Search PubMed⌕ Search

Biomedical subjects

G Thiene

Publications and source records attributed to G Thiene.

At least 127 records · Page 7Linked to original sources
PubMed1995

The aortic valve after heart transplantation.

We studied the aortic root (wall, semilunar cusp, septal myocardium) in 37 patients (29 male and 8 female; mean age; 41 years) who died 2 to 4,380 days (mean, 398 days) after heart (n = 34) and heart-lung (n = 3) transplantation. The aim of the study was to assess tissue viability, graft-host biological interaction, and cusp mineralization with time. Study methods included gross inspection and photos of each specimen, microradiography, histology and immunohistochemistry, scanning and transmission electron microscopy, and atomic absorption spectroscopy. There were no cases of valve dysfunction; in particular, cusp tears or perforations never occurred. Only 1 valve, in place for 12 years, had a pin-point calcification visible to the naked eye. Optimal preservation of the tissue components (endothelium, fibroblasts, collagen and elastic fibers, proteoglycans, intrinsic nervous ganglia) was observed at both short and long term. Concomitant acute rejection of valve leaflets and myocardium was seen in 7, mild valve thickening in 14, myxoid degeneration in 4, and graft aortic atherosclerosis in 26. Mineralization was negligible and was not progressive with time. No linear correlation was found between mineralization and number of acute rejections. In conclusion, we observed optimal cusp viability and integrity even at long term, concomitant valve and myocardium rejection with no valvular sequelae, and negligible, non-progressive cusp calcification. Donor-recipient blood group matching, heart-beating donor, and chronic immunosuppression are the reasonable explanations of the optimal durability of the aortic valve after heart transplantation.

Adult↗
PubMed1995

Porcine valve durability: a comparison between Hancock standard and Hancock II bioprostheses.

Two series of patients who received a Hancock standard (HS) (1970 to 1983) and a Hancock II (HII) (1983 to 1992) porcine bioprosthesis were reviewed to compare bioprosthetic durability. Patients with HS porcine bioprostheses (n = 769) differed from those with HII bioprostheses mostly in mean age at operation (47 +/- 12 versus 62 +/- 9 years; p < 0.001); the latter prosthesis was implanted mostly in patients older than 50 years. At 8 years after operation, actuarial survival was 57% +/- 4% after aortic, 61% +/- 3% after mitral, and 39% +/- 7% after mitral-aortic valve replacement with the HS bioprosthesis; actuarial survival was 51% +/- 9% after aortic, 66% +/- 6% after mitral, and 49% +/- 10% after mitral and aortic valve replacement with an HII bioprosthesis. No cases of structural deterioration of HII bioprostheses were observed at 8 years in any patients. Actuarial freedom from structural valve deterioration was 78% +/- 4% after aortic, 88% +/- 3% after mitral, and 79% +/- 7% after mitral-aortic valve replacement with an HS bioprosthesis at 8 years. In all patients greater than 50 years of age, actuarial freedom from structural valve deterioration at 8 years was 90% +/- 3% in patients with an HS bioprosthesis and 100% in those with an HII bioprosthesis (p = 0.08). A trend to an improved durability of the HII bioprosthesis compared with the HS was observed during the first 8 postoperative years. Because these results could be influenced partly by the age difference in the two series of patients, a longer follow-up is needed to confirm these data.

Actuarial Analysis↗
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

Mid-term results of heart transplantation for end-stage valvular disease.

The results of heart transplantation in a consecutive series of 19 end-stage valvular disease patients (15 male, aged 48 +/- 8 years) were analysed retrospectively. The indication for heart transplantation was heart failure due to left and/or right ventricular dysfunction; 16 patients had undergone previous valve surgery, but prosthetic dysfunction was present in only one patient. All patients were in NYHA class IV, 15 were on oral anticoagulants and 5 on i.v. catecholamine support. There were four in-hospital deaths (21%) and one late death (5%), resulting in a 1-year mortality rate slightly, but not significantly, higher than that of patients transplanted for other indications (16%). Mean follow-up of the survivors was 48 +/- 33 months (range 9-95); 5-year actuarial survival was similar to that observed among the other heart transplantation patients (74 +/- 10% vs 77 +/- 3%, P = NS). The incidence of acute rejection and infection was also similar in valvular disease and non-valvular disease patients. Kidney and liver function at 1 year post-heart transplantation was preserved in all cases; cardiac catheterization revealed normal graft function in all patients and the absence of coronary lesions in all but two. In conclusion, in our limited experience morbidity and mortality in patients transplanted for end-stage valvular disease seem to be similar to those of patients undergoing heart transplantation for other etiologies.

