Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm. Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects. Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.
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PMID:Histamine-induced coronary artery spasm: the concept of allergic angina. 179 97

Unexpected occurrence of coronary artery spasm is sometimes observed during cardiac catheterization. We report here two cases of coronary artery spasm with hypotension and urticaria subsequent to administration of contrast material. The etiology of coronary artery spasm is discussed.
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PMID:Coronary artery spasm during cardiac angiography. 229 58

Fifteen patients with coronary artery spasm completed a double-blind placebo-controlled trial comparing diltiazem and nifedipine. Increasingly, higher daily doses (diltiazem, 90 to 360 mg; nifedipine, 30 to 120 mg) were administered to achieve optimal clinical effects. Daily diaries and ambulatory electrocardiographic recordings were used to assess efficacy and side effects. Both drugs significantly decreased angina frequency compared with that in the preceding placebo period (diltiazem 1.4 +/- 0.4 [mean +/- SEM] to 0.4 +/- 0.2 episodes per day; nifedipine 1.4 +/- 0.3 to 0.4 +/- 0.1 episodes per day; both p less than 0.05). Ambulatory electrocardiographic recordings showed fewer ST shifts than were expected during all treatment periods (0.02/h recorded during placebo, none during diltiazem and 0.02/h during nifedipine therapy). Although some patients responded better to one drug than the other, neither drug resulted in a clearly superior clinical response. Diltiazem was discontinued in one patient because of urticaria, but the total number of side effects was higher with nifedipine (12 of 15 patients) than with diltiazem (5 of 15, p less than 0.01). Nine patients remained symptomatic on single drug treatment and entered open label treatment with the combination of diltiazem and nifedipine. Three patients did not tolerate the combination because of important side effects; the other six also had side effects, but these were relatively minor. Four patients received no more benefit from the combination than from a single agent; the condition of two patients improved. Both diltiazem and nifedipine provide effective antianginal therapy for coronary spasm, but diltiazem has fewer side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of diltiazem and nifedipine alone and in combination in patients with coronary artery spasm. 354 92

Recent investigations suggest that the vasoactive substances, histamine, prostaglandin E2, and thromboxane A2 are mediators of coronary artery spasm. These substances may be released during a episode of urticaria. We report here a case of coronary artery spasm associated with an episode of acute urticaria. The coronary spasm may have been mediated by the vasoactive substances released from basophils and secondary platelet aggregation, known to occur with urticaria.
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PMID:Coronary spasm associated with urticaria: report of a case mimicking anaphylaxis. 708 49

We report two cases of vasospastic angina associated with anaphylactic reaction caused by nonsteroidal anti-inflammatory drugs (NSAIDs). Both patients exhibited anaphylactic manifestations, such as general rash and urticaria, along with angina pectoris with electrocardiographic ST-segment elevations after suppository administration of diclofenac sodium or indomethacin, the most commonly used NSAIDs. Although these patients had normal coronary arteriograms, intracoronary administration of ergonovine or acetylcholine provoked diffuse coronary artery spasms accompanied by chest pain and ischemic ST-segment changes. It is therefore suggested that an allergic mechanism may be involved as a causative factor of the coronary artery spasm induced by NSAIDs.
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PMID:Vasospastic angina induced by nonsteroidal anti-inflammatory drugs. 922 Jan 83

A 43-year-old man with no cardiac history presented with chest pain followed by cardiac arrest. He was successfully defibrillated and underwent primary percutaneous coronary angioplasty to a culprit coronary artery lesion. He later re-presented with a diffuse urticarial rash and lip swelling, reporting that these symptoms had been present for 4 weeks before his cardiac arrest and voicing concern that a further cardiac arrest may be imminent. A diagnosis of post-viral or idiopathic autoimmune urticaria and angioedema was made. Given the absence of cardiac symptoms before the development of the rash, it was hypothesised that coronary artery spasm precipitated by histamine release due to his dermatological condition contributed to his myocardial infarction and cardiac arrest. The final diagnosis was therefore cardiac arrest secondary to type II Kounis syndrome, resulting from idiopathic autoimmune or post-viral urticaria and angioedema.
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PMID:Cardiac arrest secondary to type 2 Kounis syndrome resulting from urticaria and angioedema. 2047