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Biomedical subjects

J Milei

Publications and source records attributed to J Milei.

At least 19 recordsLinked to original sources
PubMed2001

Chromosomal alterations in atherosclerotic plaques.

Alterations of chromosomes 7 and 11 have been involved in the progression of atherosclerosis. Twenty-three carotid endarterectomy specimens were studied for the presence of alterations in chromosomes 7 and 11, and fibroblastic growth factor-3 (FGF-3) gene amplification. Besides classic histological stainings, immunophenotyping of cellular and vascular components and fluorescence in situ hybridization (FISH) were performed. At the caps, unstable plaques (n=18) showed inflammatory infiltration of macrophages, smooth muscle cells, and T-lymphocytes. Specifically in these regions, the FISH showed varying percentages of trisomy (15/18) and tetrasomy (8/15) of chromosome 7. In four cases polisomy 7 was noted in some nuclei. Monosomy of chromosome 11 and gene amplification of FGF-3 gene was observed. The FISH of the five stable plaques and normal arterial walls showed no chromosome alterations; furthermore, chromosome 3, which is not involved in atherosclerotic progression, presented a normal ploidy of smooth muscle cells in stable and unstable plaques and normal arterial walls. In conclusion, chromosome 7 and 11 alterations and FGF-3 gene amplification are components of unstable plaques, and might contribute to the evolution of stable plaques into complicated plaques.

Adult↗
PubMed2000

Inflammatory cells, apoptosis and Chlamydia pneumoniae infection in atherosclerosis.

Chlamydia pneumoniae (CP), chromosomal alterations and apoptosis were suggested as contributing factors in the pathogenesis of atherosclerosis. Early (EP) and unstable plaques (UP) were studied in order to assess infiltrate composition, the apoptotic index, chromosome 7 stability and to investigate the concurrent presence of CP in EP and UP. Paraffin embedded sections of three iliac arteries and four aortas from young donors (EP), and four coronaries and nine carotid arteries (UP) were used. Aside from histological techniques, immunophenotypification for macrophages, T and B cells, smooth muscle and endothelial cells; FISH and DNA nick end labeling were performed. The amplifications with PCR for CP infection were negative in all specimens. In the EP, a focal myointimal thickening with foam cells and scarce smooth muscle cells was observed. Macrophages were most frequent in the intima (10.8%) while T and B cells were found in 2.3 and 1.5%. In the UP a thin cap covering a lipid-rich core with widespread vascularization and with severe luminal obstruction was observed. Macrophages were increased (21%), and T (1.5%) and B cells (3.5%) in the caps and inner areas of the lipid cores. At these sites, the FISH showed trisomy and tetrasomy of chromosome 7 and apoptosis was very frequent (10-30%). Macrophages in intimal lesions is one of the most prominent, consistent and permanent features in EP, and an elevated apoptotic index and chromosome 7 instability might contribute to evolution from stable to complicated plaques, while CP seems to play no role. However, further studies are needed with more cases to confirm this last observation.

Adult↗
PubMed2000

[Proliferative activity and chromosomal alterations of smooth muscle cells in atherosclerosis].

Atherosclerosis is the most frequent cause of death in industrialized countries. Lesions are characterized by lipid deposits, focal thickening of the arterial wall with proliferation of smooth muscle cells (SMC), mononuclear infiltrates and neoformed vessels. In this paper, we studied the proliferative characteristics and cytogenetic alterations of SMC. These cells, expressing specific muscular actin, were diploid with an increased proliferative index for PCNA. A high percentage of SMC showed intense expression of p53. There were signs of chromosomal instability, being the most frequent findings chromosome 7 trisomy and chromosome 11 monosomy. Additionally, the gene for FGF-3 showed a marked amplification. These findings strongly suggest that SMC proliferation is active, and is related to the accumulation or mutation of the p53 oncoprotein. It also presents specific chromosomal alterations in close relation with growth factors. According to these findings SMC hyperplasia in the atherosclerosis plaque may be considered as a cellular clonal expansion.

Arteriosclerosis↗
PubMed1998

Mortality and morbidity from smoking-induced cardiovascular diseases: the necessity of the cardiologist's involvement and commitment.

