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Alberto Aranda

Publications and source records attributed to Alberto Aranda.

11 recordsLinked to original sources
PubMed2006

Pulmonary embolism as a cause of death in patients with heart disease: an autopsy study.

STUDY OBJECTIVE: To establish the prevalence of pulmonary embolism (PE) in autopsy material at a tertiary cardiac referral center and its importance as a cause of death in patients with heart disease (HD). DESIGN: Case series. SETTING: National Heart Institute, Mexico City. PATIENTS: One thousand thirty-two patients who died at our institution from 1985 to 1994 in whom an autopsy study was performed. MEASUREMENTS AND RESULTS: Of the 1,032 autopsies reviewed, 231 cases (24.4%) of PE were found; 100 of these patients had a diagnosis of massive PE. Massive PE (obstruction of either of the main pulmonary arteries or more than two lobar arteries) was found to be the third cause of death in this HD population. By age-group distribution, the global prevalence of massive events was higher in patients < 10 years old. Clinical suspicion (premortem) was raised in only 18% of the cases. CONCLUSIONS: PE was a frequent cause of morbidity and mortality in patients with HD who underwent autopsies. The incidence of massive PE was high in children.

Adult↗
PubMedDate not supplied

[Non-complicated and complicated polyfascicular blocks].

Septal necrosis + Peripheral blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block, first ventricular activation forces become evident, and the electrical signs of a sepatal necrosis are concealed. In the presence of a trifascicular block, the manifestation of the first ventricular electromotive forces diminishes again and the electrical signs of septal necrosis become evident once more. Small Q waves are present in leads V1 to V4. Extensive anterior necrosis + Peripheral blocks. Such a necrosis is manifested by QS complexes from V2 to V6. An associated left bifascicular block reduces the electrical manifestation of dead tissue: QS complexes persist only in V3 and V4. A trifascicular block determines the presence of QS complexes from V2 to V5. Posteroinferior necrosis + Peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis. QS or QR complexes are recorded in leads a VF, II, and III. A left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation. QRS complexes become positive and wider in all leads, the reflect the potential variations of the inferior portions of the left ventricle: aVF, II, and III, sometimes V5 and V6. The electrical signs of necrosis are reduced or abolished. With a trifascicular block, wide and slurred QS complexes appear in aVF, II, III, and sometimes in V5 and V6 too.

Bundle-Branch Block↗
PubMedDate not supplied

An experimental contribution to the concept of "jumping wave" phenomenon in the interventricular septum.

OBJECTIVE: The purpose of this study was to evaluate the existence of a histologically bipartite interventricular septum and the electrical independence of both septal masses, as well as to understand the changes of septal activation fronts in the presence of bundle branch blocks. METHODOLOGY: We examined the histological characteristics of both septal masses in 12 canine hearts. Furthermore, in another 11 anesthetized dog hearts, we analyzed morphological and chronological data of intraseptal records with normal activation and in the presence of proximal blocks. RESULTS: A histological discontinuity between the two septal masses in canine hearts seems to exist. Analysis of intraseptal and intracavitary electrical records confirmed slow transmission of the activation fronts from one septal mass to the other when proximal blocks were present. Morphological and chronological changes of the intracavitary complexes agree with the "jumping wave" phenomenon theory. CONCLUSIONS: These results support the validity of this approach to the activation of both septal masses and explain the chronological and morphological changes of the intracavitary records in the presence of ventricular blocks. In addition, this approach is a useful tool to detect the possible coexistence of dead septal tissue.

Animals↗
PubMedDate not supplied

[Electrical features of hypertrophied left heart].

Chronological and spatial characteristics of the main resultant vectors of the left atrial and ventricular depolarization in normal conditions and in presence of hypertrophy, due to a sustained overload, are described. The coexistence of interatrial, intraatrial, and intraventricular conduction disorders can modify the orientation of these vectors. The main electrocardiographic sign of left atrial hypertrophy is a P wave duration > 0.10 sec in adults. In case of left ventricle hypertrophy, the time of onset of the intrinsicoid deflection (TOID) is prolonged in the near left unipolar leads, and the S wave voltage is increased in opposite regions, i.e. in the right precordial or transitional leads. It is necessary to bear in mind other useful electrocardiographic signs. Hence, absence of the right basal vector (IIId) manifestation in a clockwise rotating heart is probably due to an increase in the basal electromotive forces of the left ventricle (vector IIIi) due to hypertrophy or ipsilateral ventricular conduction disorders. For a correct evaluation of these signs, it is mandatory to perform a rational analysis of the traings, not just a stereotyped electrical exploration. Besides it is very important to determine the Q-Tc interval in the left unipolar leads to establish whether, in these leads, the inverted T wave is of secondary type (normal Q-Tc) or of primary type (prolonged Q-Tc) due to a coexisting subepicardial or transmural ischemia. From these considerations, the usefulness of the thoracic circle and high abdominal unipolar leads is inferred.

