বিসমিল্লাহির রহমানির রহিম 

#DAVIDSON_REVIEW 
#CARDIOLOGY 3

Page 483-504 (424 - 442)

Box 16.36 *** (Changed)

Box 16.38 *** 𝗝𝗮𝗻 𝟮𝟬
Angina pectoris ***
Box 16.39 *** (23rd + 24th)
Box 16.41 *
Acute coronary syndrome **********
Box 16.45 ***
Box 16.47 *** (Changed)
Box 16.48 **
Box 16.49 *****
Box 16.50 ***
Box 16.51 ***
Fig 16.70 (16.69) **
Box 16.52 *****
Peripheral arterial disease *
Box 26.56 *
Box 16.57 ***
Box 16.58 ***
Box 16.60 ***

      𝗖𝗢𝗥𝗢𝗡𝗔𝗥𝗬 𝗔𝗥𝗧𝗘𝗥𝗬 𝗗𝗜𝗦𝗘𝗔𝗦𝗘

*** 𝗖𝗼𝗺𝗺𝗼𝗻𝗲𝘀𝘁 𝗰𝗮𝘂𝘀𝗲 𝗼𝗳 𝗮𝗻𝗴𝗶𝗻𝗮 & 𝗮𝗰𝘂𝘁𝗲 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲 & 𝗹𝗲𝗮𝗱𝗶𝗻𝗴
𝗰𝗮𝘂𝘀𝗲 𝗼𝗳 𝗱𝗲𝗮𝘁𝗵 𝘄𝗼𝗿𝗹𝗱𝘄𝗶𝗱𝗲

🔹In the vast majority of patients, CAD is caused by atherosclerosis 

🔹𝗠𝗮𝗰𝗿𝗼𝗽𝗵𝗮𝗴𝗲𝘀/𝗠𝗼𝗻𝗼𝗰𝘆𝘁𝗲𝘀 : 𝗠𝗼𝘀𝘁 𝗶𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝘁 𝗰𝗲𝗹𝗹 𝗶𝗻 𝗽𝗮𝘁𝗵𝗼𝗴𝗲𝗻𝗲𝘀𝗶𝘀 𝗼𝗳
𝗮𝘁𝗵𝗲𝗿𝗼𝘀𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀 (𝗦𝗕𝗔)

*** Vulnerable plaques are characterised by 

  + Lipid-rich core 
  + Thin fibrocellular cap
  + Speckled calcification  
  + Increase in inflammatory cells 

*** Stable plaques are typified by 

  + Small lipid pool,  
  + Thick fibrous cap
  + Heavy calcification  
  + Plentiful collagenous cross-links

*** 𝗔𝗴𝗲 : 𝗠𝗼𝘀𝘁 𝗽𝗼𝘄𝗲𝗿𝗳𝘂𝗹 𝗶𝗻𝗱𝗲𝗽𝗲𝗻𝗱𝗲𝗻𝘁 𝗿𝗶𝘀𝗸 𝗳𝗮𝗰𝘁𝗼𝗿 𝗳𝗼𝗿 𝗮𝘁𝗵𝗲𝗿𝗼𝘀𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀 (𝗦𝗕𝗔)

*** 𝗦𝗺𝗼𝗸𝗶𝗻𝗴 : 𝗠𝗼𝘀𝘁 𝗶𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝘁 𝗺𝗼𝗱𝗶𝗳𝗶𝗮𝗯𝗹𝗲 𝗿𝗶𝘀𝗸 𝗳𝗮𝗰𝘁𝗼𝗿 (𝗦𝗕𝗔)

.

Box 16.38
   + SBA & MCQ
   + Q: Factors affecting oxygen demand / coronary blood flow?
   + 𝗖𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗯𝗹𝗼𝗼𝗱 𝗳𝗹𝗼𝘄 𝗼𝗰𝗰𝘂𝗿𝘀 𝗺𝗮𝗶𝗻𝗹𝘆 𝗶𝗻 𝗱𝗶𝗮𝘀𝘁𝗼𝗹𝗲

                    𝗔𝗡𝗚𝗜𝗡𝗔 𝗣𝗘𝗖𝗧𝗢𝗥𝗜𝗦

   + Syndrome X ***
   + Anti anginal drug *****

🔹Symptom complex caused by transient myocardial ischaemia due to an imbalance

between myocardial oxygen supply & demand

*** 𝗖𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝘁𝗵𝗲𝗿𝗼𝘀𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀 : 𝗠𝗼𝘀𝘁 𝗰𝗼𝗺𝗺𝗼𝗻 𝗰𝗮𝘂𝘀𝗲 𝗼𝗳 𝗮𝗻𝗴𝗶𝗻𝗮 𝗽𝗲𝗰𝘁𝗼𝗿𝗶𝘀

(𝗦𝗕𝗔)

🔹Angina may also occur in 

  + Aortic valve disease 
  + Hypertrophic cardiomyopathy 
  + Vasculitis or aortitis.
🔹Coronary artery spasm + Transient ST elevation : Prinzmetal's angina 

*** Syndrome X
   + 𝗧𝘆𝗽𝗶𝗰𝗮𝗹 𝗮𝗻𝗴𝗶𝗻𝗮 𝗼𝗻 𝗲𝗳𝗳𝗼𝗿𝘁
   + 𝗡𝗼𝗿𝗺𝗮𝗹 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗿𝘁𝗲𝗿𝗶𝗲𝘀 𝗼𝗻 𝗮𝗻𝗴𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆
   + 𝗢𝗯𝗷𝗲𝗰𝘁𝗶𝘃𝗲 𝗲𝘃𝗶𝗱𝗲𝗻𝗰𝗲 𝗼𝗳 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗶𝘀𝗰𝗵𝗮𝗲𝗺𝗶𝗮 𝗼𝗻 𝘀𝘁𝗿𝗲𝘀𝘀 𝘁𝗲𝘀𝘁𝗶𝗻𝗴 
   + 𝗠𝗼𝗿𝗲 𝗰𝗼𝗺𝗺𝗼𝗻 𝗶𝗻 𝘄𝗼𝗺𝗲𝗻
   + 𝗚𝗼𝗼𝗱 𝗽𝗿𝗼𝗴𝗻𝗼𝘀𝗶𝘀
   + 𝗥𝗲𝘀𝗽𝗼𝗻𝗱 𝘃𝗮𝗿𝗶𝗮𝗯𝗹𝘆 𝘁𝗼 𝗮𝗻𝘁𝗶 𝗮𝗻𝗴𝗶𝗻𝗮𝗹 𝘁𝗵𝗲𝗿𝗮𝗽𝘆 

🔹𝗛𝗶𝘀𝘁𝗼𝗿𝘆 𝗶𝘀 𝘁𝗵𝗲 𝗺𝗼𝘀𝘁 𝗶𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝘁 𝗳𝗮𝗰𝘁𝗼𝗿 𝗶𝗻 𝗺𝗮𝗸𝗶𝗻𝗴 𝘁𝗵𝗲 𝗱𝗶𝗮𝗴𝗻𝗼𝘀𝗶𝘀

🔹An exercise ECG is commonly performed 
   + 𝗣𝗹𝗮𝗻𝗮𝗿 𝗼𝗿 𝗱𝗼𝘄𝗻-𝘀𝗹𝗼𝗽𝗶𝗻𝗴 𝗦𝗧 𝗱𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 𝗼𝗳 𝟭 𝗺𝗺 𝗼𝗿 𝗺𝗼𝗿𝗲 𝗶𝘀 𝗶𝗻𝗱𝗶𝗰𝗮𝘁𝗶𝘃𝗲
𝗼𝗳 𝗶𝘀𝗰𝗵𝗮𝗲𝗺𝗶𝗮 
   + 𝗨𝗽-𝘀𝗹𝗼𝗽𝗶𝗻𝗴 𝗦𝗧 𝗱𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 𝗶𝘀 𝗹𝗲𝘀𝘀 𝘀𝗽𝗲𝗰𝗶𝗳𝗶𝗰 
🔹False-positive results can occur with 
   + Digoxin therapy
   + Left ventricular hypertrophy
   + Bundle branch block 
   + WPW syndrome
🔹𝗜𝗳 𝘁𝗵𝗲 𝗱𝗶𝗮𝗴𝗻𝗼𝘀𝗶𝘀 𝗶𝘀 𝘂𝗻𝗰𝗹𝗲𝗮𝗿, 𝗖𝗧 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗻𝗴𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆 𝗶𝘀 𝘁𝗵𝗲 𝗶𝗺𝗮𝗴𝗶𝗻𝗴
𝗶𝗻𝘃𝗲𝘀𝘁𝗶𝗴𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗳𝗶𝗿𝘀𝘁 𝗰𝗵𝗼𝗶𝗰𝗲 (𝗦𝗕𝗔)

