Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sildenafil, a selective inhibitor of phosphodiesterase type 5 (PDE5), is the first in a new class of orally effective treatments for erectile dysfunction. During sexual stimulation, the cavernous nerves release nitric oxide (NO), which induces cyclic guanosine monophosphate (cGMP) formation and smooth muscle relaxation in the corpus cavernosum. Sildenafil facilitates the erectile process during sexual stimulation by inhibiting PDE5 and thus blocking the breakdown of cGMP. Sildenafil alone can cause mean peak reductions in systolic/diastolic blood pressure of 10/7 mm Hg that are not dose related, whereas the heart rate is unchanged. Sildenafil and nitrates both increase cGMP levels in the systemic circulation but at different points along the NO-cGMP pathway. The combination is contraindicated because they synergistically potentiate vasodilation and may cause excessive reductions in blood pressure. Erectile dysfunction is a significant medical condition that shares numerous risk factors with ischemic heart disease, and hence a substantial overlap exists between these patient groups. From extensive clinical trials, the most commonly reported cardiovascular adverse events in patients treated with sildenafil were headache (16%), flushing (10%), and dizziness (2%). The incidences of hypotension, orthostatic hypotension, and syncope and the rate of discontinuation of treatment due to adverse events were <2% and were the same in patients taking sildenafil and those taking placebo. Retrospective analysis of the concomitant use of antihypertensive medications (beta blockers, alpha blockers, diuretics, angiotensin-converting enzyme inhibitors, and calcium antagonists) in patients taking sildenafil did not indicate an increase in the reports of adverse events or significant episodes of hypotension compared with patients treated with sildenafil alone. In clinical trials, the incidence of serious cardiovascular adverse events, including stroke and myocardial infarction, was the same for patients treated with sildenafil or placebo. Concurrent disease states, such as renal or hepatic impairment, or concomitant use of inhibitors of the cytochrome P450 isozyme CYP3A4 could increase systemic exposure to sildenafil. Since the US market launch in April 1998, monitoring of spontaneous adverse event reports in association with sildenafil has demonstrated a pattern that is generally consistent with the experience observed during clinical development, with the exception of infrequent reports of priapism. In conclusion, extensive clinical testing has shown that overall treatment with sildenafil for up to 1 year is well tolerated and is associated with a low incidence of adverse events that result in discontinuation of treatment in <3% of patients.
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PMID:Overall cardiovascular profile of sildenafil citrate. 1007 41

Anxiety appears to be a strong risk factor for ischemic heart disease (IHD) and specifically fatal IHD. However, no randomly assigned, controlled, clinical trial targeting anxiety yet exists demonstrating an impact on objective cardiac outcomes. Situational anxiety is frequent in cardiac populations and can diminish quality-of-life by increasing symptoms/disability and result in unnecessary medical system utilization. "Noncardiac" chest pain is common both in patients with objective coronary disease and in patients whose cardiac workup is negative. Both presentations of chest pain respond to cognitive/behavioral therapy, and imipramine has been found to be effective for chest pain unaccompanied by coronary disease. Because anxiety-like symptoms overlap with symptoms of IHD (eg, chest pain, dyspnea, dizziness, palpitations) and can be caused by organic factors, the diagnosis and treatment of anxiety in these populations require special considerations.
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PMID:Cognitive/behavioral therapy of anxiety in the medically ill: cardiac settings. 1037 57

