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)

The classification of Raynaud's phenomenon has been complicated by various confusing labels, including Raynaud's disease and Raynaud's syndrome. To improve clarity and to allow for uniformity in reporting, most investigators agree that only the terms primary and secondary Raynaud's phenomenon should be used for patient classification. The prevalence of Raynaud's phenomenon seems to vary among different populations and different climates, suggesting genetic and environmental influences on its expression. The concept that Raynaud's phenomenon is the manifestation of a generalized vasospastic disorder has been addressed by studies of migraine headaches, variant angina, and the pulmonary vascular circulation. Current data suggest that the pathophysiology of Raynaud's phenomenon is complex and multifactorial, involving the endothelium, neuroreceptor expression, and locally produced mediators that affect vascular responses. New and old diagnostic tools used to measure digital circulation continue to be tested in an effort to define a better method of evaluating patients. Occupational causes of Raynaud's phenomenon continue to be an important health problem despite efforts to control vibratory tool usage. The role of beta-blockers in the induction of Raynaud's phenomenon has been questioned, but the use of chemotherapeutic agents is a definite risk factor. A new radical surgical approach for severe refractory Raynaud's phenomenon was described. Intravenous prostaglandins continue to appear helpful in the treatment of severe Raynaud's phenomenon, and oral prostaglandins are beginning to be studied.
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PMID:Raynaud's phenomenon. 811 41

Coexisting medical conditions often complicate the selection of antihypertensive drugs. Felodipine, a new vascular-selective calcium antagonist with demonstrated antihypertensive efficacy, has not been found to alter lipid profiles in hypertensive patients. Studies in additional patient populations have yielded insights into the effects of the drug on other diseases that may coexist with hypertension. In individuals with stable angina pectoris or congestive heart failure, acute administration of felodipine reduces systemic vascular resistance and increases cardiac output and total coronary blood flow; myocardial contractility is not depressed at doses that produce a clinically significant reduction in vascular resistance. In patients with coronary stenoses, the drug increases vessel diameter in the vicinity of obstructive lesions. Single-dose and long-term studies in patients with exertional angina have found that felodipine reduces anginal frequency and improves exercise tolerance. In patients with congestive heart failure, chronic dosing with felodipine produces a persistent reduction in vascular resistance and an increase in cardiac output, both at rest and during exercise. Symptomatic improvement and increased exercise tolerance have been noted in some studies. In patients with Raynaud's phenomenon, felodipine has been associated with a dose-dependent improvement in symptomatology. Among individuals with exercise-induced bronchospasm, the drug has no effect on resting bronchial tone and may exert some positive effects during exercise. In hypertensive patients with Type II diabetes, felodipine has not been found to raise glucose levels significantly. The data obtained thus far suggest that felodipine is safe for use in hypertensive patients with a variety of concomitant diseases.
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PMID:Treatment of hypertension with felodipine in patients with concomitant diseases. 845 9

The chemistry, pharmacology, pharmacokinetics, clinical uses, adverse effects, and dosage of felodipine and isradipine are reviewed. Felodipine and isradipine are new calcium-channel-blocking agents with FDA-approved labeling for use in the treatment of essential hypertension. Both agents are members of the dihydropyridine class of calcium antagonists, which also includes nifedipine and nicardipine. Like those agents, felodipine and isradipine affect blood pressure by producing peripheral vasodilation. Felodipine and isradipine undergo extensive first-pass metabolism; their bioavailabilities are approximately 15% and 17%, respectively. The drugs are highly protein bound but do not affect serum digoxin concentrations. Anticonvulsants may reduce the elimination half-life of felodipine. Felodipine and isradipine are effective antihypertensive agents when used alone or in combination with beta blockers or diuretics. Both agents have shown some benefit in the treatment of angina pectoris in limited studies. Clinical data do not support the use of either agent for the treatment of congestive heart failure or Raynaud's phenomenon. Felodipine and isradipine have similar adverse-effect profiles, and their adverse effects resemble those of other agents in the class. Common adverse effects are peripheral edema and increased heart rate. The initial dosage of isradipine for the treatment of hypertension is 2.5 mg twice daily. Felodipine should be started at a dosage of 5 mg once daily. Felodipine and isradipine are effective antihypertensive drugs but have not demonstrated clear advantages over other dihydropyridine calcium-channel blockers.
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PMID:Felodipine and isradipine: new calcium-channel-blocking agents for the treatment of hypertension. 845 78

