Percutaneous coronary intervention. I: History and development
BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7398.1080 (Published 15 May 2003) Cite this as: BMJ 2003;326:1080
- Ever D Grech, consultant cardiologist, assistant professor
- Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada, University of Manitoba, Winnipeg
Introduction
The term “angina pectoris” was introduced by Heberden in 1772 to describe a syndrome characterised by a sensation of “strangling and anxiety” in the chest. Today, it is used for chest discomfort attributed to myocardial ischaemia arising from increased myocardial oxygen consumption. This is often induced by physical exertion, and the commonest aetiology is atheromatous coronary artery disease. The terms “chronic” and “stable” refer to anginal symptoms that have been present for at least several weeks without major deterioration. However, symptom variation occurs for several reasons, such as mental stress, ambient temperature, consumption of alcohol or large meals, and factors that may increase coronary tone such as drugs and hormonal change.
Unequivocal indications for use of coronary stents
Classification
The Canadian Cardiovascular Society has provided a graded classification of angina which has become widely used. In clinical practice, it is important to describe accurately specific activities associated with angina in each patient. This should include walking distance, frequency, and duration of episodes.
History of myocardial revascularisation
In the management of chronic stable angina, there are two invasive techniques available for myocardial revascularisation: coronary artery bypass surgery and catheter attached devices. Although coronary artery bypass surgery was introduced in 1968, the first percutaneous transluminal coronary angioplasty was not performed until September 1977 by Andreas Gruentzig, a Swiss radiologist, in Zurich. The patient, 38 year old Adolph Bachman, underwent successful angioplasty to a left coronary artery lesion and remains well to this day. After the success of the operation, six patients were successfully treated with percutaneous transluminal coronary angioplasty in that year.
By today's standards, the early procedures used cumbersome equipment: guide catheters were large and could easily traumatise the vessel, there were no guidewires, and balloon catheters were large with low burst pressures. As a result, the procedure was limited to patients with refractory angina, good left ventricular function, and a discrete, proximal, concentric, and non-calcific lesion in a single major coronary artery with no involvement of major side branches or angulations. Consequently, it was considered feasible in only 10% of all patients needing revascularisation.
Developments in percutaneous intervention
During 1977-86 guide catheters, guidewires, and balloon catheter technology were improved, with slimmer profiles and increased tolerance to high inflation pressures. As equipment improved and experience increased, so more complex lesions were treated and in more acute situations. Consequently, percutaneous transluminal coronary angioplasty can now be undertaken in about half of patients needing revascularisation (more in some countries), and it is also offered to high-risk patients for whom coronary artery bypass surgery may be considered too dangerous.
Major milestones in percutaneous coronary intervention
Although percutaneous transluminal coronary angioplasty causes plaque compression, the major change in lumen geometry is caused by fracturing and fissuring of the atheroma, extending into the vessel wall at variable depths and lengths. This injury accounts for the two major limitations of percutaneous transluminal coronary angioplasty-acute vessel closure and restenosis.
Modern balloon catheter: its low profile facilitates lesion crossing, the flexible shaft allows tracking down tortuous vessels, and the balloon can be inflated to high pressures without distortion or rupture
Acute vessel closure—This usually occurs within the first 24 hours of the procedure in about 3-5% of cases and follows vessel dissection, acute thrombus formation, or both. Important clinical consequences include myocardial infarction, emergency coronary artery bypass surgery, and death.
