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Cristina Basso

Publications and source records attributed to Cristina Basso.

At least 55 records · Page 3Linked to original sources
PubMed2003

Does sports activity enhance the risk of sudden death in adolescents and young adults?

OBJECTIVES: We sought to assess the risk of sudden death (SD) in both male and female athletes age 12 to 35 years. BACKGROUND: Little is known about the risk of SD in adolescents and young adults engaged in sports. METHODS: We did a 21-year prospective cohort study of all young people of the Veneto Region of Italy. From 1979 to 1999, the total population of adolescents and young adults averaged 1,386,600 (692,100 males and 694,500 females), of which 112,790 (90,690 males and 22,100 females) were competitive athletes. An analysis by gender of risk of SD and underlying pathologic substrates was performed in the athletic and non-athletic populations. RESULTS: There were 300 cases of SD, producing an overall cohort incidence rate of 1 in 100,000 persons per year. Fifty-five SDs occurred among athletes (2.3 in 100,000 per year) and 245 among non-athletes (0.9 in 100,000 per year), with an estimated relative risk (RR) of 2.5 (95% confidence interval [CI] 1.8 to 3.4; p < 0.0001). The RR of SD among athletes versus non-athletes was 1.95 (CI 1.3 to 2.6; p = 0.0001) for males and 2.00 (CI 0.6 to 4.9; p = 0.15) for females. The higher risk of SD in athletes was strongly related to underlying cardiovascular diseases such as congenital coronary artery anomaly (RR 79, CI 10 to 3,564; p < 0.0001), arrhythmogenic right ventricular cardiomyopathy (RR 5.4, CI 2.5 to 11.2; p < 0.0001), and premature coronary artery disease (RR 2.6, CI 1.2 to 5.1; p = 0.008). CONCLUSIONS: Sports activity in adolescents and young adults was associated with an increased risk of SD, both in males and females. Sports, per se, was not a cause of the enhanced mortality, but it triggered SD in those athletes who were affected by cardiovascular conditions predisposing to life-threatening ventricular arrhythmias during physical exercise.

Adolescent↗
PubMed2003

Implantable cardioverter-defibrillator therapy for prevention of sudden death in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a condition associated with the risk of sudden death (SD). METHODS AND RESULTS: We conducted a multicenter study of the impact of the implantable cardioverter-defibrillator (ICD) for prevention of SD in 132 patients (93 males and 39 females, age 40+/-15 years) with ARVC/D. Implant indications were a history of cardiac arrest in 13 patients (10%), sustained ventricular tachycardia in 82 (62%), syncope in 21 (16%), and other in 16 (12%). During a mean follow-up of 39+/-25 months, 64 patients (48%) had appropriate ICD interventions, 21 (16%) had inappropriate interventions, and 19 (14%) had ICD-related complications. Fifty-three (83%) of the 64 patients with appropriate interventions received antiarrhythmic drug therapy at the time of first ICD discharge. Programmed ventricular stimulation was of limited value in identifying patients at risk of tachyarrhythmias during the follow-up (positive predictive value 49%, negative predictive value 54%). Four patients (3%) died, and 32 (24%) experienced ventricular fibrillation/flutter that in all likelihood would have been fatal in the absence of the device. At 36 months, the actual patient survival rate was 96% compared with the ventricular fibrillation/flutter-free survival rate of 72% (P<0.001). Patients who received implants because of ventricular tachycardia without hemodynamic compromise had a significantly lower incidence of ventricular fibrillation/flutter (log rank=0.01). History of cardiac arrest or ventricular tachycardia with hemodynamic compromise, younger age, and left ventricular involvement were independent predictors of ventricular fibrillation/flutter. CONCLUSIONS: In patients with ARVC/D, ICD therapy provided life-saving protection by effectively terminating life-threatening ventricular arrhythmias. Patients who were prone to ventricular fibrillation/flutter could be identified on the basis of clinical presentation, irrespective of programmed ventricular stimulation outcome.

Adolescent↗
PubMed2003

Coronary thrombosis and sudden death after an enteroviral infection. Case report.

We report the case of a 26-year-old man who died suddenly 9 days after an episode of flu. Microscopic examination of the left anterior descending coronary artery showed an eccentric fibroatheromatic plaque complicated by thrombosis, endothelial erosion and extensive T-cell and macrophage infiltration. Frozen sections of the thrombotic coronary segment, analysed for different infective agents by polymerase chain reaction (PCR) and reverse transcriptase (RT)-PCR, showed positive amplification for an enteroviral genome. Enteroviral infection may play an important role in coronary plaque instability and may precipitate thrombotic occlusion.

