Search PubMed⌕ Search

Biomedical subjects

D R Alonso

Publications and source records attributed to D R Alonso.

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

Histopathology of the conducting tissue of the heart in Chagas' myocarditis.

The conducting tissue of the heart was studied in 25 human cases of Chagas' myocarditis with a method which employs complete serial sections mounted on continuous transparent plastic tape. The pathological changes were correlated with electrocardiographic findings. The inflammation of the acute phase of Chagas' myocarditis, as seen in one single case, did not seem to interfere with conduction through the AV system. In chronic Chagas' myocarditis the conducting tissue showed extensive and variable changes: chronic inflammation, fibrosis, atrophy and fragmentation of specific fibers, extreme dilatation and tortuosity of veins, capillaries and lymphatics, fatty infiltration, and arterial medial and intimal fibrosis. A preferential involvement of the right bundle branch and the anterior fascicles of the left branch was observed and an excellent correlation with electrocardiographic abnormalities was found. There was also evidence presented that bundle branch block may be caused by disease proximal to the bundle branches. Complete AV block seemed to be the final result of the progressive inflammatory and degenerative changes involving the conduction system in chronic Chagas' myocarditis. Inflammation and fibrosis did also involve the sinoatrial node, Purkinje fibers, intracardiac nervous ganglia, and the contractile myocardium.

Acute Disease↗
PubMed1978

Role of delayed intraaortic balloon pumping in treatment of experimental myocardial infarction.

Intraaortic balloon pumping improves coronary blood flow characteristics while simultaneously reducing myocardial oxygen demands by reducing aortic systolic pressure. Clinical application of intraaortic balloon pumping has largely been in the "high risk" patient (cardiogenic shock, postinfarction angina, left main coronary artery disease and unstable angina) for support during diagnostic studies or cardiac surgery, or both. In addition, there is some evidence that balloon pumping immediately after coronary occlusion reduces the size of experimentally induced myocardial infarcts. In this study, myocardial infarcts were produced by ligation of the left anterior descending coronary artery in 12 dogs, 6 of which were treated with balloon counterpulsation beginning 3 hours after coronary occlusion. All dogs were killed 8 hours after coronary ligation. Intraaortic balloon pumping resulted in the expected hemodynamic changes (decreased aortic systolic pressure, left ventricular end-diastolic pressure and heart rate and increased aortic peak diastolic pressure). In addition, there was a significant reduction in infarct size in the group with balloon pumping as determined with epicardial S-T segment mapping, myocardial imaging with technetium-99m-glucoheptonate and histochemical staining with nitroblue tetrazolium. These results suggest that even when instituted as long as 3 hours after coronary occlusion, intraaortic balloon pumping results in significant reduction in infarct size and, it might be speculated, the mortality and morbidity associated with acute myocardial infarction may also be decreased.

Angina Pectoris↗
PubMed1978

Early quantification of experimental myocardial infarction with technetium-99m glucoheptonate: scintigraphic and anatomic studies.

Recent advances in understanding of the pathophysiology of myocardial necrosis indicate the need for a noninvasive method that will allow detection and quantification of infarcts in the first few hours after the onset of infarction. Myocardial infarct scintigraphy using technetium-99m glucoheptonate is capable of detecting infarction in dogs and man within 4 to 6 hours of onset. Studies were performed in 45 dogs with acute myocardial infarction: 28 with with an anterior infarct, 5 with an inferior infarct, 6 with an anterior infarct studied after infusion of mannitol and 6 with ligation of the left anterior descending coronary coronary artery and reperfusion of the ischemic area. The dogs were given 20 m Ci of technetium-99m glucoheptonate 1 hour after coronary occlusion, subjected to imaging 5 to 9 hours later and then killed. The experiments revealed that (1) scintigraphic infarct size correlated with infarct weight for anterior (r = 0.85) and inferior (r = 0.88) infarcts; (2) technetium-99m glucoheptonate also concentrated in a rim of myocardium around the infarct that probably represented the ischemic zone; and (3) technetium-99m glucoheptonate uptake by infarcted myocardium could be greatly increased with mannitol and reperfusion.

Animals↗
PubMed1978

Evaluation of methods for the quantification of experimental myocardial infarction.

