Biomedical subjects

A Osornio Vargas

Publications and source records attributed to A Osornio Vargas.

5 recordsLinked to original sources

PubMed1992

[Rupture of the middle left ventricle after a mitral valve replacement. A report on 27 autopsy cases].

Left ventricular rupture is a serious complication of mitral valve replacement. The prevalence ranged from 0.5 to 14%, and is the principal cause of early postoperative death following mitral valve replacement. In this report we described certain morphologic observations and some clinical and epidemiological data of a series of 27 necropsy patients with midventricular rupture (type III). This complication was predominantly present in females (88.9%) with an average age of 44 +/- 11.4 years. The predominant valvular lesion was stenosis (70.4%). In all cases we found small-sized left ventricles and the ventricular wall hypertrophied. Perforation was observed in the 18.5% of the cases. In 59.2% of the patients high profile prostheses were used. Seventy-eight percent of patients died before 24 hours with refractory ventricular failure and only in the 25.9% of cases the clinical diagnoses was suspected and rupture unsuccessfully repaired. Our results suggested that age, sex, type of mitral lesion, ventricular size and type of prostheses are not risk factors for this complication. The mortality is high and the diagnosis was not suspected frequently. Midventricular rupture of the left ventricle is a lethal complication and is necessary to know all its characteristics to implement better methods of prevention and management.

Age Factors↗

PubMedDate not supplied

[Myocardial infarct and rupture of the left ventricular free wall. Some considerations on incidence, morphological characteristics and risk factors].

Rupture of the left ventricle free wall is a sudden and unexpected event in myocardial infarction. It is considered the third most common cause of death, following cardiogenic shock and arrhythmias. The frequency of rupture varies because many patients may survive the initial insult of myocardial infarction. Conflicting reports regarding risk factors have been published by several authors. With these considerations in mind, the present investigation was undertaken to evaluate ventricular rupture in an autopsy population from the Instituto Nacional de Cardiología. We analyzed the salient morphologic features and the risk factors. Our results indicated an incidence rate of 17.7% of cardiac rupture in patients who died of acute myocardial infarction and were autopsied. Ruptures are more common in elderly female patient during their first infarct, they were localized preferentially in the anterior wall and occurred within the first four days after infarction. Chance of rupture was greater in hypertensive patients, whereas a history of previous infarct protected against this contingency.

Age Factors↗

PubMedDate not supplied

[Diagnosis using bidimensional echocardiography in a free thrombus of the left atrium].

Left atrial thrombosis in patients with rheumatic mitral valve disease is frequent. It is important to establish an early diagnosis particularly in those patients who had previous thromboembolic episodes. We describe the case of a sixty-year-old woman with pure mitral stenosis and free left atrial thrombus. We emphasize the sensitivity and specificity of bidimensional echocardiography in such conditions.

Cardiac Catheterization↗

PubMedDate not supplied

[Experimental left atrial infarct].

Electrical changes produced by an experimental left atrial infarction were studied in 15 mongrel dogs, anesthetized by sodium pentobarbital intravenously and submitted to intratracheal intubation, medical sternotomy and heart exposition without open the pericardial sac. 5 to 8 ml of alcohol 96 degrees were infiltrated into left atrial myocardium by means of a thin needle introduced superficially and parallel to the visceral pericardium. Left atrial damage reduces the electromotive, forces corresponding to the anterolateral portions of the left atrium giving rise to QS or QR slurred P waves with very delayed activation when left portion of interatrial band was damaged. Surface ECG records bimodal wide P waves with or without a qp wave in V2-V4 leads, associated to STa elevation in lead a VL and higher leads in the fourth and third left intercostal spaces at the vertical line of V4. QTac interval is more prolonged in right than in left registries as it was observed in right atrial damage, which implies a more earlier repolarization of left atrium. These data are useful for diagnosis of infarction or myocarditis.

Animals↗

PubMedDate not supplied

[Electric signs of experimental pericarditis].

Utilizing 25 mongrel dogs, we studied the electrocardiographic (direct and surface records) and lesional changes induced by the instillation of 7.5% Methyl-salicilate solution and by the acute pericardial effusion produced by the injection of 50 ml of mixed blood-saline solution. Ten unipolar records on the parietal pericardium, right atrium, right and left intraventricular unipolar leads and cavitary tensional curves were obtained. Light and electronic microscopy changes were analized in 11 cases. The anatomical data showed pericardial hemorrhage and injury of 3 to 6 lines of superficial myocytes. On ECG (direct and surface leads) an elevation of RST-T was observed from chest and pericardial unipolar leads and depressed ST in the chambers of the heart, and from a VR and a VL. RST-T displacement as well as developing negative T waves were outstanding on the rigth chest leads (V5R to V3R), on the left (V4-to V6), in DII, DIII, aVF and abdominal leads. A straight RST-T elevation with notch at the juntional point was observed, suggesting atrial injury. No alteration of intrinsic or intrinsicoid velocity were apparent. All of these signs, together with depressed ST in leads aVR and unipolar right chamber leads are signs which suggest pericardial involvement. The P wave became bimodal on the middle chest leads and +/- on right chest leads indicating atrial damage (68%). Thus, an RST-T upward displacement in V3R-V4R, can be a sign of pericarditis as well as right ventricular infarction. The pressure curves were altered only by artificial acute effusion: RA = 20.6, pericardial sac 20.6 and late diastolic of RV = 13.2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