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Biomedical subjects

C Basso

Publications and source records attributed to C Basso.

At least 73 records · Page 4Linked to original sources
PubMed1996

Spin-echo nuclear magnetic resonance for tissue characterisation in arrhythmogenic right ventricular cardiomyopathy.

OBJECTIVE: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disorder characterised clinically by ventricular arrhythmias that can cause cardiac arrest and morphologically by fatty or fibro-fatty myocardial atrophy of the right ventricle. In vivo tissue characterisation without endomyocardial biopsy would be useful. The aim of this study was to investigate the diagnostic accuracy of spin-echo nuclear magnetic resonance (NMR) for tissue characterisation in ARVC. PATIENTS AND METHODS: Twenty three subjects (15 men and eight women, aged 18-49, mean 34) were studied with spin-echo T1-weighted NMR and multislice scan. Fifteen had a clinical diagnosis of ARVC and eight were controls (age and sex matched subjects). Data were independently evaluated by two expert observers. RESULTS: In the control group NMR was always negative (100% specificity). Ten of the 15 patients with ARVC had an abnormal NMR result (67% sensitivity), with areas that had a signal intensity close to that of pericardial or subcutaneous fat. In the remaining five cases the NMR signal was inadequate. Nine patients underwent both NMR and endomyocardial biopsy; biopsy was positive in eight (89%) and NMR was positive in five (56%). CONCLUSIONS: NMR is a useful non-invasive diagnostic tool in the evaluation of fatty replacement in ARVC. The technique can be used with other procedures in the initial diagnostic evaluation and is a useful alternative tool in the long term follow up of patients with ARVC.

Adolescent↗
PubMed1995

Congenital heart disease and sudden death in the young.

Sudden death is a frequent mode of fatal outcome in cardiac disease and does not exclude young people. The aim of this investigation was to establish whether and to what extent sudden death in the young may be ascribable to the substrate of underlying congenital heart disease. Among 182 young people (< or = 35 years) who died of cardiac sudden death and underwent postmortem examination, 58 (32%) had congenital heart disease. Seven showed an intrapericardial rupture of aortic dissection, in the setting of Marfan syndrome in two, isolated bicuspid aortic valve in two, and bicuspid aortic valve and isthmic coarctation in three; all exhibited equally severe degeneration of the aortic wall. Sixteen cases had conduction system anomalies, mostly bypass tracts; 15 coronary artery anomalies (three ostial valve-like stenosis, five origin from the wrong aortic sinus, and seven deep intramyocardial course); 12 hypertrophic cardiomyopathy; five postoperative congenital heart disease including scar following ventriculotomy, conduction system injury, and defects left unrepaired; and three congenital aortic valve stenosis. One third of sudden deaths in the young was ascribable to structural defects present since birth. A large spectrum of congenital heart disease involves the risk of sudden death, but most structural defects are usually not considered to be life threatening. Some of these concealed defects are potentially detectable in life by clinical imaging techniques.

Adolescent↗
PubMed1995

Sudden death in mitral valve prolapse with Holter monitoring-documented ventricular fibrillation: evidence of coexisting arrhythmogenic right ventricular cardiomyopathy.

We report the case of a 42-year-old female, affected by mitral valve prolapse and ventricular arrhythmias, who died suddenly from ventricular fibrillation recorded during Holter monitoring. The lethal arrhythmia initiated with late diastolic couplets followed by a ventricular tachycardia that eventually degenerated into ventricular fibrillation. The patient had experienced four orthostatic and stress-related syncopal episodes, associated with nausea and diaphoresis, and a positive tilt test. Holter monitoring documented ventricular arrhythmias, consisting of both isolated monomorphic and sporadic repetitive beats. Her standard ECG and exercise test were normal, but signal-averaged study findings were significantly positive. QT prolongation in the absence of arrhythmias was observed during the Valsalva manoeuvre and isoproterenol infusion. 2D echo showed a remarkable mitral valve prolapse without regurgitation and localized structural abnormalities of the right ventricle. Postmortem study confirmed mitral valve prolapse, and also disclosed pulmonary infundibulum dilatation, massive adipose infiltration of the right ventricular free wall, patchy fibrosis and scattered myocardial inflammatory infiltrates in the left ventricle; these features are all consistent with arrhythmogenic right ventricular cardiomyopathy.

Adult↗
PubMed1995

Bicuspid aortic valves in hearts with other congenital heart disease.

