Biomedical subjects

B Halawa

Publications and source records attributed to B Halawa.

At least 19 recordsLinked to original sources

PubMed1999

[Antiarrhythmic agents in the prevention of sudden cardiac death].

Sudden cardiac death due to ventricular arrhythmias remains a significant problem. In most studies about 50% of all death related to coronary artery disease and heart failure are sudden and unexpected and are caused by acute fatal ventricular tachycardia and fibrillation. Most of the patients suffering sudden cardiac death have some kind of structural heart disease but 80% of SCD events are associated with coronary artery disease, 10-15% with dilated and hypertrophic cardiomyopathy, and only small fraction with the less common disorders as valvular heart disease, ventricular dysplasia and cardiac involvement in sarcoidosis or amyloidosis. In some patients the anomaly responsible for sudden cardiac death is not structural but mainly electrical as in patients with the long QT syndrome, WPW syndrome or in patients with a proarrhythmic effect from antiarrhythmic drugs. In this review, data from clinical trials and other studies on on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention sudden cardiac death in high risk patients. Taken together with the mortality data routine prophylactic use of class I antiarrhythmic drugs in the patients survivors of acute myocardial infarction and patients with heart failure is associated with increased risk of death. Conversely beta-blockers are associated with significant reduction in nonfatal cardiac arrest in the short term trials and sudden cardiac death in long term trials. These benefits are likely due to relief ischemia, reduction of heart rate and maintenance favourable autonomic nervous system balance. Overall trial data on amiodarone suggests that this agent is effective in reducing the risk of death in survivors of cardiac arrest, post infarction patients, and patients with heart failure but the routine prophylactic use of amiodarone remains of uncertain efficacy. The physician who considers the use of antiarrhythmic medications in patients with ventricular arrhythmias must be aware of which arrhythmias are malignant or potentially malignant and which are benign and the decision to initiate antiarrhythmic therapy should be based on consideration of the patients absolute mortality risk.

Anti-Arrhythmia Agents↗

PubMed1999

[Trends in pharmacological treatment of congestive heart failure].

Congestive heart failure (CHF) is growing epidemiologic and clinical problem, and is the only common cardiovascular condition that is increasing in incidence, prevalence and mortality. During last years numerous clinical trial have been conduced evaluating the effect of various treatment procedures on clinical endpoints in patients with CHF. The major risk factor for CHF are hipertension and atherosclerotic vascular diseases, and now it is clear that aggressive treatment of hypertension and hyperlipidemia can be effective in preventing CHF. Treatment strategies for CHF are aimed at preventing and delaying progression of the disease and improving survival. In the treatment of CHF diuretics are at present the first drugs line for patients with fluid retention and are necessary to relieve symptoms but cannot halt progression or improve the prognosis of CHF. Angiotensin-converting enzyme inhibitors (ACE inhibitors) therapy has been shown to decrease mortality and progression of CHF and should be used early in patients with left ventricular dysfunction whether they have symptomatic or asymptomatic CHF. Digoxin therapy is associated with decrease in the risk of worsening CHF irrespective of rhythm, systolic function, severity of CHF or therapy with ACE inhibitors. In patients with symptomatic CHF due to systolic dysfunction the addition of diuretics and digoxin appears to reducing worsening CHF without improving survival. Other than digoxin oral inotropic agents (amrinone, pimobendan, vesnarinone, ibopamine) increase mortality in patients with CHF and have not improved symptom status and other clinical endpoints during long-term therapy. Hydralazine and isosorbide dinitrate administrated in combination are less effective alternative to ACE inhibitors. Beta-blockers and particular carvedilol may prolong survival and decrease worsening CHF when used in combination with digoxine, diuretics and ACE inhibitors. Beta-blockers therapy improve hemodynamics, LVEF and functional status patients with CHF and the ideal candidate for this therapy is stable patients with NYHA II-III CHF due to nonischemic cause. Calcium antagonists do not appear to be useful in patients with CHF, although amlodipine and mibefradil appears to be safe for treatment of angina or hypertension in this group. On the basis of current data, antiarrhythmic agents should not be given to patients with CHF free from arrhythmia but those with sustained ventricular tachycardia or ventricular fibrillation amiodaron appears to be safe.

Adrenergic beta-Antagonists↗

PubMed1999

[Do cytokines have any value in the patients with chronic blood circulation insufficiency?].

