Cardiovascular Pathology


Starts as an intimal tear in the ascending aorta, then blood dissects along the media

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Starts as an intimal tear in the ascending aorta, then blood dissects along the media

  • May extend proximal and distal to the intimal tear

  • Common cause of death: rupture into a serous cavity

    Notes:

    The entity is not strictly an aneurysm since there is no dilatation.

    In Marfan’s, the dissection typically occurs between the middle and outer 1/3 of the media.

    Look at but do not memorize the DeBakey types pictured in Robbins. The dissection may extend into the great head/upper extremity arteries. The dissection may also disrupt the aortic valve apparatus.




    Aortic Dissection in Marfan’s Syndrome




    • Marfan’s syndrome is among the best known genetic causes of aortic dissection. The cardiac manifestations include:

    • Cystic medial degeneration and aortic dissection

    • Dilatation of the aortic root

    • Mitral valve prolapse (floppy mitral valve)

    • Microscopic of aorta wall shows fragmentation of elastic fibers and cleft-like spaces known as cystic medial degeneration

    Notes:

    The changes are referred to as “cystic medial degeneration” rather than the old term “cystic medial necrosis.” The changes are not specific for Marfan’s and are also seen as an ageing change. The cleft-like spaces contain amorphous extracellular material and are not true, epithelial lined cysts.




    Aortic Dissection Clinical Course




    • Typically presents with excruciating pain which progresses downward

    • Used to have a high mortality, but now most are salvaged with aggressive control of hypertension and surgical plication of aorta


    • May result in a "double barreled" aorta if the dissection ruptures back into the lumen of the aorta



    Ischemic Heart Disease



    • Nearly synonymous with atherosclerotic cardiovascular disease (90%)

    • Divisible into 4 clinical syndromes:

      • Myocardial infarct

      • Angina pectoris (3 types)

      • Chronic ischemic heart disease with heart failure

      • Sudden death

    Notes:

    These four groups are heterogeneous and overlapping.

    Angina may be stable (the usual type), unstable (dangerous – preinfarction angina), or Prinzmetal angina (atypical – occurs at rest – due to cor. artery vasoconstriction).


    Pathogenesis of Atherosclerotic Cardiovascular Disease

    • Pathogenesis involves the interplay of 4 factors:

    • Fixed narrowing of coronary arteries – takes 75% to be hemodynamically significant

    • Acute plaque change

    • Thrombosis

    • Vasoconstriction




    Acute Plaque Change




    • Thought to trigger sudden cardiac events (and maybe unstable angina)

    • May be due to:

    • May be followed by thrombus formation on the plaque surface, which may:

      • Totally occlude the lumen  MI

      • Partially occlude the lumen  ? unstable angina, subendocardial infarct, sudden death

      • Embolize  microinfarcts

      • Organize  contribute to growth of plaque

    Notes:

    The most dangerous plaques are moderately stenotic (50 – 75%) with a relatively large, soft lipid core and a thin cap. More stenotic lesions may actually be more stable. More stenotic lesions may actually protect the myocardium against MI by preconditioning (mechanism unknown).


    For a good review of vulnerable plaque change, see Circulation 108:1664, 2003

    What causes acute plaque change?



    • Mechanisms are uncertain; may include:

      • Adrenergic stimulation – accounts for more MI’s in AM or when stressed (increased MI's after earthquakes, 9/11 attacks)

      • Vasoconstriction may contribute to plaque fracture


      • Inflammation may play a role in destabilizing the plaque

    Myocardial Infarct




    • Cause:

      • ~90% due to disrupted plaque  platelet adhesion  occlusive thrombus

      • Other 10%, who knows?

        • Prolonged, severe vasospasm

        • Emboli from left atrium or paradoxical emboli through patent foramen ovale

        • Abnormalities of intramural coronary arteries, vasculitis, hemoglobinopathies

        • Unexplained




    Risk Factors for MI – Same as for Atherosclerosis




    • Older age

    • Hypertension

    • Smoking

    • Diabetes mellitus

    • Hypercholesterolemia

    • Male > female (declines progressively with age past reproductive years)

    Notes:

    Review the coronary artery anatomy:

    LAD – supplies the apex, anterior LV wall, and anterior 2/3 of the ventricular septum.

    RCA – Posterior LV and posterior 1/3 of septum in the right dominant heart, whole RV

    LCx – lateral LV

    The left and right coronary artery systems each supply about 50% of the left ventricle in the right dominant heart.




    Morphology of an MI



    • Location depends on coronary artery affected (may be fooled by well-developed collateral flow)

    • The subendocardial zone is the "end" of the blood flow

    • Subendocardial MI = inner 1/3 to ½, may be circumferential in the distribution of all 3 cor. arts.

    • Transmural MI = more than half of ventricle wall thickness, usually in the distribution of one cor. art.



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