This review deals with tobacco-associated cardiovascular effects and diseases. The importance of tabaccoism in primary care, its effects on cardiovascular, and immunology system and hemostasia, as well as, the role of smoking in atherosclerosis, coronary heart disease, acute myocardial infarct, diabetes, and other alterations are discussed. Finally we summarize the general tobacco control policies and the methods to achieve smoking cessation. Although it is well established the causal relationship between smoking and disease, and the general public is aware of this, the cardiologist's involvement and commitment is of utmost importance.

Argentina↗
PubMed1998

Cardiac involvement in acquired immunodeficiency syndrome--a review to push action. The Committee for the Study of Cardiac Involvement in AIDS.

As more effective therapies have produced longer survival times for human immunodeficiency virus (HIV)-infected patients, new complications of late-stage HIV infection including HIV-related heart disease have emerged. Almost any agent that can cause disseminated infection in patients with acquired immunodeficiency syndrome (AIDS) may involve myocardium, but clinical evidence of cardiac disease is usually overshadowed by manifestations in other organs, primarily the brain and lungs. Cardiac abnormalities are found at autopsy in two-thirds of patients with AIDS, and more than 150 reports of cardiac complications have been published. Cardiac involvement in HIV disease includes pericardial effusion, myocarditis, dilated cardiomyopathy, and/or endocardial involvement at any stage of the disease. This review deals with all the cardiac manifestations of AIDS and serves to highlight two problems and one indication. First of all, there are very few clinical studies. Current knowledge is based almost exclusively on echocardiography and autopsy studies. Observational or clinical trials would be useful. Second, there exists very poor information on the impact of treatment; and epidemiologic and clinicopathologic studies are mandatory for obtaining detailed data concerning the mechanisms of myocardial damage in AIDS. Finally, because cardiac complications are often clinically inapparent or subtle in the initial stages, periodic screening of HIV-positive patients by electrocardiogram and echocardiogram is probably indicated. In addition, AIDS may also provide the opportunity to gain insights into the pathogenesis of little understood cardiac diseases such as lymphocytic myocarditis and dilated cardiomyopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Carotid rupture and intraplaque hemorrhage: immunophenotype and role of cells involved.

BACKGROUND: A complete immunohistochemical characterization in complicated carotid plaques is still lacking. The cellular components of 165 carotid endarterectomy specimens were analyzed to assess their role in the pathogenesis of plaque rupture and intraplaque hemorrhage without rupture. METHODS AND RESULTS: The fibrous caps at the sites of plaque rupture showed CD68+ macrophages, T-lymphocytes, and scarce B-lymphocytes. Ruptured plaques showed mononuclear infiltrates in the caps, shoulders, and bases of the plaques in 85% of the cases. Only 46% of nonruptured plaques showed such infiltrates (P <.0001). Two types of lipid cores were recognized: avascular or mildly vascularized and highly vascularized. The vessels of the latter type reacted with CD31 and CD34. In 57.5% of the cases, the base and the shoulders of the plaques showed neoformed, CD34+ vessels, often surrounded by mononuclear infiltrates. Intraplaque hemorrhage without rupture had highly vascularized lipid cores in all cases. T-lymphocytes and macrophages were in close contact with neoformed vessels. CONCLUSIONS: Plaque rupture is characterized by mononuclear cell infiltration of the caps, whereas intraplaque hemorrhage without rupture is characterized by extensive vascularization of the plaque.

Adult↗
PubMed1998

Is stunning prevented by ischemic preconditioning?

In a model of global ischemia in the isolated perfused rat heart, a 20 min ischemic period followed by 30 min of reperfusion induces a decrease in isovolumic developed pressure (LVDP) and +dP/dtmax to 61+/-6% and 61+/-7% of baseline, respectively. Left ventricular end-diastolic pressure (LVEDP) increases to 36+/-4 mmHg at the end of the reperfusion period. No significant necrotic area as assessed by triphenyltetrazolium chloride (TTC) was detected at the end of the reperfusion period. By an immunohistochemical method using antiactin monoclonal antibodies 10.8+/-1.9% of unstained cells were detected in the stunned hearts and 10.3+/-1.2% in control hearts. Preceding the ischemic episode with a cycle of 5 min of ischemia followed by 10 min of reperfusion (ischemic preconditioning) protected contractile function. LVDP and +dP/dtmax now stabilized at 89+/-5% and 94+/-5% of baseline respectively. LVEDP was 20+/-2 mmHg at the end of the reperfusion period. The protection of contractile dysfunction after 20 min of ischemia was achieved also by early reperfusion of low Ca2+-low pH perfusate. With this intervention LVDP stabilized at 87+/-5% of baseline. LVEDP was 12+/-2 mmHg at the end of the reperfusion period. A positive inotropic intervention induced by a modified postextrasystolic potentiation protocol at the end of the reperfusion period increases LVDP to levels higher than baseline in the stunned hearts. However, these values were less than those obtained in control hearts. Ischemic preconditioning significantly increased the maximal inotropic response. Therefore, ischemic preconditioning diminishes the contractile dysfunction of early stunning.

