Angina and vasodilators

• what is angina?

  •Angina pectoris = pain in the chest of cardiac origin, pain is often reffered to the left shoulder/upper limb
• brief pathology of angina

  Pathology - Inadequate blood and O₂ supply to myocardium

  •Occlusion of coronary arteries, atheroma = very common, mostly asymptomatic

  progressive: atheromatous deposits -> plaques -> atherosclerosis

  stable -> unstable angina -> thrombosis/MI

  •Vasospasm of coronary arteries - rare

  Prinzmetal’s (variant) = rare
• how would you differentiate cardiac pain form the differentials?

  here

  
• explain how angina effects the sympathetic system and what effect this has (angina physiology):

  
• explain how angina affects the coronary arteries and arterioles when comparing rest to exercise

  
• what drugs are prescribed for acute exacerbations/episodes of angina?

  short-acting nitrates
• what drugs are prescribed for angina long-term?

  common

  • beta blockers
  • calcium channel blockers
  • long-acting nitrates
  • nicorandil
  • ivabridine

  others:

  • minoxidil
  • hydralazine
  • dypyridamole
• what is the aim of drugs prescribed for angina?

  redress the imbalance between the oxygen delivery and consumption

  with vasodilators the idea is that vasodilation of the coronary arteries causes increased blood supply to the myocardium and increases the ischaemia related angina symptoms
• what role to collateral vessels play in the pathophysiology of angina

  as there is an occlusion in one artery to accommodate for the decrease in blood supply, collateral vessels are formed from other coronary arteries to the myocardium that would be supplied from the affected coronary artery -> essentially redirects the blood flow to the ischaemic areas

  
  

  note that fitness training can also lead to the formation of collateral blood vessels

  
• how do nitrovasodilators cause the dilation of collateral vessels?

  they (NO) preferentially select for collateral coronary vessels and cause them to dilate which increases blood flow to the ischaemic tissue
• outline the MOA for most nitrovasodilators:

  most are prodrugs and metabolised into NO which binds to NO-sensitive soluble guanylyl cyclase causing conversion of GTP to cGMP, increasing intracellular cGMP concentration which activates PKG -> activated PKG then phosphorylates and inactives proteins needed for muscle contraction. The muscle is then relaxed. Nitrovasodilators act primarily on capacitance veins which decreases ventricular pressure and decreases the cardiac effort in return which should improve the balance between oxygen demand and supply as is the theory with angina pharmacology
• what is prinzmental angina?


  (vasospastic angina or variant angina) is chest discomfort or pain at rest with transient electrocardiographic changes in the ST segment, and with a prompt response to nitrates. These symptoms occur due to abnormal coronary artery spasm.

  unlike angina they are not related to emotion or exertion and normally occur between midnight and early morning