Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 70-year-old woman with angina pectoris developed a migrainous headache 3 days after starting oral propranolol. She had not complained of headaches since her second and third decade when she had suffered occasional attacks of migraine. It is likely that propranolol was the cause of her headache, since it recurred when she was rechallenged with the drug.
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PMID:Recurrent migraine after propranolol. 91 70

A new agent, Molsidomine, with anti-anginal effect was investigated in 43 patients with coronary heart disease by means of 121 exercise tolerance studies. A good effect was observed 1 hour after sublingual or enteral absorption of 2 mg, which was comparable to 20 mg of Isosorbiddinitrate administered sublingually. Recorded and evaluated were the depression of ST-segment in the ECG, heart rate, systolic and diastolic blood pressure as well as subjective parameters. In comparison to the controls there was a highly significant reduction of anginal pain and ST-depression equivalent to that obtained 1 hour after Isosorbiddinitrate. The effect of Molsidomine could be established already 10 min after sublingual administration and sustained 5 to 6 hours afterwards with a highly statistic significance after sublingual as well as after enteral absorption. Side effects were noticed in 3 out of 43 patients, 2 of them with headache. The remarkable advantages of the drug are to be seen in its simple dosage and administration, its good tolerability, and its intrinsic retard-effect. A combination with beta-blocking agents seems to be possible in the same way as with Isosorbiddinitrate.
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PMID:[Studies on the influence of Molsidomin on coronary heart disease (author's transl)]. 100 55

A case of suprasellar tumor associated with so-called atypical angina pectoris was reported. A 58-year-old man was admitted to our hospital on Feb. 2, 1973, because of headache, disturbance of visual field and the attack of chest pain. He had been suffering from disturbance of visual field for about 3 years and the attack of chest pain for about 4 months prior to admission. Neurological findings on admission were bitemporal hemianopia, decreased visual acuity and atrophy of the optic disc. Bilateral carotid angiography showed upward displacement of A1 portion of the anterior cerebral artery. Pneumoencephalography demonstrated defect of the anterior part of the third ventricle. Laboratory examination showed hypopituitalism. On March 26, 1973, Right frontal craniotomy was performed under the diagnosis of suprasellar tumor. The walnut-sized tumor was detected in the suprasellar region and removed totally. Histological examination showed dermoid cyst. With regard to the attack of chest pain, the selective coronary angiography was performed. But organic change was not detected and Master's two step test did not induce any pathological finding in EEG. So we made a diagnosis of so-called atypical angina pectoris. There are many arguments about pathogenesis of so-called atypical angina pectoris. There is no organic change of the heart of attention now. Recently it is said that so-called atypical angina pectoris is closely connected with paradoxical sleep. We recognized dysunction of the autonomic nervous system through various examinations. The hypothalamus was displaced upward by a suprasellar tumor in this case. After removal of the suprasellar tumor, the frequency of the attack of chest pain was decreased. The atypical angina pectoris in the presented case may be considered to consequence of distrubance of the hypothalamic function.
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PMID:[A case of suprasellar tumor associated with so-called atypical angina pectoris]. 103 74

Nicorandil belongs to the class of compounds known as potassium channel activators which are characterised by their arterial vasodilator properties. In addition, nicorandil has venodilating properties which are attributable to a nitrate group in its chemical structure. Therefore, by combining these two vasodilator mechanisms, nicorandil represents a novel type of compound for use in the treatment of angina pectoris. Furthermore, increasing experimental evidence suggests that potassium channel activation may also exert a direct cytoprotective effect by augmenting normal physiological processes which protect the heart against ischaemic events. Comparative studies of up to 3 months' duration suggest that nicorandil is equivalent in efficacy to isosorbide dinitrate, propranolol, atenolol, nifedipine or diltiazem in the treatment of stable angina. Preliminary evidence suggests that an improvement of anginal and ischaemic symptoms is maintained for up to 1 year. Whilst the efficacy of nicorandil in other types of angina has not been extensively studied, preliminary results indicate that intravenous nicorandil is as effective as isosorbide dinitrate in the treatment of unstable angina and is also effective in patients with variant angina. In addition, the limited data available indicate that nicorandil may be effective in patients with unstable and variant angina who are refractory to therapy with conventional antianginal agents, a potentially important area for further study. Headache, mostly of mild to moderate intensity was the most commonly reported adverse event, occurring in one-third of patients receiving the recommended therapeutic regimen of nicorandil 10 to 20mg twice daily. In comparative trials involving a total of 84 patients who received nicorandil, the incidence of headache was similar to that produced by isosorbide mononitrate and isosorbide dinitrate. Headache was most frequent on initiating therapy but declined with continued treatment. To date, approximately 5% of patients participating in European trials have withdrawn due to headache, although this rate may be reduced by using a lower starting dose of nicorandil (5 mg twice daily). In summary, clinical experience thus far indicates that nicorandil, with its novel combination of two distinct vasodilator mechanisms, offers an effective alternative to established vasodilator therapy with conventional nitrates and calcium antagonists in the long term treatment of stable angina pectoris. Further studies are warranted to establish whether the unique pharmacodynamic profile of nicorandil is advantageous for the treatment of other types of angina and/or the ischaemic myocardium.
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PMID:Nicorandil. A review of its pharmacology and therapeutic efficacy in angina pectoris. 128 Oct 76