The bicuspid aortic valve is the most frequent congenital cardiac malformation; it may be isolated or associated with other congenital heart disease. The present investigation consists of a study of bicuspid aortic valves in 1022 heart specimens belonging to the anatomical collection of the Institute of Pathological Anatomy of the University of Padua. A bicuspid aortic valve was observed in 95 specimens. It occurred as an isolated congenital cardiac defect in 28 cases, seven of which had spontaneous laceration of the aortic valve (aortic dissection). It was associated with other congenital cardiac malformations in 67 out of the remaining 994 specimens (6.7%), 41 of which (61.2%) showed obstruction of the aortic arch. The frequency of bicuspid aortic valve in specimens with complete transposition of great arteries was only 1%. Bicuspid aortic valve was particularly frequent in association with ventricular septal defect and was significantly more frequent in cases with (51.1%) than in cases without (20.5%) aortic arch obstruction (p < 0.001). There was no significant relationship between the occurrence of bicuspid aortic valves and left ventricular outflow tract obstructions or mitral valve malformations. The morphology of the pulmonary valve was also examined. Concurrence of a bicuspid aortic and pulmonary valve was detected in 11 specimens, five of these had trisomy-18. Our findings cast doubt on the assumption that altered fetal blood flow through the aortic valve may be the main factor producing the bicuspid condition. Indeed, they rather support the hypothesis that most bicuspid aortic valves are expressions of a developmental complex that affects the aortic arch and the wall of the ascending aorta as well as the aorta valve.

Adult↗
PubMed1994

Anomalous origin of the right coronary artery from the left aortic sinus and sudden infant death.

The origin of the right coronary artery from the left aortic sinus is an uncommon anomaly, which has been shown to be a cause of sudden cardiac death in young and adult patients, often in association with physical exertion. So far, to the best of our knowledge, only six cases of sudden death related to this anomaly have been reported in newborns and infants. We describe here a further case which reinforces the need of precise postmortem examination in these fatalities.

Coronary Vessel Anomalies↗
PubMed1994

Surgical pathology of valve disease in the elderly.

Since age is no longer considered an additional risk factor for cardiac surgery, the epidemiology of valve disease in the elderly at present may be estimated from the surgical pathology evaluation of valve specimens which are resected at the time of valve replacement. In the time interval 1991-1993, 500 patients underwent native cardiac valve replacement or repair at our University, with a total of 549 valves available for gross and histological examination. Single valve surgery was performed in 451 patients (300 aortic, 148 mitral, 3 tricuspid), and double valve replacement in 49 (47 mitral-aortic, 1 aorto-tricuspid and 1 mitral-tricuspid). Two hundred and eighteen patients (44%) were older than 65 years; the mean age was 70.4 +/- 4.3 years, and the male to female ratio was 0.9 to 1. Two-thirds of the interventions in the elderly group were aortic operations. However, regardless of the age group, 50 and 60% of the cases with respectively aortic and mitral valve disease were due to rheumatic disease. Age-related degenerative valve diseases were prominent; senile dystrophic calcification with aortic stenosis mostly in the elderly, anuloaortic ectasia with aortic incompetence mostly in adults, and floppy valve with mitral incompetence in both age groups. Bicuspid aortic valve, a congenital anomaly which is silent until adulthood, accounted for both aortic stenosis and stenoincompetence by dystrophic calcification, and pure aortic incompetence by endocarditis or anuloaortic ectasia. Our findings suggest that although age-related degenerative valve diseases are increasing, rheumatic disease still remains the leading cause of valve dysfunction in our country even in the elderly. These data may have an impact on prevention strategies and health-care costs. However, it has to be pointed out that the high prevalence of rheumatic disease is a feature of this particular study but is different from the findings of other studies around the world.

Adolescent↗
PubMed1994

Sudden cardiac arrest in a teenager as first manifestation of Takayasu's disease.

A 14-year-old girl was rescued from a sudden cardiac arrest at school. Aortography disclosed mild aortic root dilation with aortic valve incompetence and subocclusion of coronary ostia and left common carotid artery. An emergency aortocoronary bypass operation was undertaken, but the patient did not recover from cardiopulmonary bypass. Postmortem disclosed massive myocardial infarction. The microscopic feature of arterial involvement was consistent with giant cell Takayasu's arteritis. The abrupt clinical presentation in this teenager with coronary ostial subocclusion is very unusual.

Adolescent↗
PubMed1994

Sudden death in the young. Is acute coronary thrombosis the major precipitating factor?

