Dual Antiplatelets


🌟WHEN do you use dual antiplatelet therapy (DAPT)?

1️⃣ Patients who have had acute coronary syndrome event (ACS) such as a heart attack

2️⃣ Patients who have stable ischemic heart disease and receive a stent placement (in other words, non-ACS setting)

🤫 pssst – if you don’t know what an ACS is – it is ANY condition brought on by a sudden reduction or blockage of blood flow to the heart. This is often caused by plaque rupture or clot formation in the heart’s arteries leading to sx of chest pain.

🌟 Okay great, we know when but WHY?

ACS is considered a medical emergency; treatment is needed to reopen the arteries and restore blood flow to the heart so it can work properly. This is usually done with a combination of medications + procedures such as a PCI (percutaneous coronary intervention) where a small structure called a stent is placed to open up the blocked blood vessel.

Afterward, the patient is at higher risk of future thrombotic events since they just had an occurrence and increased risk of stent thrombosis. This is where DAPT is recommended to prevent recurrent ischemic events.

🌟 Cool – but WHAT are dual antiplatelets?

Dual antiplatelet therapy recommendations include:

Aspirin PLUS ticagrelor, prasugrel, or clopidogrel

🌟 P2Y12 inhibitor considerations:

-Prasugrel is the most potent followed by ticagrelor, then clopidogrel (🧠TIP: Prasugrel is the most Potent ‘P’ for potent – but with increased potency comes increased bleeding risks. Avoid prasugrel in pt. age >75, hx of TIA/stroke, and hepatic dysfunction

-All of them are dosed once daily except ticagrelor which is dosed twice daily (🧠TIP: Ticagrelor is dosed ‘T’ for Twice daily) – can your patient be compliant?

-Clopidogrel and prasugrel are affordable and available in generic versions while ticagrelor is not. Can your patient afford it?



Let’s 👏🏻 talk 👏🏻 diabetes👏🏻!⁠

🌟American Diabetes Association (ADA) and the European Society of Cardiology (ESC) released new 2023 guidelines recently and I just had to do a doodle note on it. 🤓⁠

🌟There has been lots of debates regarding whether metformin should still be first-line for all patients with type 2 diabetes. ⁠

🌟 It still is a great first-line option for most patients due to it’s proven efficacy, safety, and low cost. There are also some speculation that it m-a-y have cardiovascular benefits as well considering many patients in the clinical trials were also on metformin. ⁠

💗🫘However, in patients with ASCVD or high ASCVD risks, heart failure, and chronic kidney disease, the ADA/ESC guidelines recommend starting a SGLT-2 inhibitor or GLP-1 agonists with cardiovascular and renal benefits regardless if they have type 2 diabetes. ⁠

🌟 It is still important to look at patient specific factors (cost, comorbidities, side effects) when deciding which agent to start first or to add on. ⁠

👉🏻GLP-1 agonists commonly have GI side effects and carry warnings for rare pancreatitis and gallbladder disease. It can cost patients $1000/month. Most of the agents are injectables and supply is not consistent.⁠

👉🏻SLGT-2 inhibitors are linked to genital yeast infections, and volume depletion. Cost is about $600/month but they do come in oral formulations.⁠

Reference: Diabetes Care. 2023 Jan 1;46 (suppl 1):S140-S157⁠


🔝 Beta-blockers are one of the top 200 drugs prescribed as they are indicated for many different cardiovascular diseases such as hypertension, angina, atrial fibrillation/flutter, and heart failure with reduced ejection fraction. ⁠⠀
⭐Generally, there are two types of beta-adrenergic receptors, beta-1 and beta-2 receptors.⁠⠀
-Non-selective beta-blockers block both beta-1 (β1) and beta-2 (β2) adrenoceptors. ⁠⠀
-Cardioselective beta-blockers are relatively selective for β1 adrenoceptors (remember you have 1 heart) and tend to be favored in patients with diabetes or COPD/asthma. ⁠⠀
-Some beta-blockers also cause vasodilation through blockade of vascular alpha receptors making them great for use in hypertension.⁠⠀
🧠 Use the mnemonic – Be (β1) selective about your MAN BABE to help you remember the beta-blockers that are cardioselective. ⁠⠀

