Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with a giant cell carcinoma of the bronchus presented with headache and flushing attacks and a blood eosinophilia. He developed a right bundle branch block and later congestive cardiac failure. At post mortem he was found to have the appearance of Loeffler's endocarditis. A tentative mechanism for these events is proposed.
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PMID:Bronchial carcinoma with eosinophilia and cardiomegaly. 12 74

Hypertensive patients, particularly the elderly, may often suffer from other diseases. Therefore, antihypertensive compounds should not negatively affect such disorders. Felodipine is a calcium antagonist that has potentially beneficial effects in angina pectoris and congestive heart failure. Further, it does not adversely affect lung function in asthmatic patients or glucose tolerance in patients with diabetes. Preliminary investigations also indicate that felodipine has no negative influence on plasma lipid levels. Although felodipine seems to be safe in most patients, treatment with felodipine should at present be avoided in pregnant women, since digital anomalies have been observed in rabbit fetuses. The adverse effects seen during treatment with felodipine are usually mild and transient and generally related to the vasodilatory action of the drug, the most common being ankle edema, headache, flushing, dizziness, and palpitations. The only significant drug interactions with felodipine occur with inducers and inhibitors of the cytochrome P-450 system, which is responsible for the metabolism of felodipine.
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PMID:The safety of felodipine. 169 36

Felodipine, a dihydropyridine calcium-channel antagonist, significantly reduces systolic and diastolic blood pressure (BP) in patients with hypertension and has been associated with beneficial hemodynamic effects in patients with chronic stable angina pectoris or congestive heart failure (CHF). In hypertensive patients, felodipine does not appear to significantly affect glomerular filtration rate, creatinine clearance, glucose tolerance, or plasma lipoprotein concentrations. Studies comparing felodipine with other agents as monotherapy in mild to moderate hypertension have demonstrated felodipine to be at least as efficacious as hydrochlorothiazide (HCTZ) and HCTZ plus amiloride hydrochloride in combination. Comparisons of felodipine with other agents as adjuncts to beta-blocker or diuretic therapy have shown felodipine to be at least as effective as HCTZ, propranolol hydrochloride, prazosin hydrochloride, and nifedipine. Evaluations of patients with chronic stable angina are limited, and additional studies are needed before felodipine can be recommended for the routine management of angina pectoris. Similarly, additional studies are essential to delineate the role of felodipine, if any, in the management of CHF. In the management of hypertension, felodipine 5-40 mg/d significantly reduces systolic and diastolic BP. Although some patients may be controlled throughout the entire dosing interval when felodipine is administered bid, many patients will require more frequent dosing to obtain adequate BP control. Adverse effects associated with felodipine are similar to those of other dihydropyridine calcium-channel antagonists and include peripheral edema, headache, dizziness, flushing, and fatigue. A potentially clinically important drug interaction was observed when felodipine was administered concomitantly with theophylline aminopropanol; significant decreases in theophylline concentrations were noted. In summary, felodipine appears to be safe and effective for the management of hypertension when used alone or in combination with other antihypertensive agents. The efficacy of felodipine in the management of chronic stable angina pectoris and CHF requires further investigation.
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PMID:Felodipine: a new dihydropyridine calcium-channel antagonist. 176 37

3-Deazaguanine (Dezaguanine), a purine antimetabolite, was evaluated in a phase I trial in 42 patients with advanced solid tumors. Dezaguanine was given as a weekly intravenous infusion for three consecutive weeks of a four-week cycle. The dose ranged from 30 to 2000 mg/m2; no consistent dose-limiting hematologic or gastrointestinal toxicity was observed. Some patients reported brief episodes of burning at the infusion site or transient facial flushing immediately following the administration of dezaguanine. Three patients experienced cardiac toxicity. Two patients, at doses of 1130 and 2000 mg/m2 respectively, developed congestive heart failure. In one case the heart failure was fatal; the second patient recovered within 8 weeks. The third patient had a progressive fall in left ventricular ejection fraction but did not develop clinical evidence of heart failure before his death from progressive cancer two months later. Postmortem cardiac pathology in the two patients who died early following therapy revealed nonspecific interstitial fibrosis without inflammatory cell infiltrates. The myocardium of the third patient, who died 20 months after receiving dezaguanine, was normal. Electron microscopic analysis of myocardium from the first patient did not show myofibrillar loss or mitochondrial disorganization characteristic of anthracycline cardiomyopathy. Due to the probable cardiotoxicity of dezaguanine in this study and the lack of objective antitumor response, further development of this agent has been discontinued.
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PMID:3-Deazaguanine: report of a phase I trial and drug-related cardiac toxicity. 208 70

