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Coronary Angioplasty - Techniques and Complications
PC Rath

The twentieth century saw a revolution in modalities for treatment of cardiovascular diseases. The most remarkable is the development of percutaneous methods in treating coronary artery disease which is one of the most common cause of morbidity and mortality in India at present.

It started with the invention of X-ray by Wilhelm Roentgen in 1895 and cardiac catheterization by Werner Forssmann in 1929. These were early days and there was no effective way of treating coronary artery disease. In late 1960’s pioneering work by Favaloro et al led to evolution of coronary artery bypass grafting (CABG). Despite the success of CABG procedure cardiologist were still thinking of a nonsurgical method to treat coronary artery disease and this led to 1st coronary angioplasty being performed by a Dr. Andreas Gruentzig in 1977 in Zurich. From that day the technique of percutaneous transluminal coronary angioplasty (PTCA) has evolved so dramatically that now it is on the verge of replacing CABG in most of the lesion categories.

In late 70’s and early 80’s the technique for doing PTCA was cumbersome with use of bulky materials. They were using 9-10 French guiding catheter which had to be shaped manually. Guidewires were also bulky and were difficult to track distally. Later on Introducer sheaths were developed. Gradually newer preshaped guiding catheters with soft tip and larger central lumen were developed, and coated guidewires came up with less friction more torquability and with varying tip stiffness for different lesion types. As the technique evolved interventional cardiologists started tackling more and more complex lesion anatomies. Various supportive instruments were also developed to improve the success of procedure like Rotablator, Laser, Brachy therapy, Intravascular ultrasound etc.

For doing percutaneous coronary angioplasty following materials are required:

  • Introducer sheath
  • Guiding catheter : various shapes are available for different coronary ostium locations and different lesion type to give better coaxial support.
  • Guide wires : Usually 0.014 or 0.018 inch wire is used for coronary angioplasty. The wires come in different length (180 cms, 190 cms, 300 cms or exchange length etc.) and with different tip strength (floppy tip, stiff wires), with or without hydrophilic coating for various coronary lesion types to improve crossability
  • Contrast : Iodinated contrast is used to opacify coronary arteries. It may be Ionic(Diatrizoate) or Non Ionic which may be low osmolar (Omni paque, Hexabrix etc.) or Iso osmolar (Visi paque).
  • Balloon : Used to dilate the coronary stenosis. They come in different length and diameter and with different compliance (non compliant or compliant) for dilating different lesions. They are of two types over the wire or rapid exchange balloon(monorail). The choice of which depends on the operator and lesion.
  • Other supporting materials needed to improve crossability of lesion and to prevent complications are :
  1. Thrombus extraction catheters : used in thrombus containing lesions e.g. Export catheter, Diver catheter, Angioget etc.
  2. Distal protection devices e.g. Filter wire, angioguard, percusurge etc. They prevent distal embolisation of plaque material and are specially used in saphenous vein graft (SVG) interventions, interventions in acute MI etc.
  3. Ablative Instruments : e.g. Rotablator, Directional coronary atherectomy, Laser. These are specially used only rarely now a days and in heavily calcified or total occlusion lesions.
  4. Stents : They are used to prevent abrupt closure, elastic recoil and to reduce late restenosis. Now a days in all coronary angioplasty procedures stents are used unless it is a very small artery. These are commonly made of stainless steel, cobalt chromium etc. They may be bare metal or drug eluting stents. Drug eluting stents are preferred now a days as they have least restenosis.
  5. Resuscitative instruments : Defibrillators, laryngoscope, temporary pacemaker, intraaortic balloon pump etc.

Once a patient is selected for coronary angioplasty he/she is taken to cardiac catheterization table. Patient is generally kept 4 to 6 hours fasting and should have received aspirin (160–325 mg) and Clopidogrel (75–600 mg) atleast 4–6 hours before the procedure. Patient is given mild anxiolytic and is adequately hydrated preferably by normal saline. Once on table the site through which PTCA is to be done depends on operator (Femoral, Radial, Brachial, Ulnar) most commonly femoral route is preferred. Then ECG leads are connected and defibrillator, temporary pacemaker wire and other resuscitative materials are kept standby.

