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Biomedical subjects

G Thiene

Publications and source records attributed to G Thiene.

At least 181 records · Page 10Linked to original sources
PubMed1992

Heart valve bioprosthesis durability: a challenge to the new generation of porcine valves.

Long-term experience with first generation porcine valve xenografts enabled identification of the major limitations to their durability: (1) prosthetic-ventricular mismatch due to the high profile of the stent in patients with mitral stenosis and a small left ventricle; (2) high-pressure fixation with loss of natural collagen crimping in the fibrosa, and wash-out of proteoglycans in the spongiosa; (3) xenograft tissue autolysis, due to the long interval between animal slaughter and aortic valve removal fixation; (4) muscle shelf in the right coronary cusp, which created a gradient and could undergo accelerated calcification and/or spontaneous perforation with time; (5) a flexible polypropylene stent, which could creep or even fracture with consequent inward bending of the stent; (6) progressive time-related dystrophic calcification; (7) host fibrous tissue ingrowth. An awareness of these limitations stimulated technical modifications, which frequently brought about distinct improvements: (1) the reduction of the stent profile eliminated the problem of mismatch, but resulted in a higher tendency towards cusp prolapse and earlier commissural tearing; (2) natural collagen waviness, proteoglycans and cusp extensibility were preserved by employing low or even zero pressure during the fixation process; (3) earlier valve fixation enabled preservation of cell integrity; (4) a new orifice for small valves was designed by replacing the right muscular cusp, thus achieving less gradient and avoiding muscle-shelf-related complications; (5) polypropylene was replaced by Delrin as stent material; (6) calcium-retarding agents like T6 and toluidine blue were applied during commercial processing and storage in order to mitigate tissue mineralization.(ABSTRACT TRUNCATED AT 250 WORDS)

Bioprosthesis↗
PubMed1992

Heart valve replacement with the Sorin tilting-disc prosthesis. A 10-year experience.

From 1978 to 1988, 697 patients with a mean age of 48 +/- 11 years (range 5 to 75 years) received a Sorin tilting-disc prosthesis; 358 had had aortic valve replacement, 247 mitral valve replacement, and 92 mitral and aortic valve replacement. Operative mortality rates were 7.8%, 11.3%, and 10.8%, respectively, in the three groups. Cumulative duration of follow-up is 1650 patient-years for aortic valve replacement (maximum follow-up 11.4 years), 963 patient-years for mitral valve replacement (maximum follow-up 9.9 years) and 328 patient-years for mitral and aortic valve replacement (maximum follow-up 9.4 years). Actuarial survival at 9 years is 72% +/- 4% after mitral valve replacement, 70% +/- 3% after aortic valve replacement, and 50% +/- 12% after mitral and aortic valve replacement, and actuarial freedom from valve-related deaths is 97% +/- 2% after mitral valve replacement, 92% +/- 2% after aortic valve replacement, and 62% +/- 15% after mitral and aortic valve replacement. Thromboembolic events occurred in 21 patients with aortic valve replacement (1.3% +/- 0.2%/pt-yr), in 12 with mitral valve replacement (1.2% +/- 0.3% pt-yr), and in seven with mitral and aortic valve replacement (2.1% +/- 0.8%), with one case of prosthetic thrombosis in each group; actuarial freedom from thromboembolism at 9 years is 92% +/- 3% after mitral valve replacement, 91% +/- 3% after aortic valve replacement, and 74% +/- 16% after mitral and aortic valve replacement. Anticoagulant-related hemorrhage was observed in 15 patients after aortic valve replacement (0.9% +/- 0.2%/pt-yr), in 9 after mitral valve replacement (0.9% +/- 0.3%/pt-yr), and in 6 with mitral and aortic valve replacement (0.9% +/- 0.5%/pt-yr); actuarial freedom from this complication at 9 years is 94% +/- 2% after aortic valve replacement, 91% +/- 4% after mitral valve replacement, and 68% +/- 16% after mitral and aortic valve replacement. Actuarial freedom from reoperation at 9 years is 97% +/- 2% after mitral and aortic valve replacement, 92% +/- 4% after mitral valve replacement, and 89% +/- 3% after aortic valve replacement, with no cases of mechanical fracture. The Sorin valve has shown a satisfactory long-term overall performance, comparable with other mechanical prostheses, and an excellent durability that renders it a reliable heart valve substitute for the mitral and aortic positions.

Actuarial Analysis↗
PubMed1991

Failure of Hancock pericardial xenografts: is prophylactic bioprosthetic replacement justified?

