Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large-scale trials have demonstrated a consistent mortality reduction from angiotensin converting enzyme (ACE) inhibitor therapy for chronic heart failure. Nonetheless, the pharmacologic and physiologic mechanisms of this favourable affect and the appropriate target population remain controversial. ACE inhibitors exert vasodilator, neurohormonal inhibiting and growth inhibiting effects that may contribute to the clinical response. They improve pump function and prevent ventricular remodelling, but they also may exert an antiarrhythmic effect. They may prevent coronary ischaemic events but appear to reduce cardiovascular event rates even more in non-ischaemic than in ischaemic heart disease. Their efficacy in early stages of asymptomatic heart disease and the optimal dose of the drugs for long-term benefit require further study.
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PMID:ACE inhibitors in non-ischaemic heart failure: results from the MEGA trials. 868 80

Heart failure represents a complex of symptoms caused by heart disease. The understanding of the underlying pathophysiological changes due to myocardial damage are crucial for an optimal diagnostic evaluation and treatment. The use of vasodilators and ACE inhibitors has led us to realize that the modulation of the neurohumoral system plays an eminent role in the morbidity and for survival of heart failure patients; therefore, the goal must be to recognize as early as possible myocardial damage, preventing the devastating effects of neurohumoral activation. This paper illustrates this aspect and discusses the clinically available therapeutic approaches.
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PMID:[Therapy-oriented assessment of heart failure in the hospital and clinical practice]. 870 Nov 91

Dysfunction of the left ventricle may result from a variety of insults, all of which may initiate a self-perpetuating process of ventricular remodeling which may progress to end-stage heart disease. Symptoms of heart failure may or may not co-exist with this ventricular remodeling. Treatment and prevention of these two largely distinct entities differ. Symptoms may respond to diuretics, vasodilators and digoxin. Progressive ventricular remodeling may be slowed by angiotensin converting enzyme inhibitors, hydralazine + isosorbide dinitrate and beta blockers. Prevention of symptomatic heart failure is dependent on early recognition of ventricular dysfunction and aggressive treatment to slow its progression. Development of more effective and targeted therapies will be dependent on expanded insight into the cellular and molecular mechanisms contributing to the remodeling process.
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PMID:Left ventricular dysfunction and heart failure. Mechanistic and therapeutic distinctions. 874 43

An insertion(I)/deletion(D) polymorphism in the angiotensin I-converting enzyme (ACE) gene seems to be associated with clinical heart disease in patients with diabetes mellitus. It is not known whether increased atherosclerosis or other factors among individuals with certain ACE-gene subtypes form the basis for the increased prevalence of heart disease among these subjects. We measured, at autopsy, the extent of macroscopically visible aortic atherosclerosis in 22 diabetic and 39 non-diabetic subjects and determined the ACE-genotype of all individuals by the polymerase chain reaction. The percentage of aortic surface area covered with atherosclerotic lesions was 29 +/- 8 (n = 6), 71 +/- 7 (n = 9), and 65 +/- 7 (n = 5) in the II-, ID-, and DD-genotype subgroups, respectively, among diabetes patients (mean +/- SEM) (2 p < 0.01, when comparing values from the ID and DD groups to the II group). The values were 37 +/- 9 (n = 11), 40 +/- 5 (n = 14) and 37 +/- 6 (n = 11) in the II-, ID-, and DD-genotypes in the non-diabetic group. There were no differences in sex ratio or age in any of the ACE-gene subtypes. The previously described relationship between heart disease and the ACE-gene polymorphism in diabetes could thus be founded in an increased extent of atherosclerosis among patients with the ID- and DD-ACE-gene subtypes. Patients with diabetes have several alterations in the composition of the collagenous components in the arterial wall. We also analysed for associations between total collagen and type IV and type V collagen content in the aortic vessel wall and the ACE-gene subtypes. We were, however, not able to disclose correlations between the polymorphism and any of these parameters. In conclusion, our data show an association between the ACE-I/D polymorphism and the degree of aortic atherosclerosis in diabetes; however, we did not observe correlations between the polymorphism and data concerning arterial collagenous components.
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PMID:Aortic atherosclerosis in diabetes mellitus is associated with an insertion/deletion polymorphism in the angiotensin I-converting enzyme gene. No relation between the polymorphism and aortic collagen content. 878 65

