10 results match your criteria: "Vita Salute University and Scientific Institute San Raffaele[Affiliation]"
J Nucl Cardiol
April 2022
Nuclear Medicine Unit, Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
J Nucl Cardiol
August 2022
Nuclear Medicine Unit, Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Background: Among the other variants, the apical pattern of hypertrophic cardiomyopathy (AHCM) is probably the most important, with possible aneurysmatic evolution.
Methods And Results: We analyzed 12 patients with AHCM who underwent [N]NH-PET/CT. Regional perfusion, stress global myocardial blood flow (MBF), and transmural perfusion patterns were assessed.
Circ Heart Fail
January 2018
>From the Cardiomyopathy Unit, Careggi University Hospital, Florence, Italy (I.O., B.T., A.F.); Vita Salute University and Scientific Institute San Raffaele, Milan, Italy (P.G.C.); Dipartimento Cardiotoracovascolare, Ospedale Niguarda, Milan, Italy (P.A.M.); Ospedale S. Orsola Malpighi, Bologna, Italy (C.R.); Clinic of General and Interventional Cardiology, University Heart Center, Hamburg, Germany (M.P.); Cardiology Department, Hospital General Universitario de Alicante, ISABIAL - FISABIO, Alicante, Spain (V.C.); Cardiovascular Department, Ospedale di Cattinara, Trieste, Italy (G.S.); Hospital Universitario Virgen de la Arrixaca, IMIB-Arrixaca, Murcia, Spain (F.M.); University Hospital, Heidelberg, Germany (P.E.); University Hospital Regensburg, Germany (L.S.M.); Herz zentrum Georg-August-Universitaet, Göttingen, Germany (C.J.); Department of Clinical and Experimental Medicine, Cardiology, Sassari Hospital, Sassari, Italy (A.G.); Ospedale Mazzoni, Ascoli Piceno, Italy (L.M.); Hospital Ramòn y Cajal, Alcalá University, Madrid, Spain (A.H.M.); Department Neurofarba, University of Florence, Italy (R.C., A.M.); Medi Service, Genoa, Italy (G.R.); Department of Experimental and Clinical Medicine, University of Florence, Italy (C.P., F.F.); Gilead Sciences, Foster City, CA (L.B.); and CESMAV, Florence, Italy (G.G.).
Background: The late sodium current inhibitor ranolazine reverses the main electrophysiological and mechanical abnormalities of human hypertrophic cardiomyopathy (HCM) cardiomyocytes in vitro, suggesting potential clinical benefit. We aimed to assess the effect of ranolazine on functional capacity, symptomatic status, diastolic function, and arrhythmias in HCM.
Methods And Results: In this multicenter, double-blind, phase 2 study, 80 adult patients with nonobstructive HCM (age 53±14 years, 34 women) were randomly assigned to placebo (n=40) or ranolazine 1000 mg bid (n=40) for 5 months.
Background: Symptoms and signs of myocardial ischemia in the absence of obstructive coronary disease are common in hypertensive patients. This can be explained by CMD due to adverse remodeling of coronary arterioles which have also been reported in the SHR.
Objective: The aim of this study was to compare the effects of ramipril, perindopril, candesartan, atenolol, amlodipine, indapamide, and HMR1766 on CMD in the SHR.
Circulation
March 2015
Noninvasive Cardiovascular Imaging Program, Departments of Internal Medicine and Radiology, Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Division of Cardiovascular Medicine, Department of Medicine, Brigham & Women's Hospital, Boston, MA.
Cardiovasc Res
April 2015
Thoraxcenter, Department of Cardiology, Erasmus MC, Rotterdam, The Netherlands.
