Acute Coronary Syndromes PDF
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Terry L. Schwinghammer
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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