14 research outputs found

    Gruppi superiori di omotopia

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    Tesi compilativa riguardo definizione, proprietà e metodi di calcolo di Gruppi superiori di omotopia. Argomenti:definizioni, gruppi delle sfere, proprietà, sospensione, proiezioni di rivestimento, spazi fibrati, approssimazione cellulare, gruppi stabili di omotopia, esempi

    Morphofunctional abnormalities of mitral annulus and arrhythmic mitral valve prolapse

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    Background\u2014Arrhythmic mitral valve prolapse (MVP) is characterized by myxomatous leaflets and left ventricular (LV) fibrosis of papillary muscles and inferobasal wall. We searched for morphofunctional abnormalities of the mitral valve that could explain a regional mechanical myocardial stretch. Methods and Results\u2014Thirty-six (27 female patients; median age: 44 years) arrhythmic MVP patients with LV late gadolinium enhancement on cardiac magnetic resonance and no or trivial mitral regurgitation, and 16 (6 female patients; median age: 40 years) MVP patients without LV late gadolinium enhancement were investigated by morphofunctional cardiac magnetic resonance. Mitral annulus disjunction (median: 4.8 versus 1.8 mm; P1.5 (22 [61%] versus 4 [25%]; P=0.016) were higher in MVP patients with late gadolinium enhancement than in those without. A linear correlation was found between mitral annulus disjunction and curling (R=0.85). A higher prevalence of auscultatory midsystolic click (26 [72%] versus 6 [38%]; P=0.018) was also noted. Histology of the mitral annulus showed a longer mitral annulus disjunction in 50 sudden death patients with MVP and LV fibrosis than in 20 patients without MVP (median: 3 versus 1.5 mm; P<0.001). Conclusions\u2014Mitral annulus disjunction is a constant feature of arrhythmic MVP with LV fibrosis. The excessive mobility of the leaflets caused by posterior systolic curling accounts for a mechanical stretch of the inferobasal wall and papillary muscles, eventually leading to myocardial hypertrophy and scarring. These mitral annulus abnormalities, together with auscultatory midsystolic click, may identify MVP patients who would need arrhythmic risk stratification

    Relapsing Leukemia Infiltrating the Heart

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    none11nononeDe Lazzari, Manuel; Fedrigo, Marny; Marra, Martina Perazzolo; Calabrò, Federica; Tarantini, Giuseppe; D'Amore, Emanuele G.S.; Adami, Fausto; Thiene, Gaetano; Iliceto, Sabino; Angelini, Annalisa; Tona, FrancescoDE LAZZARI, Manuel; Fedrigo, Marny; PERAZZOLO MARRA, Martina; Calabro', Federica; Tarantini, Giuseppe; D'Amore, Emanuele G. S.; Adami, Fausto; Thiene, Gaetano; Iliceto, Sabino; Angelini, Annalisa; Tona, Francesc

    Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial infarction

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    Background and aims: No-reflow (NR), where the coronary artery is patent after treatment of ST-elevation myocardial infarction (STEMI) but tissue perfusion is not restored, is associated with worse outcomes. We aimed to investigate the relationship between autoantibodies activating endothelin-1 receptor type A (ETAR-AAs) and NR after primary percutaneous coronary intervention (PPCI) in STEMI. Methods: We studied 50 patients (age 59 ± 11 years, 40 males) with STEMI who underwent PPCI within 6 h after the onset of symptoms. Blood samples were obtained from all patients within 12 h following PPCI for ETAR-AA level measurement. The seropositive threshold was provided by the manufacturer (>10 U/ml). NR was assessed by cardiac magnetic resonance imaging (MVO, microvascular obstruction). As a control group, 40 healthy subjects matched for age and sex were recruited from the general population. Results: MVO was observed in 24 patients (48%). The prevalence of MVO was higher in patients with ETAR-AAs seropositivity (72% vs. 38%, p = 0.03). ETAR-AAs were higher in patients with MVO (8.9 U/mL (interquartile range [IQR] 6.8-16.2 U/mL) vs. 5.7 U/mL [IQR 4.3-7.7 U/mL], p = 0.003). ETAR-AAs seropositivity was independently associated with MVO (OR 3.2, 95% CI 1.3-7.1; p = 0.03). We identified ≥6.74 U/mL as the best cut-off for prediction of MVO (sensitivity 79%; specificity 65%; NPV 71%; PPV 74%; accuracy 72%). Conclusions: The ETAR-AAs seropositivity is associated with NR in STEMI patients. These findings may open up new options in the management of myocardial infarction even if confirmation in a larger trial is needed