Heart Atria↗
PubMedDate not supplied

[Severe right ventricular hypertension secondary to metastatic obstruction due to hepatocarcinoma].

Right ventricular hypertension (RVH) is an entity that could be expected in various cardiopulmonary diseases. Mechanical obstruction to the right ventricle outflow tract is a cause of RVH. We present the case of a 69 year-old male with a history of hepatocarcinoma previously treated. The developed RVH due to mechanical obstruction secondary to metastatic infiltration of the right ventricle. The clinical syndrome was characterized by systemic venous hypertension. Non-invasive studies, such as electrocardiogram and computed tomography scan limited the metastasis to the right ventricle; the diagnosis was confirmed by cardio-angiography and endocardial biopsy. The studies did not demonstrate neoplastic activity at any other level.

Aged↗
PubMedDate not supplied

[On Q-wave and non-Q wave myocardial infarcts].

Much has been said, and is still being said, on Q-wave and non-Q wave myocardial infarcts, trying to relate this electrocardiographic behavior with the culprit coronary arteries and the location of the damaged myocardium. However, it seems logic to bear in mind that the presence or absence of abnormal Q waves depends on the relation established between the zone of damaged myocardium and the width of the electrical endocardium. It must be recalled that the presence of normal Q waves is possible in leads that seem to move away from the first vector of ventricular activation. Besides, the electrical endocardium, i.e., the territory of distribution of Purkinje's network, is situated mainly in the lower half of the ventricles and is virtually absent in basal regions. This endocardium constitutes a histological-functional entity, since the Purkinje fibers, which receive at the same time the activation impulses, are depolarized simultaneously without producing differences in potential. Therefore, these fibers cannot supply an electrical contribution either in normal condition or in the presence of limited damage. Nevertheless, when the damaged zone reaches beyond the exterior limits of this endocardium, for example, in regions where it is small, the exploring electrode can register abnormal Q waves, due to the activation fronts that are moving away, followed by R waves originated in contiguous bands of non-damaged myocardium. We present two characteristic examples of the electrocardiographic manifestations of a transmural left ventricle infarct (QS complexes) and of a subendocardial infarct, reaching beyond the borders of the electrical endocardium (QR complexes). In both of these cases, the electrocardiographic data agree with the anatomical findings.

Electrocardiography↗
PubMedDate not supplied

[Electrocardiographic features of right ventricular hypertrophy in chronic cor pulmonale].

The electrophysiological criteria for diagnosing right ventricular hypertrophy, characteristic of chronic cor pulmonale, are described. Right ventricular hypertrophy due to a sustained systolic overload can be global or regional. In the first situation, as for example, an idiopathic pulmonary hypertension, the magnitude and manifestation of all the main vectors resulting from the depolarization of this ventricle are increased: Ils (septal), llr (parietal), and Illr (basal). When the right ventricular hypertrophy is of the segmental (regional) type, as for example, that due to a chronic bronchial obstruction, the magnitude and manifestation of only some right vectors are increased. In this condition, only the magnitude of the right basal vector (Illr) is augmented. In the presence of subepicardial or transmural ischemia of the right ventricle, negative T waves of primary type are recorded in right precordial and transitional leads, where the Q-Tc interval is prolonged in the absence of digitalis effect. Two demonstrative examples of the correlations existing between the electrocardiographic and anatomical findings in global and regional hypertrophies, respectively, of the right ventricle are presented.

Adult↗
PubMedDate not supplied

[On the ventricular arrhythmias in Chagasic chronic cardiomyopathy].

Some authors have shown a high prevalence of electric circuits localized in the epicardium in Chagasic cardiomyopathy. Other authors have found in these patients, during electric mapping, mid-diastolic potentials and earlier myocardial activation in epicardial regions than in the endocardium. In a previous study, we found electrocardiographic signs of subepicardial ischemia in 66% of seropositive Chagasic patients against 16% of seronegative Chagasic ones. In the case presented here, a Chagasic dilated cardiomyopathy, we found electrocardiographic signs of subepicardial injury in the left free ventricular wall, related with histological findings of lymphocytic inflammation in these regions. In contrast, the endocardium was completely free from inflammation foci.

Aged↗