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: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists are important classes of antihypertensive agents. Within their respective classes, ACE inhibitors and calcium antagonists share common pharmacokinetic properties, but in contrast to ACE inhibitors, some calcium antagonists may cause a significant increase in plasma digoxin concentrations. Clinically, both classes of agents have been shown to be safe and effective in large-scale, long-term clinical trials. ACE inhibitors appear to be very well tolerated and may be associated with fewer adverse effects than some calcium antagonists. ACE inhibitors appear to blunt diuretic-induced hypokalemia, hypercholesterolemia, hyperuricemia, and hyperglycemia. Both classes of agents can be used safely in patients with renal disease, diabetes mellitus, peripheral vascular disease, and chronic obstructive pulmonary disease. They may also be used in the elderly. While ACE inhibitors are particularly useful in hypertension accompanied by congestive heart failure, calcium antagonists can be very useful when angina pectoris is present in the hypertensive patient.
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PMID:Comparative pharmacokinetic and clinical profiles of angiotensin-converting enzyme inhibitors and calcium antagonists in systemic hypertension. 154 35

A systolic blood pressure greater than 160 mm Hg is a more significant risk factor for cardiovascular disease than a diastolic blood pressure greater than 95 mm Hg, regardless of a patient's age. Treatment of isolated systolic hypertension significantly reduces the incidence of both fatal and nonfatal cardiovascular events, even in patients who are over 80 years of age. Non-pharmacologic measures and behavior modification should be tried for three to six months in a patient with mildly elevated blood pressure (140 to 160 mm Hg/90 to 100 mm Hg). If these measures fail or the patient has target-organ disease or multiple cardiac risk factors, medication may be prescribed earlier. Half the usual recommended dose should be initially prescribed in the frail elderly. Long-acting diuretics or beta blockers are recommended first-line agents. Angiotensin-converting enzyme inhibitors, calcium channel blockers and alpha blockers have not been shown to reduce mortality in hypertensive patients who do not have comorbid disease. Angiotensin-converting enzyme inhibitors may benefit hypertensive patients with heart failure, and calcium channel blockers may help those with angina, especially vasospastic angina.
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PMID:Hypertension in the elderly. 863

The Angiotensin I-converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular diseases. Previous studies showed that deletion polymorphism in the the ACE gene might be a risk factor for myocardial infarction in the Caucasian population, but, this finding has not yet been reported in a Japanese population. In this study, a 287 base pair (bp) insertion/deletion polymorphism in intron 16 of the ACE gene was examined by the polymerase chain reaction (PCR) in a cross-sectional study of 100 healthy subjects and 218 patients with ischemic heart diseases (IHD) (70 angina pectoris, 148 myocardial infarction). Polymorphism of the ACE gene was characterized by three genotypes: two deletion alleles (genotype DD), two insertion allele (genotype II) and heterozygotes alleles (genotype ID). No differences could be detected among the three genotypes for total cholesterol, high-density lipoprotein cholesterol, blood pressure and body mass index. The serum ACE activity in each II, ID and DD genotype was 11.4 +/- 2:7 microU/ml, 14.5 +/- 3.5 microU/ml, 16.6 +/- 4.6 microU/ml, respectively. In the population study, genotype DD was significantly associated with IHD when compared with the other two genotypes (ID and II). The frequency of deletion allele was higher (0.56) in the IHD group than in the normal individuals (0.42) (p < 0.05). These frequencies were not varied whether they had classic risk factors or not. Furthermore, coronary multivessel impairment was significantly associated with a deletion allele than with an insertion allele (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Deletion polymorphism of the angiotensin I-converting enzyme gene associates with increased risk for ischemic heart diseases in the Japanese]. 773 15

