PM154 Lecture 6 - Coronary Heart Disease

Learning Objectives

  • Explain the pathophysiology of atherosclerosis, coronary heart disease (CHD) and myocardial infarction (MI).

Artery structure

  • Endothelial cells line the lumen of all blood vessels acting as a barrier to keep circulating factors in the bloodstream

  • All blood vessels have 3 layers: intima - endothelial cells, media - smooth muscle and elastic tissue, adventitia - structural support

    • Layers present in all vessels but more obvious in large arteries & veins and depending on the vessel they have different amounts of each layer

      • Veins are “storage” for extra blood and have valves

      • Arteries have thick smooth muscle and elastic tissue for high pressure

  • Arterial walls are thicker than corresponding veins to accommodate pulsatile blood flow and higher blood pressure

Vocabulary

  • HDL (the good cholesterol) - goes around mopping up LDL (the bad cholesterol) and liver processes LDL and kicks it out.

  • Nitric oxide (NO) - vasodilates blood vessels and lets white blood cells to move around better

  • ischaemia - lack of blood/

Coronary Heart Disease

  • Stable angina (pain on exertion) is the first step

    • Stress related - narrowing, but narrowing hasn’t exploded

  • Followed by unstable angina. Chest pain when not doing anything specific

  • Finally followed by a myocardial infarction (lack of blood supply and death to tissues of heart)

    • ECG changes as well as cells do not conduct signal as well

MI - Myocardial infarction

Risk factors

  • Non-modifiable

    • age, gender

    • lipid (cholesterol) profile

  • Modifiable

    • hypertension

    • activity levels

    • smoking/vaping

    • exercise

What triggers atherosclerosis?

  • Begins early and there is nothing we can do but it can be advanced by things that trigger atherosclerosis (above)

  • Elevated glucose over a long time binds to endothelial cells

  • GI flora that naturally live in colon/intestine - if taking antibiotics or poor diet they may change and produce toxins that enter the blood

Damage to endothelial cells

  • LDL can slip under endothelial cells to smooth muscle layer

  • High LDL levels = more LDL underneath

  • That LDL gets oxidised from metabolites from cells which then damages endothelial cells more

  • Damaged endothelial cells bring monocytes underneath them and monocytes eat the lipids and become really big becoming foam cells

    • at this point you still have wide arteries

  • Lipid core forms under endothelial cells with plaque formed over it

  • Vessel gets narrower

  • Potentially bursts

First place the blood goes from the aorta is the heart

  • But a narrowing in the arteries over a long period can lead to myocardial infarction

  • Stable angina - predictable chest pain, usually on exertion/stress; something that increases the demand of the heart

  • Unstable Angina - chest pain that occurs unpredictably

  • Myocardial infarction - heart does not get enough oxygen for a prolonged period leading to heart muscle death

    • if an artery is blocked for ~20 minutes, the tissues it supplies will die and form scar tissue

    • ischaemic cardiomyopathy - lots of things going on leading to reduced heart muscle efficiency; leading towards heart failure

Angina

  • pain associated with angina is caused by myocardial ischaemia - pain lasts 3-5 minutes and may radiate to neck, lower jaw, left arm and shoulder

  • key thing whether stable or unstable: no permanent damage after pain recedes

  • stable angina

    • pain on physical exertion/stress/anything that requires increased nutrient delivery to heart

  • unstable angina

    • rupturing of an atherosclerotic plaque

    • dissolves away - intermittent reduction in blood flow which leads to pain

    • unstable and unpredictable - doesn’t have to be triggered by stress or exercise

  • how do you reduce the risk of angina?

    • taking aspirin with heart disease

      • inhibits platelets that form clots from clotting which makes it less likely to clot from a plaque

    • taking nitrates - causes venodilation (dilation of veins); more blood remains in veins (storage) so less blood goes back to the heart, therefore the heart stretches out less, so it requires less energy to pump out again

      • reduces oxygen demand of heart

        

Myocardial Infarction (MI)

  • myocardium necrosis results from coronary blood flow being interrupted for an extended period of time

    • less oxygen

    • lactic acid and other chemicals released, causing damage

    • can’t contract as well - loses contractility

    • leads to uncontrolled cell death

    • scar tissue forms from affected myocardium - electrical currents don’t pass through scar tissue leading to arrythmias and potential heart failure

  • a heart attack activates the sympathetic nervous system

  • two major types of MI

    • STEMI (ST elevation MI)

    • Non-STEMI

    • electrocardiogram: an ECG will tell where the blockage is and whether the MI is STEMI or non-STEMI

  • troponin is definitive, specific marker of heart damage

    • the more troponin, the more damage has been done

Angina vs Myocardial Infarction (heart attack)

  • Clammy skin that doesn’t evaporate

  • More prolonged than angina

  • Sharper pain

bypass graft takes blood from before the block and puts it in a place after the block