Adult↗
PubMed2003

Arrhythmogenic right ventricular cardiomyopathy type 1 (ARVD1): confirmation of locus assignment and mutation screening of four candidate genes.

Arrhythmogenic right ventricular cardiomyopathy type 1 (ARVD1) is an autosomal dominant disorder characterised by progressive degeneration of right ventricular myocardium, arrhythmias and risk of sudden death. By linkage analysis, we previously mapped the involved gene to chromosome 14q24.3. In the present study we report on linkage analysis of one additional and unrelated family, which enabled to confirm previous locus assignment. Another family is reported, in which genetic and clinical data suggest linkage to the same locus. Direct sequencing of DNA from individuals belonging to established ARVD1 families failed to detect causative mutations in exonic sequences of four genes (POMT2, TGFbeta3, KIAAA1036 and KIAA0759) expressed in the heart and which defects could possibly induce plasma membrane instability or apoptosis, key features of ARVD pathogenesis.

Adult↗
PubMed2003

Noninvasive risk stratification in arrhythmogenic right ventricular cardiomyopathy.

The natural history of arrhythmogenic right ventricular cardiomyopathy is determined by the electrical instability of the dystrophic myocardium, which can precipitate arrhythmic cardiac arrest any time during the course of the disease and by the progressive myocardial loss that results in ventricular dysfunction and heart failure. Sudden death accounts for the majority of the fatal events but its occurrence is mostly unpredictable. There are no prospective and controlled studies assessing clinical markers that can predict the occurrence of life-threatening ventricular arrhythmias. However, the noninvasive risk profile, which emerges from retrospective analysis of clinical and pathologic series, is characterized by history of syncope, physical exercise, spontaneous ventricular tachycardia or ventricular fibrillation, right ventricular dysfunction, left ventricular involvement, right precordial negative T wave, right bundle branch block, QT-QRS dispersion, right precordial ST-segment elevation and late potentials. At present only QRS dispersion, history of syncope and right and/or left ventricular abnormalities at radionuclide angiography proved to be independent noninvasive predictors of sudden death.

Arrhythmogenic Right Ventricular Dysplasia↗
PubMed2002

Mutation in human desmoplakin domain binding to plakoglobin causes a dominant form of arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVD/C) is a genetically heterogeneous disease characterized by progressive degeneration of the right ventricular myocardium and increased risk of sudden death. Here, we report on a genome scan in one Italian family in which the disease appeared unlinked to any of the six different ARVD loci reported so far; we identify a mutation (S299R) in exon 7 of desmoplakin (DSP), which modifies a putative phosphorylation site in the N-terminal domain binding plakoglobin. It is interesting that a nonsense DSP mutation was reported elsewhere in the literature, inherited as a recessive trait and causing a biventricular dilative cardiomyopathy associated with palmoplantar keratoderma and woolly hairs. Therefore, different DSP mutations might produce different clinical phenotypes, with different modes of inheritance.

Adolescent↗
PubMed2002

Screening for ryanodine receptor type 2 mutations in families with effort-induced polymorphic ventricular arrhythmias and sudden death: early diagnosis of asymptomatic carriers.

OBJECTIVES: We sought to establish the role of genetic screening for ryanodine receptor type 2 (RyR2) gene mutations in families with effort-induced polymorphic ventricular arrhythmia (PVA), syncope and juvenile sudden death. BACKGROUND: The RyR2 mutations have been associated with PVA, syncope and sudden death in response to physical or emotional stress. METHODS: We studied 81 subjects (39 males and 42 females; mean age 31 +/- 20 years) belonging to eight families with pathogenic RyR2 mutations. All subjects underwent screening for RyR2 mutations, electrocardiography (ECG), 24-h Holter monitoring, signal-averaged electrocardiography (SAECG), two-dimensional echocardiography and exercise stress testing. Electrophysiologic (EP) study was performed in nine patients. RESULTS: Six different RyR2 mutations were found in eight families. Forty-three family members carried the gene mutation. Of these, 28 (65%) showed effort-induced arrhythmic symptoms or signs and one died suddenly during follow-up. Family history revealed 19 juvenile cases of sudden death during effort or emotion. In two families sharing the same mutation, no subject presented with PVA during the stress test; thus, sudden death and syncope were the only clinical manifestations. The 12-lead ECG was normal in all but two subjects, whereas five patients showed positive late potentials on the SAECG. In 17 (39.5%) of 43 subjects, the two-dimensional echocardiogram revealed localized kinetic abnormalities and mild structural alterations of the right ventricle. The EP study was not able to induce PVA. CONCLUSIONS: The absence of symptoms and PVA on the stress test in more than one-third of carriers of RyR2 mutations, as well as the lack of PVA inducibility by the EP study, underlies the importance of genetic screening for the early diagnosis of asymptomatic carriers and prevention of sudden death.