Micrographs showing arterial barotrauma caused by coronary angioplasty. Top left: coronary arterial dissection with large flap. Top right: deep fissuring within coronary artery wall atheroma. Bottom: fragmented plaque tissue (dark central calcific plaque surrounded by fibrin and platelet-rich thrombus), which may embolise in distal arterioles to cause infarction, and intramural and perivascular haemorrhage (bottom)
Micrographs showing arterial barotrauma caused by coronary angioplasty. Top left: coronary arterial dissection with large flap. Top right: deep fissuring within coronary artery wall atheroma. Bottom: fragmented plaque tissue (dark central calcific plaque surrounded by fibrin and platelet-rich thrombus), which may embolise in distal arterioles to cause infarction, and intramural and perivascular haemorrhage (bottom)
Micrographs showing arterial barotrauma caused by coronary angioplasty. Top left: coronary arterial dissection with large flap. Top right: deep fissuring within coronary artery wall atheroma. Bottom: fragmented plaque tissue (dark central calcific plaque surrounded by fibrin and platelet-rich thrombus), which may embolise in distal arterioles to cause infarction, and intramural and perivascular haemorrhage (bottom)
Restenosis occurring in the first six months after angioplasty is caused largely by smooth muscle cell proliferation and fibrointimal hyperplasia (often called neointimal proliferation), as well as elastic recoil. It is usually defined as a greater than 50% reduction in luminal diameter and has an incidence of 25-50% (higher after vein graft angioplasty). Further intervention may be indicated if angina and ischaemia recur.
Drills, cutters, and lasers
In the 1980s, two main developments aimed at limiting these problems emerged. The first were devices to remove plaque material, such as by rotational atherectomy, directional coronary atherectomy, transluminal extraction catheter, and excimer laser. By avoiding the vessel wall trauma seen during percutaneous transluminal coronary angioplasty, it was envisaged that both acute vessel closure and restenosis rates would be reduced.
However, early studies showed that, although acute closure rates were reduced, there was no significant reduction in restenosis. Moreover, these devices are expensive, not particularly user friendly, and have limited accessibility to more distal stenoses. As a result, they have now become niche tools used by relatively few interventionists. However, they may have an emerging role in reducing restenosis rates when used as adjunctive treatment before stenting (especially for large plaques) and in treating diffuse restenosis within a stent.
Tools for coronary atherectomy. Top: the Simpson atherocath has a cutter in a hollow cylindrical housing. The cutter rotates at 2000 rpm, and excised atheromatous tissue is pushed into the distal nose cone. Left: the Rotablator burr is coated with 10 μm diamond chips to create an abrasive surface. The burr, connected to a drive shaft and a turbine powered by compressed air, rotates at speeds up to 200 000 rpm
Tools for coronary atherectomy. Top: the Simpson atherocath has a cutter in a hollow cylindrical housing. The cutter rotates at 2000 rpm, and excised atheromatous tissue is pushed into the distal nose cone. Left: the Rotablator burr is coated with 10 μm diamond chips to create an abrasive surface. The burr, connected to a drive shaft and a turbine powered by compressed air, rotates at speeds up to 200 000 rpm
Intracoronary stents
The second development was the introduction of intracoronary stents deployed at the site of an atheromatous lesion. These were introduced in 1986 with the objective of tacking down dissection flaps and providing mechanical support. They also reduce elastic recoil and remodelling associated with restenosis.
The first large randomised studies conclusively showed the superiority of stenting over coronary angioplasty alone, both in clinical and angiographic outcomes, including a significant 30% reduction in restenosis rates. Surprisingly, this was not due to inhibition of neointimal proliferation—in fact stents may increase this response. The superiority of stenting is that the initial gain in luminal diameter is much greater than after angioplasty alone, mostly because of a reduction in elastic recoil.