In every year since 1984, cardiovascular disease has claimed the lives of more females than males. More than 450,000 women succumb to heart disease annually, and 250,000 die of coronary artery disease. Despite the proportions, most women believe they will die of breast cancer. The perception that heart disease is a man's disease and that women are more likely to die of breast cancer is alarming. Although women develop heart disease about 10 years later than men, they are likely to fare worse after a heart attack. The poorer outcomes are due, in part, to the failure to identify heart attack symptoms. Approximately 35% of heart attacks in women are believed to go unnoticed or unreported. However, because of increased age, women are more likely to have co-morbid diseases such as diabetes and hypertension. In women, not only is "tightness" or discomfort in the chest a warning sign, but in addition, nausea and dizziness are common indicators of myocardial ischemia. Other symptoms include breathlessness, perspiration, a sensation of fluttering in the heart, and fullness in the chest. In comparison to men, women are less likely to undergo tertiary care interventions such as cardiac catheterization, angioplasty, thrombolytic therapy, and bypass surgery; to participate in cardiac rehabilitation; and to return to work full-time after myocardial infarction. In the past, most research about treatments for heart disease focused on men, and gender differences have been ignored. Recent studies are enrolling enough women to test if there are differences between men and women in outcomes. One of the major areas of research relates to estrogen and hormonal replacement therapy to reduce the relative risk of heart attack and stroke. The Women's Health Initiative is a major NIH-sponsored trial that addresses the issue of primary prevention of cardiac disease by hormonal replacement therapy. The results will be available in 2004. The Heart Estrogen/Progestin Replacement Study (HERS), disappointingly, did not show a significant reduction of coronary events in women taking hormonal replacement therapy, nor did the Estrogen Replacement and Atherosclerosis (ERA) trial of 309 postmenopausal women who underwent coronary angiography. New insight into the role of vitamins, phytoestrogens and other natural sources, and selective estrogen receptor modulators may provide other options for management. Until then, modification of risk factors and healthy life style choices are recommended for reducing the risk of cardiac disease. In fact, the key to a healthy heart in the year 2000 appears closely tied to life style choices. Prevention of disease is the key, and current recommendations are simply to stop smoking, or do not start; treat and control blood pressure >140/90 mm Hg; manage elevated lipids by diet, exercise, and cholesterol-lowering medications (if necessary); treat diabetes; lose weight so that BMI is <25; walk for 20-30 minutes at least three times a week; and take an aspirin tablet daily.
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PMID:Heart disease in women. 1114 May 44

Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable clinical interest, severe neurological manifestations may occur days or weeks after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
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PMID:Carbon monoxide poisoning: systemic manifestations and complications. 1141 Jun 84

Association of ischemic heart disease (IHD) with vascular affections of the brain is the cardiocerebrovascular syndrome having common pathogenetic mechanisms of formation in the structure of cardiovascular pathology. Some specificities were studied of the clinical course of IHD concomitant with hypertensive dyscirculatory encephalopathy (HDE) in 35 patients (main group), with 25 IHD controls free from manifestations of neurological symptomatology. In IHD HDE patients the anginous syndrome is characterized by a lesser dependency on time in each period of 24 hours and physical load and greater dependency on arterial pressure, meteofactors, it is often accompanied by cephalgia appearing with the intake of antianginal drugs, dizziness, memory, sleep disturbances. The main group patients demonstrated elevated levels of LPO products, those of lipid metabolism, and the AO system tension.
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PMID:[Characteristics of the clinical course of ischemic heart diseases in patients with hypertensive dyscirculatory encephalopathy]. 1145 23

A 71-year-old woman had hypertrophic cardiomyopathy associated with midventricular obstruction and an apical aneurysm in the left ventricle. She had had abnormal electrocardiograms for more than 30 years and for the past year had been suffering from occasional attacks of dizziness and low systemic blood pressure. Holter 24-h electrocardiographic monitoring revealed ventricular paroxysmal contractions (676/day) with nonsustained ventricular tachycardia. Doppler echocardiography revealed paradoxical jet flow from the apical aneurysm to the left ventricular outflow during early diastole. Magnetic resonance imaging depicted midventricular hypertrophy and a dyskinetic thin apical wall, which were confirmed by angiography. Coronary angiograms showed no narrowing of the major extramural coronary arteries, but there was compression of aberrant coronary arteries apparently feeding the hypertrophic portion of the left ventricular wall. Stress thallium-201 myocardial imaging showed a persistent severe defect in the left ventricular apex. A hemodynamic study revealed low cardiac output and an intraventricular pressure gradient (approximately 90 mmHg) between the left ventricular apical high-pressure chamber and the subaortic low-pressure chamber. The present case represents a rare combination of hypertrophic cardiomyopathy, midventricular obstruction, and an apical aneurysm in an elderly woman. Myocardial ischemia may have played an important role in the genesis of the apical aneurysm.
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PMID:Hypertrophic cardiomyopathy with midventricular obstruction and apical aneurysm: a case report. 1166 99

The long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram. It is associated with precipitation of a polymorphic ventricular tachycardia, torsade de pointes, which may cause sudden death. The syndrome is a disorder of cardiac repolarization caused by the alterations in the transmembrane potassium and sodium currents. Six genetic loci for the congenital forms of the syndrome have been identified; sporadic cases occur because of spontaneous mutations. Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. Clinical symptoms are the result of the precipitation of torsade de pointes and range from such minor symptoms as dizziness to syncope and sudden death. Short-term treatment is aimed at preventing the recurrences of torsade de pointes and includes intravenous magnesium and potassium administration, temporary cardiac pacing, and correction of electrolyte imbalance; rarely, intravenous isoproterenol is indicated. Long-term management includes use of beta-blockers, permanent pacemaker placement, and cardioverter-defibrillator implantation. Asymptomatic patients are treated if under the age of 40 years at the time of diagnosis.
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PMID:Clinical and therapeutic aspects of congenital and acquired long QT syndrome. 1181 8