Heart failure is a common and increasing public problem. Neurohormonal activation plays a role in the pathophysiology of heart failure, but is probably also affected by cytokines. We studied 75 patients with heart failure NYHA functional class II and III-IV, who were treated with angiotensin converting enzyme inhibitor (enarenal), diuretics (furosemide) and digoxine. Their mean age was 63.9 years/range 65-86/, left ventricular ejection fraction in the patients NYHA functional class II and III-IV classes was 68.9% and 47.3% respectively; 12 were females. Significant improvements in NYHA classification were shown. The levels plasma TNF-alpha (tumor necrosis factor-alpha) and interleukin-6 (IL-6) were analysed before and after therapy. The authors showed increased plasma levels TNF-alpha and IL-6 in patients with chronic heart failure. After the treatment the plasma IL-6 levels decreased only in the patients III-IV NYHA functional classes, whereas the treatment had no effect on the plasma TNF-alpha levels.

Aged↗

PubMed1999

[The level of plasma endothelin-1 in patients with essential hypertension].

Endothelin-1 (ET-1) as a potent vasoconstrictor, has mitogenic and inotropic properties, stimulates the renin-angiotensin-aldosterone system and sympathetic nervous system. The results of recent studies suggest that overall hemodynamic effects of ET-1 may play a part in the control of blood pressure and the pathophysiology of hypertension. Several investigators have invoked increase level of ET-1 in human essential hypertension but the results of studies concerning hypertensive patients with normal renal function have shown that they have similar concentrations of ET-1 to those in normotensives. To establish whether ET-1 may elevate of blood pressure, the value of plasma ET-1 activity was determined in peripheral blood in 101 patients with essential hypertension. There was no significant difference between in mean level of ET-1 in patients with essential hypertension and in control group. The plasma ET 1 was significantly higher in patients with severe hypertension than that of patients with mild and moderate hypertension, and in patients with severe hypertension there was a correlation between the level of ET-1 and microalbuminuria. There was no correlation between the plasma ET-1 level and systolic blood pressure and diastolic blood pressure in the patients with essential hypertension as a whole, not was there any correlation between ET-1 and noradrenaline, aldosterone level and renin plasma activity.

Adult↗

PubMed1999

[The study of the activity of creatine kinase in diagnosis of coronary reperfusion in patients with acute myocardial infarction after thrombolysis].

Early estimation of the efficacy of thrombolysis in acute myocardial infarction is of great clinical importance because the appearance of coronary reperfusion changes therapeutic and diagnostic procedures and decreases the mortality rate. Previous studies showed that the analysis of activity of creatinine kinase (CPK) measured in regular, short periods of time after thrombolysis night be useful in the diagnosis of reperfusion equally to coronary angiography. The aim of the study was to estimate the usefulness of the analysis of creatine kinase (CPK) and its isoenzyme (CK-MB) in the diagnosis of coronary reperfusion in patients with acute myocardial infarction after thrombolytic therapy. The study was performed in 50 patients with acute myocardial infarction admitted to our Cardiology Department, of these 42 were men aged from 34 to 68 and 8 were women aged from 43 to 70. 28 patients had acute inferior myocardial infarction, 22 patients--acute anterior myocardial infarction. All patients were administered 300 mg of aspirin after admission and then 150 mg of aspirin daily and 1,500,000 IU of streptokinase i.v. within 1 hour. Venous blood samples for determination of CPK and CK-MB were obtained every 3 hours during the first 48 h and once a day at 8 a.m from 3rd to 11th day. All patients underwent coronary angiography 2-4 weeks after thrombolysis. The study showed that in patients with reperfusion, activities of CPK and CK-MB three hours after thrombolysis were higher than 30% of later peak. These findings show the usefulness of this criterion in early, non-invasive estimation of efficacy of thrombolysis. Determination of activity of isoenzyme CK-MB during thrombolytic therapy is not necessary, because it evaluates similarly to CPK. We showed that electrocardiographic and enzymatic criteria are comparable in estimation of efficacy of thrombolytic therapy.

Acute Disease↗

PubMed1999

[Alveolar-arterial oxygen gradient in patients with clinical symptoms of pulmonary embolism].

