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Biomedical subjects

J Milei

Publications and source records attributed to J Milei.

At least 55 records · Page 3Linked to original sources
PubMed1989

Panarteritis precipitating extensive circumferential acute myocardial infarction. A case report.

It is widely known that other causes than recent coronary thrombosis may precipitate acute myocardial infarction in the presence of coronary atherosclerosis. A 48 year old male patient was admitted due to acute coronary insufficiency. The ECG showed anterolateral necrosis and lateral ischemia. Despite medication angina persisted and he died immediately after coronary angiography. At autopsy, established coagulation necrosis was observed in the internal half and the subendocardium of the lateral and posterior walls, of the left ventricle. Early coagulation necrosis occupied the inner half of the anterior, posterior and septal walls. Severe atherosclerotic coronary lesions were found in all major coronary trunks. An extensive panarteritis, involving extra and intramyocardial branches, consisting of mononuclear cells and prominent edema, was observed. A mixed mechanism may be invoked to explain the extensive myocardial necrosis: panarteritic infiltrates and extensive edema and humoral-induced coronary spasm.

Arteritis↗
PubMed1988

Assessment of myocardial oxidative stress in patients after myocardial revascularization.

A homogeneous group of six patients, who underwent coronary artery bypass surgery, was studied to determine the presence of oxidative stress caused by oxygen-derived free radicals and its relationship with reperfusion cell damage. Biopsies were performed before ischemia and 10 minutes after reperfusion. The samples were assayed for hydroperoxide-initiated chemiluminescence and histochemical succinic dehydrogenase activity; the specimens were also studied by electron microscopy. The preischemic biopsy specimens showed chemiluminescence of 40 +/- 2 (cpm/mg protein) x 10(3), normal succinic dehydrogenase activity (grade 4), and generally preserved ultrastructure (necrotic/normal cells 5/100). However, the reperfusion biopsy specimens showed an increase in chemiluminescence to 91 +/- 19 (cpm/mg protein) x 10(3) (p less than 0.025), a partial loss of enzymatic activity (grade 2.6), and ultrastructural changes characterized by mitochondrial swelling and focal myofibrillar disorganization (necrotic/normal cells: 15/100; p less than 0.001). These observations seem to indicate the presence of oxidative stress during reoxygenation, a situation that may play a major role in the genesis of reperfusion injury. It appears to be the first observation relating free radical-induced oxidative stress to reperfusion injury in humans.

Adult↗
PubMed1988

Histopathology of the heart conducting system in experimental Chagas disease in mice.

Although mice infected with Trypanosoma cruzi develop a wide variety of electrocardiographic (ECG) alterations, the typical isolated right bundle branch block or its association with the left anterior hemiblock patterns are not found in this model. This has been explained as related to topographic differences in the anatomy of the murine conducting system. However, there is no conclusive evidence that the murine conducting system differs from the human system. In this study, the anatomy of the murine conducting system is described, as well as its involvement in the chronic stages of experimental infection. 24 three-month-old C3H mice were infected with 50 bloodstream forms of T. cruzi, Tulahuén strain. Animals were killed after 3, 8 and 12 months. Whole frontal sections of the heart, including the conducting system, were serially studied. The sinoatrial node was located in the right atrial appendage, or in the junction between the superior vena cava and the right atrium, or "riding" on the interatrial septum. The atrioventricular (A-V) node and the His bundle showed a similar anatomic course to that in man. Therefore, there was no important anatomical difference that might have explained the lack of the ECG patterns observed in human chagasic myocardiopathy. The inflammatory involvement and the lesions of the conducting system were diverse and rarely severe. No significant difference was observed in animals killed at different times. The lesions in the working myocardium were similar to those observed in humans (chronic inflammatory infiltrates). Nevertheless, the topography of lesions was different: there was a selective involvement in the neighbourhood of the A-V groove.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Prevention of adriamycin-induced cardiotoxicity by prenylamine: a pilot double blind study.

Adriamycin (ADM) is an effective antineoplastic drug. However, the amount of ADM that can be administered must be limited because of the risk of developing a severe dose-dependent myocardiopathy. Prenylamine (PNL), a calcium antagonistic drug, provided partial protection against ADM-induced cardiotoxicity in mice and in the rabbit. Thus, it was considered important to evaluate the cardioprotective potential of PNL in patients given ordinary doses of ADM. Twenty-six patients were selected and randomized in two groups, and a double-blind trial was begun. Group A (n = 13): patients received ADM, i.v. at standard oncological doses up to 550 mg/m2, plus placebo, orally. Group B (n = 13): ADM was administered as in Group A, but PNL 200 mg/day was given instead of placebo. Standard ECG and chest radiographs were performed at the beginning of treatment and every two months. Mode-M echocardiograms and 24-hour ambulatory ECGs were obtained previously to the beginning of the ADM treatment and two months after the administration of the last dose of the drug. In Group A, three patients died from oncological causes, total ADM dose was 359 +/- 100 mg/m2, and the mean age was 59.7 years. One patient in this group developed a congestive myocardiopathy while another patient developed a severe supraventricular arrhythmia. In Group B, four patients died from oncological causes, total ADM dose was 367 +/- 132 mg/m2, and the mean age was 63.8 years. No myocardiopathy was found in this group. These findings suggest that simultaneous administration of PNL may mitigate ADM cardiotoxicity, but larger trials are needed to draw definite conclusions.