Local anaesthesia is given with Lignocaine and then introducer sheath is inserted by modified seldinger technique. After this patient is given heparin (To achieve ACT of 250 to 300) or low molecular weight heparine (1 mg/Kg Enoxaparine or 0.75 mg/kg Enoxaparine if Gp IIb IIIa inhibitor are used). Then a guiding catheter is taken to engage the coronary ostium. And then coronary angiogram is done in different views to properly delineate the coronary stenosis. Then a Y connector is attached to the guiding catheter (one lumen is for introducing guide wire, balloon etc and other is for injecting contrast to visualize coronary artery). This Y connector is attach to a manifold which is used to monitor blood pressure and inject contrast. Then a guide wire is chosen depending on the lesion type and its tip is slightly bent to improve its manoeuvrability. A torquer is attached to other end of the guide wire and under constant fluoroscopy the guide wire is manoeuvred with the help of torquer to cross the stenosis. After crossing the lesion with a wire a balloon is introduced over this wire. The balloon is placed across the lesion and inflated. The inflation is done by a inflating device to the desired balloon diameter and kept inflated for 30 sec to 1 minute. The size of the balloon in plain balloon angioplasty is usually 1:1 with reference to the size of reference vessel diameter (which is size of normal vessel just proximal to the lesion). After dilating the balloon is removed and final result checked by angiography in atleast two orthogonal views. If satisfactory result is obtained (less than 20% residual stenosis) the patient is shifted to cardiac ICU where the introducer sheath is removed after 4- 6 hour under local anaesthesia (once ACT is < 150). Patient is watched for any vasovagal reaction during sheath removal which can be managed by IV fluids or Inj. Atropine. If post procedure is uneventful patients can be discharged from hospital after 2 to 3 days.

The complications which occur due to coronary angioplasty are very rare and can be divided into coronary or non coronary complications.

Coronary complications :
Abrupt closure : This occurs due to a dissecting flap or a thrombus totally occluding the coronary lumen. It happens in 3-5% of patients during plain balloon angioplasty. With use of stents this complications is rarely seen.

Dissection : This occurs mainly in patients with long lesion, eccentric lesion, calcific lesion, tortuous vessel or ectatic vessels. It happens due to guiding catheter, guide wire, balloon dilatation, edge of stent after stent deployment. The incidence is 0.5–1%. It is usually treated by deploying another stent. Some times if dissection is very small (< 15 mm) and is type A or B (NHLBI types) without flow limitation it can be medically managed.

No reflow Phenomena : This is defined as reduction in coronary blood flow (TIMI 0 or 1) through coronary artery without angiographic evidence of mechanical vessel obstruction. It happens in 0.5 to 2 % of cases after PTCA(Highest after DCA, 7%). It is treated or prevented by intra coronary (IC) Nitroprusside (50 – 100 mcg), IC adenosine (25 – 50 mcg). Other agents used are IC Verapamil, Nikorandil, Papaverine etc. Distal protection device also reduce the incidence of no reflow. No reflow phenomena if it does not resolve can lead to acute myocardial infarction and even death of the patient.

Coronary vasospasm – It occurs in 1-5% of cases and usually responds to IC Nitroglycerin (50-100 mcg) other agents used are IC calcium antogonist like verapamil (100-400 mcg), Diltiazem (0.5–2.5 mg). Sometimes removal of guiding catheter, guide wire also relieves Vasospasm.

Stent thrombosis : The incidence is usually 0.5-2%. It can happen with both baremetal and drug eluting stents. It is thought that drug eluting stents have higher incidence of stent thrombosis but till date no large randomised study has proven this. Drug eluting stents have even been used during primary PTCA (thrombus containing milieu) without any increased incidence of stent thrombosis. Drug eluting stent have slightly higher incidence of late thrombosis due to delayed endothelialisation. It is prevented by achieving adequate ACT during procedure, use of adequate antiplatelet drugs (aspirin, clopidogrel, GPIIb / IIIa inhibitors and high pressure stent deployment).

Coronary perforation : Its incidence is o.5 – 3%. It occurs commonly while using ablative techniques like rotablator, DCA, Laser and while attempting CTO’s with stiffer wire or while crossing tortuous vessels. Usually these are managed by prolonged balloon inflation. Massive perforation causing tamponade and haemodynamic instability are managed by covered stents or if it happens in side branch thrombotic material to occlude the artery are used (Gel foam, alcohol etc.). Rarely patient is sent for surgery.

Restenosis : It is delayed complication of coronary angioplasty. It happens in 20-30% if bare metal stent is used and 5–10 % if drug eluting stent is used. The incidence increases to up to 40- 50% if bare metal stents are used in diabetic patients, small vessels (< 2.7 mm), long lesion (> 20 mm), calcified lesions, SVG graft interventions. In these situations it is better to use drug eluting stents.