Throughout the developed world, populations are growing older. Blood pressure, especially systolic blood pressure, increases with aging, and this increase leads to increased risks of cardiovascular morbidity and mortality. Clinical trials demonstrate that treatment of hypertension in the elderly reduces overall cardiovascular mortality, cardiac mortality, nonfatal cardiovascular events, congestive heart failure, progression to severe hypertension, and strokes. Drug treatment has been well tolerated, but diuretic therapy has been known to increase plasma glucose, uric acid, and creatinine. Therapeutic trials of nonpharmacologic treatment may be indicated in those with mild elevation in blood pressure and no serious end organ disease. However, most people up to age 80 will require drug treatment. Many drugs are effective in the elderly, but, some like beta-blockers, may not be as effective as in younger patients. Controlled clinical trials demonstrate that nitrendipine, a calcium channel blocking drug, significantly reduced mean systolic and diastolic blood pressure in older hypertensive patients, (successfully controlling pressure in a high percentage) and was well tolerated. Drug effects persist for 12 h or more. The drug decreased the exercise-induced rise in the rate-pressure product. Although there is a temporary increase in heart rate, this returns to baseline after a short time. Side effects include headache, flushing, dizziness, edema, and palpitations. Therefore, nitrendipine offers a reasonable and useful alternative to many other drugs in the treatment of combined systolic and diastolic hypertension in the elderly.
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PMID:Epidemiologic aspects of elderly hypertensive patients and the results of treatment with nitrendipine. 248 68

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Nicardipine is an antagonist of calcium influx through the slow channel of the cell membrane and has been shown to be an effective and relatively well-tolerated treatment for stable effort angina and rest angina due to coronary artery spasm, and mild to moderate hypertension. Although its exact mechanism of action in these disease states has not been precisely defined, the potent coronary and peripheral arterial dilator properties of nicardipine, with concomitant improvements in oxygen supply/demand and reductions in systemic vascular resistance, are of major importance. Clinical studies have shown that nicardipine appears to be effective in the treatment of chronic stable exercise-induced angina pectoris and possibly in angina at rest due to coronary artery spasm. In the treatment of stable angina, nicardipine has proved to be equally as effective as nifedipine. However, haemodynamic and clinical studies indicate that nicardipine may have a further advantage of not depressing cardiac conduction or left ventricular function, even in patients with compromised cardiac pumping ability. Nicardipine also appears to be useful as initial monotherapy or in combination with other antihypertensive drugs when used in the treatment of mild to moderate hypertension, and may have some advantages over other vasodilators in this regard in that it may not be as frequently associated with fluid retention or weight gain as other similar drugs. In the treatment of hypertension nicardipine has been shown to be as effective as drugs such as hydrochlorothiazide, cyclopenthiazide, propranolol and verapamil in short term studies although confirmation of its long term usefulness in well-designed clinical trials is still required. Similarly, although the use of nicardipine in other disorders such as congestive heart failure and cerebrovascular disease has provided encouraging preliminary results, more studies are needed to clarify its place in their treatment. Side effects appear to be dose related and more frequent within the first few weeks of therapy. Most of these effects are minor and transient in nature and include headache, flushing and peripheral oedema. Thus, there is no doubt that nicardipine provides a suitable alternative to other drugs available for the treatment of angina and hypertension. However, further well-designed comparative clinical trials are needed to clarify its relative place in the long term management of these disorders.
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PMID:Nicardipine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy, in the treatment of angina pectoris, hypertension and related cardiovascular disorders. 329 16