Aged↗
PubMed1987

Ketanserin in parenteral treatment of acute essential hypertension: a dose-response curve.

This study assesses the efficacy, safety, and dose-response curve of ketanserin, according to parenteral routes of administration, in the treatment of acute severe essential hypertension. We studied 50 patients with supine diastolic blood pressure (SDBP) phase V greater than or equal to 110 mm Hg after 2 h of continuous BP monitoring. Ketanserin was administered as follows: 5 mg i.m. (Group I: SDBP X = 115.7 mm Hg); 10 mg i.m. (Group II: SDBP X = 119.0 mm Hg); 5 mg i.v. (Group III: SDBP X = 123.9 mm Hg); and 10 mg i.v. (Group IV: SDBP X = 130.8 mm Hg), according to initial severity of symptoms and BP. All patients were monitored, and most of them were on antihypertensive treatment. [Total group mean age: 57.9 years (range: 38-78 years)]. There were 35 men and 15 women. Systolic BP fell progressively, from a mean of 177.9 mm Hg (basal) to 156.4 mm Hg at 60 min postadministration (Group I), p less than 0.01; from 188 to 164 mm Hg (Group II), p less than 0.05; from 192.1 to 157.9 mm Hg (Group III), p less than 0.01; and from 207.5 to 168.3 mm Hg (Group IV), p less than 0.01). SDBP decreased from a basal mean value of 115.7 to 92.1 mm Hg at 60 min (Group I), p less than 0.01; from 119.0 to 98 mm Hg (Group II), p less than 0.05; from 123.9 to 101.6 mm Hg (Group III), p less than 0.01; and from 130.8 to 105.8 mm Hg (Group IV), p less than 0.01. Heart rate decreased slightly in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Amelioration of adriamycin-induced cardiotoxicity in rabbits by prenylamine and vitamins A and E.

The cardioprotective potentials of prenylamine (a calcium antagonist) and of a combination of vitamins A and E (a singlet oxygen quencher and a free radical scavenger, respectively) were evaluated in rabbits given chronically large doses of Adriamycin (ADM) (10.8 mg/kg body weight for 9 to 11 weeks). Among ADM-treated rabbits, 8 of 10 showed post-treatment ECG changes; in rabbits treated with ADM and prenylamine, changes were found in a smaller number (5 of 10); and in animals treated with ADM and vitamins A and E, the incidence was only one in six (p less than 0.05). Heart homogenates from ADM-treated rabbits showed an increased hydroperoxide-initiated chemiluminescence (expressed as cpm/mg protein X 10(-3)) of 77 +/- 4 compared to control animals (52 +/- 1) (p less than 0.01). Prenylamine administration did not alter hydroperoxide-initiated chemiluminescence in ADM-treated rabbits, whereas treatment with a combination of vitamins A and E showed a significant decrease in hydroperoxide-initiated chemiluminescence in control (40 +/- 2) and ADM-treated rabbits (42 +/- 1). Microscopically, myocardial fibers had mild to severe hydropic vacuolization of sarcoplasm, which led to progressive myocytolysis. A total of 103 +/- 13 damaged fibers were detected over 700 counted fibers. Myocardial damage was lowered to 47 +/- 16 by administration of prenylamine and to 28 +/- 8 by administration of vitamins A and E. It is suggested that ADM leads to myocardial lipid peroxidation (ameliorated by vitamins A and E) with membrane damage and to an increase in calcium permeability, the latter being counteracted by prenylamine.

Animals↗
PubMed1986

Early myocardial infarction. A feasible histologic diagnostic procedure.

The Barbeito-López trichrome stain (BLTS) was compared with hematoxylin and eosin (HE), the basic fuchsin picric acid (BFP) and nitro-blue tetrazolium (NBT) dye tests. Two types of hearts were studied: myocardial necrosis induced by isoproterenol (ISP) in rats and human hearts with early coagulation necrosis (Early CN). The BLTS was much more sensitive than HE for diagnosis of Early CN in rats. By 24 hours, both BLTS and HE showed established coagulation necrosis (Established CN) although BLTS did so more clearly. In human material BLTS was a useful indicator of Early CN. It showed patchy areas of coagulation necrosis in the cytoplasm of damaged myocardial cells which were not visualized with HE. Normal myocardium remained green or pale blue. Early CN appears as patchy yellow areas while the remainder of the cytoplasm stains green. Established CN appears "golden yellow" or "orange yellow".

