UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malondialdehyde (MDA), a product of platelet lipid peroxidation, was measured in human platelet-rich plasma. Levels of 3.19 n moles/10(9) platelets /+- 0.40 S.E. in 11 patients with prosthetic heart valves were elevated (p < 0.25) compared to 17 normal subjects (2.09 /+- 0.13 n moles/10(9) platelets). Reduced production (1.44 /+- 0.28 n moles/10(9) platelets, p < 0.5) was found in 10 patients with unstable angina. Normal levels were found in patients with mitral stenosis, cardiomyopathy or hypertension. Usual serum levels of drugs used in cardiac treatment reduced MDA levels as follows: acetaminophen, 47% (p < .01); aspirin, 58% (p < .05); furosemide, 32.6% (p < .005), and sulfinpyrazone, 41% (p < .05). Digoxin, dipyridamole, heparin, hydrochlorothiazide, lidocaine, nitroglycerin, procainamide, propranolol, quinidine, or warfarin had no significant effect at therapeutic concentrations. None of the drugs explained the enhanced production in patients with prosthetic valves while enhanced production in patients with prosthetic valves while analgesic therapy could explain the decreased levels in other cardiacs. The half-time of platelet survival, measured by suppression of malondialdehyde production, was 3.2 /+- 0.24 days in 9 normal subjects but could not be measured reliably in most patients because of multiple drug therapies. We conclude that the blood platelets of patients with prosthetic heart valves differ from those of normal subjects in their capacity to release malondialdehyde after stimulation with n-ethylmaleimide. Additionally, we find that inhibition of malondialdehyde production by several pharmacologic agents limits the usefulness of this method for the measurement of platelet survival in cardiac patients.
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PMID:Platelet malondialdehyde in cardiovascular disease: effect of prosthetic heart valves and cardioactive drugs on production. 745 95

Coronary artery disease, hypertension, valvular heart disease, and cardiomyopathies are the commonest causes of CHF in elderly patients. Almost half of elderly patients with CHF have normal LV ejection fraction. LV ejection fraction must be measured before knowing how to treat CHF. Underlying causes of CHF should be treated when possible. Precipitating causes of CHF should be treated. Diuretics are the first-line drug in the treatment of CHF. ACE inhibitors reduce mortality in patients with CHF and should be administered with diuretics to patients with CHF and abnormal or normal LV ejection fraction. Oral isosorbide dinitrate plus hydralazine improves survival in patients with CHF, and should be administered to patients with CHF and abnormal or normal LV ejection fraction who cannot tolerate ACE inhibitor therapy or in whom CHF persists despite therapy with diuretics plus ACE inhibitors. Digoxin should be administered to patients with a rapid ventricular rate associated with supraventricular tachyarrhythmias. Digoxin should be administered to patients with CHF in sinus rhythm and abnormal LV ejection fraction that does not respond to diuretics plus ACE inhibitors or in patients unable to tolerate ACE inhibitors or other vasodilator therapy. Digoxin should not be given to patients with CHF in sinus rhythm with normal LV ejection fraction. Calcium channel blockers are contraindicated in patients with CHF and abnormal LV ejection fraction but may be used to treat CHF with normal LV ejection fraction. The use of beta blockers in the treatment of CHF with abnormal LV ejection fraction is experimental. However, beta blockers might improve clinical symptoms in patients with CHF and normal LV ejection fraction by slowing heart rate, thereby increasing LV diastolic filling time and increasing LV end-diastolic volume. Maintenance of sinus rhythm will also increase LV diastolic filling time in patients with CHF and normal LV ejection fraction.
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PMID:Management of congestive heart failure in the elderly patient. 755 8

