Sindrom Kounis syndrome: Angina Alergi dan Infark Miokardial Alergi

wp-1505798535310.Sindrom Kounis syndrome: Angina Alergi dan Infark Miokardial Alergi

Bila alergi atau hipersensitivitas dan anafilaksis atau anafilaktoid menyebabkan gejala dan tanda kardiovaskular, termasuk kejadian koroner akut, hasilnya mungkin adalah terjadi sindroma Koumis entitas nosokologis yang baru didefinisikan. Angina alergi vasospastik, infark miokard alergi, dan trombosis stent dengan trombus occluding yang disusupi oleh sel eosinofil dan / atau mast adalah 3 varian sindrom ini. Tiga varian sindrom Kounis yang dilaporkan – angina alergi vasospastik, infark miokard alergi, dan trombosis stent dengan trombus occluding – disebabkan oleh mediator inflamasi. Agen yang menghambat degranulasi sel mast mungkin berkhasiat dalam mencegah kejadian koroner dan serebrovaskular akut sindrom Kounis.

Sindrom Kounis telah ditetapkan sebagai gangguan koroner hipersensitivitas yang disebabkan oleh berbagai kondisi, obat-obatan, paparan lingkungan, makanan dan stent koroner. Reaksi alergi, hipersensitivitas, anafilaksis dan anafilaktoid berhubungan dengan sindrom ini. Angina alergi vasospastik, infark miokard alergi dan trombosis stent dengan trombus occluding yang disusupi oleh eosinofil dan / atau sel mast merupakan tiga varian sindrom ini yang dilaporkan sejauh ini. Selain arteri koroner, ini mempengaruhi arteri serebral dan mesenterika. Manifestasinya semakin meluas dan etiologinya terus meningkat. Sindrom Kounis adalah penyakit di mana-mana yang merupakan paradigma alam yang indah dan eksperimen alami di jalur pemicu akhir yang terlibat dalam kasus kejang arteri koroner dan ruptur plak. Sindrom Kounis tampaknya bukan penyakit langka tapi jarang merupakan entitas klinis yang terdiagnosa yang telah mengungkapkan bahwa mediator yang sama yang terlepas dari sel inflamasi yang sama juga hadir dan pada kejadian koroner akut etiologi non alergi. Sel-sel ini tidak hanya terdapat di wilayah pelakunya sebelum erosi plak atau pecah tetapi mereka melepaskan isinya tepat sebelum kejadian koroner yang sebenarnya. Oleh karena itu, kesadaran akan etiologi, epidemiologi, patogenesis dan manifestasi klinis tampaknya penting untuk prognosis, diagnosis, pengobatan, pencegahannya.

Manifestasi klinik Kounis syndrome.

Gejala Klinik Tanda EKG Laboratorium
– Acute chest pain
– Chest discomfort
– In swallowing
– Sesak
– Faintness
– Sakit kepala
– Malaise
– mual
– Pruritus
– Kulit gatal
– Sinkop
– Muntah
– Bradikardi
– Cardiorespiratory arrest
– Cold extremities
– Diaphoresis
– Hypotension
– Pallor
– Palpitations
– Skin rash
– Sudden death
– Sweating
– Tachycardia
– Atrial fibrillation
– Bigeminal rhythm
– Heart block
– Nodal rhythm
– Sinus bradycardia
– Sinus tachycardia
– ST segment depression or elevation
– T-wave flattening and/or inversion
– QRS complex prolongation
– QT segment prolongation
– Ventricular ectopics
– Venticular fibrillation
– Coronary angiography (spasm, thrombosis)
– Eosinophilia
– Increased cardiac enzymes and especially CPK-MB
– Increased troponins
– Cardiomegaly in the chest X-ray
– Dilated cardiac chambers in echogram
– Eosinophils, and/or mast cells in coronary biopsy
– MRI: subendocardial gadolinium concentration
– SPECT: detects ischemia

Mediator inflamasi termasuk histamin, protease netral, produk asam arakidonat, faktor pengaktifan trombosit dan berbagai sitokin dan kemokin meningkat dalam darah atau urin baik pada episode alergi maupun sindrom koroner akut. Pelepasan mediator selama penghinaan alergi telah diberatkan untuk menginduksi kejang arteri koroner dan / atau erosi plak atheromatosa atau ruptur. Jalur umum antara sindrom koroner alergi dan non-alergi tampaknya ada. Saat ini, ada bukti bahwa sel mast tidak hanya memasuki daerah pelakunya sebelum erosi plak atau pecah tetapi mereka melepaskan isinya sebelum episode koroner sebenarnya. Sindrom Kounis adalah persetujuan sindrom koroner akut dengan kondisi yang terkait dengan aktivasi sel mast termasuk alergi atau hipersensitivitas dan penghinaan anafilaksis atau anafilaksoid. Hal ini disebabkan oleh mediator inflamasi yang dilepaskan melalui aktivasi sel mast. Sindrom Kounis, sebagai konsekuensinya, dari asosiasi patofisiologis di atas dianggap sebagai eksperimen alami dan paradigma alam yang menakjubkan yang menunjukkan cara baru dalam upaya mencegah sindrom koroner akut. Obat dan molekul alami yang menstabilkan membran sel mast dan antibodi monoklonal yang melindungi permukaan sel mast dapat muncul sebagai modalitas terapeutik baru yang mampu mencegah kejadian koroner dan serebrovaskular akut.

 

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