3.1 Coronary Artery Disease, Myocardial Infarction & Revascularization (PCI/CABG)

Coronary artery disease (CAD) is the most common cardiovascular disease encountered in clinical exercise settings, and it underlies nearly every cardiac rehabilitation referral. Understanding its pathophysiology, the acute coronary syndrome (ACS) spectrum, and the two revascularization pathways is foundational to safe exercise testing and prescription.

Atherosclerosis: The Underlying Pathophysiology

CAD results from atherosclerosis, a chronic inflammatory process in the coronary artery wall. The sequence begins with endothelial injury from shear stress, hypertension, smoking, or hyperglycemia, which increases endothelial permeability to LDL cholesterol. LDL particles infiltrate the subendothelial space, become oxidized, and attract monocytes that differentiate into macrophages. These macrophages engulf oxidized LDL and become foam cells, forming the visible fatty streak, the earliest lesion. Over years, smooth muscle proliferation and collagen deposition build a fibrous cap over a necrotic lipid core, producing a mature atherosclerotic plaque. A plaque with a thin fibrous cap and large lipid core is vulnerable to rupture or erosion, which exposes thrombogenic material to circulating blood and triggers platelet aggregation and thrombus formation — the event that converts stable CAD into an acute coronary syndrome.

The Acute Coronary Syndrome Spectrum

Risk Factors

Modifiable risk factors — dyslipidemia (elevated LDL, low HDL), hypertension, current tobacco use, diabetes/insulin resistance, obesity, sedentary lifestyle, and poor diet — are the primary targets of exercise-based secondary prevention. Non-modifiable risk factors include age (men >=45, women >=55), male sex or postmenopausal status, and family history of premature CAD (a first-degree male relative affected before age 55 or a female relative before age 65).

Exercise Physiology Implications: Ischemia and the Rate-Pressure Product

Myocardial oxygen demand rises with both heart rate and afterload, so the rate-pressure product (RPP = HR x SBP) is used as a surrogate for myocardial oxygen consumption. Patients with fixed coronary stenoses often demonstrate a reproducible ischemic threshold — a consistent RPP at which angina or ischemic ECG changes appear. Classic ischemic ST-segment depression is horizontal or downsloping depression of at least 1 mm, measured 60-80 ms after the J-point. Because many patients — especially those with diabetic autonomic neuropathy, older adults, and women — experience silent ischemia or anginal equivalents (dyspnea, unusual fatigue, jaw or arm discomfort) rather than classic chest pain, the CEP must monitor symptoms, ECG, and RPP together rather than relying on chest pain alone.

Revascularization: PCI and CABG

Percutaneous coronary intervention (PCI) uses a catheter-delivered balloon and, almost always, a drug-eluting stent to mechanically open a stenosis; access is typically femoral or radial, and patients are placed on dual antiplatelet therapy (DAPT) for 6-12 months to prevent stent thrombosis. Coronary artery bypass graft (CABG) surgery reroutes blood around obstructions using the saphenous vein or, preferentially for durability, the internal mammary (thoracic) artery, accessed through a median sternotomy. CABG is generally favored for extensive multivessel disease, left-main disease, or diabetic patients with complex anatomy, while PCI is favored for single-vessel or focal lesions and offers a faster initial recovery.

Post-Revascularization Precautions and Cardiac Rehabilitation

Post-CABG patients require sternal precautions for roughly 6-8 weeks: no lifting greater than 5-10 lb, no pushing or pulling, and no bilateral overhead or behind-the-back movements that load the healing sternotomy; the CEP should also watch for a sternal click or instability, which signals a possible wound complication. Post-PCI patients need brief precautions at the vascular access site — limiting vigorous lower-body resistance at a femoral site for 24-48 hours and limiting wrist range of motion after a radial approach — plus awareness that DAPT increases bleeding risk with contact or high fall-risk activity. Structured cardiac rehabilitation progresses through Phase I (inpatient, low-level mobility), Phase II (outpatient, ECG-monitored, typically up to 36 sessions), and Phase III/IV (community-based maintenance).

Safety Considerations for the Clinical Exercise Physiologist

Always know the patient's ischemic RPP threshold and symptom pattern from the most recent graded exercise test before prescribing intensity, and remember that beta-blockers blunt the heart-rate response, making RPE and symptom monitoring more reliable than heart-rate-based targets alone. Emergency readiness — recognizing angina equivalents, unstable rhythm changes, and knowing when to stop a session and activate emergency response — is a non-negotiable safety skill in any CAD population.