Acute Coronary Syndromes PDF

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This document discusses Acute Coronary Syndromes, covering pathophysiology and potential treatment approaches. The text explains how endothelial dysfunction, inflammation, and fatty streaks contribute to the development of atherosclerotic coronary artery plaques.

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SECTION 2 CARDIOVASCULAR DISORDERS Edited by Terry L. Schwinghammer 5 CHAPTER Acute Coronary Syndromes Acute coronary s...

SECTION 2 CARDIOVASCULAR DISORDERS Edited by Terry L. Schwinghammer 5 CHAPTER Acute Coronary Syndromes Acute coronary syndrome (ACS) involves acute myocardial ischemia resulting from an imbalance between myocardial oxygen demand and supply. Classification based on electrocardiographic (ECG) changes includes: (1) ST-segment-elevation myocar- dial infarction (STEMI) or (2) non–ST-segment-elevation ACS (NSTE-ACS), which includes non–ST-segment-elevation MI (NSTEMI) and unstable angina (UA). PATHOPHYSIOLOGY Endothelial dysfunction, inflammation, and formation of fatty streaks contribute to development of atherosclerotic coronary artery plaques. Eventual plaque rupture and subsequent thrombus formation abruptly decreases myocardial blood flow and oxygen supply, leading to ischemia and, potentially, infarction. Atherosclerotic plaques that rupture typically have thin fibrous caps and tend to be nonobstructive, occluding ‫وﺗﺴﺪ‬ ،‫ﻣﻌﻮﻗﺔ‬ ‫ﻏﻴﺮ‬ ‫ﺗﻜﻮن‬ ‫أن‬ ‫إﻟﻰ‬ ‫وﺗﻤﻴﻞ‬ ‫رﻗﻴﻘﺔ‬ ‫ﻟﻴﻔﻴﺔ‬ ‫أﻏﻄﻴﺔ‬ ‫ﺗﻨﻔﺠﺮ‬ ‫اﻟﺘﻲ‬ ‫اﻟﺘﺼﻠﺒﻴﺔ‬ ‫ﻟﻠﺒﻼﻛﺎت‬ ‫ﻳﻜﻮن‬ ً ‫ﻋﺎدة ﻣﺎ‬ oxygen supply, leading to ischemia and, potentially, infarction. Atherosclerotic ‫اﻟﺘﻨﻈﻴﻢ‬ ‫ﺗﻤﺰق اﻟﺒﻼك ﺑﺴﺒﺐ‬ ‫اﻟﺼﺪرﻳﺔ ﻗﺒﻞ‬ plaques ‫ﻣﻦ اﻟﺬﺑﺤﺔ‬ that rupture ‫اﻟﻤﺮﺿﻰ‬have typically ‫ﻳﻌﺎﻧﻲ‬thin ‫ﻗﺪ ﻻ‬fibrous ،‫وﺑﺎﻟﺘﺎﻟﻲ‬ ‫اﻟﺸﺮﻳﺎن؛‬ caps and tend‫ﺗﺠﻮﻳﻒ‬ to ‫ﻗﻄﺮ‬ be ‫ﻣﻦ‬ ‫ﻓﻲ ﻋﻀﻠﺔ‬ ‫اﻟﻄﻠﺐ ﻋﻠﻰ اﻷﻛﺴﺠﻴﻦ‬ nonobstructive, ‫< زﻳﺎدة‬70% occluding ‫اﻷﻛﺴﺠﻴﻦ أﺛﻨﺎء‬ of the ‫وإﻣﺪادات‬ ‫ﻋﻠﻰ ﺗﺪﻓﻖ اﻟﺪم‬ luminal diameter; thus,‫ﻳﺤﺎﻓﻆ‬ ‫اﻟﺬي‬may patients ‫اﻟﻜﺎﻓﻲ‬ not‫اﻟﺬاﺗﻲ‬ ‫ﺗﻤﺰق اﻟﻐﻄﺎء‬ experience angina ‫زﻳﺎدة اﺣﺘﻤﺎﻟﻴﺔ‬ ‫إﻟﻰ‬prior to plaque ‫اﻟﻌﺎﻃﻔﻲ‬ rupture ‫اﻟﺒﺪﻧﻲ أو‬ ‫اﻹﺟﻬﺎد‬due to ‫اﻟﻤﺘﺰاﻳﺪ‬ ‫أﺛﻨﺎء‬ adequate autoregulation ‫اﻟﻜﺎﺗﻴﻜﻮﻻﻣﻴﻦ‬ ‫إﻃﻼق‬that ‫ﻳﺆدي‬ main- ‫ ﻗﺪ‬.‫اﻟﻘﻠﺐ‬ tains blood flow and oxygen supply during increased myocardial oxygen demand..‫اﻟﻠﻴﻔﻲ اﻟﺮﻗﻴﻖ‬ Increased catecholamine release during physical or emotional stress may enhance the ‫اﻟﻤﺘﺪاوﻟﺔ‬ ‫اﻟﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ‬ likelihood of rupture‫ﺗﻨﺠﺬب‬ of a ‫ﺣﻴﺚ‬ ‫ اﻟﺪم؛‬fibrous thinning ‫وﻣﻜﻮﻧﺎت‬cap. ‫ ﻳﺨﺘﺮق ﺗﻤﺰق اﻟﺒﻼك اﻟﺤﺎﺟﺰ ﺑﻴﻦ ﻗﻠﺐ اﻟﺒﻼك اﻟﻤﻴﺖ‬ ‫اﻟﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ‬ Plaque ‫ﺟﻠﻴﻜﻮﺑﺮوﺗﻴﻦ‬ rupture breaches‫ﻣﺴﺘﻘﺒﻼت‬ the‫ﺧﻼل‬ ‫اﻟﺪﻣﻮﻳﺔ ﻣﻦ‬ barrier between ‫اﻟﺼﻔﺎﺋﺢ‬ ‫ﻳﺤﺪث اﻟﺘﺼﺎق‬ the necrotic plaque.