Calcitonin gene related peptide (CGRP), a potent vasoactive and cardiotonic peptide, interacts with specific G-protein-coupled receptors. CGRP is synthesized and released from small, capsaicin-sensitive sensory nerves. This extensive network of sensory nerves, found in virtually all organs, suggest a potential role for CGRP in diverse physiologic and pathophysiologic processes. The potent vasodilation elicited by CGRP in the cerebral, coronary, and peripheral vasculature has led to its therapeutic evaluation in the treatment of cerebral vasospasm following subarachnoid hemorrhage, stable angina, and Raynaud's phenomenon. The potential inotropic action and coronary vasodilation have also led to a potential beneficial effect in congestive heart failure. The enriched localization of CGRP in trigeminal sensory ganglia may indicate a role in the neurogenic inflammation associated with migraine. Thus, CGRP antagonists may represent a novel therapeutic approach to the treatment of migraine. In addition, CGRP and amylin (homologous pancreatic peptide) reduce the tissue--glucose response to insulin. It has been suggested that a CGRP antagonist may therefore improve insulin sensitivity in non-insulin-dependent diabetes, NIDDM. This brief review provides a preliminary exploration of the potential therapeutic opportunities surrounding CGRP and CGRP antagonists. Future advances are dependent on a better understanding of the structure and function of CGRP receptor(s) and the concomitant identification of selective and potent agonists and antagonists useful for addressing therapeutic hypotheses.
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PMID:Clinical perspectives of calcitonin gene related peptide pharmacology. 884 3

There are a number of cardiovascular conditions in which calcium channel antagonists (CCAs) are accepted as first-line therapy, including Prinzmetal's angina and Raynaud's phenomenon. The real issue is whether symptomatic relief of angina or effective reduction of blood pressure (BP) is matched by a good safety record. In effort angina, verapamil is as safe as metoprolol, and nifedipine (tablet form) is as safe as atenolol. In unstable angina, intravenous diltiazem is better than intravenous nitroglycerin; there are no similar data on beta-blockade. Short-acting nifedipine is contraindicated in unstable angina. There is no place for CCAs in acute phase myocardial infarction and short-acting nifedipine is contraindicated. In the post-MI phase, two specific groups of patients benefit from diltiazem or verapamil: (1) those who had non-Q-wave infarcts and (2) those who are hypertensive. The DAVIT studies argue for the safety and efficacy of verapamil but do not allow comparisons with standard beta-blocker therapy. In the treatment of hypertension, the recommendation often made that a low-dose diuretic should be first-line therapy holds for the elderly with systolic hypertension but is not based on prospective studies in the case of younger patients. High-dose diuretics may have adverse effects, as reported in two case-controlled studies. Prospective outcome data favoring beta-blocker monotherapy as first-line therapy are limited, especially in the elderly, while case-control studies suggest an increased incidence of cardiac death in those treated by beta-blockers. CCAs may be the preferred first-line antihypertensive treatment for those groups in whom low-dose diuretics are unlikely to work as monotherapy.
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PMID:Calcium channel antagonists should be among the first-line drugs in the management of cardiovascular disease. 892 59

The prevalence of migraine and Raynaud's phenomenon in Japanese patients with vasospastic angina (group I) were compared with those in 2 control groups: one with effort angina (group II) and the other group without known ischemic heart disease (group III). There were no significant differences among the 3 groups with respect to age and sex. The prevalence of migraine in group I was 23 of 100, as compared with 4 of 100 in group II (p<0.01) and 11 of 100 in group III (p<0.05). The prevalence of Raynaud's phenomenon in group I was 9 of 100, as compared with 3 of 100 in group II and 4 of 100 in group III. Thus, in Japan, the prevalence of migraine in patients with vasospastic angina was higher than those in the 2 control groups, whereas the prevalence of Raynaud's phenomenon did not differ significantly among the 3 groups. The prevalence of Raynaud's phenomenon in Japanese patients with vasospastic angina was different from that reported from North America, although the prevalence of migraine was the same. This may be partially explained by racial differences.
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PMID:Prevalence of migraine and Raynaud's phenomenon in Japanese patients with vasospastic angina. 1078 43