BACKGROUND: Atherosclerotic coronary artery disease, complicated by acute thrombosis, is the usual cause of sudden death in adults. This study addresses the pathology of coronary arteries in sudden death in the young (< or = 35 years old). METHODS AND RESULTS: Among 200 consecutive cases of sudden death in youth in the Veneto region of Italy, 37 (33 men and 4 women, age 18 to 35 years; mean, 29.4 years) showed obstructive atherosclerotic coronary artery disease in the absence of other cardiac pathological conditions and causes of death. No patient had previous angina pectoris or myocardial infarction. Cardiac arrest occurred at rest in 30 subjects and was related to effort in 7. A histological study was carried out on the obstructive coronary plaques. Degree of lumen stenosis and extension of lipid core and intimal fibrocellular hyperplasia facing the lumen were calculated morphometrically. Immunohistochemistry and electron microscopy were used to further characterize the plaque cell population. Single-vessel disease was found in 33 patients and triple-vessel disease in 4, with an overall total of 45 obstructive plaques, 34 of which were located in the proximal left anterior descending coronary artery. At histological study, only 10 plaques from 10 patients showed acute thrombosis (occlusive in 5 and subocclusive in 5); the remaining 35 were uncomplicated. Thirty-one plaques were fibrous in nature, while the other 14 were atheromatous. Compared with the atheromatous lesions, the fibrous plaques were rarely complicated by thrombosis (3% versus 64%; P < .001) and distinctly exhibited a fairly well-preserved tunica media (81% versus 21%; P < .001) as well as a stratum of neointimal fibrocellular hyperplasia (68% versus 7%; P < .001), which on immunohistochemistry and electron microscopy appeared to be proliferating smooth muscle cells. CONCLUSIONS: In our study population, sudden death was precipitated by acute coronary thrombosis in only 27% of patients with obstructive coronary atherosclerotic plaque. Most of the young victims of sudden death with obstructive coronary atherosclerosis showed single-vessel disease that affected the left anterior descending coronary artery and was due to fibrous plaques with neointimal smooth muscle cell hyperplasia and a preserved tunica media in the absence of acute thrombosis.

Acute Disease↗
PubMed1994

[Histopathological features of balloon coronary angioplasty].

Balloon coronary angioplasty revascularization is accomplished through a remodelling of the atherosclerotic stenotic wall. Increase in lumen diameter is achieved by plaque cracking with intimal dissection, plaque compression and medial stretching. Acute complications are frequent (3-8%) and mostly consist of occlusive thrombosis occurring upon fissuring of atheromasic plaque, intimal flap with invagination, medio-adventitial dissection in the case of tearing of the tunica media, and atheromatous embolism. Healing process may be so exuberant as to lead to restenosis within a few months.

Angioplasty, Balloon, Coronary↗
PubMed1993

[The early and late complications after percutaneous balloon coronary angioplasty].

The coronary arteries from the hearts of 7 patients, 6 male and 1 female, age ranging from 39 to 69 years (mean 56), who died early or in the mid term from percutaneous transluminal coronary angioplasty (PTCA), were investigated by histology, immunohistochemistry and electron microscopy. Atherosclerotic coronary artery disease was present in all: single vessel disease in 2 and double vessel disease in 5. Indication to PTCA was stable angina in 1 patient, unstable angina in 2, postinfarction angina in 2 and acute myocardial infarction in the remaining 2. Thrombolysis was an associated procedure in 3 cases. Time interval between PTCA and death was less than 48 hours in 6, and 4 months in 1. Cause of death was myocardial infarction due to coronary occlusion complicating PTCA in 3 patients, and myocardial infarctions preceding PTCA in 4 patients. 9 coronary segments underwent dilatation: 5 in the anterior descending coronary artery, 3 in the right coronary artery and 1 in the left circumflex artery. Angiographically, the PTCA had been effective (decrease of stenosis > or = 40%) in 5 and failed in 4. Basically, the atherosclerotic plaques were eccentric in 3 and concentric in 6; the histotype was fibrotic in 4, atheromatous in 4 and fibro-atheromatous in 1. Only one case did not show any complication and the dilatation was effective as a consequence of plaque compression and stretching of the underlying tunica media. Complications observed in the other cases with early death consisted of: a) plaque cracks with intimal flaps and hematomas in all 6; b) laceration of the tunica media, even of the disease-free wall, with dissecting hematoma in 2; c) occlusive thrombosis in 3 and d) atheroembolism in 1. The 4 coronary segments, which appeared occluded angiographically soon after PTCA, were clinically interpreted as dissection in 3 and thrombosis in 1, whereas at histology the closing mechanism was an intimal hematoma with flap in 2, occlusive thrombosis in 1, and medio-adventitial dissecting hematoma with thrombosis in 1. Only ruptures of atheromatous plaques were complicated by thrombosis. The patient who died at 4 months exhibited a pattern of restenosis due to intimal smooth muscle cell proliferation. In conclusion, our postmortem study shows that PTCA may be associated with severe damage of the coronary artery consisting of plaque crack and laceration even of the disease-free wall, intimal and medial hematomas, thrombosis and atheroembolism.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

[Myocardial infarct and sudden death with angiographically undamaged coronary arteries].

