A5012646653- Cardiac electrophysiology and arrhythmias
- Ion channel regulation and function
- Cardiomyopathy and Myosin Studies
- Cardiovascular Effects of Exercise
- Cardiovascular Function and Risk Factors
- ECG Monitoring and Analysis
- RNA and protein synthesis mechanisms
- Receptor Mechanisms and Signaling
- Muscle Physiology and Disorders
- Cardiac Arrhythmias and Treatments
- Cardiac Fibrosis and Remodeling
- Neuroscience and Neural Engineering
- Cardiac pacing and defibrillation studies
- Viral Infections and Immunology Research
- Signaling Pathways in Disease
- Cardiovascular Disease and Adiposity
- Heart Failure Treatment and Management
- Cardiac Ischemia and Reperfusion
- Extracellular vesicles in disease
- Protein Kinase Regulation and GTPase Signaling
- Phonocardiography and Auscultation Techniques
- Protein Tyrosine Phosphatases
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Neurofibromatosis and Schwannoma Cases
- Hereditary Neurological Disorders
IRCCS Policlinico San Donato
2017-2023
The Ohio State University
2007-2017
IRCCS Humanitas Research Hospital
2014
Vita-Salute San Raffaele University
2014
University of Illinois Chicago
2011-2013
Lung Institute
2009-2012
Jesse Brown VA Medical Center
2012
Emory University
2012
QED Labs
2009
Fondazione Humanitas per la Ricerca
2006
Rationale: Previously, we demonstrated that a deoxycorticosterone acetate (DOCA)-salt hypertensive mouse model produces cardiac oxidative stress and diastolic dysfunction with preserved systolic function. Oxidative has been shown to increase late inward sodium current (I Na ), reducing the net cytosolic Ca 2+ efflux. Objective: in DOCA-salt may I , resulting amenable treatment ranolazine. Methods Results: Echocardiography detected evidence of mice improved after ranolazine (E/E′:sham,...
Brugada syndrome (BrS) is associated with an increased risk of sudden cardiac death due to ventricular tachycardia/fibrillation (VT/VF) in young, otherwise healthy individuals. Despite SCN5A being the most commonly known mutated gene date, genotype-phenotype relationship poorly understood and remains uncertain. This study aimed elucidate correlation BrS.Brugada probands deemed at high future arrhythmic events underwent genetic testing phenotype characterization by means epicardial...
In the present study, we compared cardioprotective effects of TRV120023, a novel angiotensin II (ANG II) type 1 receptor (AT R) ligand, which blocks G protein coupling but stimulates β-arrestin signaling, against treatment with losartan, conventional AT R blocker in cardiac hypertrophy and regulation myofilament activity phosphorylation. Rats were subjected to 3 wk saline, ANG II, + or TRV120023 alone. induced increased left ventricular mass rats that received losartan TRV120023. Compared...
Since omega–3 polyunsaturated fatty acids (n-3 PUFAs) can alter ventricular myocyte calcium handling, these could adversely affect cardiac contractile function, particularly following myocardial infarction. Therefore, 4 wk after infarction, dogs were randomly assigned to either placebo (corn oil, 1 g/day, n = 16) or n-3 PUFAs supplement [docosahexaenoic acid (DHA) + eicosapentaenoic (EPA) ethyl esters; 1, 2, g/day; 7, 8, and 12, respectively] groups. In vivo, function was evaluated by...
Background— Ventricular hypertrophy is a physiological response to pressure overload that, if left untreated, can ultimately result in ventricular dysfunction, including diastolic dysfunction. The aim of this study was test the hypothesis that frequency-dependent myofilament desensitization, healthy myocardium, altered hypertrophied myocardium. Methods and Results— New Zealand white rabbits underwent pulmonary artery banding procedure induce overload. After 10 weeks, animals were euthanized,...
p21-activated kinase 1 (Pak1) is a serine/threonine that activates protein phosphatase 2a, resulting in the dephosphorylation of cardiac proteins and increased myofilament Ca(2+) sensitivity. Emerging evidence indirectly indicates role for Pak1 ischemia-reperfusion (I/R), but direct lacking. We hypothesize activation signaling pathway cardioprotective mechanism prevents or reverses detrimental effects ischemic injury by inducing posttranslational modifications ultimately improve...
Abstract Aims Brugada syndrome (BrS) represents a major cause of sudden cardiac death in young individuals. The risk stratification to forecast future life-threatening events is still controversial. Non-invasive assessment late potentials (LPs) has been proposed as tool. However, their nature BrS undetermined. purpose this study assess the electrophysiological determinants non-invasive LPs. Methods and Results Two hundred fifty consecutive patients with (Group 1, n = 96) without 2, 154)...
Myocardial infarct requires prompt thrombolytic therapy or primary percutaneous coronary intervention to limit the extent of necrosis, but reperfusion creates additional damage. Along with reperfusion, a maladaptive remodeling phase might occur and it is often associated inflammation, oxidative stress, as well reduced ability recover metabolism homeostasis. Infarcted individuals can exhibit lipid turnover their accumulation in cardiomyocytes, which linked deregulation peroxisome proliferator...
Abstract Sudden cardiac death results from arrhythmias commonly caused by channelopathies and cardiomyopathies, often due to several genetic factors. An emerging concept is that these disease states may in fact overlap, with variants traditionally classified ‘cardiomyopathy genes’ resulting ‘channelopathies phenotypes’. Another important the influence of both non-genetic factors expression, leading utilization systems biology approaches, such as genomics/epigenomics, transcriptomics,...