Animals↗
PubMed1996

Inapparent myocarditis and sudden death in pediatrics. Diagnosis by immunohistochemical staining.

We analyzed the anatomopathological findings in two cases of sudden death related to myocarditis in pediatric patients. Since the diagnosis of myocarditis depends either upon histologic and histochemical techniques or the manner the sample was obtained, we describe a more specific immunohistochemical method to stain samples and more accurately diagnose and qualify cellular lymphoid strains in the inflammatory reaction of the myocardium thus allowing a correct diagnosis of myocarditis.

Biopsy↗
PubMed1996

Carotid atherosclerosis. Immunocytochemical analysis of the vascular and cellular composition in endarterectomies.

Papers dealing with rupture of carotid plaque surface are few in spite of the growing importance of the subject. The aim of this study was to analyze the cellular and vascular components of surgically excised carotid endarterectomies in order to obtain information about their role in the pathogenesis of the plaque rupture and intraplaque hemorrhage. Seventy-six surgical specimens of carotid endarterectomies were used for this study. The findings of immunophenotyping of the cellular constituents of the plaques were: 1) endothelial lining: the fibrous cap at the site of the rupture showed an eroded surface with loss of the endothelial lining. Conversely, in the remaining surface a continuous, not damaged row of endothelial cells stained with anti-CD31 and anti-CD34 was observed; 2) fibrous cap: the collagenous fibrous cap at the site of erosion was attenuated and the phenotypic characterization of the cells showed inflammatory components consisting mainly of macrophages (CD68 positive), 2/3 of the total infiltration. The remaining 1/3 was composed of T-lymphocytes and scarce B-lymphocytes. A close interaction between macrophages and capillaries and macrophages and T-lymphocytes was observed; 3) lipid cores: two different types of lipid cores could be depicted. Avascular or mildly vascularized lipid cores and highly vascularized, with neoformed vessels stained with CD34 and CD31. CD34 stained endothelia of all kind of vessels; conversely, neoformed vessels showed a weak stain with CD31. T-lymphocytes were found to be in close contact with neoformed vessels, and in some cases, migrating through the endothelial cells; 4) deeper layers of the plaque: the base and the shoulder of the plaques showed in 28/76 cases neoformed vessels, thin or thick walled, CD34 positive, generally surrounded by mild to extensive mononuclear infiltrates. Atherosclerotic plaques were found to belong to six different lesions: plaque rupture plus thrombosis (18/76, 23.6%), plaque rupture plus intraplaque hemorrhage plus thrombosis (18/76, 23.6%), intraplaque hemorrhage without plaque rupture (16/76, 21.0%), plaque rupture plus intraplaque hemorrhage (5/76, 6.5%), stable calcified non complicated plaque (14/76, 18.4%) and unstable, soft, non complicated plaque (5/76, 6.5%). The first four lesions were considered as "complicated lesions". Complicated plaques presented neoformed vessels in the periphery, shoulder and base of the plaque in 22/57 (38.5%) cases. Conversely only 1/14 (7.1%) of non complicated, stable calcified plaques presented neoformed vessels, (p < 0.05). Of note, the 5 causes of unstable, soft non complicated plaque presented neoformed vessels surrounding the plaque. In 10/57 (17.5%) complicated plaques unequivocal histological signs of old hemorrhages were found surrounding those vessels. Irrespective of presenting no rupture, 11/35 plaques showed a mononuclear infiltrate in the fibrous cap. In conclusion, rupture of carotid plaques (50% of the cases), is characterized by the presence of a macrophagic infiltration of the caps and by the direct apposition of T-lymphocytes to macrophages and a close relation of these cells to endothelial cells. This highly suggests a cell-to-cell interaction, which results in an inflammatory process. Intraplaque hemorrhage without rupture represented 21% of the endarterectomies. These lesions are not related to cap erosion, but to plaque vascularization. Most lipid cores were highly vascularized with neoformed vessels with macrophages and T-cells in close contact and in some cases disrupting the endothelium. The abrupt growing of the lipid core and/or an overproduction of oxygen free radicals could lead to the breakdown of core vessels and intraplaque hemorrhage.