Nicorandil is a new vasodilator agent. Efficacy and safety of nicorandil in the treatment of angina pectoris have been evaluated through an extensive clinical program with a total of 1,680 patients who received the product. Results of hemodynamic studies provide clear evidence of the vasodilatory effect of nicorandil. In a population of patients with normal left ventricular function, a reduction in preload was apparent from a decrease in left ventricular end-diastolic pressure from 7.4 +/- 1.7 to -3.2 +/- 1.5 mm Hg. Furthermore, nicorandil produced marked reductions in total peripheral resistance (19%) and aortic blood pressures with decreases in systolic pressure of 34% and in diastolic pressure of 21%. At antianginal doses, nicorandil has a coronary vasodilating effect as well as a balanced peripheral action that leads to decreases in both preload and afterload. Therefore, nicorandil affects two of the main hemodynamic determinants of oxygen demand without impairing myocardial contractility or atrioventricular conduction. In addition, its strong spasmolytic activity is of particular interest when dynamic coronary obstruction is considered. Nicorandil clearly has demonstrated K(+)-channel-opening activity. In addition, the range of plasma concentrations in humans at therapeutic doses is similar to that of experimental models in which the K(+)-channel activity has been determined. This mechanism of action may explain the different hemodynamic profiles of nicorandil and nitrates in humans. Nicorandil is an effective and potent antianginal agent at a dose of 10-40 mg, which in monotherapy controls 69-80% of patients with stable chronic angina. Comparative trials have shown that the efficacy of nicorandil compares with that of drugs from the main classes of antianginal drugs--beta-blockers (atenolol, propranolol) and a Ca2+ antagonist (diltiazem). Patients treated for as long as 3 months or 1 year have shown sustained efficacy with no evidence of development of tolerance to the drug. The long duration of action allows effective treatment with a well-tolerated b.i.d. regimen. At the recommended doses, the main side effects were limited to headaches. They usually occurred early in the course of treatment and can be diminished by a progressive titration. From the large safety data base, there is no evidence that nicorandil induced exacerbation of myocardial ischemia or abrupt withdrawal syndrome. Nicorandil does not adversely affect the lipid profile or the glucose level. As an antianginal drug with a novel mechanism of action, nicorandil provides a useful alternative to existing antianginal agents in the long-term management of patients with angina pectoris.
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PMID:Clinical profile of nicorandil: an overview of its hemodynamic properties and therapeutic efficacy. 128 84

Amlodipine, a potent long-acting dihydropyridine calcium antagonist, was compared with placebo in a parallel, randomized, double-blind study in 134 patients with chronic stable angina pectoris maintained on beta-adrenergic blocking agents. After a single-blind, two-week placebo period, patients were randomized to receive either amlodipine (2.5, 5, and 10 mg) or placebo once daily for four weeks. The effects of amlodipine on maximal exercise time, work, time to angina onset, and subjective indices including angina frequency, nitroglycerin tablet consumption, and patient and investigator ratings were assessed. Each dose of amlodipine produced increases in exercise time and calculated total work accomplished compared to baseline. Improvements at 5 and 10 mg were significantly greater than placebo which produced no significant change (p less than 0.05). Qualitative improvements in the severity of angina were produced by amlodipine at 5 and 10 mg daily assessed by patient-rating questionnaires (p less than 0.05). Reductions in angina frequency attacks per week and weekly nitroglycerin tablet consumption occurred but were not statistically significant when compared with placebo. Adverse effects observed during amlodipine treatment prompted discontinuation of treatment in only 2 out of 100 patients. Three patients discontinued treatment for reported lack of efficacy. No laboratory abnormalities prompted treatment discontinuation and minor side effects of dizziness, nausea, headache, and fatigue were observed infrequently. The results of this controlled, large-scale multicenter trial suggest that amlodipine significantly increased exercise capacity and was well tolerated when added to the antianginal regimen of patients remaining symptomatic while receiving beta-blocking agents.
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PMID:Amlodipine combined with beta blockade for chronic angina: results of a multicenter, placebo-controlled, randomized double-blind study. 135 85

