Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3793_Библиотеки_им_академика_М_И_Перельмана
.pdf
CHAPTER 16 Supraventricular and Ventricular Arrhythmias 173.e1
https://t.me/medicina_free
REFERENCES
1. Meltzer LE, Cohen HE. The incidence of arrhythmias associated
with acute myocardial infarction. In: Meltzer JE, Dunning AJ,
eds. Textbook of Coronary Care. Philadelphia: Charles Press;
1972.
2. Antman EM, Braunwald E. Acute myocardial infarction. In:
Braunwald E, ed. Braunwald’s Heart Disease: A Textbook of
Cardiovascular Medicine. 10th ed. Philadelphia: Saunders;
2015:1068–1094.
3. O’Doherty M, Taylor DI, Quinn E. Five hundred patients with
myocardial infarction monitored within one hours of symptoms.
BMJ. 1983;286:1405.
4. Pantridge JF, Adgey AAJ. Pre-hospital coronary care: the mobile
coronary care unit. Am J Cardiol. 1969;24:666–673.
5. Gorenek B, et al. Cardiac arrhythmias in acute coronary
syndromes: position paper from the joint EHRA, ACCA, and
EAPCI task force. EuroIntervention. 2015;10:1095–1108.
6. Nordrehaug JE. Malignant arrhythmia in relations to serum
potassium in acute myocardial infarction. Am J Cardiol.
1985;56:20D–23D.
7. Janse MJ, Opthof T. Mechanisms of ischemia-induced
arrhythmias. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology.
Philadelphia: Saunders; 2013:849–857.
8. Crimm A, Severance HW Jr, Coffey K, et al. Prognostic
significance of isolated sinus tachycardia during first three days
of acute myocardial infarction. Am J Med. 1984;76(6):983–988.
9. Norris RM, Mercer CJ, Yeates SE. Sinus rate in acute myocardial
infarction. British Heart J. 1972;34:901–904.
10. Desanetis RW, Block P, Hutter AD. Tachyarrhythmias in
myocardial infarction. Circulation. 1972;45:681–702.
11. Liberthson RR, Salisbury KW, Hutter AM, et al. Atrial
tachyarrhythmias in acute myocardial infarction. Am J Med.
1976;60:956–960.
12. Cristol N, Szwaeberg J, Gueron M. Supraventricular arrhythmias
in acute myocardial infarction. Ann Intern Med. 1975;82:35–39.
13. Berisso MZ, Carratino L, Ferroni A, et al. Frequency,
characteristics, and significance of supraventricular
tachyarrhythmias detected by 24-hour electrocardiographic
recording in the late hospital phase of acute myocardial
infarction. Am J Cardiol. 1990;65:1064–1070.
14. Serrano CV Jr, Ramires JAF, Mansur AP, et al. Importance of the
time of onset of supraventricular tachyarrhythmias on prognosis
of patients with acute myocardial infarction. Clin Cardiol.
1995;18:84–90.
15. Rechavia E, Strasberg B, Mager A, et al. The incidence of atrial
arrhythmias during inferior wall myocardial infarction with and
without right ventricular involvement. Am Heart J.
1992;124:387–391.
16. Zoni Berisso M, Ferroni A, De Caro E, et al. Clinical significance
of supraventricular tachyarrhythmias after acute myocardial
infarction. Eur Heart J. 1986;7:743–748.
17. Snyder DW, Jaffe AS. Acute myocardial infarction. In: Messerll
FH, ed. Cardiovascular Drug Therapy. Philadelphia: Saunders;
1990:36–57.
18. Goldstein JA, Vlahakes GJ, Verrier ED, et al. The role of right
ventricular systolic dysfunction and elevated intrapericardial
pressure in the genesis of low output in experimental right
ventricular infarction. Circulation. 1982;65:513–522.
19. Jewitt DE, Balcon R, Raferty EB, et al. Incidence and
management of supraventricular arrhythmias after acute
myocardial infarction. Lancet. 1967;2:734.
20. Klass M, Haywood LJ. Atrial fibrillation associated with acute
myocardial infarction: a study of thirty-four cases. Am Heart J.