Adult↗
PubMed1996

[Anatomo-clinical and epidemiologic study of Chagas disease].

Chagas' disease is a chronic form caused by a parasite, the Trypanosoma Cruzi, endemic of Latin America. The Trypanosoma Cruzi is transmitted by hematophageous bugs, particularly in dilapidated rural areas. Three phases of the disease can be distinguished: 1) acute phase, with high tissue and blood parasitic involvement; 2) undetermined phase, in which the diagnosis requires sophisticated clinical investigations; 3) chronic phase (10-30 years following the infection), characterized particularly by cardiac disease manifestations. The present 120 patients were subdivided into four groups: 1) 43 asymptomatic serum-positive subjects; 2) 25 serum-positive patients with electrocardiographic abnormalities; 3) 14 serum-positive patients with cardiomegaly; 4) 38 with classic chagasic cardiopathy. Comparative studies among these four groups were carried out employing Holter monitoring (24h), ergometric and phonomechanographic tests, M-mode and bidimensional echography and radionuclide ventriculography. A significant difference between the first 3 groups and, respectively, the fourth group (p < 0.001) was found. Deadly-risk (p < 0.001) manifestation were pointed out, such as a third tone, right bundle branch block with left anterior hemiblock and left ventricle's dilation. Autoptic controls were performed and in 4 patients the myocardial biopsy showed C3 and IgG deposition in capillaries and myocardial fibers, at electron microscopic examination, some thickening of capillary and myocytic basal membrane, interstitial collagen proliferation, besides non-specific myocellular abnormalities were detected.

Adolescent↗
PubMed1996

[Pathology of cardiac lesions induced by radiofrequency ablation in an experimental model].

Radiofrequency catheter ablation is increasingly being used for the treatment of several tachyarrhythmias. The main aim of this paper is to describe the lesional pathology produced by this type of current. Fourteen Wistar rats (mean weight 300 g) were subjected to discharges of a 700 KHz, pure, unmodulated, sine-wave radiofrequency generator. Three rats, through open chests, received epicardial shocks and were immediately sacrificed ("acute" lesions). The remaining 11 rats received shocks through percutaneously plunged tungsten wires, and were sacrificed 1 to 4 weeks after the procedure ("chronic" lesions). Hearts were fixed in buffered (pH7) 10% formalin solution. Selected slices were stained with hematoxilin-eosin and Mallory trichrome. Other slices were fixed in 3% glutaraldehyde and post-fixed in osmium tetroxyde, dehydrated and included in Polybed 812. Ultrathin slices were stained with uranil acetate and lead citrate and examined in a JEOL JEM-100 C electronic microscope. "Acute" specimens showed small coagulation necrosis areas, well delimited by carbonization and hemorrhages. Neighbouring myocardium showed one o two rows of moderate cell lesions which consisted of cytoplasmic homogeneization and increased contracture bands. " Chronic" lesions showed granulation tissue with mononuclear infiltrates and neoformation vessels surrounding a central necrosis area. The older the lesion, the larger the number of fibroblasts and mature collagen tissue. Ultrastructural studies showed irreversible myocardial changes in the lesional borders, with cytosolic and myofibrillar edema, contracture bands and rupture of mitochondrial crests. Radiofrequency lesions are limited, shallow and with net borders, which makes them almost ideal for subendocardial ablation of small arrhythmogenic areas.

Animals↗
PubMed1995

Effect of vitamins A and E on ischemia-reperfusion damage in rabbit heart.

