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Michele Galli

Bio: Michele Galli is an academic researcher from University of Naples Federico II. The author has contributed to research in topics: Myocardial infarction & Coronary artery disease. The author has an hindex of 19, co-authored 62 publications receiving 2527 citations.


Papers
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Journal ArticleDOI
Sekar Kathiresan1, Benjamin F. Voight1, Shaun Purcell2, Kiran Musunuru1, Diego Ardissino, Pier Mannuccio Mannucci3, Sonia S. Anand4, James C. Engert5, Nilesh J. Samani6, Heribert Schunkert7, Jeanette Erdmann7, Muredach P. Reilly8, Daniel J. Rader8, Thomas M. Morgan9, John A. Spertus10, Monika Stoll11, Domenico Girelli12, Pascal P. McKeown13, Christopher Patterson13, David S. Siscovick14, Christopher J. O'Donnell15, Roberto Elosua, Leena Peltonen16, Veikko Salomaa17, Stephen M. Schwartz14, Olle Melander18, David Altshuler1, Pier Angelica Merlini, Carlo Berzuini19, Luisa Bernardinelli19, Flora Peyvandi3, Marco Tubaro, Patrizia Celli, Maurizio Ferrario, Raffaela Fetiveau, Nicola Marziliano, Giorgio Casari20, Michele Galli, Flavio Ribichini12, Marco Rossi, Francesco Bernardi21, Pietro Zonzin, Alberto Piazza22, Jean Yee14, Yechiel Friedlander23, Jaume Marrugat, Gavin Lucas, Isaac Subirana, Joan Sala24, Rafael Ramos, James B. Meigs1, Gordon H. Williams1, David M. Nathan1, Calum A. MacRae1, Aki S. Havulinna17, Göran Berglund18, Joel N. Hirschhorn1, Rosanna Asselta, Stefano Duga, Marta Spreafico25, Mark J. Daly1, James Nemesh2, Joshua M. Korn1, Steven A. McCarroll1, Aarti Surti2, Candace Guiducci2, Lauren Gianniny2, Daniel B. Mirel2, Melissa Parkin2, Noël P. Burtt2, Stacey Gabriel2, John R. Thompson6, Peter S. Braund6, Benjamin J. Wright6, Anthony J. Balmforth26, Stephen G. Ball26, Alistair S. Hall26, Patrick Linsel-Nitschke7, Wolfgang Lieb7, Andreas Ziegler7, Inke R. König7, Christian Hengstenberg27, Marcus Fischer27, Klaus Stark27, Anika Grosshennig7, Michael Preuss7, H-Erich Wichmann28, Stefan Schreiber29, Willem H. Ouwehand19, Panos Deloukas30, Michael Scholz, François Cambien31, Mingyao Li8, Zhen Chen8, Robert L. Wilensky8, William H. Matthai8, Atif Qasim8, Hakon Hakonarson8, Joe Devaney32, Mary-Susan Burnett32, Augusto D. Pichard32, Kenneth M. Kent32, Lowell F. Satler32, Joseph M. Lindsay32, Ron Waksman32, Stephen E. Epstein32, Thomas Scheffold, Klaus Berger11, Andreas Huge11, Nicola Martinelli12, Oliviero Olivieri12, Roberto Corrocher12, Hilma Holm33, Gudmar Thorleifsson33, Unnur Thorsteinsdottir34, Kari Stefansson34, Ron Do5, Changchun Xie4, David S. Siscovick14 
TL;DR: SNPs at nine loci were reproducibly associated with myocardial infarction, but tests of common and rare CNVs failed to identify additional associations with my Cardiovascular Infarction risk.
Abstract: We conducted a genome-wide association study testing single nucleotide polymorphisms (SNPs) and copy number variants (CNVs) for association with early-onset myocardial infarction in 2,967 cases and 3,075 controls We carried out replication in an independent sample with an effective sample size of up to 19,492 SNPs at nine loci reached genome-wide significance: three are newly identified (21q22 near MRPS6-SLC5A3-KCNE2, 6p24 in PHACTR1 and 2q33 in WDR12) and six replicated prior observations1, 2, 3, 4 (9p21, 1p13 near CELSR2-PSRC1-SORT1, 10q11 near CXCL12, 1q41 in MIA3, 19p13 near LDLR and 1p32 near PCSK9) We tested 554 common copy number polymorphisms (>1% allele frequency) and none met the pre-specified threshold for replication (P < 10-3) We identified 8,065 rare CNVs but did not detect a greater CNV burden in cases compared to controls, in genes compared to the genome as a whole, or at any individual locus SNPs at nine loci were reproducibly associated with myocardial infarction, but tests of common and rare CNVs failed to identify additional associations with myocardial infarction risk

1,092 citations

Journal ArticleDOI
TL;DR: Deceleration time of early filling is a powerful independent predictor of poor prognosis in patients with left ventricular systolic dysfunction, whether symptomatic or asymptomatic.