    Arrhythmic Mitral Valve Prolapse and Sudden Cardiac Death

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    Background\u2014Mitral valve prolapse (MVP) may present with ventricular arrhythmias and sudden cardiac death (SCD) even in the absence of hemodynamic impairment. The structural basis of ventricular electric instability remains elusive. Methods and Results\u2014The cardiac pathology registry of 650 young adults ( 6440 years of age) with SCD was reviewed, and cases with MVP as the only cause of SCD were re-examined. Forty-three patients with MVP (26 females; age range, 19\u201340 years; median, 32 years) were identified (7% of all SCD, 13% of women). Among 12 cases with available ECG, 10 (83%) had inverted T waves on inferior leads, and all had right bundle-branch block ventricular arrhythmias. A bileaflet involvement was found in 70%. Left ventricular fibrosis was detected at histology at the level of papillary muscles in all patients, and inferobasal wall in 88%. Living patients with MVP with (n=30) and without (control subjects; n=14) complex ventricular arrhythmias underwent a study protocol including contrast-enhanced cardiac magnetic resonance. Patients with either right bundle-branch block type or polymorphic complex ventricular arrhythmias (22 females; age range, 28\u201343 years; median, 41 years), showed a bileaflet involvement in 70% of cases. Left ventricular late enhancement was identified by contrast-enhanced cardiac magnetic resonance in 93% of patients versus 14% of control subjects (P<0.001), with a regional distribution overlapping the histopathology findings in SCD cases. Conclusions\u2014MVP is an underestimated cause of arrhythmic SCD, mostly in young adult women. Fibrosis of the papillary muscles and inferobasal left ventricular wall, suggesting a myocardial stretch by the prolapsing leaflet, is the structural hallmark and correlates with ventricular arrhythmias origin. Contrast-enhanced cardiac magnetic resonance may help to identify in vivo this concealed substrate for risk stratification

    Predictors of Left Ventricular Scar Using Cardiac Magnetic Resonance in Athletes With Apparently Idiopathic Ventricular Arrhythmias

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    Background In athletes with ventricular arrhythmias (VA) and otherwise unremarkable clinical findings, cardiac magnetic resonance (CMR) may reveal concealed pathological substrates. The aim of this multicenter study was to evaluate which VA characteristics predicted CMR abnormalities. Methods and Results We enrolled 251 consecutive competitive athletes (74% males, median age 25 [17-39] years) who underwent CMR for evaluation of VA. We included athletes with >100 premature ventricular beats/24 h or 651 repetitive VA (couplets, triplets, or nonsustained ventricular tachycardia) on 12-lead 24-hour ambulatory ECG monitoring and negative family history, ECG, and echocardiogram. Features of VA that were evaluated included number, morphology, repetitivity, and response to exercise testing. Left-ventricular late gadolinium-enhancement was documented by CMR in 28 (11%) athletes, mostly (n=25) with a subepicardial/midmyocardial stria pattern. On 24-hour ECG monitoring, premature ventricular beats with multiple morphologies or with right-bundle-branch-block and intermediate/superior axis configuration were documented in 25 (89%) athletes with versus 58 (26%) without late gadolinium-enhancement (P<0.001). More than 3300 premature ventricular beats were recorded in 4 (14%) athletes with versus 117 (53%) without positive CMR (P<0.001). At exercise testing, nonsustained ventricular tachycardia occurred at peak of exercise in 8 (29%) athletes with late gadolinium-enhancement (polymorphic in 6/8, 75%) versus 17 athletes (8%) without late gadolinium-enhancement (P=0.002), (P<0.0001). At multivariable analysis, all 3 parameters independently correlated with CMR abnormalities. Conclusions In athletes with apparently idiopathic VA, simple characteristics such as number and morphology of premature ventricular beats on 12-lead 24-hour ambulatory ECG monitoring and response to exercise testing predicted the presence of concealed myocardial abnormalities on CMR. These findings may help cost-effective CMR prescription
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