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)

The authors present a retrospective study of 46 consecutive patients aged from 70 to 79 years (mean 73.3 +/- 2.5 years) with suspected coronary artery disease who, being unfit for exercise tests, were explored by myocardial scintigraphy with thallium 201 after coronary dilatation with intravenous dipyridamole. The examination was well tolerated by 30 patients. Such classical side-effects as chest pain, malaise, dizziness, headache, flushing, vomiting and transient arrhythmia or repolarization disorders were recorded, but they were not more frequent than in younger subjects. However, the occurrence of severe hypotensive malaise relieved by theophylline in two cases and of angina in about one third of patients with myocardial ischaemia means that the procedure must be performed under close supervision. A fall in blood pressure (-11 mmHg on average) and a rise in heart rate (+8 beats/min on average) were usual. Post-scintigraphy follow-up of patients over a mean period of 11.1 +/- 6.2 months showed that a reversible defect of thallium 201 uptake, due to redistribution, is a highly selective indicator of patients who are particularly exposed to a cardiac accident in the short--or mid-term. Only one out of 26 patients without reversible ischaemia (4 p. 100) subsequently presented with a major coronary event (unstable angina). In contrast, in the group of 20 patients with reversible ischaemia three required early myocardial revascularization; furthermore, five serious accidents (29 p. 100) occurred among the 17 patients who were left under medical treatment, including two sudden deaths, two cases of unstable angina and one case of myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tolerance and prognostic value of Thallium 201 myocardial tomoscintigraphy with dipyridamole in the aged subject]. 314 28

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

Nicardipine is currently being evaluated in clinical trials as a treatment for angina and hypertension. Over 2,000 patients have received nicardipine, most at dosages of 20 to 40 mg 3 times daily. In 12 double-blind, parallel-group studies (4 of them placebo-controlled) the efficacy of nicardipine was evaluated in mild to moderate hypertension; supine systolic blood pressure was lowered by 10 to 15 mm Hg and supine diastolic blood pressure by 10 mm Hg. A clear dose response is present at dosages from 10 to 40 mg 3 times daily. Patients with angina were treated in 9 double-blind, crossover design studies: 4 of these were placebo-controlled; 3 were comparison studies with beta blockers; 2 were comparisons with nifedipine. Treadmill exercise tests were the major measure of efficacy. Results of these studies showed consistent, statistically significant improvement in exercise tolerance and time to onset of angina, and clinical improvement in patients with chronic stable angina. The effective dosages of nicardipine were 30 or 40 mg 3 times daily. A placebo-controlled study demonstrated remarkable efficacy in patients with vasospastic angina. No deaths or serious adverse reactions were attributed to nicardipine during clinical trials. The most common side effects reported were flushing, palpitations, headache and pedal edema. These appeared to be due to the drug's pharmacologic property of vasodilatation.
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PMID:An overview of the safety and efficacy of nicardipine in clinical trials. 330 Feb 39

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.
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PMID:Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications. 332 59

To assess the dosing equivalency and the early and late antianginal efficacy of a gastrointestinal therapeutic system for once-daily, continuous-release nifedipine (N-GITS), 10 patients with stable angina pectoris, who were previously receiving chronic treatment with nifedipine, completed a 12-week trial comparing N-GITS with standard nifedipine. All patients (nine men and one woman; mean age 54 +/- 2 [SEM] years) who were receiving standard nifedipine (mean dose 40 +/- 5 mg/24 hr) for more than 2 weeks (mean 8 +/- 2 months, range 2 to 36 months) were switched to an equivalent once-daily dose (39 +/- 5 mg/24 hr) of N-GITS. Standard nifedipine and N-GITS were compared by symptom-limited exercise treadmill tests with a baseline test (A) performed 3 hours after a standard dose of nifedipine. Exercise tests were also performed after 2 weeks of treatment with N-GITS 3 hours (B) and 24 hours (C) after the drug was given, and after 12 weeks of treatment with N-GITS, 24 hours after dosing (D). Results of exercise tests showed no significant difference in mean exercise time--(A) 422 +/- 25 vs (B) 426 +/- 36 vs (C) 438 +/- 35 vs (D) 487 +/- 37 seconds. Likewise, there was no significant mean difference in peak double product, resting heart rate, peak exercise heart rate, or resting or maximal systolic blood pressure for any of the exercise test points. Furthermore, five patients (50%) reported side effects with standard nifedipine (all vasodilator-flushing, dizziness, or both), which resolved after treatment with N-GITS (p +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative dosing and efficacy of continuous-release nifedipine versus standard nifedipine for angina pectoris: clinical response, exercise performance, and plasma nifedipine levels. 335 8