Mutations in cardiac sarcomere protein genes are associated with a variety of clinical phenotypes, including hypertrophic (HCM), dilated (DCM), and restrictive (RCM) cardiomyopathy as well as left ventricular non-compaction, with the overlap of morpho-functional manifestations in individual patients and families. Over time, initial phenotypes may undergo profound changes which determine clinical course and disease progression. Although genetic defects causing HCM and DCM have opposite effects at the myofilament level, a number of downstream maladaptive mechanisms, ranging from microvascular dysfunction and ischaemia to myocardial fibrosis and from diastolic dysfunction to abnormal sympathetic activation and arrhythmogenesis, seem to recur in sarcomeric cardiomyopathies, independent of the presenting phenotype.
View Article and Find Full Text PDFNat Rev Cardiol
January 2015
CNR IBFM, Via Fratelli Cervi, 93, 20090 Segrate (MI), Italy.
Obstructive disease of the epicardial coronary arteries was recognized as the cause of angina pectoris >2 centuries ago, and sudden thrombotic occlusion of an epicardial coronary artery has been established as the cause of acute myocardial infarction for >100 years. In the past 2 decades, dysfunction of the coronary microvasculature emerged as an additional mechanism of myocardial ischaemia that bears important prognostic implications. The coronary microvasculature (vessels <300 μm in diameter) cannot be directly imaged in vivo, but a number of invasive and noninvasive techniques, each with relative advantages and pitfalls, can be used to assess parameters that depend directly on coronary microvascular function.
View Article and Find Full Text PDFMed Phys
July 2014
INSERM, UMR1101, LaTIM, Université de Bretagne Occidentale, 29609 Brest, France.
Purpose: Cardiac imaging suffers from both respiratory and cardiac motion. One of the proposed solutions involves double gated acquisitions. Although such an approach may lead to both respiratory and cardiac motion compensation there are issues associated with (a) the combination of data from cardiac and respiratory motion bins, and (b) poor statistical quality images as a result of using only part of the acquired data.
View Article and Find Full Text PDFCirculation
June 2014
From the Division of Cardiovascular Medicine, Department of Internal Medicine, and Divisions of Nuclear Medicine and Cardiothoracic Imaging, Department of Radiology, University of Michigan, Ann Arbor, MI (V.L.M.); Noninvasive Cardiovascular Imaging Program, Departments of Internal Medicine and Radiology (V.L.M., M.N., V.R.T., S.D., R.B., M.F.D.C.), and Division of Cardiovascular Medicine, Department of Medicine (V.L.M., V.R.T., J.H., S.D., R.B., M.F.D.C.), Brigham & Women's Hospital, Boston, MA; Division of Nuclear Medicine and Molecular Imaging, Department of Radiology (C.R.F., M.G., J.H., S.D., M.F.D.C.), and Istituto di Bioimmagini e Fisiologia Molecolare (O.R.), Consiglio Nazionale delle Ricerche and Scientific Institute San Raffaele, Milan, Italy; Division of Cardiology, Vita Salute University and Scientific Institute San Raffaele, Milan, Italy (P.G.C.).
Background: Coronary microvascular dysfunction (CMD) is a prevalent and prognostically important finding in patients with symptoms suggestive of coronary artery disease. The relative extent to which CMD affects both sexes is largely unknown.
Methods And Results: We investigated 405 men and 813 women who were referred for evaluation of suspected coronary artery disease with no previous history of coronary artery disease and no visual evidence of coronary artery disease on rest/stress positron emission tomography myocardial perfusion imaging.
Eur Heart J
June 2012
Vita-Salute University and Scientific Institute San Raffaele, Via Olgettina 60, Milan, Italy.
Over the last several decades, basic cardiovascular research has significantly enhanced our understanding of pathobiological processes leading to formation, progression, and complications of atherosclerotic plaques. By harnessing these advances in cardiovascular biology, imaging has advanced beyond its traditional anatomical domains to a tool that permits probing of particular molecular structures to image cellular behaviour and metabolic pathways involved in atherosclerosis. From the nascent atherosclerotic plaque to the death of inflammatory cells, several potential molecular and micro-anatomical targets for imaging with particular selective imaging probes and with a variety of imaging modalities have emerged from preclinical and animal investigations.
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