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)

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

A 60-year-old man, known for stable coronary artery disease, was admitted for suspected unstable angina. In the previous month, the patient presented with progressive dyspnea on light exertion. In the preceding four months, he had experience occasional episodes of flushing and diarrhea, and had inexplicably lost 22.7 kg. Night sweats and fever were absent. ST segment elevation in the inferior leads and ST segment depression in the precordial leads were documented during an episode of chest pain. The coronary angiogram showed diffuse disease with 70% stenosis of the left anterior descending coronary artery and 50% stenosis on the second diagonal (D(2)). An echocardiogram showed a patent foramen ovale. Balloon angioplasty and stenting were performed on the two lesions. Two days later, prolonged chest pain recurred. Cardiac catheterization was repeated and showed occlusive thrombus within the stent on the D(2). Angioplasty was repeated. Symptoms recurred 36 h later, with the electrocardiogram showing ST segment elevation. The first angiogram was reviewed and vasospasm was suspected on a branch of the D(2), on the second marginal and in the distal circumflex artery. The diagnosis of vasospastic angina was retained. Beta-blockers were replaced by high doses of a calcium channel blocker with an excellent clinical response. The case described is of a patient with an acute coronary syndrome, vasospastic angina, in-stent thrombosis and carcinoid disease. Coronary vasospasm was attributed to serotonin, which was secreted by the carcinoid tumour that reached an atherosclerotic coronary vasculature through a patent foramen ovale, thereby avoiding pulmonary inactivation.
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PMID:A most unusual acute coronary syndrome. 1663 80

Herein, we report a case of progressive coronary vasospasm in a 70-year-old man who had a long-standing history of metastatic gastrointestinal carcinoid tumor. Despite octreotide, nitrate, and calcium channel-blocker therapy, the patient's urinary 5-hydroxy-indole acetic acid level increased, coinciding with an increased frequency of flushing episodes with chest discomfort. In the cardiac catheterization laboratory, we captured an episode that was associated with diffuse right coronary artery spasm, ST-segment elevation, and intense symptoms. We attribute the patient's coronary vasospasm to his metastatic carcinoid disease.
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PMID:Metastatic carcinoid disease inducing coronary vasospasm. 2271 74

Coronary artery spasm (CAS) plays an important role in the pathogenesis of ischemic heart disease, including angina pectoris, myocardial infarction, and sudden death, occurring most often from midnight to early morning. CAS is prevalent among East Asians and is associated with an aldehyde dehydrogenase 2 (ALDH2)-deficient genotype (ALDH2*2) and alcohol flushing, which is prevalent among East Asians but is virtually non-existent in other populations. ALDH2 eliminates not only acetaldehyde but also other toxic aldehydes from lipid peroxidation and tobacco smoking, thereby protecting tissues and cells from oxidative damage. Risk factors for CAS include smoking and genetic polymorphisms including those of ALDH2*2, endothelial NO synthase, paraoxonase I, and interleukin-6. Accordingly, oxidative stress, endothelial dysfunction, and low-grade chronic inflammation play an important role in the pathogenesis of CAS, leading to increased coronary smooth muscle Ca2+ sensitivity through RhoA/ROCK activation and resultant hypercontraction. Ca-channel blockers blocking the intracellular entry of Ca2+ are specifically effective for treatment for CAS.
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PMID:Coronary artery spasm - Clinical features, pathogenesis and treatment. 3074 2