The accurate detection of pulmonary embolism is possible by means of non-invasive but very expensive ventilation-perfusion lung scanning or invasive and with high rate of complications pulmonary angiography. Thus monitoring of many clinical and biochemical parameters has been recently attempted to increase the probability of correct diagnosis of pulmonary embolism. The alveolar-arterial oxygen gradient is a more sensitive indicator of disturbance in oxygenation than occurrence of hypoxia in gasometry. The aim of our study was to examined the changes of the alveolar-arterial oxygen gradient in patients with pulmonary embolism. The survey was made in 35 patients aged from 41 to 75 with acute pulmonary embolism, of these 17 were men and 18 were women. We excluded patients with coexisting serious heart or lung disease. Pulmonary embolism was diagnosed on the grounds of presence of commonly known risk factors, sudden onset, findings on the chest radiography, hypoxia resistant to oxygen therapy, electrocardiography, echocardiography and catheterization of pulmonary artery using a Swan-Ganz catheter. The alveolar-arterial oxygen gradient was measured in arterial blood samples obtained 15 minutes after 100% oxygen ventilation, using standard formulae. All patients were administered heparin, oxygen and warfarine therapy. The control group consisted of 20 patients, 11 women and 9 men aged from 37 to 74, with deep venous thrombosis without coexisting heart or lung disease. In our study we showed that the alveolar-arterial oxygen gradient is a very useful parameter helping with diagnosis and monitoring efficacy of treatment in patients with pulmonary embolism without coexisting heart or lung diseases.

Acute Disease↗

PubMed1999

[Plasma concentrations of endothelin-1 and endothelin-2 in patients with pulmonary hypertension].

Increased pressure in pulmonary artery is connected among other things with increased endothelin plasma concentration. The aim of the study was to assess plasma endothelin concentration in patients with pulmonary hypertension. The analysis comprised 22 patients with increased pressure in pulmonary artery in the course of pulmonary thromboembolism or chronic exacerbated left ventricular failure and 10 patients with chronic exacerbated left ventricular failure without pulmonary hypertension. Plasma endothelin concentration was measured in pulmonary artery and capillary wedge pressure were evaluated with Swan-Ganz catheter and also peripheral and pulmonary vascular resistance were calculated. Endothelin plasma concentration in peripheral vein was compared between patients and healthy volunteers. Plasma endothelin concentration in pulmonary artery, peripheral artery and vein was higher in patients with pulmonary hypertension than in patients with chronic exacerbated left ventricular failure without pulmonary hypertension. Plasma endothelin concentration in patients with chronic exacerbated left ventricular failure without pulmonary hypertension was higher in pulmonary artery than in peripheral artery and vein. At these patients plasma endothelin concentration in the peripheral vein didn't differ significantly from the healthy volunteers.

Adult↗

PubMed1999

[Levels of tumor necrosis factor (TNF-alpha) and interleukin 6 (IL-6) in serum of patients with acute myocardial infarction].

In acute myocardial infarction may increase the synthesis of cytokines, which can enlarge the myocardial lesion owing to their direct toxic action on myocytes or induction of inflammatory changes that lead to myocardiofibrosis. All this may quickening the appearance of congestive heart failure after myocardial infarction. The aim of the study was examination of tumor necrosis factor (TNF-alpha) and interleukin 6 (IL-6) plasma levels in patients with acute myocardial infarction and analysis of correlation between concentrations of these cytokines and myocardial lesions during infarction. The study was made in 94 patients admitted to the Department of Cardiology with acute myocardial infarction (AMI). Of these, 40 were women aged from 41 to 85 (mean 67 years) and 54 were men aged from 39 to 86 (mean 63 years). Anterior AMI was diagnosed in 40 patients, inferior AMI was diagnosed in 54 patients. 63 patients underwent the thrombolytic therapy, reperfusion appeared in 45 patients, 24 patients were excluded from the thrombolytic therapy. Control group consisted of 28 healthy persons aged from 35 to 76 (mean 61 years). Blood samples for determination of TNF-alpha and IL-6 plasma levels were taken just after admission prior to the treatment. Then patients were taken streptokinase or tissue-type plasminogen activator with typical doses. Blood samples for determination of cytokines were obtained in 3. and 7. day after treatment. TNF-alpha and IL-6 plasma levels were determined with radioimmunological assay. Creatine kinase activity were monitored in patients with AMI as well as ejection fraction was checked in echocardiography in 3. and 7. day after treatment. We showed increased plasma levels of TNF-alpha and IL-6 in patients with AMI with maximum in 3. day of infarction. Concentrations of cytokines were higher in patients with anterior AMI than in patients with inferior AMI. In anterior infarction concentrations of cytokines were significantly lower after thrombolytic therapy with reperfusion than after treatment without reperfusion. There is a correlation between infarct size and concentrations of TNF-alpha and IL-6.

Adult↗

PubMed1998

[Views on the use of calcium channel blockers in the treatment of heart ischemia and hypertension].

