Cardiovascular Pathology


The necrosis is coagulative (apoptosis may play a role)

:)


Download 167.33 Kb.
Page5/9
Date conversion05.11.2016
Size167.33 Kb.
1   2   3   4   5   6   7   8   9

The necrosis is coagulative (apoptosis may play a role)

Notes:

In MI, occlusions almost always involve one of the 3 named coronary arteries or a secondary branch (diagonal branch of LAD, marginal branch of LCx).

A pure right ventricular MI is rare, but the RV may be involved by extension from LV.

Myocyte cell death occurs first in the subendocardial zone and the advances outward as a wave with an “at risk” zone at the leading edge.

The extent of the MI depends on several factors including:

Duration of occlusion

Metabolic/O2 needs of myocardium

Hypotension, arrhythmias, spasm



What happens to a cardiac myocyte when blood is cut off?




  • It resorts to anaerobic glycolysis within seconds

  • It stops contracting within about a minute (can  acute heart failure)

  • Myocyte death occurs in 20 to 40 minutes

  • >1 hour, vascular injury occurs




Gross Changes in MI




0 to 12 hours Nothing (triphenyltetrazolium chloride stain can show in 2 – 3 hours)

24 hours Dark mottling (trapped blood)

3 to 7 days Yellow-tan center, hyperemic margin

7 to 10 days Max. necrosis of yellow-tan center

2 months Mature scar




Light Microscopic Changes in MI




0 to 4 hours Not much – wavy fibers at edge

4 to 24 hours Beginning coagulation necrosis, nuclear pyknosis, early neutrophilic infiltrate

1 to 3 days Well developed coagulative necrosis with loss of nuclei and cross striations, lots of neutrophils

Up to 10 days Progressive dissolution of myocytes & ingrowth of granulation tissue

2 months Dense collagenous scar




Reperfusion After Acute MI



  • By thrombolytic therapy (TPA, streptokinase) or mechanical (angioplasty)

  • May limit infarct size and improve function & survival

  • Must be done within 3 – 4 hours of onset of Sx ( if done in first 20 min, may prevent all necrosis)

  • Causes its own type of injury (reperfusion injury)

    • Hemorrhage due to damaged, leaky blood vessels

    • More rapid disintegration of critically damaged myocytes – get “contraction band necrosis” in irreversibly injured myocytes

    • Some new cellular injury may occur due to O2 free radicals

    • Arrhythmia

    • Increased apoptosis of myocytes

    • May cause swelling of endothelial cells  occlusion  stops reperfusion ("no-reflow")

Note: "Stunned" myocardium refers to reversible myocyte dysfunction after an ischemic event. The myocardium may take several days to recover.



Complications of MI




  • Nearly ¾ have one or more:

  • LV contractile dysfunction with heart failure, hypotension, shock if >40% of LV is lost

  • Arrhythmias – may cause sudden death

  • Pericarditis

  • Myocardial rupture (Most frequently 2 – 4 days post MI)

    • Through septum to RV

    • Through free wall  tamponade

    • Partial rupture through free wall  pseudoaneurysm filled with thrombus

    • Papillary muscle rupture  acute mitral insufficiency

  • Infarct extension

  • Mural thrombus may  thromboembolus

  • LV aneurysm – late complication

  • Papillary muscle dysfunction

  • Progressive heart failure (“ischemic heart disease”)



Notes:

In 10 – 15% of pts, usually with >40% LV infarct, there is 70% mortality.

Pericarditis after an MI is typically fibrinous or fibrinohemorrhagic. Typical onset 2 – 3 days after acute MI, then resolves.

Large anterior transmural MI’s have a higher risk of rupture, expansion, aneurysm, thrombi & in general have a worse prognosis than posterior MI's.

Large posterior transmural MI’s have a higher risk of heart blocks, RV infarct (or both).

Compensatory remodeling occurs with healing of MI with compensatory hypertrophy and areas of thinning, scarring and dilatation. May get late decompensation of the myocardium.

The conventional wisdom has been that cardiac myocytes cannot regenerate and are replaced by scar tissue when they die. There is some evidence to the contrary, but myocyte regeneration, if it occurs, does not play much of a role in the healing of an MI.

Chronic Ischemic Heart Disease



  • Results in progressive failure due to ischemic myocardial damage

  • Usually in pts with prior MI, but may see with severe obstructive coronary artery disease without MI

  • Hearts are typically large and heavy due to areas of compensatory hypertrophy & areas of dilatation & fibrosis

  • “Ischemic cardiomyopathy” is used for this, but it is not strictly a "primary" abnormality of the myocardium




Sudden Cardiac Death




  • Def: Rapid (<1 hr) unexpected death due to cardiac causes

  • IHD the most common cause in older persons (acute plaque change  thrombus arrhythmia)

  • In younger persons, non-atherosclerotic causes are more common




Non-atherosclerotic Causes of Cardiac Sudden Death



  • Hypertrophic cardiomyopathy/isolated hypertrophy of unknown cause

  • Congenital heart disease, including coronary artery anomalies

  • Aortic stenosis (congenital or acquired)

  • Myocarditis

  • Pulmonary hypertension

  • Conduction system or ion channel abnormalities (prolonged QT interval)



1   2   3   4   5   6   7   8   9
:)


The database is protected by copyright ©hestories.info 2017
send message

    Main page

:)