow grade as predictors of left ventricular remodeling.
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Management of patients with persistent chest pain and ST-segment elevation during 5-fluorouracil treatment: report about two cases.
Ital Heart J2003 Dec;4(12):895-9.
Mafrici Antonio, Alberti Antonia, Corrada Elena, Ferrari Stefano, Marenna Biondino
Abstract
5-Fluorouracil, a widely used drug in cancer treatment, is known to have cardiotoxic effects: chest pain with ECG changes, arrhythmias, arterial hypertension or hypotension, myocardial infarction, cardiogenic shock and sudden death have been described in the literature. Coronary artery vasospasm is the pathogenetic mechanism hypothesized in most cases, but mechanisms other than myocardial ischemia had been advocated in some patients. The approach to the patient with persistent chest pain, despite therapy and persistent ST-segment elevation mimicking an acute myocardial infarction, has not been well addressed, and the appropriate diagnostic and therapeutic pathways have not yet been defined. We present our experience regarding 2 patients treated with 5-fluorouracil and referred to our coronary care unit because of prolonged chest pain (in one case with clinical evidence of hemodynamic impairment) and persistent ST-segment elevation, in whom an acute myocardial infarction was suspected. One patient was treated with systemic fibrinolysis, and coronary angiography was performed 6 days later; the other was submitted to urgent coronary angiography shortly after admission. In both cases the ECG and echocardiographic abnormalities were transient and normalized within a few days, the serum markers of myocardial necrosis were persistently in the normal range and the coronary artery trees were normal. The diagnostic and therapeutic approach to patients with this unusual clinical presentation is also discussed.
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Prognostic value of contractile response during high-dose dipyridamole echocardiography test in heart transplant recipients.
J Heart Lung Transplant2003 May;22(5):526-32.
Ciliberto Guglielma Rita, Parodi Oberdan, Cataldo Gabriella, Mangiavacchi Maurizio, Alberti Antonia, Parolini Marina, Frigerio Maria
Abstract
BACKGROUND:
Coronary allograft vasculopathy (CAV) remains a main factor limiting long-term survival after heart transplantation (HTX). The diagnosis of CAV is still based on serial coronary angiography. In this study, we evaluated the prognostic value of high-dose dipyridamole echocardiography in HTX.
METHODS:
Sixty-eight patients underwent dipyridamole echocardiography within 48 hours of their scheduled annual coronary angiography. Coronary allograft vasculopathy was defined as CAV 1 (focal or diffuse stenosis or=50%). Wall-motion score index (WMSI) was evaluated at rest and after dipyridamole administration.
RESULTS:
Results of coronary angiography were normal in 43 patients (63%), showed CAV 1 in 11 (16%), and showed CAV 2 in 14 (21%). Rest wall motion was normal in 39 patients and abnormal in 29. After dipyridamole administration, wall motion remained normal in all 39 (Group 1, no CAV in 34 and CAV 1 in 5). Of 29 patients with rest wall-motion abnormalities, all reversed to normal after dipyridamole in 8 patients (Group 2, no CAV in 7 and CAV 1 in 1) and remained or worsened in 21 (Group 3, CAV 2 in 14 and no CAV or CAV 1 in 7). During follow-up (6 +/- 3 years), 15 patients had major cardiac events: 11 occurred in Group 3, whereas 4 occurred in Groups 1 and 2. Wall motion at rest and after dipyridamole administration and CAV were independent predictors for cardiac events; only dipyridamole WMSI >1 remained significant (p
CONCLUSIONS:
Dipyridamole echocardiography is a simple, non-invasive test that after HTX may identify patients with altered wall motion who deserve stricter surveillance.
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