❤️𝗠𝗮𝗻𝗮𝗴𝗲𝗺𝗲𝗻𝘁

*** 𝗔𝗹𝗹 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝗮𝗻𝗴𝗶𝗻𝗮 𝘀𝗲𝗰𝗼𝗻𝗱𝗮𝗿𝘆 𝘁𝗼 𝗖𝗔𝗗 𝘀𝗵𝗼𝘂𝗹𝗱 𝗿𝗲𝗰𝗲𝗶𝘃𝗲 𝗮𝗻𝘁𝗶𝗽𝗹𝗮𝘁𝗲𝗹𝗲𝘁
𝘁𝗵𝗲𝗿𝗮𝗽𝘆

*** 𝗔𝗹𝗹 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝗽𝗿𝗲𝘀𝗰𝗿𝗶𝗯𝗲𝗱 𝗮 𝘀𝘁𝗮𝘁𝗶𝗻, 𝗲𝘃𝗲𝗻 𝗶𝗳 𝗰𝗵𝗼𝗹𝗲𝘀𝘁𝗲𝗿𝗼𝗹 𝗶𝘀 𝗻𝗼𝗿𝗺𝗮𝗹 

Anti anginal drug therapy 

🔹It is conventional to start therapy with sublingual GTN & β-blocker & then add a CCB or a
long-acting nitrate if needed. 
  
   *** Nitrates 
 🔹Venous & arteriolar dilatation. 
 🔹They help angina by 
   + 𝗛𝗲𝗹𝗹𝗼 𝗟𝗼𝘄𝗲𝗿𝗶𝗻𝗴 𝗽𝗿𝗲𝗹𝗼𝗮𝗱 & 𝗮𝗳𝘁𝗲𝗿𝗹𝗼𝗮𝗱, 𝘄𝗵𝗶𝗰𝗵 𝗿𝗲𝗱𝘂𝗰𝗲𝘀 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹
𝗼𝘅𝘆𝗴𝗲𝗻 𝗱𝗲𝗺𝗮𝗻𝗱
   + 𝗜𝗻𝗰𝗿𝗲𝗮𝘀𝗶𝗻𝗴 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗼𝘅𝘆𝗴𝗲𝗻 𝘀𝘂𝗽𝗽𝗹𝘆 𝘁𝗵𝗿𝗼𝘂𝗴𝗵 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝘃𝗮𝘀𝗼𝗱𝗶𝗹𝗮𝘁𝗮𝘁𝗶𝗼𝗻
🔹S/E : Headache, Symptomatic hypotension & Syncope 

   *** Beta-blockers 
🔹Lower myocardial oxygen demand by 
   + 𝗥𝗲𝗱𝘂𝗰𝗶𝗻𝗴 𝗵𝗲𝗮𝗿𝘁 𝗿𝗮𝘁𝗲, 𝗕𝗣 & 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗰𝗼𝗻𝘁𝗿𝗮𝗰𝘁𝗶𝗹𝗶𝘁𝘆
🔹Beta-blockers should not be withdrawn abruptly, as rebound effects may 
   + Precipitate dangerous arrhythmias
   + Worsening angina 
   + Precipitate MI

   *** Calcium channel antagonists 

 🔹Lower myocardial oxygen demand by 𝟴𝗿𝗲𝗱𝘂𝗰𝗶𝗻𝗴 𝗕𝗣 & 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗰𝗼𝗻𝘁𝗿𝗮𝗰𝘁𝗶𝗹𝗶𝘁𝘆.
🔹Dihydropyridine calcium antagonists, such as 𝗻𝗶𝗳𝗲𝗱𝗶𝗽𝗶𝗻𝗲 & 𝗮𝗺𝗹𝗼𝗱𝗶𝗽𝗶𝗻𝗲, 𝗺𝗮𝘆 𝗰𝗮𝘂𝘀𝗲
𝗿𝗲𝗳𝗹𝗲𝘅 𝘁𝗮𝗰𝗵𝘆𝗰𝗮𝗿𝗱𝗶𝗮, it is best to use them with a β-blocker 
🔹 In contrast, 𝘃𝗲𝗿𝗮𝗽𝗮𝗺𝗶𝗹 & 𝗱𝗶𝗹𝘁𝗶𝗮𝘇𝗲𝗺 𝗰𝗮𝗻 𝗯𝗲 𝘂𝘀𝗲𝗱 𝗮𝘀 𝗺𝗼𝗻𝗼𝘁𝗵𝗲𝗿𝗮𝗽𝘆 𝗯𝗲𝗰𝗮𝘂𝘀𝗲
𝘁𝗵𝗲𝘆 𝘀𝗹𝗼𝘄 𝗦𝗔 𝗻𝗼𝗱𝗲 𝗳𝗶𝗿𝗶𝗻𝗴, 𝗶𝗻𝗵𝗶𝗯𝗶𝘁 𝗰𝗼𝗻𝗱𝘂𝗰𝘁𝗶𝗼𝗻 𝘁𝗵𝗿𝗼𝘂𝗴𝗵 𝗔𝗩 𝗻𝗼𝗱𝗲 & 𝘁𝗲𝗻𝗱 𝘁𝗼
𝗰𝗮𝘂𝘀𝗲 𝗯𝗿𝗮𝗱𝘆𝗰𝗮𝗿𝗱𝗶𝗮.
🔹CCB reduce myocardial contractility & must be used with care in patients with poor LV
function.

✅ Potassium channel activators

   + Nicorandil 
   + Vasodilator with effects on arterial & venous systems
   + Does not exhibit the tolerance seen with nitrates

   *** If channel antagonist

🔹Induces 𝗯𝗿𝗮𝗱𝘆𝗰𝗮𝗿𝗱𝗶𝗮 𝗯𝘆 𝗺𝗼𝗱𝘂𝗹𝗮𝘁𝗶𝗻𝗴 𝗶𝗼𝗻 𝗰𝗵𝗮𝗻𝗻𝗲𝗹𝘀 𝗶𝗻 𝘀𝗶𝗻𝘂𝘀 𝗻𝗼𝗱𝗲
🔹𝗗𝗼𝗲𝘀 𝗻𝗼𝘁 𝗶𝗻𝗵𝗶𝗯𝗶𝘁 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗰𝗼𝗻𝘁𝗿𝗮𝗰𝘁𝗶𝗹𝗶𝘁𝘆 & 𝗮𝗽𝗽𝗲𝗮𝗿𝘀 𝘁𝗼 𝗯𝗲 𝘀𝗮𝗳𝗲 𝗶𝗻 𝗛𝗙 

✅ Ranolazine
   + Inhibits late inward Na current in coronary artery smooth muscle cells

*** Vessels used for Coronary artery bypass grafting

   • Internal mammary artery
   • Radial artery
   • Saphenous vein

         𝗔𝗖𝗨𝗧𝗘 𝗖𝗢𝗥𝗢𝗡𝗔𝗥𝗬 𝗦𝗬𝗡𝗗𝗥𝗢𝗠𝗘

+ SBA & MCQ

+ Clinical feature ***
+ Complications 
+ ECG *****
+ Cardiac biomarkers ***
+ Reperfusion therapy ***

♦️Acute coronary syndrome

   + Unstable angina
   + Myocardial infarction

♦️Unstable angina 
   + New-onset or rapidly worsening angina (crescendo angina)
   + Angina on minimal exertion 
   + Angina at rest in absence of myocardial damage 

♦️𝗠𝗜 𝗱𝗶𝗳𝗳𝗲𝗿𝘀 𝗳𝗿𝗼𝗺 𝘂𝗻𝘀𝘁𝗮𝗯𝗹𝗲 𝗮𝗻𝗴𝗶𝗻𝗮, 𝘀𝗶𝗻𝗰𝗲 𝘁𝗵𝗲𝗿𝗲 𝗶𝘀 𝗲𝘃𝗶𝗱𝗲𝗻𝗰𝗲 𝗼𝗳 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹

𝗻𝗲𝗰𝗿𝗼𝘀𝗶𝘀. 

