Anti-Angina Flashcards
● Due to blockage or imbalance of the oxygen supply and demand is too much on the heart
● If oxygen supply cannot keep up with the demand
MYOCARDIAL INFARCTION
What is the primary symptom of Myocardial Infarction?
Angina Pectoris
○ Chest pain
○ Pain over the myocardium
○ Which is associated with Ischemic Heart Disease or Myocardial Ischemia
Myocardial ischemia main dysfunction is when you have
atherosclerosis or when there is blockage inside the arteries
● Increase lipid deposition in subendothelial space which gives way to plaques (early plaque) in the arterial lining/blood vessels
● Leads to endothelial dysfunction with decrease production of Nitrous Oxide (NO) which is a vasodilator
● Less vasodilation, increase risk of platelet adhesion
● Influx of lipid scavenger cells, necrosis, sterile inflammation
● Proliferation of smooth M cells, calcification and narrowing of blood vessel by inc plaque formation
ATHEROSCLEROSIS
What are the triggering factors for atherosclerosis?
Cases wherein symptoms will come up:
○ Acute inflammation: viral infection (Influenza)
○ Blood Pressure (BP) peaks during exercise or
emotional stress
Factors that determine progress of Coronary Artery Disease
● Most important: Concentration of lipids in blood
○ Familial hypercholesterolemia
- family disorder; high level of lipids even with strict diet and exercise
○ More fatty food, higher conc. Of lipids in the blood; bad lipids LDL, VLDL
● Endothelial dysfunction
● Blood Pressure (high)
● Activity of inflammatory system
● Reactivity of pro- and anti-thrombotic systems
Patient with Coronary Artery Disease (CAD) advised
● Lipid profile: At a certain age needs to be check (LDL, HDL/good cholesterol, VLDL)
○ There are some patients who have low HDL; Typically female patients have high HDL until they reach menopause. Afterwhich, as we all know, the cardiovascular risk factors of females equal those of the males after menopausal. Typically, women are really protected while they are still menstruating.
○ It’s important to remember that, when patients have low HDL, we advise them to drink fish oil or to eat fish more.
● Exercise regularly
○ Ideally, around 4-5 times a week, even 30 minutes or even just walking
● Stop smoking
● BP and body weight control
● Treatment with statins, aspirin, Beta blockers
● Annual vaccinations against Influenza
○ Nowadays, also COVID vaccinations
What is the primary symptom of Ischemic Heart Disease?
Angina Pectoris
It is due to an imbalance in the myocardial oxygen
supply-demand relationship
Angina Pectoris
Angina Pectoris is c/b:
Caused by:
○ Increase myocardial oxygen demand
■ As when you exercise because usually that’s when your angina or your symptoms will come out when exercising or under stress
○ Decrease in myocardial oxygen supply
■ Presence of plaques or vasospasm
What happens in progressive decrease in vessel radius (coronary atherosclerosis)?
Impair coronary blood flow
○ Angina will occur when myocardial O2 demand increases
When there is an abrupt decrease in blood flow?
○ Coronary thrombosis
○ Localized vasospasm
Signs and Symptoms of Angina Pectoris
● Heavy, pressing, substernal discomfort often radiating to left shoulder, flexor aspect of left arm, jaw or epigastrium
● Key is Management: If the patient is complaining of Angina, you have to be very fast. When the patient already has Myocardial infarction, the golden rule is that, within an hour, you have to stop the progression of your infarction so you will not end up with dead myocardial tissue which is now very difficult to treat
● May have atypical symptoms
● Some of them may complain, not of chest pain but some may complain of cough, or back pain or sometimes dyspnea, and they don’t really complain of chest pain, so we have to investigate further.
Women, elderly, and diabetics
● We all know that beta blockers and some calcium entry blockers like your verapamil and diltiazem, decreases the heart rate and contractility leading to an increase in oxygen demand
● Your nitrates and your calcium entry blockers also can affect your preload and afterload also leading to decrease in oxygen demand
Does vasodilators increase oxygen supply?
Yes.
They don’t have any effect on the oxygen demand because they do not per say have any effect on the heart. They do have an effect on your blood vessels, they dilate the blood vessels to improve coronary blood flow, increasing the oxygen supply.
● Any imbalance of the two will now lead to your
ischemia.
You now have an anaerobic metabolism, and the accumulation of your substance P, as well as increase in glycolysis, lactate, and pyruvate formation, what is now triggered?
sympathetic nerve endings are now triggered. So, it will all lead to pain and that’s when the patient will complain of angina.
This is typically a person with angina. If you notice, he or she will complain of tightness or pain in the chest. Usually, they will hold a fist to the left side of their chest, typically that is what they complain of.
● But sometimes there are also other causes of chest pains, it’s not just angina. One of the more common causes may be your gastroesophageal reflux disease (GERD), pancreatitis. There are a lot of causes but the main thing that you should rule out immediately when you have patients complaining of chest pain is your ischemia or in the worst case scenario, a myocardial infarction.
What are the types of angina?