289 citations

Journal ArticleDOI
TL;DR: This study provides no evidence supporting an association between 9 polymorphisms of genes encoding proteins involved in hemostasis and the occurrence of premature myocardial infarction or protection against it.
Abstract: Background—We investigated the association between 9 polymorphisms of genes encoding hemostasis factors and myocardial infarction in a large sample of young patients chosen because they have less coronary atherosclerosis than older patients, and thus their disease is more likely to be related to a genetic predisposition to a prothrombotic state. Methods and Results—This nationwide case-control study involved 1210 patients who had survived a first myocardial infarction at an age of <45 years who underwent coronary arteriography in 125 coronary care units and 1210 healthy subjects matched for age, sex, and geographical origin. None of the 9 polymorphisms of genes encoding proteins involved in coagulation (G-455A &bgr;-fibrinogen: OR, 1.0; CI, 0.8 to 1.2; G1691A factor V: OR, 1.1; CI, 0.6 to 2.1; G20210A factor II: OR, 1.0; CI, 0.5 to 1.9; and G10976A factor VII: OR, 1.0; CI, 0.8 to 1.3), platelet function (C807T glycoprotein Ia: OR, 1.1; CI, 0.9 to 1.3; and C1565T glycoprotein IIIa: OR, 0.9; CI, 0.8 to 1.2), fibrinolysis (G185T factor XIII: OR, 1.2; CI, 0.9 to 1.6; and 4G/5G plasminogen activator inhibitor type 1: OR, 0.9; CI, 0.7 to 1.2), or homocysteine metabolism (C677T methylenetetrahydrofolate reductase: OR, 0.9; CI, 0.8 to 1.1) were associated with an increased or decreased risk of myocardial infarction. Conclusions—This study provides no evidence supporting an association between 9 polymorphisms of genes encoding proteins involved in hemostasis and the occurrence of premature myocardial infarction or protection against it.

204 citations

Journal ArticleDOI
TL;DR: After anterior Q-wave infarction, the recovery of perfusion and wall motion may continue well after the subacute phase, suggesting the presence of hibemating myocardium in the infarcted area.
Abstract: BACKGROUND In patients with ventricular dysfunction caused by stunning or hibernation, it is not clear when complete recovery of the salvaged myocardium occurs after acute myocardial infarction. The purpose of this study was to determine whether a delayed recovery of perfusion and contraction continues even after the subacute phase. METHODS AND RESULTS We prospectively studied 71 consecutive male patients with first uncomplicated Q-wave anterior infarction. Resting regional blood flow distribution and contraction were assessed quantitatively 5 weeks and 7 months after the acute phase by serial sestamibi tomography and two-dimensional echocardiography. Coronary angiography also was performed in 52 patients. Overall, at 7 months there was an improvement in the perfusion defect severity (1019 +/- 811 versus 1365 +/- 821 at 5 weeks, P CONCLUSIONS After anterior Q-wave infarction, the recovery of perfusion and wall motion may continue well after the subacute phase. Several patients exhibit relative hypoperfusion in viable tissue as late as 5 weeks after infarction, and a significant improvement of perfusion in the infarcted area commonly is observed between 5 weeks and 7 months. This delayed improvement of perfusion is associated with a delayed improvement of contractile function in the infarcted area after the first 5 weeks, which may continue for up to 7 months, suggesting the presence of hibernating myocardium in the infarcted area. Despite similar perfusion defect sizes, the level of regional function can be different at 5 weeks, and measurements taken around this time may not accurately estimate the eventual recovery of function.

128 citations

01 Jul 2011
TL;DR: In early-onset myocardial infarction, the 9p21.3 variant rs1333040 affects the progression of coronary atherosclerosis and the probability of coronary artery revascularization during long-term follow-up.
Abstract: OBJECTIVES The purpose of this study was to test whether the 9p21.3 variant rs1333040 influences the occurrence of new cardiovascular events and coronary atherosclerosis progression after early-onset myocardial infarction. BACKGROUND 9p21.3 genetic variants are associated with ischemic heart disease, but it is not known whether they influence prognosis after an acute coronary event. METHODS Within the Italian Genetic Study of Early-onset Myocardial Infarction, we genotyped rs1333040 in 1,508 patients hospitalized for a first myocardial infarction before the age of 45 years who underwent coronary angiography without index event coronary revascularization. They were followed up for major cardiovascular events and angiographic coronary atherosclerosis progression. RESULTS Over 16,599 person-years, there were 683 cardiovascular events and 492 primary endpoints: 77 cardiovascular deaths, 223 reoccurrences of myocardial infarction, and 383 coronary artery revascularizations. The rs1333040 genotype had a significant influence (p = 0.01) on the primary endpoint, with an adjusted hazard ratio of 1.19 (95% confidence interval [CI]: 1.08 to 1.37) for heterozygous carriers and 1.41 (95% CI: 1.06 to 1.87) for homozygous carriers. Analysis of the individual components of the primary endpoints provided no significant evidence that the rs1333040 genotype influenced the hazard of cardiovascular death (p = 0.24) or the reoccurrence of myocardial infarction (p = 0.57), but did provide significant evidence that it influenced on the hazard of coronary revascularization, with adjusted heterozygous and homozygous ratios of 1.38 (95% CI: 1.17 to 1.63) and 1.90 (95% CI: 1.36 to 2.65) (p = 0.00015), respectively. It also significantly influenced the angiographic endpoint of coronary atherosclerosis progression (p = 0.002). CONCLUSIONS In early-onset myocardial infarction, the 9p21.3 variant rs1333040 affects the progression of coronary atherosclerosis and the probability of coronary artery revascularization during long-term follow-up.

