Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After a brief synopsis of the classical antihypertensive drugs a survey is given of the newer therapeutics, such as calcium antagonists, ACE-inhibitors and alpha 1-adrenoceptor antagonists. Experimental drugs, such as imidazoline receptor agonists, renin inhibitors, angiotensin II receptor antagonists, alpha 2-adrenoceptor antagonists, potassium channel openers, ketanserin, endopeptidase inhibitors, and hybrid (multifactorial) drugs are discussed, with special attention for their modes of action. In spite of the ever increasing number of antihypertensive drugs and principles, the large scale of clinical evidence for a beneficial effect of long-term treatment (in particular with respect to protection against stroke) remains limited to diuretics and beta-blockers. In spite of this limitation it seems worthwhile to consider the newer antihypertensive drugs as well, especially for optimal treatment of the individual patient. The newer drugs may in particular offer special advantages in the presence of concomitant diseases, such as diabetes mellitus, hyperlipidaemia, angina pectoris or congestive heart failure.
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PMID:New avenues in antihypertensive drug treatment. 826 86

Arterial hypertension is the most frequent cause of a disturbance of coronary microcirculation. Inspite of having normal epicardial coronary arteries, patients with arterial hypertension often have symptoms of angina pectoris and a positive exercise tolerance test. The angina pectoris-symptoms in patients with arterial hypertension are due to functional and structural alterations of the coronary microcirculation. Consequently, an antihypertensive therapy should not only aim at lowering blood pressure and reversing myocardial hypertrophy, but also improve coronary microcirculation in order to avoid the consequences of chronic ischemia on the myocardium. Until now, only experimental studies have indicated that antihypertensive therapy can improve coronary flow reserve. To determine to what extent under clinical conditions coronary flow reserve can be improved, in hypertensive patients maximal coronary blood flow, minimal coronary resistance, and coronary reserve (Dipyridamol) were studied before and after a long-term antihypertensive treatment (9-12 months) with the ACE-inhibitor enalapril (10-20 mg/d). To assess the chronic effects rather than the acute effects of the antihypertensive pharmacon, the coronary microcirculation was studied after intermission of medical therapy for a period of 1 week. Along with a decrease in LV muscle mass by about 8%, coronary reserve was improved after enalapril by 48%. It is likely that the observed increase in coronary reserve is related to the reversal of structural vascular abnormalities at the level of the coronary microcirculation. Consequently, it seems that reparation of hypertensive remodeling of the coronary microcirculation can be induced by ACE-inhibitor therapy.
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PMID:ACE-inhibitors and coronary microcirculation. 835 38

Diltiazem is a benzothiazepine derivative calcium antagonist available in several formulations, some of which enable once daily administration. The drug as monotherapy has demonstrated similar efficacy to diuretics in older patients with hypertension. Data comparing diltiazem with beta-blockers and angiotensin converting enzyme inhibitors are more limited, but available studies suggest at least comparable antihypertensive efficacy. Diltiazem as monotherapy or in combination with a beta-adrenoceptor-antagonist, isosorbide dinitrate, or another calcium antagonist, has demonstrated efficacy in patients with effort angina. The drug has also been used intravenously to terminate supraventricular tachycardias and to control the ventricular response to atrial fibrillation or flutter; it also appears to reduce the rate of early reinfarction in patients with non-Q-wave myocardial infarction. The most common adverse events during diltiazem therapy include headache, flushing, peripheral oedema and hypotension. Atrioventricular block although rare, is the most frequent serious adverse event related to diltiazem therapy and may be exacerbated by coadministration of beta-adrenoceptor antagonists, especially in the elderly. Thus, diltiazem appears to be an effective and well tolerated treatment for hypertension and angina in older patients and has shown promise as therapy for supraventricular tachycardias and as prophylaxis against early reinfarction in patients with non-Q-wave myocardial infarction.
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PMID:Diltiazem. A review of its pharmacology and therapeutic use in older patients. 836 96