♦️Adverse prognostic factors include 

   + Recurrent ischaemia
   + Extensive ECG changes at rest or during pain
   + Raised troponin I or T levels
   + Arrhythmias 
   + Haemodynamic complications (hypotension, mitral regurgitation). 

*** 𝗔𝗖𝗦 𝗮𝗹𝗺𝗼𝘀𝘁 𝗮𝗹𝘄𝗮𝘆𝘀 𝗼𝗰𝗰𝘂𝗿𝘀 𝗶𝗻 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘄𝗵𝗼 𝗵𝗮𝘃𝗲 𝗮𝘁𝗵𝗲𝗿𝗼𝘀𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀. 

   *** Clinical features (Box 16.49)

*** 𝗖𝗵𝗲𝘀𝘁 𝗽𝗮𝗶𝗻 𝗮𝘁 𝗿𝗲𝘀𝘁 𝗶𝘀 𝘁𝗵𝗲 𝗰𝗮𝗿𝗱𝗶𝗻𝗮𝗹 𝘀𝘆𝗺𝗽𝘁𝗼𝗺 & 𝗯𝗿𝗲𝗮𝘁𝗵𝗹𝗲𝘀𝘀𝗻𝗲𝘀𝘀, 𝘃𝗼𝗺𝗶𝘁𝗶𝗻𝗴
& 𝗰𝗼𝗹𝗹𝗮𝗽𝘀𝗲 𝗮𝗿𝗲 𝗮𝗹𝘀𝗼 𝗰𝗼𝗺𝗺𝗼𝗻 𝗳𝗲𝗮𝘁𝘂𝗿𝗲𝘀. 
*** 𝗣𝗮𝗶𝗻𝗹𝗲𝘀𝘀 𝗼𝗿 ‘𝘀𝗶𝗹𝗲𝗻𝘁’ 𝗠𝗜 𝗺𝗮𝘆 𝗮𝗹𝘀𝗼 𝗼𝗰𝗰𝘂𝗿 𝗶𝘀 𝗽𝗮𝗿𝘁𝗶𝗰𝘂𝗹𝗮𝗿𝗹𝘆 𝗰𝗼𝗺𝗺𝗼𝗻 𝗶𝗻 𝗼𝗹𝗱𝗲𝗿
𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝗼𝗿 𝗗𝗠. 

*** 𝗩𝗼𝗺𝗶𝘁𝗶𝗻𝗴 & 𝘀𝗶𝗻𝘂𝘀 𝗯𝗿𝗮𝗱𝘆𝗰𝗮𝗿𝗱𝗶𝗮 𝗮𝗿𝗲 𝗽𝗮𝗿𝘁𝗶𝗰𝘂𝗹𝗮𝗿𝗹𝘆 𝗰𝗼𝗺𝗺𝗼𝗻 𝗶𝗻 𝗶𝗻𝗳𝗲𝗿𝗶𝗼𝗿 𝗠𝗜 . 

.

𝗔𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮 (Box 16.50)

♦️Risk of arrhythmia can be minimised by 

   + Adequate pain relief
   + Rest &
   + Correction of hypokalaemia

*** 𝗩𝗙 : 𝗠𝗮𝗷𝗼𝗿 𝗰𝗮𝘂𝘀𝗲 𝗼𝗳 𝗱𝗲𝗮𝘁𝗵 𝗶𝗻 𝘁𝗵𝗼𝘀𝗲 𝘄𝗵𝗼 𝗱𝗶𝗲 𝗯𝗲𝗳𝗼𝗿𝗲 𝗿𝗲𝗰𝗲𝗶𝘃𝗶𝗻𝗴 𝗺𝗲𝗱𝗶𝗰𝗮𝗹
𝗮𝘁𝘁𝗲𝗻𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)
  
♦️Inferior MI with AV block : 
   + Usually temporary & often resolves following reperfusion therapy
   + If there is clinical deterioration : Temporary pacemaker should be considered

*** 𝗔𝗩 𝗯𝗹𝗼𝗰𝗸 𝗰𝗼𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗻𝗴 𝗮𝗻𝘁𝗲𝗿𝗶𝗼𝗿 𝗶𝗻𝗳𝗮𝗿𝗰𝘁𝗶𝗼𝗻 𝗶𝘀 𝗺𝗼𝗿𝗲 𝘀𝗲𝗿𝗶𝗼𝘂𝘀 because

asystole may suddenly supervene
.

𝗥𝗲𝗰𝘂𝗿𝗿𝗲𝗻𝘁 𝗮𝗻𝗴𝗶𝗻𝗮

♦️Should be considered for prompt coronary angiography with a view to revascularisation

♦️Patients with dynamic ECG changes & ongoing pain should be treated with IV glycoprotein
IIb/IIIa receptor antagonists tirofiban or abciximab
.

𝗣𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀 (𝗦𝗕𝗔)

♦️Particularly common on 2nd & 3rd days

♦️Patient may recognise 𝗮 𝗱𝗶𝗳𝗳𝗲𝗿𝗲𝗻𝘁 𝗽𝗮𝗶𝗻, 𝗲𝘃𝗲𝗻 𝘁𝗵𝗼𝘂𝗴𝗵 𝗮𝘁 𝘁𝗵𝗲 𝘀𝗮𝗺𝗲
𝘀𝗶𝘁𝗲,𝗽𝗼𝘀𝗶𝘁𝗶𝗼𝗻𝗮𝗹 & 𝘁𝗲𝗻𝗱𝘀 𝘁𝗼 𝗯𝗲 𝘄𝗼𝗿𝘀𝗲 𝗼𝗿 𝘀𝗼𝗺𝗲𝘁𝗶𝗺𝗲𝘀 𝗽𝗿𝗲𝘀𝗲𝗻𝘁 𝗼𝗻𝗹𝘆 𝗼𝗻
𝗶𝗻𝘀𝗽𝗶𝗿𝗮𝘁𝗶𝗼𝗻
♦️Pericardial rub may be audible 
♦️𝗢𝗽𝗶𝗮𝘁𝗲-𝗯𝗮𝘀𝗲𝗱 𝗮𝗻𝗮𝗹𝗴𝗲𝘀𝗶𝗮 𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝘂𝘀𝗲𝗱. ♦️𝗡𝗦𝗔𝗜𝗗𝘀 & 𝘀𝘁𝗲𝗿𝗼𝗶𝗱 𝗺𝗮𝘆 ↑ 𝗿𝗶𝘀𝗸
𝗼𝗳 𝗮𝗻𝗲𝘂𝗿𝘆𝘀𝗺 & 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗿𝘂𝗽𝘁𝘂𝗿𝗲 & 𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝗮𝘃𝗼𝗶𝗱𝗲𝗱. 
.

