Download Management of Cardiac Arrhythmias in Post

Management of Cardiac Arrhythmias in Post-PCI Patients
B. GORENEK
Introduction
Percutaneous coronary interventions (PCI) have been the fastest growing
major invasive procedure in the past decade. Accompanying the obvious
benefit, there are certain risks, including cardiac arrhythmias. A variety of
arrhythmias and conduction disturbances can occur during PCI. In general,
lethal ventricular arrhythmias, including serious ventricular tachycardia
(VT) and ventricular fibrillation (VF), have been reported to occur in
1.5–4.4% of the patients undergoing coronary angioplasty. The frequency of
these arrhythmias after primary PCI was analysed in data on 3065 patients
from Primary Angioplastic in Myocardial Infarction (PAMI) trials [1].
Ventricular arrhythmias occurred in 133 patients (4.3%). Smoking, lack of
preprocedural beta-blockers, shorter time from symptom onset to arrival in
emergency room initial thrombolysis in myocardial infarction (TIMI) flow
grade 0, and right coronary artery-related infarct were variables independently associated with a risk of serious ventricular arrhythmias. These
patients had higher rates of complications including cardiopulmonary resuscitation and intubation in the catheterisation laboratory, but had similar frequencies of major adverse cardiac events in hospital and at 1 year.
These arrhythmias may be the result of excessive catheter manipulation,
intracoronary dye injection, new ischaemic events, or reperfusion injury.
Role of Dye Injection and Intracoronary Solutions
Various contrast media have been developed for use in coronary angiography and PCI. These contrast media may be divided into ionic contrast media
Cardiology Department, Osmangazi University, Eskisehir,Turkey
232
B. Gorenek
of high osmolarity, those of low osmolarity, and non-ionic contrast materials. The risk of ventricular arrhythmia from intracoronary dye is greatest
with the injection of ionic contrast agents into the right coronary artery, particularly in the setting of prolonged injection or a damped pressure tracing.
VF may occur if dye is allowed to remain static in the coronary tree. The
incidence of VF during PCI can be significantly decreased by using lowosmolarity non-ionic contrast media lacking calcium-binding additives.
However, in some reports, contrary to the current belief in the overall safety
of low-osmolarity ionic contrast agents compared with other agents in diagnostic coronary angiography procedures, such agents are associated with an
increased risk of sustained ventricular arrhythmias [2].
VF is a serious complication during induction of hypothermia for surgical purposes [3]. In a study published 2 years ago, six patients were found to
have VF during intracoronary saline, heparin, contrast medium, or nitrate
delivery [4]. These medications did not warm up to body temperature.
Immediate intracoronary flush would result in local hypothermia. Thus, to
decrease the risk of VF, warmed-up fluid and warmed-up iso-osmolar nonionic contrast agents must be preferred, especially in patients undergoing
PCI on the right coronary artery.
Management of Ventricular Premature Beats
The first period of ventricular premature beats, which usually heralds malignant arrhythmias during acute coronary occlusion, develops after a quiescent period of 1.5–2.5 min and reaches a peak at 5 min. Both re-entrant and
non-re-entrant mechanisms contribute to the development of premature
beats and malignant ventricular arrhythmias during the early phase of
myocardial ischaemia. Complex premature ventricular contractions and
occasional non-sustained ventricular tachycardia are seen after 2–3% of
apparently uncomplicated angioplasty procedures. These arrhythmias usually abate over 12–36 h and do not, in general, require treatment. However,
hypokalaemia and hypomagnesaemia should be ruled out because potassium and magnesium may be depleted by diuretic-induced diuresis and may
need to be replaced [5].
Arrhythmias Related to Ischaemia
Acute myocardial ischaemia often results in malignant arrhythmias owing to
both the direct effects of ischaemia and the resultant haemodynamic compromise during PCI. Some of the most refractory ventricular ectopy is seen
Management of Cardiac Arrhythmias in Post-PCI Patients
233
in the setting of profound transmural ischaemia or early myocardial infarction. Venticular fibrillation due to acute ischaemia is a not infrequent complication of PCI. As in diagnostic coronary angiography, it is readily treated
by defibrillation and death rarely results. There appears to be no relation to
the severity of coronary artery disease, and the cause is partially related to
the use of contrast agents or post-PCI complications.
