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Hamid Barakpour,MD. Interventional Electrophysiologist October 2011 The conducting system in normal human hearts The arterial blood supply of the conducting system in normal human hearts • The sinus node and the sinoatrial region are, in 55% of patients, perfused by an atrial branch from the proximal part of the right coronary artery (RCA). In 45% of cases this region is perfused by a proximal branch of the circumflex coronary artery. A proximal occlusion of the RCA or the cicumflex coronary artery may therefore lead to ischemia of the sinus node and the surrounding atrium. • The AV conduction system (the AV node, the bundle of His, and the bundle branches) is perfused by the RCA and the left anterior descending coronary artery (LAD); the AV node and the proximal part of the bundle of His are perfused by the RCA, while the distal part of the bundle of His, the right bundle branch, and the anterior fascicle of the left bundle branch are supplied by the septal branches of the LAD. The posterior fascicle of the left bundle branch is supplied by septal branches from both the LAD and the RCA. The Incidence of Symptomatic Bradyarrhythmias in Patients with Coronary Artery Disease • The incidence of bradyarrhythmias in patients with acute coronary syndrome (ACS) is 0.3% to 18%. It is caused by sinus node dysfunction (SND), high-degree atrioventricular (AV) block, or bundle branch blocks. • sinus bradycardia is found in approximately 40% of patients, representing the most commonly encountered bradyarrhythmia in patients with AMI. Junctional rhythm is noted in 20% of patients, whereas idioventricular rhythm occurs in 15% of such cases. • Of the AVBs, first-degree and second-degree, type I AV blocks are found in 15% and 12% of patients with AMI, respectively. Complete heart block (third-degree AVB) complicates 8% of infarctions. Second-degree, type II AV block is rare. • First- or second-degree AV block is seen very frequently within 24 h of the beginning of ACS; these arrhythmias are frequently transient and usually disappear after 72 h. • Third-degree AV blocks are also frequently transient in patients with infero-posterior myocardial infarction (MI) and permanent in anterior MI patients. • In the realm of unstable bradyarrhythmias complicating AMI, complete heart block is most often encountered, with an incidence of 40%. Sinus bradycardia (25%) and junctional rhythm (20%) are the next most commonly encountered hemodynamically compromising bradycardic rhythms in AMI patients. In Germany, approximately 100000 patients die suddenly per year; this sudden death is caused by ventricular tachyarrhythmias in 65% to 80% of these patients, whereas bradyarrhythmias are present in 5% to 20% of them. Trappe HJ.Tachyarrhythmias, bradyarrhythmias and acute coronary syndromes.J of emergencies,trauma and shock 2010;3:137-142. The Incidence of Coronary Artery Disease in Patients with Symptomatic Bradyarrhythmias • In one study,in patients with symptomatic bradyarrhythmias requiring permanent cardiac pacing, the incidence of CAD was 20% as determined by coronary angiography. Hypercholesterolemia and DM were the two most significant independent predictors for CAD in these patients. • The nodal artery was seldom involved in patients with coexistent CAD and symptomatic bradyarrhythmias (9%), and most patients had significant stenosis over LAD (74%). pathophysiology • The pathophysiologic mechanisms underlying most bradyarrhythmic episodes in AMI patients involve either reversible ischemic injury or irreversible necrosis of the conduction system, as well as altered autonomic function. Additional mechanisms include myocardial hyperkalemia, local increases in adenosine, metabolic acidosis, systemic hypoxia, and the complications of medical therapy, in particular both beta- and calcium channel–blocking agents. • Unusually, coronary vasospasm(Prinzmetal’s angina) presents as recurrent episodes of variant angina and recurrent symptomatic complete heart block and asystole. CONDUCTION DISTURBANCES AND INFARCT LOCATION Inferior Wall MI • Inferior, inferolateral, and inferoposterior AMIs resulting from occlusion of the right coronary artery (RCA) are frequently complicated by bradyarrhythmias. The common association of inferior wall ischemic events and compromising bradyarrhythmias can be due to increased parasympathetic influence, especially early in the course of the infarction. • Such patients tend to develop rhythm disturbances abruptly, within 6 hours of the onset of infarction, have relatively slow ventricular escape rates, and respond rapidly to atropine or isoproterenol therapy. • Patients who develop bradyarrhythmia after 6 hours of infarction usually do so gradually, with an equally slow return to normal sinus rhythm. The escape rhythm is usually of ventricular origin, with a relatively high rate and poor response to medical therapy. These patients most likely experience the rhythm disturbance because reversible ischemia of the conduction system. • In patients with inferior AMI, irreversible damage of the AV node (i.e., necrosis of this structure) is rare owing to the presence of both extensive collateral circulation (i.e., right coronary artery and left anterior descending artery contributions in the most patients), as well as a relatively low metabolic rate with high glycogen reserves of such