Search PubMed⌕ Search

Biomedical subjects

G Thiene

Publications and source records attributed to G Thiene.

At least 289 records · Page 16Linked to original sources
PubMed1984

Histologic observations after closed chest ablation of the atrioventricular conduction system.

Postmortem examination of the heart was done in a case with disabling supraventricular tachyarrhythmia successfully treated by closed-chest ablation of the His bundle. A ventricular aneurysm developed as a result of a previous myocardial infarction, and death occurred suddenly five months after the procedure. Histologic studies of the atrioventricular (AV) junctional tissue demonstrated severe damage to the nearby AV node and penetrating His bundle. No damage to the branching His bundle or either bundle branch was observed.

Atrioventricular Node↗
PubMed1984

Calcific degeneration as the main cause of porcine bioprosthetic valve failure.

Sixty-seven glutaraldehyde-processed porcine bioprostheses (PBs), recovered at autopsy or reoperation from 65 patients, were evaluated by roentgenologic and pathologic examination. Seven patients with 8 PBs were younger than 20 years of age. The time interval of function was 2 to 138 months (average 62). Pathologically, 53 explants had signs of intrinsic dysfunction, which was ascribed to calcification in 36 (68%). By x-ray examination, calcific deposits were found in 55 of 67 PBs (82%). The mean duration of function was 70 +/- 32 months in calcified PBs vs 27 +/- 18 months in noncalcified PBs (p less than 0.001). All 26 PBs that had been in place for longer than 6 years were calcified. In 45 PBs the Ca++ deposits were considered severe (mean time of function 76 +/- 32 months) and mild in 10 (mean time of function 44 +/- 22 months) (p less than 0.005). The Ca++ deposits were located at the commissures in 54 PBs (98%), at the body of cusps in 41 (75%), at the free margin in 37 (67%) and at the aortic wall in 37 (67%). When mild, Ca++ deposits involved the commissures in 90% of cases, the body of cusps in 30% and the free margin only in 10%. Forty-seven calcified PBs were mounted on a flexible stent, and 8 had a rigid stent, with an average time of function of 63 +/- 28 and 113 +/- 18 months, respectively (p less than 0.00001). Ca++ dysfunction occurred earlier in the aortic than in the mitral position (59 +/- 19 vs 86 +/- 35 months, p less than 0.05). All the PBs explanted from young patients and 47 of 59 PBs removed from adult patients were calcified, with an average time of function of 50 +/- 21 vs 73 +/- 33 months, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Abnormal pulmonary artery branching in tetralogy of Fallot with "absent" pulmonary valve.

Microangiographic postmortem study in a case of tetralogy of Fallot with so-called absent pulmonary valve disclosed an abnormal branching pattern of the intrapulmonary arteries, but failed to detect any compression of intrapulmonary bronchi as a consequence of the distorted segmental arteries. The case also featured the absence of the ductus arteriosus, which should be considered a basic associated anomaly in the development of this malformative complex.

Humans↗
PubMed1984

Isolated mitral valve replacement with the Hancock bioprosthesis: a 13-year appraisal.

Four hundred seventy-six patients underwent isolated mitral valve replacement (MVR) with the glutaraldehyde-preserved porcine Hancock bioprosthesis from March, 1970, through December, 1981. There were 312 female and 164 male patients ranging in age at operation from 9 to 68 years (average, 53 years). Associated surgical procedures were performed in 35 patients. Hospital mortality was 13%, the main cause of death being low-output syndrome. The survivors were followed from 1.6 to 13.2 years (mean, 5.2 years). Cumulative duration of follow-up is 2,180 patient-years and is 97% complete. Overall late mortality is 3.1 +/- 0.3% per patient-year, and actuarial survival is 73.8 +/- 3.4% at 13 years. Embolic accidents occurred in 45 patients and were fatal in 13; the linearized incidence of postoperative systemic thromboemboli is 2.1 +/- 0.3% per patient-year. Reoperation was necessary in 49 patients: in 4 because of valve endocarditis, with 3 deaths; in 6 because of perivalvular leak, with no deaths; in 2 because of left atrial thrombosis; and in 37 because of valve dysfunction due to primary tissue failure, caused mainly by calcific degeneration of the tissue, with 5 operative deaths. Actuarial freedom from primary tissue failure is 58 +/- 6.6% at 13 years. Extended follow-up after MVR with the Hancock bioprosthesis confirms the satisfactory performance and low thrombogenicity of this device up to 13 years after operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1984

Tetralogy of Fallot after surgery: autopsy review of 14 cases.