Arrhythmic Complications and Patient Characteristics
Vessel calibre is one of the important factors in the genesis of arrhythmias in
PCI. Huang et al. observed that a small calibre of the right coronary artery
and associated ST segment changes played important roles in the patients
who experienced VF during the PCI. They suggested that the cause of acute
ischaemia might be the size of the guiding catheter. Most of the catheters
they used in patients with VF were 7F, except in two cases where a 6F
catheter was used. So, small-size catheters should be preferred especially in
high-risk patients [4].
The risk of cardiac arrhythmias in PCI is more pronounced in patients
with heart failure. Three years ago, DeGeare et al. investigated the predictive
value of Killip classification in patients undergoing primary PCI for acute
myocardial infarction. Killip classification predicted the incidence of
arrhythmias in those patients. This classification was a predictor of mortality in their study. Killip classification on hospital admission was a simple and
useful independent predictor of in-hospital and 6-month mortality in
patients with acute myocardial infarction who were undergoing primary PCI
[6].
Importance of QT Dispersion and Heart Rate Variability
QT dispersion may serve as a measure of variability in ventricular recovery
time and may be a means of identifying patients at risk of lethal ventricular
arrhythmias and sudden death with coronary artery disease. Ashikaga et al.
showed that increased QTc dispersion may predict the risk of lethal ventricular arrhythmias during angioplasty. The fact that successful angioplasty
decreased QTc dispersion indicates that part of increased QTc dispersion is
related to myocardial ischaemia in patients with coronary artery disease [7].
Thus, in patients with QTc dispersion we should be alert for serious ventricular arrhythmias. Nicorandil may precondition the myocardium and may
prevent the occurrence of ventricular arrhythmias after coronary angioplasty by suppressing the increase in QT dispersion [8].
234
B. Gorenek
Abrupt coronary occlusion may cause a wide range of autonomic reactions as evidenced by changes in heart rate, blood pressure, and heart rate
variability (HRV). Coronary occlusion-induced increase in HRV seems to
have a protective effect against the occurrence of complex ventricular
arrhythmias during the early stage of abrupt coronary occlusion, suggesting
that vagal activation may modify the outcome of acute coronary events with
coronary artery disease [9].
Reperfusion Arrhythmias
Reperfusion arrhythmias may be one of the manifestations of reperfusion
injury. These arrhythmias are common in patients undergoing PCI, which
include accelerated idioventricular rhy thms, VT, and VF. Reperfusion
arrhythmias, in addition to their importance as a marker of successful reperfusion, need special attention because haemodynamics may rapidly deteriorate during VT or VF.
Intracellular calcium overload is believed to play a critical role in the
development of reperfusion arrhythmias. Accumulation of calcium in the cell
causes damage to the respiratory chain and decreases ATP production, leading to depletion of mitochondrial energy [10]. The oxygen paradox is closely
linked to the calcium overload or calcium paradox, since oxygen mediates the
uptake of calcium by mitochondria [11]. Oxygen also leads to cell damage
during reperfusion through the formation of oxygen radicals [12]. The role of
free radicals in the genesis of reperfusion arrhythmias is uncertain. Free-radical-induced damage occurs in the 10 min after reperfusion [13]. Reduced
levels of free radical scavengers have been observed within 3 h of angioplasty
in patients with acute myocardial infarction [14].
Some strategies may be helpful for the prevention and treatment of
reperfusion arrhythmias, but their beneficial affects are limited. Today we
know a little about the effectiveness of antioxidant therapy. The results have
largely been mixed and the investigation remains focused at the animal level.
Magnesium can be a choice, but there are conflicting data on its benefit.
Numerous studies have examined the efficacy of vasodilators as cardioprotective agents in ischaemic reperfusion injury. Intracoronary adenosine and
papaverine may be effective as cardioprotective agents. Human studies with
papaverine have also demonstrated success in improving angiographically
documented TIMI flow grades in epicardial arteries [15]. Calcium channel
blockers may block intracellular calcium overload and have positive effects
on vascular flow. The effects have been demonstrated during the administration of nifedine and verapamil [16]. Two years ago Yoshida et al. showed that
administration of dipyridamole can prevent and terminate reperfusion
Management of Cardiac Arrhythmias in Post-PCI Patients
235
arrhythmias such as accelerated idioventricular rhythms and VT. They concluded that cAMP-mediated triggered activity may, at least in part, be
responsible for reperfusion arrhythmias [17].