𝗗𝗿𝗲𝘀𝘀𝗹𝗲𝗿’𝘀 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲 (𝗦𝗕𝗔)

♦️𝗣𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗳𝗲𝘃𝗲𝗿, 𝗽𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀 & 𝗽𝗹𝗲𝘂𝗿𝗶𝘀𝘆 -

♦️𝗣𝗿𝗼𝗯𝗮𝗯𝗹𝘆 𝗱𝘂𝗲 𝘁𝗼 𝗮𝘂𝘁𝗼𝗶𝗺𝗺𝘂𝗻𝗶𝘁𝘆
♦️𝗢𝗰𝗰𝘂𝗿 𝗮 𝗳𝗲𝘄 𝘄𝗲𝗲𝗸𝘀 𝗼𝗿 𝗲𝘃𝗲𝗻 𝗺𝗼𝗻𝘁𝗵𝘀 𝗮𝗳𝘁𝗲𝗿 𝗠𝗜 & 𝗼𝗳𝘁𝗲𝗻 𝘀𝘂𝗯𝘀𝗶𝗱𝗲 𝗮𝗳𝘁𝗲𝗿 𝗳𝗲𝘄
𝗱𝗮𝘆𝘀
♦️𝗥𝘅 : 𝗛𝗶𝗴𝗵-𝗱𝗼𝘀𝗲 𝗮𝘀𝗽𝗶𝗿𝗶𝗻, 𝗡𝗦𝗔𝗜𝗗𝘀 𝗼𝗿 𝗴𝗹𝘂𝗰𝗼𝗰𝗼𝗿𝘁𝗶𝗰𝗼𝗶𝗱𝘀
.

𝗣𝗮𝗽𝗶𝗹𝗹𝗮𝗿𝘆 𝗺𝘂𝘀𝗰𝗹𝗲 𝗿𝘂𝗽𝘁𝘂𝗿𝗲

♦️𝗧𝘆𝗽𝗶𝗰𝗮𝗹𝗹𝘆 𝗽𝗿𝗲𝘀𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝗮𝗰𝘂𝘁𝗲 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗼𝗲𝗱𝗲𝗺𝗮 & 𝘀𝗵𝗼𝗰𝗸 𝗱𝘂𝗲 𝘁𝗼 𝘀𝘂𝗱𝗱𝗲𝗻
𝘀𝗲𝘃𝗲𝗿𝗲 𝗠𝗥
♦️𝗘𝘅𝗮𝗺𝗶𝗻𝗮𝘁𝗶𝗼𝗻 : 𝗣𝗮𝗻𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗺𝘂𝗿𝗺𝘂𝗿 & 𝟯𝗿𝗱 𝗵𝗲𝗮𝗿𝘁 𝘀𝗼𝘂𝗻𝗱 but murmur may be
quiet or absent in severe MR 
♦️Confirmatory : Echocardiography
.

𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝘀𝗲𝗽𝘁𝘂𝗺 𝗿𝘂𝗽𝘁𝘂𝗿𝗲 

♦️𝗨𝘀𝘂𝗮𝗹𝗹𝘆 𝗽𝗿𝗲𝘀𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝘀𝘂𝗱𝗱𝗲𝗻 𝗵𝗮𝗲𝗺𝗼𝗱𝘆𝗻𝗮𝗺𝗶𝗰 𝗱𝗲𝘁𝗲𝗿𝗶𝗼𝗿𝗮𝘁𝗶𝗼𝗻 + 𝗮 𝗻𝗲𝘄 𝗹𝗼𝘂𝗱

𝗽𝗮𝗻𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗺𝘂𝗿𝗺𝘂𝗿 𝗿𝗮𝗱𝗶𝗮𝘁𝗶𝗻𝗴 𝘁𝗼 𝗿𝘁 𝘀𝘁𝗲𝗿𝗻𝗮𝗹 𝗯𝗼𝗿𝗱𝗲𝗿 
♦️𝗖𝗮𝘂𝘀𝗲𝘀 𝗿𝗶𝗴𝗵𝘁 𝗛𝗙 𝗿𝗮𝘁𝗵𝗲𝗿 𝘁𝗵𝗮𝗻 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗼𝗲𝗱𝗲𝗺𝗮 

     *** 
🔹 𝗣𝗮𝗻𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗺𝘂𝗿𝗺𝘂𝗿 + 𝗣𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗲𝗱𝗲𝗺𝗮 : 𝗠𝗥
🔹 𝗣𝗮𝗻𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗺𝘂𝗿𝗺𝘂𝗿 + 𝗥𝗶𝗴𝗵𝘁 𝗵𝗲𝗮𝗿𝘁 𝗳𝗮𝗶𝗹𝘂𝗿𝗲 : 𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝘀𝗲𝗽𝘁𝗮𝗹 𝗿𝘂𝗽𝘁𝘂𝗿𝗲 
.

𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗿𝗲𝗺𝗼𝗱𝗲𝗹𝗹𝗶𝗻𝗴 

♦️𝗔 𝗽𝗼𝘁𝗲𝗻𝘁𝗶𝗮𝗹 𝗰𝗼𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗮𝗻 𝗮𝗰𝘂𝘁𝗲 𝘁𝗿𝗮𝗻𝘀𝗺𝘂𝗿𝗮𝗹 𝗠𝗜 due to thinning &

stretching of infarcted segment
♦️To reduce late ventricular remodelling & prevent onset of HF
   + 𝗕𝗲𝘁𝗮-𝗯𝗹𝗼𝗰𝗸𝗲𝗿
   + 𝗔𝗖𝗘 𝗶𝗻𝗵𝗶𝗯𝗶𝘁𝗼𝗿 
   + 𝗠𝗶𝗻𝗲𝗿𝗮𝗹𝗼𝗰𝗼𝗿𝘁𝗶𝗰𝗼𝗶𝗱 𝗿𝗲𝗰𝗲𝗽𝘁𝗼𝗿 𝗮𝗻𝘁𝗮𝗴𝗼𝗻𝗶𝘀𝘁 
 .

𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗮𝗻𝗲𝘂𝗿𝘆𝘀𝗺

♦️𝗣𝗮𝗿𝘁𝗶𝗰𝘂𝗹𝗮𝗿𝗹𝘆 𝗰𝗼𝗺𝗺𝗼𝗻 𝘄𝗵𝗲𝗻 𝘁𝗵𝗲𝗿𝗲 𝗶𝘀 𝗽𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗼𝗰𝗰𝗹𝘂𝘀𝗶𝗼𝗻 𝗼𝗳 𝗶𝗻𝗳𝗮𝗿𝗰𝘁 -

𝗿𝗲𝗹𝗮𝘁𝗲𝗱 𝘃𝗲𝘀𝘀𝗲𝗹
♦️Complications of aneurysm
   + Heart failure
   + Ventricular arrhythmias
   + Mural thrombus & systemic embolism 
♦️Other features 
   + Paradoxical impulse on chest wall, 
   + 𝗣𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗦𝗧 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 𝗼𝗻 𝗘𝗖𝗚 (𝗦𝗕𝗔)
   + Sometimes an unusual bulge from cardiac silhouette on chest X-ray 
♦️𝗘𝗰𝗵𝗼𝗰𝗮𝗿𝗱𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆 𝗶𝘀 𝗱𝗶𝗮𝗴𝗻𝗼𝘀𝘁𝗶𝗰
.
𝗜𝗻𝘃𝗲𝘀𝘁𝗶𝗴𝗮𝘁𝗶𝗼𝗻

*** 𝟭𝟮-𝗹𝗲𝗮𝗱 𝗘𝗖𝗚 𝗶𝘀 𝗰𝗲𝗻𝘁𝗿𝗮𝗹 𝘁𝗼 𝗰𝗼𝗻𝗳𝗶𝗿𝗺𝗶𝗻𝗴 𝗗𝘅 & 𝗱𝗲𝗰𝗶𝗱𝗶𝗻𝗴 𝗶𝗺𝗺𝗲𝗱𝗶𝗮𝘁𝗲 𝗠𝘅

🔹 Initial ECG may be normal or non diagnostic in one-third of cases

*** 𝗘𝗮𝗿𝗹𝗶𝗲𝘀𝘁 𝗘𝗖𝗚 𝗰𝗵𝗮𝗻𝗴𝗲 : 𝗦𝗧-𝘀𝗲𝗴𝗺𝗲𝗻𝘁 𝗱𝗲𝘃𝗶𝗮𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)

   *** Proximal occlusion of a major coronary artery : 

🔹ST elevation (or new bundle branch block) > 
🔹Diminution in size of R & in transmural infarction, development of Q
 >
🔹T wave invertion (Persists after ST segment has returned to normal) 