Calcium-channel blockers differ in their molecular structure, their sites and modes of action. Based on rapport's about short acting calcium-channel blockers, several recent publications have questioned the safety of agents in this class, particularly nifedypine. It has been well documented that nifedypine can cause a precipitation uncontrollable drop in arterial blood pressure, which can be dangerous in the presence of ischemic heart disease, hypertension and other hemodynamically unstable situation. The cardiovascular risk for patients prescribed short-acting calcium channel blockers was eight times than for those taking, long-acting ones. Sustained-release preparations are the preferred form of therapy, as they appear, to be safer than short-acting agents. Most calcium-channel blockers, including verapamil, diltiazem, amlodypine, felodipine, nitrendipine and nicardipine have been shown to be effective in reducing symptoms of myocardial ischemia, and all have been used successfully for lowering blood pressure in hypertensive patients. Data from trials of nondihydropyridines have not demonstrated increased mortality or myocardial infarction rates in patients with myocardial ischemia and good left ventricular function. In patients with coronary artery disease and in hypertensive patients with poor left ventricular function, amlodypine or felodipine may be relatively safe alternative. Particular attention should be paid to the benefits of werapamil in postinfarct patients. In patients with hypertension, calcium-channel blockers should be reserved for use when diuretics, beta-blockers or angiotensin-converting enzyme inhibitors have been used already or contraindicated or are not tolerated and when further blood pressure reduction is necessary.

Aged↗

PubMed1998

[Plasma adrenomodullin concentration in patients wtih essential hypertension].

Adrenomedullin (ADM) is a novel peptide secretion from vascular smooth muscle, endothelial cells and other peripheral organs. It has potent and long-lasting vasodilatatory and natriuretic properties which could participate in regulating systemic blood pressure. To examine the pathophysiological role of ADM in hypertension the plasma concentrations of ADM were measured in patients with essential hypertension, before and after effective antihypertensive therapy, and in normotensive control group. Plasma ADM concentrations were increases in patients with severe hypertension and normal in patients with mild and moderate hypertension, and were decreased after effective therapy. In all hypertensive patients plasma ADM concentrations where not correlated with blood pressure, plasma renin activity, plasma endothelin-1,2, or plasma aldosterone. These results may suggest that ADM participates in defense mechanisms acting against the high elevation blood pressure in patients with hypertension.

Adrenergic beta-Agonists↗

PubMed1998

[Levels of neuropeptide Y and thromboxane B2 in patients with variant angina].

One of the causes of coronary artery spasm in patients with variant angina could be a disturbed interaction between the vasodilating action of endothelial derived relaxing factor and the vasospastic action of neuropeptide Y and thromboxane B2. The aim of this study was a verification of the participation of neuropeptide Y and thromboxane B2 in etiopathogenesis of the coronary artery spasm in patients with variant angina. The survey was made in 38 patients with variant angina and in 18 patients with chronic stable angina pectoris. The control group consisted of 20 healthy persons. Before the hyperventilation test, during which the person under test has been breathing with a frequency of 40/minute through 5 minutes, the Tris (tromethamol) of pH = 10.5 has been given in intravenous infusion lasting for 5 minutes. The neuropeptide Y and thromboxane B2 plasma levels have been determined just before the hyperventilation test, just after the termination of the test and 10 minutes after the termination of the test. Neuropeptide Y and thromboxane B2 plasma levels have been determined with a radioimmunologic method. It has been recorded that during the hyperventilation test in all of the 38 patients with variant angina the clinical and the electrocardiographic symptoms of the coronary artery spasm have appeared--but these have not appeared in patients with chronic stable angina pectoris and in healthy persons. The level of neuropeptide Y in patients with variant angina before the test, just at its end and as well as 10 min. after completing of the hyperventilation test, was significantly higher compared with the level in patients with chronic stable angina pectoris and controls. Contrary to chronic stable angina pectoris patients and controls, in variant angina group the level of neuropeptide Y increased rapidly at the end of the test and further elevation in neuropeptide Y level was observed 10 min. after the test. There was no difference in basal thromboxane B2 levels between angina patients and controls. At the end of hyperventilation test in variant angina group thromboxane B2 level significantly increased and remained on this level until 10 min. after the test. Significant increase of neuropeptide Y and thromboxane B2 plasma levels in variant angina patients during artery coronary spasm induced by hyperventilation test suggests the contribution of these humoral factors to the pathogenesis of vasospastic episodes in angina patients.