Hypertension has been defined and treated as a disease of abnormal systolic and diastolic blood pressure. Recent data have, however, demonstrated that effective blood-pressure control has not resulted in the expected decrease in coronary artery disease. These findings are probably a result of hypertension being a complex inherited syndrome of cardiovascular risk factors, all of which are genetically linked and all of which contribute to the development of cardiovascular disease in these patients. Included in the hypertension syndrome are abnormalities of lipid profile, insulin resistance, changes in renal function, left ventricular hypertrophy and reduced arterial compliance. In many patients, high blood pressure is a late manifestation of this disease process. Since all cardiovascular risk factors contribute to heart disease in these patients, they should all be considered in the management of this disease process. Diuretics and beta blockers, when used at high doses, negatively impact lipid metabolism and insulin sensitivity, while angiotensin converting enzyme (ACE) inhibitors and calcium antagonists tend to have a neutral effect on these metabolic risk factors. These findings have resulted in decreased use of diuretics and beta blockers in favor of newer agents such as ACE inhibitors and calcium antagonists. However, recent data have demonstrated that when used at low doses (6.25 or 12.5 mg of hydrochlorothiazide), diuretics lack significant metabolic side effects while bringing about significant reductions in blood pressure. Thus, at these doses, hydrochlorothiazide is a useful drug in the treatment of hypertension, both as monotherapy and in combination therapy.
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PMID:Metabolic manifestations of low-dose diuretics. 887 77

Angiotensin converting enzymes inhibitors are now regarded as the cornerstone of congestive heart failure therapy owing to established reduction in mortality and the symptomatic amelioration following their use. Although the response to converting enzyme inhibitor therapy may be influenced by race, we have reported a trend to reduce intra hospital mortality, the correction of hyponatremia and shortened hospitalization in Nigerians treated with converting enzyme inhibitors. We have now conducted an extended retrospective study, to evaluate the trends in the use of enalapril or captopril and its impact on prognosis in Nigerian patients with heart failure alone, admitted between January 1992 to December 1994. The proportion of heart failure treated with (captopril or enalapril) increased from 37pc in 1992, to 50pc in 1993, to 65pc in 1994. The demographic variables and cause of heart disease were similar in patients treated with converting enzyme inhibitors (n = 55) and those treated conventionally (n = 36). The cumulative mortality among converting enzyme inhibitors treated patients, was (8/55, 14pc) compared to patients not treated (17/36, 48pc) x2 = 12.4; p < 0.0001. There was no sex predilection in mortality (M = 25pc, F = 28pc, mean 27pc). However, initial serum Na+,125mmol was significantly (x2 = 11.1; p < 0.001) more common in the dead patients, 25pc compared to the survivors discharged home 7.5pc. The median hospital stay was 17 days in captopril treated survivors (range two to 44 days) and 19 days (range four to 67 days) in conventionally treated patients. Thus converting enzyme inhibitor therapy may reduce intra hospital mortality in Black Africans hospitalized for congestive heart failure and shorten hospital stay, despite the epidemiologically low plasma renin in Blacks. Hyponatremia may be a poor prognostic index in heart failure in our patients, and its reversal by converting enzyme inhibitors may reflect neurohormonal inhibitor. Earlier and more wide spread use of angiotensin converting enzyme inhibitors in Nigerian and Black Africans with chronic heart failure is now clearly indicated.
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PMID:A three year clinical review of the impact of angiotensin converting enzyme inhibitors on the intra hospital mortality of congestive heart failure in Nigerians. 899 May 72

Heart failure is often complicated by atrial fibrillation. Once atrial fibrillation has started it further enhances heart failure due to uncontrolled rate with shortened filling time and provocation of tachycardiomyopathy. Absent atrial kick and irregularity of the ventricular rhythm also contribute. Considering these mechanisms, restoration of sinus rhythm is most beneficial but is associated with frequent recurrences. Before cardioversion heart failure must be treated. ACE inhibition, initiated before cardioversion, may enhance maintenance of sinus rhythm by reducing neurohumoral activation. As a consequence, arrhythmogenic factors diminish and ventricular function may improve. beta-blockade and amiodarone may have similar effects. If cardioversion fails, adequate rate control is mandatory to prevent progressive ventricular dysfunction. Digitalis is the treatment of first choice, but when the heart rate remains uncontrolled low-dose beta-blockade should be given. If the ventricular rate remains uncontrolled despite drugs, atrioventricular node ablation with implantation of a pacemaker may be considered. Not only patients with idiopathic heart failure and atrial fibrillation, but also those with significant underlying heart disease may benefit from this intervention. In atrial fibrillation patients undergoing cardiac surgery for heart failure due to valvular disease, additional arrhythmia surgery may be contemplated.
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PMID:Management of atrial fibrillation in the setting of heart failure. 915 75