   *** Partial occlusion of a major vessel or complete occlusion of a minor vessel 

🔹 Causing unstable angina or partial thickness (subendocardial) MI
🔹 ST depression & T wave change
🔹 Some loss of R wave
🔹 Absence of Q wave
🔹 No ST elevation 

   *** ECG changes in leads (𝗦𝗕𝗔)

♦️𝗔𝗻𝘁𝗲𝗿𝗼𝘀𝗲𝗽𝘁𝗮𝗹 : 𝗩𝟭 𝘁𝗼 𝗩𝟰
♦️𝗔𝗻𝘁𝗲𝗿𝗼𝗹𝗮𝘁𝗲𝗿𝗮𝗹 : 𝗩𝟰 𝘁𝗼 𝗩𝟲,𝗮𝗩𝗟 & 𝗜
♦️𝗜𝗻𝗳𝗲𝗿𝗶𝗼𝗿 : 𝗜𝗜, 𝗜𝗜𝗜 & 𝗮𝗩𝗙 (& 𝗥𝗲𝗰𝗶𝗽𝗿𝗼𝗰𝗮𝗹 𝗦𝗧 𝗱𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 𝗶𝗻 𝗜,𝗮𝗩𝗟 & 𝗮𝗻𝘁𝗲𝗿𝗶𝗼𝗿
𝗰𝗵𝗲𝘀𝘁 𝗹𝗲𝗮𝗱)
♦️𝗣𝗼𝘀𝘁𝗲𝗿𝗶𝗼𝗿 𝘄𝗮𝗹𝗹 𝗼𝗳 𝗟𝗩 : 𝗥𝗲𝗰𝗶𝗽𝗿𝗼𝗰𝗮𝗹 𝗦𝗧 𝗱𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 & 𝘁𝗮𝗹𝗹 𝗥 𝗶𝗻 𝗩𝟭 - 𝗩𝟰
.

𝗖𝗮𝗿𝗱𝗶𝗮𝗰 𝗯𝗶𝗼𝗺𝗮𝗿𝗸𝗲𝗿 

🔹 Unstable angina : No detectable ↑ in troponin

🔹 MI : ↑ In troponin T,I & other cardiac enzymes 

   *** Troponins T & I

+ 𝗜𝗻𝗰𝗿𝗲𝗮𝘀𝗲 𝘄𝗶𝘁𝗵𝗶𝗻 𝟯–𝟲 𝗵𝗼𝘂𝗿𝘀
+ 𝗣𝗲𝗮𝗸 𝗮𝘁 𝗮𝗯𝗼𝘂𝘁 𝟯𝟲 𝗵𝗼𝘂𝗿𝘀 
+ 𝗥𝗲𝗺𝗮𝗶𝗻 𝗲𝗹𝗲𝘃𝗮𝘁𝗲𝗱 𝗳𝗼𝗿 𝘂𝗽 𝘁𝗼 𝟮 𝘄𝗲𝗲𝗸𝘀. 

♦️↑ WBC,CRP & ESR

♦️Lipids should be measured within 24 hr as there is often a transient fall in cholesterol in the
3 months following infarction
♦️Echocardiography is normally performed before discharge from hospital 𝘁𝗼 𝗮𝘀𝘀𝗲𝘀𝘀
𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻 & 𝗳𝗼𝗿 𝗱𝗲𝘁𝗲𝗰𝘁𝗶𝗻𝗴 𝗶𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝘁 𝗰𝗼𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀
.

𝗖𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗿𝘁𝗲𝗿𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆
♦️Should be considered with a view to revascularisation 𝗶𝗻 𝗮𝗹𝗹 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝗮𝘁 𝗺𝗼𝗱𝗲𝗿𝗮𝘁𝗲
𝗼𝗿 𝗵𝗶𝗴𝗵 𝗿𝗶𝘀𝗸 𝗼𝗳 𝗮 𝗳𝘂𝗿𝘁𝗵𝗲𝗿 𝗲𝘃𝗲𝗻𝘁, 𝗶𝗻𝗰𝗹𝘂𝗱𝗶𝗻𝗴 those
   + 𝗪𝗵𝗼 𝗳𝗮𝗶𝗹 𝘁𝗼 𝘀𝗲𝘁𝘁𝗹𝗲 𝗼𝗻 𝗺𝗲𝗱𝗶𝗰𝗮𝗹 𝘁𝗵𝗲𝗿𝗮𝗽𝘆
   + 𝗪𝗶𝘁𝗵 𝗲𝘅𝘁𝗲𝗻𝘀𝗶𝘃𝗲 𝗘𝗖𝗚 𝗰𝗵𝗮𝗻𝗴𝗲𝘀
   + 𝗪𝗶𝘁𝗵 𝗮𝗻 𝗲𝗹𝗲𝘃𝗮𝘁𝗲𝗱 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝘁𝗿𝗼𝗽𝗼𝗻𝗶𝗻 
   + 𝗪𝗶𝘁𝗵 𝘀𝗲𝘃𝗲𝗿𝗲 𝗽𝗿𝗲-𝗲𝘅𝗶𝘀𝘁𝗶𝗻𝗴 𝘀𝘁𝗮𝗯𝗹𝗲 𝗮𝗻𝗴𝗶𝗻𝗮
.

                       𝗠𝗮𝗻𝗮𝗴𝗲𝗺𝗲𝗻𝘁

🔹No complications & angiography not required : Patient can be mobilised from 2nd day &
discharged after 2–3 days. 
🔹Low-risk patients without spontaneous angina : ETT approximately 4 wks after ACS 
.

𝗔𝗻𝗮𝗹𝗴𝗲𝘀𝗶𝗮

♦️Essential to
   + 𝗥𝗲𝗹𝗶𝗲𝘃𝗲 𝗱𝗶𝘀𝘁𝗿𝗲𝘀𝘀 
   + 𝗟𝗼𝘄𝗲𝗿 𝗮𝗱𝗿𝗲𝗻𝗲𝗿𝗴𝗶𝗰 𝗱𝗿𝗶𝘃𝗲 & 𝘁𝗵𝗲𝗿𝗲𝗯𝘆 
✓ 𝗥𝗲𝗱𝘂𝗰𝗲 𝘃𝗮𝘀𝗰𝘂𝗹𝗮𝗿 𝗿𝗲𝘀𝗶𝘀𝘁𝗮𝗻𝗰𝗲, 𝗕𝗣
✓ 𝗜𝗻𝗳𝗮𝗿𝗰𝘁 𝘀𝗶𝘇𝗲 &
✓ 𝗦𝘂𝘀𝗰𝗲𝗽𝘁𝗶𝗯𝗶𝗹𝗶𝘁𝘆 𝘁𝗼 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮𝘀
♦️IV opiates : Morphine sulphate or diamorphine & antiemetics : Metoclopramide
♦️𝗜𝗠 𝗶𝗻𝗷𝗲𝗰𝘁𝗶𝗼𝗻𝘀 𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝗮𝘃𝗼𝗶𝗱𝗲𝗱 because    
   + Clinical effect delayed by poor skeletal muscle perfusion
   + Painful haematoma may form following thrombolytic or antithrombotic therapy
.

