Submodule
Coronary Disease Spectrum and Assessment
CCD includes fixed plaque, prior infarction or revascularization, nonobstructive ischemia, vasospasm, microvascular dysfunction, and symptom states that can change from stable to acute.
- Atherosclerotic plaque
- Supply-demand mismatch
- Anginal equivalents
- Unstable symptom change
Can remain silent or produce fixed obstruction
Symptoms emerge when reserve is insufficient
Angina can occur without major obstruction
Observed disease determines prevention intensity
Define the coronary phenotype
CCD includes obstructive and nonobstructive coronary disease, prior MI or revascularization, ischemia detected noninvasively, and chronic angina syndromes. Anatomy, physiology, symptoms, ventricular function, and event history each contribute information. A normal-looking major vessel does not exclude coronary dysfunction.
Connect plaque to systemic risk
Coronary plaque is one expression of a diffuse atherosclerotic process. PCI or bypass can restore flow around selected lesions but does not erase plaque elsewhere. Lipid lowering, blood pressure control, tobacco cessation, activity, diabetes therapy, and antithrombotic planning remain necessary after symptom relief or revascularization.
Interpret supply and demand
Myocardial ischemia can result from fixed flow limitation, vasospasm, microvascular dysfunction, tachycardia, hypertension, anemia, hypoxemia, or increased contractility. Chest pressure is common, but dyspnea, fatigue, epigastric discomfort, nausea, or reduced exercise capacity can be anginal equivalents.
Detect the transition to acute care
New rest symptoms, longer or more frequent episodes, a lower exertional threshold, syncope, instability, or poor nitroglycerin response require urgent ACS evaluation. Do not remotely titrate chronic antianginals when the clinical pattern suggests acute plaque disruption or another emergency.
Quick check
Submodule
Comprehensive Event Prevention
Event prevention requires sustained control of atherosclerotic biology and the conditions that accelerate it, supported by rehabilitation, behavior change, and accessible care.
- Physical activity and rehabilitation
- Tobacco treatment
- Lipid and pressure goals
- Cardiometabolic therapies
Build repeatable rather than idealized plans
Use current risk-based goals
Balance ischemia and bleeding
Make the plan deliverable
Build movement and rehabilitation into care
Habitual aerobic and resistance activity, less sedentary time, and cardiac rehabilitation improve function and outcomes in eligible patients. A useful plan accounts for ischemic symptoms, recent events, revascularization, ventricular function, mobility, transport, cost, work, and confidence.
Treat tobacco dependence as disease
Ask about cigarettes, vaping, smokeless tobacco, and nicotine products. Combine behavioral support with evidence-based cessation medication when appropriate. E-cigarettes are not preferred first-line cessation therapy because long-term safety and sustained use remain concerns.
Control lipids and pressure
CCD is secondary prevention. Use the current 2026 LDL-C and non-HDL-C goals, a maximally tolerated statin foundation, and nonstatin escalation when required. Confirm blood pressure with accurate office and home technique, then select therapy around angina, ventricular function, kidney disease, heart rate, and adverse effects.
Use cardiometabolic outcome therapy
Selected SGLT2 inhibitors and GLP-1 receptor agonists provide cardiovascular or heart-failure benefit in appropriate populations beyond glucose lowering alone. Match the exact product to diabetes, HF, CKD, obesity, ASCVD goal, organ function, safety, and access rather than treating broad class labels as interchangeable.
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Submodule
Antithrombotic Strategy
Long-term single antiplatelet therapy, post-PCI DAPT, P2Y12 monotherapy, and oral-anticoagulant overlap solve different thrombotic problems and carry different bleeding costs.
- Single antiplatelet therapy
- DAPT after PCI
- Short DAPT strategies
- Oral anticoagulation overlap
Common long-term CCD foundation
Duration follows presentation and risk
Avoid indefinite bleeding burden without benefit
Never interrupt a recent stent regimen casually
Use single antiplatelet therapy for the right foundation
Low-dose aspirin is a common long-term secondary-prevention therapy when no contraindication or oral-anticoagulant strategy changes the plan. Clopidogrel can be an alternative in selected patients. Review prior MI, PCI, CABG, stroke, bleeding, ulcer disease, anemia, NSAIDs, and allergy.
