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 45-year-old woman with almost normal coronary arteries suffered from acute inferior myocardial infarction after taking 2 tablets (2.0 mg) of ergotamine tartrate for headache. She had had attacks of variant angina and spasm of the right coronary artery had been demonstrated during the attack. After the recovery from myocardial infarction the intravenous injection of ergonovine maleate 0.05 mg induced spasm of the right coronary artery again. We conclude that acute myocardial infarction in this patient was probably caused by coronary arterial spasm induced by ergotamine tartrate.
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PMID:Acute myocardial infarction induced by ergotamine tartrate: possible role of coronary arterial spasm. 678 44

The effect of molsidomine on hemodynamics and myocardial ischemia were studied in 48 patients with acute myocardial infarction. Between 8 and 12 mg of orally and intravenously administered molsidomine led to a significant reduction in left ventricular filling pressure. In response to 2 x 4 mg p.o., diastolic pulmonary arterial pressure fell from 12.1 to 8.8 mm Hg in patients with filling pressure below 20 mm Hg. Patients with left heart failure and left ventricular filling pressure above 20 mm Hg (Group 2) displayed a decline in filling pressure from 23.8 to 17.4 mm Hg following 12 mg i.v. In addition, right atrial pressure dropped significantly across the entire range of dosages. Although patients without left ventricular failure (Group I) showed a decline in cardiac output (5.7 to 4.7 l/min), this parameter remained unchanged in Group 2. Heart rate in Group 2 fell from 85 to 81 per min. Arterial blood pressure was reduced by a mean of only 10 mm Hg at high dosages and remained unchanged at lower dosages. No change was observed in peripheral resistance. The maximum effect was seen 30 min after oral administration. Three hours later, the effect was reduced by half. Only minimal activity could be observed after 8 h. The incidence of side effects was low, with transient headaches occurring in 8% of the patients. An intraindividual comparison with 1.6 mg of sublingually administered nitroglycerin demonstrated no significant difference in hemodynamic effectiveness (n = 11). Molsidomine, not unlike nitroglycerin, exerts a favorable effect on hemodynamics and myocardial ischemia. It acts primarily to reduce preload. The additional moderate effect on afterload with a slight decline in arterial pressure at high dosages may also be considered advantageous.
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PMID:[Effect of molsidomine on hemodynamics and myocardial ischemia in patients with acute myocardial infarction (author's transl)]. 689 77

In part I of this article we report on 89 hypertensive patients who underwent 9 months of treatment with oxprenolol HCl 160 mg in a slow-release formulation plus cyclopenthiazide 0.25 mg and potassium chloride 600 mg (Trasidrex; Ciba-Geigy). Blood pressures, both supine and standing, and pulse rates were consistently controlled by this regimen throughout the 9 months of treatment, regardless of the time of day at which these parameters were measured, i.e. morning or afternoon. Seventy-six patients completed the trial. The most common symptom or sign occurring during treatment was headache, the next most common being heartburn. No patient developed angina while on the regimen. Three patients discontinued the study owing to unwanted effects. This study represents a total of 28237 patient-days of treatment. In part II of the trial we studied the effects of a similar regiment in 67 patients for 1 year preceded by a 2-week wash-out period. Forty-six of the patients completed a full year's treatment. Statistically significant reductions in blood pressures and pulse rates occurred after commencement of active treatment and were maintained throughout the study period. Four patients withdrew from the study owing to adverse effects, 1 patient died of an acute myocardial infarction, and 1 patient was considered a treatment failure. This study represents 19858 patient-days of treatment.
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PMID:Oxprenolol slow-release with cyclopenthiazide KCl in the treatment of essential hypertension. A multicentre general practice study. 701 37