There have been few studies of hypertension in nursing home patients. To assess the prevalence, demographic characteristics, comorbidity and drug therapy in hypertensive nursing home patients compared with those who are normotensive, we reviewed all medical charts of patients in three nursing home facilities. Of the 804 patients, 355 (44.2%) have hypertension. Calcium channel blockers were the most frequently prescribed anti-hypertensive (30.3%) and together with diuretics (28.4%) and ACE inhibitors (27.7%) account for more than 85%. Hypertensive patients take more cardiac, hypoglycaemic, and analgesic drugs (P = <0.001, <0.001, and 0.004, respectively) than those who are normotensive. Overall patients take an average of 8.68 medications daily. In hypertensive patients, the average number of comorbid conditions (excluding hypertension) is 5.02 compared with 3.23 in normotensive patients. Hypertension is significantly associated with diabetes, heart disease, cerebrovascular disease, neoplasms, endocrine disorders, gastrointestinal diseases, psychiatric disorders, dementia, other central nervous system diseases, skin problems, blood diseases and inversely with hip fracture. Blood pressure control (<140/90 mm Hg) is achieved in 88.8%, is not related to age and is significantly more frequent in males than females (91.8% vs 82.6% P = 0.025). The problem of hypertension in nursing home patients is complex and has received insufficient study. Since studies demonstrating benefit from anti-hypertensive therapy in the elderly excluded the very elderly and those with significant comorbid conditions, additional research is needed.
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PMID:Hypertension in nursing home patients. 950 52

Patients with homozygous beta-thalassemia are chronically transfused and, if not assiduously chelated, are at risk for cardiac dysfunction. Available data suggest that even in optimally chelated patients, cardiac pathology is abnormal secondary to iron deposition, fibrosis, hypertrophy, and the structural effects of chronic anemia. Evidence of myopericarditis may also be found. Cardiac performance is usually only subtly affected, primarily with diastolic abnormalities not routinely detected on echocardiograms or nuclear scan. In poorly chelated patients, severe heart failure occurs and is easily predictable but invariably fatal, despite treatment with diuretics, vasodilators, inotropes, and antiarrhythmics. Based on successful prevention of heart failure with ACE inhibitors in other forms of cardiomyopathy, we suggest multicenter trials to explore methods to stabilize cardiac function in patients at risk for iron-induced heart disease. Long-term adverse effects of iron deposition, diastolic dysfunction, and abnormal hormone regulation need to be quantitated in patients reaching their third and fourth decades when the potential for ischemic cardiac disease could compound cardiac dysfunction.
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PMID:Diagnosis and management of iron-induced heart disease in Cooley's anemia. 966 46

Heart failure has become the most widely studied syndrome in cardiology over the recent years. Despite the encouraging achievements by angiotensin converting enzyme (ACE) inhibitors, the mortality of patients with chronic heart failure remains high. There are several factors which can potentially be responsible for the fact that about 80% of patients with a failing heart defy protection by ACE inhibitors: different activation of tissue and systemic renin-angiotensin system (RAS) in a particular heart disease and the distinct ability of various ACE inhibitors to block cardiac ACE, alternative pathways for angiotensin II formation (chymase), genetic polymorphism of the RAS system and the complexity of neuroendocrine activation. Moreover, chronic heart failure can provoke disturbances in the reactivity of peripheral vessels and metabolism of striated muscles. These factors may then potentiate the vicious circle of heart failure. New therapeutic approaches, which could further reduce the mortality in patients with heart failure involve angiotensin II type 1 receptor antagonists, beta-blockers, aldosterone antagonists and blockers of the endothelin receptor. A number of questions associated with functions of the RAS still remain open and their solution could be of substantial benefit for patients with a failing heart.
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PMID:Heart failure and angiotensin converting enzyme inhibition: problems and perspectives. 1047 Aug 60


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