Two hundred and ninety one patients admitted with atrial fibrillation through the emergency room of a regional hospital in the year 1993 were reviewed to evaluate the presenting features and in-hospital treatment of patients with symptomatic atrial fibrillation. The incidence of atrial fibrillation increased with age (mean age was 73 +/- 12 years) and the ratio of female to male was 1.8:1. The commonest presenting features were palpitation (42.3%), dyspnoea (38.1%) and heart failure (16.4%). The most frequently associated cardiac conditions were hypertension (28.9%), atherosclerotic cardiovascular disease (24.7%) and rheumatic heart disease (17.5%). Pulmonary diseases (18.6%), diabetes mellitus (12.7%) and thyrotoxicosis (6.2%) were the principal associated non-cardiac conditions. Thromboembolic complications were found in 15 patients at presentation (5.2%). Cardiac enzyme assessment was investigated in two thirds of the patients (68.1%), while thyroid function test (59.5%) and echocardiography (29.6%) were less commonly investigated. Digoxin was still the most popular drug used for ventricular rate control, and cardioversion was performed in only 6.9% of patients. Antithrombotic therapy was used in 5.8% of patients only although it was clinically indicated in more than half of the patients (52%). Contraindications of anticoagulation were found in 23 patients (7.9%), including a history of gastrointestinal or cerebrovascular bleeding, active bleeding, chronic renal failure and poor drug compliance. The mean hospital stay was 5 +/- 4 days, compared to a mean stay of 2.7 days for other medical patients. Fourteen patients (4.8%) died during hospitalisation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Presentation and management of patients admitted with atrial fibrillation: a review of 291 cases in a regional hospital. 778 42

The prevalence and incidence of adverse drug interactions involving NSAIDs remain unknown. To identify those proposed drug interactions of greatest clinical significance, it is appropriate to focus on interactions between commonly used and/or commonly coprescribed drugs, interactions for which there are numerous well documented case reports in reputable journals, interactions validated by well designed in vivo human studies and interactions affecting high-risk drugs and/or high-risk patients. While most interactions between NSAIDs and other drugs are pharmacokinetic, NSAID-related pharmacodynamic interactions may be considerably more important in the clinical context. However, prescriber ignorance is likely to be a major determinant of many adverse drug interactions. Adverse drug interactions involving NSAIDs may be restricted by rational prescribing and by careful monitoring, particularly high-risk patients, drugs and therapy periods. Prescribing NSAIDs is relatively contra-indicative for patients on oral anticoagulants due to hemorrhage and for patients taking high dose methotrexate due to bone marrow toxicity, renal failure and hepatic dysfunction. Combination NSAID therapy cannot be justified since toxicity may be increased without any improvement in efficacy. Where lithium or antihypertensives are coprescribed with NSAIDs, aspirin or sulindac are preferred and close monitoring is mandatory for lithium toxicity and hypertension respectively. Phenytoin or oral hypoglycemic agents may be administered with NSAIDs other than pyrazoles and salicylates, provided, the patients are monitored carefully at the initiation and cessation of NSAID treatment. Digoxin, aminoglycosides and probenecid may be coprescribed with NSAIDs but close monitoring is required, particularly for high-risk patients such as the elderly. Indomethacin and triamterine should be avoided due to the risk of renal failure, high dose aspirin should be replaced by naproxen in patients on sodium valproate and care is required when corticosteroids are administered to patients taking salicylates long term in high dosage. Interactions between NSAIDs and antacids or cholestyramine are generally avoidable by administering these drugs at different times.
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PMID:NSAID-related adverse drug interactions with clinical relevance. An update. 783 59

The prevalence and incidence of adverse drug interactions involving nonsteroidal anti-inflammatory drugs (NSAIDs) remains unknown. To identify those proposed drug interactions of greatest clinical significance, it is appropriate to focus on interactions between commonly used and/or commonly coprescribed drugs, interactions for which there are numerous well documented case reports in reputable journals, interactions validated by well designed in vivo human studies and those affecting high-risk drugs and/or high-risk patients. While most interactions between NSAIDs and other drugs are pharmacokinetic, NSAID-related pharmacodynamic interactions may be considerably more important in the clinical context, and prescriber ignorance is likely to be a major determinant of many adverse drug interactions. Prescribing NSAIDs is relatively contraindicated for patients on oral anticoagulants due to the risk of haemorrhage, and for patients taking high-dose methotrexate due to the dangers of bone marrow toxicity, renal failure and hepatic dysfunction. Combination NSAID therapy cannot be justified as toxicity may be increased without any improvement in efficacy. Where lithium or anti-hypertensives are coprescribed with NSAIDs, close monitoring is mandatory for lithium toxicity and hypertension, respectively, and aspirin (acetylsalicylic acid) or sulindac are preferred. Phenytoin or oral hypoglycaemic agents may be administered with NSAIDs other than pyrazoles and salicylates provided that patients are monitored carefully at the initiation and cessation of NSAID treatment. Digoxin, aminoglycosides and probenecid may be coprescribed with NSAIDs, but close monitoring is required, particularly for high-risk patients such as the elderly. Indomethacin and triamterene should be avoided due to the risk of renal failure. High dose aspirin should be replaced by naproxen in patients on valproic acid (sodium valproate) and care is required when corticosteroids are administered to patients taking salicylates long term in high dosage. Interactions between NSAIDs and antacids or cholestyramine are generally avoidable. Adverse drug interactions involving NSAIDs may be limited by rational prescribing and by careful monitoring, particularly for high-risk patients, drugs and therapy periods.
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PMID:Adverse drug interactions with nonsteroidal anti-inflammatory drugs (NSAIDs). Recognition, management and avoidance. 845 60