Adult↗
PubMed1995

A new locus for arrhythmogenic right ventricular cardiomyopathy (ARVD2) maps to chromosome 1q42-q43.

Autosomal dominant arrhythmogenic right ventricular cardiomyopathy (ARVD, MIM 107970) is one of the major causes of juvenile sudden death. We have previously assigned the disease locus to chromosome 14q23-q24. Here we report on a novel variant of ARVD, which is transmitted associated to 1q42-q43 and is characterized by a concealed form, showing effort-induced polymorphic tachycardias. Since both loci ARVD1 and ARVD2 map in proximity of alpha-actinin genes, the possible implication of these myofibrillar proteins in the pathogenesis of ARVD is discussed. Two additional ARVD families, tested with markers of chromosomes 1q42-q43 and 14q23-q24, failed to show linkage, providing evidence of further genetic heterogeneity.

Actinin↗
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

Hancock II porcine bioprosthesis: excellent durability at intermediate-term follow-up.

OBJECTIVES: This study aimed to assess the clinical performance and durability of a new generation of porcine valve, the Hancock II bioprosthesis, at intermediate-term follow-up. BACKGROUND: Standard porcine bioprostheses undergo progressive structural deterioration, mainly due to cusp and commissural calcification, affecting durability and requiring reoperation. The Hancock II bioprosthesis, which is currently undergoing clinical investigation, is made from a porcine aortic valve treated with a calcium-retarding agent (sodium dodecyl sulfate [T6]), which should delay onset of calcification and increase durability. METHODS: From May 1983 to December 1992, we used the Hancock II bioprothesis in aortic (59 patients), mitral (101 patients) and mitral-aortic (25 patients), valve replacement procedures. Postoperative follow-up ranged from 0.1 to 8.7 years (mean [+/- SD] 4.5 +/- 2.6 years) and was 100% complete. Freedom from major postoperative events was calculated at 7 years for patients with aortic valve replacement and at 8 years for those with mitral and mitral-aortic valve replacement. RESULTS: The actuarial survival rate was 48 +/- 10%, 76 +/- 3% and 63 +/- 6%; freedom from valve-related mortality was 91 +/- 4%, 94 +/- 2% and 89 +/- 6%; freedom from thromboembolism was 80 +/- 11%, 90 +/- 2% and 79 +/- 7%; and freedom from reoperation was 100%, 97 +/- 1% and 89 +/- 6% after aortic, mitral and mitral-aortic valve replacement, respectively. No structural valve deterioration occurred. CONCLUSIONS: At intermediate-term follow-up the Hancock II bioprosthesis showed excellent durability in all positions. However, the effectiveness of anticalcification treatment must be assessed with longer follow-up studies.

Actuarial Analysis↗
PubMed1994

The gene for arrhythmogenic right ventricular cardiomyopathy maps to chromosome 14q23-q24.

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) is a dominantly inherited disorder progressively affecting the myocardium and it is one of the major causes of juvenile sudden death. The chromosomal localization of the disease gene is reported here for the first time. A maximum lod score of 6.04 was obtained at theta = 0 for linkage with the polymorphic marker D14S42 (14q23-q24) in two families, one of which has 82 subjects (19 affected) in four generations. The pre-symptomatic identification of ARVD carriers by linkage analysis in the affected families strongly increases the possibility of prevention of life-threatening complications.

Arrhythmias, Cardiac↗
PubMed1994

A catastrophic antiphospholipid syndrome: the importance of high levels of warfarin anticoagulation.

We report the clinical observation of a 23-year-old woman affected by the so-called 'catastrophic antiphospholipid syndrome'. Within a 3-month period she suffered a number of thrombotic events and haemolytic anaemia with thrombocytopenia and had high levels of immunoglobulins G and M and anticardiolipin antibodies associated with lupus anticoagulant activity. The severity of the clinical and laboratory changes is described and diagnostic and therapeutic difficulties are discussed. The apparent control of thrombotic events only with high levels of warfarin anticoagulation is stressed.

Adult↗
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↗