AV REENTRY TACHYCARDIAS: ABLATION 537 (a) AVN Left sided AP (b) FP SP Figure 13.9 (a) Orthodromic AVRT via a left-sided accessory pathway (AP). Activation from A to V is down the atrioventricular node (AVN), then across the ventricular myocardium and b ack from V to A up the AP, thus completing the circuit. The ventricle therefore is an essen tial part of the circuit. Antidromic AVRT (not shown) would activate in the opposite direct ion. A left-sided AP as shown here would be accessed by a trans-septal puncture or retrogra dely (via aortic valve and LV). (b) Typical AVNRT activates from the atrium to the AVN via the slow pathway (SP) and from the AVN to the atrium via the fast pathway (FP), thus comple ting the circuit. The ventricle is activated as a bystander via the bundle of His and is no t an essential part of the circuit. Atypical AVNRT (not shown) activates in the opposite di rection. Ablation targets the slow pathway. CHAPTER 13 Invasive electrophysiology 538 Ablation of ventricular tachycardia Clinical indications Only a small percentage of patients with VT and structural heart disea se are suitable for ablation. The VT needs to be relatively well tolerated (see Fig. 13.10) and ideally is monomorphic. In this group, success rates of 70% are expected. Ablation sho uld be offered to patients whose VT is well tolerated and have one of the following feature s: \200 \200 \200 \200 Recurrent symptomatic paroxysms The number of therapies delivered by an ICD needs to be red uced Incessant VT VT in normal hearts: ablation offers a cure for these patients (>90% cure ). RVOT and fascicular tachycardia are mapped during VT, looking for the earliest ventricul ar activation. Mechanism of VT In structural heart disease VT almost always has a reentry mechanism. Scarr ed ventricular myocardium (due to ischemia, cardiomyopathy, etc.) provides the substrate fo r reentry as described previously. A stable reentry circuit can break down into chaotic act ivation of \201 brillation (VF), hence the link between VT and sudden death. Mapping reentry VT To successfully map the reentry circuit, the patient must be in VT (acti va- tion mapping). Thus the VT needs to be hemodynamically well tolerated. Remote de \201 brillation paddles are attached to the patient so that if VF or hypotensive VT occurs, it c an be immediately cardioverted. The aim is to identify the critical pathway at which the circuit is most susceptible to des truction. This is achieved by entrainment mapping. Alternately, 3-D noncontact scar mapping can be performed in SR and \200\234escape pathways \200\235 can be eliminated by ablation . Entrainment of VT This can only be performed on tachycardias with a reentry mechanism. The ablation catheter is moved around the ventricle to sites where the cir- cuit is expected (i .e., adjacent to areas of scar). By pacing with this catheter at a rate just faster than th e tachycardia cycle length, a VT is entrained if it is following the same circuit but at a faster rate. If the ECG during pacing is a 12/12 surface lead match to the clinical VT, then this is con cealed entrainment. This implies that the pacing catheter is within the critical portion of the circuit. To con \201 rm this when pacing is stopped, the return cycle length or post- pacing interval (the time from the \201 nal paced beat to the next activation at the cath eter) should be almost identical to the tachycardia cycle length. Ablation technique The standard steps of a VT ablation are as follows: \200 \200 Induce VT. Ensure similar to clinical VT and well tolerated. Map VT to identify critical di astolic pathway: \200 Very early local electrogram occurring mid-diastole (50 \200\223150 ms ahead of ECG) ABLATION OF VENTRICULAR TACHYCARDIA 539 +160 Arterial 0 HRA HBEp HBEd RVA I aVF Figure 13.10 An induced VT at a cycle length of 320 ms (187/min). From top to bottom a trac ing of arterial pressure, high right atrial Egram, proximal then distal His bundle Egram, R V Egram, then 2 surface ECG leads. There is no V-to-A conduction at this rate and the atriu m is dissociated form the ventricle. Despite the rapid rate, the systolic BP is maintained at 100 mmHg, enabling the VT to be mapped if necessary. \200 Concealed entrainment during pacing Return cycle length (= post-pacing interval) < tachycar dia cycle length + 30 ms \200 Deliver energy at site, meeting criteria above. If VT is terminated, attempt to reinduce ag ain. Failed ablation If conventional ablation fails, alternative approaches are as follows: \200 \200 Arrhythmia cardiac surgery. Ablate the epicardial surface of the heart by delivering the ca theter via the pericardium (as for a pericardial aspiration). Alcohol ablation via a small terminal coronary branch subtending the scarred area supporting reentry. This gives the pat ient a controlled, small MI that destroys the critical portion of the reentry