12. The Heart

// 12. The Heart

21.06.21 | 14:04 tags:


”Ischemic heart disease represents a group of pathophysiologically related syndromes resulting from myocardial ischemia—an imbalance between myocardial supply (perfusion) and cardiac demand for oxygenated blood”

  • most common: blockage of coronary vessels
  • decade long progression

Clinical manifestation

  • Myocardial indfarction - ischemia causing cardiac necrosis
  • Angina pectoris - Ischemia is not severe enough to cause necrosis
  • chronic Ischemic heart disease with heart disease
  • Sudden cardiac death

Ischemic Heart Disease - Acute Coronary Syndrome

  • Unstable Angina Pectoris
  • Myocardial Infarction
  • Sudden Cardiac Death
  • Due to sudden change in atherosclerotic plaque

Etiology

  • Atherosclerosis
  • Emboli
  • Myocardial vessel inflammation
  • Vascular Spasm
  • Systemic hypotension
  • Increased demand - Myocardial Hypertrophy and increased heart rate

Epidemiology:

  • Similar to etiology of Atherosclerois
  • Decreasing trend due to better prevention
  • Better diagnostic and

Pathogenesis

  • 90% - Atherosclerosis
  • CAD - Coronary Artery Disease
  • Progressive narrowing leading to stenosis -> fixed obstruction
  • Acute plaque change with thrombosis
  • Fixed obstruction more than 75% significant CAD
  • Threshold for sympotomatic ischemia are precipitated by exercise
  • Obstruction of 90% cross-sectional area - inadequate coronary flow even during rest
  • Collaterals :Progressive ischemia induced by slowly developing occlusion.
  • Single or two to three coronary vessels may be involved(LAD, LCX and RCA) I!

Acute Plaque Change:

  • Abrupt conversion of stable plaque to unstable atherothrombotic lesion

Consequences of Ischemia

Angina

Patterns of Infarction

  • It is dependent on the perfusion pattern
    • Subendocardial zone is the least supplied part of the coronary arteries, thus it is most susceptible to ischemia
    • It progresses towards epicardium as the ischemia persists
  • Transmural Infarction
    • Occlusion of epicardial vessels in absence of intervention
    • ST elevation MI
  • Non-transmural infarct
    • A.k.a Sub-endocardial infarction

Coronary Blood Supply

  • Dominant artery is determined by coronary artery that supplies posterior third of septum (RCA vs Left Circumflex)
    • Right dominant in 80%
    • LAD and LCX supply majority of LV
  • Left ventricle/septum commonly involved
    • Right and left ventricle-RCX
  • Isolated right ventricle/atria is unusual (1% to 3%)

Morphology

  • Gross annd microscopic appearance of an infarct
  • Depend on duration of survival of patient following MI (should survive for a certain duration after MI - Morphological changes are not seen for sudden death)
  • Progressive sequence of morphologic changes
  • Coagulative necrosis, Inflammation and repair

Gross features

  • MI <12 hours old - not grossly apparent
    • MI >3 hours - Triphenyl tetrazolium chloride (TTF) a dye that colors of non-infarcted part of the heart as it demonstrates color only for parts that contain LDH
    • [[Pasted image 20210623091850.png]]
  • MI >12 hours - microscopic features
    • Reversible
      • None [0-30 minutes]
    • Irreversible
      • None [30 to 4 hours]
      • Dark mottling (occasional) [4 to 12h]
      • Dark mottling [12-24h]
      • Mottling with yellow-tan infarct
      • Hyperemic border, central-yellow tan softening
      • Maximally, yellow-tan and soft, with depressed red-tan margins
      • Red-gray depressed infarct borders
      • Gray-white scar,progressive from border toward core
      • Scarring complete [> 2 months]

Microscopy

  • Visible after 4 to 6 hours
    • Early coagulation necrosis; edema; hemorrhage

Gross and morphological changes based on time is very important for the exam

Clinical Features

  • Characterized by severe, radiating, crushing substernal chest pain that can radiate to the neck, jaw, epigastrium or left arm
  • Several minutes to hours
  • Not releibved by rest or nitroglycerin
  • Silent MIs in DM and elderly patients
  • Nausea, vommiting heart burn

ECG

  • ST-segment

Laboratory Evaluation

  • Cardiac Troponins; cTnT and CtNi
    • Detected after 2-4 hours
    • Peaks at 48 hours
    • levels remain elevated for 7 to 10 days
    • not useful for re-infarction
  • Creatinine KInase: CK-MB
    • Detectable after 2-4h
    • Peak at 24-48h
    • useful for detecting re-infarction

Complications

Minutes/Hours

  • Arrythmias- usually ventricular fibrillation
  • Cardiac Failure
  • Cardiogenic shock is seen in massive MI (>40% of left ventricle infarcted)
  • Pulmonary edema of cardiogenic ratio

Days

  • Thrombosis (over infarct area) -> Thromboembolism
  • Rupture of heart (Wall/septum/papillary muscle) - Most commonly affected: Left Anterolateral wall of the left ventricle

Week/Months

  • Dressler’s syndrome
  • Cardiac Aneurysm (Ventricular wall aneurysm - more associated)

Reperfusion Injury

  • Restoration of blood flow to ischemic myocardium

  • Occurs due to oxidative stress from incomplete reduction in leukocytes and cells and intracellular calcium overload

  • Salvage myocardium at risk and limit infarct size

  • Impacts short and long time function

  • 3-4 hours critical

  • Thrombolysis - Removes only thrombus

  • Angioplasty - removes thrombus and clears atherosclerotic lesions

  • Coronary bypass - When multiple vessels are affected

  • Vascular injury and leakiness is seen in repurfusion injury

  • May lead to hypercontraction bands that appear as hypereosinophillic

Thus reperfusion is beneficial but can trigger complications May lead to arrythmias or reperfusion injury