‫اﻹﺻﺎﺑﺔ‬ core and ‫ﺑﻤﻨﻄﻘﺔ‬ blood‫وﺗﻠﺘﺼﻖ‬ components; ‫ﺟﻠﻴﻜﻮﺑﺮوﺗﻴﻦ‬ ‫ﻣﺴﺘﻘﺒﻼت‬circulating platelets ‫ﺑﺎﻹﺿﺎﻓﺔ إﻟﻰ‬ are‫اﻟﻠﻴﻔﻲ‬ ،‫اﻟﺘﺎﻟﻒ‬ attracted ‫ اﻟﻐﻄﺎء‬and ‫داﺧﻞ‬adhere ‫ﺑﺎﻟﻜﻮﻻﺟﻴﻦ‬ to the ‫ﺗﺮﺗﺒﻂ‬ area‫اﻟﺘﻲ‬of(GP injury. ) ‫اﻟﺴﺎدس‬ Platelet‫ﺑﻮاﺳﻄﺔ‬ ‫اﻟﻜﻮﻻﺟﻴﻦ‬ adhesion ‫ ذﻟﻚ‬occurs via platelet ‫اﻟﺪﻣﻮﻳﺔ ﺑﻌﺪ‬ ‫اﻟﺼﻔﺎﺋﺢ‬glycoprotein ‫ ﻳﺘﻢ ﺗﻨﺸﻴﻂ‬.‫وﻳﻠﺒﺮاﻧﺪ‬(GP) VI ‫ﻓﻮن‬ receptors ‫ وﻋﺎﻣﻞ‬Ib-IX binding‫اﻟﺪﻣﻮﻳﺔ‬to col- ‫اﻟﺼﻔﺎﺋﺢ‬ lagen within the damaged fibrotic cap, as well as platelet GP Ib-IX receptors and von ‫ ﻳﺆدي ارﺗﺒﺎط ﻫﺬه‬.‫( واﻷدرﻳﻨﺎﻟﻴﻦ واﻟﺴﻴﺮوﺗﻮﻧﻴﻦ‬ADP) ‫ وأدﻳﻨﻮﺳﻴﻦ ﺛﻨﺎﺋﻲ اﻟﻔﻮﺳﻔﺎت‬A2 ‫واﻟﺜﺮوﻣﺒﻴﻦ واﻟﺜﺮوﻣﺒﻮﻛﺴﺎن‬ Willebrand factor. Platelets are then activated by collagen, thrombin, thromboxane ،ADPA‫ ﻟـ‬,P2Y12 adenosine ‫ﻣﺴﺘﻘﺒﻞ‬ ،‫ﺳﺒﻴﻞ اﻟﻤﺜﺎل‬ diphosphate ‫ )ﻋﻠﻰ‬epinephrine, (ADP), ‫اﻟﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ‬ and ‫ﺳﻄﺢ‬ ‫اﻟﻤﺤﺪدة ﻋﻠﻰ‬ serotonin. ‫ﺑﻤﺴﺘﻘﺒﻼﺗﻬﺎ‬ The binding ‫اﻟﻤﻨﺸﻄﺎت‬ of these 2 ‫اﻟﻤﺰﻳﺪ ﻣﻦ‬ ‫اﻟﺪﻣﻮﻳﺔ وإﻃﻼق‬ activators to their‫اﻟﺼﻔﺎﺋﺢ‬ specific‫ﺳﻄﺢ‬ ‫ﻣﺴﺎﺣﺔ‬on receptors ‫زﻳﺎدة‬ the‫إﻟﻰ‬ (‫ﻟﻠﺜﺮوﻣﺒﻴﻦ‬ platelet 1-[PAR surface ‫اﻟﻤﻨﺸﻂ‬ (eg, ]P2Y 12 ‫اﻟﺒﺮوﺗﻴﺎز‬ receptor ‫ﻣﺴﺘﻘﺒﻞ‬ for ADP, protease-activated ‫واﻟﺒﺮوﺛﺮوﻣﺒﻴﻨﺎز‬ ‫ﺗﺠﻤﻴﻊ ﻣﻌﻘﺪات اﻟﺘﻴﻨﺎز‬ receptor [PAR]-1 ‫ ﻳﻨﺘﺞ‬.‫اﻟﺪﻣﻮﻳﺔ‬ for thrombin) ‫اﻟﺼﻔﺎﺋﺢ‬ ‫اﻟﺤﺒﻴﺒﺎت داﺧﻞ‬results ‫ﻣﻦ‬in increased ‫اﻟﺪﻣﻮﻳﺔ‬ ‫اﻟﺼﻔﺎﺋﺢ‬ platelet ‫ﻣﻨﺸﻄﺎت‬ ‫ﻳﺆدي اﻟﺘﻐﻴﻴﺮ ﻓﻲ‬surface area‫ﺳﻠﺴﻠﺔ‬.‫اﻟﺘﺨﺜﺮ‬ and release of further ‫)اﻟﺜﺮوﻣﺒﻴﻦ( ﻓﻲ‬ platelet ‫اﻟﻤﻨﺸﻂ‬ IIa‫و‬activators Xa ‫ اﻟﻌﺎﻣﻞ‬from ‫ﻣﻌﻈﻢ‬granules within platelets. ‫اﻟﺪﻣﻮﻳﺔ اﻟﻤﻨﺸﻄﺔ‬ ‫داﺧﻞ اﻟﺼﻔﺎﺋﺢ‬ Assembly of tenase and prothrombinase complexes within activated platelets pro- ‫ ﻟﻠﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ إﻟﻰ رﺑﻂ اﻟﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ ﺑﺒﻌﻀﻬﺎ اﻟﺒﻌﺾ ﻣﻦ ﺧﻼل‬GP IIb/IIIa ‫ﺗﻜﻮﻳﻦ ﻣﺴﺘﻘﺒﻼت ﺳﻄﺢ‬ duces most of the activated factor Xa and IIa (thrombin) in the coagulation cascade..‫اﻟﻠﻮﻳﺤﺔ‬A‫ﺗﻤﺰق‬ change‫ﻣﻨﻄﻘﺔ‬ in ‫ﻓﻲ‬ the ‫ﺻﻔﻴﺤﻴﺔ‬ ‫وﺗﻜﻮﻳﻦ ﺳﺪادة‬ conformation of the GP‫اﻟﺪﻣﻮﻳﺔ‬ ‫اﻟﺼﻔﺎﺋﺢ‬ IIb/IIIa ‫ﺗﻜﺘﻞ‬receptors surface ‫ ﻳﺆدي إﻟﻰ‬of ‫ﻣﻤﺎ‬platelets ،‫اﻟﻔﻴﺒﺮﻳﻨﻮﺟﻴﻦ‬ cross-‫ﺟﺴﻮر‬ ‫اﻟﺘﻲ ﺗﺤﺒﺲ‬ links‫اﻟﺪﻣﻮﻳﺔ‬ ‫اﻟﺼﻔﺎﺋﺢ‬ platelets ‫ﺳﺪادة‬ to each ‫ﺣﻮل‬through other (‫اﻟﻔﻴﺒﺮﻳﻦ )ﺧﺜﺮة‬ fibrinogen ‫ﺷﺒﻜﺔ ﻣﻦ‬ bridges,‫ﺗﻜﻮﻳﻦ‬ ‫اﻟﺘﺨﺜﺮ إﻟﻰ‬ resulting ‫ﺗﻨﺸﻴﻂ ﺳﻠﺴﻠﺔ‬ in platelet aggrega- ‫ ﻳﺆدي‬ tion ‫وإﻣﺪاد‬ and‫ﻋﻀﻠﺔ‬ ‫اﻟﻘﻠﺐ‬ formation ‫اﻟﺪم إﻟﻰ‬of ‫ﺗﺪﻓﻖ‬ ‫ ًﺌﺎ ﻓﻲ‬plug a platelet ‫ ﻣﻔﺎﺟ‬in ً the area ‫اﻧﺨﻔﺎﺿﺎ‬ ‫وﺗﺴﺒﺐ‬of plaque ‫اﻟﺤﻤﺮاء‬rupture. ‫اﻟﻤﻜﻮﻧﺎت اﻟﺨﻠﻮﻳﺔ ﻣﺜﻞ ﺧﻼﻳﺎ اﻟﺪم‬ Activation.