In CAD, the coronary arteries narrow with fatty plaque, so the heart muscle can't get as much oxygen-rich blood as it needs — and that mismatch between oxygen supply and demand is what causes ischemia.

How the plaque builds up (atherosclerosis development):

1. Endothelial injury — the inner lining of the artery gets damaged, usually from hypertension, smoking, hyperlipidemia, or diabetes.
2. Lipid accumulation — LDL cholesterol seeps into that damaged lining and gets oxidized, which makes it strongly pro-inflammatory.
3. Inflammation and immune response — immune cells called macrophages come in to clean up the lipid, gorge on it, and turn into what are called foam cells.
4. Plaque formation — a fibrous cap forms over the pool of lipid underneath, sealing it into a plaque.

What can go wrong with the plaque:

• It can rupture — the cap tears, a clot (thrombus) forms on top of it, and that clot can block the artery outright, causing a myocardial infarction.
• It can just keep growing and cause stenosis — progressive narrowing of the artery.
• The narrowing causes ischemia — not enough blood getting through — which is felt as angina.

Why the pain shows up with exertion:

At rest, even a narrowed artery can usually deliver enough blood to keep the heart muscle satisfied. But when you exert yourself, the heart muscle's oxygen demand goes up — and the artery is fixed in how narrow it is, so it can't deliver any more blood to meet that demand. The mismatch causes ischemia, which you feel as angina, and it eases again once you rest and demand drops back down.

Some CAD risk factors are things you cannot change; others are things you (or treatment) can act on.

The short version: none of these tests on its own says “this is CAD.” Some ask “is the heart short of oxygen right now?”, some ask “does it go short when you make it work?”, and one actually takes a picture of the artery.

What each test is for:

Both are ways cholesterol travels through the blood, but they move it in opposite directions.

LDL (low-density lipoprotein) — the "Lousy" one:

LDL carries cholesterol from the liver to the tissues, where it can penetrate the artery wall and deposit there. That's why it's called atherogenic — it's the cholesterol that builds the plaque. Once it gets oxidized inside the artery wall, it becomes strongly pro-inflammatory, which drives the injury-and-plaque process further.

HDL (high-density lipoprotein) — the "Healthy" one:

HDL runs the opposite direction — reverse transport. It picks up excess cholesterol that's sitting in the artery walls and carries it away, back to the liver, where it can be processed and eliminated. That's why HDL is protective.

All the numbers below are in mg/dL.

These are verified against NCEP/ATP III — your deck lists the terms but not the numbers, so these are the numbers to actually memorize.

Dyslipidemia is the umbrella term: any abnormal lipid level, whether it's too high or too low — including a low HDL. Hyperlipidemia is narrower: it specifically means elevated lipids (cholesterol and/or triglycerides).

Primary causes — genetic:

• Familial hypercholesterolemia
• Familial combined hyperlipidemia

Secondary causes (from your deck) — something else is driving the lipid problem:

• Diabetes mellitus
• Obesity
• Hypothyroidism
• Chronic kidney disease
• Liver disease
• Medications (thiazides, beta blockers, corticosteroids, antiretrovirals)
• Lifestyle factors
• Other endocrine disorders — polycystic ovary syndrome and Cushing syndrome

At its core, heart failure means less blood is being pumped out than the body needs — and the heart's own attempt to compensate ends up making things worse.

The self-reinforcing cycle:

Decreased contractility means the heart squeezes less forcefully, so less blood is pumped out with each beat (decreased stroke volume). Whatever wasn't pumped out is left behind in the ventricle, so more volume builds up there before the next beat — this is an increased left ventricular end-diastolic volume (LVEDV), also called increased preload. That extra volume stretches and enlarges (dilates) the heart, and a dilated heart contracts even less well — feeding right back into decreased contractility. It's a cycle that keeps reinforcing itself.

Left-sided heart failure (the most common kind):

The left ventricle can't pump blood forward efficiently, so blood backs up behind it — into the pulmonary circulation (the lungs). That raises the pressure in the pulmonary vessels, which forces fluid to leak out into the alveoli, causing pulmonary congestion and edema. And because less blood is getting pumped forward in the first place, patients also get fatigue and cool extremities from that reduced output.

Right-sided heart failure:

The right ventricle can't pump blood to the lungs adequately, so blood backs up behind it instead — into the systemic venous circulation (the body). That raises venous pressure, which causes fluid retention, peripheral edema, ascites (fluid in the abdomen), and hepatic congestion (a backed-up liver).

Two ways right-sided failure develops:

1. Secondary to left-sided failure (most common) — fluid that's backed up from the failing left side works its way back through the lungs and puts strain on the right ventricle.
2. Without any left-sided failure — from long-standing lung disease, especially COPD, or pulmonary hypertension. This standalone pattern is called cor pulmonale. These patients show jugular venous distention, peripheral edema, and hepatosplenomegaly, but without the lung symptoms you'd see in left-sided failure.

Systolic vs. diastolic dysfunction — two different ways the pump can fail:

• Coronary artery disease and prior myocardial infarction — CAD is a leading cause
• Diabetes mellitus
• Valvular heart disease
• Cardiomyopathy
• Obesity
• Chronic lung disease (COPD) and pulmonary hypertension — these drive right-sided failure specifically
• Anemia — the heart has to work harder to compensate for the blood carrying less oxygen
• Advancing age
• Chronic kidney disease
• Arrhythmias such as atrial fibrillation

The NYHA classification answers a different question than the ACC/AHA stages do. The stages describe the structure of the heart and only ever move forward. NYHA instead describes how much the symptoms limit the patient's activity — and unlike the stages, it can move back and forth as treatment helps or the disease worsens. It's used to describe functional capacity in Stage C — your slide 64 brings NYHA in at Stage C specifically, and describes Stage D separately as end-stage. On its own it's an independent predictor of mortality.