The incidence of major valve-related complications was evaluated in a series of patients in whom the Hancock pericardial xenograft was used for aortic (AVR; n = 84), mitral (MVR; n = 17) and mitral-aortic (MAVR; n = 13) valve replacement. At 7 years actuarial survival is 66% +/- 8% after AVR, 64% +/- 13% after MVR, and 41% +/- 15% after MAVR, whereas actuarial freedom from valve-related death is 79% +/- 7% after AVR, 78% +/- 13% after MVR, and 81% +/- 12% after MAVR. Actuarial freedom from thromboemboli and anticoagulant-related hemorrhage at 7 years is 93% +/- 4% and 98% +/- 2% after AVR and 83% +/- 10% and 88% +/- 11% after MVR; no such complications occurred after MAVR. Structural valve deterioration determined at reoperation, at autopsy, or by clinical investigation was observed in 34 patients with AVR (10.0 +/- 0.2%/patient-year), in 10 with MVR (10.6 +/- 3.3%/patient-year), and in 9 with MAVR (16.6 +/- 5.5%/patient-year). After AVR, 19 patients underwent reoperation and 2 died before reoperation; 4 patients with MVR underwent reoperation, and 7 patients with MAVR underwent reoperation and 1 died before reoperation. Seventy-eight percent of the current survivors (13 patients with AVR, 7 with MVR, and 1 with MAVR) have clinical evidence of valve failure. At 7 years actuarial freedom from structural deterioration of the Hancock pericardial xenograft is 25% +/- 7% after AVR, 29% +/- 14% after MVR, and 0% after MAVR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Cardiomyopathy: a necessary revision of the WHO classification.

The classification of myocardial disease proposed by the WHO/ISFC task force in 1980 distinguishes specific heart muscle diseases from myocardial diseases of unknown origin, termed cardiomyopathies, and differentiated into the dilated, hypertrophic and restrictive forms. This last group includes endomyocardiofibrosis and fibroblastic parietal endocarditis. In more recent years, two new forms of heart muscle disease have been recognized: so-called "primary" restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Primary restrictive cardiomyopathy is characterized anatomically by normally sized, non-hypertrophic ventricles with dilated atria, and functionally by impaired diastolic compliance due to myocardial stiffness. The clinical picture is that of chronic congestive heart failure; histology shows interstitial fibrosis and myocardial disarray, but not hypereosinophilia. In arrhythmogenic right ventricular cardiomyopathy, the myocardium of the right ventricular free wall is substituted by fibrous and/or adipose tissue, which results in regional dynamic alterations and ominous ventricular arrhythmias. The left ventricle is usually spared. Both forms should be classified as heart muscle diseases of unknown origin, and kept clearly distinct from the other cardiomyopathies listed in the WHO classification.

Arrhythmias, Cardiac↗
PubMed1991

Is lung biopsy useful for surgical decision making in congenital heart disease?

Sixty patients with congenital heart disease (CHD), age range 3 months-45 years (median 2 years), underwent lung biopsy to exclude pulmonary vascular disease (PVD): 25 had an atrioventricular (AV) septal defect, 14 a ventricular septal defect (VSD), 7 a complete transposition of the great arteries (TGA) + VSD, 3 an atrial septal defect, and 2 a patent ductus arteriosus; 9 had other malformations. Scoring of histological section (0-4) according to a modified Heath-Edwards classification disclosed that 30 patients had severe "irreversible" PVD (greater than or equal to grade 3) (11 AV septal defect, 8 VSD, 6 TGA + VSD and 5 others); 8 patients were younger than 1 year. Pulmonary vascular resistance (PVR) was calculated in 51 patients and exceeded 7 U/m2 in 1 of 2 patients with grade 0, in 9 of 18 with grade 1, in 1 of 4 with grade 2, in 11 of 18 with grade 3, and in 8 of 9 with grade 4. PVR was also calculated after 100% oxygen administration in 19 patients, 14 of whom had a resting PVR greater than or equal to 7 U/m2. PVR persisted greater than or equal to 7 U/m2 in 5 patients: 4 had PVD greater than or equal to grade 3 and died after surgery. PVR fell to under 7 U/m2 in 14 patients, 3 of whom had PVD greater than or equal to grade 3:1 patient with grade 4 was not operated upon and 2 with grade 3 were operated upon: all are alive. Follow-up in discharged living patients was 100%, with a mean of 50 months. Fifty-five patients underwent surgery with 10 early and 2 late deaths. Among the 12 subjects with a fatal outcome, 10 had irreversible lesions. The 5 non-operated patients all had irreversible lesions at biopsy, and are still alive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Extended follow-up of the standard Hancock porcine bioprosthesis.