‫اﻟﺨﻼﻳﺎ‬of‫وﻣﻮت‬the clotting cascade‫ﻓﻲ‬forms ‫اﻟﺨﻼﻳﺎ اﻟﻌﻀﻠﻴﺔ‬ ‫ﻳﺤﺪث ﻧﺨﺮ‬ a fibrin ‫ ﻓﻘﺪ‬meshwork (thrombus) ،‫اﻟﺘﺮوﻳﺔ دون ﻋﻼج‬ ‫ﺮك ﻧﻘﺺ‬ around the ‫ إذا ُﺗ‬.‫اﻷﻛﺴﺠﻴﻦ‬ platelet plug that traps cellular components such as red blood cells and causes abrupt ‫( ﺗﻤﺰق أو ﺷﻖ أو ﺗﺂﻛﻞ ﻟﻮﻳﺤﺔ ﺗﺼﻠﺐ‬1) :‫( ﻋﻠﻰ اﻟﺴﺒﺐ‬MI) ‫ ﺗﻌﺘﻤﺪ اﻷﻧﻮاع اﻟﻔﺮﻋﻴﺔ ﻣﻦ اﺣﺘﺸﺎء ﻋﻀﻠﺔ اﻟﻘﻠﺐ‬ reduction in myocardial blood flow and oxygen supply. If ischemia is left untreated, ‫ﻋﻤﻠﻴﺔ‬myocyte ‫ﻓﻲ ﻏﻴﺎب‬necrosis ‫زﻳﺎدة اﻟﻄﻠﺐ‬ and ‫أو‬cell‫اﻟﻘﻠﺐ‬ death ‫ﻟﻌﻀﻠﺔ‬ may‫اﻷﻛﺴﺠﻴﻦ‬ ensue. ‫( اﻧﺨﻔﺎض إﻣﺪاد‬2) ‫ ﻣﻦ اﻟﺤﺎﻻت(؛‬٪90) ‫اﻟﺸﺮاﻳﻴﻦ‬ (4) ‫اﻟﺤﻴﻮﻳﺔ؛‬ Subtypes ‫اﻟﻤﺆﺷﺮات‬ ‫إﻣﻜﺎﻧﻴﺔ ﻗﻴﺎس‬ of myocardial ‫اﻟﻮﻓﺎة دون‬ infarction (MI) ‫إﻟﻰ‬are ‫ﻳﺆدي‬ based‫ﻣﻤﺎ‬ on‫اﻟﻘﻠﺐ‬ ‫(ﻋﻀﻠﺔ‬1) etiology: ‫اﺣﺘﺸﺎء‬ (3) ‫اﻟﺘﺎﺟﻲ؛‬ rupture, fissure, ‫اﻟﺸﺮﻳﺎن‬ or erosion ‫(؛‬4b ‫)اﻟﻨﻮع‬ of an ‫اﻟﺪﻋﺎﻣﺔ‬ atherosclerotic ‫ﺗﺨﺜﺮ‬ ‫( أو‬4a ‫؛ اﻟﻨﻮع‬PCI plaque (90% ) ‫اﻟﺠﻠﺪ‬ ‫ﻃﺮﻳﻖ‬ of ‫ﻋﻦ‬ cases); (2)‫ﺑﺎﻟﺘﺪﺧﻞ‬ ‫اﻟﺘﺎﺟﻲ‬ reduced‫اﻟﻤﺮﺗﺒﻂ‬ myocardial ‫ﻋﻀﻠﺔ اﻟﻘﻠﺐ‬ oxygen ‫اﺣﺘﺸﺎء‬ supply or increased.(demand in the ‫اﻟﺸﺮﻳﺎن‬ CABG) ‫اﻟﺘﺎﺟﻲ‬ absence‫ﻣﺠﺎزة‬ of a ‫ﺑﺠﺮاﺣﺔ‬ coronary artery ‫اﻟﻤﺮﺗﺒﻂ‬ process; ‫اﻟﻘﻠﺐ‬ (3) MI (5)‫و‬ ‫اﺣﺘﺸﺎء ﻋﻀﻠﺔ‬ ً ‫ﺗﺆدي‬ resulting in death without the possibility of measuring biomarkers; (4) MI associated ‫أﻳﻀﺎ‬ ‫ ﺗﺤﺪث ﺗﻜﻴﻔﺎت ﺣﺎدة وﻣﺰﻣﻨﺔ ﻟﻤﻨﻊ اﻻﻧﻬﻴﺎر اﻟﺪﻳﻨﺎﻣﻴﻜﻲ اﻟﺪﻣﻮي وﻟﻜﻨﻬﺎ ﻗﺪ‬،‫ ﺑﻌﺪ اﻹﺻﺎﺑﺔ ﺑﻨﻮﺑﺔ ﻗﻠﺒﻴﺔ‬ with percutaneous coronary intervention (PCI; Type 4a) or stent thrombosis (Type ‫ وﻧﻈﺎم‬4b); ‫اﻟﻮدي‬and ‫اﻟﻌﺼﺒﻲ‬ (5) MI‫اﻟﺠﻬﺎز‬ ‫ﻳﻌﻮض ﺗﺤﻔﻴﺰ‬ associated with.‫ﻗﻠﺒﻴﺔ‬ coronary‫ﺑﻨﻮﺑﺔ‬artery ‫اﻹﺻﺎﺑﺔ‬bypass ‫ﻣﺎ ﺑﻌﺪ‬graft ‫وﻣﻀﺎﻋﻔﺎت‬ (CABG) ‫اﻟﺒﻄﻴﻦ‬ ‫إﻟﻰ إﻋﺎدة ﺗﺸﻜﻴﻞ‬ surgery. ‫اﻟﻤﺰﻣﻦ ﻳﻤﻜﻦ‬ After ‫اﻷﻧﻈﻤﺔ‬ MI,‫ﻫﺬه‬acute ‫ﻧﺸﺎط‬and‫ﻓﺮط‬chronic ‫ ﻓﺈن‬،‫ذﻟﻚ‬adaptations ‫ وﻣﻊ‬.‫اﻟﻨﺎﺗﺞ اﻟﻘﻠﺒﻲ‬ occur‫اﻧﺨﻔﺎض‬ ‫أﻟﺪوﺳﺘﻴﺮون ﻋﻦ‬-‫أﻧﺠﻴﻮﺗﻨﺴﻴﻦ‬-‫اﻟﺮﻳﻨﻴﻦ‬ to prevent hemodynamic collapse but may ‫اﻻﻟﺘﻬﺎﺑﻴﻴﻦ وﺗﺮﺳﺐ‬ also lead ‫اﻟﻮﺳﻄﺎء‬ ‫إﻃﻼق‬to‫ﻳﺴﺎﻫﻢ‬ ventricular.‫ اﻟﻘﻠﺒﻲ‬remodeling ‫اﻻﻧﻘﺒﺎض واﻟﻨﺎﺗﺞ‬ and‫ﺿﻌﻒ‬ post-MI complications. ‫وﻣﺰﻳﺪ ﻣﻦ‬ ‫ﺗﻀﺨﻢ اﻟﺒﻄﻴﻦ‬ Stimula- ‫أن ﻳﺆدي إﻟﻰ‬ tion of ‫اﻟﻨﻬﺎﺋﻲ ﻻﻋﺘﻼل‬ the sympathetic ‫واﻟﺘﻄﻮر‬ ‫اﻟﺒﻄﻴﻦ اﻷﻳﺴﺮ‬nervous ‫ﺗﺮﻗﻖ ﺟﺪار‬ system ‫ﻳﺆدي إﻟﻰ‬ (SNS) and،‫ﺗﻨﺪﺑﻬﺎ‬ ‫ﻣﻤﺎ ﻗﺪ‬ renin–angiotensin–aldosterone ‫اﻟﻜﻮﻻﺟﻴﻦ ﻓﻲ ﺗﻠﻴﻒ ﻋﻀﻠﺔ اﻟﻘﻠﺐ أو‬ system (RAAS) compensates for decreased cardiac output. However, chronic.‫ﻋﻀﻠﺔ اﻟﻘﻠﺐ اﻟﻤﺘﻮﺳﻊ‬ ،‫ وﺣﺼﺎر اﻟﻘﻠﺐ‬،‫ وﺑﻂء ﺿﺮﺑﺎت اﻟﻘﻠﺐ‬،‫ ﺗﺸﻤﻞ ﻣﻀﺎﻋﻔﺎت اﺣﺘﺸﺎء ﻋﻀﻠﺔ اﻟﻘﻠﺐ ﻋﺪم اﻧﺘﻈﺎم ﺿﺮﺑﺎت اﻟﻘﻠﺐ اﻟﺒﻄﻴﻨﻲ‬ ‫ واﻻﻧﺴﺪاد اﻟﺨﺜﺎري )ﺑﻤﺎ ﻓﻲ ذﻟﻚ اﻟﺴﻜﺘﺔ‬،‫ وﺗﻤﺰق ﺟﺪار اﻟﺒﻄﻴﻦ اﻷﻳﺴﺮ أو اﻟﺤﺎﺟﺰ‬،‫ واﻟﺼﺪﻣﺔ اﻟﻘﻠﺒﻴﺔ‬،‫اﻟﻘﻠﺐ‬51‫وﻓﺸﻞ‬ ‫ ﻳﺼﺎب‬.