The aim of this study was to test the effect of vitamins A and E in reducing oxyradical effects and myocardial damage after ischemia-reperfusion in the rabbit heart. Oxyradical effects were indirectly assessed by hydroperoxide initiated chemiluminescence and myocardial damage was evaluated by qualitative and quantitative electron microscopy. Left anterior coronary artery was ligated in control and vitamin-treated rabbits for 30 min and then reperfused for 10 min. Rabbits were pretreated with 150 mg vitamin E and 60,000 IU vitamin A 24 h before surgery. After 10 min of reperfusion full-thickness needle samples were obtained from five different myocardial areas (three ventricular and two septal areas) and used for the determination of hydroperoxide-initiated chemiluminescence and ultrastructural damage. In the control group, hydroperoxide-initiated chemiluminescence was 18,400 +/- 500 cpm/mg protein for the non-ischemic and non-reperfused ventricular areas, and 40,500 +/- 1,800 cpm/mg protein for ischemic-reperfused ventricular areas. In the vitamin-treated group, hydroperoxide-initiated chemiluminescence was decreased by 8% in the non ischemic and non reperfused ventricular areas and by 51-75% in the ventricular ischemic and reperfused areas. The two septal areas in the control group gave chemiluminescences of 6,800 +/- 1,200 cpm/mg protein (non ischemic-non reperfused) and 17,000 +/- 2,000 cpm/mg protein (ischemia-reperfusion). In the vitamin-treated group, chemiluminescence decreased by 4 and 58%, respectively. The ischemia-reperfused areas showed extensive edema, margination of nuclear chromatin and swollen mitochondria with disrupted cristae including rupture of the inner and outer mitochondrial membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Beneficial effects of cloricromene in ischemic reperfused myocardium.

Cloricromene (Clo) has been used to prevent myocardial damage after transient occlusion of the circumflex coronary artery (Cx). Twenty rabbits were injected for 4 days with a single dose of Clo (0.25 mg/kg i.v.) or placebo. On the 5th day, the Cx was occluded, and Clo (6.4 micrograms/kg/min) or placebo was continuously infused. After 50 min, the occlusion was removed and after 20 min of reperfusion, the rabbits were sacrificed. In the placebo group, all rabbits showed marked ST segment changes and severe ischemic arrhythmias (6/10 animals). In 5 of them, ventricular fibrillation was followed by death. In the Clo group smaller ST segment elevations were observed, and in 2 rabbits ventricular fibrillation spontaneously reversed as did ST segment elevations. A significant reduction of the necrotic area was also observed in the Clo group by postmortem examination.

Animals↗
PubMed1994

[Ischemia-reperfusion experimental model in the rabbit: ligation of the circumflex coronary artery versus ligation of the anterior descending coronary artery].

INTRODUCTION AND OBJECTIVES: The myocardial damage during ischemia and reperfusion in the rabbit was studied, in order to compare two different models: the occlusion of the circumflex coronary artery (Cx) vs the occlusion of the left anterior descending coronary artery (LAD). METHODS: Each group consisted of 10 New Zealand rabbits; after 50 minutes of occlusion the artery was reopened for 20 minutes and then a biopsy from the area at risk and another from the perfused area were obtained. The specimens were used for chemiluminiscence and electron microscopy. Electrocardiograms were taken throughout the experience. Transverse sections of both ventricles were used for light microscopy. RESULTS: In both groups elevations of the ST segment, more important in the Cx group (p < 0.001) were observed. In the LAD group, the QRS complexes were enlarged in three animals, in 4 rabbits there were reperfusion arrhythmias, but the experimental mortality was zero. In the other group, 50% of the animals died during the experiment. In the LAD group the chemiluminiscence of the area at risk was greater than that of the perfused area (p < 0.001). No differences could be demonstrated between the samples of the Cx group, probably because of the extensive necrotic areas unable to generate photoemission. Ultrastructural and microscopic characteristic lesions of the ischemia-reperfusion phenomena were found in both groups, particularly severe in the Cx group with extensive areas of necrotic tissue. CONCLUSIONS: This experience shows that the myocardial necrosis, the mortality and the malignant arrhythmias were quantitatively different according to which coronary artery was occluded. This fact may be taken into account when an animal model for ischemia-reperfusion is selected.

Animals↗
PubMed1993

Antibodies to laminin and immunohistochemical localization of laminin in chronic chagasic cardiomyopathy: a review.