The concept of "cardioprotection" with ACE inhibitors has evolved over the last decade. In the 1980s, protective benefits of ACE inhibitors in hypertension were established, regression of left ventricular hypertrophy was demonstrated, and improved ventricular function and survival in mild-to-moderate and severe congestive heart failure was documented. A further "protective" role of ACE inhibitors in coronary artery disease is emerging as more attention is focused on the concept of local tissue renin-angiotensin systems. Recent contributions to the literature describe significant benefits of ACE-inhibitor therapy in acute myocardial infarction, including suppression of ventricular arrhythmias and reduction of both early and late ventricular dilation, preservation of left ventricular function, and improved survival. All of the above effects can be considered "cardioprotective." However, as new benefits are reported in the 1990s, a broadened view of "cardiovascular protection" emerges from investigative studies in the literature. ACE inhibitors may reduce tolerance to nitrates, reduce angina in some but not all studies, and limit smooth muscle cell proliferation (and perhaps restenosis) induced by experimental balloon angioplasty. Local vascular effects may attenuate atherosclerotic changes in the arterial wall in experimental animals and may decrease the incidence of aneurysm formation in hypertensive animals. The effectiveness of ACE inhibitors in acute myocarditis, suggested by reports that captopril may reduce lesions of murine myocarditis when administered early after infection with coxsackievirus B3, requires clinical confirmation. Despite these apparently diverse "cardiovascular protective" consequences of ACE inhibitor therapy, the mechanism(s) of action of these agents remain to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotection with angiotensin-converting enzyme inhibitors: redefined for the 1990s. 843 34

Amlodipine belongs to the dihydropyridine class of calcium channel blockers. Both short and long term studies indicate that amlodipine effectively lowers mild to moderately elevated blood pressure and relieves symptoms of angina pectoris. In comparative studies, its antihypertensive efficacy is similar to that of other established agents such as beta-blockers, diuretics, ACE inhibitors and other calcium channel blockers (including the dihydropyridines); limited comparative data are, however, available in patients with angina pectoris. Amlodipine may offer potential in patients with congestive heart failure. Vasodilator adverse events such as oedema, headaches, and flushing are commonly observed with amlodipine. The drug does not appear to cause postural hypotension, reflex tachycardia or cardiac conduction disturbances. Comparative studies suggest that amlodipine is at least as well tolerated as other standard agents. Thus, amlodipine provides an attractive therapeutic option for the treatment of hypertension, and offers potential for patients with angina pectoris. Its beneficial effects in patients with congestive heart failure require confirmation in future studies.
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PMID:Amlodipine. A reappraisal of its pharmacological properties and therapeutic use in cardiovascular disease. 852 73

The insertion/deletion DNA polymorphism of the gene coding human angiotensin converting enzyme (ACE) was examined in 109 patients with coronary artery disease (CAD) and 93 non-coronary subjects (NCS) living in a northern part of Japan. The presence of risk factors including age, hypertension, hypercholesterolemia, tobacco use, diabetes mellitus and hyperuricemia were also examined. An insertion (I) / deletion (D) polymorphism of the ACE gene was determined by the polymerase chain reaction with oligonucleotide primers encompassing the polymorphic region in intron 16. The template DNA was isolated from peripheral blood leukocytes of patients. The frequency of the D-allele in NCS was 0.27, significantly lower than that reported in Caucasians or in Japanese living in the Osaka area. The frequency of the D-allele in patients with myocardial infarction (MI) and angina pectoris was 0.39 and was higher than that in NCS. The frequencies of genotypes DD, ID, and II were 17.8, 43.3 and 38.9%, respectively, in CAD except in young patients (below 40 years of age) with MI and AP groups, and 6.5, 40.9 and 52.7%, respectively in NCS (p < 0.05 between CAD and NCS). Young MI showed similar frequencies in ACE gene polymorphisms to those in NCS, a pattern which differed from that seen in subjects with CAD (p < 0.05). The numbers of risk factors did not alter the frequency of ACE gene genotype among patients with CAD, however, in normotensives, the odds ratio of DD-genotype was significantly increased to 3.4. Accordingly, ACE gene polymorphism may be associated with morbidity from CAD in Japanese living in northern Japan as has been noted in Caucasians, despite the lower frequencies of the D-allele in the Japanese population.
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PMID:Association of ACE gene polymorphisms with coronary artery disease in a northern area of Japan. 855 60