𝗥𝗲𝗽𝗲𝗿𝗳𝘂𝘀𝗶𝗼𝗻 𝘁𝗵𝗲𝗿𝗮𝗽𝘆

   *** Immediate reperfusion with PCI when ECG shows 

+ 𝗡𝗲𝘄 𝗕𝗕𝗕 𝗼𝗿 
+ 𝗖𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝘁𝗶𝗰 𝗦𝗧 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 𝗶𝗻 𝟮 𝗰𝗼𝗻𝘁𝗶𝗴𝘂𝗼𝘂𝘀 𝗹𝗲𝗮𝗱𝘀 𝗼𝗳 ≥ 𝟭 𝗺𝗺 𝗶𝗻 𝗹𝗶𝗺𝗯 𝗹𝗲𝗮𝗱𝘀
𝗼𝗿 ≥ 𝟮 𝗺𝗺 𝗶𝗻 𝗰𝗵𝗲𝘀𝘁 𝗹𝗲𝗮𝗱𝘀

 *** 𝗥𝘅 𝗼𝗳 𝗰𝗵𝗼𝗶𝗰𝗲 𝗳𝗼𝗿 𝘁𝗵𝗼𝘀𝗲 𝗽𝗿𝗲𝘀𝗲𝗻𝘁𝗶𝗻𝗴 𝘄𝗶𝘁𝗵𝗶𝗻 𝟭𝟮 𝗵𝗼𝘂𝗿𝘀 𝗼𝗳 𝘀𝘆𝗺𝗽𝘁𝗼𝗺 𝗼𝗻𝘀𝗲𝘁 :

𝗣𝗖𝗜 (𝗦𝗕𝗔)

🔹 If PCI can't be performed within 120 min & thrombolysis is contraindicated : PCI should
be performed as soon as possible
🔹 PCI should be considered within first 24 hours, even if they have reperfused
spontaneously or with thrombolytic therapy
🔹 Coronary artery patency is restored in over 95% of patients undergoing PCI. 

🔹 Successful therapy is associated with

   + 𝗥𝗮𝗽𝗶𝗱 𝗽𝗮𝗶𝗻 𝗿𝗲𝗹𝗶𝗲𝗳
   + 𝗥𝗲𝘀𝗼𝗹𝘂𝘁𝗶𝗼𝗻 𝗼𝗳 𝗮𝗰𝘂𝘁𝗲 𝗦𝗧 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻
   + 𝗢𝗰𝗰𝗮𝘀𝗶𝗼𝗻𝗮𝗹 𝘁𝗿𝗮𝗻𝘀𝗶𝗲𝗻𝘁 𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮

*** 𝗣𝗖𝗜 𝗰𝗼𝗻𝗳𝗲𝗿𝘀 𝗻𝗼 𝗶𝗺𝗺𝗲𝗱𝗶𝗮𝘁𝗲 𝗺𝗼𝗿𝘁𝗮𝗹𝗶𝘁𝘆 𝗯𝗲𝗻𝗲𝗳𝗶𝘁 𝗶𝗻 𝗻𝗼𝗻-𝗦𝗧 𝘀𝗲𝗴𝗺𝗲𝗻𝘁

𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 𝗔𝗖𝗦 
.

𝗧𝗵𝗿𝗼𝗺𝗯𝗼𝗹𝘆𝘁𝗶𝗰 𝘁𝗵𝗲𝗿𝗮𝗽𝘆

🔹 𝗜𝗳 𝗽𝗿𝗶𝗺𝗮𝗿𝘆 𝗣𝗖𝗜 𝗰𝗮𝗻𝗻𝗼𝘁 𝗯𝗲 𝗮𝗰𝗵𝗶𝗲𝘃𝗲𝗱 𝗶𝗻 𝗮 𝘁𝗶𝗺𝗲𝗹𝘆 𝗺𝗮𝗻𝗻𝗲𝗿, 𝘁𝗵𝗿𝗼𝗺𝗯𝗼𝗹𝘆𝘁𝗶𝗰

𝘁𝗵𝗲𝗿𝗮𝗽𝘆 𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝗮𝗱𝗺𝗶𝗻𝗶𝘀𝘁𝗲𝗿𝗲𝗱
🔹 Although survival advantage is not as good as primary PCI, mortality is reduced 
🔹 𝗕𝗲𝗻𝗲𝗳𝗶𝘁 𝗶𝘀 𝗴𝗿𝗲𝗮𝘁𝗲𝘀𝘁 𝘄𝗶𝘁𝗵𝗶𝗻 𝗳𝗶𝗿𝘀𝘁 𝟭𝟮 𝗵𝗼𝘂𝗿𝘀 & 𝗲𝘀𝗽𝗲𝗰𝗶𝗮𝗹𝗹𝘆 𝗳𝗶𝗿𝘀𝘁 𝟮 𝗵𝗼𝘂𝗿𝘀. 
🔹 Modern thrombolytic agents (Can be given as IV bolus)  
   + Tenecteplase (TNK) 
   + Reteplase (rPA)
🔹 𝗠𝗮𝗷𝗼𝗿 𝗵𝗮𝘇𝗮𝗿𝗱 : 𝗕𝗹𝗲𝗲𝗱𝗶𝗻𝗴
🔹 𝗘𝘃𝗲𝗻 𝘄𝗵𝗲𝗿𝗲 𝘁𝗵𝗿𝗼𝗺𝗯𝗼𝗹𝘆𝘀𝗶𝘀 𝘀𝘂𝗰𝗰𝗲𝘀𝘀𝗳𝘂𝗹𝗹𝘆 𝗮𝗰𝗵𝗶𝗲𝘃𝗲𝘀 𝗿𝗲𝗽𝗲𝗿𝗳𝘂𝘀𝗶𝗼𝗻, 𝗣𝗖𝗜
𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝗰𝗼𝗻𝘀𝗶𝗱𝗲𝗿𝗲𝗱 𝘄𝗶𝘁𝗵𝗶𝗻 𝟮𝟰 𝗵𝗿 𝘁𝗼 𝗽𝗿𝗲𝘃𝗲𝗻𝘁 𝗿𝗲𝗰𝘂𝗿𝗿𝗲𝗻𝘁 𝗶𝗻𝗳𝗮𝗿𝗰𝘁𝗶𝗼𝗻 &
𝗶𝗺𝗽𝗿𝗼𝘃𝗲 𝗼𝘂𝘁𝗰𝗼𝗺𝗲
.

𝗔𝗻𝘁𝗶𝘁𝗵𝗿𝗼𝗺𝗯𝗼𝘁𝗶𝗰 𝘁𝗵𝗲𝗿𝗮𝗽𝘆

♦️Antiplatelet
   + Aspirin : Should be continued indefinitely if there are bo side effects
   + P2Y12 receptor antagonist (Clopidogrel, Prasugrel, Ticagrelor) : Upto 12 months
   + GP IIb/IIIa receptor antagonist ( Tirofiban, Abciximab : High risk patients with ACS who
undergo PCI 

♦️Anticoagulant
   + UFH
   + LMWH
   + Pentasaccharide (Fondaparinux) : Best safety & efficacy profile
♦️Anticoagulant should be continued
   + For 8 days or 
   + Until discharge from hospital or 
   + Coronary revascularisation has been completed 
.

𝗥𝗲𝗻𝗶𝗻–𝗮𝗻𝗴𝗶𝗼𝘁𝗲𝗻𝘀𝗶𝗻 𝗯𝗹𝗼𝗰𝗸𝗮𝗱𝗲

♦️Long term treatment

   + Counteract ventricular remodelling
   + Prevent the onset of HF
   + Improve survival
   + Reduce recurrent MI 
   + Avoid rehospitalisation
♦️They should be considered in all patients with ACS
.

𝗠𝗶𝗻𝗲𝗿𝗮𝗹𝗼𝗰𝗼𝗿𝘁𝗶𝗰𝗼𝗶𝗱 𝗿𝗲𝗰𝗲𝗽𝘁𝗼𝗿 𝗮𝗻𝘁𝗮𝗴𝗼𝗻𝗶𝘀𝘁𝘀 

♦️In Patients with acute MI & LVEF < 35% & either pulmonary oedema or DM 

♦️𝗔𝗹𝗹 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘀𝗵𝗼𝘂𝗹𝗱 𝗿𝗲𝗰𝗲𝗶𝘃𝗲 𝘁𝗵𝗲𝗿𝗮𝗽𝘆 𝘄𝗶𝘁𝗵 𝗛𝗠𝗚 𝗖𝗼𝗔 𝗿𝗲𝗱𝘂𝗰𝘁𝗮𝘀𝗲 𝗲𝗻𝘇𝘆𝗺𝗲
𝗶𝗻𝗵𝗶𝗯𝗶𝘁𝗼𝗿𝘀 (𝘀𝘁𝗮𝘁𝗶𝗻𝘀) 𝗮𝗳𝘁𝗲𝗿 𝗔𝗖𝗦 𝗶𝗿𝗿𝗲𝘀𝗽𝗲𝗰𝘁𝗶𝘃𝗲 𝗼𝗳 𝘀𝗲𝗿𝘂𝗺 𝗰𝗵𝗼𝗹𝗲𝘀𝘁𝗲𝗿𝗼𝗹 
.

