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Biomedical subjects

H Dinh

Publications and source records attributed to H Dinh.

17 recordsLinked to original sources
PubMed2001

Testosterone inhibits early atherogenesis by conversion to estradiol: critical role of aromatase.

The effects of testosterone on early atherogenesis and the role of aromatase, an enzyme that converts testosterone to estrogens, were assessed in low density lipoprotein receptor-deficient male mice fed a Western diet. Castration of male mice increased the extent of fatty streak lesion formation in the aortic origin compared with testes-intact animals. Administration of anastrazole, a selective aromatase inhibitor, to testes-intact males increased lesion formation to the same extent as that observed with orchidectomized animals. Testosterone supplementation of orchidectomized animals reduced lesion formation when compared with orchidectomized animals receiving the placebo. This attenuating effect of testosterone was not observed when the animals were treated simultaneously with the aromatase inhibitor. The beneficial effects of testosterone on early atherogenesis were not explained by changes in lipid levels. Estradiol administration to orchidectomized males attenuated lesion formation to the same extent as testosterone administration. Aromatase was expressed in the aorta of these animals as assessed by reverse transcription-PCR and immunohistochemistry. These results indicate that testosterone attenuates early atherogenesis most likely by being converted to estrogens by the enzyme aromatase expressed in the vessel wall.

Animals↗
PubMed1994

Uniformity of captopril benefit in the SAVE Study: subgroup analysis. Survival and Ventricular Enlargement Study.

The Survival and Ventricular Enlargement (SAVE) Study demonstrated that long-term administration of the angiotensin-converting enzyme inhibitor captopril to recent survivors of myocardial infarction with left ventricular dysfunction resulted in a reduction in cardiovascular mortality and morbidity. Analysis of multiple subgroups demonstrated that baseline demographics (older age) and clinical characteristics (such as prior MI, history of diabetes or hypertension), that have previously been associated with a higher risk of cardiovascular events, were associated with greater end point event rates in SAVE regardless of therapy assignment at the time of randomization. The effectiveness of captopril therapy in reducing cardiovascular mortality and morbidity was examined in multiple subgroups. Although not all subgroups provided adequate statistical power, the benefits of captopril therapy were relatively uniform in the SAVE study. This indicates that the benefits were not confined to one particular subgroup and conversely that targeting of captopril therapy should be to the broadest group, as defined by SAVE entry criteria, to result in a reduction in cardiovascular mortality and morbidity.

Captopril↗
PubMed1991

Exercise increases the circulating concentration of the N-terminus of the atrial natriuretic factor prohormone in normal individuals.

Recently two peptides consisting of amino acids (aa) 1 to 30 and 31 to 67 of the N-terminus of the 126 aa prohormone of atrial natriuretic factor (proANF), as well as atrial natriuretic factor (ANF, aa 99 to 126; C-terminus), were found to have vasodilatory and natriuretic properties. These peptides, as well as ANF, circulate in humans as part of the N-terminus of the prohormone. To determine the effect of graded exercise on the circulating concentrations of the N-terminus and C-terminus of the ANF prohormone in normal persons, 12 healthy individuals (mean age 45 +/- 2 years) were evaluated before, for 2 hours after, and during bicycle exercise at a work loads of 25, 50, 75, 100, 125, 150, and 175 W. Both the N- and C-terminus of the ANF prohormone were released simultaneously with graded exercise in direct proportion to the intensity of the work load, measured objectively via maximal oxygen consumption (VO2max), respiratory quotient, and heart rate. Both the N-terminus and C-terminus of the ANF prohormone had strong positive correlations (p less than 0.001) with blood pressure, heart rate, VO2max, and respiratory quotient. Following exercise, the C-terminus returned to preexercise levels within 30 minutes, while the N-terminus remained significantly elevated at 30 and 60 minutes postexercise, reflecting the longer half-life of the N-terminus in the circulation.

Adult↗
PubMed1991

Acute and sustained release of the atrial natriuretic factor prohormone N-terminus with acute myocardial infarction.