Several invasive and noninvasive techniques used in determining the size of experimental myocardial infarction were evaluated after acute ligation of the left anterior descending (LAD) coronary artery in ten dogs. Systemic blood pressure, left ventricular end-diastolic pressure (LVEDP), and heart rate did not change significantly for up to 24 hours after coronary occlusion. Left ventricular wall motion abnormalities were detected by left ventriculography in the distribution of the LAD but these changes did not correlate well with the infarct weight determined at autopsy. On the other hand, the number of epicardial sites with ST-segment elevation of greater than or equal to 2 mm (mean 15.1 sites +/- 0.6 SEM) and the infarct area as measured by 99mTc-glucoheptonate (TcGH) myocardial imaging (15.7 sq cm +/- 0.6) did correlate strongly with the infarct weight (16.8 g +/- 0.7) determined by the nitroblue tetrazolium (NBT) technique (r = 0.91). TcGH myocardial scintigraphy and epicardial ST-segment mapping allowed early and accurate quantification of experimental myocardial infarcts ranging from less than 1 g to 28 g.

Animals↗
PubMed1978

Pathogenesis of diverticulitis complicating granulomatous colitis.

The involement of diverticula by granulomatous colitis may cause an increased incidence of diverticulitis. Of 21 patients with Crohn's disease and associated diverticulosis who underwent resection, sigmoid diverticulitis was pathologically confirmed in 10 (48%). The clinical recognition of the coexistence of the two diseases is often difficult. The radiological signs of peridiverticulitis complicating granulomatous colitis usually show clear evidence of the underlying pathological changes. They include localized diverticular performation, perhaps with multiple communications via a paracolonic sinus tract, mass pressure from the paracolicabscess, and occasionally some degree of communication with deep fissuring ulcers of Crohn's disease. Because diverticula breach the colonic wall, histological analysis confirm that their involvement by the transmural process of granulomatous colitis predisposes to peridiverticulitis and/or abscess formation.

Aged↗
PubMed1977

Pathogenesis of an unexpected sudden death: role of early cycle ventricular premature contractions.

A 61 year old man who had been studied extensively died unexpectedly ("instantaneously") outside the hospital while wearing an electrocardiographic recorder. Death was caused by ventricular fibrillation, which was initiated by an early cycle ventricular premature contraction occurring in the vulnerable period of repolarization. Such early cycle ventricular premature contraction had been noted in recordings 4 years previously but had never been observed to encroach on the T wave until 5 minutes before death. In the intervening period, the patient had shown increasing evidence of myocardial ischemia and hypertrophy and congestive heart failure, which had been partly obscured by his concealment or denial of symptoms and refusal to change his pattern of activities. Autopsy revealed two old myocardial infarcts and pronounced left ventricular hypertrophy. There was advanced occlusive arteriosclerosis of the major coronary vessels with a recent thrombus in the right coronary artery.

Arrhythmias, Cardiac↗
PubMed1977

Studies on the pathogenesis of atheroarteriosclerosis induced in rabbit cardiac allografts by the synergy of graft rejection and hypercholesterolemia.

Heterotopic cardiac allografts were placed in the necks of 48 rabbits. In rabbits that were not immunosuppressed, allografts beat as long as 12 days, while in immunosuppressed rabbits allografts beat as long as 101 days. Coronary arterial lesions in donor hearts of rabbits fed a lipid-poor diet were found in arteries of all sizes and were mainly proliferative without fatty change. In cholesterol-fed rabbits, arterial lesions were similarly distributed, but the majority of lesions in longer surviving transplants were fatty-proliferative and some bore close resemblance to chronic human coronary atheroselerosis. In contrast to findings in cardiac homotransplants, only occasional predominantly fatty lesions were induced in small intramyocardial arteries of cholesterol-fed recipients. By electron microscopy, early arterial lesions in allografts were characterized by platelet aggregates in widened junctions between endothelial cells, sloughing of endothelium without intimal thickening but with adherence of platelets to the denuded arterial wall, and platelets deep within essentially normal media. Platelets were also seen adhering to the lining cells overlying the thickened intima of more advanced arterial lesions. Results indicate that immunologic arterial injury due to allograft rejection acting in synergy with hypercholesterolemia resulting from a dietary supplement of cholesterol can lead to rapidly developing atherosclerosis. Observations of early and evolving lesions indicate that endothelial injury and platelet interaction with the arterial wall are early and continuing events and may be of primary importance in the pathogenesis of experimental graft-induced atheroarteriosclerosis. In man, similar mechanisms may be involved in the pathogenesis of graft-induced athererosclerosis and in other instances of atherosclerosis. (Am J Pathol 87:415-442, 1977).