Role of Inhibition of the Renin–Angiotensin–Aldosterone System
In the normal heart, locally derived angiotensin II may modulate coronary
blood flow, inotropy, and chronotropy [18–21], whereas under pathological
conditions the renin–angiotensin–aldosterone system (RAS) may influence
ventricular growth and myocardial metabolism, induce ventricular arrhythmias during ischaemia and reperfusion injury, and contribute to post-infarction ventricular remodelling [22]. We also know that bradykinin accumulation
is a potent cardioprotective mechanism underlying RAS inhibition in
ischaemia and reperfusion injury. A role for RAS in reperfusion arrhythmias
was suggested by studies in angiotensin II type 1a receptor knockout mice
which, compared to wild-type mice, showed less reperfusion arrhythmia
despite a similar infarct size. In addition, administration of a selective
angiotensin II type 1 receptor before ischaemia blocked reperfusion arrhythmias [23]. An experimental study showed us that losartan attenuates myocardial ischaemia-induced ventricular arrhythmias and reperfusion injury in
hypertension, and may be useful in the treatment of ventricular arrhythmias
induced by acute myocardial infarction and attenuation of reperfusion injury
[24]. Intracoronary enalaprilat infusion in the infarct-related artery is feasible
in the setting of primary angioplasty and is safe and well tolerated [25].
Effective cardiac RAS inhibition can be achieved by low-dose intracoronary
enalaprilat, which primarily causes a potentiation of bradykinin [25].
Preconditioning and Arrhythmias
The incidence of serious ventricular arrhythmias in the presence of intracoronary thrombus was high in a report [26]. Sudden obstruction of the
coronary artery without pre-existing coronary artery narrowing was associated with a higher incidence of VF than was obstruction occurring in association with pre-existing stenoses [26]. The profibrillatory effect of thrombus
was not detectable in another report. Experimental studies have suggested
that the phenomenon of ischaemic preconditioning may increase the VF
threshold [27] and reduce the incidence of ischaemic and reperfusion
arrhythmias [28]. The mitochondrial KATP channel seems to be important
in prevention of myocardium by preconditioning. A study in dogs suggests
that preconditioning may exert an antiarrhythmic effect during ischaemia by
236
B. Gorenek
modifying cardiac autonomic receptor mechanisms, which results in an
improved parasympathetic balance. A preceding short vessel occlusion–
reperfusion cycle increases the electrical stability of ischaemic myocardium,
so the repeated coronary artery occlusions during PCI protect against
ischaemia-induced ventricular arrhythmias [29].
Benefits of Intra-aortic Balloon Counterpulsation
Intra-aortic balloon counterpulsation (IABC) has been used following primary PCI in high risk patients in an attempt to improve outcomes by
increasing coronary blood flow reserve, decreasing preload and afterload,
and augmenting systemic pressure [30]. In high risk patients prophylactic
use of IABC may decrease the incidence of VF, especially in patients with
cardiogenic shock [30]. Intra-aortic balloon counterpulsation used before
primary PCI provides benefit to patients with cardiogenic shock by reducing
the incidence of catheterisation laboratory events, including VT. So, we recommend the use of IABC in patients with cardiogenic shock who are undergoing primary PCI.
Supraventricular Arrhythmias and Atrial Fibrillation
Supraventricular arrhythmias including atrial fibrillation (AF) may be
induced by PCI, but they are not as frequent as ventricular arrhythmias.
However, AF especially has prognostic significance in patients treated with
PCI. Because the patency of infarct-related artery is better, primary PCI is
superior to thrombolytic therapy in restoring sinus rhythm in patients with
acute myocardial infarction who have developed AF [31].
Kinjo et al. investigated the prognostic significance of AF and atrial flutter in patients with acute myocardial infarction treated with PCI. In their
study, the patients with AF were older, were in higher Killip classes, had
higher rates of previous myocardial infarction and previous cerebrovascular
accident, had systolic blood pressure of less than 100 mmHg and heart rates
of 100 beats/min or more, were less likely to smoke, and had a higher prevalence of multivessel disease and poorer reperfusion of infarct-related artery
than those without AF. Atrial fibrillation was a common complication in
patients with acute myocardial infarction who are treated with PCI and independently influenced 1-year mortality, they said [32].
