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)

Myocardon (1 tablet=0.5 mg Nitroglycerin, 100 mg Euphyllin, 29.7 mg Papaverin-hydrochlorid and 0.3 mg Atropinmethylnitrat, without phenobarbital) was given in a dosis of 3 and 6 tablets in patients with acute myocardial infarction. According to the initial value of left ventricular filling pressure (LVFP) the patients were divided into 2 groups: Group I with a LVFP below 20 mm Hg and group II with a LVFP above 20 mm Hg. In group II there was clinical evidence of left ventricular failure. In both groups a decrease in pulmonary artery pressure and especially in left ventricular filling pressure was observed (in group I from 13 +/- 4 to 8 +/- 3 mm Hg and in group II from 26 +/- 7 to 16 +/- 4 mm Hg). Heart rate and mean arterial pressure did not change. In group II cardiac output increased from 3.5 +/- 0.6 to 4.3 +/- 1.31/min, whereas in group I it decreased from 5.1 +/- 0.9 to 4.6 +/- 0.91/min. Like isosorbid dinitrate Myocardon is useful in the management of left ventricular failure in patients with acute myocardial infarction. Side effects were observed: in two patients vomiting and in one patient sickness. The main effect of Myocardon is probably due to nitroglycerin, which is part of the substance. In higher dosis Myocardon has to be given without phenobarbital. Myocardon is especially useful if in the case of headache after nitrates the drug has to be changed.
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PMID:[The effect of nitroglycerin in patients with acute myocardial infarction. IV. Myocardon in patients with and without left ventricular failure (author's transl)]. 81 16

The toxicities of cocaine are far-ranging. They include sudden death, acute medical and psychiatric illness, infectious complications, reproductive disturbances, trauma, criminal activities and societal disruption, including child neglect and abuse and lost job productivity. This chapter focuses on the medical complications. Medical complications in general reflect the intense sympathomimetic activities of cocaine ('sympathetic neural storm'). Psychiatric complications include acute anxiety or panic and paranoid psychosis. Cardiovascular complications include arrhythmias and sudden death, acute myocardial infarction, myocarditis, dissecting aneurysm and bowel infarction. Neurological complications include seizure, intracerebral haemorrhage and brain injury due to hyperthermia and/or seizures, and headache. The incidence of medical complications has been estimated using two databases collected prospectively in the United States. In 1989 and 1990 cocaine ranked first in total encounters, major medical complications and drug-related deaths. An attempt was made to assess the intrinsic toxicity of cocaine by computing the incidence of adverse health outcomes per population of drug abusers. Rates of emergency department visits and deaths were 15.1 and 0.5 respectively, per 1000 persons using drugs in the past year. The magnitude of the cocaine problem, while considerable, is relatively small compared with that of cigarette smoking or alcohol abuse.
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PMID:How toxic is cocaine? 163 9

Adenosine thallium-201 myocardial scintigraphy is a promising test for coronary artery disease detection, but its safety has not been reported in large patient cohorts. Accordingly, the tolerance and safety profile of adenosine infusion were analyzed in 607 patients (351 men, 256 women, mean age 63 +/- 11 years) undergoing this test either because of suspected coronary artery disease (Group I, n = 482) or for risk stratification early (5.2 +/- 2.8 days) after myocardial infarction (Group II, n = 125). Adenosine increased the heart rate from 74.5 +/- 14.0 to 91.8 +/- 15.9 beats/min (p less than 0.001) and decreased systolic blood pressure from 137.8 +/- 26.8 to 120.7 +/- 26.1 mm Hg (p less than 0.001). Side effects were frequent and similar in both groups. Flushing occurred in 35%, chest pain in 34%, headache in 21% and dyspnea in 19% of patients. Only 35.6% of Group I patients with chest pain during adenosine infusion had concomitant transient perfusion abnormalities, compared with 60.7% of Group II patients (p less than 0.05). First- and second-degree AV block occurred in 9.6% and 3.6% of patients, respectively, and ischemic ST changes in 12.5% of cases. Concomitance of chest pain and ischemic ST depression was uncommon (6%) but, when present, predicted perfusion abnormalities in 73% of patients. Most side effects ceased rapidly after stopping the adenosine infusion. The side effects were severe in only 1.6% of patients and in only six patients (1%) was it necessary to discontinue the infusion. No serious adverse reactions such as acute myocardial infarction or death occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance and safety of pharmacologic coronary vasodilation with adenosine in association with thallium-201 scintigraphy in patients with suspected coronary artery disease. 186 36

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.
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PMID:[Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case]. 225 22