Digoxin therapy has been suggested to increase mortality risk in survivors of acute myocardial infarction. Since digoxin is a drug with a narrow therapeutic/toxic ratio, we raised the hypothesis that the association between digoxin and post myocardial infarction mortality may have a dose-dependent relationship. The purpose of this study was to evaluate this hypothesis. We retrospectively analyzed data from 1731 survivors of acute myocardial infarction. At the time of hospital discharge, 175 patients (10%) were taking digoxin. The exact dosage of digoxin was ascertained in 153 (87%) patients. Patients were divided into two groups based on the weekly dosage of digoxin at hospital discharge: The first group included 41 patients who were treated with a low dose (< or = 1.5 mg per week, usually 0.125 mg daily). The second group included 112 patients treated with a full dose (> 1.5 mg per week, usually 0.25 mg daily). Both groups were comparable with regard to mean age, gender, history of prior myocardial infarction, diabetes mellitus, hypertension, and prior angina. There were no significant differences in the incidence of in-hospital complications, such as heart failure, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, and postinfarction angina. One year mortality was significantly higher among patients treated with a full dose [19 of 112 (17%)] than patients treated with a low dose of digoxin [1 of 41 (2%); p < 0.02] Multivariate analysis performed by the Cox proportional hazards model identified treatment with a full dose of digoxin as an independent determinant associated with increased death during the first year after myocardial infarction (hazard ratio 10.7; 95% confidence interval 1.4-80.5). Thus, mortality among myocardial infarction survivors treated with digoxin was related to a full-dose therapy. Patients treated with a low dose experienced a low mortality rate. Our findings raise concern that digoxin may exert a dose-dependent deleterious effect upon the survival of patients recovering from acute myocardial infarction.
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PMID:Digoxin and increased mortality among patients recovering from acute myocardial infarction: importance of digoxin dose. The SPRINT Study Group. 857 56

Because of its prevalence in the population and its associated underlying diseases and morbidity, atrial fibrillation (AF) is an important and costly health problem. Advancing age, diabetes, heart failure, valvular disease, hypertension, and myocardial infarction predict the occurrence of AF within a population. The management of AF is complex and involves prevention of thromboembolic complications and treatment of arrhythmia-related symptoms. Stroke occurs in 4.5% of untreated patients with AF per year. Independent risk factors for stroke in nonrheumatic patients with AF are advanced age; a history of prior embolism, hypertension, or diabetes; and echocardiographic findings of left atrial enlargement and left ventricular dysfunction. Warfarin decreases stroke by two-thirds and death by one-third; aspirin is only about half as effective overall and is insufficient therapy for those with risk factors for stroke. Options for thromboembolic prophylaxis are use of warfarin for all in whom it is safe or, alternatively, warfarin for those with risk factors and aspirin for those without risk factors. One-half of the patients with AF are 75 years of age or older. The uniform applicability and relative safety of warfarin therapy in this age-group are controversial. Specific therapy for the arrhythmia should be dictated by the need to control symptoms. Symptomatic treatments include rate-control medications and strategies designed to terminate and prevent arrhythmia recurrence. Digoxin, beta-adrenergic blockers, verapamil, and diltiazem slow excessive ventricular rates in patients with AF and may favorably manage comorbid conditions. The efficacy of anti-arrhythmic medications is only 40 to 70% per year in preventing recurrences of AF, and these agents, except amiodarone, may increase the risk of sudden death in patients with certain types of organic heart disease and AF. The use of nonpharmacologic symptomatic therapies such as atrioventricular node modification or ablation with a rate-response pacemaker or surgical intervention is increasing.
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PMID:Management of atrial fibrillation in adults: prevention of thromboembolism and symptomatic treatment. 857 89