Atrial fibrillation during PCI tends to revert spontaneously over a period
of minutes to hours, but may require additional therapy if it produces
ischaemia or haemodynamic instability. Intravenous beta-blockers (e.g.
Management of Cardiac Arrhythmias in Post-PCI Patients
237
esmolol, metoprolol), calcium channel blockers (e.g. verapamil), or digoxin
may be given and up-titrated until adequate control of ventricular response
is achieved. Electrical cardioversion is rarely required.
Conduction Defects and Heart Blocks
New conduction defects occur in about 0.9% of the patients undergoing
coronary angioplasty [33]. Of these, right bundle branch block was the most
common, followed by first-degree atrioventricular block. These defects
almost always disappeared without treatment before the time of hospital discharge, but occasionally required the elimination of drugs depressing cardiac activity [5].
When complete heart block develops, atropine is rarely helpful in the setting of inadequate escape and deterioration, but should be given anyway.
Coughing may help support the circulation and maintain consciousness
while a temporary pacing catheter is inserted.
Conclusions
Either ventricular or atrial arrhythmias or conduction disturbances can be
observed during PCI. Some of them occur as a complication of the procedure, but many of the arrhythmias are related to reperfusion injury. The
patient’s characteristics, the type of the procedure, the features of the target
vessel and the type of the lesion play an important role in the occurrence of
arrhythmias. The majority of the arrhythmias tend to revert spontaneously,
but when necessary, special treatment must be given promptly.
References
1.
2.
3.
4.
Mehta RH, Harjai KJ, Grines L et al (2004) Sustained ventricular tachycardia or
fibrillation in the cardiac catheterisation laboratory among patients receiving primary percutaneous coronary intervention: incidence, predictors, and outcomes. J
Am Coll Cardiol 43:1765–1772
Hajj-Ali R, Ezzeddine R, Jadonath R et al (2001) Use of low-osmolar ionic contrast
agents increases the risk of sustained ventricular arrhythmias during diagnostic
coronary angiography. Am J Cardiol 88 (5A): TCT298 Suppl.
Kearns JB, Murnaghan MF (1969) Ventricular fibrillation during hypothermia. J
Physiol Lond, 203(1):51P-53P
Huang JL, Ting CT, Chen YT, Chen SA (2002) Mechanisms of ventricular fibrillation during coronary angioplasty: increased incidence for the small orifice caliber
of the right coronary artery. Int J Cardiol 82:221–228
238
B. Gorenek
5.
Ellis SG (1994) Elective coronary angioplasty: technique and complications. In:
Topol EJ (ed) Textbook of interventional cardiology. Saunders, Philadelphia, pp
186–206
DeGeare WS, Boura JA, Grines LL et al (2001) Predictive value of the Killip classification in patients undergoing primary percutaneous coronary intervention for
acute myocardial infarction. Am J Cardiol 87:1035–1038
Ashikaga T, Nishizaki M, Arita M et al (1998) Increased QTc dispersion predicts
lethal venticular arrhythmias complicating coronary angioplasty. Am J Cardiol
82:814–816
Kato T, Kamiyama T, Maruyama M et al (2001) Nicorandil, a potent cardioprotective agent, reduces QT dispersion during coronary angioplasty. Am Heart J
141:940–943
Airaksinen KE, Ylitalo A, Nimela MJ et al (1999) Heart rate variability and occurrence of ventricular arrhythmias during balloon occlusion of a major coronary
artery. Am J Cardiol 83:1000–1005
Matsuma K, Jeremy RW, Schaper J et al (1998) Progression of myocardial necrosis
during reperfusion of ischemic myocardium. Circulation 97:795–804
Opie LH, Coetzee WA ( 1988) Role of calcium ions in reperfusion arrhythmias:
Relevance to pharmacologic intervention. Cardiovasc Drugs Ther 2:623–636
Hearse DJ, Tosak A (1988) Free radicals and calcium. Simultaneous interacting triggers as determinants of vulnerability to reperfusion-induced arrhythmias in the
rat heart. J Mol Cell Cardiol 20:213–223