circuit. CHAPTER 13 Invasive electrophysiology 540 Accessory pathways (Wolff \200\223Parkinson \200\223 White syndrome) De \201 nitions and ECG The atria and ventricles are separated by the \201 brous annuli of the TV on the right and MV on the left. The AV node is the only electrical connec- tion in normal hearts. Abnormal accessory pathways can occur at any position along these annuli and are named accordingly (see Fig. 13.11). They may conduct in one or both directions. The y are the substrate for AVRT to occur. If an AP conducts anterogradely (A to V) it will be manifest on the ECG as pre-excitation ( short PR interval and delta wave). The morphology of the delta wave helps to predict the lo cation of the AP. An AP that con- ducts only retrogradely is described as concealed. Wolff \200\223Parkinson \200\223White syndrome refers strictly to APs that are both manifest as pre-excitation on the resting ECG and cause tachycardia. Tachycardias An AP can be associated with tachycardia by several mechanisms: \200 Orthodromic AVRT (most common, accounts for 95% of AP-mediated tachycardias) \200\224narrow complex tachycardia with anterograde conduction over the AVN and retrograde conduction via the AP wide complex tachycardia with anterograde Antidromic AVRT \200\224 conduction via t he AP and retrograde conduction via the AVN Bystander \200\224SVT of another etiology that conducts down the AP Prognosis AF in the presence of an AP with anterograde conduction can be danger- ous, as th e ventricle is not protected by the decremental behavior of the AV node. This can precipita te VF and sudden death. If patients are discov- ered incidentally to have an AP and are tru ly asymptomatic, then sudden death is extremely rare (2 deaths in 600 patients followed for 3 \200\22320 years). Invasive EP can be used to risk stratify patients. A worse prognosis is predicted by the following: Invasive EP testing \200 Anterograde ERP of the AP <250 ms (the longest interval that will not conduct down the AP d uring atrial extrastimulus pacing or AF) Inducible AVRT Multiple APs \200 Symptomatic tachycardia Ebstein \200\231s anomaly \200 ACCESSORY PATHWAYS (WOLFF \200\223PARKINSON \200\223WHITE SYNDROME) 541 Anterior Left lateral His Septal MV TV CS Right lateral Posterior Figure 13.11 Tricuspid (TV) and mitral valve (MV) annuli. Accessory pathways can be positio ned anywhere on the annuli. They are named anatomically, i.e., anterior, left anterolateral , left lateral, left posterolateral, etc. Anteroseptal pathways are close to the His bundle and AV node and are termed parahisian. CHAPTER 13 Invasive electrophysiology 542 Accessory pathways: localization R/S(cid:1)1 V2 Yes No \210\206 (+) \210\206 (+) III Yes Yes No No LL/ LAL \210\206 ( \200\223) \210\206 (+) \210\206 (+) V1 Yes Yes Yes No No No RAS/ RA LL/ LAL RPS MS AVF \210\206 V1 R/S(cid:1)1 No Yes \200\223 + LP/ LPL RP/ RPL RL RAL LPS Figure 13.12 Algorithm to locate the accessory pathway from the ECG with pre-excitation. \210\206 = delta wave. Reprinted with permission from Chiang et al. (1996). Am J Cardiol 76 (1):41 \200\22346. ACCESSORY PATHWAYS: MANAGEMENT 543 Accessory pathways: management Ablation Accessory pathways (APs) can be inactivated by catheter ablation and this is \201 rst-line treatment for symptomatic patients. A catheter is moved around the MV or TV a nnulus until the AP is located by \201 nding the exact point of \200 \200 \200 Earliest ventricular activation during SR or atrial pacing. Earliest atrial activation duri ng ventricular pacing. Earliest atrial activation during orthodromic AVRT. Acute success is >90%. The complication rate is very low (death 0% \200\2230.2%, AV nodal b lock <1%). For parahisian AP, the risk of AV nodal block is higher and cryoablation may be used if available. Left-sided pathways can be approached via the femoral artery, aorta, and left ventricle, or from the RA by a transseptal puncture. All symptomatic patients (with tachycardias) should be offered ablation. Asymptomatic young patients (<35 years) or those in a high-risk profes- sion (pilots, divers, etc.) should be considered for invasive EP testing and ablation. However, risk of sudden death must be bal anced against the 2% serious complication rate of ablating the pathway (particularly if lef t-sided or parahisian). Pharmacological Flecainide and propafenone slow conduction in the AP and the AV node and ar e the preferred agents. Drugs that slow AV-nodal conduction only (verapamil and digoxin) sh ould not be used unless invasive EP has demonstrated that the AP does not conduct anterogra dely (or conducts poorly). Unusual pathways Mahaim pathways These are APs between the RA and RV (atrioventricular) or RA and right bundle branch (atriofascicular). Unlike ordinary APs, they exhibit AV nodal pr operties of decremental conduction and sensitivity to adenosine. They only conduct anterogr adely