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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

Migraine is a common disorder with a prevalence of 9-10% in Hungary. Migraine can be accompanied by hypertension and/or ischemic heart disease sometimes in younger patients, but more frequently in the elderly, which is important for therapeutical considerations. The article reviews the literature with special focus on hypertension and coronary heart disease. In the second part, the authors summarize their experiences on headache patients.
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PMID:[Treatment of migraine in patients with hypertension and ischemic heart disease]. 1212 40

Elevated blood pressure is a risk factor for a variety of cardiovascular disorders, including coronary heart disease, peripheral vascular disease, cardiac failure and cerebrovascular disease. The prevailing view is that an elevated systolic rather than diastolic blood pressure is the major contributor in mortality and morbidity attributed to cardiovascular disorders. Isolated high systolic blood pressure, especially in the elderly, is a major risk factor and should undoubtedly be a target for drug treatment. In the general population, systolic and diastolic blood pressure are highly correlated, and thus it is difficult to dissociate the effects of these two components of the blood pressure and specifically ascribe cardiovascular risk factors to just elevated systolic blood pressure. Therefore, the goal in therapy of an individual with hypertension must be to reduce elevated systolic and diastolic blood pressure in order to reduce mortality and morbidity. ACE and neutral peptidase inhibitors are a new class of drugs that may be beneficial in the treatment of patients with hypertension and heart failure. They may also be useful in the treatment of diabetic patients with hypertension and/or heart failure. Drugs of this class are dual inhibitors of ACE and neutral endopeptidase, and are capable of affecting vascular tone and fluid balance. They are capable of producing vasodilatation by virtue of inhibiting the production of angiotensin II, degradation of natriuretic peptides and bradykinin. They also appear to promote natriuresis and diuresis by amplifying the actions of natriuretic peptidase and reducing aldosterone effects. In addition, they should also attenuate trophogenic actions of the renin angiotensin system and the sympathetic nervous system. Omapatrilat is one drug that appears to be at the advanced stages of clinical development. This drug has been shown to be quite effective in the treatment of hypertension. Evidence also seems to indicate that treatment with omapatrilat results in a higher tendency towards preventing death and worsening heart failure when compared with treatment with a pure ACE inhibitor in patients with advanced heart failure. Overall safety with omapatrilat appears to be good, but like other ACE inhibitors the incidence of cough is higher when compared with placebo. Other common adverse effects noted are headaches, facial flushing/warm sensation, dizziness, nausea and dyspnoea. Of greater concern is the occurrence of angio-oedema, the true incidence of which remains to be fully established as part of the published medical literature.
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PMID:Dual ACE and neutral endopeptidase inhibitors: novel therapy for patients with cardiovascular disorders. 1501 94

Normal ageing is associated with a decline in spontaneous growth hormone (GH) secretion, and although elderly hypopituitary adults demonstrate an increase in total and central fat compared with age-matched controls and are distinguishable from control subjects in terms of GH responsiveness on dynamic testing, there are few data available on the response to GH replacement in older subjects. We have studied the baseline characteristics of 295 patients (173 males and 122 females) aged >65 years of age who began GH replacement therapy at the time of entry into the KIMS program (Pfizer International Metabolic Database) and the effects of GH replacement in 125 patients who completed at least 12 months of GH replacement therapy. Data were compared with those of 2469 (1249 males and 1220 females) patients aged <65 years with adult-onset GH deficiency (GHD). The patients were selected using strict criteria in accordance with the recommendations from the Growth Hormone Research Society. There was a higher proportion of pituitary adenoma relative to craniopharyngioma in the older age group (P<0.001), but there was no difference between groups in the degree of hypopituitarism (number of additional hormone deficiencies). Blood pressure, cholesterol and low-density lipoprotein (LDL) cholesterol levels were positively correlated with age, and older patients had a predictably higher prevalence of diabetes mellitus, coronary heart disease, stroke and history of hypertension. Quality of life (Assessment of Growth Hormone Deficiency in Adults (AGHDA) score) was impaired in both groups before the start of GH therapy. GH replacement doses were lower in older patients with GHD as compared with patients <65 years old. After 12 months of GH replacement, significant improvements were evident in waist circumference, waist/hip ratio, lean body mass, diastolic blood pressure, total and LDL cholesterol levels and AGHDA scores in patients aged <65 years. Similar significant reductions were evidenced in patients >65 years old compared with those observed in younger patients. The total number of adverse events was similar in younger and older patients with GHD. However, younger patients had more fluid retention-related adverse events such as headache, oedema and arthralgia; whereas, older patients with GHD had more adverse events related to glucose metabolism, cardiovascular events and neoplasms. These data indicate a positive benefit from GH replacement in older patients with hypopituitarism - particularly in relation to quality of life - using a lower dose of GH for replacement and with appropriate age-related safety controls.
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PMID:Aspects of growth hormone deficiency and replacement in elderly hypopituitary adults. 1513 78

