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Biomedical subjects

A de Micheli

Publications and source records attributed to A de Micheli.

At least 19 recordsLinked to original sources
PubMed2000

On the electrocardiographic diagnosis of biventricular infarctions.

To diagnose posterior and anterior biventricular infarctions it is necessary to record from right and left thoracic and high abdominal unipolar leads. These supplementary leads are dependable, can be repeated as many times as needed and show the evolution from signs of myocardial injury to those of dead tissue (Q waves of 0.04 sec or more). This electrocardiographic evolution increases the diagnostic value of the electrical exploration, since the injury current can be observed also in other conditions. The diagnosis of right ventricular infarction can be established even in the presence of RBBB. Signs of a dead zone in the free right ventricular wall are more frequently observed in posterior biventricular infarctions than in anterior ones. In these cases, the signs of subepicardial injury are more accentuated in the right thoracic unipolar leads than in V3, indicating anterior right ventricular involvement. These signs are also observed in experimental studies made in animals. This electrocardiographic exploration opens a wide field for the diagnosis of myocardial infarction, particularly in biventricular involvement, including old myocardial scars, and in discarding signs of pericarditis manifested only by the upward displacement of the ST segment. A review of the medical literature concerning diagnosis of biventricular infarctions is presented.

Aged↗
PubMed1996

A new ECG algorithm for the localization of accessory pathways using only the polarity of the QRS complex.

A new algorithm is proposed for localization of accessory atrioventricular pathways by use of a 12-lead electrocardiogram (ECG). The polarity of the QRS complex in leads III, V1, and V2 from 102 patients with Wolff-Parkinson-White syndrome with manifested preexcitation who underwent successful radiofrequency catheter ablation was analyzed. Accessory pathways on the right side of the heart were localized to three regions around the tricuspid annulus, and left-sided pathways were localized to two regions around the mitral valve annulus. In 42 of 46 patients (91%) with left posterolateral accessory pathways, a common characteristic of the ECG was a positive QRS complex in leads III and V1 (sensitivity 91%, specificity 95%). Of 19 patients with left inferior paraseptal or inferior accessory pathways, 16 (84%) had a negative QRS complex in lead III and a positive QRS complex in lead V1 (sensitivity 84%, specificity 98%). All six patients with right anterosuperior paraseptal accessory pathways had a positive QRS complex in lead III but a negative QRS complex in lead V1 (sensitivity 100%, specificity 97%). The 25 patients with right inferior paraseptal or inferior accessory pathways had a negative or isodiphasic QRS complex in leads III and V1, but the QRS complex was positive in lead V2 in 21 (84%) of these patients (sensitivity 84%, specificity 100%). Finally, five of the six patients (83%) with right anterior accessory pathways had a negative QRS complex in leads III, V1, and V2 (sensitivity 83%, specificity 96%). With the algorithm, the localization of accessory pathways was thus identified in 90 of the 102 patients (88%).

Adolescent↗
PubMed1994

Electrocardiographic features in experimental subendocardial infarctions in canine hearts.

Chemical necrosis was produced with the infiltration of 96 degrees alcohol on the middle anterosuperior segment 5 (nomenclature of the International Society for Computerized Electrocardiology) of the free left ventricular (LV) wall in 45 dogs and on the apical segment 10 and middle posterolateral segment 11 in 30 others. In five animals from each group, a 10 bipolar arrow assembly was used to obtain Purkinje fiber potentials and to determine the degree to which QS complexes are recorded from the inner portions of the free LV wall. When transmural necrosis was present, QS complexes were generally obtained in both the epicardial and thoracic leads. Subendocardial necrosis was manifested by qrS complexes on the epicardium, as well as in the peripheral leads. When the posterolateral middle third of the LV wall was damaged, Rs or qRs complexes were recorded in leads II, III, and aVF, and an increase in the voltage of the R wave in leads V1 and V2 was observed. Intramural myocardial necrosis diminished the voltage of the R wave in the corresponding leads. Left peripheral blocks obscured the manifestation of myocardial necrosis.

Action Potentials↗
PubMed1987

Interatrial conduction and STa in experimental atrial damage.

