| Download the amazing global Makindo app: ✅ Means NICE/National Guidelines 2026 compliant Android | Apple | |
|---|---|
| MEDICAL DISCLAIMER: Educational use only. Not for diagnosis or management. See below for full disclaimer. |
Related Subjects: | AP of the Coronary Arteries |Atherosclerosis |Ischaemic heart disease |Acute Coronary Syndrome (ACS): Complications |Acute Coronary Syndrome (ACS) |Assessing Chest Pain |ACS - General |ACS - STEMI |ACS - NSTEMI |ACS - GRACE Score |ACS - ECG Changes |Cardiac Troponins |ACS: Right Ventricular Infarction
Coronary revascularisation restores blood supply to myocardium affected by obstructive coronary artery disease. It is performed either by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). The decision is not simply based on how narrow a coronary artery looks on angiography. It depends on the clinical presentation, coronary anatomy, physiological significance of the stenosis, burden of ischaemia, left ventricular function, diabetes, comorbidity, frailty, procedural risk and patient preference. A useful principle is that PCI treats a focal stenosis from inside the artery, whereas CABG provides a new route for blood to travel beyond diseased coronary segments.
At rest, coronary autoregulation can often maintain myocardial blood flow despite a moderate stenosis by dilating the downstream arterioles. During exercise, however, the ability to increase coronary flow becomes limited.
When myocardial oxygen demand exceeds the available coronary blood supply, myocardial ischaemia develops and may produce angina, ECG changes or impaired ventricular contraction.
This explains why a patient may have a significant coronary stenosis but no symptoms at rest and develop angina only during exertion.
PCI involves passing a catheter into the arterial circulation, usually through the radial artery. The coronary arteries are engaged with a guiding catheter and a fine guidewire is passed across the stenosis.
The lesion may be dilated with a balloon and is usually treated by implantation of a coronary stent. The stent acts as a scaffold that holds the artery open and reduces acute recoil following angioplasty.
Modern PCI generally uses drug-eluting stents. These are metal stents coated with drugs that suppress excessive cellular proliferation within the treated segment.
The drugs are commonly from the -limus family, such as sirolimus-related compounds. They inhibit smooth-muscle proliferation and neointimal hyperplasia.
This substantially reduces restenosis compared with older bare-metal stents.
These are different complications and should not be confused.
Drug-eluting stents greatly reduce restenosis. Antiplatelet therapy is particularly important in preventing stent thrombosis.
In stable coronary disease, PCI is particularly effective at relieving angina and improving quality of life when symptoms remain troublesome despite appropriate medical therapy.
However, an angiographic stenosis does not automatically mean that PCI will improve survival. In many patients with chronic coronary disease, optimal medical therapy and aggressive modification of cardiovascular risk remain the foundation of treatment.
Revascularisation becomes particularly important when symptoms remain unacceptable despite medical treatment or when coronary anatomy identifies a group in whom revascularisation may improve prognosis.
A 60% narrowing seen on angiography may be haemodynamically important in one patient and relatively unimportant in another. Intermediate coronary lesions can therefore be assessed physiologically.
FFR compares pressure distal to a coronary stenosis with aortic pressure during maximal coronary hyperaemia. A significant pressure fall across the stenosis indicates that the lesion is limiting coronary blood flow. iFR uses the pressure gradient during a particular phase of diastole when resistance in the coronary microcirculation is naturally relatively stable and therefore does not require pharmacological hyperaemia.
An important principle is that an anatomical narrowing is not synonymous with functionally important myocardial ischaemia.
The rationale for PCI is different in acute coronary syndromes. The central problem is usually disruption or erosion of an atherosclerotic plaque followed by platelet activation and thrombus formation. The vessel may therefore change rapidly from a previously tolerable stenosis to severe obstruction or complete occlusion. Rapid restoration of coronary flow may preserve myocardium and be lifesaving.
ST-elevation myocardial infarction usually results from acute complete or near-complete coronary occlusion. Primary PCI is the preferred reperfusion strategy when it can be delivered promptly.
The culprit artery is identified, crossed with a guidewire and reopened, usually with implantation of a drug-eluting stent.
The aim is not simply to relieve chest pain. Every minute of persistent occlusion results in progressive irreversible myocardial necrosis, hence the principle:
Time is myocardium.
Many patients presenting with STEMI have significant disease in more than one coronary artery. In haemodynamically stable patients, complete revascularisation of important non-culprit lesions may reduce subsequent cardiovascular events.
This may be performed during the index admission or as a staged procedure depending on coronary anatomy, clinical stability and procedural complexity. Cardiogenic shock is different. Routine immediate PCI of multiple non-culprit vessels is generally avoided, with initial treatment concentrated on restoring flow through the culprit artery.
In non-ST elevation acute coronary syndromes, the coronary artery may be partially occluded or intermittently obstructed rather than completely occluded.
Patients are risk stratified to determine the urgency of coronary angiography and possible PCI.
Features favouring an early or urgent invasive strategy include:
A newly implanted coronary stent is thrombogenic. Platelets can adhere to the foreign surface and damaged endothelium, producing acute stent thrombosis. Patients therefore usually receive dual antiplatelet therapy consisting of aspirin plus a P2Y12 receptor inhibitor.
P2Y12 inhibitors include:
The optimal duration depends on whether PCI was performed for acute coronary syndrome or chronic coronary disease and on the balance between thrombotic and bleeding risk. Following an acute coronary syndrome, approximately 12 months of dual antiplatelet therapy remains a common default where bleeding risk is acceptable. Shorter treatment, de-escalation or alternative strategies may be appropriate in patients at high bleeding risk.
After elective PCI for chronic coronary disease, shorter courses are increasingly possible with modern drug-eluting stents, particularly where bleeding risk is high.