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.
Headache 2004 May
PMID:Are migraine and coronary heart disease associated? An epidemiologic review. 1514 88

Identifying the patient for whom triptans are contraindicated because of recognized, diagnosed cardiovascular disease is relatively straightforward. Determining whether a patient with potential unrecognized cardiovascular disease is an appropriate candidate for triptan therapy, however, constitutes a difficult challenge, especially in the absence of a framework for workup of patients. This article discusses the pathophysiology of coronary heart disease and issues involved in assessing cardiovascular risk, and it attempts to provide a framework for cardiovascular risk assessment that can be applied to decisions for prescribing triptans. Current guidelines for cardiovascular risk assessment allow stratification of patients to low, intermediate, or high risk of coronary heart disease events. This framework for risk assessment can be applied to decisions for prescribing triptans. Cardiovascular risk-assessment algorithms discussed elsewhere in this supplement suggest that patients at low risk (1 or no risk factors) of coronary heart disease can be prescribed triptans without the need for a more intensive cardiovascular evaluation. Conversely, patients with established coronary heart disease or coronary heart disease risk equivalents should not be prescribed triptans according to the current prescribing recommendations. Patients at intermediate risk (2 or more risk factors) of coronary heart disease require cardiovascular evaluation before triptans can be prescribed. Current understanding suggests that the risk of future acute coronary events is a function of the absolute number of vulnerable plaques present, a variable that cannot be accurately determined using available technology or risk-prediction models. Cardiovascular risk-assessment guidelines should be evaluated in the context of this limitation.
Headache 2004 May
PMID:Cardiovascular risk assessment and triptans. 1514 91

At altitudes higher than the threshold altitude of 2,500 m, high-altitude diseases may occur, usually after a delay of 6 to 12 hours. Apart from the headache associated with acute mountain sickness, life-threatening cerebral edema may develop. High-altitude pulmonary edema is a non-cardiac edema that often precedes acute mountain sickness. The most important preventive measure is a slow ascent. In the case of mountain sickness a prophylactic effect can be achieved with acetazolamide or dexamethasone possible, while for high-altitude pulmonary edema, nifedipine is the first-choice drug. Immediate descent and the administration of oxygen are always indicated. Patients with a high-altitude risk are those with cardiac or pulmonary disease. Nevertheless, it is still possible for patients with coronary heart disease, hypertension or bronchial asthma to attain to high altitudes. In contrast, patients with COPD, interstitial pulmonary disease or pulmonary hypertension are at appreciably greater risk.
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PMID:[Visiting high altitudes--healthy persons and patients with risk diseases]. 1534 35

