Allergic Myocardial Infarction

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Kunis syndrome

Text of Allergic Myocardial Infarction


2. Introduction Sign and symptom of anaphylaxis , cardiovascular Tachycardia Presyncope Hypotension Shock Chest pain Bradycardia Orthostasis Cardiac arrest Adult 46% (Yocum et al.) Children 26% (Dibs et al. child 119 years of age) 3. Younger died of anaphylactic shock tended to vasodilation with hypotension, leading to pulseless electrical activity and death Older, shock was found to be from arrhythmia, which is more commonly found in older hearts with pre-existing disease(Pumphrey ; Curr Opin Allergy Clin Immunol 4:285290 2004) 4. Myocardial ischemia, in anaphylactic reaction, can result from circulatory system instability (drop in coronary perfusion pressure) and pathophysiologically it does not differ from disturbances shock Allergic reactions can lead to myocardial ischemia as a result of coronary vessel contraction (Kounis NG ; Int J Cardiol 2006) 5. Hypersensitivity coronary syndrome concurrence of acute coronary syndromeswith condition associated with mast cellactivation, involving interrelated andinteracting inflammatory cells and includingallergic or hypersensitivity and anaphylacticor anaphylactoid insults Allergic myocardial infraction and allergic angina (Kounis NG ; Int J Cardiol 2006) 6. Cardiac features of suspected hypersensitivity myocarditis and hypersensitivity coronary syndromeHypersensitivity myocarditis Kounis syndromeCardiac symptomsAcute chest pain +Chest discomfort+ +Dyspnea + +Palpitations+ +Sudden death+ +Cardiac signsElevated JVP+ +Irregular pulse + +Gallop rhythm + +Electrocardiographic signsAtrioventricular block ++Left bundle-branch block ++Right bundle-branch block++Sinus tachycardia++ST-segment elevation ++ST-segment depression++T-wave inversion ++Ventricular tachycardia++Laboratory signsCoronary angiography Eosinophilia Increased cardiac enzymes and++especially CPK-MBIncreased troponins + +Cardiomegaly in the chest x-ray + +Dilated cardiac chambers in + +echogramEosinophils, atypicallymphocytes, and giant cells inbiopsy 7. ACS with allergic etiologyKounis syndrome 2 type 1. Type I 2. Type II 8. Type I Normal coronary arteries without predisposing factors for CAD Acute allergic insult induces coronary artery spasm with normal cardiac enzymes and troponins or coronary artery spasm progressing to acute MI with raised cardiac enzymes and troponins Positive ergonovine or histamine Represent a manifestation of endothelial dysfunction or microvascular angina(Kounis NG ; Int J Cardiol 2006) 9. Case 1 A 57-year old fisherman, heavy smoker 30 yr Decided to give up smoking and his doctor prescribed nicotine skin patches (nicorette) PH and FH no CVD and allergy 3 days later he developed itching and hives around the patch area which started progressing to generalized itching George Almpanis, International Journal of Cardiology 2009 10. 2 days later while cleaning fishes he injured one of his fingers with a fish bone and the following hours hives and itching relapsed in the corresponding hand and arm Following day the symptoms worsened itching becamewidespread and the rash covered the arms, face, neck and legsGeorge Almpanis, International Journal of Cardiology 2009 11. While the patient was in the examination room he developed suddenly severe retrosternal pain radiating to both arms and neck and started vomiting with diaphoresis pulse increased to 122 bpm regular and the blood pressure also raised to 180/100 mmHgGeorge Almpanis, International Journal of Cardiology 2009 12. EKG revealed 1 mm ST depression in leads II, III, AVF, V4V6 , inferolateral MIGeorge Almpanis, International Journal of Cardiology 2009 13. Immediately he was given 5 mg of morphine sulfate, 1 g of hydrocortisone sodium succinate, 50 mg of diphenydramine and 50 mg of ranitidine IV Admit CCU Coronary angiography was also normal with ejection fraction 60%. cardiac enzymes and troponin were within normal limits. Total IgE was elevated to 203 IU/ml (normal values, 110 IU/ml) and tryptase levels were raised to 25 g/l and after two hours 20 m/l (normal 5.613.5 m/l) and eosinophils were also raised to 9%George Almpanis, International Journal of Cardiology 2009 14. Type II Pre-existing atheromatous disease Acute allergic episode can induce plaque erosion or rupture manifesting as an acute MI Mechanism lead to plaque destabilization (oxidized LDL or allergic process)(Kounis NG ; Int J Cardiol 2006) 15. Case 2 A 72 year-old man was brought to the ER of after a syncopal attack, which developed 15 min after ingesting a pill Confused and SBP 80 mm Hg, PR 150/min Respiratory distress with bronchospasm and rales at the base of both lungsDogu Klc; International Journal of Cardiology 135 (2009) 16. EKG : AF and ST segment elevation in leads D2, D3 aVF, and ST segment depression in the leads V1-4, D1, aVL indicating acute inferior injury