We have reviewed 665 patients in whom the standard Hancock porcine bioprosthesis (HPB) was used for aortic (AVR = 173), mitral (MVR = 437), and mitral and aortic (MAVR = 55) valve replacement in the time interval from 1970 to 1983. After AVR, HPB-related deaths occurred in 24 patients (1.7% +/- 0.4% per patient-year); 11 had thromboembolic episodes (0.8% +/- 0.2% per patient-year), 6 hemorrhages related to anticoagulants (0.4% +/- 0.2% per patient-year), 9 endocarditis (0.7% +/- 0.2% per patient-year), 7 prosthetic leak (0.5% +/- 0.1% per patient-year), and 59 structural deterioration (4.3% +/- 0.6% per patient-year). At 16 years, actuarial survival is 40% +/- 6%, freedom from thromboembolic episodes 89% +/- 4%, from hemorrhages 90% +/- 5%, from endocarditis 94% +/- 2%, from prosthetic leak 95% +/- 2%, and from structural deterioration 36% +/- 6%. After MVR, HPB-related deaths occurred in 64 patients (1.6% +/- 0.2% per patient-year); 68 had thromboembolic episodes (1.7% +/- 0.2% per patient-year), 28 hemorrhages (0.7% +/- 0.1% per patient-year), 12 endocarditis (0.3% +/- 0.1% per patient-year), 9 prosthetic leak (0.2% +/- 0.1% per patient-year), and 158 structural deterioration (4.0% +/- 0.3% per patient-year). At 18 years, actuarial survival is 33% +/- 4%, freedom from thromboembolic episodes 57% +/- 13%, from hemorrhages 81% +/- 6%, from endocarditis 91% +/- 4%, from prosthetic leak 98% +/- 1%, and from structural deterioration 18% +/- 5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1991

Quantitative structural analysis of peripheral airways and arteries in sudden fatal asthma.

The peripheral airways and the adjacent muscular pulmonary arteries were studied by morphometric methods in the autopsy lungs of six asthmatic subjects who died suddenly during an asthma attack, and they were compared with those of six control subjects who died of other causes and had no history of respiratory diseases. Bronchioles of asthmatic subjects had an increased amount of lumen occlusion (p less than 0.01), smooth muscle thickness (p less than 0.001), and inflammatory infiltrate (p less than 0.001), and both mononuclear cells and eosinophils contributed to this increased inflammation. The muscular pulmonary arteries adjacent to occluded and inflamed bronchioles did not have the morphologic features of chronic hypoxia, as shown by the normal medial and intimal thickness, but they had an important inflammatory process in their walls that was particularly marked at sites adjacent to airways. Although the functional significance of these findings is unknown, they may be responsible in part for the gas exchange abnormalities observed in acute severe asthma.

Adolescent↗
PubMed1991

Embolizing papillary fibroelastoma of the mitral valve.

We report a case of myocardial infarction secondary to coronary embolization of a papillary fibroelastoma of the anterior mitral leaflet. The patient underwent successful operation. The English literature describes only 9 other surgically excised papillary fibroelastomas of the mitral valve. In 5 of these cases, the patient presented with signs of cerebral or coronary embolization. Our case further confirms that intracardiac papillary fibroelastomas pose a major threat of systemic embolization and that the clinician should be alert to the possibility of this condition, particularly in young patients who present with myocardial infarction or other conditions that could have arisen from systemic embolization.

Journal Article↗
PubMed1991

[Familial dissecting aortic aneurysm].

A family is described in which two brothers (44 and 48 years old) had aortic dissecting aneurysms (the first one died, the other one underwent surgical treatment and is still living) in the absence of clinical features of Marfan syndrome and of systemic hypertension. Two of the six living siblings have aortic dilation on echocardiography. Histologic examination of the aortic wall at autopsy or surgery revealed a loss of elastic fibers, deposition of mucopolysaccaride-like material and medionecrosis. We can postulate a genetically-determined disease of connective tissue usually described as "Marfan's forme fruste".

Adult↗
PubMed1991

[Congenital malformations of the mitral valve: clinical and morphological aspects].