Clinicopathologic findings in two young adults, who complained of ischemic cardiac arrest by ventricular fibrillation and of myocardial infarction complicated by cardiogenic shock respectively, are described. At coronary angiography, coronary arteries appeared normal. In both cases, detailed pathologic examination of the coronary arteries disclosed a focal eccentric atherosclerotic plaque in the proximal descending coronary artery, where selective coronary angiography had failed to reveal filling defects. These observations suggest a more critical attitude in evaluating angiographically normal coronary arteries in patients with myocardial infarction or aborted sudden death, and underline the possibility of arterial lumen stenosis underestimation, especially in the presence of eccentric plaque, with likely compensatory ectasia of the plaque-free wall segment.

Adult↗
PubMed1986

Relationships between metabolic deactivation of ICR compounds and their differential mutagenicity in bacteria and cultured mammalian cells.

Preparations of Chinese hamster ovary (CHO) cells decreased the genotoxicity of 3 ICR compounds (ICR 191, ICR 191-OH and ICR 170-OH), while they did not affect the genotoxicity of ICR 170 in the Salmonella reversion test nor in a DNA-repair test in E. coli. These data may contribute towards the explanation of the lack of activity of the two hydroxylated compounds in the CHO/HGPRT forward mutation system, as well as the different rank of mutagenicity of the two chloroethyl compounds in bacteria (ICR 191 greater than ICR 170), compared to cultured mammalian cells and in general to eukaryotic cells (ICR 170 greater than ICR 191).

Aminacrine↗
PubMed1986

Bacterial genotoxicity of nitrosated famotidine.

Famotidine, a histamine H2-receptor antagonist, was devoid of mutagenic activity in seven his- Salmonella typhimurium strains (TA1535, TA1537, TA1538, TA97, TA98, TA100 and TA102) and was equitoxic in repair-proficient (WP2) and repair-deficient (WP2uvrA, WP67, CM561, CM571, WP100 and CM871) Escherichia coli strains, both in the presence and in the absence of S9 mix containing liver S9 fractions from Aroclor-treated rats. However, after a short pre-incubation step with nitrite in an acidic environment, the drug increased, by a direct mechanism, the number of his+ revertants in Salmonella strains TA100, TA102 and TA97 (a decrease of mutagenicity being conversely observed in TA1535) and of trp+ revertants in E. coli strains WP2uvrA and WP67. Moreover, it enhanced the induction of non-reparable DNA damage in E. coli strains simultaneously lacking the uvrA-dependent excision repair and the lexA post-replication repair pathways. The mutagenicity of acidified nitrite-famotidine mixtures was related to doses of both precursors, with a maximum production of mutagenic derivatives in a slight molar excess of nitrite. The optimal pH of the nitrosation reaction (2.0) was intermediate between the one required for cimetidine (1.5) and ranitidine (2.5). Potency of famotidine as a precursor of mutagenic derivatives was considerably lower than the one of the other two H2 blockers. The nitrosation products of all three drugs mainly induced base-pair substitutions in Salmonella DNA, to a greater extent at sites containing G.C base pairs (strain TA100) in the case of famotidine and cimetidine, and at sites containing A.T base pairs (TA102) in the case of ranitidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Metabolic activation of hepatocarcinogens in chronic hepatitis B.

S9 fraction pools of liver biopsy samples, collected from 129 patients in two consecutive studies, were comparatively assayed for their ability to activate aflatoxin B1 (AFB1) and a tryptophan pyrolysate product (Trp-P-2) in a miniaturized Salmonella mutagenicity test system. Metabolic activation was not affected to a significant extent by most of the monitored variability factors, such as sex, alcohol, cigarette smoking and liver histology (minimal changes, chronic persistent (CPH) or active (CAH) hepatitis, CAH steatosis, or cirrhosis). Conversely, a significant enhancement of activation was observed for AFB1 in cases of mild CAH and especially for Trp-P-2 in hepatitis B virus carriers, irrespective of their histologic diagnosis.

Aflatoxin B1↗