and mediate an AVRT with a broad complex LBBB appearance. They are successfully treat ed by catheter ablation. CHAPTER 13 Invasive electrophysiology 544 Implantable cardioverter de \201 brillators (ICDs) Mirowski implanted the \201 rst de \201 brillator in 1980 to manage sudden cardiac death. Since then, there has been dramatic improvement in technology, and many randomized controlled trials provide evidence to suppor t their use in both primary and secondary prevention of sudden cardiac death. Initial implants used epicardial leads and required surgical implantation. The generators w ere large and placed in abdominal pockets. Currently, the devices are implanted transvenous ly and the generators placed in the pectoral region. ICDs employ a series of complex sensing algorithms for arrhythmia detection and use tiered therapy of pacing and shocking to treat arrhyth- mia as well as to minimize myocardial inju ry. Components A typical pulse generator consists of a lithium silver vanadium oxide bat- tery, an aluminum electrolytic capacitor, and sensing circuitry that can sense local electrogram s and \201 lter out noise like skeletal myopotentials. De \201 brillators have at least one lead in the RV for pacing/sensing and de \201 - brillation. There may be a second lead in the SVC or a dual coil lead to lower de \201 brillation threshold. An atrial lead can be implanted for dual-chamber pacemaker indications or to help with detection or discrimination of arrhythmias. Detection Most leads sense between the tip of the lead and an electrode anywhere along the length of the shocking coil (integrated bipolar sensing). Potential problems are with noise , far- \201 eld sensing, or post-shock undersensing. True bipolar sensing between a ring a nd tip electrode is more reliable but requires the lead to have three conductors. Basic detection of VT involves a heart rate, above which therapy will be delivered. Modern devices can be programmed to have multiple detec- tion zones, each with its own speci \201 c therapies. Rate detection is very reliable but susceptible to inappropriate therapies fo r sinus tachycardia or poorly controlled atrial \201 brillation. This is where medical th erapy such as B-blockers is very important to help prevent inappropriate therapy. To decrease inappropriate shocks, various detection enhancements are included in modern dev ices, such as rate stability (looking at variations in R \200\223R intervals to recognize A F), electrogram morphology (to distinguish a normal QRS [SVT], including BBB, from the QRS when in VT), and sud- den-onset criteria (gradual onset of sinus tachycardia). The most useful algorithm, however, is to have an atrial lead so the device can analyze the timing of simultanous atrial electrograms. The tradeoff of improved detection means that t herapy for VT is inhibited. Most devices include \200\234sustained rate duration \200\235 as a backup, which ensures delivery of therapy if the tachycardia is sustained. As a defaul t, these detec- tion algorithms do not apply in the programmed VF zone. INDICATIONS FOR ICD IMPLANTATION 545 Indications for ICD implantation Box 13.2 Indications for ICD implantation De \201 nite indications \200 Survivors of cardiac arrest due to ventricular \201 brillation or hemodynamically unstabl e sustained VT in the absence of a completely reversible cause Spontaneous sustained VT in a patient with structural heart disease, whether hemodynamically stable or unstable Syncope of undetermined origin with hemodynamically signi \201 cant sustained VT or ventricular \201 brillation induced at EPS. LVEF <35% due to prior MI in patients who are at least 40 days post-MI and are in NYHA functional Class II or III Patients with nonischemic dilated c ardiomyopathy who have an LVEF \211 35% and who are in NYHA functional Class II or III Pat ients with LV dysfunction due to prior MI who are at least 40 days post-MI, have an LVEF <3 0%, and are NYHA functional Class I. Nonsustained VT due to prior myocardial infarction, LV EF <40%, and inducible ventricular \201 brillation or sustained VT at EPS Relative indications \200 Unexplained syncope, signi \201 cant LV dysfunction, and nonischemic dilated cardiomyopath y Sustained VT and normal or near-normal ventricular function Patients with hypertrophic ca rdiomyopathy who have one or more major* risk factor for SCD Prevention of SCD in patients with arrhythmogenic right ventricular dysplasia or cardiomyopathy who have one or more risk factor for SCD To reduce SCD in patients with long-QT syndrome who are experiencing syncop e and/or VT while receiving B-blockers Nonhospitalized patients awaiting transplantation Pa tients with Brugada syndrome who have had syncope Patients with Brugada syndrome who have d ocumented VT that has not resulted in cardiac arrest Patients with catecholaminergic polymo rphic VT who have syncope and/or