Drugs classified as calcium channel blockers (CHBs) are now among the most frequently prescribed drugs for the treatment of cardiovascular disease. Although the currently available CCBs have major differences in their structural and cardiovascular effects, they share the common property of blocking the transmembrane flow calcium ions through voltage gated L-type channels. These drugs have been approved for the treatment of hypertensive heart disease: they reduce left ventricular hypertrophy and improve its sequelae, such as ventricular dysrhythmias, impaired filling and contractility, and myocardial ischemia. Long-acting CCBs have been shown to reduce mortality and morbidity in elderly patients with systolic hypertension, appear to be extremely useful in patients with cyclosporin-induced hypertension, and can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus, renal disease, Raynaud's phenomenon or migraine. Long-acting dihydropyridine have been shown to be effective and safe in the treatment classic angina pectoris and vasospastic angina, supraventricular arrhythmias, particularly reentrant AV-nodal tachycardia, others to be beneficial in patients with congestive heart failure, and all of them have potential for decreasing atherogenesis.
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PMID:[Calcium channel blockers in the treatment of cardiovascular disease]. 1157 40

Cardiovascular diseases impair the lives of millions of Americans each year. Researchers have studied a variety of nonpharmacologic interventions in an attempt to discover their use as therapies for these diseases. Various methods of biofeedback have shown promise in the treatment or management of several cardiovascular disorders. The literature relating to the use of biofeedback therapies for hypertension, cardiac arrhythmias, angina pectoris, cardiac ischemia, myocardial infarction, and Raynaud's phenomenon is reviewed. The number and types of studies in each of these areas vary widely, but research to date suggests that biofeedback could be a useful alternative or adjunct to more conventional forms of treatment. Further research to clarify the appropriate uses of biofeedback in the management of these disorders is recommended.
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PMID:Biofeedback applications in the treatment of cardiovascular diseases. 1507 88

In evaluating the cardiovascular risks of triptans (5-HT(1B/1D) agonists) for the treatment of migraine, the possible relationship between migraine and cardiovascular disease warrants careful assessment. The vascular nature of migraine is compatible with the possibility that migraine is a manifestation of cardiovascular disease or is linked to cardiovascular disease via a common mechanism. If so, then migraine itself--independent of the use of triptans--may be associated with an increased risk of cardiac events. This article considers the epidemiologic literature pertinent to evaluating the association of migraine with coronary heart disease. The research reviewed herein fails to support an association between migraine and coronary heart disease. First, data from several large cohort studies show that the presence of migraine does not increase risk of coronary heart disease. Furthermore, although migraineurs are generally more likely than nonmigraineurs to report chest pain, the presence of chest pain in most studies did not predict serious cardiac events such as myocardial infarction. That the gender- and age-specific prevalence of migraine does not overlap with that of coronary heart disease is also consistent with a lack of association between migraine and atherosclerotic cardiovascular disease. While migraine appears not to be associated with coronary heart disease, preliminary evidence suggests a possible link of migraine with vasospastic disorders such as variant angina and Raynaud's phenomenon. These results warrant further investigation in large prospective studies.
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PMID:Are migraine and coronary heart disease associated? An epidemiologic review. 1514 88

Sarpogrelate is a selective 5-hydroxytryptamine receptor subtype 2A (5-HT2A) antagonist. It is metabolised to racemic M-1 and both enantiomers of M-1 are also antagonists of 5-HT2A receptors. Sarpogrelate inhibits responses to 5-HT mediated by 5-HT2A receptors such as platelet aggregation, vasoconstriction and vascular smooth muscle proliferation. There is no information available on the pharmacokinetics of sarpogrelate. Sarpogrelate is efficacious in animal models of thrombosis, coronary artery spasm, atherosclerosis, restenosis, peripheral vascular disease, pulmonary hypertension, ischaemic heart disease, myocardial infarction, diabetes and kidney disease. Small clinical trials indicate that sarpogrelate may be beneficial in the treatment of coronary artery disease, angina, restenosis, heart valve prostheses surgery, diabetes mellitus, Raynaud's phenomenon, systemic sclerosis and Buerger's disease. Larger, randomised, double-blind, placebo-controlled clinical trials of sarpogrelate in intermittent claudication, coronary artery disease, restenosis and diabetes should be considered.
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PMID:Sarpogrelate: cardiovascular and renal clinical potential. 1521 24


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