Celiprolol is a beta 1-selective adrenoceptor antagonist (beta-blocker) which acts as a weak agonist at beta 2-adrenoceptors. The drug demonstrates vasodilator properties and does not depress heart rate to the same extent as propranolol, atenolol or metoprolol. Celiprolol has shown equivalent antihypertensive efficacy to other beta-blockers, notably propranolol, atenolol, metoprolol and pindolol, in patients aged 18 to 75 years with mild to moderate essential hypertension. The drug has also shown similar antihypertensive efficacy to the angiotensin converting enzyme inhibitor enalapril and to combination diuretic therapy with hydrochlorothiazide and amiloride. Celiprolol was equally effective in adult patients of all ages, although no data are available for patients aged over 75 years. Data from a small number of clinical trials indicate celiprolol to be as effective as both propranolol and atenolol in improving work capacity and reducing the frequency of anginal attacks in patients with stable effort angina. However, the drug has not yet been evaluated in postmyocardial infarction patients. Celiprolol offers advantages over other beta-blockers, including reduction of peripheral vascular resistance and maintenance of resting heart rate, cardiac output and renal perfusion. The drug is also associated with improvements in plasma lipid profiles and does not appear to adversely affect carbohydrate metabolism or lung function, although its use in patients with reversible obstructive pulmonary disease is not recommended. Celiprolol is therefore a highly cardioselective beta-blocker with ancillary characteristics which are potentially useful in patients with hypertension and angina complicated by other conditions commonly associated with advanced age. These include impaired glucose tolerance or diabetes mellitus, peripheral vascular disease and hyperlipidaemia. The drug may also be preferred to other beta-blockers in patients in whom a reduction in heart rate would be particularly undesirable. Further long term (> 12 months) clinical trials and pharmacoeconomic data are now required to confirm the clinical relevance of the pharmacodynamic advantages of celiprolol therapy.
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PMID:Celiprolol. An evaluation of its pharmacological properties and clinical efficacy in the management of hypertension and angina pectoris. 857 93

To elucidate how symptoms and signs of chronic heart failure are related to the filling pressure and cardiac output at rest, 58 patients (55 males, 3 females, mean age 57 +/- 9 years, range 30-75) with left ventricular ejection fraction (LVEF) < or = 30% and a lesion > or = 50% on a major coronary branch have been selected from patients submitted in 1985-1993 to a complete right and left cardiac catheterization including ventriculography and coronary angiography. Patients with recent myocardial infarction (MI), unstable angina, associated heart diseases or recent changes in body weight and in diuretic therapy were excluded. Clinical data were obtained at cardiac catheterization time from history, physical examination, chest X-ray and ECG. Patients with angina as limiting symptom were excluded from NYHA functional classification. Pulmonary venous congestion (PVC) was defined on X-ray as: absent, venous redistribution, interstitial pulmonary edema (IPE). Mean pulmonary capillary wedge pressure (PCWP) was recorded under fluoroscopy and cardiac index was measured by the Fick method. On the whole group, 96% of patients had had one or more MI (on ECG necrosis was anterior in 58%, inferior in 9%, anterior and inferior in 26%), 69% were in NYHA functional class III or IV, 54% had IPE and 45% had mitral regurgitation. 71% were under treatment with digitalis, 74% with diuretics and 39% with ACE-inhibitors. PCWP was correlated with LVEDV (r = 0.34; p < 0.001) but neither with LV mass nor with LV mass/volume ratio. It was significantly higher (p < 0.01) in patients with mild-moderate mitral regurgitation, in patients with necrosis involving both anterior and inferior walls (26 +/- 6 vs 21 +/- 8 mmHg in patients with single wall necrosis, p < 0.05) and in patients with multiple MI (26 +/- 7 vs 20 +/- 8 mmHg in patients with no or single MI, p < 0.02). Moreover, it was neither correlated with functional classification nor with PVC: of patients with PCWP > 24 mmHg, 14% were in II NYHA functional class and 21% had no PVC while of patients with PCWP < 15 mmHg, 36% were in NYHA functional class IV and 7% had IPE. Cardiac index was reduced below 2.3 l/min/m2 in 21% of patients: these patients had increased pulmonary (p < 0.0002) and systemic (p < 0.0001) vascular resistance, increased systolic (p < 0.001) and diastolic (p < 0.01) pulmonary artery pressure and reduced LVEF (p < 0.01) and right ventricular ejection fraction (p < 0.03). Furthermore, on the whole patients an inverse correlation was found between cardiac index and functional classification (r = -0.42; p < 0.01). The reliability of NYHA functional class IV, physical signs of heart failure and IPE for estimating PCWP > 24 mmHg and cardiac index < 2.3 l/min/m2 was rather limited although high specificity was shown for gallop sounds (92 and 97%) and jugular vein distension (88 and 97%). In conclusion, in coronary patients with chronic severe LV systolic dysfunction a mismatch between clinical data and central hemodynamics is not rare. The reliability of functional class, X-ray PVC and physical signs to predict central hemodynamics in fairly limited.
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PMID:[Hemodynamics and clinical data in chronic coronary disease with severe left ventricular systolic dysfunction]. 867 4

