Search PubMed⌕ Search

Biomedical subjects

R Seabra-Gomes

Publications and source records attributed to R Seabra-Gomes.

At least 127 records · Page 7Linked to original sources
PubMed1977

The assessment of regional abnormalities of the left ventricle by angiography.

A method of regional wall motion analysis of left ventricular cineangiograms which does not make assumptions about ventricular geometry is described. The technique measures the movement of the ventricular perimeter in relation to the geometric center of gravity of the endsystolic frame expressing movement as a change in radical length. 10 control patinets each with 3 left ventricular cineangiograms, comprise the group for definition of normal values of movement and permit estimations of reproducibility within and across patient groups. Isolated examples of abnormal wall motion are shown.

Adult↗
PubMed1976

Effect of methylprednisolone sodium succinate on hypoxic heart muscle.

The ability of 30 mg/litre methylprednisolone sodium succinate (MPSS) to modify the effects of hypoxia on isolated Langendorff-perfused rat hearts was investigated. When perfused under hypoxic conditions (pO2 less than 0.8 kPa[6 mmHg]) these hearts lose intracellular enzymes, including creatine phosphokinase (CPK) and succinic dehydrogenase (SDH). The size of the extracellular space is enhanced, the cells gain Na+ and Ca2+ and lose K+, and the endogenous stores of ATP and CP are depleted. Initially the resistance to flow in the coronary circulation falls but after 75 min of hypoxic perfusion it increases so that coronary flow is reduced. MPSS failed to prevent hypoxic muscle from either gaining Na+ and Ca2+ or losing K+. It did, however, delay the release of CPK and SDH from the hypoxic muscle, prolong the phase of increased coronary flow, and decrease the rate of depletion of the energy-rich phosphate stores. MPSS potentiated the hypoxic-induced gain in Ca2+. Whilst the effects of MPSS on coronary flow and tissue Ca2+ were probably due to the steroid part of the complex, the other changes, including the protection of the ATP and CP stores and the delayed enzyme release, were probably due to the presence of the sodium succinate.

Adenosine Triphosphate↗
PubMed1976

Left ventricular function after aortic valve replacement.

Changes in haemodynamics and in systolic time intervals, early after valve replacement, were studied in a group of 15 patients. Though all the haemodynamic measurements were within normal limits at 44 hours after operation, there was a persistent change in systolic time intervals (shortening of left ventricular ejection time and electromechanical systole, and prolongation of pre-ejection period and increase in the ratio PEP/LVET). The effect of periods of myocardial ischaemia during cardiopulmonary bypass on myocardial function is suggested as the explanation for the changes observed.

Adult↗
PubMed1976

Hemodynamic effects of verapamil and practolol in man.

The hemodynamic effects of verapamil and practolol were investigated in a group of 10 selected patients (7 with coronary artery disease) undergoing cardiac catherization. The drugs were given i.v. in a dose of 0.1 mg/kg, alone or in combination, before and after controling the heart rate by atrial pacing. Measured hemodynamic parameters included aortic and left ventricular pressure and its first derivative, cardiac output, and echocardiographically derived left ventricular dimensions. Each drug given individually caused minor hemodynamic changes, but the combination of practolol and verapamil when the heart rate was fixed by atrial pacing invaribly caused a reduction in LV dp/dt max which was independent of preload and afterload. It is concluded that both drugs have a mildly negative inotropic effect when administered at this dose intravenously to patients with normal or mildly impaired left ventricular function. The myocardial depression was more apparent when practolol preceded verpamil. Caution must be exercised when using these drugs in combination in patients with impaired myocardial function.

Adult↗
PubMed1975

Multiple cerebral aneurysms and cardiac myxoma.

Neurological signs are a frequent manifestation of left atrial myxoma, but the association of cardiac myxoma with multiple cerebral aneurysms is rare. A case of left atrial myxoma was detected in the course of a long-lasting psychiatric and neurological illness. Four-vessel study showed the presence of multiple saccular and fusiform aneurysms, regularly and almost symmetrically distributed. The intracardiac mass was removed, and the patient improved.

Adult↗
PubMed1975

Irreversible myocardial injury in anoxic perfused rat hearts.