Ambrosio G, Weisfeldt ML, Jacobus WE et al (1987) Evidence for a reversible oxygen mediated component of reperfusion injury: reduction by recombinant human
superoxide dismutase administered at the time of reflow. Circulation 75:282–291
Lafont A, Marwick TH, Chisolm GM et al (1996) Decreased free radical scavengers
with reperfusion after coronary angioplasty in patients with acute myocardial
infarction. Am Heart J 1996 131:219–23
Ishihara M, Sato H, Tateishi H et al (1996) Attenuation of the no-reflow phenomenon after coronary angioplasty for acute myocardial infarction with intracoronary
papaverine. Am Heart J 132:959–963
Tillmanns H, Neumann FJ, Parekh et al (1990) Pharmacologic effects on coronary
microvessels during myocardial ischemia. Eur Heart J 11:B10–B15
Yoshida Y, Hirai M, Yamada T et al (2000) Arrhythmic efficacy of dipyridamole in
treatment of reperfusion arrhythmias. Circulation 101:624–630
Saito K, Gutkind JS, Saaverda JM (1987) Angiotensin II binding sites in the conduction system of rat hearts. Am J Physiol 253:1618–1622
Xiang JZ, Scholkens BA, Ganten D, Unger T (1984) Effects of sympathetic nerve stimulation is attenuated by the converting enzyme inhibitor Hoe 498 in isolated rabbit hearts. Clin Exp Hypertens 6:1853–1857
Xiang JZ, Linz W, Becker H et al (1985) Effects of converting enzyme inhibitors:
ramipril and enalapril on peptide action and sympathetic neurotransmission in
the isolated heart. Eur J Pharmacol 113:215–223
Rogers TB, Gaa ST, Allen IS (1986) Identification and characterization of functional
angiotensin II receptors on cultured heart myocytes. J Pharmacol Exp Ther
236:438–444
Dostal DE, Baker KM (1993) Evidence for a role of an intracardiac renin-angiotensin system in normal and failing hearts. Trends Cardiovasc Med 3:67–74
Harada K, Komuro I, Hayashi D et al (1998) Angiotensin II type 1a receptor is
involved in the occurrence of reperfusion arrhythmias. Circulation 97:315–317
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Management of Cardiac Arrhythmias in Post-PCI Patients
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
239
Lee YM, Peng YY, Ding YA et al (1997) Losartan attenuates myocardial ischemiainduced ventricular arrhythmias and reperfusion injury in spontaneously hypertensive rats. Am J Hypertens 10:852–858
Kurz T, Schafer U, Dendorfer A et al (2001) Effects of intracoronary low dose enalaprilat as an adjunct to primary percutaneous transluminal coronary angiography
in acute myocardial infarction. Am J Cardiol 88:1351–1357
Coronel R, Wilms-Schopman FJ, Janse MJ (1997) Profibrillatory effects of intracoronary thrombus in acute regional ischemia of the in situ porcine heart.
Circulation 96:3985–3991
Gulker H, Kramer B, Stephan K et al (1977) Changes in ventricular fibrillation threshold during regional short-term coronary occlusion and release. Basic Res Cardiol
72:547–562
Lawson CS, Hearse DJ (1996) Anti-arrhythmic protection by ischemic preconditioning in anesthetised dogs and rats. Cardiovasc Res 31:655–662
Airaksinen KEJ, Huikuri HV (1997) Antiarrhythmic effect of repeated coronary
occlusion during balloon angioplasty. J Am Coll Cardiol 29:1035–1038
Brodie BR, Stuckey TD, Hansen C et al (1999) Intra-aortic balloon counterpulsation before primary percutaneous transluminal coronary angioplasty reduces
catheterization laboratory events in high-risk patients with acute myocardial
infarction. Am J Cardiol 84:18–23
Gorenek B, Birdane A, Unalir A et al (2000) Restoring sinus rhythm in patients with
atrial fibrillation complicating acute myocardial infarction: comparison of outcomes of primary angioplasty and thrombolytic therapy (abstract). Eur J Heart Fail,
Suppl 1:32
Kinjo K, Sato H, Sato H et al (2003) Prognostic significance of atrial
fibrillation/atrial flutter in patients with acute myocardial infarction treated with
percutaneous coronary intervention. Am J Cardiol 92:1150–1154
Bredlau CE, Roubin GS, Leimgruber PP et al 81985) In-hospital mortality in
patients undergoing elective coronary angioplasty. Circulation 72:1044–1052