In all patients hospitalized in one single hospital due to acute myocardial infarction (AMI) during a period of 21 months, we describe the prognosis in relation to smoking habits and other risk indicators with death. Of 862 AMI patients, 37% reported smoking at the onset of AMI. Of the patients who smoked at the onset of AMI and who survived the first year, 53% reported having quit smoking. Patients who had quit smoking reported fewer symptoms of chest pain (p < 0.01), headache (p < 0.01) and dizziness (p < 0.001) as compared with patients who continued to smoke after one year. Of the patients who had quit smoking, the mortality during the subsequent 4 years was 17% as compared with 31% for patients who continued to smoke (p < 0.05). However, patients who quit smoking less frequently had a previous history of myocardial infarction and congestive heart failure. When correcting for such dissimilarities, quitting smoking did not remain significantly associated with prognosis.
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PMID:Smoking habits in consecutive patients with acute myocardial infarction: prognosis in relation to other risk indicators and to whether or not they quit smoking. 758 61

Previous small clinical trials have suggested that treatment with nitric oxide donors in suspected myocardial infarction can reduce mortality by 30-35%. To confirm this finding in a large-scale trial, we compared molsidomine and its active metabolite linsidomine (a nitric oxide donor) with placebo in 4017 patients with acute myocardial infarction. In our trial, patients without signs of overt heart failure (Killip III/IV) were randomly assigned in a double-blind design within 24 h of symptom onset to receive linsidomine 1 mg/h intravenously for 48 h, followed by 16 mg molsidomine by mouth daily for 12 days (n = 2007), or an identical placebo (n = 2010). All other treatments could be used at the responsible physician's discretion with the exception of systematic vasodilator treatment. The molsidomine and placebo groups showed similar all-cause 35-day mortality (168 [8.4%] vs 176 [8.8%] deaths, p = 0.66), and adjustment for baseline variables in a Cox model had no effect. Similarly, we found no difference for long-term mortality (mean follow-up 13 months; 294 [14.7%] vs 285 [14.2%] deaths, p = 0.67). The two groups showed similar frequencies of major and minor adverse events; only headache was significantly more common in the molsidomine group. Changes in treatment practices and the lower risk profile of our study subjects than of participants in previous trials may explain the results. It is still not clear whether nitric oxide donors can improve survival in higher-risk myocardial infarction patients.
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PMID:The ESPRIM trial: short-term treatment of acute myocardial infarction with molsidomine. European Study of Prevention of Infarct with Molsidomine (ESPRIM) Group. 791 27

For sumatriptan, tightness in the chest caused by an unknown mechanism has been reported in 3-5% of users. We describe a 47-year-old woman with an acute myocardial infarction after administration of sumatriptan 6 mg subcutaneously for cluster headache. The patient had no history of underlying ischaemic heart disease or Prinzmetal's angina. She recovered without complications.
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PMID:Transmural myocardial infarction with sumatriptan. 809 32

The use of pharmacologic stress testing for detecting and assessing ischemic heart disease (IHD) is reviewed. Methods of diagnosing IHD are designed to emulate conditions that increase myocardial oxygen demand in order to identify areas of ischemia and atherosclerotic lesions and to evaluate their functional or anatomical importance. Diagnostic methods can be divided into functional assessment with stress testing and anatomical assessment with coronary angiography. Physical stressors, such as exercise or atrial pacing, or pharmacologic stressors, such as vasodilators or beta-adrenergic-receptor agonists, can be used in stress testing. Electrocardiography, thallium planar scintigraphy, echocardiography, and other techniques are used to evaluate the response to stress testing. Unlike exercise stress testing, pharmacologic testing does not require physical exertion. Adenosine, dipyridamole, and dobutamine are the principal agents used in pharmacologic stress testing. Adenosine and dipyridamole mediate coronary artery vasodilation. Adenosine, a direct agonist, has a rapid onset and short duration of action. Dipyridamole, the only agent with approved labeling for use in stress testing, inhibits adenosine indirectly. Dobutamine increases cardiac output and heart rate as well as promoting coronary artery vasodilation. Clinical trials show that all three drugs can be used safely and effectively in patients after acute myocardial infarction or before vascular surgery and in individuals with risk factors for or symptoms of IHD. The sensitivity and specificity of pharmacologic stress testing for detecting IHD are at least as high as those of exercise testing. Minor adverse effects, including chest pain, headache, and facial flushing, are common, but major adverse effects are rare. Pharmacologic stress testing can be used in patients who cannot undergo exercise testing and offers a noninvasive alternative to coronary angiography.
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PMID:Pharmacologic stress testing: experience with dipyridamole, adenosine, and dobutamine. 816 Jun 85

