Cardiovascular Disorders

Ischemic Heart Disease (IHD)

Clinical Overview and Exam Mastery Guide covering stable angina, acute coronary syndromes, core pharmacology, reperfusion strategy, and secondary prevention.

Core Disease
Coronary flow-limiting atherosclerosis
Stable Pattern
Predictable exertional angina
ACS Driver
Plaque rupture plus thrombosis
STEMI Priority
Immediate reperfusion (PCI)

Coronary Occlusion Visual

Plaque Reduced myocardial flow Coronary artery lumen

Progressive narrowing limits oxygen delivery and triggers ischemic symptoms/events.

1. What Is Ischemic Heart Disease?

Ischemic Heart Disease (IHD), also called Coronary Artery Disease (CAD), occurs when coronary arteries are narrowed or blocked by atherosclerosis, reducing blood flow to myocardium.

Angina Myocardial infarction Arrhythmias Sudden cardiac death

2. Pathophysiology

Step 1: Atherosclerotic plaque formation
Step 2: Plaque rupture
Step 3: Platelet activation
Step 4: Thrombus formation and coronary occlusion

Stable Angina vs ACS Pathway Diagram

Atherosclerotic plaque Coronary narrowing Stable plaque Demand ischemia, exertional pain Plaque rupture + clot Acute coronary syndromes Stable angina Relief with rest or nitro UA / NSTEMI / STEMI Urgent ACS pathway
Stable plaque leads to stable angina. Plaque rupture with thrombosis leads to ACS.

3. Clinical Classification

A. Stable Angina

  • Predictable chest pain
  • Triggered by exertion
  • Relieved by rest or nitroglycerin

B. Acute Coronary Syndromes (ACS)

  • Unstable angina
  • NSTEMI
  • STEMI
ACS is plaque rupture plus thrombosis until proven otherwise.

4. Management of Stable Angina

Goals: reduce symptoms, prevent progression, reduce mortality.

A. Nitrates (Nitroglycerin)

MOA

  • Converted to nitric oxide
  • Venous vasodilation
  • Reduced preload and myocardial oxygen demand

Use / Safety

  • Acute angina relief and prophylaxis before exertion
  • Side effects: headache, hypotension, reflex tachycardia
  • Contra: PDE-5 inhibitors, severe hypotension, RV infarction

B. Beta Blockers

  • MOA: beta1 blockade lowers HR, contractility, and oxygen demand
  • Benefits: reduced post-MI mortality, fewer angina episodes
  • Side effects: bradycardia, hypotension, fatigue
  • Contraindications: severe bradycardia, cardiogenic shock

C. Calcium Channel Blockers

  • MOA: block L-type calcium channels causing vasodilation and lower afterload
  • Useful when beta blockers are contraindicated or insufficient
  • Avoid non-DHP agents in HFrEF

D. Ranolazine

  • MOA: inhibits late sodium current and improves relaxation
  • Role: refractory angina add-on therapy
  • Side effect: QT prolongation
  • Contra: baseline significant QT prolongation, strong CYP3A inhibitors

5. Management of Acute Coronary Syndromes (ACS)

Immediate priorities: restore perfusion, prevent clot propagation, and reduce myocardial workload.

A. Antiplatelet Therapy

Aspirin

  • MOA: irreversible COX-1 inhibition, lower thromboxane A2
  • Side effects: GI bleeding, dyspepsia
  • Contra: active bleeding

P2Y12 Inhibitors

  • Clopidogrel, ticagrelor, prasugrel
  • MOA: ADP receptor blockade, reduced platelet aggregation
  • Side effects: bleeding, dyspnea (ticagrelor)
  • Contra: active bleeding, prior stroke (prasugrel)

B. Anticoagulants

  • Heparin, enoxaparin
  • MOA: potentiate antithrombin, inhibit thrombin and factor Xa
  • Side effects: bleeding, HIT (heparin)

C. High-Intensity Statins

  • Atorvastatin, rosuvastatin
  • MOA: HMG-CoA reductase inhibition, lower cholesterol synthesis, stabilize plaque
  • Benefits: lower recurrent events and improve survival
  • Side effects: myopathy, elevated liver enzymes
  • Contraindications: active liver disease, pregnancy

D. Reperfusion

  • STEMI: PCI preferred, fibrinolysis if PCI unavailable
  • NSTEMI: risk stratification, early invasive strategy for high-risk patients

ACS Immediate Management Flow Diagram

Suspected ACS ECG + troponin + vitals Aspirin now Start antiplatelet base Add P2Y12 inhibitor DAPT strategy Anticoagulation + statin Heparin/LMWH + high-intensity statin STEMI? Immediate reperfusion decision STEMI: PCI preferred Fibrinolysis if PCI cannot be delivered in time NSTEMI/UA Risk stratify and consider early invasive strategy

6. Secondary Prevention

All post-MI patients should receive:

DAPT Beta blocker ACE inhibitor High-intensity statin
Lifestyle modification remains mandatory.

Management Recap Drill

Stable angina: Nitroglycerin for acute relief
Chronic control: Beta blocker first-line
Escalate if needed: Add CCB or ranolazine
ACS sequence: Aspirin -> P2Y12 -> anticoagulation -> statin -> reperfusion

Guideline References

ACC/AHA Guideline for Chronic Coronary Disease

https://www.acc.org/guidelines

ACC/AHA Guideline for Acute Coronary Syndromes

https://www.acc.org/guidelines

7. Common Exam Traps

Do not combine nitrates with PDE-5 inhibitors.
Prasugrel is contraindicated with prior stroke history.
Beta blockers reduce mortality after myocardial infarction.
Post-ACS statin therapy is required even with normal LDL.
STEMI requires urgent reperfusion strategy.

8. Quick Revision Summary

Must Remember

  • Stable angina is demand ischemia
  • ACS is plaque rupture until proven otherwise
  • MONA is outdated; prioritize DAPT plus anticoagulation
  • STEMI points to urgent PCI pathway

Post-MI Core Bundle

  • High-intensity statin
  • Beta blocker
  • ACE inhibitor
  • DAPT and risk-factor control

Practice Questions Placeholder

  • Topic: Ischemic Heart Disease
  • Subtopics: stable angina, NSTEMI, STEMI, DAPT, secondary prevention