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evidence of congestive heart failure, had their circulating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31-67; pro ANF 31-67) and creatine phosphokinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31-67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p less than 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1-98 and pro ANF 31-67 levels in these patients were within our normal range and significantly lower (p less than 0.001) than seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.

Adult↗
PubMed1989

Increased plasma concentration of atrial natriuretic factor with squamous cell carcinoma invasion of the right and left atria of the heart.

Atrial natriuretic factor is a new peptide hormone synthesized in the heart which has potent natriuretic, diuretic, and vasodilatory properties. A 47-year-old man with squamous cell carcinoma of the lung resected 6 months previously presented with syncope secondary to hypotension and a low serum sodium. He was evaluated to determine if atrial natriuretic factor (ANF) might be the etiology of this clinical picture. His plasma concentration of atrial natriuretic factor was increased three-fold over that of 70 normotensive person. Further evaluation revealed metastatic lesions in the right and left cardiac atria with the mass on the left occluding 75% of the left atrial chamber. The mass effect in the atria increasing atrial stretch and atrial pressure one would expect was the main contributor to the increased ANF level. The contribution of direct tumor invasion into the atria and/or production of atrial natriuretic factor by the tumor itself to produce this elevated plasma level of atrial natriuretic factor could not be determined, but this markedly elevated level of atrial natriuretic factor does appear to be the etiology of this patient's clinical picture.

Atrial Natriuretic Factor↗
PubMed1989

Acute and sustained release of atrial natriuretic factor with acute myocardial infarction.

The present investigation was designed to determine if acute ischemic cardiac injury causes the release of atrial natriuretic factor (ANF). Seventeen patients with acute myocardial infarction but without clinical evidence of congestive heart failure had their circulating concentration of ANF and creatine phosphokinase monitored daily for 14 days. All 17 patients had an elevated plasma ANF concentration at time of presentation. Maximal increase in ANF was on day 2 and 3 post-infarction. This maximal increase correlated with the size of infarction estimated by the maximal creatine phosphokinase concentration (r = 0.475; p less than 0.05), but did not correlate with the amount of left ventricular dysfunction. ANF began to decrease by day 4 post-infarction and was normal at 10 days post-infarction in 14 of the 17 (82%) patients. At 12 days post-infarction, all 17 patients had normal ANF levels. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured ANF levels in these patients were within our normal range and were significantly lower (p less than 0.001) than those seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina likewise had normal circulating ANF concentrations during prolonged episodes of chest pain. These levels were also significantly lower (p less than 0.001) than the 17 patients with acute infarcts not given tPA. The distinct pattern of release of ANF may be useful as an adjunct to serum cardiac enzymes in determining if a myocardial infarction has occurred.

Adult↗
PubMed1989

Chronic cor pulmonale.

Chronic cor pulmonale is defined as right heart hypertrophy and/or chronic right heart failure. There are many etiologies, but the common cause is increased right heart work from pulmonary hypertension. Etiology can be conveniently discussed by assuming two prototypes, the asphyxial or hypoxic type and the vascular obliterative type. A common cause of the asphyxial type is chronic obstructive pulmonary disease, and the obliterative type is represented by chronic pulmonary thromboembolic disease or primary pulmonary hypertension. Pathology is discussed, emphasizing the cardiac manifestations of chronic cor pulmonale including data of specific cardiac chamber size. An overview of hemodynamics is given, and the use and limitation of electrocardiography and chest x-rays are discussed. The exciting potential use of echocardiography for the serial non-invasive measurement of anatomical and pathophysiological features is outlined, along with the value of a careful physical examination and the proper utilization of laboratory tests in the diagnosis of chronic cor pulmonale. In the patient with the asphyxial type, the treatment of pulmonary infectious exacerbations, the role of corticosteroids, digoxin, diuretics, phlebotomy, bronchodilators (theophylline, beta adrenergic agonists, and anticholinergics), and long-term oxygen therapy is noted. The controversy surrounding the use of vasodilators and calcium blockers in these patients is discussed. Treatment aspects of the vascular obliterative type, including the role of vasodilators, calcium blockers, prostacyclin, anticoagulants, and overall strategy are discussed. A brief note is mentioned of the promising role of surgical therapy in chronic thromboembolic disease causing chronic cor pulmonale.

