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)

The calcium ion plays a decisive role in the effect and regulation of several cellular processes. The heart muscle cells, pacemaker and channel systems and vascular smooth muscle are functionally dependent on Ca2+ influx mainly via potential sensitive L (long lasting)-Ca(2+)-channels, which are blocked by Ca(2+)-channel blockers, a group of organic substances binding to specific sites at the Ca2+ channels. The Ca2+ channel blockers are now well established in the treatment of angina pectoris, arterial hypertension, supraventricular arrhythmia and subarachnoidal haemorrhage. On the basis of chemistry and pharmacodynamics the Ca2+ channel blockers are divided into three groups, with verapamil, nifedipine and diltiazem representing 1. generation derivatives and prototypes for groups I, II and III, respectively. All Ca2+ channel blockers act as vasodilators, while group I (verapamil) and to a lesser degree group III (diltiazem) also have antiarrhythmic effects. All Ca(2+)-channel blockers are contraindicated in hypotension. In cases of pronounced bradycardia, sinoatrial and atriventricular block Ca2+ channel blockers with antiarrhythmic effects are contraindicated and must be used with care in combination with beta-blocker treatment and in heart failure. Headache, flushing, reflex tachycardia, nausea, obstipation and ankle oedema are the most important secondary effects. With respect to pharmacodynamics the newly marketed 2. generation derivatives do not differ essentially from the 1. generation derivatives. The clinical potential of the Ca2+ channel blockers is not fully explored and the possibilities for extending their indications are still to be elucidated.
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PMID:[Calcium channel blockers (calcium antagonists). Background, effects and use]. 764 18

The efficacy and safety of cilazapril in chronic heart failure have been extensively investigated in an international clinical program in patients with underlying chronic heart failure with ischemic heart disease or dilated cardiomyopathy. Cilazapril in single doses of 1.25-5 mg produced a significant dose-dependent reduction in pulmonary capillary wedge pressure and systemic vascular resistance and a significant increase in cardiac index. In placebo-controlled studies, 1-5 mg of cilazapril once daily for 12 weeks prolonged predose exercise test duration and improved New York Heart Association classification status and signs and symptoms of chronic heart failure, including paroxysmal nocturnal dyspnea. Up to 86% of patients receiving these dosages had improvement, with only 12% of patients requiring the higher dose, 5 mg. These data indicate that cilazapril is effective when administered once daily to patients with chronic heart failure receiving concomitant therapy with digitalis and/or a diuretic. The safety of cilazapril in patients with chronic heart failure has been evaluated in 1,163 patients administered from 0.5 to 15 mg once daily for treatment periods ranging from 1 day to 57 months. Cilazapril was administered to 500 patients for at least 6 months, 264 patients for at least 1 year, and 101 patients for at least 2 years. The most frequently occurring adverse events were dizziness, coughing, dyspnea, fatigue, angina pectoris, and headache. Cilazapril was equally well tolerated by young and elderly patients. Treatment was discontinued due to adverse events in 12.9% of patients, mainly as a result of coughing (1.7%) and dizziness (1%). Forty-four patients (3.8%) died during cilazapril therapy or during a period without treatment. Of these deaths, 93% were due to cardiac causes, especially rhythm disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart failure therapy with cilazapril: an overview. 770 63

This multicenter, open-label study provides the first assessment of the safety and acute hemodynamic effects of a short-term infusion of 15AU81, a chemically stable analog of prostacyclin, in patients with New York Heart Association class III or IV heart failure. Twelve patients underwent sequential dose escalation by increasing the rate of the infusion at 15-minute intervals until the drug was no longer tolerated. Patients then received a 90-minute infusion at their maximum tolerated dose. The infusion was then discontinued and the subjects were observed during a 90-minute washout segment. Serial hemodynamic measurements were made throughout the dose-ranging, maintenance, and washout segments. A significant decrease in systemic vascular resistance (1,935 +/- 774 vs 1,243 +/- 351 dynes.s.cm-5; p < 0.001) and pulmonary vascular resistance (395 +/- 335 vs 223 +/- 198 dynes.s.cm-5; p = 0.008) occurred from the infusion of vehicle to the maximum tolerated dose. During dose titration, there was a a significant increase in cardiac index (1.9 +/- 0.7 vs 2.6 +/- 0.6 liters/min/m2; p < 0.001) and a tendency for a mild reduction in pulmonary artery wedge pressure (18 +/- 7 vs 17 +/- 6; p = 0.055) for the 8 patients with values on vehicle and maximum tolerated dose. These hemodynamic changes persisted during the maintenance infusion and disappeared rapidly during the washout segment. The most common adverse event to limit dose-ranging was headache, which occurred at a mean maximum tolerated dose of 36 +/- 15 ng/kg/min. Administration of 15AU81 was associated with significant acute hemodynamic improvement in patients with severe heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute hemodynamic effects of the prostacyclin analog 15AU81 in severe congestive heart failure. 784 51