Adolescent↗
PubMed2002

Endothelin A-receptor antagonist administration immediately after experimental myocardial infarction with reperfusion does not affect scar healing in dogs.

OBJECTIVE: Endothelin (ET) receptor antagonists have been reported to reduce both infarct size and no-reflow phenomenon; however, in rat models their effect on the healing process after myocardial infarction (MI) is controversial. The study aimed to evaluate the effect of early administration of the ET(A) receptor antagonist darusentan on scar healing in an ischemia-reperfusion model in dogs. METHODS: Thirty male mongrel dogs surviving 180 min left anterior descending coronary artery balloon occlusion were randomised to: darusentan i.v. bolus-5 mg/kg 5 min before reperfusion-(group I); darusentan i.v. bolus+chronic oral-10 mg/kg/day-(group II); saline (group III). Five age-matched dogs served as controls (group IV). At 6 weeks weight, volume, mass/volume, wall thickness, thinning ratio and expansion index were assessed in the explanted hearts. Infarct size and scar area tissue composition were evaluated by computerized histomorphometry. Cellularity, vessels and TGFbeta in the scar area were scored by immunohistochemistry. RESULTS: 24 dogs (80%; 7 group I, 8 group II, 9 group III) developed an anterior MI, transmural in 15 and subendocardial in 9, mean size 11.5+/-4% of left ventricular area and 37+/-9% of left ventricular endocardial circumference. MIs were homogeneously distributed among the three groups regarding either infarct size or transmural extent. No differences were found in the three MI groups regarding thinning ratio, expansion index and scar area tissue characterization. Percent scar collagen content (37+/-17 vs. 53+/-20 vs. 46+/-14), myofibroblasts (1.2 vs. 1.3 vs. 1.4), macrophages (1.2+/-0.5 vs. 1.3+/-0.5 vs. 1.4+/-0.5), neovessels (2.8+/-0.4 vs. 2.6+/-0.5 vs. 2.9+/-0.3) and TGFbeta score (2 vs. 2.25 vs. 2.11) were not significantly different. CONCLUSIONS: Early administration of the ET(A) receptor antagonist darusentan does not affect the scar healing process at 6 weeks after experimental MI with reperfusion in dogs.

Administration, Oral↗
PubMed2002

Signal-averaged electrocardiographic parameter progression as a marker of increased electrical instability in two cases with an overt form of arrhythmogenic right ventricular cardiomyopathy.

In arrhythmogenic right ventricular cardiomyopathy (ARVC) the fibrofatty substitution of the RV myocardium constitutes the substrate for reentrant circuits, leading to the onset of ventricular arrhythmias. This pathological process also accounts for "delayed ventricular potentials" that could be recorded as late potentials using the signal-averaged ECG technique (SAECG). This study examined two patients affected by overt forms of ARVC who showed a worsening of the electrical instability associated with a fast progression of SAECG parameters, while all the other clinical findings remained unchanged. This suggests a possible role of SAECG parameter progression as a marker of increased electrical instability.

Adolescent↗
PubMed2002

Case report: fibroelastoma of the papillary muscle of the mitral valve: diagnostic implications and review of the literature.

A 77-year-old woman was found accidentally to be in atrial fibrillation. Two-dimensional echocardiography revealed the presence of a mass attached to the anterior papillary muscle of the mitral valve. She was mildly symptomatic for dyspnea and asthenia. The patient was successfully operated on to excise the left ventricular mass and preserve the mitral valve apparatus. Morphological examination of the excised tissue led to a diagnosis of papillary fibroelastoma. Surgical treatment must be considered when such a tumor is diagnosed, even though asymptomatic, and especially if left-sided because of the high risk of systemic embolization.

Aged↗
PubMed2002

Bicuspid aortic valve: abnormal aortic elastic properties.