Anti-phosphatidylethanolamine antibodies (aPE) belong to the group of anti-phospholipid antibodies (aPL) and are directed against neutral phospholipid, connected with co-factor protein, while cardiolipin antibodies (aKL) are directed against negative phospholipid. The paper presents a study of prevalence and clinical significance of IgG aPE in 28 patients (22 women and 6 men, mean age 47.6 +/- 11.6 years) with Sneddon's syndrome (SS), which consists in cerebrovascular disturbances and extensive livedo reticularis. IgG aPE were detected by immune-enzyme assay. The upper normal limit, calculated as mean + 3SD after studying 19 healthy donors, was 0.303 optic density units. aPE were found in 15 (54%), aKL and/or lupus anticoagulant (LA)--in 6 (21%) patients with SS. aPE were found in 10 (46%) out of 22 aKL- and LA-negative patients. Among the aPE-positive patients there was a higher incidence of cortic dementia (53% vs. 8%, p = 0.02), the widening of cortical sulci, detected by means of computed tomography and magnetic resonance imaging (73% vs. 31%, p = 0.05), and mild renal syndrome (73% vs. 16%, p = 0.03). Besides, they displayed a higher rate of headaches (87% vs. 62%), chorea (33% vs. 8%), epilepsy (27% vs. 8%), non-carrying of pregnancy (91% vs. 50%), peripheral venous thrombosis (27% vs. 15%), coronary heart disease (47% vs. 31%), cardiac valvular thickening, detected by means of EchoCG (93% vs. 69%), arterial hypertension (87% vs. 54%), thrombocytopenia (20% vs. 0), anemia (40% vs. 15%); however, the difference was not significant. The results show that aPE detection, performed in addition to detection of classic immunological antiphospholipid syndrome markers (aKL and LA), increases the portion of aPE-positive patients with SS by 33%. aPE are often (in 46% of cases) found in aKL- and LA-negative patients with SS. aPE is likely to be the most significant factor of thrombosis in small arteries of the brain cortex and kidneys, which could explain their association with dementia and renal syndrome.
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PMID:[Anti-phosphatidylethanolamine antibodies in patients with Sneddon's syndrome]. 1598 83

Information on the safety of mobilization and collection of peripheral blood progenitor cells (PBPC) in patients with advanced coronary heart disease (CHD) is limited. We report herein our early experience with patients participating in a Phase I trial of injection of autologous CD 34(+) cells into threatened, ischemic myocardium for neovascularization and symptom relief in patients with chronic refractory myocardial ischemia. All patients had advanced inoperable CHD despite the best medical therapy. Granulocyte colony stimulating factor (G-CSF, 5 microg/kg/day) was administered subcutaneously for 5 days for mobilization of CD34(+) cells into the peripheral blood. PBPCs were collected in the outpatient apheresis suite on day 5. Nine patients from our institution were evaluable. Adverse effects of mobilization included: increase in frequency and/or intensity of angina in 8 patients (88.8%); bone pain in 7 patients (77.7%); headaches in 4 patients (44.4%); 2 patients (22%) were hospitalized. Collection phase toxicities included: tingling in 5 patients (55.5%) and angina in 3 patients (33%). All procedures were completed without new myocardial infarction, congestive heart failure, or death. The median peripheral blood CD34(+) cell count on day 5 of G-CSF was 21 cells/microl (range 10-40 cells/microl). A median of 1.65 x 10(6) CD34(+) cells/kg (range: 0.13-3.0 x 10(6)/kg) were harvested. We conclude that mobilization and collection of PBPC in patients with advanced CHD can be safely performed as an outpatient procedure. Apheresis professionals should be aware of the intensity and frequency of angina in this patient population.
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PMID:Safety and efficacy of peripheral blood progenitor cell mobilization and collection in patients with advanced coronary heart disease. 1634 93

A recent population-based prospective study reported that in women, migraine with aura (MA), but not migraine without aura (MoA), was associated with increased risk of coronary heart disease events (CHD). We sought to confirm this association in an Australian population-based cohort of older men and women (n = 2331, aged 49-97 years). We defined MA and MoA from face-to-face interview using International Headache Society criteria. Over a mean 6-year follow-up, 30 women (2.8%) and 30 men (4.4%) without any prior CHD history died from CHD-related causes. In women, a history of MA was associated with a non-significant twofold higher risk of CHD death (age-adjusted relative risk 2.2, 95% confidence interval 0.8, 5.8, P = 0.11), which remained similar after adjustment for cardiovascular risk factors. There were no CHD deaths in men with a history of migraine. Our findings support reports that in women, MA, but not MoA, may be associated with increased risk of CHD.
Cephalalgia 2007 Apr
PMID:Migraine and coronary heart disease mortality: a prospective cohort study. 1734 6


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