The Angiotensin I-converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular diseases. Previous studies showed that deletion polymorphism in the ACE gene might be a risk factor for myocardial infarction in the Caucasian population. However, this finding has not yet been reported in the Japanese population. In this study, a 287 base pair (bp) insertion/deletion polymorphism in intron 16 of the ACE gene was examined by polymerase chain reaction (PCR) in a cross-sectional study of 35 healthy subjects and 85 patients with ischemic heart diseases (IHD) (32 angina pectoris, 53 myocardial infarction). Polymorphism of the ACE gene was characterized by three genotypes; two deletion alleles (genotype DD), two insertion allele (genotype II) and heterozygotes alleles (genotype ID). No differences could be detected among the three genotypes for total cholesterol, high-density lipoprotein cholesterol, blood pressure and body mass index. The serum ACE activities in each II, ID and DD genotype were 10.1 +/- 2.1 microU/ml, 13 +/- 3.2 microU/ml, 14.2 +/- 5.4 microU/ml, respectively. In the population study the genotype DD was significantly associated with IHD when compared with the other two genotypes (ID and II). The frequency of deletion allele was higher (0.61) in the IHD group than in the normals (0.39) (chi 2 = 7.8, p < 0.01). These frequencies were not varied whether they had classic risk factors or not. Furthermore, coronary multivessel impairment was significantly associated with the deletion allele than with the insertion allele (chi 2 = 11.7, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Deletion polymorphism of the angiotensin I-converting enzyme gene associates with increased risk for ischemic heart diseases in the Japanese]. 806 33

Verapamil is effective as antianginal medication but contraindicated in patients with congestive heart failure. Angiotensin-converting enzyme (ACE) inhibitors improve survival in patients with congestive heart failure but have limited effect on patients with angina pectoris. No studies have been published on the combined treatment with verapamil and ACE inhibitors in patients with stable angina pectoris and left ventricular dysfunction. We performed an open study in 14 patients with angina pectoris and ejection fraction < 40%. The patients received verapamil 180 mg and trandolapril 2 mg twice daily for 3 months. We found a significant increase in ejection fraction from 28 +/- 6 to 35 +/- 11 (p < 0.03), wall motion index from 1.0 +/- 0.3 to 1.2 +/- 0.3 (p < 0.03), exercise duration from 6.9 +/- 2.5 to 7.7 +/- 2.9 minutes (p < 0.01), and ratio of exercise to rest rate-pressure product from 2.2 +/- 0.4 to 2.5 +/- 0.6 (p < 0.02). Use of nitroglycerin and number of angina pectoris attacks were both significantly reduced after 3 months of treatment. These findings support the hypothesis that the combination of verapamil and trandolapril is useful in patients with attenuated left ventricular function and angina pectoris.
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PMID:Verapamil and angiotensin-converting enzyme inhibitors in patients with coronary artery disease and reduced left ventricular ejection fraction. 867 92

The D allele of an insertion/deletion (I/D) polymorphism in the angiotensin I-converting enzyme (ACE) gene is associated with a risk of myocardial infarction, and the relative risk associated with the ACE D allele is increased by the C allele of an angiotensin II type 1 receptor (AT1R) gene polymorphism (an A-->C transversion at nucleotide position 1166) [28]. The relation of the ACE and AT1R gene polymorphisms to coronary heart disease and the severity of coronary artery stenosis has now been investigated in 133 patients with myocardial infarction (MI) or angina pectoris who underwent coronary angiography and in 258 control subjects. The frequency of the ACE DD genotype as compared with non-DD was significantly higher in the patients who experienced an MI and in the low-risk patients than that in the controls (P < 0.05). The DD genotype showed a significantly increased risk of MI (odds ratio 1.85). The frequency of the AT1R A/C genotypes did not differ between the patients and the controls. The severity of coronary stenosis in the patients was estimated by the number of affected vessels (> 75% stenosis) and the coronary score of Gensini. Neither the number of affected vessels nor the coronary score differed among the ACE I/D genotypes. However, the number of affected vessels was significantly greater in patients with the AT1R AC genotype than in those with the 4A genotype (1.93 +/- 0.27 vs. 1.27 +/- 0.99; P < 0.05) (CC genotype was not found in the patients). After excluding patients with diabetes mellitus, the coronary score of those with the AC genotype was also significantly higher than in those with the AA genotype (51.7 +/- 34.4 vs. 18.2 +/- 23.3; P < 0.01). These results suggest that the ACE D allele is associated with the occurrence of myocardial infarction, while the AT1R C allele is involved in the development of the coronary artery stenosis.
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PMID:Significance of angiotensin I-converting enzyme and angiotensin II type 1 receptor gene polymorphisms as risk factors for coronary heart disease. 884 48