A difficult situation occurs when a patient undergoing PCI also requires anticoagulation, for example because of atrial fibrillation. Combining aspirin, a P2Y12 inhibitor and an anticoagulant produces powerful antithrombotic therapy but markedly increases bleeding risk.
Modern management therefore attempts to keep triple therapy as short as reasonably possible.
The precise regimen must be individualised according to the indication for anticoagulation, complexity of PCI, bleeding risk and clinical presentation.
CABG takes a fundamentally different approach. Rather than opening the stenotic segment, a new blood vessel is connected to the coronary artery beyond the obstruction.
Blood therefore bypasses the diseased proximal artery and reaches the myocardium through the graft.
CABG is particularly useful when disease is extensive, anatomically complex or involves several major coronary arteries.
CABG has an important advantage in extensive disease because the graft is usually attached beyond a large proximal segment of coronary artery. It can therefore provide protection against several upstream stenoses rather than treating each individual plaque separately.
The most important and durable CABG conduit is the left internal mammary artery, usually grafted to the left anterior descending coronary artery. The LIMA normally remains attached proximally to the left subclavian artery. Its distal end is divided and anastomosed to the LAD beyond the obstructive coronary disease.
Blood therefore travels:
Subclavian artery → LIMA → LAD → myocardium.
The LIMA has excellent long-term patency and is substantially more resistant to atherosclerosis than conventional saphenous vein grafts.
Additional grafts may be created using arteries or veins.
The radial artery is increasingly used as a second arterial conduit and generally has better long-term durability than a saphenous vein graft when used for suitable coronary targets.
The right internal mammary artery may be used for another coronary territory or incorporated into a composite arterial graft. Saphenous vein grafts remain widely used because the vein is readily available and technically straightforward to harvest, but they are more susceptible to progressive graft disease.
A vein is designed for a low-pressure venous circulation. When transplanted into the high-pressure arterial system it undergoes major biological and mechanical stress.
Failure can occur through several mechanisms:
Arterial grafts, particularly the LIMA, are much more resistant to these processes.
PCI is less invasive, usually requires a shorter hospital stay and allows substantially faster recovery. It is particularly attractive for focal or relatively uncomplicated coronary disease.
CABG involves major surgery but can achieve more complete and durable revascularisation in patients with extensive or anatomically complex coronary disease.
One of the most consistent differences is that patients treated with PCI are more likely to require repeat revascularisation later than patients treated with CABG.
CABG is particularly favoured when coronary disease is extensive or complex, especially in patients with diabetes and multivessel disease.
It may also offer prognostic benefit in selected patients with important left main disease, complex multivessel disease or ischaemic left ventricular dysfunction.
Modern PCI remains a reasonable alternative to CABG in some patients with less complex anatomy, particularly where surgical risk is high or patient preference favours PCI.
For complex coronary disease, the decision should not simply be made by whichever specialist happens to see the patient first.
A multidisciplinary Heart Team usually includes interventional cardiologists and cardiac surgeons and may involve imaging specialists, anaesthetists and other clinicians where appropriate.
The decision should consider:
Traditional CABG commonly uses cardiopulmonary bypass. Venous blood is diverted from the patient to a heart-lung machine, oxygenated and pumped back into the arterial circulation.
The heart can then be temporarily stopped using cardioplegia, providing the surgeon with a relatively motionless and bloodless operative field in which to construct the grafts.
In off-pump CABG, grafts are constructed while the heart continues to beat. Mechanical stabilisation devices immobilise the small area of myocardium on which the surgeon is operating.
This avoids cardiopulmonary bypass but is technically demanding. It has not replaced conventional on-pump CABG and is most useful in selected patients when performed by experienced surgical teams.
CABG is major surgery and complications include:
Postoperative atrial fibrillation is particularly common and usually occurs during the first few days after surgery.
Recurrent angina following CABG should prompt consideration of graft failure or progression of the underlying coronary disease.
Early causes include:
Late causes include:
Investigation may involve CT coronary angiography or invasive coronary angiography. Further treatment may include medical therapy, PCI to a native coronary artery or graft, or occasionally repeat CABG.
Neither PCI nor CABG cures atherosclerosis. Revascularisation treats the consequences of coronary artery disease but does not remove the systemic disease responsible for it.
Secondary prevention is therefore fundamental after either procedure.
Patients with established coronary artery disease require intensive lipid lowering because LDL cholesterol plays a causal role in the development and progression of atherosclerotic plaque.
High-intensity statin therapy is usually first-line. Ezetimibe can be added if lipid reduction is inadequate, with PCSK9-directed therapy or other lipid-lowering treatments considered in appropriate high-risk patients.
The important concept is not simply to prescribe a statin, but to achieve substantial and sustained reduction in atherogenic lipoproteins.
Some patients have angina despite having no major obstructive epicardial coronary stenosis. Mechanisms include coronary microvascular dysfunction and vasospastic angina.
This is increasingly described as angina with non-obstructive coronary arteries (ANOCA) or ischaemia with non-obstructive coronary arteries (INOCA).
Implanting a stent into a non-flow-limiting coronary lesion will not correct microvascular dysfunction. This is another reason why demonstrating a coronary narrowing does not necessarily prove that the narrowing is causing the patient's symptoms.
The practical question is not:
“Does this patient have a coronary stenosis?”
The more useful questions are:
In chronic coronary disease, the foundation remains disease-modifying medical therapy and aggressive cardiovascular risk reduction, with revascularisation used for persistent symptoms and selected prognostic indications.
In acute coronary syndromes, the situation is different: plaque disruption and thrombosis may suddenly threaten a large territory of myocardium, making rapid restoration of coronary blood flow an emergency.