 𝗦𝗺𝗼𝗸𝗶𝗻𝗴 𝗰𝗲𝘀𝘀𝗮𝘁𝗶𝗼𝗻

♦️𝗚𝗶𝘃𝗶𝗻𝗴 𝘂𝗽 𝘀𝗺𝗼𝗸𝗶𝗻𝗴 𝗶𝘀 𝘁𝗵𝗲 𝘀𝗶𝗻𝗴𝗹𝗲 𝗺𝗼𝘀𝘁 𝗲𝗳𝗳𝗲𝗰𝘁𝗶𝘃𝗲 𝗰𝗼𝗻𝘁𝗿𝗶𝗯𝘂𝘁𝗶𝗼𝗻 𝗮 𝗽𝗮𝘁𝗶𝗲𝗻𝘁

𝗰𝗮𝗻 𝗺𝗮𝗸𝗲 𝘁𝗼 𝘁𝗵𝗲𝗶𝗿 𝗳𝘂𝘁𝘂𝗿𝗲.

 *** ICDs prevent sudden cardiac death in LV impairment (ejection fraction ≤ 30%) after MI
.

Prognosis

♦️𝗘𝗮𝗿𝗹𝘆 𝗱𝗲𝗮𝘁𝗵 𝗶𝘀 𝘂𝘀𝘂𝗮𝗹𝗹𝘆 𝗱𝘂𝗲 𝘁𝗼 𝗮𝗻 𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮 & 𝗶𝗻𝗱𝗲𝗽𝗲𝗻𝗱𝗲𝗻𝘁 𝗼𝗳 𝗲𝘅𝘁𝗲𝗻𝘁 𝗼𝗳

𝗠𝗜
♦️𝗣𝗿𝗼𝗴𝗻𝗼𝘀𝗶𝘀 𝗶𝘀 𝘄𝗼𝗿𝘀𝗲 𝗳𝗼𝗿 𝗮𝗻𝘁𝗲𝗿𝗶𝗼𝗿 𝘁𝗵𝗮𝗻 𝗳𝗼𝗿 𝗶𝗻𝗳𝗲𝗿𝗶𝗼𝗿 𝗶𝗻𝗳𝗮𝗿𝗰𝘁𝘀
♦️𝗕𝘂𝗻𝗱𝗹𝗲 𝗯𝗿𝗮𝗻𝗰𝗵 𝗯𝗹𝗼𝗰𝗸 & 𝗵𝗶𝗴𝗵 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝗺𝗮𝗿𝗸𝗲𝗿 𝗰𝗼𝗻𝗰𝗲𝗻𝘁𝗿𝗮𝘁𝗶𝗼𝗻𝘀 : 𝗜𝗻𝗱𝗶𝗰𝗮𝘁𝗲
𝗲𝘅𝘁𝗲𝗻𝘀𝗶𝘃𝗲 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗱𝗮𝗺𝗮𝗴𝗲

.
Box 16.51
   + Secondary prevention drug ***
.

     𝗣𝗘𝗥𝗜𝗣𝗛𝗘𝗥𝗔𝗟 𝗔𝗥𝗧𝗘𝗥𝗜𝗔𝗟 𝗗𝗜𝗦𝗘𝗔𝗦𝗘 

*** 𝗜𝗻 𝗱𝗲𝘃𝗲𝗹𝗼𝗽𝗲𝗱 𝗰𝗼𝘂𝗻𝘁𝗿𝗶𝗲𝘀, 𝗮𝗹𝗺𝗼𝘀𝘁 𝗮𝗹𝗹 𝗣𝗔𝗗 𝗶𝘀 𝗱𝘂𝗲 𝘁𝗼 𝗮𝘁𝗵𝗲𝗿𝗼𝘀𝗰𝗹𝗲𝗿𝗼𝘀𝗶𝘀

   *** Clinical features

🔹Symptomatic PAD affects legs about eight times more commonly than arms
🔹Several locations may be affected including 
   + Aortoiliac vessels
   + Femoropopliteal vessels 
   + Infrapopliteal vessels 

   *** 𝗜𝗻 𝗮𝗿𝗺, 𝘀𝘂𝗯𝗰𝗹𝗮𝘃𝗶𝗮𝗻 𝗮𝗿𝘁𝗲𝗿𝘆 𝗶𝘀 𝘁𝗵𝗲 𝗺𝗼𝘀𝘁 𝗰𝗼𝗺𝗺𝗼𝗻 𝘀𝗶𝘁𝗲 𝗼𝗳 𝗱𝗶𝘀𝗲𝗮𝘀𝗲

.

𝗜𝗻𝘁𝗲𝗿𝗺𝗶𝘁𝘁𝗲𝗻𝘁 𝗰𝗹𝗮𝘂𝗱𝗶𝗰𝗮𝘁𝗶𝗼𝗻 (𝗜𝗖)

*** 𝗠𝗼𝘀𝘁 𝗰𝗼𝗺𝗺𝗼𝗻 𝗽𝗿𝗲𝘀𝗲𝗻𝘁𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗣𝗔𝗗 𝗮𝗳𝗳𝗲𝗰𝘁𝗶𝗻𝗴 𝘁𝗵𝗲 𝗹𝗼𝘄𝗲𝗿 𝗹𝗶𝗺𝗯𝘀 (𝗦𝗕𝗔 )

🔹𝗖𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝗲𝗱 𝗯𝘆 𝗶𝘀𝗰𝗵𝗮𝗲𝗺𝗶𝗰 𝗽𝗮𝗶𝗻 𝗮𝗳𝗳𝗲𝗰𝘁𝗶𝗻𝗴 𝘁𝗵𝗲 𝗺𝘂𝘀𝗰𝗹𝗲𝘀 𝗼𝗳 𝗹𝗲𝗴 

   + 𝗨𝘀𝘂𝗮𝗹𝗹𝘆 𝗳𝗲𝗹𝘁 𝗶𝗻 𝗰𝗮𝗹𝗳 𝗯𝗲𝗰𝗮𝘂𝘀𝗲 𝘁𝗵𝗲 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 𝗺𝗼𝘀𝘁 𝗰𝗼𝗺𝗺𝗼𝗻𝗹𝘆 𝗮𝗳𝗳𝗲𝗰𝘁𝘀
𝘀𝘂𝗽𝗲𝗿𝗳𝗶𝗰𝗶𝗮𝗹 𝗳𝗲𝗺𝗼𝗿𝗮𝗹 𝗮𝗿𝘁𝗲𝗿𝘆
   + May be felt in thigh or buttock if iliac arteries are involved
   + 𝗧𝘆𝗽𝗶𝗰𝗮𝗹𝗹𝘆, 𝗽𝗮𝗶𝗻 𝗰𝗼𝗺𝗲𝘀 𝗼𝗻 𝗮𝗳𝘁𝗲𝗿 𝘄𝗮𝗹𝗸𝗶𝗻𝗴 & 𝗿𝗮𝗽𝗶𝗱𝗹𝘆 𝘀𝘂𝗯𝘀𝗶𝗱𝗲𝘀 𝗼𝗻 𝗿𝗲𝘀𝘁𝗶𝗻𝗴
   + 𝗥𝗲𝘀𝘂𝗺𝗽𝘁𝗶𝗼𝗻 𝗼𝗳 𝘄𝗮𝗹𝗸𝗶𝗻𝗴 𝗹𝗲𝗮𝗱𝘀 𝘁𝗼 𝗮 𝗿𝗲𝘁𝘂𝗿𝗻 𝗼𝗳 𝘁𝗵𝗲 𝗽𝗮𝗶𝗻. 
.