Ejection fraction is the percentage of the blood sitting in the ventricle at the end of filling (end-diastolic volume) that actually gets ejected with each beat. Normal is 55–70%. It's measured by echocardiogram, and it's the key number that separates systolic failure from diastolic failure.

These four categories come from the 2022 AHA/ACC/HFSA guideline, which is newer than your webinar deck — so if the deck only lists two or three categories, that's why.

The heart has four valves — aortic, mitral, pulmonary, and tricuspid — and each one can fail in one of two directions: it can get too narrow (stenosis), or it can stop closing all the way and let blood leak backward (regurgitation). Left alone, either one can progress all the way to heart failure.

Stenosis:

The valve opening narrows, which restricts how much blood can flow through and forces the heart to work harder to push blood through the smaller opening. The narrowing itself is what produces the murmur you hear, and the extra workload causes the chamber pushing against the narrowed valve to thicken (chamber hypertrophy) — this is called pressure overload. It can also raise the pressure, and potentially cause regurgitation, in the chamber next door.

Regurgitation:

The valve doesn't close all the way, so some blood leaks backward instead of moving forward. Whichever chamber receives that backward flow has to hold extra volume, so it stretches out and enlarges — this is volume overload, and the chamber dilates rather than thickens.

Aortic stenosis — high yield:

The classic triad is angina, syncope, and dyspnea — all brought on by exertion. Of the three, syncope is the most ominous symptom.

Why exercise triggers the fainting (exertional syncope):

1. The aortic valve is stuck narrow and physically cannot open any wider — it's a fixed obstruction, not one that can flex to let more blood through.
2. During exercise, your muscles need more blood, so the body relaxes (vasodilates) the blood vessels feeding them — this drops your systemic vascular resistance.
3. Normally the heart would answer that drop by pumping out more blood to keep blood pressure up. But cardiac output can't increase past the valve's fixed narrow opening — there's simply no more room for blood to get through.
4. So blood pressure falls anyway, the brain is underfed (cerebral hypoperfusion), and the patient faints.
5. The medical word for that faint is syncope.

Three causes your course names:

• Congenital anomalies
• Age-related degeneration (calcification of the leaflets)
• Rheumatic heart disease

If it's left untreated, the chronic extra pressure the left ventricle is pushing against (pressure overload) makes it hypertrophy to try to keep output up — but that thickened muscle eventually causes myocardial ischemia, angina, and heart failure of its own.

The only real fix is replacing the valve, and your book is specific about how. The catheter route (TAVI/TAVR) is the one it says is indicated for people who have symptoms and for most people who don't yet, as long as the stenosis is severe. So "just watch and wait" is the wrong answer for severe aortic stenosis, even with no symptoms. Medicines can ease the heart's workload (vasodilators) but they don't fix the valve, and statins specifically have been shown not to slow it down.

Mitral stenosis — high yield:

Worldwide, the most common cause is rheumatic heart disease following a strep throat infection (group A streptococcal pharyngitis) that was never treated. The immune system's antibodies against the strep bacteria cross-react with the valve tissue itself (molecular mimicry) — that cross-reaction thickens the leaflets and fuses them together at their edges (commissural fusion), a process slow enough that it doesn't show up until decades later.

The downstream effects: the left atrium enlarges, which can trigger atrial fibrillation; pressure backs up into the lungs causing pulmonary congestion; engorged pulmonary capillaries can rupture and cause hemoptysis (coughing up blood); and in advanced disease, pulmonary hypertension develops and eventually causes right heart failure with peripheral edema.

Simplified — by heart phase · AI GENERATED

Simplified — the four, one at a time · AI GENERATED

Watch the short forms — this one catches people out. MS means mitral stenosis: the rumbling murmur you hear while the heart is FILLING, down at the apex, with a snap as the stiff valve opens. MR means mitral regurgitation: it lasts the whole SQUEEZE and carries out toward the armpit. They are one letter apart and they happen in opposite halves of the heartbeat, yet they sit side by side on nearly every summary chart — **and one of the charts you were sent labels mitral stenosis as (MR), the very same short form as the row below it. Same for the aortic pair: AS happens during the squeeze, AR** during the filling. If a chart's short form and its timing disagree, believe the timing.

One more rule of thumb: diastolic murmurs are essentially always pathologic, while some systolic murmurs can be benign.

• Age — degenerative calcification of the leaflets
• Untreated streptococcal infection, which can lead to rheumatic fever
• Congenital abnormality — especially a bicuspid aortic valve, which causes disease to present earlier
• Infective endocarditis
• Prior myocardial infarction — can cause the papillary muscle or chordae to rupture, producing acute mitral regurgitation
• Chest radiation
• Connective tissue disease such as Marfan syndrome
• Intravenous drug use

Factors that specifically accelerate aortic stenosis:

• Hypertension
• Dyslipidemia
• Smoking — this is the one that was missing. Your book says aortic stenosis carries many of the same risk factors as coronary artery disease, and gives three examples: high blood pressure, smoking, and abnormal cholesterol. The word it uses is including, so that list isn't the whole set — insulin resistance counts too, because the same chapter lists "diabetes and insulin resistance" among the seven big coronary risk factors. Learn all four.