The possible determinants of a fatal outcome following surgical repair of the tetralogy of Fallot were analyzed by postmortem examination in 14 cases. Only one patient died late in the postoperative period, due to patch detachment; the others died shortly after undergoing surgery. Death could not be explained in three cases. In three patients with perimembranous ventricular septal defects, complete atrioventricular block occurred as a consequence of traumatic disruption of the branching bundle. In four cases residual stenosis of the pulmonary outflow tract was shown; in one of these cases adequate relief of obstruction had been prevented by a large conal coronary artery. A residual mitral cleft was found in one patient. Death was not related to the cardiac conditions in two cases; one of these patients died of brain apoplexy and the other of tracheal hemorrhage. These findings stress the need for accurate preoperative diagnosis and precise knowledge of the surgical anatomy of this malformation.

Adult↗
PubMed1984

Dysplasia of the atrioventricular valves associated with conduction system anomalies.

Clinical, vectorcardiographic, and echocardiographic data from two siblings with atrial septal defects and dysplasia of the mitral and tricuspid valves are reported. Vectorcardiograms showed that both siblings had abnormal ventricular activation with initial electrical forces directed posteriorly. One sibling died after surgery, and necropsy showed incomplete differentiation of the leaflets and tensor apparatus producing anomalies resembling "mitral arcade." Serial histological examination of the conducting tissue showed that the atrioventricular node was located on the left side of the atrial septum, that the central fibrous body and the membranous septum were hypoplastic, and that an accessory nodoventricular pathway originating in the compact node joined the left side of the ventricular septum. This accessory pathway was probably the cause of the unusual ventricular activation. Dysplasia of the mitral and tricuspid valves together with hypoplasia of the central fibrous body and the presence of accessory pathways are probably part of a malformative complex caused by incomplete differentiation of both the cardiac atrioventricular valves and the junctional area.

Child↗
PubMed1984

Congenital atrioventricular block in right atrial isomerism (asplenia). A case due to atrionodal discontinuity.

The association of complex congenital heart disease with asplenia syndrome and congenital AV block is described in a newborn. Cardiovascular lesions were right atrial isomerism, d-loop, discordant ventriculoarterial connection, pulmonary stenosis, total anomalous pulmonary venous drainage, absent right pulmonary artery, and bilateral superior vena cava. The ECG recording disclosed complete AV block with narrow QRS (suprahisian block). The histology of the conduction system revealed two AV nodes, one anterior and one posterior, none of which connected with the atrial myocardium; only the posterior node was continuous with a penetrating and bifurcating bundle. The histologic findings were consistent with the suprahisian AV block due to lack of connection between the atria and the regular posterior AV specialized junction.

Aorta, Thoracic↗
PubMed1984

Diagnosis of cardiac amyloidosis made by ultrastructural examination of endomyocardial biopsy. A case report.

A case of cardiac amyloidosis is described in which clinical and scintigraphic findings were those of ischemic heart disease. Electrocardiogram disclosed low voltages in the peripheral leads and a pattern of anterior pseudo-myocardial infarction. 2D-echocardiography showed thickened cardiac walls and a "granular sparkling" appearance of the septum. The curve of the left ventricular diastolic pressure suggested impaired ventricular relaxation without a true dip-plateau morphology. Stains for amyloid of rectal biopsy specimens were negative. Histological study of left ventricular endomyocardial biopsy indicated the presence of basophilic material among the myocytes; at ultrastructural examination this infiltrating substance resulted to be amyloid. This case stresses the effectiveness of ultrastructural investigation of left ventricular endomyocardial biopsy in the diagnosis of infiltrative and/or metabolic cardiac disorders.

Amyloidosis↗