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

A case of aneurysm arising from the posterior communicating artery itself clipped by contralateral frontotemporal craniotomy (pterional approach) is presented. A 65-year-old female developed sudden severe headache and chest pain in January of 1993. Neurological examination on admission revealed consciousness disturbance such as stupor and nuchal stiffness. CT-scan showed marked subarachnoid hemorrhage. She also suffered from acute myocardial ischemia and cardiac failure. Cerebral angiograms after recovery from cardiac dysfunction demonstrated three saccular aneurysms arising from the dilated right posterior communicating artery itself, the junction of the left internal carotid artery and the posterior communicating artery, and the bifurcation of the left middle cerebral artery. The left IC-PC junction aneurysm was thought to be ruptured because of its size and contour, so left frontotemporal craniotomy was undertaken. By the left pterional approach, successful clipping of all three aneurysms involving the one arising from the contralateral posterior communicating artery was achieved. The aneurysm at the posterior communicating artery itself was found to arise from the non-branching site and to project inferiorly, thus the successful clipping through the prechiasmal cistern could be performed without compromising any small perforating arteries.
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PMID:[Clipping of aneurysm arising from the posterior communicating artery itself by contralateral craniotomy: a case report]. 801 76

A total of 4676 patients and 1759 patients were treated with lisinopril and nifedipine respectively in a post-marketing surveillance study conducted in general practice in the UK. Patients were followed up for 12 months. Most of the lisinopril patients had hypertension, but a small number (180) had heart failure. Most of the nifedipine patients had uncomplicated hypertension, but some (22.57%) had other cardiovascular disease with or without hypertension. Lisinopril and nifedipine were equally effective in reducing blood pressure. During the study, 1.5% of hypertensive patients assigned to lisinopril died compared with 1.8% of patients assigned to nifedipine, and 15.1% of lisinopril patients compared with 19.7% of patients in the nifedipine group withdrew because of adverse events. Cough, malaise and fatigue, nausea and vomiting were more frequent causes of withdrawal from lisinopril than nifedipine. Conversely, headaches, pallor and flushing, oedema and palpitations caused more frequent withdrawals from nifedipine. Anaemia was more often encountered on nifedipine treatment than on lisinopril. In hypertensive patients, the frequency of first-dose hypotension was similar on both treatments. Serious events occurred in 0.8% and 0.5% of patients given lisinopril and nifedipine respectively. Lisinopril was well tolerated by heart failure patients: 16 patients (8.88%) died and an incidence of 4.44% of serious adverse events was reported, a pattern to be anticipated in such patients; dizziness, giddiness, dyspnoea, cough, nausea and vomiting were the most frequent causes of withdrawal; the incidence of first-dose hypotension was low (2.22%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-marketing surveillance of lisinopril in general practice in the UK. 811 50

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that prolongs the action potential and refractoriness of cardiac tissue and has potent nonselective beta-blocking activity. Sotalol is well absorbed after oral administration. The pharmacokinetics of sotalol can be described by an open, linear, two-compartment model. The drug is eliminated primarily by the kidneys; mean elimination half-life is 12 hours. Sotalol has been found to be effective in controlling life-threatening ventricular arrhythmias, including sustained ventricular tachycardia, ventricular fibrillation, and premature ventricular complexes. Although sotalol has FDA-approved labeling for use in the treatment of ventricular arrhythmias only, it is also effective against a variety of supraventricular arrhythmias. Noncardiac adverse effects include fatigue, impotence, depression, headache, nausea, diarrhea, and increased triglyceride levels. Cardiovascular adverse effects include atrioventricular block, bradycardia, hypotension, exacerbation of heart failure, and polymorphic ventricular tachycardia. Overall, 11-21% of patients experience adverse effects; 6-18% of these patients have reactions serious enough to warrant the discontinuation of sotalol therapy. The initial dosage of oral sotalol hydrochloride in adults is 80 mg twice daily or 160 mg once daily; the dosage can be increased every three to four days in increments of 40-160 mg/day to a maximum of 480 mg/day. Sotalol is useful in the control of intractable, life-threatening ventricular arrhythmias, as well as a variety of supraventricular arrhythmias, in patients who do not respond to or are intolerant of more conventional antiarrhythmics.
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PMID:Sotalol: a new class III antiarrhythmic agent. 813 5