The prevalence and incidence of atrial fibrillation increase with age. Atrial fibrillation is associated with a higher incidence of coronary events, stroke, and mortality than sinus rhythm. A fast ventricular rate associated with atrial fibrillation may cause tachycardia-related cardiomyopathy. Management of atrial fibrillation includes treatment of underlying causes and precipitating factors. Immediate direct-current cardioversion should be performed in persons with atrial fibrillation associated with acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta-blockers, verapamil, or diltiazem may be used to immediately slow a fast ventricular rate associated with atrial fibrillation. An oral beta-blocker, verapamil, or diltiazem should be given to persons with atrial fibrillation if a rapid ventricular rate occurs a rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening atrial fibrillation refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic atrial fibrillation in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal atrial fibrillation associated with the tachycardia-bradycardia syndrome should be managed with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with atrial fibrillation in whom symptoms such as dizziness or syncope associated with non-drug-induced ventricular pauses longer than 3 seconds develop. Elective direct-current cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than medical cardioversion in converting atrial fibrillation to sinus rhythm. Unless transesophageal echocardiography shows no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of atrial fibrillation and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy of ventricular rate control plus warfarin rather than to maintain sinus rhythm with antiarrhythmic drugs, especially in older patients. Digoxin should not be used in persons with paroxysmal atrial fibrillation. Patients with chronic or paroxysmal atrial fibrillation who are at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio (INR) of 2.0 to 3.0. Persons with atrial fibrillation who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg aspirin daily.
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PMID:Atrial fibrillation. 1197 40

Atrial fibrillation (AF) is associated with a higher incidence of mortality, stroke, and coronary events than is sinus rhythm. AF with a rapid ventricular rate may cause a tachycardia-related cardiomyopathy. Immediate direct-current (DC) cardioversion should be performed in patients with AF and acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta blockers, verapamil, or diltiazem may be given to slow immediately a very rapid ventricular rate in AF. An oral beta blocker, verapamil, or diltiazem should be used in persons with AF if a fast ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected patients with symptomatic life-threatening AF refractory to other drugs. Nondrug therapies should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drugs. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in patients with AF and with symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds that are not drug-induced. Elective DC cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than does medical cardioversion in converting AF to sinus rhythm. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective DC or drug cardioversion of AF and should be continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer, especially in older persons, ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiarrhythmic drugs. Digoxin should not be used to treat patients with paroxysmal AF. Patients with chronic or paroxysmal AF at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Patients with AF at low risk for stroke or with contraindications to warfarin should receive 325 mg of aspirin daily.
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PMID:Management of the older person with atrial fibrillation. 1202 64

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of almotriptan are reviewed. Migraine is a common disorder with a serious impact on quality of life. Newer serotonin-receptor agonists have been developed with the aim of improving pharmacokinetic characteristics. Almotriptan, a selective agonist of serotonin receptors 1B and 1D, carries FDA-approved labeling for use in the management of migraine with or without aura in adults. The efficacy and receptor affinity resemble those of sumatriptan, but almotriptan has a more favorable pharmacokinetic profile. It has a rapid onset of action, an oral bioavailability of 70-80%, and a longer half-life than sumatriptan. In clinical trials, almotriptan has been significantly more effective than placebo and as effective as sumatriptan. However, it has been associated with better tolerability and greater patient satisfaction. In clinical trials, the most commonly reported adverse effects were nausea, dry mouth, dizziness, somnolence, fatigue, vomiting, and paresthesia. Almotriptan is contraindicated in patients with known ischemic heart disease, coronary vasospasm, and other significant cardiovascular disorders. Almotriptan has a lower acquisition cost than other triptans and possibly lower overall health care costs because of a lower frequency of cardiovascular adverse effects. The recommended dose of almotriptan is one 6.25- or 12.5-mg tablet given at the onset of symptoms. Almotriptan is effective for the management of migraine and offers the potential for fewer adverse effects than other agents in its class.
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PMID:Efficacy and safety of almotriptan malate for migraine. 1245 2


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