Coronary artery disease (CAD) questions are everywhere on Step 1 and Step 2—and the fastest points often come from recognizing risk factors on sight. Here’s a quick-hit, shareable mnemonic set that helps you recall major CAD risk factors, plus the “why it matters” one-liners USMLE loves.
The Big Picture (What CAD Risk Factors Really Do)
Most CAD risk factors converge on:
- Endothelial injury/dysfunction → easier lipid entry + inflammation
- Atheroma formation (foam cells, fatty streaks) → plaque growth
- Plaque rupture + thrombosis → acute coronary syndrome (UA/NSTEMI/STEMI)
If a stem gives you multiple risk factors, your pre-test probability of CAD skyrockets.
Core Mnemonic: CAD HITS
Think: the things that “hit” the coronary arteries.
C A D H I T S
| Letter | Risk factor | USMLE one-liner |
|---|---|---|
| C | Cigarette smoking | Causes endothelial damage, ↑ platelet adhesion, ↓ HDL; strongest modifiable risk factor. |
| A | Age | Risk rises with age; classic male ≥45, female ≥55 (or postmenopausal). |
| D | Diabetes mellitus | Equivalent to a “CAD risk equivalent” clinically; accelerates atherosclerosis via glycation, inflammation. |
| H | Hypertension | Chronic shear stress → endothelial injury → promotes plaque formation. |
| I | Increased LDL / dyslipidemia | LDL is atherogenic; oxidized LDL → foam cells → fatty streaks. |
| T | Triglycerides high / low HDL | Low HDL reduces reverse cholesterol transport; hyperTG often tags along with insulin resistance. |
| S | Strong family history | Premature CAD in first-degree relative (men <55, women <65) implies genetic risk. |
Memory hack: If you can recite CAD HITS, you can usually answer “most important risk factor” or “most likely diagnosis” questions quickly.
The Classic “Nonmodifiable vs Modifiable” Split (Test-Friendly)
Nonmodifiable (can’t change, but should recognize)
- Age
- Sex (men higher risk earlier; women catch up after menopause)
- Family history / genetics
Modifiable (the ones NBME expects you to treat)
- Smoking
- Hypertension
- Diabetes
- Dyslipidemia (↑ LDL, ↓ HDL)
- Obesity + sedentary lifestyle
- Diet (high saturated/trans fats)
- Chronic kidney disease (often “CAD equivalent” in clinical framing)
Rapid-Fire Visual: “The Plaque Stack”
Picture plaque like a stack built from three major inputs:
- Pressure injury = HTN
- Poison injury = Smoking
- Sugar + fat load = Diabetes + LDL
If you see those three together in a vignette, CAD is almost always the intended direction.
High-Yield USMLE Pearls (Common Traps & Favorites)
1) “Most important modifiable risk factor?”
- Many resources emphasize smoking as a top modifiable risk factor for CAD/MI due to its strong association and immediate benefit with cessation.
- In clinical prevention frameworks, LDL lowering and BP control are also major targets—so read the question stem carefully (population vs individual framing).
2) Diabetes is a “CAD accelerator”
- Expect multivessel disease, earlier onset, and atypical symptoms.
- Step 2 loves: diabetic patient with silent ischemia or atypical dyspnea/fatigue.
3) HDL vs LDL—what to remember quickly
- LDL = “Lousy” → plaque
- HDL = “Healthy” → reverse cholesterol transport
- Oxidized LDL drives foam cells (macrophages stuffed with lipid).
4) Family history wording that matters
- “Dad had an MI at 49” or “mom had MI at 60” = premature CAD → strong risk signal.
5) Metabolic syndrome = CAD risk cluster
If you see central obesity + insulin resistance features, think:
- ↑ TG, ↓ HDL, ↑ BP, ↑ fasting glucose → high CAD risk.
One-Liner Summary You Can Screenshot
CAD HITS: Cigarettes, Age, Diabetes, Hypertension, Increased LDL, Triglycerides/low HDL, Strong family history.