The efficacy of flosequinan 100 mg once daily was evaluated in 15 patients with severe congestive heart failure (New York Heart Association [NYHA] class II-IV) who had not responded adequately to digoxin and diuretics. Efficacy assessments using non-invasive techniques included exercise capacity, haemodynamics and left ventricular function. Determinations were made after 3 and 21 days' treatment, and compared with baseline. Flosequinan significantly increased exercise capacity by 27% after 3 days (+79 seconds, p = 0.015) and by 43% after 21 days (+123 seconds, p = 0.0007) and was accompanied by an increase in heart rate (+7.2 beats/min, p = 0.03; +9.1 beats/min, p = 0.03, respectively). Cardiac index and cardiac output were also significantly increased but only after 21 days' treatment (+0.3 l/min/m2, +16% and +0.5 l/min, +14%, respectively; both p = 0.008). Flosequinan was well tolerated, with headache being the most frequently reported adverse event and only 1 patient being withdrawn. One patient died but this was not unexpected in a group of patients with severe heart failure. Using non-invasive techniques this study demonstrated that in patients with severe chronic congestive heart failure, flosequinan increased exercise capacity and cardiac output, the latter being achieved mainly by an increase in heart rate.
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PMID:A non-invasive evaluation of flosequinan on haemodynamics and exercise capacity in chronic congestive heart failure. 822 97

Arteriovenous (AV) fistulas of cerebral and spinal arteries are characterized angiographically by an immediate AV transition without a capillary bed or "nidus" as occurs in AV malformations (AVM's). The clinical presentation, morphology, radiology, and treatment of 12 patients with cerebral AV fistulas and of 12 patients with spinal AV fistulas are reviewed. In the patients with cerebral lesions, headache and seizure disorders were the most common presentations followed by subarachnoid hemorrhage, cardiac failure, progressive neurological dysfunction, and incidental detection on prenatal ultrasound study. In patients with spinal AV fistulas, weakness and sensory disturbance in the lower extremities were the most frequent clinical presentations followed by back pain, disturbances of micturition, and grand mal seizure. The etiology of the symptom complex produced by AV fistulas in each of these locations differed, with venous hypertension being important in spinal cord lesions. Of the patients with cerebral lesions, nine had a single AV fistula, one had two fistulas, and two had multiple fistulas. An AVM was observed in five patients with fistulas (two large, three small). Nine patients exhibited extramedullary AV fistulas of the spine, of whom eight had a single fistula and one had three fistulas; three patients had intramedullary spinal AV fistulas. An arterial aneurysm was found in association with two fistulas, one cerebral and one spinal. Venous ectasias or varices, frequently exhibiting mural calcification, were observed to be prominent in all AV fistulas involving cerebral arteries and in two involving spinal arteries. The location and size of the venous complexes reflected the diameter of the fistula. In addition to conventional imaging techniques (cerebral angiography, computerized tomography, and magnetic resonance (MR) imaging), MR angiography was a helpful adjunct in the evaluation of fistulas. Treatment strategies employed for AV fistulas in both locations included open surgical and endovascular procedures, frequently used in combination. A satisfactory outcome was observed in all patients.
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PMID:Arteriovenous fistulas of the brain and the spinal cord. 827 Oct 12

We present a 81-year old male who developed dementia, gait disturbance and right hemiparesis. He was well until the age of 74 when he developed a hemorrhagic infarction in the right occipital region, which left him left homonymous hemianopsia. One year later he had one TIA attack consisting of dizziness, headache, and some clouding of consciousness. At that time, atrial fibrillation was found. At age 79, he was attacked by right hemiparesis. Cranial CT scans revealed a lesion consistent with a hemorrhagic infarct in the left middle cerebral artery territory. Two months prior to his final admission, he had a gradual onset of forgetfulness, labile affect, nocturnal agitation and hallucination which were followed by gait disturbance and urinary incontinence. On admission, he was alert but moderately demented. In addition he showed difficulty in repetition, limb kinetic and ideomotor apraxia of the left hand indicative of sympathetic apraxia, and constructional apraxia bilaterally. Granial nerves appeared intact except for left homonymous hemianopsia. His gait was wide-based and small stepped. No weakness or ataxia was noted. Deep reflexes were diminished on the left side. Plantar reflex was equivocally extensor of the left. Light touch and pain was slightly diminished on the right side. Cranial CT scans revealed a large low density area in the left fronto-temporo-parietal region. Also ventricular dilatation, diffuse low density change in the subcortical white matter, and diffuse cortical atrophy were seen. His clinical course was complicated by melena, anemia, pneumonia, cardiac failure and renal failure. He expired 2 months after his admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia]. 833 25


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