At the end of a short-term (3-month) study of antihypertensive treatment of mild-to-moderate hypertension, 141 of the 200 study patients continued into a 2-year follow-up of isradipine as monotherapy or in combination with other antihypertensive agents. Although all 141 patients completed the first year, only 102 completed the study. Twenty-four patients dropped out: 2 with flushing; 1 each with arrhythmia, edema, angina, and headache; 12 who were noncompliant; 2 with disease unrelated to the study drug; and 4 for reasons unknown. Before the follow-up, 70% of the 141 patients were taking isradipine; after 2 years, 63% were still taking isradipine as monotherapy. During the follow-up study, the blood pressure remained stable (142.9/86.8 mm Hg after 3 months, and 142.9/86.2 mm Hg after 2 years), whereas the normalization rate was only slightly changed (73 vs. 75.2%). The incidence of reported adverse events decreased with time. At the end of the short-term study, 44.7% of patients had reported one or more adverse events; after 2 years of treatment, only 14.4% reported adverse events. Two patients had ECG signs of left ventricular hypertrophy: one showed no relevant changes while the other presented clear signs of regression. No clinically relevant laboratory abnormalities were noted during the study. In conclusion, isradipine is effective, well tolerated and safe in the long-term treatment of mild-to-moderate hypertension.
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PMID:Long-term (2-year) isradipine data in the treatment of mild-to-moderate hypertension. 137 34

Based on obligatory notifications from pharmacies to the National Board of Health about prescription of strong analgesics as well as questionnaires to the prescribing doctors, the occurrence and causes of pain requiring strong analgesics outside hospitals were analysed over a period of one month in Denmark in a limited population (480,000), corresponding to nearly 10% of the Danish population. During one month, strong analgesics were prescribed to 0.2 per cent of the population. The commonest acute conditions were back pain (23%) and trauma (17%). The commonest recurrent acute conditions were headache (25%) and angina pectoris (17%). The commonest chronic non-malignant conditions were back pain (29%) and pancreatitis (7%). The commonest malignant conditions were lung cancer (20%) and colorectal cancer (14%). The commonest conditions indicated under the chronic pain syndrome were headache (33%) and back pain (13%). Conditions requiring strong analgesics reflect to some extent the distribution of painful conditions in the general population.
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PMID:Epidemiology of pain requiring strong analgesics outside hospital in a geographically defined population in Denmark. 142 20

The calcium antagonist, diltiazem is effective in the treatment of patients with various types of angina pectoris, as well as with essential and renovascular arterial hypertension. Sustained-release diltiazem in dose of 180 mg once daily is effective as sustained-release diltiazem in dose of 90 mg twice daily. Besides, in patients with stable angina pectoris and essential arterial hypertension the monotherapy with sustained-release diltiazem in dose of 180 mg is similarly effective as beta blockers and thiazide diuretics. However, monotherapy with sustained-release diltiazem is at least effective as monotherapy with sustained-release verapamil. Comparative clinical investigations showed that diltiazem is more effective than propranolol in decreasing ischemic attacks, whereas the risk of bradycardia is smaller. On the other hand, nifedipine (dihydropyridine calcium antagonist) is more effective than diltiazem in lowering ischemic electrocardiographic changes, incidence of attacks and improving working capability. The efficacy of diltiazem, nifedipine and verapamil is similar in the treatment of patients with spastic angina pectoris, whereas the least effective is propranolol. As far as the arterial hypertension is concerned, clinical investigations showed that the efficacy of diltiazem and nifedipine is similar. Side effects are relatively rare (1.8-9.6% patients) and depend on the dose (nausea, fatigue, dizziness, headache and itching).
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PMID:[Pharmacology--new therapy. Calcium channel blockers: new aspects of therapeutic use of diltiazem]. 146 75

The movement of calcium into neurons may be the common denominator for the triggering and propagation of seizure activity. We report results of the first double-blind, placebo-controlled, crossover trial with the dihidropyridine calcium antagonist nifedipine (NFD) as adjuvant therapy in refractory epilepsy. Twenty-two students (12 male, 10 female, age 17-22 years) attending Lingfield Hospital School received NFD retard and matched placebo for 8 weeks in 2 doses (20 and 40 mg b.i.d. each for 4 weeks) with a washout period of 8 weeks between treatment phases. In the 20 students who completed the trial, fewer partial seizures (p less than 0.05) were documented during the first 2 weeks of NFD administration. Similarly, fewer seizure days (p less than 0.05) were reported in the first month of active treatment. This response was not sustained into the second month of the trial. Blind scoring of EEGs suggested a small improvement with NFD (p less than 0.05). More patients reported headache when receiving NFD (p less than 0.02) than placebo, but heart rate and erect and supine blood pressure remained unaffected. Mean maximum NFD concentrations were 13.1 +/- 10.4 ng/ml. A weak correlation was noted between total (p less than 0.05) and partial (p = 0.025) seizure numbers and NFD concentrations following 8 weeks of treatment. This study does not support important anticonvulsant efficacy for NFD as adjuvant therapy for refractory epilepsy at doses appropriate for the treatment of angina or hypertension. Further trials are recommended using higher doses of NFD in less severely affected patients.
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PMID:Nifedipine for epilepsy? A double-blind, placebo-controlled trial. 154 65


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