Adult↗

PubMed1998

[Sodium efflux through lymphocytic cell membranes in patients with chronic respiratory insufficiency].

Disturbances of Na(+)-K(+)-ATPase activity in patients with respiratory insufficiency may cause the hypertonia of non-striated muscles, which leads to increased peripheral resistance or bronchoconstriction, and also may inhibit the uptake of catecholamines and therefore may intensify their action on the respiratory and circulatory systems. All this is very harmful in respiratory insufficiency. The aim of the study was the examination if there are any changes in sodium efflux through lymphocytic cell membrane in patients with chronic respiratory insufficiency and if retraction of insufficiency can influence the activity of Na(+)-K(+)-ATPase. The study was performed in 40 patients with chronic respiratory insufficiency, of these 11 were women aged from 58 to 72 years and 29 were men aged from 62 to 77 years. Control group consisted of 31 healthy persons, of these 9 were women aged from 37 to 55 and 22 years were men aged from 21 to 60 years. In the study we included patients with exacerbation of chronic obstructive pulmonary disease (COPD). Blood samples were obtained during the exacerbation of COPD and after partial improvement. We determined arterial blood gases and rates of total, ouabain-sensitive and furosemide-sensitive sodium efflux through lymphocytic cell membrane in venous blood. The rates of sodium efflux were estimated with the method described by Haegerty et al. In the study we showed that in patients with exacerbation of COPD rates of total and ouabain-sensitive sodium efflux through lymphocytic cell membrane were decreased, but after improvement of the disease these rates normalized. In patients with exacerbation of COPD rates of furosemide-sensitive sodium efflux were normal. Disturbances of activity of Na(+)-K(+)-ATPase in patients with exacerbation of chronic pulmonary insufficiency are due to hypoxia.

Adult↗

PubMed1998

[Sodium efflux through lymphocytic cell membranes in patients with acute myocardial infarction].

One of the reasons of ventricular arrhythmias and coronary artery spasms in patients with acute myocardial infarction (AMI) may be the lower Na(+)-K(+)-ATPase activity, which causes decrease of potassium intracellular concentration and increase of calcium intracellular concentration. The aim of the study was the examination of the rate of sodium efflux through the lymphocytic cell membrane in patients with AMI after thrombolytic therapy. The survey was made in 50 patients with AMI after thrombolytic therapy: 30 of them with reperfusion (group I) and 20 without reperfusion (group II). The control group consisted of 31 healthy persons. Rates of total, ouabain-sensitive and furosemide-sensitive sodium efflux through the lymphocytic cell membrane were measured before thrombolysis, then 3 and 5 days after, using the method elaborated by Haegerty et al. All patients were treated with aspirin, glyceryl trinitrate and thrombolysis therapy with alteplase (r-TPA). In all patients with AMI rates of total and ouabaine-sensitive sodium efflux through the lymphocytic cell membrane were decreased, but rates of furosemide-sensitive sodium efflux were normal. In patients after thrombolytic therapy with reperfusion, 3 and 5 days after thrombolysis the decreased rates were normal, but they were still decreased in patients without reperfusion.

Adult↗

PubMed1998

[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease].

Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. The renin-angiotensin-aldosterone system is complex and acts as a circulating hormonal system, a local endogenous tissue system and neuromodular. Current experimental evidence suggests that ACE inhibitors reduce the risk associated with atherosclerotic cardiovascular disease. The antiatherogenic action of ACE inhibitors is related to complex effects mediated by these agent, including an antiproliferative and antimitotic action, beneficial effects on endothelial function, plaque-stabilizing effects and the action of these agents on the sympathetic nervous system. The role of ACE inhibitors in preventing the clinical sequale of atherosclerotic cardiac disease has been evaluated in various patient populations. Several small trial assess the effects of ACE inhibitors in severity of angina pectoris have reported conflicting results, with benefit is some patients and no benefit or even exacerbation of angina in others, indicating that ACE inhibitors do not have consistent antianginal effects in short-term study. ACE inhibitors have the theoretical potential to prevent restenosis after PTCA but they do not prevent restenosis and has no effect on overall clinical outcome. New data suggest that ACE inhibitors may be effective therapy fir patients following acute myocardial infarction. The renin-angiotensin system, is activated during new myocardial infarction and has an impact on the process of remodeling of the left ventricle which causes ist dysfunction and heart failure. In most of the large mortality trials the rationale for early treatment with ACE inhibitors after myocardial infarction was stated. ACE inhibitors have a positive effect in preventing the ventricular dilatation and they reduce the rate of reinfarctions and the mortality rate.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

[Combination therapy in primary hypertension].