Make DAPT time limited and explicit
After PCI for CCD, DAPT commonly protects against stent-related thrombosis before transition to single therapy. Duration depends on whether the presentation was chronic or acute, PCI complexity, prior stent thrombosis, bleeding risk, oral anticoagulation, and upcoming procedures. A stop date is a clinical decision, not an administrative detail.
Use shortened regimens selectively
In selected post-PCI populations, 1 to 3 months of DAPT followed by P2Y12 monotherapy can reduce bleeding. This is not a universal schedule for complex anatomy or high thrombotic risk. The interventional plan, presentation, device, adherence, and bleeding context determine suitability.
Minimize unnecessary overlap with anticoagulation
When AF or another indication requires long-term oral anticoagulation, antiplatelet overlap should be limited to the period and indication that justify it. In stable coronary disease beyond the high-risk PCI period, anticoagulant monotherapy is often preferred when no stent-thrombosis history or other indication requires an antiplatelet.
Quick check
Submodule
Antianginal Pharmacotherapy
Antianginal therapy improves symptoms by reducing demand, increasing supply, or changing cellular ischemic stress. Drug choice follows hemodynamics, ventricular function, rhythm, interactions, and the patient's symptom goal.
- Beta blockers and calcium channel blockers
- Nitrates
- Ranolazine
- Combination and safety
Reduce rate, contractility, or both
Improve coronary and systemic vasodilation
Reduce late sodium current-related calcium overload
Treat persistent symptoms by mechanism
Choose the first agent from physiology
A beta blocker or calcium channel blocker is commonly selected first, and a long-acting nitrate is another effective option. Beta blockers reduce heart rate and contractility. Non-DHP calcium channel blockers also slow rate but can worsen systolic dysfunction. DHP agents vasodilate without the same nodal effect.
Separate beta-blocker indications
Long-term beta blockade is not continued solely for outcome benefit when there has been no MI in the past year, LVEF is above 50 percent, and no other primary indication exists. Angina, recent MI, reduced LVEF, arrhythmia, or hypertension can still justify therapy. Avoid abrupt withdrawal.
Use nitrates safely
Short-acting nitroglycerin treats episodes and can be used before predictable exertion. Long-acting nitrates require a nitrate-free interval to limit tolerance. Teach seated use, storage, headache, hypotension, and emergency thresholds. PDE5 inhibitors and riociguat can create dangerous hypotension with nitrates.
Add by a different mechanism
Persistent symptoms can improve when a second antianginal from another class is added. Ranolazine is useful when heart rate or blood pressure limits other drugs, but CYP3A interactions, QTc, liver and kidney context, dizziness, and constipation require review. Refractory symptoms may prompt revascularization evaluation.
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Submodule
Testing, Revascularization, and INOCA
Testing answers a changed clinical question. Revascularization treats selected anatomic and physiologic problems, while INOCA requires recognition of coronary dysfunction beyond large-vessel obstruction.
- Actionable test selection
- No routine surveillance
- Symptom-driven revascularization
- Microvascular and vasospastic disease
Reassess when the clinical state changes
Choose the modality for the question
Use anatomy, physiology, symptoms, and preference
Do not image stable patients without a reason
Test because the clinical state changed
New symptoms, reduced function, new ventricular dysfunction, an interval event, or a specific treatment decision can justify anatomic or ischemic evaluation. Test choice depends on exercise capacity, ECG interpretability, kidney function, contrast allergy, radiation, body habitus, prior anatomy, and local expertise.
Avoid calendar-based surveillance
Routine periodic anatomic or ischemic testing is not recommended when symptoms and functional status are unchanged. Low-value surveillance can produce false positives, incidental findings, unnecessary invasive procedures, contrast exposure, radiation, and cost.
Use revascularization for a defined objective
When lifestyle-limiting angina persists despite guideline-directed therapy and anatomy is amenable, PCI or CABG can improve symptoms. Anatomy, ischemic physiology, diabetes, ventricular function, kidney disease, procedural risk, prognosis, and preference determine the approach. Prevention continues afterward.
Recognize INOCA
Ischemia with nonobstructive coronary arteries can reflect microvascular dysfunction, epicardial spasm, endothelial dysfunction, or mixed mechanisms. A nonobstructive angiogram does not make symptoms imaginary. Mechanism-directed testing and therapy can improve function and quality of life.
Quick check
Module test
Check the connections.
Each attempt draws 10 questions from the complete 100 question bank.
Each attempt draws a fresh set and rearranges the answer choices.
References
Current clinical foundation.
Lecture material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.