The Cardiac Arrhythmia Pilot Study tested the feasibility of performing a large-scale study to evaluate the effect of therapy of ventricular arrhythmias after acute myocardial infarction (AMI). Ten clinical sites identified patients with greater than or equal to 10 ventricular premature complexes (VPCs)/hour, recorded 6 to 60 days after AMI in patients with an ejection fraction greater than 0.20. Patients were randomized to receive 1 of 5 agents: encainide, flecainide, imipramine, moricizine or placebo. Successful therapy was defined as greater than or equal to 70% suppression of VPCs and greater than 90% suppression of runs of ventricular tachycardia. Randomization to a second agent occurred if a patient did not achieve adequate suppression with the initial agent. Patients initially randomized to placebo continued to receive placebo. Patients were evaluated at 3-month intervals for the next year. Of 30,763 patients screened, 10,734 (35%) were younger than 70 years old and had a qualifying AMI. A Holter recording was obtained in 3,957 patients, of whom 871 (22%) had qualifying arrhythmias and 687 were eligible. Of the 687 eligible patients, 502 (73%) were randomized. Mean age of enrolled patients was 59 years. One-half of patients were randomized within 1 month after AMI. Mean ejection fraction was 0.45, with 175 (35%) patients having an ejection fraction less than 0.40. On baseline drug-free recording, 173 (35%) patients had less than 30 VPCs/hour; 149 (30%) between 30 and 100/hour and 180 (36%) greater than or equal to 100/hour. At least 1 run of ventricular tachycardia was seen in 172 (34%) patients. Drugs taken at baseline were similar in all groups with 116 (23%) patients taking digitalis, 161 (32%) taking diuretics, 203 (41%) taking beta blockers and 200 (40%) taking calcium antagonists. Slightly more patients, 53 (51%), randomized to flecainide were taking calcium antagonists. No significant relation was noted between baseline VPC frequency and ejection fraction, but baseline VPC frequency was correlated with heart rate, arrhythmia noted before AMI and right bundle branch block. As expected, a high ejection fraction correlated with lower peak creatine kinase values, an inferior location of the infarct and fewer signs of congestive heart failure. At baseline, at least 1 adverse symptom was volunteered by 192 (39%) patients. The most common symptoms were unusual tiredness or fatigue, heart beating fast or skipping beats or headache. In this study, over 20 age- and AMI-eligible patients were identified to obtain each randomized patient. The randomization process successfully distributed baseline variables across drug groups.
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PMID:Recruitment and baseline description of patients in the Cardiac Arrhythmia Pilot Study. The Cardiac Arrhythmia Pilot Study (CAPS) investigators. 245 14

The hemodynamic effects of IS-5-MN were studied in 18 patients with acute myocardial infarction (AMI) complicated with left ventricular failure. Before treatment, 13 patients were in Forrester's hemodynamic class II and 5 in class IV. Hemodynamic monitoring was performed for 3 days, and the following parameters were measured: heart rate (HR), blood pressures (BP), right atrial (RAP), pulmonary artery and pulmonary capillary (PCP) pressures, cardiac index (CI), systemic (SVR) and pulmonary (PVR) vascular resistances, and coronary perfusion pressure (CPP). Patients with clinical symptoms of acute pulmonary edema or systolic BP (BPs) less than 90 mmHg were not included. Twenty mg of 5-IS-MN per os were administered every 8 h. Hemodynamic measurements and IS-5-MN plasma levels were obtained in basal conditions and 1/2, 1, 2, 6 and 8 h after the first and seventh dose of IS-5-MN. A significant decrease of systolic and diastolic BPs, RAP, PCP, SVR and PVR was observed after 1/2 of IS-5-MN administration and was maintained through the study, while CI and CPP increased and HR remained unchanged. The hemodynamic effect was maintained after the seventh dose, with a further decrease of the following parameters: BP, RAC, PCP and PVR. However, 2 patients were withdrawn from the study due to severe symptoms of heart failure. One patient presented headache. IS-5-MN plasma levels were identified after 1/2 h, with a peak level after 1 h, and were similar after the seventh dose. A significant correlation was found between the IS-5-MN levels and the delta RAP and delta PCP after the seventh dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic effect of isosorbide-5-mononitrate in acute cardiac insufficiency secondary to myocardial infarct]. 281 84

Labetalol is a unique antihypertensive agent which is a competitive peripheral antagonist at both alpha- and beta-adrenoceptor sites. Clinically, it possesses about one fourth of the beta-adrenoceptor blocking activity of propranolol and one half of the alpha-adrenoceptor blocking activity of phentolamine with a beta- to alpha-blocking ratio of approximately 7:1. Nowadays, the clinical profile of labetalol is clearly defined. Perorally, it has often been used in the treatment of mild, moderate and severe hypertension and intravenously in the management of hypertensive emergencies. It offers many advantages over beta-blockers with no prominent side-effects. Hemodynamically, labetalol reduces blood pressure, heart rate and, first of all, peripheral resistance with almost no change in resting cardiac output or stroke volume. Labetalol appears to be useful particularly in patients whose blood pressure is not adequately controlled by beta-blockers alone or combined with a diuretic, but sometimes at the expense of postural hypotensive side-effects. It has proved to be safe in patients with coronary artery disease or after acute myocardial infarction and in pregnant patients, but in phaechromocytoma further clinical experience is needed. In induced hypotension during anesthesia and surgery no invasive blood pressure measurements are needed. The most frequent adverse effects include fatigue, postural hypotension, headache and gastrointestinal complaints. On the whole, labetalol expands the armamentarium of the practising physician in the treatment of hypertension of different origin.
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PMID:Current status of labetalol, the first alpha- and beta-blocking agent. 286 49