‫ واﻟﺘﻬﺎب ﻏﻼف اﻟﻘﻠﺐ‬،‫اﻟﺪﻣﻮﻳﺔ‬ ‫ وﺗﻜﻮﻳﻦ ﺗﻤﺪد اﻷوﻋﻴﺔ‬،(‫اﻟﺪﻣﺎﻏﻴﺔ اﻟﺜﺎﻧﻮﻳﺔ ﻻﻧﺴﺪاد ﺧﺜﺮة اﻟﺒﻄﻴﻦ اﻷﻳﺴﺮ‬ https://ebookmedicine.com/.‫اﻟﻌﺪﻳﺪ ﻣﻦ ﻣﺮﺿﻰ ﻣﺘﻼزﻣﺔ اﻟﺸﺮﻳﺎن اﻟﺘﺎﺟﻲ اﻟﺤﺎدة ﺑﺎﻻﻛﺘﺌﺎب أﺛﻨﺎء ﻓﺘﺮة اﻟﻨﻘﺎﻫﺔ‬ 06_Schwinghammer_ch05.indd 51 13/03/23 11:36 AM SECTION 2  |  Cardiovascular Disorders hyperactivation of these systems can lead to ventricular hypertrophy and further impairment of contractility and cardiac output. The release of inflammatory media- tors and collagen deposition contribute to myocardial fibrosis or scarring, which can lead to thinning of the left ventricular (LV) wall and eventual development of dilated cardiomyopathy. Complications of MI include ventricular arrhythmias, bradyarrhythmias, heart block, heart failure (HF), cardiogenic shock, LV free-wall or septal rupture, throm- boembolism (including stroke secondary to LV thrombus embolization), aneurysm formation, and pericarditis. Many patients with ACS develop depression during the convalescent period. CLINICAL PRESENTATION The patient is typically in acute distress and may present with or develop hyperten- sive crisis, acute HF, cardiogenic shock, or cardiac arrest. The classic symptom of ACS is abrupt-onset substernal chest pain or discomfort often described as a squeezing, heaviness, or tightness that persists for 10 minutes or longer. Symptoms may radiate to the arms and shoulders (especially on the left side), back, abdo- men, or jaw. Nausea, vomiting, diaphoresis, or shortness of breath may also be present. Many patients have atypical symptoms without chest pain, such as epigastric pain, indigestion, pleuritic chest pain, and increasing exertional dyspnea. Older adults, women, and patients with diabetes mellitus (DM), impaired renal function, and dementia are more likely to present with atypical features. No physical examination findings are specific to ACS. Nonspecific findings include S4 or paradoxical splitting of S2 heart sounds on auscultation. Signs of acute decom- pensated HF include jugular venous distention, pulmonary edema, and an S3 on auscultation. Patients may also present with arrhythmias, heart block, hypertension (HTN), hypotension, or shock. DIAGNOSIS Obtain 12-lead ECG within 10 minutes of presentation. Changes suggestive of acute ischemia include ST-segment elevation (STE), ST-segment depression, and T-wave inversion. Presence of a new left bundle-branch block (LBBB) in patients with sus- pected ACS is strongly suggestive of acute MI. Some patients with ACS have no ECG changes, so appropriate evaluation and risk stratification