Although the exposure of human subjects to prostacyclin (PGI2) infusion has been broad, no systematic approaches have been made in order to investigate the dose-related side effects in patients with angina pectoris and coronary artery disease (CAD). We studied 25 patients with typical chest pain and overt CAD. All patients underwent a cycloergometer stress testing (25 W increments at 2-min intervals). PGI2 was infused in scalar doses up to 10 ng/kg/min. During the infusion 25 patients (100%) had facial flushing, 7 (28%) moderate headache and one (4%) had nausea. In addition, 4 patients experienced the typical chest pain and had significant (greater than or equal to 0.1 mV) ST segment depression at 8.10 ng/kg/min infusion rates. These patients had lower tolerance to exercise (6.7 +/- 1.7 vs. 8.8 +/- 1.9 min; p less than 0.05) and coronary artery lesions more severe than those observed in patients without drug-induced angina pectoris. Our data therefore indicate that PGI2 at therapeutic doses may induce myocardial ischemia in patients with angina pectoris, low tolerance to exercise and severe CAD. In patients with mild to moderate degree of CAD, PGI2 was found to be well tolerated. These findings suggest that patients with angina pectoris and low tolerance to exercise should be excluded from clinical studies directed at elucidating the effectiveness of PGI2 in cardiovascular disorders.
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PMID:Side effects of prostacyclin in patients with angina pectoris and coronary artery disease. 390 57

This study evaluated 1 year the efficacy of therapy with nicardipine in patients with chronic stable angina pectoris. Twenty-five male patients were entered. After a placebo run-in phase, the patients received nicardipine 30 mg, nicardipine 40 mg, and placebo, three times daily given in random, double-blind manner for 8 weeks. A double-blind, cross-over study comparing nicardipine with placebo was then undertaken. After 5 months of open treatment with nicardipine 90 or 120 mg day-1, patients received either placebo or nicardipine for 3 weeks, each followed by the alternative treatment for an additional 3 weeks and further open-label treatment with nicardipine for another 3-5 months. There were no significant changes in the PR, QRS or QT intervals, or in the QRS pattern during the short-term and long-term studies. There were no significant differences in mean heart rate after nicardipine compared with baseline. During treatment with nicardipine 120 mg day-1, patients reported significantly fewer anginal attacks compared with placebo, and nitroglycerin consumption also decreased. Nicardipine increased treadmill time, time to onset of angina, and time to one mm ST segment depression. These effects were maintained after 6 months of continued nicardipine therapy. Adverse effects were minor and well tolerated and included headache, dizziness, gastrointestinal upset, flushing paraesthesia and pedal oedema. Abrupt withdrawal of nicardipine at the end of the study resulted in a rapid return of the original symptoms but without further deterioration from the baseline measurements. Nicardipine was effective in the treatment of stable effort angina pectoris; this benefit was maintained for the entire year of treatment.
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PMID:Short- and long-term treatment of stable effort angina with nicardipine, a new calcium channel blocker: a double-blind, placebo-controlled, randomised, repeated cross-over study. 392 59

The safety, tolerability and efficacy of PN 200-110, a new calcium antagonist with minimal negative inotropic effects, were studied in twelve patients with stable angina pectoris and coronary artery disease. The study design was single-blind and placebo-controlled and increasing doses of the drug were used on consecutive days to investigate a dose response relationship. Eleven patients completed the trial. Response to the drug was evaluated using symptom limited cycle ergometric exercise. PN 200-110 in all three tested doses of 2.5 mg, 5.0 mg and 10.0 mg significantly increased the resting heart rate (p less than 0.02) and the exercise time to the onset of angina pectoris (p less than 0.02). Doses above 2.5 mg did not appear to improve the exercise parameters evaluated. Four patients had side effects probably due to PN 200-110 but these were mild and included dizziness, headache and flushing. There were no abnormal results from haematological and biochemical screening or from urine testing. We conclude that PN 220-110 can be given safely to patients with coronary artery disease without producing deleterious effects on blood pressure either at rest or during exercise.
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PMID:Safety, tolerability and efficacy of PN 200-110, a new calcium antagonist in patients with angina and coronary heart disease. 624 Apr 5

The efficacy and safety of high-dose verapamil (480 mg/day) and diltiazem therapy (360 mg/day) were compared in separate cohorts of 26 and 20 patients, respectively. All patients had stable exertional angina and underwent an initial 6-week double-blind, placebo-controlled, randomized phase followed by a 12-month open-label period. Angina attacks were reduced by verapamil (6.3 +/- 7.5 to 2.5 +/- 4.1 attacks per week, p less than 0.001) and by diltiazem (9.2 +/- 7.5 to 3.0 +/- 3.1 attacks per week, p less than 0.001), while treadmill time increased with both verapamil (372 +/- 132 to 444 +/- 108 s, p less than 0.001) and diltiazem (412 +/- 175 to 536 +/- 164 s, p less than 0.001) during the short-term study. Both agents continued to show similar salutory effects at the end of one year. The beneficial effects of both drugs appeared to be related in part to a reduction of the rate-pressure product during submaximal exercise (12% by verapamil, 7% by diltiazem, both p less than 0.05). Adverse effects were few and consisted primarily of mild constipation in six patients taking verapamil, and pedal edema and transient flushing in 2 patients each using diltiazem. Thus, high-dose verapamil and diltiazem have similar beneficial effects and are safe for the long-term treatment of effort-related angina pectoris.
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PMID:The efficacy and safety of high-dose verapamil and diltiazem in the long-term treatment of stable exertional angina. 639 71

In this report we present the history of a patient with symptomatic carcinoid syndrome. During flushing he suffered from variant angina. The observation of coronary spasm due to excess 5-hydroxytryptamine (5-HT) is discussed with regard to the discharge of 5-HT from clotting platelets in the coronary arteries.
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PMID:Evidence for coronary spasm during flushing in the carcinoid syndrome. 646 96


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