documented sustained VT while receiving B-blockers ICD imp lantation is reasonable for patients with cardiac sarcoidosis, giant cell myocarditis, or C hagas disease \200 \200 \200 Risk factors for SCD with HCM: prior SCD, prior nonsustained VT, massive hypertrophy (>30 m m), family history of SCD, syncope. Adapted from ACC/AHA/NASPE 2008 guidelines for device-b ased therapy. J Am Coll Cardiol 2008; 51;2085 \200\2232105. CHAPTER 13 Invasive electrophysiology 546 ICD therapies Antitachycardia pacing (ATP) The two most common methods of ATP are rate-adaptive burst pac ing and autodecremental or ramp pacing. With rate-adaptive burst pacing the device is progr ammed to deliver a set number of pulses (6 \200\22312) at a cycle length that is a programm ed percentage of the tachycardia cycle length (TCL) (i.e., 81% of the TCL). The sequences may be repeated with a decrementing cycle length. In ramp pacing the initial coupling interval is also a percentage of the TCL but each subsequent coupling interval dec rements by a set amount (i.e., 10 ms). Again, this sequence can be repeated. Generally, modern devices can be programmed to have one to three VT zones with multiple tie rs of therapy. One manufacturer allows for a fast VT zone in the VF zone, which allows pain less ATP to treat fast VT instead of cardioversion. De \201 brillation Most ICDs deliver a maximum energy of 30 \200\22336 J via their capacit ors as a biphasic waveform from the tip of the RV lead to the pulse generator, which is an \200\234active can. \200\235 The shocking vector travels superiorly from the RV including most of the IVS and LV. Sometimes a third electrode is needed as either a separate SVC coil or a dual coil RV lead to improve the de \201 brillation threshold (DFT), and the device can shock either between both coils or between the can and either coil and sometimes the vector is reversed. Very r arely, a subcutaneous patch is needed and is placed in the left axillary region. Low-energy de \201 brillation Devices can also deliver low-energy cardioversions when the tachycardia is generally <180 bpm, which has some ef \201 cacy but patients feel shocks ab ove 1 J. This has not been shown to be better than ATP. De \201 brillation threshold (DFT) testing Unless contraindicated, DFTs should be tested a t implant. The goal is for the DFT to be less than the maximum output of the device, ideall y by 10 J. VF is induced via rapid burst pacing, T-wave shock, or AC current (unpleasant) w hile the patent is sedated. Appropriate VF detection and device charge time as well as the DFT can be evaluated. ICD: TROUBLE SHOOTING AND FOLLOW-UP 547 ICD: trouble shooting and follow-up Follow-up \200 Oversensing leading to therapy (e.g., T-wave sensing, electrical noise from lead fractures, atrial activity). Sensitivity settings can be adjusted to help prevent T-wave sensing. Lea d fractures require replacement and atrial leads help distinguish atrial activity. Undersen sing or VF. It is more likely with unipolar systems. It may indicate lead displacement, in \202 ammation, or \201 brosis at the lead tip. is more serious but less common. May not detect VT Drug interactions \200 Increased de \201 brillation threshold \200\224Class I antiarrhythmics and amiodarone Decr eased de \201 brillation threshold \200\224sotalol Antiarrhythmics may slow VT below the d etection threshold, affect the ability of ATP to terminate the tachycardia, or cause incess ant VT. They may impair ventricular function and cause bradycardia requiring pacing. They m ay also affect the pacing threshold for bradycardia. \200 Table 13.3 Complications of ICD implantation Early \200 \200 \200 \200 \200 \200 \200 VT \200 \200 Late \200 \200 \200 \200 \200 \200 Infection Hemopneumothorax Cardiac perforation Hemorrhage and pocket hematoma Vascular inju ry Venous thrombosis Lead displacement or damage Infection Pain Erosion Lead/insulation break Lead displacement Twiddler \200\231s syndrome Heart block This page intentionally left blank 549 Chapter 14 Cardiac catheterization and coronary intervention Radiation protection in the catheter laboratory 550 Vascular access: the femoral artery 551 Vascular access: the radial artery 553 Vascular access: site management 555 Coronary angio graphy 556 Interpreting the coronary angiogram 558 Angiographic study of grafts 560 Complic ations of angiography 561 Right heart catheterization 564 Cardiac output and LV function 56 6 Cardiac catheterization in valve disease 567 Intravascular ultrasound 569 Angioplasty and coronary stenting 571 Restenosis following PTCA 573 Drug-eluting stents 574 Stent thrombos is 576 Physiological assessment of coronary \202 ow 578 Primary angioplasty for STEMI 580 Primary angioplasty: procedure 581 Invasive assessment of vulnerable plaque 583 Complex co ronary angioplasty 584 Left main stem angioplasty 586 Adjunctive therapy for angioplasty