must carefully assess medi- cal history, presenting symptoms, and cardiac biomarkers. Cardiac troponin (either T or I) is measured at the time of presentation and repeated 3–6 hours later to detect myocardial injury; elevated blood levels (exceeding the 99th percentile of the upper reference limit) occur within 2–4 hours of myocyte injury or necrosis and may remain elevated as long as 2 weeks. Myocardial injury is considered acute if there is a dynamic rise and/or fall by 20% or more in serial troponin values. Elevated levels in a patient with ACS symptoms, ischemic changes on ECG, or other evidence of ischemia confirm the diagnosis of MI. Additional troponin levels should be obtained beyond 6 hours after symptom onset in patients with intermediate- to high-risk features of ACS but normal troponin levels during serial measurements. Elevated dynamic cardiac troponin levels with ST-segment elevation of at least 1 mm in two contiguous leads or new LBBB on the presenting ECG confirms the diagnosis of STEMI. In contrast, the diagnosis of NSTEMI is appropriate for patients with symptoms of ACS and elevated troponin levels without at least 1 mm ST-segment elevation on the ECG at presentation. Patients with symptoms consistent with ACS but in whom troponin is not elevated may have UA or an alternative diagnosis. TREATMENT Goals of Treatment: Short-term goals include: (1) early restoration of blood flow to the affected artery to prevent infarct expansion (in the case of MI) or prevent 52 https://ebookmedicine.com/ 06_Schwinghammer_ch05.indd 52 13/03/23 11:36 AM SECTION 2  |  Cardiovascular Disorders ‫اﻟﻌﺮض اﻟﺴﺮﻳﺮي‬ hyperactivation of these systems can lead to ventricular hypertrophy and further ‫اﻟﻘﻠﺐ‬ ‫ﻓﺸﻞ‬ ‫أو‬ ‫اﻟﺪم‬ ‫ﺿﻐﻂ‬ ‫ارﺗﻔﺎع‬ ‫أزﻣﺔ‬ ‫ﻣﻦ‬ ‫ﻳﻌﺎﻧﻲ‬ ‫وﻗﺪ‬ ‫اﻟﺤﺎد‬ ‫اﻟﻀﻴﻖ‬ impairment of contractility and cardiac output. The release of inflammatory ‫ﻣﻦ‬ ‫ﺣﺎﻟﺔ‬ ‫ﻓﻲ‬ ‫ﻋﺎدة‬ ‫اﻟﻤﺮﻳﺾ‬ media-‫ ﻳﻜﻮن‬ tors and collagen deposition contribute to myocardial.‫اﻟﻘﻠﺒﻴﺔ‬ ‫اﻟﺴﻜﺘﺔ‬ fibrosis ‫اﻟﺼﺪﻣﺔ اﻟﻘﻠﺒﻴﺔ أو‬ or scarring, which can‫اﻟﺤﺎد أو‬ ‫اﻟﻘﺺ‬ lead‫ﺗﺤﺖ‬ ‫ ﻓﻲ اﻟﺼﺪر‬of to thinning ‫اﻧﺰﻋﺎج‬ ‫ﻣﻔﺎﺟﺊ أو‬ the left ‫(ﻫﻲ أﻟﻢ‬LV) ventricular ‫اﻟﺤﺎدة‬ wall‫اﻟﺘﺎﺟﻲ‬ ‫ﻟﻤﺘﻼزﻣﺔ اﻟﺸﺮﻳﺎن‬ and eventual ‫اﻟﻜﻼﺳﻴﻜﻴﺔ‬ development ‫ اﻷﻋﺮاض‬ of dilated cardiomyopathy. ‫اﻟﺬراﻋﻴﻦ‬ ‫ ﻗﺪ ﺗﻨﺘﺸﺮ اﻷﻋﺮاض إﻟﻰ‬.‫ دﻗﺎﺋﻖ أو أﻛﺜﺮ‬10 ‫ﻳﻮﺻﻒ ﻏﺎﻟ ًﺒﺎ ﺑﺄﻧﻪ ﺿﻐﻂ أو ﺛﻘﻞ أو ﺿﻴﻖ ﻳﺴﺘﻤﺮ ﻟﻤﺪة‬ ‫أﻳﻀﺎ ﻏﺜﻴﺎن أو ﻗﻲء‬ ‫ أو‬Complications ً of ‫ﻫﻨﺎك‬ MI ‫ﻳﻜﻮن‬ include ventricular ‫ ﻗﺪ‬.‫اﻟﻔﻚ‬ arrhythmias, ‫أو اﻟﺒﻄﻦ أو‬ ‫اﻷﻳﺴﺮ( أو اﻟﻈﻬﺮ‬ bradyarrhythmias, ‫)ﺧﺎﺻﺔ ﻋﻠﻰ اﻟﺠﺎﻧﺐ‬heart ‫واﻟﻜﺘﻔﻴﻦ‬ block, heart failure (HF), cardiogenic shock, LV free-wall or septal rupture, throm- boembolism (including stroke secondary to LV thrombus embolization),.