Myocardial infarction represents a crossroads in the natural history of coronary artery disease. The prognosis is determined by the severity of coronary artery disease, infarct size (and hence ejection fraction), and age of the patient. After infarction, patients may remain symptomless, or suffer angina, silent ischemia, reinfarction, heart failure or sudden death. Hence patient management after infarction includes (1) estimation of risk, (2) the use of stress tests to detect ischemia and rhythm disorders, (3) PTCA or bypass if required and (4) medical therapy. Cardiac catheterization is indicated in patients with angina or silent ischemia, non-Q wave infarction or large infarctus; its use is less well established in patients without ischemia and left ventricular dysfunction, but this indication is nevertheless increasingly accepted. PTCA is primarily utilized in patients with single or two vessel disease, while coronary bypass surgery is indicated in patients with left main or three vessel disease. All these measures are designed to improve symptoms and prognosis. For secondary prevention medical therapy should be used to treat cardiovascular risk factors (antihypertensive drugs, lipid-lowering drugs etc.), to inhibit platelets (aspirin, ticlopidine) or coagulation (coumarins), to block neurohumoral activation (betablocker, ACE-inhibitors), for vasoconstriction (calcium channel blockers, nitrates) and to suppress arrhythmias. The large number of drugs requires reasoned use depending on the risk profile of the individual patient. Cardiovascular risk factors should be treated appropriately. Platelet inhibitors should be given to all patients except those with atrial fibrillation or large ventricles (coumarins). Betablockers reduce mortality, reinfarction and sudden death after infarction and hence should be used if no contraindications exist. ACE-inhibitors are particularly effective in improving symptoms and prognosis in patients with impaired left ventricular function. Calcium antagonists should be used with caution and only in patients with normal left ventricular function. Nitrates are primarily effective in improving symptoms in patients with angina or heart failure. Antiarrhythmic drugs (amiodarone) are only useful in patients with complex arrhythmias. Digitalis has been shown to improve symptoms in patients with heart failure, while other inotropic drugs are virtually no longer used. These guidelines allow reasoned differential therapy after myocardial infarction to the maximum benefit of the patient and at minimum cost.
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PMID:[Therapeutic measures following acute myocardial infarct: differential use of PTCA, surgery and drugs]. 868 87

The submitted review deals with contemporary possibilities of antianginal treatment. After a brief account of pathophysiological and morphological data in different types of cardiac ischaemia and angina pectoris the author submits algorithms which should be the basis for therapeutic decisions. It is a question of proper timing of invasive examinations leading to revascularization operations in relation to medicamentous treatment. The latter is supplementary treatment before or after revascularization, or is the main approach in case of minimal complaints, in case of contraindicated invasive treatment or in case of an inoperable finding. The author discusses the action, indications, contraindications, undesirable effects, and average dosage of nitrates, beta-blockers, calcium channel inhibitors and antithrombotics. The author mentions also the use of angiotensin converting enzyme inhibitors. View on treatment will change with advancing knowledge.
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PMID:[Antianginal therapy '95]. 868 93


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