Isolated rat hearts were perfused at 37 C on a double reservoir, nonrecirculating Langendorff apparatus. For aerobic perfusion, Krebs-Henseleit medium containing 10 mM glucose was gassed with 95% O2-5% CO2; for anoxic perfusion, glucose was replaced with 10 mM mannitol, a nonmetabolizable substrate, and the medium was equilibrated with 95% N2-5% CO2. Heart effluent was serially collected during perfusion for creatine phosphokinase activity (CPK) analysis. Fixation was with 1% glutaraldehyde for morphologic studies. With aerobic control perfusion, hearts continued contracting, released no CPK, and were morphologically normal by light and electron microscopy examination after 120 minutes. With anoxic perfusion, contractions soon ceased, and by 60 minutes a sustained slow release of CPK was first observed. By electron microscopy, cells at 60 or 90 minutes were swollen and contained amorphous matrix densities in mitochondria; a few cells showed breaks in cell plasma membrane. When anoxic hearts were challenged with reoxygenation, there was a sudden change in color to a pale opaque appearance, CPK was rapidly released, and there was massive cellular swelling. By electron microscopy, damaged cells showed contraction bands, clumping of nuclear chromatin, both amorphous densities and granular dense bodies in mitochondria, and prominent disruptions of cell plasma membranes. The number of damaged cells observed increased as a linear function of time between 30 and 55 minutes of anoxia. The results show that anoxic perfusion in vitro produces irreversible myocardial injury and that this injury is closely associated with loss of cell volume control, release of intracellular enzymes, and striking structural defects in the plasma membrane of the sarcolemma. Reoxygenation accelerates the development of lesions in irreversibly injured cells but protects reversibly injured cells.

Animals↗
PubMedDate not supplied

Prognosis in patients with left bundle branch block and normal dipyridamole thallium-201 scintigraphy.

BACKGROUND: The presence of complete left bundle branch block (LBBB) is commonly associated with a poorer prognosis, especially in patients with coronary artery disease (CAD). In the general population with suspected CAD and normal intraventricular conduction, a normal dipyridamole-thallium scintigraphy is a strong marker of a favorable outcome. OBJECTIVE: Our objective was to assess the prognosis in patients with LBBB and a normal dipyridamole thallium-201 scintigram. POPULATION AND METHODS: Patients with complete LBBB and normal myocardial perfusion on dipyridamole SPECT thallium-201 scintigraphy performed in our center for suspected CAD between 1988 and 1995 were monitored for clinical events. RESULTS: Sixty-nine patients (36 women and 33 men) with a mean age of 59 years (range 56 to 61) were monitored for a mean period of 33 months (range 25 to 35). During this period, 4 patients had unstable angina, 2 of whom underwent myocardial revascularization. There were no deaths or myocardial infarction. All events occurred at least 2 years after the thallium-201 scintigraphy. CONCLUSION: The presence of a normal myocardial perfusion with dipyridamole thallium-201 scintigraphy in this group of patients with suspected CAD and LBBB was associated with a very good prognosis, a low rate of clinical events occurring only 2 years after the myocardial scintigraphy, and no hard events.

Bundle-Branch Block↗
PubMedDate not supplied

[Unsustained ventricular tachycardia and accelerated idioventricular rhythm--clinical and electrocardiographic features].

OBJECTIVE: To compare clinical and electrocardiographic characteristics of Nonsustained Ventricular Tachycardia (NSVT) and Idioventricular Accelerated Rhythm (IVAR). MATERIAL AND METHODS: We studied 155 patients, 113 men and 42 women, with mean age 54 +/- 14 retrospectively, of these, 108 had NSVT and 47 IVAR. The arrhythmias were defined as follows: NSVT-more than 3 ventricular consecutive beats with an heart rate superior to 110 b/m and lasting less than 30 s.; IVAR-3 or more ventricular consecutive beats with an heart rate equal or superior to 50 and lower than 110 b/m, lasting less than 30 s. We evaluated clinical data (symptoms, functional class and anti-arrhythmic therapy), electrocardiographic data (rhythm, changes in conduction and repolarization) and ventricular function (with ECO, Radionuclide Angiography or Ventriculography). In the Holter recording (ECG-H), we analysed the presence of associated ventricular arrhythmias, their electrocardiographic characteristics (number of episodes, number of beats per episode, previous arrhythmia rate, morfology, regularity) and the relations of the arrhythmia with symptoms. RESULTS: Analysis of underlying pathology showed in both groups, the importance of coronary artery disease (44.5% vs 40%) followed by valvular heart disease (24% vs 27.6%) and cardiomyopathy (22.2% vs 17%) respectively to NSVT and IVAR. Only in the NSVT group there were patients without cardiac pathology (3.6%). Comparing with one control group of our department, this distribution was substantially different (p less than 0.0001). All IVAR episodes were assympthomatic compared with 90% of NSVT. Ventricular premature beats were found in all NSVT patients and in 90% of IVAR patients, and were frequent (greater than 10/h) in 79% and 60%, couplets in 84% and 53% respectively (ns). The previous rate of the arrhythmia was 85.3 +/- 20 b/m in NSVT against 68.7 +/- 14 in IVAR (p less than 0.0001). We found left ventricular disfunction in 60% of NSVT patients and in 63.7% in IVAR patients, being serious in 35% and 39% respectively. The follow-up was of 18.5 months (1-72) and posterior evolution showed 14.8% and 17% of deaths with no relation to the arrhythmia, although in NSVT the number of complexes and episodes were related with the ventricular disfunction (p = 0.02 and p = 0.05). CONCLUSION: Both arrhythmias appeared in patients with similar clinical and arrhythmic setting and identified a population with structural cardiopathy, bad function and poor outcome.

Adult↗