Coronary stents. Top: Guidant Zeta stent. Middle: BiodivYsio AS stent coated with phosphorylcholine, a synthetic copy of the outer membrane of red blood cells, which improves haemocompatibility and reduces thrombosis. Bottom: the Jomed JOSTENT coronary stent graft consists of a layer of PTFE (polytetrafluoroethylene) sandwiched between two stents and is useful in sealing perforations, aneurysms, and fistulae
Coronary stents. Top: Guidant Zeta stent. Middle: BiodivYsio AS stent coated with phosphorylcholine, a synthetic copy of the outer membrane of red blood cells, which improves haemocompatibility and reduces thrombosis. Bottom: the Jomed JOSTENT coronary stent graft consists of a layer of PTFE (polytetrafluoroethylene) sandwiched between two stents and is useful in sealing perforations, aneurysms, and fistulae
Coronary stents. Top: Guidant Zeta stent. Middle: BiodivYsio AS stent coated with phosphorylcholine, a synthetic copy of the outer membrane of red blood cells, which improves haemocompatibility and reduces thrombosis. Bottom: the Jomed JOSTENT coronary stent graft consists of a layer of PTFE (polytetrafluoroethylene) sandwiched between two stents and is useful in sealing perforations, aneurysms, and fistulae
Although neointimal proliferation through the struts of the stent occurs, it is insufficient to cancel out the initial gain, leading to a larger lumen size and hence reduced restenosis. Maximising the vessel lumen is therefore a crucial mechanism for reducing restenosis. “Bigger is better” is the adage followed in this case.
Early stent problems
As a result of initial studies, stents were predominantly used either as “bail out” devices for acute vessel closure during coronary angioplasty (thus avoiding the need for immediate coronary artery bypass surgery) or for restenosis after angioplasty.
Coronary angiogram showing three lesions (arrows) affecting the left anterior descending artery (top left). The lesions are stented without pre-dilatation (top right), with good results (bottom)
Coronary angiogram showing three lesions (arrows) affecting the left anterior descending artery (top left). The lesions are stented without pre-dilatation (top right), with good results (bottom)
Coronary angiogram showing three lesions (arrows) affecting the left anterior descending artery (top left). The lesions are stented without pre-dilatation (top right), with good results (bottom)
Thrombosis within a stent causing myocardial infarction and death was a major concern, and early aggressive anticoagulation to prevent this led to frequent complications from arterial puncture wounds as well as major systemic haemorrhage. These problems have now been overcome by the introduction of powerful antiplatelet drugs as a substitute for warfarin. The risk of thrombosis within a stent diminishes when the stent is lined with a new endothelial layer, and antiplatelet treatment can be stopped after a month. The recognition that suboptimal stent expansion is an important contributor to thrombosis in stents has led to the use of intravascular ultrasound to guide stent deployment and high pressure inflations to ensure complete stent expansion.
Current practice
A greater understanding of the pathophysiology of stent deployment, combined with the development of more flexible stents (which are pre-mounted on low-profile catheter balloons), has resulted in a massive worldwide increase in stent use, and they have become an essential component of coronary intervention. Low profile stents have also allowed “direct” stenting—that is, implanting a stent without the customary balloon dilatation—to become prevalent, with the advantages of economy, shorter procedure time, and less radiation from imaging. Most modern stents are expanded by balloon and made from stainless steel alloys. Their construction and design, metal thickness, surface coverage, and radial strength vary considerably.
Stents are now used in most coronary interventions and in a wide variety of clinical settings. They substantially increase procedural safety and success, and reduce the need for emergency coronary artery bypass surgery. Procedures involving stent deployment are now often referred to as percutaneous coronary interventions to distinguish them from conventional balloon angioplasty (percutaneous transluminal coronary angioplasty).
Exponential increase in use of intracoronary stents since 1986. In 2001, 2.3 million stents were implanted (more than double the 1998 rate)
A major recent development has been the introduction of drug eluting stents (also referred to as “coated stents”), which reduce restenosis to very low rates. Their high cost currently limits their use, but, with increasing competition among manufacturers, they will probably become more affordable.
Canadian Cardiovascular Society classification of angina
Footnotes
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The ABC of interventional cardiology is edited by Ever D Grech and will be published as a book in summer 2003.
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Competing interests None declared.
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The micrographs showing deep fissuring within a coronary artery wall atheroma and fragmented plaque tissue caused by coronary angioplasty were supplied by Kelly MacDonald, consultant histopathologist at St Boniface Hospital, Winnipeg, Canada.