70 citations


Cited by
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Journal ArticleDOI
08 Oct 2009-Nature
TL;DR: This paper examined potential sources of missing heritability and proposed research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.
Abstract: Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.

7,797 citations

Journal ArticleDOI
TL;DR: Recommendations for the evaluation of left ventricular diastolic function by echocardiography are made and further research is needed to determine the best method for this evaluation.
Abstract: Recommendations for the evaluation of left ventricular diastolic function by echocardiography

4,162 citations

Journal ArticleDOI
TL;DR: Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography and the European Association of Cardiovascular Imaging are presented.
Abstract: Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography : An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging

4,020 citations

Journal ArticleDOI
TL;DR: The assessment of left ventricular (LV) diastolic function and filling pressures is of paramount clinical importance to distinguish this syndrome from other diseases such as pulmonary disease resulting in dyspnea, to assess prognosis, and to identify underlying cardiac disease and its best treatment.
Abstract: The assessment of left ventricular (LV) diastolic function should be an integral part of a routine examination, particularly in patients presenting with dyspnea or heart failure. About half of patients with new diagnoses of heart failure have normal or near normal global ejection fractions (EFs). These patients are diagnosed with “diastolic heart failure” or “heart failure with preserved EF.”1 The assessment of LV diastolic function and filling pressures is of paramount clinical importance to distinguish this syndrome from other diseases such as pulmonary disease resulting in dyspnea, to assess prognosis, and to identify underlying cardiac disease and its best treatment. LV filling pressures as measured invasively include mean pulmonary wedge pressure or mean left atrial (LA) pressure (both in the absence of mitral stenosis), LV end-diastolic pressure (LVEDP; the pressure at the onset of the QRS complex or after A-wave pressure), and pre-A LV diastolic pressure (Figure 1).Although these pressures are different in absolute terms, they are closely related, and they change in a predictable progression with myocardial disease, such that LVEDP increases prior to the rise in mean LA pressure. Figure 1 The 4 phases of diastole are marked in relation to high-fidelity pressure recordings from the left atrium (LA) and left ventricle (LV) in anesthetized dogs. The first pressure crossover corresponds to the end of isovolumic relaxation and mitral valve opening. In the first phase, left atrial pressure exceeds left ventricular pressure, accelerating mitral flow. Peak mitral E roughly corresponds to the second crossover. Thereafter, left ventricular pressure exceeds left atrial pressure, decelerating mitral flow. These two phases correspond to rapid filling. This is followed by slow filling, with almost no pressure differences. During atrial contraction, left atrial pressure again exceeds left ventricular pressure. The solid arrow points to left ventricular minimal pressure, the dotted arrow to left ventricular …

3,659 citations

Journal ArticleDOI
TL;DR: Reversible myocardial dysfunction can be identified by contrast-enhanced MRI before coronary revascularization and is strongly related to the degree of improvement in the global mean wall-motion score and the ejection fraction after Revascularization.
Abstract: Background Recent studies indicate that magnetic resonance imaging (MRI) after the administration of contrast material can be used to distinguish between reversible and irreversible myocardial ischemic injury regardless of the extent of wall motion or the age of the infarct. We hypothesized that the results of contrast-enhanced MRI can be used to predict whether regions of abnormal ventricular contraction will improve after revascularization in patients with coronary artery disease. Methods Gadolinium-enhanced MRI was performed in 50 patients with ventricular dysfunction before they underwent surgical or percutaneous revascularization. The transmural extent of hyperenhanced regions was postulated to represent the transmural extent of nonviable myocardium. The extent of regional contractility at the same locations was determined by cine MRI before and after revascularization in 41 patients. Results Contrast-enhanced MRI showed hyperenhancement of myocardial tissue in 40 of 50 patients before revascularizat...

3,058 citations