Non coronary complications :
Contrast reaction : Use of iodinated contrast during PTCA can produce various reactions which are classified in 3 grades, Mild (Nausea, Vomiting, Vertigo etc.), Moderate (Fever or chills, multiple vomiting, rashes), Severe (shock, Bronchospasm, pulmonary oedema, loss of consciousness). Mild to moderate reaction occur in 5–10% cases and severe reaction occurs in < 0.5% cases. Other contrast induced reactions are hot flushes, transient asystole, heart block, ventricular or supra ventricular tachy cardia, congestive heart failure. The incidence is lowest with Isoosmolar agents (visipaque) and highest with Ionic contrast which are rarely used now a days.

Contrast Nephropathy : It is defined as deterioration of renal function after contrast administration (increase in serum creatinine by 25% of base line or absolute increase by 0.5 mg/dl within 48 hours). It happens in patient with pre existing renal dysfunction, diabetes mellitus , congestive heart failure, use of large volume of contrast. The serum creatinine tends to raise 24 – 48 hours after procedure and peaks by 4 – 7 days and returns to normal by 14 days. It rarely needs (< 10%) dialysis. It happens in 2 - 5% of patient with normal renal function, 10–15% in diabetic and in up to 30% with preexisting azotaemia. Iso Osmolar (visipaque) and low osmolar contrast are less associated with contrast induced nephropathy than high osmolar agents. It can be prevented by minimizing the volume of contrast used, proper hydration with normal saline (1 ml/kg/hr started 12 hour before procedure and for 12-24 hour after procedure) and use of N-acetylcysteine (400-600 mg twice daily started a day before and on the day of procedure). Other agents like dopamine, Mannitol, Loop diuretics, natriuretic peptides have been tried with conflicting result.

Bleeding : The incidence of bleeding after PTCA is 1–5% but it rarely needs blood transfusion. It is usually seen in Obese patients, female gender, calcified peripheral arteries, hypertension, use of multiple antiplatelet and anticoagulant agents, double puncture (posterior wall of artery puncture), use of large sheath, higher ACT level, in proper technique to achieve haemostasis while removing sheath. Most commonly it is access site bleeding to local haematoma, retroperitoneal haematoma or compartment syndrome (radial / ulnar access). Bleeding is not significant unless the haematoma is > 10 cm diameter or it causes a drop in haemoglobin by 3 mg/dl. Rarely patient can also develop intracranial haemorrhage (<0.5%). The local haematoma usually resolves by two weeks. If it causes nerve compression then the paraesthesia or weakness also resolves by two weeks. The vascular site complication can be prevented by adopting radial / ulnar approach. Vascular closure devices were used to reduce access site bleeding complication and for early ambulation but till date there usefulness is not proven.

Other complications : These are very rare but has been documented in literature and are :

Dissection of artery (femoral, radial etc.)
Pseudoaneurysm formation
AV fistula formation
Infectious complication
Cholesterol embolisation syndrome
Thrombotic occlusion of vascular access site

Percutaneous techniques to treat coronary artery disease is growing at a rapid pace with increasing experience more and more complex lesions can be tackled by this technique with excellent results. The complications are rare and most of the time predictable and if the operator is experienced they can be minimised by taking appropriate precautions.

  1. Braunwald’s Heart disease a text book of cardiovascular disease 7th Edition, 2005. Editor : DP Zipes, P Libby, R Bonow, E Braunwald. Elsevier, Philadelphia, USA.
  2. Text book of Interventional Cardiology, 4th Edition 2003, Editor – EJ Topol, Saunders, Elsevier Philadelphia USA.
  3. Interventional Cardiology secrets 1st Edition 2003, Editor – ED Marchana, A CAG Ferreira, Elsevier, Philadelphia, USA.
  4. Tepel M, Aspelin P, Lameire N, Contrast Induced Nephropathy; a clinical and evidenced based approach. Circulation 2006; 113 : 1799-1806.

‘Human smoking behaviour is not simply more variable than standard testing, but systematically greater in virtually every case’
In this week’s Lancet David Hammond and colleagues review internal tobacco industry documents about industry research on smoking behaviour. The documents reveal how British-American Tobacco (BAT) exploited limitations of testing protocols to intentionally conceal from consumers and regulators the potential toxicity of their products. BAT’s own research shows that tar and nicotine delivered to smokers is substantially greater than the machine-smoked yields reproted to consumers and regulators. In a Comment, Simon Chapman discusses the values that should underpin any policy response from health authorities.

Lancet, 2006; 706, 781.



Consultant Cardiologist, Apollo Hospital, Hyderabad.