Antibodies against laminin were determined by ELISA in forty six patients suffering from Chagas' disease and twenty healthy persons (control group). The patients were divided into three groups according to the severity of clinical, electrocardiographic and echocardiographic studies. Histologic, ultrastructural and immunohistochemical studies were made of endomyocardial biopsy specimens from 10 of these patients with chronic Chagasic cardiomyopathy. Antibodies to laminin were detected in 50% of the patients in each of the three groups. However analysis of the data did not allow us to determine any significant correlation among the severity of the different clinical and non-invasive studies and the level of circulating antibodies to laminin. The highest titers of antilaminin antibodies were detected in the group with severe cardiological alterations (37% of the patients). Histological and electron microscopic observation of myocardial biopsies disclosed marked thickening of the basement membranes of the myocytes, endothelial cells and vascular smooth muscle cells. Light (peroxidase-labeled antibodies) and electron (gold-conjugated antibody) microscopic immunohistochemical methods revealed a positive reaction for laminin in these thickened basement membranes. This thickening may develop as a consequence of: a) an immunologic reaction which is triggered by the presence of a laminin-like molecule on the surfaces of T. cruzi amastigotes and trypomastigotes; b) an immunologic response to direct injury of basement membranes causing some of their components to become antigenic; c) myocardial fibrosis, with synthesis of new connective tissue components, and d) a combination of the preceding factors. The relationship of these changes to antilaminin antibodies remains unclear.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Immunohistochemical localization of laminin in the hearts of patients with chronic chagasic cardiomyopathy: relationship to thickening of basement membranes.

Histologic, ultrastructural, and immunohistochemical studies were made of endomyocardial biopsy specimens from 10 patients with chronic chagasic cardiomyopathy. Histologic and electron microscopic observation disclosed marked thickening of the basement membranes of the myocytes, endothelial cells, and vascular smooth muscle cells in all patients. Light (peroxidase-labeled antibodies) and electron (gold-conjugated antibody) microscopic immunohistochemical methods revealed a positive reaction for laminin in these thickened basement membranes. This thickening of basement membranes may develop as a consequence of: (1) an immunologic reaction that is triggered by the presence of a laminin-like molecule on the surfaces of Trypanosoma cruzi amastigotes and trypomastigotes; (2) an immunologic response to direct injury of basement membranes causing some of their components to become antigenic; (3) myocardial fibrosis, with synthesis of new connective tissue components; and (4) a combination of the preceding factors. The relationship of these changes to antilaminin antibodies requires clarification.

Adult↗
PubMed1992

Reduction of reperfusion injury with preoperative rapid intravenous infusion of taurine during myocardial revascularization.

To assess a possible free-radical scavenging action of taurine during coronary artery bypass grafting, 12 patients were randomly divided into two equal groups. One to 3 hours before surgery, they received a rapid intravenous infusion of either placebo (group 1) or taurine (5 gm) (group 2). During surgery, biopsy samples were taken before ischemia (preischemic samples) and after 10 minutes of reperfusion (reperfusion samples). Lipoperoxidation was determined by hydroperoxide-initiated chemiluminescence of heart homogenates, and myocardial cell damage was assessed by electron microscopy. The values for chemiluminescence in preischemic and reperfusion samples from group 1 were 7500 +/- 1600 and 18,600 +/- 4600 cpm/mg of protein, respectively (p less than 0.03). This difference was not observed in group 2 where the values were 10,050 +/- 2700 and 11,800 +/- 4200 cpm/mg of protein, for preischemic and reperfusion samples, respectively. The number of severely damaged mitochondria (grades 3 and 4) in reperfusion samples from group 1 increased significantly compared to preischemic samples (25 +/- 8% vs 12 +/- 3%, p less than 0.01). Conversely no differences were observed between the number of severely damaged mitochondria in reperfusion and preischemic samples from group 2 (8 +/- 3% vs 8 +/- 2%). The number of damaged and necrotic myocytes increased in group 1 after reperfusion from 22 +/- 9% to 34 +/- 10% (p less than 0.03) and from 10 +/- 7% to 26 +/- 20% (p = NS), respectively. No changes were observed between reperfusion and preischemic samples in group 2. Treatment with taurine seems to reduce lipoperoxidation and decrease cell damage at the time of reperfusion.

Biopsy↗