Dogu Klc; International Journal of Cardiology 135 (2009) 17. Plan PTCA , bolus dose of heparin (5000 IU), ASA and nebulised mixture of salbutamol and ipratropium During the preparation ; STsegment elevations resolved, sinus rhythm restored and SBP 115 mm Hg Elevated cardiac markers were indicative of subsequent myocardial injuryDogu Klc; International Journal of Cardiology 135 (2009) 18. History could only be taken 8 h after the symptoms to reveal Salbactam ampicillin ingestion 15 min before the syncopal attack Tryptase level 1.0 mcr/l Circulating specific IgE levels for the ampicillin was moderately positive (class 2) Specific IgE levels for the penicilloyl G, penicilloyl V, cefaclor and amoxycillin showing low positive (class 1) values for the former two and negative values for the latter two (class 0). Dogu Klc; International Journal of Cardiology 135 (2009) 19. Dogu Klc; International Journal of Cardiology 135 (2009) 20. Case 3 13-year-old healthy boy admited ER Severe chest pain and mild pruritic skin rashes 30 min after ingesting an oral dose of 500 mg of amoxicillin/clavulanic acid Murat Biteker; International Journal of Cardiology 136 (2009) 21. ST segment elevations in leads II, III, aVF, V4, V5 and V6Murat Biteker; International Journal of Cardiology 136 (2009) 22. Echocardiogram : inferior wall hypokinesia Troponin-I estimated on arrival was 2.1 ng/ml (reference:00.1 ng/ml), creatine kinase-MB fraction (CK-MB) was 30 U/L (reference: 025 U/L) Serum tryptase was 31 g/L (reference: 5.6 13.5 g/L) Murat Biteker; International Journal of Cardiology 136 (2009) 23. Biteker et al; Kounis syndrome: first series in Turkish patients 24. Clinical relevance Incidence and prevacence Recent study : 9.5% ( Single ant on healthy volunteer, 2/21)S G A Brown ; Emerg Med J 2004 Atopic individual higer risk of ACS, men with high IgE (woman lower IgE low rate) Criqui MH Am J Med 1987 (Kounis NG ; Int J Cardiol 2006) 25. Causes capable of inducing Kounis syndrome Conditions DrugsEnvironmental exposures Angio-edemaAntibioticsAnt stings Bronchial asthma Analgesics Bee stings Exercise induced ThrombolyticsWasp stings anaphylaxisAnticoagulants Food allergy Contrast media Jellyfish sting Idiopathic anaphylaxis CorticosteroidsGrass cutting Mastocytosis Intravenous anaesthetics Poison ivy Serum sickness NSAIDs Latex contact UrticariaSkin disinfectants Limpet ingestionAntineoplasiticMillet allergyBupropionShellfish eatingDextranViper venom poisoningHeparinProtamineStreptokinaseKounis NG ; Int J Cardiol 2006, Wadysaw Sinkiewicz et al ; Caridol J 2008 26. Mechanism Mast cell activation and degranulation 1. IgE mediated cross linking of Fc receptor 2. Histamine releasing factor secret by Macrophage orT lymphocyte 3. Anaphylatoxin component of complement systemC3a, C5a Neuropeptides and bacterial products through Toll-like receptors 2,4 Drugs such as opioids or analgesics such as high doses of acetylsalicylic acid Endothelin 27. Preformed Lipid mediators mediators (fromCytokine(eicosanoids)granules) Histamine Prostaglandin D2 Eosinophil TNF- Leukotriene B4 chemotactic factor proteoglycans, Platate-activating mainly heparinfactor (active as anticoagulant) serine proteases, such as tryptase, chymaseRapid process of anaphylactic degranulation 28. Type MediatorMajor functions Biogenic amineHistamineVasopermeability; vasodilation; smoothmuscle contraction; secretion of gastricacid; pruritus through actions onendothelial cells, smooth muscle, andnerve endings Neutral proteases Tryptase Degrades fibrinogen; attracts neutrophilsthrough induction of IL-8; stimulatesangiogenesis, fibroblast and epithelialproliferation; cleaves complementfactors C3 and C3a; degrades VIP andCGRP; kallikrein-like activity ChymaseConverts angiotensin to angiotensin II;degrades extracellular matrix; affectsendothelin and lipoprotein metabolism;activates matrix metalloproteinases;stimulates angiogenesis; degrades C3a,VIP, substance P, SCF, procollagen, andcytokines including IL-6 and TNF-;stimulates bronchial mucus secretion;chemoattractant for monocytes,neutrophils Carboxypeptidase Carboxypeptidase-A-like activity, acts inconcert with other proteases, mayprotect against venoms F Ida Hsu ; Middleton 29. Acid hydrolases-hexosaminidase Cleavage of -linked hexosamines from complex carbohydrates and glycoproteins, used experimentally as an easily quantifiable marker of in vitro mast cell activation-glucuronidase, -D-galactosidase Removes -linked glucuronic acid or galactose from complex carbohydrate chains ArylsulfataseHydrolyzes sulfate esters of aromatic compoundsProteoglycansHeparinAnticoagulant, necessary for granule storage and substrate specificity of proteases and histamine Chondroitin sulfateUnknown probably protease storage functionPreformed cytokine TNF-Leukocyte recruitment, effects on dendritic cell and lymphocyte functionsF Ida Hsu ; Middleton 30. Mast cell in MIAdventitiaLipid accumulationProximal