‫ﻓﻲ اﻟﺘﻨﻔﺲ‬ ‫ﺗﻌﺮق أو ﺿﻴﻖ‬ aneurysm ‫اﻟﻬﻀﻢ‬ ‫ﺷﺮﺳﻮﻓﻲ وﻋﺴﺮ‬ formation, ‫ ﻣﺜﻞ أﻟﻢ‬،‫اﻟﺼﺪر‬ and pericarditis. Many‫ﻓﻲ‬patients ‫ﺑﺪون أﻟﻢ‬with ‫ﻧﻤﻄﻴﺔ‬ACS ‫ﻏﻴﺮ‬develop ‫ﻣﻦ أﻋﺮاض‬ ‫ﻣﻦ اﻟﻤﺮﺿﻰ‬ depression ‫اﻟﻌﺪﻳﺪ‬the during ‫ ﻳﻌﺎﻧﻲ‬ ‫ﻣﻦ‬ ‫اﻟﺬﻳﻦ ﻳﻌﺎﻧﻮن‬period. convalescent ‫ ﻛﺒﺎر اﻟﺴﻦ واﻟﻨﺴﺎء واﻟﻤﺮﺿﻰ‬.‫وأﻟﻢ ﺻﺪري ﺟﻨﺒﻲ وﺿﻴﻖ ﺗﻨﻔﺲ ﻣﺘﺰاﻳﺪ ﻋﻨﺪ ﺑﺬل ﻣﺠﻬﻮد‬.‫ﻣﺮض اﻟﺴﻜﺮي واﺧﺘﻼل وﻇﺎﺋﻒ اﻟﻜﻠﻰ واﻟﺨﺮف ﻫﻢ أﻛﺜﺮ ﻋﺮﺿﺔ ﻟﻺﺻﺎﺑﺔ ﺑﺨﺼﺎﺋﺺ ﻏﻴﺮ ﻧﻤﻄﻴﺔ‬ ‫أو‬CLINICAL S4 ‫ﻏﻴﺮ اﻟﻤﺤﺪدة‬ PRESENTATION ‫ ﺗﺸﻤﻞ اﻟﻨﺘﺎﺋﺞ‬.‫ ﻻ ﺗﻮﺟﺪ ﻧﺘﺎﺋﺞ ﻓﺤﺺ ﺑﺪﻧﻲ ﺧﺎﺻﺔ ﺑﻤﺘﻼزﻣﺔ اﻟﺸﺮﻳﺎن اﻟﺘﺎﺟﻲ اﻟﺤﺎدة‬ ‫ﺗﻤﺪد‬ ‫اﻟﻤﻌﻮض‬ ‫ﻏﻴﺮ‬ ‫اﻟﺤﺎد‬ The patient is typically ‫ﻗﺼﻮر اﻟﻘﻠﺐ‬ ‫ﻋﻼﻣﺎت‬ in acute ‫ﺗﺸﻤﻞ‬and distress.‫اﻻﺳﺘﻤﺎع‬ ‫ ﻋﻨﺪ‬S2with may present ‫اﻟﻘﻠﺐ‬or‫ﻷﺻﻮات‬ develop‫اﻟﻤﺘﻨﺎﻗﺾ‬ hyperten-‫اﻻﻧﻘﺴﺎم‬ ،‫اﻟﻘﻠﺐ‬ sive‫ﺿﺮﺑﺎت‬ crisis, ‫اﻧﺘﻈﺎم‬ acute HF, ً ‫اﻟﻤﺮﺿﻰ‬ ‫ﻋﺪم‬cardiogenic ‫أﻳﻀﺎ ﻣﻦ‬ shock,‫ﻳﻌﺎﻧﻲ‬ ‫ ﻗﺪ‬.‫اﻻﺳﺘﻤﺎع‬ or cardiac ‫ ﻋﻨﺪ‬S3‫ و‬،‫ وذﻣﺔ اﻟﺮﺋﺔ‬،‫اﻟﻮرﻳﺪ اﻟﻮداﺟﻲ‬ arrest. The classic symptom of.‫اﻟﺼﺪﻣﺔ‬ ACS is‫أو‬abrupt-onset ،‫اﻧﺨﻔﺎض ﺿﻐﻂ اﻟﺪم‬ substernal ‫ أو‬،‫اﻟﺪم‬ chest‫ﺿﻐﻂ‬ pain ‫ارﺗﻔﺎع‬ ‫ أو‬،‫ اﻟﻘﻠﺐ‬often or discomfort ‫أو اﻧﺴﺪاد‬ described as a squeezing, heaviness, or tightness that persists for 10 minutes or longer. ‫اﻟﺘﺸﺨﻴﺺ‬ Symptoms may radiate to the arms and shoulders (especially on the left side), back, abdo- ‫ ﺗﺸﻤﻞ اﻟﺘﻐﻴﻴﺮات‬.‫ دﻗﺎﺋﻖ ﻣﻦ اﻟﻌﺮض‬10 ‫ ﺳﻠﻜًﺎ ﻓﻲ ﻏﻀﻮن‬12 ‫ اﻟﺤﺼﻮل ﻋﻠﻰ ﺗﺨﻄﻴﻂ ﻛﻬﺮﺑﻴﺔ اﻟﻘﻠﺐ ﻣﻦ‬ men, or jaw. Nausea, vomiting, diaphoresis, or shortness of breath may also be present..T ‫اﻟﻤﻮﺟﺔ‬ Many‫واﻧﻌﻜﺎس‬ patients،ST have‫اﻟﻘﻄﻌﺔ‬ ‫واﻧﺨﻔﺎض‬ atypical symptoms،ST (STE) ‫اﻟﻘﻄﻌﺔ‬ without chest‫ارﺗﻔﺎع‬ pain,‫اﻟﺤﺎد‬ such‫اﻟﺘﺮوﻳﺔ‬ ‫ إﻟﻰ ﻧﻘﺺ‬pain, as epigastric ‫اﻟﺘﻲ ﺗﺸﻴﺮ‬ ‫ﺑﻤﺘﻼزﻣﺔ‬ ‫إﺻﺎﺑﺘﻬﻢ‬pleuritic indigestion, ‫ﻳﺸﺘﺒﻪ ﻓﻲ‬chest‫ اﻟﺬﻳﻦ‬pain, ‫اﻟﻤﺮﺿﻰ‬and ‫ﻟﺪى‬increasing (LBBB) ‫اﻟﺠﺪﻳﺪة‬ ‫اﻟﻴﺴﺮى‬ exertional ‫ﻓﺮع اﻟﺤﺰﻣﺔ‬ dyspnea. Older‫ﻛﺘﻠﺔ‬adults, ‫ﻳﺸﻴﺮ وﺟﻮد‬ women, ‫ﺑﻤﺘﻼزﻣﺔ‬ and patients ‫اﻟﻤﺼﺎﺑﻴﻦ‬ ‫ﺑﻌﺾ اﻟﻤﺮﺿﻰ‬ with ‫ﻳﻌﺎﻧﻲ‬ diabetes mellitus ‫ ﻻ‬.‫اﻟﺤﺎد‬ ‫( اﻟﻘﻠﺐ‬DM), impaired ‫اﺣﺘﺸﺎء ﻋﻀﻠﺔ‬ renal‫اﻟﺤﺎدة‬ ‫ﺑﻘﻮة إﻟﻰ‬ function, ‫اﻟﺘﺎﺟﻲ‬and ‫اﻟﺸﺮﻳﺎن‬ dementia are more ‫اﻟﺘﺎرﻳﺦ اﻟﻄﺒﻲ‬ ‫ﺗﻘﻴﻴﻢ‬likely ‫ﻳﺠﺐ‬to present ‫ﻟﺬﻟﻚ‬ ،‫اﻟﻘﻠﺐ‬with ‫ﻛﻬﺮﺑﻴﺔ‬atypical ‫ﺗﺨﻄﻴﻂ‬features. ‫اﻟﺸﺮﻳﺎن اﻟﺘﺎﺟﻲ اﻟﺤﺎدة ﻣﻦ أي ﺗﻐﻴﻴﺮات ﻓﻲ‬ No.