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Biomedical subjects

J M Aranda

Publications and source records attributed to J M Aranda.

At least 55 records · Page 3Linked to original sources
PubMed1978

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Electrocardiography↗
PubMed1977

Long-term clinical and hemodynamic studies after ventricular aneurysmectomy and aorta-coronary bypass.

Late clinical and hemodynamic evaluations in 18 patients with ventricular aneurysmectomy and aorta-coronary bypass are presented. Tne patients had significant obstructive lesions in two major vessels (55 per cent), and 6 had extensive three vessel disease (33 per cent). In 13 patients, 21 aorta-coronary saphenous bypass grafts were performed in addition to aneurysmectomy. The operative mortality rate was 11 per cent. One patient died suddenly 5 months after the operation (one year mortality rate 17 per cent). The 15 surviving patients have been followed up for 12 to 41 months (average 24 months). Clinical results were considered excellent in 2 patients who have been asymptomatic (Class I, N.Y.H.A.). Nine others were considered to have good clinical results (Class II). Five patients have continued to have congestive heart failure and angina on minimal effort (Class III or IV). Six of the 11 patients considered to have excellent or good results underwent postoperative hemodynamic studies 6 to 34 months after the operation. A significant increase in cardiac index was documented in all 6 patients. Paradoxic movement was not detected in any of the postoperative ventriculograms. Five of the seven venous grafts inserted were patent. Elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index, and a persistent dyskinetic area in the left ventricle were found in 2 patients considered to have poor clinical results. Clinical and hemodynamic evaluations have shown a significant improvement in most patients surviving ventricular aneurysmectomy. However, postoperative systemic embolism, myocardial infarction, progression of coronary artery disease, transient cerebral ischemic attacks, graft occlusion, arrhythmias, and mitral regurgitation in previously prolapsed mitral valve leaflets account for progressive disability and limited activity after a successful operation.

Adult↗
PubMed1976

Mitral valve prolapse. Recent concepts and observations.

The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.

Animals↗
PubMed1976

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Arrhythmias, Cardiac↗
PubMed1976

The His-Purkinje electrocardiogram in man: an initial assessment of its uses and limitations.

A methodology is described for noninvasive recording of the electrical activity generated by the His-Purkinje system of man utilizing filtering, high amplification, and signal averaging. A waveform ranging between 1 and 10mu V was observed during the P-R segment. In many individuals, there was temporal overlap between the terminal P wave and the initial portion of the His-Purkinje waveform. In ten patients with long P-R intervals there was a strong correlation (r greater than 0.95) between the H-V time measured by electrode catheter and the duration of the His-Purkinje waveform. In two patients with atrial fibrillation the resultant His-Purkinje waveform was similar in morphology and duration to those observed in the ten patients. In each group H-V time was determined noninvasively and a waveform associated with electrical activation of the major portions of the His-Purkinje system was obtained.

Action Potentials↗
PubMed1975

Atrioventricular block after reciprocating atrioventricular junctional tachycardia.

Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 sec) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the "upper" His bundle, above the site from which the H deflection was recorded.

Atrioventricular Node↗
PubMed1975

Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations.

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.

Adult↗
PubMed1975

Electrophysiologic studies in a patient with atrial flutter and 1:1 atrioventricular conduction.

Intracardiac electrophysiologic studies were performed in a patient having paroxysms of atrial flutter with 1:1 atrioventricular (A-V) conduction. Although duration of conduction intervals was normal during sinus rhythm, the atrio-His (A-H) interval did not show the expected increase when the atria were stimulated at progressively higher rates. The results of pacing with the extrastimulus technique also indicated that the refractory periods of the A-H tissues were shorter than normal. Yet, intravenously administered ouabain produced a significant increase in these refractory periods. The findings in the case are compatible with a partial A-V nodal bypass with a shorter refractory period than the A-V node or with an A-V node with unusual capacity for rapid conduction. The response to ouabain therapy was that of A-V nodal tissues.

Adult↗