Animals↗
PubMed1977

Physiologic observations of the heart six months after ischemic normothermic cardioplegia.

The late effects of normothermic ischemic cardioplegia were studied in four experimental groups of dogs subjected to intervals of aortic cross-clamping during cardiopulmonary bypass. Groups which had zero, 20, 30, or 40 minutes of aortic cross-clamping, respectively, were studied 6 months later for cardiac performance and morphology. The immediate operative mortality rate of animals subjected to 40 minutes of ischemia was 65 percent, compared to 22 percent in controls. There were no late deaths in any group Compliance, histology, biochemical determination of deoxyribonucleic acid: ribonucleic acid, and Vmax determinations after cross-clamping revealed no differences between the experimental groups. Open chest isovolumetric contraction curves showed decreased experimental groups. Open chest isovolumetric contraction curves showed decreased function in the 40 minute ischemia group at the extreme levels of cardiac stress. These results suggest that under the conditions of this study normothermic cardiac ischemia of greater than 30 minutes in duration results in a high initial mortality rate (65 percent) and leads to compromise of cardiac function under stress in the late postoperative period.

Animals↗
PubMed1977

Early diagnosis of myocardial infarction in the dog with 99mTc-glucoheptonate.

Early gamma imaging of acute experimental myocardial infarcts was evaluated in mongrel dogs with 99mTc-glucoheptonate. From 15 to 20 mCi were injected between 1 and 27 hr after coronary artery occlusion. Nine dogs imaged 3 hr after injection (4 hr after occlusion) showed unequivocal uptake in the region of the infarct. Fifteen dogs imaged 5-7 hr after injection (6-8 hr after occlusion) showed sufficiently well-defined regions of abnormal uptake so that planimetry could be performed reliably. Five animals imaged serially showed improvement of the image only up to about 5-7 hr after injection. Infarct-to-normal myocardium and infarct-to-blood ratios were slightly higher in dogs injected 15-27 hr after infarction than in those injected 1 hr after infarction, implying that equally good results can be obtained with injection and imaging of 99mTc-glucoheptonate at any time within the first day. No other infarct-labeling radiopharmaceutical shares this capability for the early detection a delineation of acute infarcts.

Acute Disease↗
PubMed1976

Multiple aortic aneurysms in relapsing polychondritis.

A patient with relapsing polychondritis and thoracic and abdominal aortic aneurysms is described. The aortic changes were due to aortitis, which primarily involved the media, with increased vascularization, perviascular infiltration of mononuclear cells, increased amounts of collagen and decreased amounts of elastic tissue and sulfated acid mucopolysaccharides. Aortic aneurysms frequently occur in relapsing polychondritis; they are usually in the ascending aorta but may be multiple and involve the abdominal aorta; involvement of the ascending aorta results in aortic regurgitation and left ventricular failure, and involvement of the abdominal aorta may be clinically silent and result in fatal rupture.

Adult↗
PubMed1976

Appearance of the interventricular septum in obstructive lesions of the left ventricular outflow tract.

Measurements of the thickness of the septum were made in 26 cardiac specimens and in 13 patients. There were 10 normal specimens, five with aortic stenosis, two with asymmetric septal hypertrophy, four with hypertensive cardiovascular disease, and five with idiopathic cardiomyopathy. Patient measurements were obtained by visualizing the septum during simultaneous left and right ventriculography on angiograms obtained in the left anterior oblique projection. Four patients were normal, five had aortic stenosis, and four had a symmetric septal hypertrophy. Measurements derived from normal cardiac specimens and angiographic appearance suggested that the normal septum is a smooth-walled structure with right and left ventricular surfaces parallel, diverging only slightly at the apex of the ventricle. In aortic stenosis and idiopathic cardiomyopathy, the septum tends to be biconvex with maximal thickening in its middle third. Hypertensive cardiovascular disease produces uniform septal thickening, resembling an exaggeration of normal. However, in asymmetric septal hypertrophy no consistent patterns of hypertrophy or septal thickening are evident; bulging can be present at any point along the left ventricular surface of the septum.

Aortic Valve Stenosis↗