‫اﻟﻤﺨﺎﻃﺮ‬ physical examination findings are specific to ACS. Nonspecific findings include ‫واﻷﻋﺮاض اﻟﺤﺎﻟﻴﺔ واﻟﻌﻼﻣﺎت اﻟﺤﻴﻮﻳﺔ اﻟﻘﻠﺒﻴﺔ ﺑﻌﻨﺎﻳﺔ ﻋﻨﺪ إﺟﺮاء اﻟﺘﻘﻴﻴﻢ اﻟﻤﻨﺎﺳﺐ وﺗﻘﺴﻴﻢ‬ S4 or paradoxical splitting of S2 heart sounds on auscultation. Signs of acute decom- ‫إﺻﺎﺑﺔ‬ ‫ﻋﻦ‬ ‫ﻟﻠﻜﺸﻒ‬ pensated HF include ‫ﺳﺎﻋﺎت‬jugular 6-3 ‫ ﺑﻌﺪ‬venous ‫اﻟﻌﺮض وﻳﺘﻜﺮر‬ ‫ﻓﻲ وﻗﺖ‬ distention, (I ‫ أو‬T ‫)إﻣﺎ‬edema, pulmonary ‫ﺗﺮوﺑﻮﻧﻴﻦ اﻟﻘﻠﺐ‬ and an‫ﻗﻴﺎس‬S3 on‫ ﻳﺘﻢ‬ ‫ﻓﻲ‬ (‫اﻟﻤﺮﺟﻌﻲ اﻟﻌﻠﻮي‬ auscultation. ‫ اﻟﺤﺪ‬may Patients ‫ ﻣﻦ‬99also‫اﻟﻤﺌﻮﻳﺔ‬ ‫اﻟﻨﺴﺒﺔ‬ present ‫)ﺗﺘﺠﺎوز‬ with ‫اﻟﺪم اﻟﻤﺮﺗﻔﻌﺔ‬ arrhythmias, heart‫ﻣﺴﺘﻮﻳﺎت‬ block, ‫ﺗﺤﺪث‬ ‫ﻋﻀﻠﺔ اﻟﻘﻠﺐ؛‬ hypertension ‫(ﺗﻌﺘﺒﺮ‬HTN),.‫أﺳﺒﻮﻋﻴﻦ‬ hypotension, ‫ﻟﻤﺪة ﺗﺼﻞ إﻟﻰ‬ or‫ﻣﺮﺗﻔﻌﺔ‬ shock.‫ ﺳﺎﻋﺎت ﻣﻦ إﺻﺎﺑﺔ اﻟﺨﻼﻳﺎ اﻟﻌﻀﻠﻴﺔ أو ﻧﺨﺮﻫﺎ وﻗﺪ ﺗﻈﻞ‬4-2 ‫ﻏﻀﻮن‬ ‫ أو أﻛﺜﺮ ﻓﻲ ﻗﻴﻢ‬%20 ‫أو اﻧﺨﻔﺎض ﺑﻨﺴﺒﺔ‬/‫إﺻﺎﺑﺔ ﻋﻀﻠﺔ اﻟﻘﻠﺐ ﺣﺎدة إذا ﻛﺎن ﻫﻨﺎك ارﺗﻔﺎع دﻳﻨﺎﻣﻴﻜﻲ و‬ DIAGNOSIS ‫اﻟﺸﺮﻳﺎن‬ ‫ ﺗﺆﻛﺪ اﻟﻤﺴﺘﻮﻳﺎت اﻟﻤﺮﺗﻔﻌﺔ ﻟﺪى اﻟﻤﺮﻳﺾ اﻟﺬي ﻳﻌﺎﻧﻲ ﻣﻦ أﻋﺮاض ﻣﺘﻼزﻣﺔ‬.‫اﻟﺘﺮوﺑﻮﻧﻴﻦ اﻟﺘﺴﻠﺴﻠﻴﺔ‬ ‫اﻟﺘﺮوﻳﺔ‬12-lead Obtain ‫ﻋﻠﻰ ﻧﻘﺺ‬ ECG ‫آﺧﺮ‬within ‫أي دﻟﻴﻞ‬10‫أو‬minutes ‫ﻛﻬﺮﺑﻴﺔ اﻟﻘﻠﺐ‬ ‫ ﻋﻠﻰ ﺗﺨﻄﻴﻂ‬Changes of presentation. ‫اﻟﺘﻐﻴﺮات اﻹﻗﻔﺎرﻳﺔ‬ suggestive‫اﻟﺤﺎدة أو‬ of acute‫اﻟﺘﺎﺟﻲ‬ ‫ﻇﻬﻮر‬ ‫ﺳﺎﻋﺎت ﻣﻦ‬ ischemia 6 ‫ﺑﻌﺪ‬ST-segment include ‫ﺗﺮوﺑﻮﻧﻴﻦ إﺿﺎﻓﻴﺔ‬ ‫ﻣﺴﺘﻮﻳﺎت‬ elevation ‫ﻋﻠﻰ‬ST-segment (STE), ‫ﻳﺠﺐ اﻟﺤﺼﻮل‬depression,.‫ﻋﻀﻠﺔ اﻟﻘﻠﺐ‬and ‫اﺣﺘﺸﺎء‬ ‫ﺗﺸﺨﻴﺺ‬ T-wave inversion. ‫اﻟﺘﺎﺟﻲ‬ ‫اﻟﺸﺮﻳﺎن‬Presence ‫ﻟﻤﺘﻼزﻣﺔ‬of‫اﻟﺨﻄﻮرة‬ a new left‫ﻋﺎﻟﻴﺔ‬ bundle-branch ‫ﺳﻤﺎت ﻣﺘﻮﺳﻄﺔ إﻟﻰ‬ block‫(ﻣﻦ‬LBBB) ‫ ﻳﻌﺎﻧﻮن‬in patients ‫اﻟﺬﻳﻦ‬ ‫اﻟﻤﺮﺿﻰ‬with‫ ﻟﺪى‬sus- ‫اﻷﻋﺮاض‬ pected ACS is strongly suggestive of acute.‫اﻟﺘﺴﻠﺴﻠﻴﺔ‬ MI. Some ‫اﻟﻘﻴﺎﺳﺎت‬ patients ‫ﻃﺒﻴﻌﻴﺔ أﺛﻨﺎء‬ with ACS ‫اﻟﺘﺮوﺑﻮﻧﻴﻦ‬ have no‫وﻟﻜﻦ‬ ‫ﻣﺴﺘﻮﻳﺎت‬ ECG ‫اﻟﺤﺎدة‬ changes, so appropriate evaluation and risk stratification must carefully assess medi- ‫ ﻣﻢ ﻋﻠﻰ اﻷﻗﻞ‬1 ‫ ﺑﻤﻘﺪار‬ST ‫ ﺗﺆﻛﺪ ﻣﺴﺘﻮﻳﺎت اﻟﺘﺮوﺑﻮﻧﻴﻦ اﻟﻘﻠﺒﻴﺔ اﻟﺪﻳﻨﺎﻣﻴﻜﻴﺔ اﻟﻤﺮﺗﻔﻌﺔ ﻣﻊ ارﺗﻔﺎع اﻟﻘﻄﻌﺔ‬ cal history, presenting symptoms, and cardiac biomarkers. ‫اﺣﺘﺸﺎء‬ Cardiac ‫ﺗﺸﺨﻴﺺ‬ troponin ‫اﻟﻌﺮض‬ ‫أﺛﻨﺎء‬T‫اﻟﻘﻠﺐ‬ (either or I)‫ﻛﻬﺮﺑﻴﺔ‬ ‫ﺗﺨﻄﻴﻂ‬at‫ﻋﻠﻰ‬ is measured the‫ﺟﺪﻳﺪ‬ timeLBBB ‫ﻣﺘﺠﺎورﻳﻦ أو وﺟﻮد‬ of presentation ‫ﻓﻲ ﺳﻠﻜﻴﻦ‬ and repeated ‫ﻟﻠﻤﺮﺿﻰ‬ ‫ﻣﻨﺎﺳﺐ‬ 3–6 hours ‫اﻻﻧﺴﺪادي‬ later to detect‫ﻏﻴﺮ‬myocardial ‫ﻋﻀﻠﺔ اﻟﻘﻠﺐ‬injury; ‫اﺣﺘﺸﺎء‬elevated ‫ﺗﺸﺨﻴﺺ‬blood ‫ ﻓﺈن‬،‫ذﻟﻚ‬ ‫( ﻣﻦ‬exceeding levels ‫ ﻋﻠﻰ اﻟﻨﻘﻴﺾ‬the.‫اﻟﻘﻠﺐ‬ 99th‫ﻋﻀﻠﺔ‬ percentile ‫دون ارﺗﻔﺎع‬ of ‫ﻣﺮﺗﻔﻌﺔ‬ the upper reference ‫ﺗﺮوﺑﻮﻧﻴﻦ‬ ‫وﻣﺴﺘﻮﻳﺎت‬limit)‫اﻟﺤﺎدة‬ occur‫اﻟﺘﺎﺟﻲ‬ within‫اﻟﺸﺮﻳﺎن‬ 2–4 hours of myocyte ‫ﻣﺘﻼزﻣﺔ‬ ‫ﻣﻦ أﻋﺮاض‬injury ‫ﻳﻌﺎﻧﻮن‬or‫اﻟﺬﻳﻦ‬ necrosis and may ‫اﻟﻤﺮﺿﻰ اﻟﺬﻳﻦ‬ remain ‫ﻳﻌﺎﻧﻲ‬ elevated ‫ ﻗﺪ‬.‫اﻟﻌﺮض‬ ‫ﻋﻨﺪ‬as‫اﻟﻘﻠﺐ‬ long‫ﻛﻬﺮﺑﻴﺔ‬ as 2 weeks. ‫ﺗﺨﻄﻴﻂ‬Myocardial ‫ﻋﻠﻰ اﻷﻗﻞ ﻓﻲ‬ injury ‫ ﻣﻢ‬1is‫ﺑﻤﻘﺪار‬ considered ST ‫اﻟﻘﻄﻌﺔ‬ acute if there is a dynamic rise and/or fall by 20% or more in serial troponin values. ‫ﻳﻌﺎﻧﻮن ﻣﻦ أﻋﺮاض ﻣﺘﻮاﻓﻘﺔ ﻣﻊ ﻣﺘﻼزﻣﺔ اﻟﺸﺮﻳﺎن اﻟﺘﺎﺟﻲ اﻟﺤﺎدة وﻟﻜﻦ ﻻ ﻳﺮﺗﻔﻊ ﻟﺪﻳﻬﻢ ﺗﺮوﺑﻮﻧﻴﻦ ﻣﻦ اﻟﺘﻬﺎب‬ Elevated levels in a patient with ACS symptoms, ischemic changes on ECG, or other evidence of ischemia confirm the diagnosis of MI. Additional.