♦️𝗖𝗿𝗶𝘁𝗶𝗰𝗮𝗹 𝗹𝗶𝗺𝗯 𝗶𝘀𝗰𝗵𝗲𝗺𝗶𝗮 : 𝗗𝗲𝗳𝗶𝗻𝗲𝗱 𝗮𝘀 𝗿𝗲𝘀𝘁 𝗽𝗮𝗶𝗻 𝗿𝗲𝗾𝘂𝗶𝗿𝗶𝗻𝗴 𝗼𝗽𝗶𝗮𝘁𝗲 𝗮𝗻𝗮𝗹𝗴𝗲𝘀𝗶𝗮

𝗼𝗿 𝘂𝗹𝗰𝗲𝗿𝗮𝘁𝗶𝗼𝗻 / 𝗴𝗮𝗻𝗴𝗿𝗲𝗻𝗲 𝗳𝗼𝗿 > 𝟮 𝘄𝗲𝗲𝗸𝘀 & 𝗮𝗻𝗸𝗹𝗲 𝗕𝗣 < 𝟱𝟬 𝗺𝗺𝗛𝗴
♦️𝗦𝘂𝗯𝗰𝗿𝗶𝘁𝗶𝗰𝗮𝗹 𝗹𝗶𝗺𝗯 𝗶𝘀𝗰𝗵𝗮𝗲𝗺𝗶𝗮 (𝗦𝗖𝗟𝗜) : 𝗥𝗲𝘀𝘁 𝗽𝗮𝗶𝗻 𝗼𝗻𝗹𝘆 & 𝗮𝗻𝗸𝗹𝗲 𝗽𝗿𝗲𝘀𝘀𝘂𝗿𝗲𝘀 >
𝟱𝟬 𝗺𝗺𝗛𝗴
♦️Severe limb ischaemia (SLI) : Situation where either CLI & SCLI occurs
♦️𝗜𝗖 𝗶𝘀 𝘂𝘀𝘂𝗮𝗹𝗹𝘆 𝗱𝘂𝗲 𝘁𝗼 𝘀𝗶𝗻𝗴𝗹𝗲 𝘀𝗲𝗴𝗺𝗲𝗻𝘁 𝗽𝗹𝗮𝗾𝘂𝗲 but 𝗦𝗟𝗜 𝗶𝘀 𝗮𝗹𝘄𝗮𝘆𝘀 𝗱𝘂𝗲 𝘁𝗼
𝗺𝘂𝗹𝘁𝗶𝗹𝗲𝘃𝗲𝗹 𝗱𝗶𝘀𝗲𝗮𝘀𝗲
.

Acute limb ischemia

♦️Typical presentation is with 𝗽𝗮𝗿𝗮𝗹𝘆𝘀𝗶𝘀 (𝗶𝗻𝗮𝗯𝗶𝗹𝗶𝘁𝘆 𝘁𝗼 𝘄𝗶𝗴𝗴𝗹𝗲 𝘁𝗼𝗲𝘀 𝗼𝗿 𝗳𝗶𝗻𝗴𝗲𝗿𝘀) &
𝗽𝗮𝗿𝗮𝗲𝘀𝘁𝗵𝗲𝘀𝗶𝗮 (𝗹𝗼𝘀𝘀 𝗼𝗳 𝗹𝗶𝗴𝗵𝘁 𝘁𝗼𝘂𝗰𝗵 𝗼𝘃𝗲𝗿 𝗱𝗼𝗿𝘀𝘂𝗺 𝗼𝗳 𝗳𝗼𝗼𝘁 𝗼𝗿 𝗵𝗮𝗻𝗱); so-called ‘Ps
of acute ischaemia (Box 16.57)
.

Atheroembolism
♦️May be confused with Raynaud’s phenomenon but 
   + 𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀 𝗼𝗳 𝗮𝘁𝗵𝗲𝗿𝗼𝗲𝗺𝗯𝗼𝗹𝗶𝘀𝗺 : 𝗧𝘆𝗽𝗶𝗰𝗮𝗹𝗹𝘆 𝘂𝗻𝗶𝗹𝗮𝘁𝗲𝗿𝗮𝗹 
   + 𝗥𝗮𝘆𝗻𝗮𝘂𝗱’𝘀 : 𝗕𝗶𝗹𝗮𝘁𝗲𝗿𝗮𝗹 

Investigation 
🔹 𝗜𝗻 𝗵𝗲𝗮𝗹𝘁𝗵 : 𝗔𝗕𝗣𝗜 > 𝟭.𝟬
🔹 𝗜𝗻 𝗜𝗖 : 𝗔𝗕𝗣𝗜 𝟬.𝟱–𝟬.𝟵 
🔹 𝗜𝗻 𝗖𝗟𝗜 : 𝗔𝗕𝗣𝗜 < 𝟬.𝟱
.

𝗕𝘂𝗲𝗿𝗴𝗲𝗿’𝘀 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 𝗼𝗿 𝘁𝗵𝗿𝗼𝗺𝗯𝗼𝗮𝗻𝗴𝗶𝗶𝘁𝗶𝘀 𝗼𝗯𝗹𝗶𝘁𝗲𝗿𝗮𝗻𝘀 

♦️Inflammatory disease of arteries that is distinct from atherosclerosis 

♦️𝗨𝘀𝘂𝗮𝗹𝗹𝘆 𝗽𝗿𝗲𝘀𝗲𝗻𝘁𝘀 𝗶𝗻 𝘆𝗼𝘂𝗻𝗴 (𝟮𝟬–𝟯𝟬 𝘆𝗲𝗮𝗿𝘀) 𝗺𝗮𝗹𝗲 𝘀𝗺𝗼𝗸𝗲𝗿𝘀
♦️Characteristically affects distal arteries, giving rise to 𝗰𝗹𝗮𝘂𝗱𝗶𝗰𝗮𝘁𝗶𝗼𝗻 𝗶𝗻 𝗳𝗲𝗲𝘁 𝗼𝗿 𝗿𝗲𝘀𝘁
𝗽𝗮𝗶𝗻 𝗶𝗻 𝗳𝗶𝗻𝗴𝗲𝗿𝘀 𝗼𝗿 𝘁𝗼𝗲𝘀
♦️𝗪𝗿𝗶𝘀𝘁 𝗮𝗻𝗱 𝗮𝗻𝗸𝗹𝗲 𝗽𝘂𝗹𝘀𝗲𝘀 𝗮𝗿𝗲 𝗮𝗯𝘀𝗲𝗻𝘁 𝗯𝘂𝘁 𝗯𝗿𝗮𝗰𝗵𝗶𝗮𝗹 & 𝗽𝗼𝗽𝗹𝗶𝘁𝗲𝗮𝗹 𝗽𝘂𝗹𝘀𝗲𝘀 𝗮𝗿𝗲
𝗽𝗿𝗲𝘀𝗲𝗻𝘁
♦️May also affect veins, giving rise to superficial thrombophlebitis
♦️𝗢𝗳𝘁𝗲𝗻 𝗿𝗲𝗺𝗶𝘁𝘀 𝗶𝗳 𝗽𝗮𝘁𝗶𝗲𝗻𝘁 𝘀𝘁𝗼𝗽𝘀 𝘀𝗺𝗼𝗸𝗶𝗻𝗴
♦️𝗠𝗮𝗷𝗼𝗿 𝗹𝗶𝗺𝗯 𝗮𝗺𝗽𝘂𝘁𝗮𝘁𝗶𝗼𝗻 𝗶𝘀 𝘁𝗵𝗲 𝗺𝗼𝘀𝘁 𝗳𝗿𝗲𝗾𝘂𝗲𝗻𝘁 𝗼𝘂𝘁𝗰𝗼𝗺𝗲 𝗶𝗳 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀
𝗰𝗼𝗻𝘁𝗶𝗻𝘂𝗲 𝘁𝗼 𝘀𝗺𝗼𝗸𝗲
.