myocardial conducting tissue. • Differentiation of right coronary artery (RCA) from left circumflex artery (LCxA) occlusion may be difficult since both can present an electrocardiographic pattern of inferior myocardial infarction (IMI). Patients with RCA occlusion have a higher incidence of isolated IMI than patients with LCxA occlusion, 50% vs. 17%, respectively (P<0.001). • Regarding patients with IMI: (1) sinus bradycardia is more frequent when the infarct-related artery is the RCA. (2) proximal occlusions of the right coronary predispose low heart rates. (3)occlusion of the LCxA rarely induces sinus bradycardia. • High degree AV block associated with inferior wall MI is located above the His bundle in 90 percent of patients . For this reason, complete heart block often results in only a modest usually transient bradycardia with junctional or escape rhythm rates above 40 beats per minute. It is not uncommon, however, for the junctional pacemaker that controls the ventricles to accelerate above 60 beats/min. The QRS is narrow in this setting and is associated with a low mortality. • Conduction disturbance in inferior MI can occur acutely or after hours or days. Sinus bradycardia, Mobitz type I (Wenckebach), and complete heart block are commonly seen, since the SA node, AV node, and His bundle are primarily supplied by the RCA . • The admission ECG can predict the occurrence of high degree (second or third degree) AV block in patients presenting with an inferior MI. One study of 1336 patients receiving thrombolytic therapy for an inferior MI reported that a ratio of J point/R wave amplitude more than 0.5 in two inferior leads was associated with an 11.8 percent incidence of high degree AV block compared to 6.7 percent when the J point/R wave amplitude was <0.5. Sinus bradycardia • Sinus bradycardia is the most common arrhythmia associated with inferior MI. It is present in up to 40 percent of patients in the first two hours, decreasing to 20 percent by the end of the first day. It is usually attributable to increased vagal tone in the first 24 hours after infarction. Transient sinus node dysfunction occurring later may be due to sinus node or atrial ischemia. Treatment is not indicated in the absence of adverse signs or symptoms. Atropine is effective if symptoms are present such as dizziness, syncope, or confusion from reduced cardiac output . First degree AV block • First degree AV block (characterized by prolongation of the PR interval) can arise in the AV node, the bundle of His, or the bundle branches. • First degree AV block at the level of the AV node is common after occlusion of the coronary artery which gives rise to the AV nodal artery and the arteries to the inferior and posterior wall of the heart (most often the RCA). RCA occlusion can lead to first degree AV block via ischemia of the AV node, by enhanced acetylcholine release from the inferoposterior myocardium, or perhaps by making the AV node hypersensitive to the action of acetylcholine. • First degree AV block due to occlusion of the RCA with involvement of the AV node is usually transient, generally resolving in five to seven days and requiring no therapy First degree AV block • Occlusion of the left circumflex artery may affect the AV node directly in the 10 percent of individuals in whom it supplies the AV node. • Less commonly, anterior MI produces first degree AV block below the level of the AV node, a situation that should be suspected if first degree AV block occurs in the presence of a widened QRS complex. Second degree AV block • Inferior MI is typically associated with the more benign second degree AV block of the Wenckebach type (Mobitz type I ) . Mobitz type II is uncommon in this setting, generally occurring with anterior MI. • Mobitz type I block is usually transient, resolving in most cases within five days. Third degree AV block • CHB with inferior MI generally results from an intranodal lesion. It is associated with a narrow QRS complex, and develops in a progressive fashion from first to second to third degree block. • It often results in an asymptomatic bradycardia (40 to 60 beats/min) and is usually transient, resolving within five to seven days. Left bundle branch block • LBBB is more common with anterior than inferior MI. It is often recognized by the morphology of a wide complex slow escape rhythm that results from a bradycardiadependent, longitudinal dissociation of conduction in the bundle of His . • The development of LBBB is also important because it can complicate the electrocardiographic diagnosis of MI. Anterior Wall MI • Patients with anterior and anteroseptal infarctions most often have occlusion of the left main coronary artery, the proximal LAD, and the LAD-derived branches. AVBs that develop in this setting respond poorly to therapy, and these patients have a poor prognosis. • The development of conduction disturbances in or below the bundle of His in association with acute MI is a specific marker for a very proximal occlusion of the LAD and therefore indicates that a large area of the left ventricle is in jeopardy. There is a poor prognosis for patients with an acute MI and conduction disturbances below the AV node. • High degree AV block associated with anterior MI is more often located below the AV node. It is usually symptomatic and has been associated with a high rate mortality due in large part to greater loss of