Atherosclerosis, a ❌ deposition in the subendothelial space, causes IHD. There is endothelial dysfunction with ❌ production of NO, less ❌, increased risk of platelet ❌. An influx of lipid scavenger cells (❌) cause inflammation, calcification and ❌ of the blood vessel by increasing plaque formation.

Atherosclerotic plaque rupture causes a release of ❌ factor (TF) and von Willebrand factor (vWF)
vWF. More ❌ adhere, activate, and aggregate. The coagulation cascade activates resulting in ❌ binding platelets to one another causing clot (❌) formation.

Chronic stable angina is the initial manifestation of IHD in about 50% of patients. It is often caused by obstructive ❌ lesions in the coronary arteries. Vasospasm at the site of an atherosclerotic plaque may further ❌ blood flow and contribute to angina.
Stable angina is characterised by a plaque with a thick fibrous cap and relatively ❌ lipid core.
Patients are generally in no acute distress and describe stable angina pain as a sensation of pressure, heaviness, tightness, or squeezing in the anterior ❌ area. Pain may radiate to the neck, jaw, shoulder, back, or arm and may be accompanied by dyspnoea, nausea, vomiting, or diaphoresis. Pain lasts a few ❌ and is often provoked by ❌ (e.g. walking, climbing stairs, gardening) or emotional stress; and relieved within minutes by ❌ or with sublingual nitroglycerin.

Principles of treatment:
1. Angina:
Increase myocardial O2 supply (by ❌ the cardiac vasculature) and
decrease O2 demand (by decreasing heart ❌, myocardial ❌, and afterload)
2. ACS:
Re-vascularisation/re-perfusion with mechanical or chemical Tx.
- Mechanical:
Percutaneous coronary intervention (❌) = Angiography or ❌ (using a balloon or a stent), or Coronary artery bypass graft (CABG)
- Chemical:
Anti-platelets or
Anti-coagulants or
Fibrinolytics

Match the drug treatment to the purpose for IHD.
- Dilate blood vessels and reduce cardiac load: ❌
- Stabilise atherosclerotic plaques: ❌
- Prevent platelet aggregation: ❌
- Prevent propagation of thrombus: ❌
- Break down thrombus: ❌
- Pain relief: ❌

Nitrates are ❌ that donate nitric oxide, NO. NO increases intracellular ❌, which relaxes ❌ muscle cells and causes vasodilation. Frequent or high doses are associated with ❌.

Common DHP CCBs are ❌. Non-DHP CCBS are ❌.
❌ can cause headache, flushing, dizziness/postural hypotension, peripheral oedema, and constipation. ❌ can cause bradycardia (caution if patient is on a beta blocker).

Anti-platelets:
1. Aspirin: Inhibits ❌ which decreases ❌ meaning less activation and aggregation.
2. Thienopyridines (e.g. ❌): Inhibits ❌ receptor P2Y12 to decrease ❌
3. GPIIb/IIIa inhibitors (e.g. ❌): Inhibit ❌ receptor to decrease ❌

Anti-coagulants inhibit formation and propagation of thrombi in arteries and veins. In ACS mainly the heparins are used.
1. Unfractionated heparin (UFH) increases the ❌ action of anti-thrombin (AT) on factors ❌ (and to some extent XIIa, XIa, and IXa).
2. Low molecular weight heparins (LMWHs) increase the inhibitor action of AT on factor ❌. LMWH (e.g. enoxaparin) have a ❌ molecular weight than UFH, a longer ❌, and can be administered ❌ (self-administered).

Fibrinolytics break down fibrin stabilised clots. They are used more in pulmonary ❌ or stroke than in IHD. Examples are ❌, synthetic tissue plasminogen activators (❌).