‫ﺗﺸﺨﻴﺺ ﺑﺪﻳﻞ‬ troponin‫أو‬levels ‫اﻟﺼﺪﻏﻲ‬ ‫اﻟﺸﺮاﻳﻴﻦ‬ should be obtained beyond 6 hours after symptom onset in patients with intermediate- to high-risk features of ACS but normal troponin levels during serial measurements. Elevated dynamic cardiac troponin levels with ST-segment elevation of at least 1 mm in two contiguous leads or new LBBB on the presenting ECG confirms the diagnosis of STEMI. In contrast, the diagnosis of NSTEMI is appropriate for patients with symptoms of ACS and elevated troponin levels without at least 1 mm ST-segment‫اﻟﻌﻼج‬ elevation on the ECG at presentation. Patients with symptoms consistent with ACS ‫( اﺳﺘﻌﺎدة ﺗﺪﻓﻖ اﻟﺪم إﻟﻰ اﻟﺸﺮﻳﺎن اﻟﻤﺼﺎب ﻣﺒﻜﺮً ا ﻟﻤﻨﻊ‬1) :‫ ﺗﺘﻀﻤﻦ اﻷﻫﺪاف ﻗﺼﻴﺮة اﻟﻤﺪى‬:‫ أﻫﺪاف اﻟﻌﻼج‬ but in whom troponin is not elevated may have UA or an alternative diagnosis. ‫ﺗﻮﺳﻊ اﻻﺣﺘﺸﺎء )ﻓﻲ ﺣﺎﻟﺔ اﺣﺘﺸﺎء ﻋﻀﻠﺔ اﻟﻘﻠﺐ( أو ﻣﻨﻊ اﻻﻧﺴﺪاد اﻟﻜﺎﻣﻞ واﺣﺘﺸﺎء ﻋﻀﻠﺔ اﻟﻘﻠﺐ )ﻓﻲ ﺣﺎﻟﺔ‬ (4)‫و‬ ،‫( ﻣﻨﻊ إﻋﺎدة اﻧﺴﺪاد اﻟﺸﺮﻳﺎن اﻟﺘﺎﺟﻲ‬3) ،‫( ﻣﻨﻊ اﻟﻮﻓﺎة واﻟﻤﻀﺎﻋﻔﺎت اﻷﺧﺮى‬2) ،(‫اﺣﺘﺸﺎء ﻋﻀﻠﺔ اﻟﻘﻠﺐ‬ TREATMENT ،‫ ﺗﺘﻀﻤﻦ اﻷﻫﺪاف ﻃﻮﻳﻠﺔ اﻟﻤﺪى اﻟﺘﺤﻜﻢ ﻓﻲ ﻋﻮاﻣﻞ اﻟﺨﻄﺮ اﻟﻘﻠﺒﻴﺔ اﻟﻮﻋﺎﺋﻴﺔ‬.‫ﺗﺨﻔﻴﻒ اﻧﺰﻋﺎج اﻟﺼﺪر اﻹﻗﻔﺎري‬ Goals of Treatment: Short-term goals‫وﺗﺤﺴﻴﻦ‬.‫ﻧﻮﻋﻴﺔ اﻟﺤﻴﺎة‬ include:،‫اﻹﺿﺎﻓﻴﺔ‬ (1) early restoration ‫اﻟﺪﻣﻮﻳﺔ‬ ‫واﻷوﻋﻴﺔ‬of‫اﻟﻘﻠﺐ‬ blood flow‫وﻣﻨﻊ‬ ‫أﺣﺪاث‬ to the affected artery to prevent infarct expansion (in the case of MI) or prevent 52 https://ebookmedicine.com/ 06_Schwinghammer_ch05.indd 52 13/03/23 11:36 AM Acute Coronary Syndromes  |  CHAPTER 5 complete occlusion and MI (in UA), (2) prevention of death and other complica- tions, (3) prevention of coronary artery reocclusion, and (4) relief of ischemic chest discomfort. Long-term goals include control of cardiovascular (CV) risk factors, prevention of additional CV events, and improvement in quality of life. GENERAL APPROACH TO TREATMENT OF ACS The clinical presentation, past medical history, ECG, and biomarkers are used to stratify patients as low, medium, or high risk and determine which patients may ben- efit from reperfusion therapy, an early invasive approach, or medical management. Treatment decisions are based on the initial and ongoing risk stratification (Fig. 5-1). Because STEMI has the highest short-term risk of death, these patients should be emergently referred for primary PCI; confirmation of elevated troponin should not delay treatment. General measures include hospital admission, oxygen administration if saturation is

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