Right (RA) and left atrial (LA) damage was produced with a subepicardial infiltration of 96 degrees alcohol in two groups of dogs. In six other dogs the left or right portion of the interatrial band was also injured. Conventional ECG and supplementary unipolar leads were recorded using photographic and direct inscription polygraphs at paper speeds of 50 and 100 mm/sec. Control, immediate postinjury and late tracings were obtained. A-V block was provoked to determine QTac. Slowing of heart rate and slight widening of the P wave and P-R interval were observed with both types of atrial damage. In four cases low right atrial rhythm was detected: two showed anatomo-histological sinus node involvement in right atrial injury. Qp waves were registered over the left precordium with necrosis of both sides, but were more frequent with RA damage. Damage of the left portion of the interatrial band delayed left atrial activation and split P waves in the precordial leads. Damage of the RA distorts the initial vectors, magnifying the left ones and simulating LA enlargement. The Qp registered on the RA is also detected by surface leads. Contrary distorted LA depolarization increases the RA vector and delays the left, ones, giving rise to greater asynchronsim and bimodal P waves.

Animals↗
PubMedDate not supplied

[Double tachyarrhythmia: left anterior fascicular ventricular tachycardia associated with atrial flutter and fibrillation. Report of a case].

A patient with episodes of palpitation in whom the electrocardiogram showed a right bundle branch (RBBB) configuration and right axis deviation underwent electrophysiologic study and radiofrequency ablation. Left ventricular endocardial mapping during ventricular tachycardia (VT) identified the earliest ventricular activation in the anterolateral wall of the left ventricle. The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 47 mseg, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. The stimulus to QRS time was equal to the Purkinje potential-QRS time. Several radiofrequency lesions were applied in this region, one of them resulted with termination of the tachycardia. Following delivery of this lesion the ventricular tachycardia couldn't be induced either at baseline or during isoproterenol infusion. During VT, atrial fibrillation and atrial flutter were observed, cardioversion was performed reverting to sinus rhythm.

Atrial Flutter↗
PubMedDate not supplied

[Is the concept of "jumping wave" still valid?].

UNLABELLED: The concept of the "jumping wave" phenomenon, i.e. of the slow and difficult passage of activation fronts from one septal mass to the other through an "intraseptal barrier", is derived from experimental studies of the Mexican School of Electrovectorcardiography. OBJECTIVE: To confirm the existence of histologically bipartite interventricular septum and of the electric independence of both septal masses. METHODOLOGY: We examined the histological characteristics of both septal masses in rat, canine, and human hearts. We also analyzed the morphological and chronological data of intracavitary records in the presence of different degree proximal blocks, comparing these findings with those obtained when peripheral blocks existed. RESULTS: We found a medial, longitudinal band between the two septal masses in animal as well as in human hearts. The analysis of intracavitary electric records confirmed a slow and difficult transmission of the activation fronts from one septal mass to the other, in the presence of proximal blocks and ventricular arrhythmias. Morphological and chronological changes of intraventricular complexes could not be explained if the septal activation process were of syncytial type. CONCLUSIONS: Results of this study firmly support the validity of our approach to the septal activation process in the presence of ventricular conduction disorders and arrhythmias. This approach helps to detect the possible coexistence of dead septal tissue.

Animals↗
PubMedDate not supplied

[Permanent rhythm and conduction disorders in patients surgically treated for atrial septal defect].

Atrial septal defect (ASD) represents a congenital heart disease with good prognosis, however, atrial arrhythmias are well-documented complications. A retrospective study was performed to assess the prevalence, types and risk factors of arrhythmias in patients with ASD after surgical correction. 920 patients were analyzed retrospectively; cases with complex congenital heart disease or another systemic alteration conditioning atrial rhythm disturbances were excluded. 460 patients with ASD corrected by surgery were followed at least for six months after the procedure. 29.3% of patients were male and 70.7% female. Direct closure was performed in 63%, pericardial patch was installed in 27%. 29 patients (6.3%) had conduction and rhythm disturbances before surgery, the most common arrhythmias were atrial flutter (34.5%), first degree A-V block (31%) and low right atrial rhythm (27.6%). Six months after atrial defect closure, 65 patients (14.13%) had arrhythmias, 44.6% atrial flutter, 20% ectopic atrial rhythm, 10.8% sick sinus syndrome. The risk of atrial arrhythmias was related to age at surgical repair, pulmonary hypertension and atrial arrhythmias before surgery.

Adult↗