[Diastolic thrill in the mitral area in the presence of aortic insufficiency. A variant of Austin Flint murmur. Report of 2 cases].
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Biomedical subjects
Publications and source records attributed to F Pileggi.
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Nine of 217 (4.15%) patients with infective endocarditis who were followed from October 1978 to February 1984 had extracranial mycotic aneurysms (MA). Age range of patients was 6-43 years (mean of 24.8 years) and 7 were male. Etiologic agents were Streptococcus viridans (3 cases), Staphylococcus aureus (2 cases), Staphylococcus epidermidis (1 case), and Pseudomonas aeruginosa (1 case). Two patients had negative blood cultures. The MA involved the arteries of the limbs (5 cases), thoracic (3 cases), and abdominal (1 case) arteries. The diagnosis was made by means of physical examination (5 cases), chest roentgenogram (2 cases), ultrasound examination (1 case), and aortography (1 case), at hospital admission (2 cases), early or before antibiotic therapy (2 cases), and from two days to six months after finishing antibiotic therapy (5 cases). All but one patient were operated upon due to MA; bleeding occurred in three cases; surgery was an emergency procedure in one case and performed from 8 to 58 days after the diagnosis of the MA in the others. Signs of infection at surgery were found in one case. In the others, further antibiotic therapy was not administered. There were no limb losses in the peripheral MA. Four patients received surgical treatment for endocarditis. There was one in-hospital death and another one 6 months later due to heart failure.
From 1982 to 1984 nine of 300 patients undergoing transluminal coronary angioplasty died. The nine coronary arteries and one saphenous aorto-coronary by-pass graft affected by angioplasty were studied by light microscopy. The following types of lesions were found, frequently in association: rupture of the plaque, circumscribed or reaching to the intimal layer or extending beyond it, dissections (fissures) between arterial layers, intra-plaque haemorrhage, plaque emboli and thrombosis. In two cases the therapeutic approach was considered to be clinically and pathologically successful; the patients survived 24 h (case 6) and forty days (case 4). Case 6 which presented recent lesions indicative of success showed, in contrast with the other non-successful cases, rupture affecting not only the intimal layer but also deeper structures of the arterial wall. There were also more extensive fissures. Case 4 which presented late alterations indicative of success showed a plaque fracture whose borders were kept apart by fibrous tissue. In conclusion, we believe that angioplasty allows the re-establishment of arterial blood flow by provoking deep intimal and medial rupture producing a small fissure between the arterial layers and a widening of the lumen; in cases with good late results these alterations cicatrize leaving a wider arterial lumen.
Right ventricular endomyocardial biopsy was used to study myocardial involvement in 42 patients with chronic Chagas' disease. Patients were divided into three groups: group A included 16 patients with normal ECGs, normal chest x-rays, and no symptoms; group B included 15 patients with abnormal ECGs and no cardiomegaly; and group C included 11 patients with abnormal ECGs and cardiomegaly. Biopsy fragments were analyzed for hypertrophy, degeneration of myocardial fibers, and interstitial changes such as edema, fibrosis, and inflammatory infiltrate. In group A, 5 of 16 biopsies exhibited none of the previously mentioned alterations. The frequencies pathologic alterations in groups A, B, and C, respectively, were: hypertrophy 31%, 66%, and 100%; degeneration 50%, 86%, and 81%; edema 43%, 46%, and 36%; fibrosis 12%, 33%, and 54%; and inflammatory infiltrate 37%, 66%, and 65%. These data suggest that myocardial lesions of Chagas' disease represent a continuous progression from fiber destruction to substitution by fibrosis, with compensatory hypertrophy; these data also suggest that cardiac dilatation occurs when the extent of fibrosis no longer allows for efficient compensatory hypertrophy.
The electrophysiologic studies of three patients with accessory pathways and multiple reentrant circuits are reported. The first patient had two atrioventricular accessory pathways: a left posterior capable of bidirectional conduction and a right paraseptal with retrograde conduction only. Four atrioventricular reentry circuits were documented: left and right orthodromic circuits and a left antidromic circuit with retrograde conduction over the right paraseptal accessory pathway. The second patient had a left lateral atrioventricular accessory pathway with type A preexcitation. Two reentrant tachycardias were noted: an atrial tachycardia where the accessory pathway remained concealed and an orthodromic atrioventricular tachycardia. The third patient had dual atrioventricular nodal pathways and a right nodofascicular accessory pathway. The accessory pathway became manifest only when a critical atrioventricular delay was reached, indicating its association with the slow atrioventricular nodal pathway. Wide QRS tachycardia with left bundle branch block contour was documented, by means of the slow atrioventricular nodal pathway and nodofascicular fiber antegradely, and the proximal right bundle branch, the His bundle, and the fast atrioventricular nodal pathway retrogradely.
CABG was performed in a patient with severe angina pectoris who had previous successful renal transplantation. Renal function, blood biochemistry and lymphocytes T and B did not show significant changes in the postoperative period. No postoperative complications were observed. The use of immunosuppressive drugs did not add risk of infection. One year after the procedure the patient is asymptomatic.
Cardiogenic oedema results from an increase in capillary hydrostatic pressure (either pulmonary or systemic). This increase produces a reduction in the plasma colloidosmotic pressure-capillary pressure gradient, facilitating the accumulation of fluid in the interstitial space and reducing the circulating plasmatic volume. The administration of diuretics to patients with acute ventricular dysfunction has both haemodynamic and renal effects, and causes a reduction in extravascular fluid. In chronic heart failure, the use of diuretics may result in a haemodynamic improvement once the volaemia is reduced. However, in some patients diuretics may cause activation of the neurohumoral axis and consequently a transient haemodynamic deterioration.
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