- Typical Stable Angina
- Variant Angina
- Unstable Angina
● Pathology: (this is caused by) fixed atherosclerotic narrowing of an epicardial coronary artery
● Depending on where the narrow portion or the block is, that’s where you get your symptoms
Typical Stable Angina
● Usually this is caused by a focal/diffuse coronary spasm episodically reduces coronary flow
○ there is no block but there is usually a focal or decreased coronary spasm of the artery which reduces the coronary blood flow
● AKA Prinzmetal’s Angina
● Usually this is reversed by Nitrates or Ca++ blockers
Variant Angina
● This one is dangerous because it is an acute coronary syndrome
● Episodes of angina at rest and when there is a change in character, frequency, and duration of chest pain and precipitating factors in patients with previously stable
angina
● Caused by episodes of increased epicardial artery tone
● Small platelet clots occurring in the vicinity of an atherosclerotic plaque
● High risk of MI and death
○ Or this may be a precursor to a greater cardiac event in the near future where the patient may have an impending MI. If you have a massive MI, that’s very difficult to treat already, usually that will lead to death
of the patient.
Unstable Angina
WAYS BY WHICH DRUGS RELAX VASCULAR SMOOTH MUSCLE
● Increase cGMP
○ NO
■ Nitroprusside
■ Nitrates
● Decrease Intracellular Ca+2
○ Ca++ channel blockers
○ β-blockers
● Stabilizing or preventing depolarization of vascular SM cell membrane
○ Minoxidil
○ Nicorandil
● Increase in cAMP in vascular smooth muscle cells
DRUGS FOR ANGINA
● Nitrovasodilators
● Β-adrenergic receptor antagonists
● Ca+2 channel antagonists
● All approved antianginal agents function by improving the balance of myocardial oxygen supply and demand
○ Increasing supply by dilating the coronary
vasculature
○ Decreasing demand by reducing cardiac work
Other Treatment
● Stabilize the plaque
○ Anti-platelet agents (Aspirin, Clopidogrel)
○ Statins
■ Lowers down cholesterol
○ Ranolazine
■ Chronic Angina
■ Direct effects on cardiac myocyte Na+
channels
● Β-adrenergic Antagonists
○ Decreased mortality by reducing incidence of sudden cardiac death associated with M.I. and ischemia
TREATMENT FOR CARDIAC FACTORS
● Aspirin
● Other antiplatelet agents:
○ Clopidogrel
○ Abciximab
○ Tirofiban
○ Eptifibatide
● Lipid-lowering agents
● ACE Inhibitors
○ Patients with impairment of cardiac systolic function
● Coronary Artery Bypass Surgery (CABG)
○ More than 2 vessels, or vessels are too small for a stent to be inserted; DM- small vessel disease
● Angioplasty
● Coronary Artery Stent Deployment
● Give drugs that either increase blood flow to the heart
○ Decrease left ventricular wall tension, heart rate or contractility
TYPICAL ANGINA
Prevention of coronary spasm
Variant/Vasotonic Angina
Correcting the tendency to intracoronary thrombosis
Unstable Angina
ORGANIC NITRATES
● Nitroglycerin
● Isosorbide dinitrate
● Isosorbide 5-mononitrate
○ There are all emergency medications which elderly individuals or people with high risk should have with them all the time.
○ These are life saving drugs.
NITROGLYCERIN GENERAL ACTION:
● In patients with stable angina, it produces dilatation of veins and dilatations of collaterals leading to a decrease in oxygen consumption.
● For patients with heart failure, dilation of your arteries (reduction of afterload) and dilation of veins leading to a decrease preload, so this will result in a reduction of your left ventricular end diastolic pressure, reduction in wall stress, and reduction of mitral regurgitation.
● For patients with acute coronary syndrome, dilatation of arteries, dilatation of collaterals, and produces antiaggregation of your platelets leads to an increased O2 supply.
MECHANISM OF ACTION OF NITRATES:
Source of NO (Nitric Oxide) -> activates guanylyl cyclase -> Increased levels of cGMP -> Dephosphorylation of myosin light chain, decreased cytosolic Ca++ -> smooth muscle
relaxation
EFFECTS OF NITRATES:
● Relaxation of vascular smooth muscle.
● Low concentrations will dilate the VEINS more than the arteries.
● Decreased venous return -> Decreased L and R ventricular chamber size and end-diastolic pressure.
● Relieve anginal pain by dilating coronary artery -> increased coronary blood flow.
● Angina due to coronary artery spasm
○ Epicardial coronary arteries dilate, particularly regions affected by spasm which will relieve your angina.
MECHANISM OF RELIEF OF SYMPTOMS OF ANGINA:
● Reduction in myocardial work and O2 demand
🠊 Primary effect in chronic stable angina.
● The problem with nitrates is that you will have vasodilation of all the blood vessels in the body
🠊 the patient will now experience the side effects.
● Responses evoked by vasodilation.
○ Tachycardia (baroreceptor reflex, compensatory mechanism)
○ Orthostatic Hypotension (direct extension of venodilator effect)
○ Throbbing headache (meningeal arteries
vasodilation)
Frequently repeated/continuous exposure to high doses of organic nitrates -> marked attenuation of most pharmacologic effects
TOLERANCE
Reduced capacity of vascular SM to convert nitroglycerin to NO
True Vascular Tolerance
Activation of mechanisms
Pseudotolerance
MANAGEMENT
● Interrupt treatment for 8-12 hours/day
● Omit night dose in patients with exertional angina
