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Biomedical subjects

C Beghi

Publications and source records attributed to C Beghi.

At least 37 records · Page 2Linked to original sources

[Surgical therapy of post-infarct aneurysm of the left ventricle. Immediate and long-term results].

Between January 1982 and December 1986, 62 patients (59 male and 3 female) ranging in age from 37 to 69 years (mean 53) underwent resection of postinfarction left ventricular aneurysm. The indication for operation was angina in 23 cases (37%), congestive heart failure (CHF) in 7 (11.2%), angina and CHF in 29 (46.8%), rupture in 1; 2 patients were low symptomatic. Ventricular arrhythmias were present in 6 (9.7%) cases and previous systemic embolism in 4 (6.4%). Forty-seven (75.8%) patients had lesions of three coronary arteries with involvement of left main coronary artery in 4 cases; 10 (16.1%) had lesions of two vessels [left anterior descending (LAD) and/or right coronary artery]; 4 (6.4%) had only LAD artery involvement, and 1 had no significant coronary artery stenoses. Left ventricular ejection fraction (EF) was less than 0.30 in 22% of cases, between 0.30 and 0.40 in 25.4% and greater than 0.40 in 50%. The location of the aneurysm was anterolateral or apical (83.8%), posterior (14.5%) and lateral (1.6%). Left ventricular aneurysmectomy with myocardial revascularization was performed in 61 patients (bypass/patient = 2.7), with ventricular septoplasty in 20 and concomitant mitral valve replacement in 3 patients. LAD was grafted in 59.6% of anterior aneurysm. Operative mortality (30 days) was 4.8%, the late mortality, with a follow-up between 12 and 72 months (mean 38), was 6.7% and the actuarial 5 year survival rate was 85% (91% without operative mortality). In our experience, despite no evidence of any operative risk factors, no improvement was noted in radionuclide left ventricular ejection fraction in patients undergoing aneurysmectomy with ventricular septoplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Immediate and distant results of aorto-coronary bypass performed in patients with compromised cardiac contraction].

From March 1979 to December 1985 at Cardiac Surgery Department of Parma 1064 patients underwent myocardial revascularization. Of them, 82 (7.7%) with poor left ventricular function (ejection fraction less than 40%) were studied to evaluate the effects of coronary artery bypass grafting on surgical risk, survival, ventricular performance and late clinical status. Three vessels disease was present in 65.9% and severe stenosis of left main coronary artery in 21.9% of patients. There were 74 (90.2%) patients with a history of previous myocardial infarction and 8 (9.75%) with congestive heart failure. Mean ejection fraction was 32.21 +/- 3.6%. On biplane left ventricular angiography 60 (73.2%) cases had two or more akinetic segments and 22 (21.9%) only hypokinesia. Operative mortality rate was 4.9%; perioperative myocardial infarction occurred in 5 patients (6.2%). Mean follow-up was 37.64 +/- 9.23 months and survival rate, including operative mortality, was 91.3%. Among the long-term survivors 89.04% are asymptomatic and in 49% there was a significantly improvement of preoperative left ventricular ejection fraction. We conclude that myocardial revascularization should be performed also in patients with left ventricular dysfunction, because of improvement of quality of life.

Coronary Artery Bypass↗

[Digital angiography and surgery of the carotid: our experience].

Digital subtraction angiography (DSA) has became a common diagnostic procedure in the investigation of patients with cerebrovascular disorders. In these report is described a series of 80 cases previously examined in 8 different department of radiology, 59 with IV.DSA and 21 with IA.DSA. Thirty per cent of IV.DSA images were judged to be technically inadequate, so that further evaluations with conventional angiography have been needed, and in 3 patients (5.0%) the IV.DSA diagnosis was overturned. The authors recommend intraarterial digital subtraction angiography for evaluation of extracranial carotid occlusive disease always resulted the definitive diagnostic procedure in their experience.

Carotid Artery Diseases↗

Myocardial infarction in rats. Infarct size, myocyte hypertrophy, and capillary growth.