Hypertension is an important risk factor for vascular disease. Primary goal of hypertension treatment is to prevent or delay the onset of blood pressure-related morbidity and mortality. It has been well demonstrated that the responses rate to any single class of antihypertensive agent, give as monotherapy is approximately 45% to 55%, and in half of hypertensive population a second will be required. The data from clinical trials clearly demonstrate that two-drug combination, usually with low-dose diuretics with any one of the other first-line agents increases the response rate to about 80% to 85% and reduces the likelihood of adverse events and alteration in lipid, carbohydrate and electrolyte metabolism. Of the various combinations being given that of an diuretic and ACE inhibitor, and ACE inhibitor and non-dihydropyridine calcium channel blockers seems particularly attractive. Some combinations are inappropriate, such as diuretic and calcium channel blockers, and beta-blocker with verapamil and diltiazem. Combination of ACE inhibitor and a non-dihydropyridine calcium channel blockers may provide benefit in regression left ventricular hypertrophy diabetic nephropathy, and post myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

[Levels of adrenomedullin in plasma of patients with chronic congestive heart failure].

Adrenomedullin is a potent vasodilator and natriuretic peptide that may an important role in cardiovascular disease. To investigate the role of adrenomedullin in the pathophysiology of congestive heart disease, plasma levels of adrenomedullin were measured in patients with congestive heart failure. Venous blood samples at rest were obtained before and after treatment from patients with congestive heart failure in New York Heart Association functional class II (n-23), III (n-26) and IV (n-14) and from normal subjects (n-30). Plasma adrenomedullin, endothelin-1,2, and atrial natriuretic peptide were determined by radioimmunoassay, plasma noradrenaline by radioenzymatic assay. Left ventricular ejection fraction was measured by echocardiography. The mean plasma level of adrenomedullin in normal subjects was 8.2 pmol/l, tended to be increased in patients with congestive heart failure those in class II (12.9 pmol/l) and were significantly increased in classes III and IV (21.3 and 29.9 respectively). Plasma adrenomedullin was correlated strongly with endothelin-1,2, atrial natriuretic peptide, and noradrenaline, and relatively weakly with left ventricular ejection fraction. Plasma adrenomedullin levels significantly decreased after treatment. These findings indicate that plasma levels of adrenomedullin are elevated in congestive heart failure and may be involved in the defense mechanism against further peripheral vascular resistance elevation in congestive heart failure.

Adrenomedullin↗

PubMed1998

[Pharmacological treatment of restenosis after coronary angioplasty and bypass grafting].

Angioplasty and bypass surgery have become standard methods of treating patients with symptomatic coronary atherosclerosis but restenosis remains the major limitation of percutaneous coronary revascularization. In pharmacological management of restenosis after coronary intervention multiple agents have been tried, with mostly discouraging results. Aspirin, dipyridamole, ticlopidine, heparin. Hirudin, and warfarin has failed to show beneficial effects on restenosis. Of all antithrombotics, only an inhibitor of the platelet IIb/IIIa integrin, which may lead to early vessel changes, leading to decrease restenosis. Antiproliferative agent (trapidil and angiopeptin) and probucol have also resulted in improved restenosis rate. In patients after bypass surgery with some degree of hyperlipidemia intensive lipid-lowering therapy is beneficial in slowing the late progressions of atherosclerosis as well as graft occlusion.

Angioplasty↗

PubMed1997

[Does captopril decrease endothelial production of endothelin?].

Serum levels endothelin-1,2 aldosterone, renin activity were performed in 52 patients with chronic congestive heart failure during captopril therapy. The investigations were done before therapy, after 10-15 days therapy and after disappearance symptoms of heart failure. The levels endotelin-1,2,aldosterone and renin activity were determined using radioimmunologic methods. Fraction ejection and peripheral vascular resistance were determined by echocardiography technics. It was found that serum endothelin levels in patients with chronic congestive heart failure were increased proportionally to functional class of heart failure and decreased after disappearance symptoms of heart failure. An increase in plasma endothelin concentration has not correlated with ejection fraction, aldosterone concentration and renin activity. These studies have demonstrated that in patients with congestive heart failure on captopril therapy endothelin serum levels positively correlates with peripheral vascular resistance. No correlation was found between ejection fraction and activity renin-angiotensin-aldosterone system. These findings indicated that captopril therapy decreases endothelin production.

Aged↗