Platelet activation and thrombus formation within the coronary artery are major factors in acute myocardial infarction (AMI) and unstable angina (UA), and continuing platelet activation is associated with an adverse prognosis. We assessed platelet activation by using flow cytometry to measure platelet surface expression of P-selectin and glycoprotein IIb/IIIa in 20 patients with AMI and 20 with UA, all of whom were treated with aspirin. Platelet studies were repeated after the infusion of a nitric oxide donor (glyceryl trinitrate or S-nitrosoglutathione) that produced a fall in mean arterial pressure of no more than 10 mm Hg. P-selectin was expressed on 2.5% (range, 1.4% to 6.3%) of platelets from AMI and 2.3% (range, 1.6% to 3.3%) from UA subjects compared with 1.0% (range, 0.6% to 1.9%) of platelets from 20 control volunteers without angina (P < .001). Glycoprotein IIb/IIIa expression was 101.6 +/- 2.7 arbitrary units of relative fluorescence in AMI and 100.2 +/- 3.3 in UA compared with 87.8 +/- 2.5 in control subjects (P < .01). In both AMI and UA, S-nitrosoglutathione reduced P-selectin (P < .001) and glycoprotein IIb/IIIa (P < .05) expression, as did glyceryl trinitrate (P < .02 and P < .01, respectively). In 3 of 20 patients receiving glyceryl trinitrate the lowest dose was not tolerated due to headache or hypotension. These findings show that platelet activation persists in AMI and UA despite aspirin treatment and that this can be inhibited by using glyceryl trinitrate or S-nitrosoglutathione. S-nitrosoglutathione is better tolerated at the doses required.
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PMID:Platelet activation in acute myocardial infarction and unstable angina is inhibited by nitric oxide donors. 854 26

We report a 64-year-old man who complained of headache without chest pain at the onset of acute myocardial infarction (AMI). He had no history of chest pain or headache. Severe headache in this case was the first symptom of AMI. The headache was reproduced during stress test. During the angioplasty procedure, he also complained of headache without vasospastic change in the coronary artery. These findings suggest that the headache which accompanied AMI or myocardial ischemia in this case was due to referred pain rather than a generalized vasospastic disorder.
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PMID:Headache as a manifestation of myocardial infarction. 867 53

Nisoldipine is a second-generation dihydropyridine calcium channel blocker (CCB). It is the most vascular selective of the currently available CCBs, and thus has the capacity to lower blood pressure without affecting the functioning of the myocardium and skeletal muscle, and without producing any negative inotropic effects. Nisoldipine coat core (CC) is an extended-release formulation that allows nisoldipine to be released gradually over 24 hours, minimizing fluctuations in plasma concentration and providing a good trough/peak ratio. It has a slow onset and long duration of action, and ambulatory blood pressure monitoring has demonstrated that its antihypertensive effect is maintained over 24 hours with no evidence of reflex tachycardia, hypotension, or sympathetic neurohormonal activation and no effects on circadian variation. Studies in patients with hypertension have shown that nisoldipine CC provides reductions in blood pressure that are at least equivalent to those seen with diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, and other CCBs, without deleterious effects on metabolic parameters. In particular, it has been found to be effective in elderly patients and in black patients with severe hypertension. The DEFIANT studies have demonstrated that nisoldipine CC improves cardiac function and exercise tolerance in patients recovering from acute myocardial infarction, without increasing the risk of mortality compared with placebo. It also improves exercise performance in patients with stable angina pectoris. Nisoldipine CC is well tolerated in all groups of patients, with the most frequently reported side effects being headache and peripheral edema, which are usually mild and transient.
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PMID:Nisoldipine CC: efficacy and tolerability in hypertension and ischemic heart disease. 912 76


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