Coronary artery spasm after administration of dextran 40: Implications concerning percutaneous transluminal coronary angioplasty

Klugmann, Silvio; Salvi, Alessandro; Valente, M; Zanei, Paolo; Maiolino, Pietro; Camerini, F

doi:10.1016/0002-8703(86)90027-x

Cited by 9 publications

(2 citation statements)

References 7 publications

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“…Although DLST tests of these materials were negative, low-molecular-weight dextran was the most likely agent because it had been administered to this patient for the first time and Kounis syndrome occurred immediately after its administration. There have been several reports describing how low-molecularweight dextran (dextran 40) caused coronary spasm before Kounis syndrome was advocated [7,8]. In addition, a report has also suggested that Kounis syndrome occurred due to dextran 40 [9].…”

Section: Discussionmentioning

confidence: 99%

Successful treatment of prolonged cardiopulmonary arrest of Kounis syndrome during coronary angioplasty

Akita

Kawata

Sakaguchi

et al. 2016

Journal of Cardiology Cases

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Section: Discussionmentioning

confidence: 99%

Successful treatment of prolonged cardiopulmonary arrest of Kounis syndrome during coronary angioplasty

Akita

Kawata

Sakaguchi

et al. 2016

Journal of Cardiology Cases

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“…We therefore believe that there is an association between allergy and cardiovascular disease, and histamine released during allergic processes can undoubtedly induce coronary arterial spasm, manifested as angina. Recent reports 210–212 ports demonstrated that allergic reactions to analgesics, dextran 40 and contrast media can also cause coron ary spasm and angina. Our strong feeling is that in allergic angina a type I (reaginic) or type III (Arthus) allergic reaction of Gell and Coombs takes place 20 .…”

Section: Discussionmentioning

confidence: 99%

Histamine‐induced Coronary Artery Spasm: The Concept of Allergic Angina

Kounis¹,

Zavras²

1991

Int J Clinical Practice

371

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SUMMARYHistamine, 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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Acute life‐threatening cardiovascular toxicity with umbilical cord blood infusion: The role of dextran

Robert¹,

Kwan²,

David³

et al. 2010

American J Hematol

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The main cause of hepatosplenomegaly in primary (PMF), post polycythemia vera (post-PV MF), and post essential thrombocythemia (post-ET MF) myelofibrosis (MF) is extramedullary hematopoiesis (EMH). Drug-refractory symptomatic splenomegaly in MF is usually managed by splenectomy or involved-field radiotherapy. The latter is most effective in the treatment of MF-associated bone pain and pulmonary hypertension. Our previous experience with hepatosplenic radiotherapy in MF showed efficacy in the majority of treated patients but its utility was limited by the transient nature of its benefit and the occurrence of treatment-related pancytopenia. In an effort to address these issues, we have adopted an induction-maintenance treatment strategy that utilizes lower radiation doses-induction with 100 cGy total in four daily doses of 25 cGy and maintenance with either the same or lower intensity regimen. Herein, we report our most recent experience using this treatment plan in two cases, who in addition to their expected response from the standpoint of splenomegaly, also unexpectedly showed a marked response of their underlying accelerated phase disease, including clearance of circulating blasts and basophilia.Case #1

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Coronary artery spasm after administration of dextran 40: Implications concerning percutaneous transluminal coronary angioplasty

Cited by 9 publications

References 7 publications

Successful treatment of prolonged cardiopulmonary arrest of Kounis syndrome during coronary angioplasty

Successful treatment of prolonged cardiopulmonary arrest of Kounis syndrome during coronary angioplasty

Histamine‐induced Coronary Artery Spasm: The Concept of Allergic Angina

Acute life‐threatening cardiovascular toxicity with umbilical cord blood infusion: The role of dextran

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