Animals↗
PubMed1986

Ketanserin versus metoprolol in the treatment of essential hypertension.

This study was designed to compare the antihypertensive effectiveness of ketanserin (K) and metoprolol (M) in a 3-month double-blind treatment, and to assess the long-term efficacy of K in a 1-year open trial. Twenty-four patients with mild to moderate hypertension were randomly placed in two groups: group 1 (n = 11) received K, 40 mg/day, and group 2 (n = 13) received M, 200 mg/day. In the double-blind phase of treatment both K and M significantly lowered blood pressure (BP) (P less than 0.01). The heart rate was significantly decreased by M (P less than 0.01). In the 1-year follow-up, patients were divided into three groups: group I (n = 7) had been previously treated with K and maintained on K; group II (n = 4) was given K plus M (these patients had previously been treated with K, but K had failed to decrease diastolic BP to less than or equal to 90 mmHg); and group III (n = 13) was given K (previously these patients had been treated with M). In group I, the BP lowering effect remained constant throughout the 1-year follow-up. In group III, supine and standing diastolic BP decreased significantly after treatment with K (P less than 0.05). Side effects from K were minimal. Ketanserin appears to be a new alternative approach in the treatment of mild and moderate essential hypertension.

Adult↗
PubMed1986

Experimental Argentine hemorrhagic fever: myocardial involvement in Cebus monkey.

Four Cebus apella monkeys, to test a recently proposed model for testing neurovirulence of Junín virus (JV) strains, were intracerebrally infected with 10(5) LD50 of the XJ clone 3 strain of JV. There were no significant electrocardiographic abnormalities or gross lesions, but all infected monkeys exhibited a varying degree of histologic myocardial lesions including focal lymphoblastic infiltrates, vascular ruptures, and mild interstitial reactive change. One Cebus showed lymphocytic infiltrates in the caudal portion of the A-V node without specific cell involvement. These preliminary results demonstrate cardiac involvement in experimental infection of the Cebus monkey with Junín virus.

Animals↗
PubMed1986

Correlation of cineangiographic and pathology findings in coronary artery disease.

In order to correlate the percent of coronary lumen reduction measured by cineangiography and by pathology, we reviewed the coronary trees of 12 patients who died of coronary heart disease. The 36 arterial segments were divided in two groups: group I showing a good correlation in its 24 segments (less than 15% difference between both methods, r = 0.90), and group II (12 segments) with a poor correlation. No significant differences were found every time there was a greater than 70% stenosis. Milder lesions have a higher rate of discrepancies, due to pathology overestimation because of collapse of the vessel and tissue shrinkage, and to the angiographic underestimation that appears when comparing the stenotic segment with a remaining presumably normal artery.

Adult↗
PubMed1986

Ketanserin in the treatment of essential hypertension. A double-blind study against metoprolol and a further long-term open treatment.

Monotherapy with Ketanserin, a serotonin receptor antagonist, reduces blood pressure in a sizeable number of patients with essential hypertension. The present study was designed to compare its antihypertensive potency with those of metoprolol in a double-blind treatment and further to study its long-term efficacy and safety in a one-year open trial, alone or combined to metoprolol, according to diastolic blood pressure (DBP) normalization. Twenty-four patients with mild to moderate hypertension were randomly assigned to two parallel treatment groups, one group (n = 11) received Ketanserin (40 mg/day) and the other one (n = 13) metoprolol (200 mg/day). After 3 months double-blind treatment, all patients received Ketanserin, on an open basis for one year alone or combined to metoprolol if Ketanserin failed to normalize DBP. A significant antihypertensive effect was demonstrated after 3 months double-blind treatment, for Ketanserin and metoprolol, in both standing and supine position (p less than 0.01). Heart rate showed a clear decrease by metoprolol (p less than 0.01). In the one-year follow-up, patients were divided in: I (n = 7) patients on Ketanserin (previously treated with the same drug); II (n = 4) patients on Ketanserin plus metoprolol (previously treated with Ketanserin, in whom it failed to normalize DBP); and III (n = 13) patients on Ketanserin (previously treated with metoprolol). In group I the blood pressure lowering effect of Ketanserin remained constant after one-year follow-up. In group II, although the number of patients was insufficient, a trend in the decrease of parameters was observed. In group III, supine and standing DBP diminished from 92.5 +/- 8 and 92.5 +/- 7 during treatment with metoprolol to 83.6 +/- 9 and 79.8 +/- 8 mmHg respectively at 12 months, after treatment with Ketanserin (p less than 0.05); accordingly, the cumulative percentage of normalized DBP increased from 4/13 after metoprolol to 12/13 at the end of the trial. Ketanserin side effects were minimal. Taking into account the wide variety of contraindications or side effects with beta-blockers and diuretics, Ketanserin appears as a new and important alternative in the treatment of mild and moderate essential hypertension.

Adult↗