To determine the compensatory reserve capacity of the ventricular myocardium following infarction, the left coronary artery in rats was ligated, and the animals were killed 40 days later. Infarcts affecting an average 23% of the left ventricle were characterized by a 27% hypertrophic growth of the remaining myocardium that produced a complete replacement of the necrotic tissue. In contrast, infarcts with an average 50% loss of mass resulted in 83% expansion of the spared myocardium that was inadequate for a complete restoration of ventricular tissue. Myocyte hypertrophy was 26% and 78% in small and large infarcts, respectively. Cellular hypertrophy in both cases involved significant increases in myocyte transverse area and myocyte length. After large infarcts, there was an 18% reduction in capillary surface and a 16% increase in the diffusion distance. Corresponding values for small infarcts were -10% and 9%. These alterations combined with the deficient reconstitution of myocardial mass following large infarcts resulted in 25%, 29%, and 30% deficits in the absolute amounts of capillary lumen, surface, and length per ventricle respectively. Even with small infarcts, a deficit was seen in capillary luminal surface (-16%), and length (-19%). In conclusion, we have demonstrated that cardiac hypertrophy following myocardial infarction is consistent with cellular shape changes characteristic of a combination of concentric and eccentric hypertrophic growth. However, cardiac muscle cells appear to be unable to compensate for the loss of mass induced by a 50% infarct. The inadequate adaptation of the capillary vasculature in the infarcted hearts suggests that the injured ventricle is more vulnerable to additional ischemic episodes.

Animals↗

Effects of low flux-low pressure cardiopulmonary bypass on intracellular acid-base and water metabolism.

In eight patients undergoing open heart surgery for elective myocardial revascularization, extra-intracellular acid-base and water metabolism parameters were studied before and after cardiopulmonary bypass procedures. All patients presented a different degree of metabolic acidosis related to plasma lactate increase. Intracellular acid-base indexes did not change significantly, though all but one patient showed an intracellular buffers consumption. Both total muscle and extracellular water increased, while intracellular water did not change. It was concluded that low flux-low pressure perfusion CPB was related to a substantial preservation of cell integrity.

Acidosis↗

Response of the border zone to myocardial infarction in rats.

The response of the surviving myocardium 30 days after coronary artery occlusion was measured morphometrically in the regions bordering and remote from infarcts of different sizes. Mean cell volume per nucleus increased with infarct size in both zones, but the rate of change was greater in the border than in the remote portion of the unaffected myocardium. Capillary numerical density within the uninjured tissue progressively decreased with infarct size leading to an increased diffusion distance for oxygen. Although the magnitude of changes in capillary density was similar in the two regions of the ventricle, the analysis of the individual values in each heart showed that in infarcts comprising more than 11% of the ventricular wall capillary concentration and the path length for oxygen supply to the myocytes were affected more in the border zone than in the myocardium remote from the scar. In conclusion, the border zone participates in the hypertrophic recovery process after infarction, but the inadequate growth of the capillary microvasculature suggests that this region is more susceptible to additional ischemic episodes.

Animals↗

Effects of strenuous exercise on the quantitative morphology of left ventricular myocardium in the rat.

The adaptation of the structural components in the myocardium of the left ventricle to strenuous exercise was studied morphometrically in rats following a treadmill running program. The response of the left ventricle was evaluated separately in the interventricular septum and in the left ventricular free wall. Exercise produced a 24% growth of the septum without altering free wall volume. The hypertrophic expansion of the septum was characterized by a decrease in the volume fraction of capillary lumen in the myocardium (-20%), a reduction in the capillary luminal surface per unit volume of myocytes (-17%) and by an increase in the maximum distance from the capillary wall to the mitochondria of myocytes (9%). Although none of these changes were demonstrable on a statistical basis in the left ventricular free wall, similar results were obtained in the whole left ventricle by combining the data from the septum and free wall. Since the septum constitutes a functional unit with the free wall, it was concluded that the effect of excessive physical activity on the capillary parameters responsible for oxygen availability and diffusion could lead to a local reduction in the oxygenation potential of ventricular myocardium.

Animals↗

Myocardial response to infarction in the rat. Morphometric measurement of infarct size and myocyte cellular hypertrophy.