Adult↗
PubMed1989

Prohormone atrial natriuretic peptides 1-98 and 31-67 increase with exercise in congestive heart failure patients.

Recently two peptides consisting of amino acids (a.a.) 1-30 and 31-67 of the N-terminus of the 126 a.a. prohormone of atrial natriuretic factor (pro ANF), as well as atrial natriuretic factor (ANF, a.a. 99-126; C-terminus) were found to have vasodilatory and natriuretic properties. These peptides, as well as ANF, circulate in man as part of the N-terminus of the prohormone. To determine the effect of graded exercise on the circulating concentration of the N-terminus and C-terminus of the ANF prohormone in persons with abnormal salt and water metabolism, 12 individuals with stable congestive heart failure (CHF) were evaluated before and after bicycle exercise testing and the results were subdivided based on the maximal exercise they could achieve. In all of the CHF patients, the circulating concentration of the whole N-terminus (ie, a.a. 1-98), the midportion of the N-terminus (pro ANF 31-67), which circulates as a distinct 3900 molecular weight (m.w.) peptide after being proteolytically cleaved from the N-terminus, and the C-terminus (ANF) increased with exercise. The patients who were able to achieve 100 and 125 watts of workload had a greater maximal oxygen consumption and, in general, a greater percent increase in the circulating concentration of both the N-terminus and the C-terminus of the ANF prohormone than those who had less exercise capacity. Evaluation of the echocardiographic, radionucleotide, and the exercise parameters revealed that the circulating concentrations of these atrial peptides correlated best with left atrial dimension, but that left ventricular systolic and diastolic dimensions also correlated positively with their concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Sustained therapeutic efficacy and safety of oral propafenone for treatment of chronic ventricular arrhythmias: a 2-year experience.

Thirty-two men with chronic ventricular arrhythmias responded to propafenone, a new potent antiarrhythmic agent, in short-term trials with 85% or greater reduction of total ventricular premature complexes (VPCs) per hour, 95% or greater reduction of ventricular couplets (VCs) per hour, and 100% abolition of ventricular tachycardia (VT) beats per 24 hours. These patients were continued on long-term propafenone therapy to assess sustained therapeutic efficacy and safety. Thirty patients completed 1 year and 26 patients completed 2 years of testing with this agent; one patient died of sudden death and another died of a noncardiac cause. Although there were significantly fewer patient responders at 1 and 2 years, the majority of patients (greater than 79%) continued to respond optimally to propafenone. Side effects were minor and included bitter taste, dizziness, congestive heart failure, fatigue, and significant prolongation of the PR and QRS intervals. Propafenone has sustained antiarrhythmic efficacy after 2 years without serious toxicity.

Aged↗
PubMed1987

Recent progress in the electrocardiographic diagnosis of ventricular hypertrophy.