Intravenous nitroglycerin is frequently used in the treatment of acute myocardial infarction for its vasodilating effect on lowering both preload and afterload and in the control of ischemic heart pain. The end point for doses of nitroglycerin infusion is either relief of persistent or recurrent angina or controlling congestive heart failure by lowering left ventricular end diastolic pressure and volume. Nitroglycerin accomplishes these end points primarily through its venodilating property. Intolerable headaches or symptomatic hypotension may prevent achieving the clinical end point. Nevertheless, high doses of intravenous nitroglycerin may need to be administered to achieve a desired hemodynamic and therapeutic effect. Changes in mental status, i.e., lethargy and confusion, should be a warning sign of possible ethanol intoxication. An alcohol blood level verifies the clinical impression and gradually withdrawing the intravenous nitroglycerin is all that is necessary to effect a total recovery from this reaction.
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PMID:An unusual complication of intravenous nitroglycerin. 309 6

Nitrate usage worldwide is on the increase as the indications for therapy expand. Present indications for nitrate therapy include chronic stable angina pectoris, unstable angina pectoris, complications of acute myocardial infarction, and 'unloading' therapy for acute and chronic congestive heart failure. Nitrates are also being used in the operating suite by anaesthesiologists to control systolic blood pressure during various surgical procedures. New nitrate delivery systems have recently become available which provide considerable dosing flexibility, further increasing the interest in this group of compounds. The dominant action of nitrates is a direct effect on vascular smooth muscle, producing vasodilation of the veins and arteries. These drugs decrease myocardial work by lowering systolic blood pressure, systemic vascular resistance, and reducing intracardiac dimensions. In addition, nitrates have a potent effect on cardiac preload as a result of systemic venodilatation. There is also some evidence that nitrates exert direct effects on the coronary circulation (vasodilatation of coronary arteries and coronary collateral vessels, and direct atherosclerotic stenosis dilatation). These actions may play a role in relieving myocardial ischaemia. Adverse sequelae of nitrate therapy are well known and serious adverse reactions are uncommon. Headache and dizziness are the most frequent side effects. Nitrate tolerance is a definite problem - present evidence indicates that long acting formulations, high doses, or frequent dosing regimens are particularly likely to induce vascular tolerance to nitrates. Consequently, provision of a nitrate-free interval has taken on increasing significance as a strategy to avoid tolerance. Nitrate delivery systems are numerous. Although availability varies from country to country, in most countries there are a wide variety of formulations of glyceryl trinitrate (nitroglycerin) available, including sublingual and oral tablets, oral spray, topical ointment as well as discs or patches for transdermal administration, a transmucosal tablet and an intravenous formulation. Similar formulations of isosorbide dinitrate, except buccal tablets, are available in some countries. Isosorbide 5-mononitrate, a potent metabolite of isosorbide dinitrate, is achieving increasing popularity as an antianginal drug. Optimum nitrate therapy requires a good understanding of the properties of the various formulations, particularly onset and duration of action and propensity to induce tolerance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glyceryl trinitrate (nitroglycerin) and the organic nitrates. Choosing the method of administration. 311 8

The recently introduced preparation of intravenous glyceryl trinitrate (nitroglycerin) provides a rapid steady therapeutic blood concentration of nitrates during continuous infusion. Intravenous glyceryl trinitrate causes venodilation at low doses, but at higher doses dilates both arteries and veins. Its principal haemodynamic effects at therapeutic dosages include a decrease in blood pressure in preload (left ventricular filling pressure) and in determinants of afterload, and a decrease in myocardial oxygen demand. Human pharmacokinetic data are few and difficult to interpret due to wide interstudy and interindividual variation. There is no close correlation between infusion rate, blood concentration and haemodynamic effects. The nature of the patient population treated with intravenous glyceryl trinitrate has largely precluded the use of a placebo, but in open trials the drug has been used successfully in the treatment of unstable angina, left ventricular failure accompanying acute myocardial infarction and in the control of hypertension associated with cardiac surgery at dosages titrated to achieve a specific end-point. Favourable haemodynamic responses have been achieved in very short term studies in congestive heart failure, and preliminary studies suggest that institution of intravenous glyceryl trinitrate early after acute myocardial infarction may limit ischaemic damage. However, use of the drug in acute myocardial infarction remains controversial. Intravenous glyceryl trinitrate is generally well tolerated, although hypotension and headache occur occasionally, and sinus tachycardia and bradycardia less frequently. Careful titration of dosage is required (beginning at 5 micrograms/min), and if the infusion sets contain polyvinylchloride, the delivered dose is lower than that calculated, because of adsorption of glyceryl trinitrate onto the plastic tubing.
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PMID:Intravenous glyceryl trinitrate (nitroglycerin). A review of its pharmacological properties and therapeutic efficacy. 642 Jan 39


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