Download The Incidence of Symptomatic Bradyarrhythmias in Patients with

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.