The clinical, anatomic and functional features of 23 pts with congenital mitral valve malformation, seen at the University of Padua over a period of 10 years, are described. All pts underwent hemodynamic investigation and echo-Doppler evaluation. Diagnosis was confirmed at surgery in 17 cases, and at necropsy in six. In 9 pts mitral anomalies determined prevalent stenosis; the remaining 16 pts had moderate to severe mitral regurgitation. Associated cardiac malformations were present in 19 cases (82.6%). The clinical presentation occurred earlier in pts with mitral stenosis (16.9 months vs 6.55 years). The morphologic and echocardiographic features of each malformation are described. The term "valve dysplasia", as proposed by Becker et al to define the non-Ebstein malformations of the tricuspid valve, is herein applied to the congenital anomalies of the mitral valve in order to obtain a uniform and homogeneous approach to this vast spectrum of malformations.

Adolescent↗
PubMed1991

[The anatomicofunctional picture of the atherosclerotic lesion].

The natural history of atherosclerotic disease is characterized by a first asymptomatic phase, when the lesion develops and a second one, the more dramatic symptomatic phase, when the mature plaques, which represent the progression of the early lesions, and their complications produce a wide range of clinical phenomena. After 1 year of age all children show changes in coronary arterial wall, consisting of cell proliferations, which may be considered as precursors of atherosclerosis. These cells migrate from the tunica media of the coronary artery, proliferate, may synthetize connective tissue and lose the ability to degrade plasma lipoproteins. As a consequence, they may be laden of cholesterol, which accounts for fatty streaks. Later on, near 25% of 15-20 year old children are found to be affected by silent non-obstructive coronary atherosclerotic plaques, which consist of raised lesions, the fibrous plaque, made up of frequently lipid laden cells and fibrous tissue. The lesion-prone area is chiefly the proximal anterior descending coronary artery at the site where the worst precursors of atherosclerosis are usually detected. The medial coat of the vessel retain at this stage a good thickness, which accounts for the vasoreactivity of the coronary artery in youths and young-adults. The trigger in the cascade of dynamic events which lead to the advanced lesions remains a mystery. The plaque is not a static immutable structure, but is subjected to growth with consequent stenosis of the lumen and continuing modification and remodelling which involve all the 3 coats of the arterial wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

[Structural changes in valve prostheses].

All available prostheses, either mechanical or biological, may undergo structural alterations which are cause of reoperation or death. Some of these complications are common to all valves, whereas some are specific for certain models. Modern mechanical prostheses usually are resistant to structural deterioration, but still thrombogenic thus requiring long-term anticoagulation therapy to avoid thrombotic and thromboembolic episodes, which implies the risk of anticoagulation related hemorrhages. Bioprostheses, on the other hand, present a lower thrombogenicity, however they undergo by definition structural degeneration, especially dystrophic calcification, which is usually cause of reoperation within 8-10 years from implantation. Other prosthetic complications, such as infective endocarditis and fibrous tissue overgrowth, are common to both types of prostheses.

Bioprosthesis↗
PubMed1990

Diagnostic accuracy of right ventriculography in arrhythmogenic right ventricular cardiomyopathy.

Diagnostic sensitivity and specificity of cineangiography were evaluated by multivariate logistic discriminant analysis in 32 patients with arrhythmogenic right ventricular (RV) cardiomyopathy, 27 patients with biventricular dilated cardiomyopathy, 28 patients with atrial septal defect and 18 normal subjects. In patients with arrhythmogenic RV cardiomyopathy and biventricular dilated cardiomyopathy, the diagnosis was confirmed by endomyocardial biopsy. All RV values overlapped for the diagnosis of atrial septal defect and arrhythmogenic RV cardiomyopathy; overlapping extended to dilated cardiomyopathy for end-diastolic volume and infundibular dimensions. RV ejection fraction appeared reduced in all the diseases; in particular, mean values in dilated cardiomyopathy and arrhythmogenic RV cardiomyopathy were 38 and 53%, respectively (p less than 0.05). Left ventricular quantitative studies showed a significant difference between dilated and arrhythmogenic RV cardiomyopathy, both in terms of pumping indexes (mean end-diastolic volumes 180 vs 91 ml/m2 and mean ejection fraction 33 vs 60%), and indexes of contractility (stress/end-diastolic volume 3.7 vs 6.7). Multivariate analysis disclosed that transversally arranged hypertrophic trabeculae, separated by deep fissures, were associated with the highest probability of arrhythmogenic RV cardiomyopathy (p less than 0.001). Posterior subtricuspid and anterior infundibular wall bulgings were the only other independently significant variables. Coexistence of these signs was associated with 96% specificity and 87.5% sensitivity. Thus, arrhythmogenic RV cardiomyopathy presents quantitative volumetric and hemodynamic as well as qualitative features that clearly distinguish it from dilated cardiomyopathy and confirm its nosographic autonomy among the primary diseases of the myocardium.

Adult↗