an d stenting 587 Embolic protection devices 589 Thrombectomy 591 Mitral valvuloplasty 592 Glo ssary of terms and abbreviations 594 Further reading 596 CHAPTER 14 Cardiac catheterization 550 Radiation protection in the catheter laboratory Staff working in the catheterization labora tory should be issued with radia- tion monitoring badges for the body and neck, which shoul d always be worn while in the lab. These badges should be checked monthly to assess doses o f radiation received by individual members of staff. Minimizing patient dose \200 \200 \200 \200 \200 \200 Minimize screening time and minimize acquisition time. Keep distance between X-ray tube and image intensi \201 er to a minimum. Use collimation and cones to minimize the irradiated area. Use lower magni \201 cations when possible. Use the lowest number of frames/second t o allow adequate imaging. For prolonged procedures, the intensi \201 er should be moved re gularly a few degrees to try to minimize the possibility of skin burns. Minimizing operator dose \200 \200 \200 \200 Lead aprons and lead collars should be worn. A lead apron should be below the table. A mobi le lead screen should go between the operator and the source. As above, minimize X-ray expo sure by reducing screening and acquisition time. Some projections (e.g., left anterior obli que [LAO]) give much higher scatter of X-ray, and operators should be aware of this. The dose for an interventional cardiologist has been calculated as 50 mSv (based on 150 wor king days per year and four interventions per day). The calculated effective dose if the op erator wears the correct lead apron and thyroid collar is <5 mSv/year. The maximum allowed dose is 50 mSv/ year. VASCULAR ACCESS: THE FEMORAL ARTERY 551 Vascular access: the femoral artery Procedure for femoral artery access \200 The standard approach for left heart catheterization is the right common femoral artery. Th e artery is located by palpating below the inguinal ligament, the ideal position for punctu re being approximately 3 cm below the inguinal ligament and slightly lateral to the positio n of the vessel (see Fig. 14.1). Shave area, and disinfect. The area should be anesthetized generously with of local anesthetic (usually 10 mL of 2% or up to 20 mL of 1% lidocaine). Warn the patient of \200\234pins and needles \200\235 or transient numbness in the leg tha t may be caused by the effects of lidocaine on the femoral nerve. The procedure used to pun cture the artery is known as the technique. A hollow needle is introduced slowly; it is oft en possible to feel the pulsations of the artery via the needle before the vessel is punctu red. When the needle is introduced into the vessel, pulsatile \202 ow con \201 rms its p osition in the arterial lumen. At this point, a 0.035 \200\235 wire can be advanced into th e vessel and toward the heart; this should be performed under \202 uoroscopic guidance. T he needle is then withdrawn and a hemostatic sheath (usually 5 Fr \200\2238 Fr diameter) is introduced over the wire. The hemostatic sheath allows the introduction of a guide wire an d catheter into the femoral artery, while preventing excess bleeding from the femoral punct ure site. \200 Seldinger Sheath removal \200 This can be performed immediately after diagnostic angiography or after an interval of 4 \200\2236 hours if heparin has been administered. Hemostasis can be achieved by manual comp ression or by using a compression device (e.g., Femstop \204 ). Vascular closure devices (e .g., Angioseal \204 or Perclose \204 ) allow earlier removal of sheaths in anticoagulated patients and may reduce bleeding complications. Complications \200 \200 \200 \200 \200 Femoral artery dissection Femoral artery pseudoaneurysm Distal embolization Hematoma Retrop eritoneal hemorrhage/hematoma (particularly with high punctures of the femoral artery above the inguinal ligament) CHAPTER 14 Cardiac catheterization 552 Anterior spine Inguinal ligament Skin crease 3 cm Common femoral artery Profunda Saphenous vein Superficial femoral artery Femoral vein Figure 14.1 Anatomy of the inguinal canal: the femoral vein lies medial to the femoral arte ry. The arterial puncture should be made approximately 3 cm below the inguinal ligament. VASCULAR ACCESS: THE RADIAL ARTERY 553 Vascular access: the radial artery The radial approach for coronary angiography is now wide ly accepted. There are several advantages, including a reduction in vascular compli- cation s and the ability to mobilize patients immediately following their procedure. Patient selection for radial access should include palpation of the radial artery to con \201 rm that pulsations are present and then an Allen \200\231s test (see Box 14.1). In the absence of robust supply via the ulnar artery, the radial approach should not be used. Procedure for radial artery approach \200 \200 \200 Perform Allen \200\231s