BACKGROUND AND AIMS OF THE STUDY: Bicuspid aortic valve (BAV) is frequently associated with clinically relevant abnormalities of the aorta, suggesting the existence of a common underlying developmental defect involving the aortic valve and wall of the ascending aorta. The study aim was to evaluate noninvasively the elastic properties of the aortic root in young males with BAV, to discover whether structural abnormalities of the aorta might be manifested by impairment in elasticity. METHODS: Forty-nine young male subjects with isolated BAV were consecutively detected during preenrollment military screening, and studied using transthoracic echocardiography. Data were compared with those obtained in 45 normal subjects, matched for gender and age. RESULTS: Patients and controls were comparable for body size, and systolic and diastolic blood pressures. BAVs were normally functioning in 18 patients (37%), and mildly regurgitant in 31 (63%). Measurements made by two-dimensional echocardiography showed that BAV patients had significantly larger aortic root dimensions at the annulus (2.4+/-0.2 versus 2.2+/-0.2 cm, p <0.001), at the sinus of Valsalva (3.3+/-0.4 versus 2.6+/-0.3 cm, p <0.001), at the sinotubular junction (2.9+/-0.3 versus 2.5+/-0.2 cm, p <0.001), and at the proximal ascending aorta (2.8+/-0.3 versus 2.5+/-0.2 cm, p <0.001). Measurements made using M-mode echocardiography at 3 cm from the annulus, showed the difference between systolic and diastolic diameters of the aortic root to be significantly smaller in patients than in controls (2.1+/-1.2 versus 3.0+/-1.1 mm, respectively, p <0.001). In patients and in controls, both aortic distensibility (2.7+/-1.5 versus 4.8+/-2.2 x 10(-6) cm2 dyne(-1), respectively, p <0.001) and aortic stiffness index (10.2+/-5.3 versus 5.03+/-1.97, respectively, p <0.001) were significantly different. CONCLUSION: Young male subjects with BAV and no or mild aortic regurgitation display large aortic size and abnormal elastic properties of the ascending aorta compared with controls. These findings confirm the notion that, in these patients, aortic root dilatation is a morphological correlate of intrinsic structural aortic abnormality.

Adult↗
PubMedDate not supplied

Spontaneous coronary artery dissection mimicking aortic dissection.

A 51-year-old woman suffered rapidly irreversible cardiogenic shock with left hemiparesis. Transesophageal echocardiography, which represents an essential imaging tool in the emergency room, ruled out aortic dissection involving branch vessels but did not allow an in vivo diagnosis of spontaneous coronary dissection. The in vivo diagnosis of spontaneous coronary dissection is rather difficult because of the dramatic clinical presentation and selective coronary angiography requirement.

Aortic Dissection↗
PubMedDate not supplied

Adipositas cordis, fatty infiltration of the right ventricle, and arrhythmogenic right ventricular cardiomyopathy. Just a matter of fat?

Whether fatty infiltration of the right ventricle has to be considered "per se" a sufficient morphologic hallmark of arrhythmogenic right ventricular cardiomyopathy (ARVC) is still a source of controversy; ARVC should be kept distinct from both fatty infiltration of the right ventricle and adipositas cordis. In fact, it is well known that a certain amount of intramyocardial fat is present in the right ventricular antero-lateral and apical regions even in the normal heart and that the epicardial fat increases with increasing body weight. However, both the fibro-fatty and fatty variants of ARVC show, besides fatty replacement of the right ventricular myocardium, degenerative changes of the myocytes and interstitial fibrosis, with or without extensive replacement-type fibrosis. The need to adopt strict diagnostic criteria is warranted not only in the clinical setting but also in the forensic and general pathology arena. When dealing with a case of sudden death, in which the only morphologic finding consists of an increased amount of epicardial or intramyocardial fat, a more convincing arrhythmogenic source such as myocardial inflammatory infiltrates, fibrosis, anomalous pathways, and ion channel disease should always be searched for, in order to avoid an over-diagnosis of ARVC cases.

Adipose Tissue↗
PubMedDate not supplied

Twenty years of progress and beckoning frontiers in cardiovascular pathology: cardiomyopathies.

In the last 20 years, with the advent of cardiac transplantation and the availability of molecular biology techniques, major advancements were achieved in the understanding of cardiomyopathies. Novel cardiomyopathies have been discovered (arrhythmogenic right ventricular, primary restrictive, and noncompacted myocardium) and added in the update of WHO classification. Myocarditis was also included with the name "inflammatory cardiomyopathy." Adenoviruses and parvoviruses were found to be frequent cardiotropic viruses in addition to enteroviruses. The extraordinary progress accomplished in molecular genetics of inherited cardiomyopathies allowed to establish hypertrophic and restrictive cardiomyopathies as sarcomeric ("force generation") diseases, dilated cardiomyopathies as cytoskeleton ("force transmission") disease, and arrhythmogenic right ventricular cardiomyopathy (ARVC) as cell junction disease. If we consider also cardiomyopathy as ion channel disease (long and short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia), because they are diseases of the myocardium associated with electrical dysfunction, then a genomic/postgenomic classification of inherited cardiomyopathies may be put forward: cytoskeletal cardiomyopathy, sarcomeric cardiomyopathy, cell junction cardiomyopathy and ion channel cardiomyopathy.

Adenovirus Infections, Human↗