Epoprostenol (prostacyclin) is a potent inhibitor of platelet aggregation and causes relaxation of vascular smooth muscle. These effects may be beneficial in patients with acute myocardial infarction. The effect of epoprostenol infusion in patients with acute myocardial infarction was evaluated in a randomised double blind study of 45 patients with evidence of myocardial infarction of less than 16 hours' duration. The patients were given a 72 hour infusion of epoprostenol (23) or placebo (22). The maximum dose was 5 ng/kg/min. The mean time to treatment was 8.3 hours (range 3.8-15.9 hours). The mean dose was 4.9 ng/kg/min. The patients were followed until day 30. No significant differences were found between the groups in mortality, development of congestive heart failure, cardiogenic shock, arrhythmias, recurrent chest pain, reinfarction, peak creatine kinase concentration, or the time taken to attain peak creatine kinase concentration. No significant difference in baseline ejection fraction was noted between groups, and no significant change in ejection fraction occurred within each group or between groups. The only significant side effect was the development of facial flushing in the epoprostenol group. In this pilot study epoprostenol was well tolerated by patients with acute myocardial infarction. No benefit from epoprostenol could be demonstrated at the dose range used when the drug was administered within 16 hours of the onset of symptoms.
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PMID:Epoprostenol sodium (prostacyclin) infusion in acute myocardial infarction. 353 63

We questioned 113 patients with subsequently diagnosed sustained ventricular tachycardia (VT) regarding the symptoms that prompted their seeking hospital treatment, eliciting the following: 15% of patients had lost consciousness, 15% had near syncope, 35% had mild lightheadedness and 35% had no cerebral symptoms. Patients with preexisting congestive heart failure or a VT rate of 200 beats per minute or greater more often lost consciousness. Other symptoms included palpitations in 57% of patients, chest pain in 27%, dyspnea in 25%, weakness in 6%, nausea or diaphoresis in 3% each and flushing in 2%. In approximately 50% of patients who had mild lightheadedness or no cerebral symptoms, their condition was incorrectly diagnosed as supraventricular tachycardia based on the absence of severe symptoms during the tachycardia. In some patients, VT may be associated with mild or atypical symptoms. The differentiation of supraventricular from ventricular tachycardia should be based on electrocardiographic criteria and should not be influenced by the nature or severity of a patient's symptoms. The severity of cerebral symptoms is at least partially related to the VT rate and a patient's underlying heart disease.
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PMID:Clinical symptoms in patients with sustained ventricular tachycardia. 399 9

Therapy to decrease the load in congestive heart failure is now classified as acute and chronic vasodilator therapy. In this symposium, we presented prostacyclin (PG I2) as an acute and prazosin as a chronic vasodilator. Their hemodynamic and clinical effectiveness were evaluated and their effect on the sympathetic nervous system was also studied. We studied the effect of intravenous prostacyclin infusion in doses of 22 +/- 11 ng/kg/min in nine patients with severe congestive heart failure refractory to digitalis and diuretic drugs. After prostacyclin infusion, mean pulmonary capillary wedge pressure decreased from 21.0 +/- 7.9 to 15.0 +/- 6.6 mmHg (p less than 0.001), mean arterial pressure from 98.9 +/- 12.8 to 76.2 +/- 7.0 mmHg (p less than 0.001), systemic vascular resistance from 2,574 +/- 384 to 1,368 +/- 283 dynes X sec X cm-5 (p less than 0.001), pulmonary vascular resistance from 1,008 +/- 451 to 443 +/- 135 dynes X sec X cm-5 (p less than 0.001) and pulmonary arteriolar resistance from 330 +/- 111 to 189 +/- 73 dynes X sec X cm-5 (p less than 0.001). The cardiac index increased from 2.0 +/- 0.37 to 3.2 +/- 0.59 l/min/m2 (p less than 0.001), and the stroke index from 27.6 +/- 8.69 to 42.0 +/- 0.62 ml/m2 (p less than 0.001). Moreover, prostacyclin therapy counteracted the sensation of coldness of the limbs and face, and patients felt warmth and mild flushing of the face. The effect of prazosin on the exercise duration time until dyspnea was evaluated by the treadmill test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostacyclin and prazosin in the treatment of congestive heart failure; with special reference to the sympathetic nervous system. 637 Dec 82


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