Congestive heart failure (CHF) continues to be a lethal end stage of cardiovascular diseases caused by hypertension, coronary heart disease, valve deformity, diabetes and cardiomyopathy. Current therapy for CHF can maintain function, improve quality of life, and prolong survival. Diuretics, angiotensin-converting enzyme inhibitors (ACE), and digoxin remain in standards of therapy. Diuretics remains an important component of the symptomatic management of patients with CHF, but severely II patients may require additional agents. One option frequently used in patients who exhibit resistance to loop diuretics is infusion of low-dose dopamine. Combination diuretics may effectively increase urine output, with the addition of thiazide or spironolactone. Documentation of the clinical benefit of ACE inhibitors represents the most important advance in therapeutics for CHF in the last decade. ACE inhibitors improves left ventricular function, and survival and unless contraindicated, patients with left ventricular systolic dysfunction should receive high dose ACE inhibitor with diuretic if there is peripheral oedema. For patients who cannot take an ACE inhibitor the combination of hydralazine and nitrates may offer some prognostic benefit. Digoxin has been the traditional first drug of choice for CHF, but with protracted controversy about its efficacy and safety. It is hope that new agents as vesnarione, and ibopamine may improve contractility without having adverse consequences. Acceptance of beta-blockade as a potentially beneficial therapeutic intervention increase in the past year. This year, improved diastolic function and afterload reduction were reported with beta-blockade. Amiodarone unlike other antiarrhythmic drugs does not seem depress left ventricular function, and may be the best drug in patients with CHF and symptomatic arrhythmias. The correct role of anticoagulation in patients with CHF remains controversial. Although the benefits of anticoagulation for the treatment of most patients with atrial fibrillation are increasingly accepted, it has not been shown to improve outcome in patients with CHF in normal sinus rhythm.
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PMID:[Pharmacologic treatment of chronic congestive heart failure]. 875 62

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and its prevalence increases with age. Etiologies include coronary artery disease, hypertension, valvular heart disease, thyrotoxicosis, and other cardiac and noncardiac conditions. AF can lead to reversible impairment of left ventricular (LV) function, LV dilatation, clinical heart failure, angina pectoris, stroke, and increased mortality. Digoxin, beta blockers, or calcium channel blockers are used to control ventricular rate in new-onset AF with hemodynamically stable rhythm and in chronic AF where rhythm cannot be restored. These drugs can be used alone or in combination, depending on the clinical situation. The most complete relief of symptoms occurs when sinus rhythm is restored. Class IA, IC, and III antiarrhythmic agents can be used to restore and maintain sinus rhythm in selected patients.
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PMID:Atrial fibrillation: drug therapies for ventricular rate control and restoration of sinus rhythm. 963 6

A review of the most important findings published during 1997 in cardiovascular papers is presented: Chlamydia pneumoniae was recognised as a potential risk factor for coronary artery disease (CAD) and possible pathogenic agent for valvular aortic stenosis. Valvular changes similar to the valvular disease reported after ergotamine and methylsergide were also detected in obese women treated with a combination of phentermine and fenfluramine. In CAD, several new laboratory methods were introduced for early diagnosis, such as serum troponin levels, and arbutamine and adenosine stress echocardiography. Laser transmyocardial revascularisation can be performed in patients unsuitable for PTCA and CABG. In patients with end-stage heart failure, implantable ventricular-assist devices can be used, and dynamic cardiomyoplasty or partial ventriculectomy may be useful temporary measures until a suitable heart donor is available. In pharmacotherapy, fluvastatin was registered as an antiatherosclerotic agent, and mibefradil and moxonidin in hypertension and angina. Digoxin was shown to reduce the number of hospitalisations in patients with CHF but still in sinus rhythm. In the future, several improvements in anti-thrombotic therapy are expected: antithrombins, platelet glycoprotein IIb/IIIa receptor blockers and tissue factor inhibitors are all potentially more potent than presently available drugs. Also, efforts are under way to introduce genes directly into the cells of the vascular wall to prevent atherosclerosis and restenosis, as well as to transform cardiac mesenchymal cells into the cardiac myocytes of hearts that have suffered large infarctions.
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PMID:[Cardiology in 1997]. 981 70

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