For determination of the effects of myocardial infarction on the recovery potential of muscle mass in the surviving tissue, ligation of the left coronary artery was performed in 3-month-old rats, and the infarcted ventricles were analyzed morphometrically a month after surgery. Comparisons were made with 4-month-old control rats that underwent sham operations and with 3-month-old control rats that were not operated upon for evaluation of the magnitude of infarct size and discrimination of the relative contribution of tissue growth that occurred in the surviving myocardium solely as a result of the change in age, from 3 to 4 months (postoperative tissue growth, or POTG), from the additional growth induced by infarction (hypertrophic growth, or HG). Coronary occlusion induced a 276-cu mm loss of ventricular tissue volume that corresponded to 43% of the total left ventricular mass, 648 cu mm. Over a 30-day period the remaining 372 cu mm of viable tissue expanded by 90% with an overall volume gain of 334 cu mm. This tissue augmentation consisted of 20% POTG, 67 cu mm, and 80% HG, 267 cu mm. Total myocyte volume increased 89%, from 302 cu mm to 571 cu mm, and average myocyte cell volume per nucleus increased 92%, from 16,500 cu mu to 31,600 cu mu. The expansion of the myocyte mass was the result of a 21% POTG and a 79% HG. Corresponding values for the myocyte population were 19% and 81%.

Age Factors↗

Coronary artery spasm in the rat induced by hypothalamic stimulation.

Anesthetized rats were sterotaxically implanted with electrodes and electrically stimulated in the lateral hypothalamus. During elevation of the S-T segment on simultaneous precordial electrocardiograms, the heart was perfused with glutaraldehyde-paraformaldehyde fixative and the major coronary arteries prepared for morphometry of luminal dimensions. A similar procedure was performed in a second group receiving intravenous arginine vasopressin (AVP) in place of hypothalamic stimulation. Elevation of the S-T segment was present in these animals as well. Control animals were implanted, not stimulated and otherwise treated in the same way. Morphometry showed that reductions of mean luminal diameter and cross-sectional area of statistical significance occurred in the two experimental groups compared to controls, suggesting that coronary spasm was the cause of the elevated S-T segments. Pooled plasma from separate groups of implanted control and hypothalamically-stimulated animals revealed substantial elevation of AVP levels in the latter raising the possibility that the neuroendocrine was involved in eliciting coronary artery spasm.

Animals↗

Structural compensatory mechanisms in rat heart in early spontaneous hypertension.

The response of the left ventricle (LV) during the development of spontaneous hypertension (SH) in rats was studied morphometrically at 21, 28, 35, and 45 days after birth and compared with that of normotensive (WK) controls. LV hypertrophy, varying from 24 to 27%, was characterized by the preservation of the volume fraction of capillary lumen and capillary luminal surface in the myocardium, as a result of capillary proliferation. From 21 to 45 days the number of capillaries per unit area of myocardium increased 68% in SH rats by the insertion in parallel of new capillary elements among the myocytes. This estimation was obtained by correcting the value of capillary density at 45 days for the amount of spreading produced by myocyte growth during this interval. On a similar basis capillary proliferation was only 24% in WK rats. Myocyte growth in experimental animals (151%) was achieved by a 77% enlargement in myocyte cross-sectional area (MCSA) and by a 42% lengthening of the cells. In controls myocyte expansion (124%) was the result of comparable increments in MCSA (47%) and myocyte length (53%).

Aging↗

Morphometry of right ventricular hypertrophy induced by myocardial infarction in the rat.

The growth response of the right ventricle was studied in rats following ligation of the left coronary artery, which produced infarcts comprising approximately 40% of the left ventricle. A month after surgery the weight of the right ventricle was increased 30%, and this hypertrophic change was characterized by a 17% wall thickening, consistent with the 13% greater diameter of myocytes. Myocardial hypertrophy was accompanied by an inadequate growth of the microvasculature that supports tissue oxygenation. This was seen by relative decreases in capillary luminal volume density (-27%) and capillary luminal surface density (-21%) and by an increase in the average maximum distance from the capillary wall to the mitochondria of myocytes (19%). In contrast, measurements of the mean myocyte volume per nucleus showed a proportional enlargement of these cells (32%), from 16,300 cu mu in control animals to 21,500 cu mu in experimental rats. Quantitative analysis of the right coronary artery revealed a 33% increase in its luminal area, commensurate with the magnitude of ventricular hypertrophy.

Animals↗

Morphometry of right and left ventricular myocardium after strenuous exercise in preconditioned rats.