functioning myocardium.the degree of arrhythmic complications is directly related to the extent of infarction. • Patients with conduction disturbances occurring in the setting of anterior AMI most often do not respond to medical therapy (e.g., atropine or isoproterenol). Perfusion actually can be further impaired by the vasodilating effects of isoproterenol, without an accompanying increase in the escape rhythm rate. Ventricular pacing, either by the transcutaneous or transvenous routes, is required in compromised patients. The prophylactic presence of a ventricular pacer is encouraged in those patients who are hemodynamically stable on presentation. First degree AV block • Prolongation of the PR interval due to slowed AV nodal conduction is a rare complication of anterior MI, since the AV node is usually supplied by the RCA. However, AV nodal conduction delay can occur in the 10 percent of individuals in whom the AV node is supplied by the left circumflex artery. • More often, first degree AV block in anterior MI is due to involvement of the conducting system below the level of the AV node. In this setting, there is usually widening of the QRS complex beyond 0.12 sec Second degree AV block • Second degree AV block with anterior MI is usually at the level of the AV node or below and is almost exclusively a Mobitz type 2 block. Complete AV block • CHB with anterior MI generally occurs abruptly in the first 24 hours. It can develop without warning or may be preceded by the development of RBBB with either a LAFB or LPFB (bifascicular or trifascicular block). • The escape rhythm is wide and unstable and the event is associated with a high mortality from both arrhythmias and pump failure. Heart block in this setting is thought to result from extensive necrosis that involves the bundle branches traveling within the septum. Fascicular blocks • Left anterior fascicular block occurs in approximately 5% of patients with acute myocardial ischemia; left posterior fascicular block is less frequently observed (incidence < 0.5%). The most common type of sub-AV nodal conduction disturbance following an LAD occlusion proximal to the first septal branch is right bundle branch block (RBBB) (QRS width ≥0.12 s) with or without left fascicular block. This disturbance is much more common than the development of complete left bundle branch block (LBBB). Fascicular blocks • When RBBB is the result of the MI, the prognosis is ominous, especially when accompanied by left fascicular block. When a patient presenting with acute MI also has RBBB, discerning whether the block was already present before the MI or was caused by the infarction is important with regard to the prognosis. When the RBBB was preexisting, hospital mortality rate was no different from that of patients without RBBB. In contrast, RBBB that results from an MI (typically, a very proximal LAD occlusion) indicates a poor prognosis. Post Operative Conduction Disturbances • The risk of developing conduction disturbances after coronary bypass grafting (CABG) or valvular surgery has been well established in previous studies, leading to permanent pacemaker implantation in about 2% to 3% of patients, and in 10% of patients undergoing repeat cardiac surgery. • The presence of a preoperative LBBB, concomitant LV aneurysmectomy and age > 64 years are as independent predictors of severe and prolonged postoperative bradyarrhythmias, mainly complete heart block. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with postoperative AV block that is not expected to resolve after cardiac surgery. Treatment Treatment strategies include: • Medical(atropine,isopretrenole,etc.) • Revascularization(primary PCI,CABG,etc.) • Pacemaker Implantation(temporary and permanent pacemakers) • Conduction abnormalities at the AV nodal level with second-degree or worse AV conduction disturbances in acute MI stresses the importance of early reperfusion, preferably via percutaneous coronary intervention. ACC/AHA/HRS Recommendations for Permanent Pacing After the Acute Phase of Myocardial Infarction Class I • Permanent ventricular pacing is indicated for persistent second-degree AV block in the HisPurkinje system with alternating bundlebranch block or third-degree AV block within or below the His-Purkinje system after STsegment elevation myocardial infarction. Class I • Permanent ventricular pacing is indicated for transient advanced second- or third-degree infranodal AV block and associated bundlebranch block. If the site of block is uncertain, an electrophysiological study may be necessary. Class I • Permanent ventricular pacing is indicated for persistent and symptomatic second- or thirddegree AV block. Class IIb • Permanent ventricular pacing may be considered for persistent second- or thirddegree AV block at the AV node level, even in the absence of symptoms. Class III • Permanent ventricular pacing is not indicated for transient AV block in the absence of intraventricular conduction defects. Class III • Permanent ventricular pacing is not indicated for transient AV block in the presence of isolated left anterior fascicular block. Class III • Permanent ventricular pacing is not indicated for new bundle-branch block or fascicular block in the absence of AV block. Class III • Permanent ventricular pacing is not indicated for persistent asymptomatic first-degree AV block in the presence of bundle-branch or fascicular block.