test. Remove all jewelry from the arm, shave area, and disinfect. L ocal anesthesia: use 1 \200\2232 mL of 2% lidocaine instilled via a 25-gauge needle (i.e., enough to anesthetize, but not to distort the anatomy). The artery should be palpated with the index and middle \201 ngers, the index \201 nger lifted, and the artery punctured a t 45 . The artery should be punctured as proximally as possible, and care should be taken to avoid the \202 exor retinaculum (Fig. 14.2). Once pulsatile \202 ow is obtained, a g uide wire can then be advanced through the needle and into the vessel. It is usual to make a small incision in the skin to allow passage of an arterial sheath. Care should be taken n ot to damage the radial artery while making this incision. Thus the blade should be used to incise in the longitudinal plane rather than transversely to reduce the risk of completely transecting the artery. A variety of long and short sheaths are commercially available. The advan- tage of long she aths is that they minimize trauma to the radial artery. Complications Radial artery spasm This is the most common complication of radial artery pun cture and sheath introduction. There are various techniques aimed at preventing radial arte ry spasm from occurring: \200 Careful patient selection, avoiding small and dif \201 cult to palpate radial arteries. Ad equate patient sedation if required (pain provokes spasm). The use of a cocktail of drugs i ntroduced directly into the radial artery. A variety of different regimens have been descri bed. We use 1 mg nitroglycerin, 2.5 mg verapamil, and 2500 U unfractionated heparin (UFH) m ade up to 10 mL with normal saline. Repeated doses of nitrates or verapamil (up to 5 mg) gi ven directly into the sheath or in the catheter may be required. Shorter sheaths may be bet ter tolerated. Some sheaths have a hydrophilic coating to reduce spasm and for less discomf ort on removal. Always use the guide wire to straighten catheters prior to removal from the aortic arch through the radial sheath. \200 \200 CHAPTER 14 Cardiac catheterization 554 Box 14.1 Allen \200\231s test Manual compression \200 \200 Compress radial and ulnar arteries. Ask patient to open and close their \201 ngers making a \201 st (this will cause the hand to blanche). Release ulnar artery. Allen \200\231s t est is POSITIVE if the color of the palm of the hand returns to normal within 10 seconds (c on \201 rming that the ulnar circulation is intact). \200 Plethysmography \200 \200 Attach plethysmography probe (pulse oximetry). Compress both the radial and ulnar arteries (the plethysmography trace will \202 atten). Release ulnar artery. The test is POSITIVE i f the plethysmograph curve returns to normal (con \201 rming that the ulnar circulation is intact). \200 Thenar muscles Branch of radial artery completing the superficial palmar arch Abductor pollicis longus Radial artery Radius Flexor carpi radialis Figure 14.2 Radial artery anatomy. VASCULAR ACCESS: SITE MANAGEMENT 555 Vascular access: site management Femoral sheath removal Femoral sheaths should be removed o nly by fully trained members of staff. After diagnostic coronary angiography, when no or li ttle heparin is given, the sheath may be removed immediately. Direct pressure should be app lied just proximal to the site of the skin puncture for 15 minutes. After angioplasty, if unfractionated heparin was used, it is routine to wait for 4 \200\223 6 hours and check an ACT (activated clotting time); if it is <150 seconds, it is acceptable for the sheath to be removed. In cases where bivalirudin was used, the sheath can be safel y removed after 30 minutes. Femoral clamps (FemoStop , RADI Medical Systems) can be used to reduce bleeding complications in patients. Radial sheath removal Radial sheaths are removed immediately after both diagnostic angiogra ms and angioplasty, as the position of the artery renders compression simpler. Compression bands (RadiStop , RadiMedical Systems USA, TR-Band \204 , and Terumo) can be used to achie ve hemostasis. Vascular closure devices Until recently, mechanical compression was the only method for con trol- ling bleeding from vascular access sites in the groin. Larger sheaths and the advent of the more widespread use of gpIIb/IIIa inhibitors have increased the risk of bleeding and made hemostasis more dif \201 cult. Recently, various closure devices have been introduced, their aim being to increase patient comfort and reduce puncture related complications. Suture-based closure devices Perclose (Abbot Vascular, USA) delivers a suture to the arte rial puncture site. The device is sheath-like in nature; needles are positioned above the s heath in the handle and are deployed by a plunger. A \200\234clincher \200\235 that per- f orms a knot-tying function completes a sliding surgical knot. Collagen-based closure devices Devices that use a bioresorbable