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.
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PMID:[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease]. 955 7

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.
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PMID:[Trends in pharmacological treatment of congestive heart failure]. 1036 2

Syndrome X, defined as typical angina with positive exercise test results and normal coronary angiographic findings, represents a multifactorial pathophysiologic state that may range from abnormalities in pain perception to abnormalities in endothelial- and nonendothelial-dependent coronary flow reserve associated with myocardial ischemia. Treatment begins with accurate diagnosis by means of a comprehensive coronary vascular reactivity evaluation. This may lay the groundwork for appropriate treatment. The management of patients with syndrome X is challenging, and it may be necessary to attempt various medications depending on the patient's response. We feel that the first step in the treatment is accurate diagnosis. This is done by performing a functional angiogram (assessment of endothelial-dependent and endothelial-independent coronary flow reserve). In those without evidence of coronary flow reserve abnormalities, reassurance might be curative; however, in those who continue to have symptoms, a trial of imipramine therapy at a dose of 50 mg/d may be attempted, provided other organic disorders (in particular gastrointestinal disorders) are excluded. Those who demonstrate evidence of abnormal coronary vascular reactivity are approached as outlined in Figure 1. Patients are advised to avoid medications that may cause coronary "spasm." We routinely refer our patients to the cardiovascular health clinic for risk factor management and an exercise program. Our first choice of medications usually consists of slow-release calcium channel blockers. We tend to start with a once-a-day regimen, and based on the response, we occasionally change the regimen to twice a day. If the functional angiogram reveals concomitant epicardial disease, then nitrates are added to the medical regimen. Angiotensin-converting enzyme inhibitors are part of the treatment if the patient has hypertension or diabetes or if calcium channel blocker therapy fails. l-Arginine at an initial dosage of 1 g three times daily is added and may be increased to 3 g three times daily if no contraindications are present. Because there are no data regarding the effect of l-arginine, which may affect insulin secretion, in patients with diabetes, we use caution in this patient population. There is no "gold standard" therapy for syndrome X, so each patient may respond differently to the initial medical therapy. Thus, we follow these patients closely to monitor their response to treatment.
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PMID:Syndrome X. 1109 12

Angiotensin-converting enzyme inhibitors improve endothelial function, inhibit experimental atherogenesis, and decrease ischemic events. The Quinapril Ischemic Event Trial was designed to test the hypothesis that quinapril 20 mg/day would reduce ischemic events (the occurrence of cardiac death, resuscitated cardiac arrest, nonfatal myocardial infarction, coronary artery bypass grafting, coronary angioplasty, or hospitalization for angina pectoris) and the angiographic progression of coronary artery disease in patients without systolic left ventricular dysfunction. A total of 1,750 patients were randomized to quinapril 20 mg/day or placebo and followed a mean of 27 +/- 0.3 months. The 38% incidence of ischemic events was similar for both groups (RR 1.04; 95% confidence interval 0.89 to 1.22; p = 0.6). There was also no significant difference in the incidence of patients having angiographic progression of coronary disease (p = 0.71). The rate of development of new coronary lesions was also similar in both groups (p = 0.35). However, there was a difference in the incidence of angioplasty for new (previously unintervened) vessels (p = 0.018). Quinapril was well tolerated in patients after angioplasty with normal left ventricular function. Quinapril 20 mg did not significantly affect the overall frequency of clinical outcomes or the progression of coronary atherosclerosis. However, the absence of the demonstrable effect of quinapril may be due to several limitations in study design.
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PMID:The QUinapril Ischemic Event Trial (QUIET): evaluation of chronic ACE inhibitor therapy in patients with ischemic heart disease and preserved left ventricular function. 1172 75


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