Young male rats were exposed to a biphasic training program in which a 7-week preconditioning period of moderate treadmill exercise was followed by 8 weeks of strenuous endurance running. In comparison with sedentary control animals, the trained rats at 20 weeks of age had developed myocardial hypertrophy of the right ventricle (20%) and interventricular septum (23%), but there was no difference in the weight of the left ventricular free wall. Myocyte hypertrophy (26%) in the right ventricle was achieved through an increase in mean cell length (24%) and the addition of new sarcomere units in series. Exercise induced no acceleration of capillary growth in either ventricle, leading to significant decreases in the capillary luminal volume density (-21%) and surface density (-16%) in the right ventricle. Such alterations in the structural properties of the microvasculature implicated in oxygen availability and diffusion suggest that vigorous exercise, even after a preconditioning period, may still be detrimental to the myocardium. The techniques of myocardial morphometry were examined with respect to potential errors associated with oblique tissue sections and the use of light versus electron microscopy for cell counting. It was shown that the practical effects of obliquity are negligible and that electron microscopic resolution is essential.

Animals↗

Stress tests.

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Coronary Disease↗

Morphometry of exercise-induced right ventricular hypertrophy in the rat.

In our morphometric study of the effects of exercise on the heart, male Wistar-Kyoto rats at 5 weeks of age were subjected daily to a moderate treadmill running program that lasted for 7 weeks. The heart responded to physical conditioning by different magnitudes of tissue growth of the right (22%) and left (7%) ventricular myocardium, the latter change not statistically significant. The increase in right ventricular volume was associated with a 25% enlargement of ventricular area, a 26% average lengthening of the myocytes, and no change in sarcomere length and in ventricular midwall thickness. Exercise produced significant alterations in the quantitative parameters of the microvasculature of the right ventricle, but no appreciable changes in the left ventricle. Right ventricular hypertrophy was characterized by an absolute 44% growth of the endothelial luminal surface brought about through a 16% increase in capillary numerical density, and a 41% augmentation of the total length of the capillary network. Maximum diffusion distance from the capillary wall to the mitochondria of myocytes decreased 10% as a result of capillary proliferation and the lack of lateral expansion of myocyte cross-sectional area. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria:myofibrils volume ratio, indicating a growth of these components proportional to each other and to the growth of the myocyte population as a whole. It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.

Animals↗

Morphometry of right ventricular hypertrophy induced by strenuous exercise in rat.

Effects on the myocardium, particularly those structural properties of the capillary network relevant to tissue oxygenation, were studied morphometrically in rats subjected to a severe running program. Physical conditioning produced a 31% increase in right ventricular weight and only a 12% increase in the weight of the left ventricle. Quantitative analysis of right ventricular myocardium demonstrated relative decreases in capillary luminal volume density (-27%) and capillary luminal surface density (-20%) and an increase in the average maximum distance from the capillary wall to the mitochondria of myocytes (14%). In contrast, the contractile mass expanded in proportion to the growth of the ventricle through augmentation of the cross-sectional area (17%) and length (19%) of the average myocyte. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria-to-myofibril volume ratio. In conclusion, the capillary bed controlling oxygen availability, diffusion, and transport suggests that excessive physical activity may be detrimental to the myocardium.

Animals↗

Carotid endarterectomy under hypothermic extracorporeal circulation: a method of brain protection for special patients.

This study was undertaken to evaluate the efficacy of hypothermic extracorporeal circulation for cerebral protection in 17 patients having simultaneous carotid endarterectomy and cardiac operations. The cardiopulmonary by-pass (CPB) was conducted using total hemodilution. The body temperature was cooled to 25 degrees C and the heart was arrested with cardioplegic solution. The carotid endarterectomy was performed first followed by the cardiac operation. No neurological or cardiac complications occurred. These results support the reliability of hypothermic cardiopulmonary bypass as a method of providing cerebral protection during simultaneous cardiac and carotid surgical procedures.

Aged↗

Right atrial hemangioma.

A case of right atrial hemangioma as a rare tumor of the heart is reported. Because of its single, pedunculated mass, surgical excision of the tumor resulted in the complete treatment. Histologically, it was classified as arteriolar type. The importance of recent non-invasive techniques to diagnose these tumors during life is emphasized.

Echocardiography↗