collagen plug that is depos ited at the site of arteriotomy via a sheath include the VasoSeal (Datascope Corp., USA) and Angio-Seal (St Jude Medical, USA). Other mechanical closure devices StarClose features a Nitinol clip that is designed to promote the pri- mary healing process to achieve a secure closure of femoral artery access sites following diagnostic or interventional vascular procedures. This clip provides 360* t issue apposition for rapid healing and hemostasis. Drug-based closure devices The Clo-Sur P.A.D (Medtronic, USA), MINX (USA) device contains a naturally occurring biopolymer polypr olate acetate. This polymer has a coagulant property when brought into contact with heparin ized blood. The device is placed over the puncture and the hemostatic sheath is removed. Di rect continuous pressure is applied until hemostasis is achieved. CHAPTER 14 Cardiac catheterization 556 Coronary angiography Preshaped coronary angiographic catheters The catheters used in diagno stic coronary angiography come in a wide variety of preformed shapes. In the United States, the most commonly used preshaped catheters are the Judkins Left 4 and Judkins Right 4 (kno wn as the JL4 and JR4, respectively), used to image the left and right coronary arteries, a nd the pigtail catheter used for left ventriculography. The diameter of catheters is measured in French gauge (Fr); catheters between 4 Fr (0.053 \200\235) and 8 Fr (0.105 \200\235) are commonly used (Fig. 14.3). Catheter advancement and manifold usage A \200\234J \200\235 tipped 0.035 \200\235 guide w ire is placed within the \202 ushed catheter, which is then passed into the hemostatic sh eath. The guide wire is advanced ahead of the catheter under \202 uoroscopic guidance, un til it reaches the aortic root, just above the aortic valve. The catheter is then advanced to this position and the guiding wire is removed (see Box 14.2). To ensure that no air or clot is within the catheter, a small volume of blood (5 mL) is asp irated from the catheter directly into a syringe and discarded. The catheter is then carefu lly connected to a two-way mani- fold that allows pressure monitoring, saline \202 ushing , and contrast injection through a closed system. Contrast injection Great care must be taken at all times to ensure that air is not injected into the coronary arterial tree. The injection syringe should be \201 lled with contrast from the reservoir and then the syringe held with the plunger elevated such that any air b ubbles rise to the top of the syringe. Contrast should then be injected at a continuous rat e, aiming to fully opacify the coronary vessel of interest. Care should be taken that the pressure trace prior to injection is nor- mal \200\224damping suggests an ostial lesions, excessively deep intubation, or selective intubation of a bran ch. JR 4 JL 4 AR II AL I MPR 1 PG Figure 14.3 Commonly used cardiac catheter shapes. JL, JR: Judkins left and right coronary catheters; AL, AR: Amplatz left and right; MP: multipurpose coronary access catheter; PG: p igtail catheter. CORONARY ANGIOGRAPHY 557 Box 14.2 Coronary angiography/left ventriculography Left coronary artery \200 The 50 left anterior oblique (LAO 50) is the best projection for cannulation of both the left and right coronary ostia. The JL4 catheter will almost invariably cannulate the left c oronary ostium without manipulation. In patients with large aortic roots (large, hypertensi ve patients), the JL5 (with a larger curve) may be needed, and conversely, a smaller root m ay need a smaller catheter curve, the JL3.5. Right coronary artery \200 The LAO 50 projection is best used for cannulation of the right coronary ostium. The JR4 ca theter is introduced to the aortic root, until it lies 1 \200\2232 cm above the aortic valv e. The catheter is then rotated ( \200\234torqued \200\235) in a clockwise direction such t hat the catheter tip rotates toward the right coronary ostium. It may be necessary to reduc e the torque to prevent the catheter from overshooting. There is often a noticeable lateral movement as the catheter enters the artery. Before contrast is injected, it must be ensure d that the pressure tracing transduced from the tip of the catheter is not damped, which ca n suggest that the catheter has selectively intubated the conus branch of the right coronar y artery, and injection of contrast into this vessel can induce ventricular arrhythmias. Left ventriculography \200 Position pigtail catheter a few centimeters above the aortic valve and pull wire back 5 \200\22310 cm to make catheter tip soft, and push gently (the catheter may cross at this po int). If catheter does not cross, apply torque as it is gently withdrawn. Once catheter has been placed in a stable (free of ectopy) position in mid-LV cavity, connect to manifold an d measure pressure. Disconnect manifold catheter connected to a power injector and