The surface electrocardiogram remains an insensitive method for detection of ventricular hypertrophy. Technical problems related to body size and habitus and distance from the heart cannot be overcome. Coronary arterty disease and amyloidosis, although frequently associated with hypertrophy, tend to obscure the electrocardiographic changes because of the attendant loss of voltage. The progress made in the last 20 years is due primarily to re-evaluation of traditional criteria in terms of careful anatomic correlation. The studies cited have the advantage of using specific clinical diagnoses in a defined population, specific chamber weights, and a 97.5 percentile confidence level for distinguishing normal pathologic and electrocardiographic data from abnormal. They are limited because the results may not apply to females or patients with mitral stenosis and congenital heart disease. In general, the electrocardiogram can be expected to detect left ventricular hypertrophy in six out of ten patients with the disease, and will misdiagnose the problem in about one out of every ten without the disease. Methodology using multiple criteria will achieve the best sensitivity and specificity. Several methods are available and of comparable accuracy. Simplicity of these methods varies widely and will be a factor in the choice of the method selected. The electrocardiogram will perform best in the population of patients with hypertension and aortic stenosis or regurgitation and have its greatest limitation in patients with coronary artery disease and myocardial infarctions. Echocardiography is proven to be more sensitive than the electrocardiogram for detection of left ventricular hypertrophy. Sensitivity is around 90 per cent with 95 per cent specificity. Its major limitations lie in the expense as compared to the electrocardiogram and in inadequate image resolution in a small proportion of patients. In order to achieve the results reported by centers proficient in this technique, careful attention must be paid to precise standardization of measurements and selection of images to be measured. When this is done the echocardiogram certainly offers a distinct advantage over the electrocardiogram in detecting left ventricular hypertrophy. We recommend the use of left atrial abnormality as a criterion to diagnose left ventricular hypertrophy when there is right bundle branch block. When left bundle branch block is present on the electrocardiogram, traditional criteria are probably no more accurate than the bundle branch block itself.(ABSTRACT TRUNCATED AT 400 WORDS)

Bundle-Branch Block↗
PubMed1986

QRS voltage measurements in autopsied men free of cardiopulmonary disease: a basis for evaluating total QRS voltage as an index of left ventricular hypertrophy.

Use of total 12-lead QRS electrocardiographic voltage as a criterion for left ventricular (LV) hypertrophy has been of recent interest. Although upper and lower limits of QRS voltage for individual electrocardiographic leads have been reported in clinically healthy men and women, the upper limit of total 12-lead QRS voltage has not been established in adults free of cardiopulmonary disease by clinical and necropsy criteria. Therefore, the total QRS voltage from all 12 electrocardiographic leads was determined in 30 autopsied men known to be free of cardiopulmonary disease by clinical assessment and by a special cardiac examination using postmortem coronary angiography and chamber partition determination of LV weight. Gross heart weight, LV weight and total QRS voltage are reported. Comparisons were made between disease-free patients and previously reported patients with aortic valve stenosis, aortic regurgitation and cardiac amyloidosis with respect to total QRS voltage and gross heart weight. Total QRS voltage and gross heart weight were significantly greater in patients with severe aortic stenosis (mean 245 mm) and severe aortic regurgitation (mean 274 mm) than in our patients (mean 127 mm). Total QRS voltage was significantly less, whereas gross heart weight was significantly greater in patients with cardiac amyloidosis (mean 101 mm) than in our normal subjects (mean 127 mm). These data provide a basis for evaluating the total 12-lead QRS voltage as a criterion for LV hypertrophy.

Adult↗
PubMed1984

Effect of propafenone on left ventricular ejection fraction.

The effects of orally administered propafenone on ejection fraction (EF) determined by radionuclide angiography were studied in 2 groups of patients receiving different dosing regimens. Fourteen group A patients had no clinical evidence of left ventricular (LV) dysfunction and were not receiving digoxin therapy. In this group a mean daily dosage of 879 mg resulted in a decrease in resting LVEF from 52 +/- 9% to 48 +/- 11% (p less than 0.05). Eight group B patients had clinical radionuclide evidence of LV dysfunction and were receiving digoxin therapy. In this group, a daily dosage of propafenone of 600 mg/day resulted in no significant change in LVEF. No clinically significant effects on cardiac compensation were evident in either group. These data suggest a negative inotropic effect that is either related to propafenone dosage or at least partially attenuated by digoxin therapy. Further studies are necessary to define precisely the effects of propafenone on LV function.

Aged↗
PubMed1984

Relation of right ventricular ejection fraction to exercise capacity in chronic left ventricular failure.

