Cardiovascular system

Arteries & Veins

Arteries

    Tunica intima the inner layer of the artery, composed of endothelial cells, underlying loose connective tissue and internal elastic lamina (elastic membrane) that seperates tunica intima from tunica media. The endothelial cells tend to proliferate as response to injury (altered blood flow or increased pressure). This layer is affected by progressive intimal fiborsis, that is especially prominent in the thyroid, spleen and myometrium.
    Tunica media the middle layer of the artery, composed of vascular smooth muscle cells, elastic tissue and collagen.
    Tunica adventitia it the outer most layer, composed mostly of collagen fibers, elastic fibers and fibroblasts. You might also see macrophages and other inflammatory cells, ganglion cells and vasa vasorum (small blood vessels that supply the larger ones).
artery histology

Infarction of the myocardium - coronary arteries

Timeline

    0h coronary artery gets clogged.
    4-12h myocytes become hypereosinophilic (more pink),contraction bands appear (hypercontraction of sarcomeres in myocytes).
    24-48h neutrofils appear in the interstitium. If blood flow is reestablished, you might see abundant interstitial hemorrhage (reperfusion damage).
    48-72h neutrofils start to degenerate, and therefore you have a mix og vital and degenerating neutrofils. Close to 72h you therefore see abundant cellular debris.
    Day 3 mononuclear cells start dominating the picture.
    Day 3-5 myocytes are removed and you will find lymfocytes, pigment-laden histiocytes (macrophages) along with myofibroblasts in the interstitium.
    Day 5-7 The interstitial cells increase in number, but no collagen has been produced, which is why the myocardial wall is here at its weakest and often the time of rupture.
    Day 7 collagen starts to appear and inflammatory cells begin to disappear. From here on after, the age of the infarction is dependent on the extent of the collagen and remaining inflammation.
    2 months inflammation has disappeared and only collagen remains, id est a scar is formed.
Important: The infarcted area heals from the outer borders and inward. It is important to keep that in mind when one is trying to determine the age of the infarct. If you only section the center of the infarcted area, you will end up giving the infarction an younger age.

Atherosclerosis

Hypertension and blood flow turbulance can cause endothelial/vascular damage, which in turn leads to increased endothelial permeability, leading to leukocyte adhesion and accumulation of lipids in the intima, and with it proliferation of smooth muscle cells. Leading to a thickened intima. This is the first step in atherosclerosis.
One of the most common place for artherosclerosis is where the arteries bifurcate (split), as the bifurcation cases blood flow turbulance.

    Fatty streaks: a visible yellow to white lesion on the intimal surface, where macrophages filled with lipid have accumulated beneath the endothelium in the intima.
    Atheromatous plaques: are raised yellow to white lesions within the intima. The lesion contains a lipid core and necrotic debris covered by a fibrous cap. The fibrous cap contains smooth muscle cells, macrophages filled with lipid, collagen and elastin as well as lymphocytes. The necrotic center contains cellular debris, macrophages filled with lipid, cholesterol crystals and calcium. This plaque can increase in size with time and therefore protrude into the lumen causing stenosis (decreased lumen) and affect the quality of the media underneath which in some cases can lead to aneurysm formation.
    Calcification: As the lipid core in the atheromatous plaque contains calcium, this accumulation with time will lead to calcifications within the plaque. Calcium mainly comes from dying cells that leak calcium into the extracellular matrix.
    Stenosis: is when the atheromatous plaque protrudes into the arterial lumen decreasing the diameter of the lumen, thus disturbing and decreasing blood flow.
artherosclerosis histology


Cardiomyopathy

Hypertrophic cardiomyopathy
Is when the heart muscle or the myocardium becomes thickened (hypertrophied). This can lead to diastolic dysfunction (the heart cannot relax normally), valves might not be able to close normally leading to regurgitation and even myocardial ischemia as the abnormal myocytes can compress small arteries in the heart. Hypertrophic cardiomyopathy can either be aquired or genetic. The acquired causes include hypertension and aortic stenosis, which both increase the pressure tension in the heart.
Genetic causes include mutations in genes that encode sarcomere-associated proteins, like beta-myosin heavy chain and myosin binding protein C.
To be diagnosed with hypertrophic cardiomyopathy as an adults the left ventricular end diastolic wall thickness should be >13 mm or > 15 mm (on imaging) depending on criteria used.
Histology
    Myocytes are large and have large, often box-like, nuclei (hypertrophy of myocytes). The enlarged myocytes then can cause local ischemia and death of surrounding myocytes by compressing arteries within the myocardium. This eventually causes replacement fibrosis, as the dead myocytes are replaced by fibrosis (scarring). The scarred myocardium then affects the myocytes parallel alignment, leading to fiber disarray.

Dilated cardiomyopathy
Is when the heart ventricles, one or both, have enlarged, and the myocardium stretched and thinned, leading to impaired contraction (left ventricular ejection fraction, LVEF, under 40%).
Histology
    Myocytes tend to have increased length with enlarged nuclei (hypertrophy). Focal myocyte death leads to fibrosis. This can lead to increased inflammation in the interstitium.