Diuretic Classes

There are 5 main types of diuretic classes with different mechanisms of action, site of action, and side effect profiles. ⁠ ⁠ 1) Loop diuretics work on the loop of Henle (as the name implies)⁠ 2) Osmotic diuretic work on the glomerulus⁠ 3) Thiazides work on distal convoluted tubule⁠ 4) Carbonic anhydrase work on the proximal tubule⁠ 5) Potassium-sparing diuretics (aldosterone antagonists and sodium channel blockers) work on the distal convoluted tubule⁠ and collecting ducts

Beta-1 Cardioselective Beta-Blockers

❤️ Cardioselective beta-blockers work on the beta-1 receptors. Beta-1 receptors primarily are found in cardiac tissues whereas beta-2 receptors are located in the lungs (remember: 1 heart, two lungs). ⁠

❤️ Cardioselective beta-blockers exert their effect by binding to the beta-1 receptor sites selectively and inhibiting the action of epinephrine and norepinephrine on these sites. They are often preferred in patients with respiratory disease as they are less likely to cause constriction of airways or peripheral vasculature.⁠

Diuretics Sites of Action

Diuretics work to enhance sodium and water excretion through 4 main sites on the nephron.

1– Proximal convoluted tubule: Mannitol and acetazolamide (extends into the descending loop of Henle)

2– Ascending loop of Henle: loop diuretics

3– Distal convoluted tubule: thiazides

4– Collecting ducts: Potassium-sparing diuretic (e.g., spironolactone and triamterene)

Calcium Channel Blockers

Calcium channel blockers (CCBs) are used in the treatment of many cardiovascular conditions. They are divided into subclasses, non-dihydropyridines and dihydropyridines.

The non-dihydropyridine CCBs cause less vasodilation and more cardiac depression than dihydropyridine CCBs (hence why they are not recommended in decompensated heart failure). They cause reductions in heart rate and contractility.

Dihydropyridine CCBs have more vascular selectivity and fewer cardiac effects. They are indicated in the treatment of hypertension and angina. They do not suppress AV conduction or the SA node automaticity.

Warfarin Factor Half-Lives

Warfarin is an oral anticoagulant most frequently used to control and prevent thromboembolic events. ACCP recommends that patients newly started on warfarin be bridged with LMWH or unfractionated heparin for 5 days AND until therapeutic INR is achieved.

🌟High-yield fact🌟 The presence of a therapeutic INR does not confer protection from clot formation and expansion during the first few days of warfarin therapy, so if your patient’s INR is 2.0 on day 3, it is recommended to continue bridging until day 5.

This recommendation is based on the fact that the anticoagulant activity of warfarin depends on the clearance of functional clotting factors already present in the body.

Warfarin works by inhibiting new clotting factors from forming but requires that the old factors be cleared from the body. The clearance of these clotting factors is determined by their half-lives. The earliest changes in the International Normalized Ratio (INR) are typically noted 24 to 36 hours after a dose of warfarin is administered. These changes are due to the clearance of functional factor VII, which is the vitamin K–dependent clotting factor with the shortest half-life (6 hours: after 3-5 half-lives or 24-36 hours it will be eliminated from the body). The factor with the longest half-life, prothrombin or factor II, will take 5 days to clear from the body, hence why we need to bridge for at least 5 days AND until therapeutic INR is achieved.

Warfarin Factors

This is a high-yield question that is often asked on exams and clinical rotations.  This mnemonic helps you remember which vitamin K-dependent factors warfarin affects. ⁠

Warfarin, brand name Coumadin, is an anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent clotting factors, which include Factors II, VII, IX, and X, and the anticoagulant proteins C and S.⁠