Although the left ventricle is traditionally viewed as the heart's main pumping chamber, no correlation has been shown between left ventricular (LV) ejection fraction (EF) at rest and exercise capacity in patients with chronic LV failure. Because vasodilators with venodilating activity increase exercise capacity more than predominant arterial dilators in patients with LV failure, right ventricular (RV) function may relate to exercise capacity in these patients. In 25 patients with chronic LV failure, caused by coronary artery disease in 12 patients and idiopathic dilated cardiomyopathy in 13 patients, RVEF and LVEF at rest were measured by radionuclide angiography. Maximal upright bicycle exercise testing was also performed to determine maximal oxygen consumption, which averaged only 13 +/- 4 ml/min/kg. The LVEF at rest was 26 +/- 10% and did not correlate with maximal oxygen consumption (r = 0.08). However, the RVEF was 41 +/- 12% and correlated with maximal oxygen consumption (r = 0.70, p less than 0.001) in the same patients. The correlation was stronger (r = 0.88) in patients with coronary artery disease than in those with idiopathic dilated cardiomyopathy (r = 0.60). Thus, RVEF at rest is more predictive of exercise capacity than LVEF in the same patients with chronic LV failure. These results are consistent with the clinical observation that only venodilating agents increase exercise capacity of patients with chronic LV failure.

Cardiac Output↗
PubMed1984

Effect of propafenone in patients with stable ventricular arrhythmias.

Thirty patients with clinically significant ventricular ectopy were treated with propafenone, a new potent antiarrhythmic agent with membrane stabilizing action. Patients had a minimum mean of greater than 30 ventricular premature beats per hour documented by continuous 48-hour ambulatory ECG recording. Twenty-five patients qualified as responders, defined as greater than 85% reduction of ventricular ectopy compared to baseline, and completed a double-blind placebo-crossover phase. Significant reduction in single ventricular ectopy per hour, paired ventricular ectopy per hour, and ventricular tachycardia beats per hour were observed. Almost total abolition of ventricular tachycardia and paired ventricular ectopy was achieved. Side effects were minimal and well tolerated. A significant prolongation of the PR interval occurred. QRS prolongation and prolongation of the corrected QT interval was observed in some patients, with new left bundle branch block developing in two patients. Long-term efficacy and safety studies will be necessary to determine the ultimate role of this new agent in the selection of antiarrhythmic therapy, but these initial results are encouraging.

Adult↗
PubMedDate not supplied

Tumour-growth inhibition by induced hyperglycaemia/hyperlactacidaemia and localized hyperthermia.

The present study was undertaken to exploit pathophysiological properties of solid tumours for a tumour-specific therapy. Experiments were carried out on DS-sarcomas implanted s.c. in the hind foot dorsum of Sprague Dawley rats. Treatment strategies included tumour acidification, lactate accumulation and disturbance of the microcirculation by induced systemic hyperglycaemia/hyperlact-acidaemia (15-25/10 mmol/L; for 60 min) as well as localized hyperthermia (water-bath; 43 degrees C, 30 min.). A special infusion solution was developed for the systemic treatment containing glucose, lactic acid and organic buffer without inorganic ions. Growth kinetics of tumour volume and animal survival were taken as endpoints in order to quantify therapeutic efficiency. After a single treatment with combined modalities, i.e., with hyperglycaemia/hyperlactacidaemia and hyperthermia, approximately 50% of the tumours showed complete remission in three independent series of experiments; around 40% of the animals survived more than two months. In the untreated control group, all animals died from the disease within 10-15 days after tumour implantation. The overall effect on tumour volume changes of the combined therapy was supra-additive compared to that of treatment with hyperthermia or hyperglycaemia/hyperlactacidaemia alone. However, treated animals either showed a dramatic response to the combination of treatments with complete tumour remission or hardly responded at all, justifying a subdivision into responders and non-responders. Pathophysiological mechanisms responsible for this behaviour have to be elucidated in future studies. Nevertheless, the present study represents an approach to an efficient tumour therapy with a potential application in clinical oncology in the not too distant future.

Animals↗