expel al l air. Set injection rate: typically 36 mL of contrast at a rate of 12 mL/sec. Warn patient about hot \202 ush and the feeling of extra systoles. When the left ventriculogram has b een performed, the catheter is reconnected to the manifold to allow pressure recording as t he catheter is withdrawn across the aortic valve (the pullback pressure). \200 CHAPTER 14 Cardiac catheterization 558 Interpreting the coronary angiogram LCA angiographic views LCx OMB LAO Cranial LMCA D LAD LCx LAO Caudal LAD LMCA AP Caudal LCx LAD LCx AP Cranial LMCA S LAD LCx RAO Cranial S LAD RAO Caudal LAD LCx OMB Figure 14.4 This \201 gure was published in Libby P. Braunwald \200\231s Heart Disease, 8 th ed. Saunders. Copyright Elsevier 2001. INTERPRETING THE CORONARY ANGIOGRAM 559 RCA angiographic views RCA LAO Straight PLV AMB PDA LAO Cranial RCA PLV AMB PDA RAO Straight Conus branch RCA PDA Figure 14.5 AMB, acute marginal branch; LAO, left anterior oblique; PDA, posterior descendi ng coronary artery; PLV, posterior left ventricular branch; RCA, right coronary artery; RAO , right anterior oblique. This \201 gure was originally published in Libby P. Braunwald \200\231s Heart Disease, 8th ed. Saunders. Copyright Elsevier 2007. CHAPTER 14 Cardiac catheterization 560 Angiographic study of grafts It is important to study the surgical record to ascertain how many grafts were placed at the time of the operation. Sometimes, useful information (often from a surgeon \200\231s diagram) can be obtained as to the position in the ascending aorta that the grafts arise from. As a rule, leftward-facing grafts are best cannulated from the RAO 50 projection, and right ward-pointing grafts are best cannulated in the LAO 50 projection. It may be necessary to p erform an aortogram to visualize the position of grafts. Special catheters (e.g., the left coronary bypass cath- eter, or LCB) have been designed to aid cannulation of grafts. There is usually a predictable anatomy: Posterior descending artery (PDA) grafts originate from the right anterior aspect of the aorta and run vertically to the inferior surface of t he heart. Obtuse marginal branch (OM) grafts originate from the left anterior aspect of the aorta and arc toward the posterolateral surface of the heart. Left anterior descending art ery (LAD) and diagonal grafts originate from an intermediate position and run laterally tow ard the anterior interventricular groove. Common aortic positions for placement of saphenous vein graft (SVG) SVG-OVG SVG-LAD SVG-PDA LCA RCA Figure 14.6 Vein graft anatomy. This \201 gure was published in Braunwald E. Heart Diseas e: A Textbook of Cardiovascular Medicine, 5th ed. Copyright Elsevier 2001. COMPLICATIONS OF ANGIOGRAPHY 561 Complications of angiography Peripheral vascular complications Hematoma The incidence of he matoma formation is related to the following factors: \200 \200 \200 \200 Length of time sheath is left in place Gauge (size) of sheath Anticoagulation Risk factors, e.g., hypertension, obesity, and pre-existing peripheral vascular disease Technique of she ath removal Features suggesting that a hematoma may require further investigation are an overlying brui t, expanding mass, and a large, tense swelling. Pseudoaneurysm A pseudoaneurysm represents a rupture of the femoral arterial wall at the si te of puncture, with the formation of a false aneurysm involving the media and adventitia ( Fig. 14.7). They are best visualized on ultrasound examination (Fig. 14.8). Small pseudoaneurysms can often be managed conservatively; however, large pseudoaneurysms m ay require thrombin injection, compression, or surgical intervention. (a) Common femoral artery Pseudoaneurysm Tract Superficial femoral artery Femoral head Profunda femoral artery (b) (c) Pressure device Hematoma Pseudoaneurysm Figure 14.7 Anatomy of a pseudoaneurysm. (a) Bleeding along a small tract allows blood to c ollect within the extravascular tissues. Manual compression fails to obliterate the tract ( b) and allows the hematoma to persist. Failure of thrombosis of the hematoma produces an ex travascular collection with persistent connection and \202 ow from the main artery (c). T his can be visualized on ultrasound (see Fig. 14.8). CHAPTER 14 Cardiac catheterization 562 Hemorrhage If prolonged, then direct pressure (either manually or using a clamping device) may be needed. Limb ischemia This is rare and usually occurs in patients with pre-existing limb ischemia. If limb ischemia is suspected, urgent vascular surgical team review should be sought. Dissection Dissection can occur at the time of sheath insertion and/or catheter manipulatio n; this can be diagnosed by dampening in the pressure tracing. If this is noted, an iliac a ngiogram should be performed and pressure gradi- ent recorded. If signi \201 cant dissecti on is noted, a percutaneous intervention (i.e., iliac stent) should be pursued.