1970;79:752.
21. James TN. Myocardial infarction and atrial arrhythmias.
Circulation. 1961;24:761.
22. Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in
acute myocardial infarction: a systematic review of the incidence,
clinical features and prognostic implications. Eur Heart J.
2009;30:1038–1045.
23. Jabre R, Roger VL, Murad MH, et al. Mortality associated with
atrial fibrillation in patients with myocardial infarction: a
systematic review and meta-analysis. Circiulation.
2011;123:1587–1593.
24. Helmers C, Lundman T, Mogenson L. Atrial fibrillation in acute
myocardial infarction. Acta Med Scand. 1973;193:39–44.
25. Luria MH, Knoke JD, Wachs JS. Survival after recovery from
acute myocardial infarction: two- and five-year prognostic
indices. Am J Med. 1979;67:7–14.
26. Luria MH, Knoke JD, Margolis RM, et al. Acute myocardial
infarction: prognosis after recovery. Ann Intern Med.
1976;85:561–565.
27. January CT, et al. 2014 AHA/ACC/HRS Guideline for the
Management of Patients with Atrial Fibrillation: Executive
Summary. J Am Coll Cardiol. 2014;64(21):2246–2280.
28. Norris NM. Myocardial infarction. New York: Churchill
Livingstone; 1982.
29. Meesmann W. Early arrhythmias and primary ventricular
fibrillation after acute myocardial ischemia in relation to
pre-existing coronary collaterals. In: Paratt JR, ed. Early
Arrhythmias Resulting from Myocardial Ischemia. London:
Macmillan; 1982:93–112.
30. Skinner JE, Lie JT, Entman MI. Modification of ventricular
fibrillation latency following coronary artery occlusion in the
conscious pig: the effects of psychological stress and
B-adrenergic blockade. Circulation. 1975;51:656–667.
31. Harris AS. Delayed development of ventricular ectopic rhythms
following experimental coronary occlusion. Circulation.
1950;1:1318–1328.
32. Vegh A, Komoro S, Szekeres L, et al. Antiarrhythmic effects of
preconditioning in anesthetized dogs and rats. Cardiovasc Res.
1992;26:487–495.
33. Scherlag BJ, Ope RR, Williams DO, et al. Mechanisms of ectopic
rhythm formation due to myocardial ischemia: effects of heart
rate and ventricular premature beats. In: Wellens HJJ, Lie KI,
Janse MJ, eds. The Conduction System of the Heart. Philadelphia:
Lea & Febiger; 1976:633–649.
34. Kjekshus JK. Importance of heart rate in determining B-blocker
efficacy in acute and long-term acute myocardial infarction
intervention trials. Am J Cardiol. 1986;57:43F–49F.
35. Harris AS, Otero H, Bocage AJ. The induction of arrhythmias by
sympathetic activity before and after occlusion of the coronary
artery in the canine heart. J Electrocardiol. 1971;4:34–43.
36. Schwartz PJ, Stone HL. The role of the autonomic nervous
system in sudden cardiac death. Ann N Y Acad Sci.
1982;382:162–180.
37. Bloor CM, Ehsani A, White FC, et al. Ventricular fibrillation
threshold in acute myocardial infarction and its relation to
myocardial infarct size. Cardiovasc Res. 1975;9:463.
38. Geltman EM, Ehsani AA, Campbell MK, et al. The influence
of location and extent of myocardial infarction on long-term
ventricular dysrhythmia and mortality. Circulation.
1979;60:805.
173.e2 PART III Coronary Artery Disease
https://t.me/medicina_free
39. Roque F, Amuschastegul LM, Lopez Morillos MA, et al.
Beneficial effects of infarct size and late ventricular tachycardia
in patients with myocardila infarction. Circulation. 1979;76:610.
40. Lombardi F, Sandrone G, Pernpruner S, et al. Heart rate
variability as an index of sympathovagal interaction after acute
myocardial infarction. Am J Cardiol. 1987;60:1239–1245.
41. Kleiger RE, Miller P, Bigger TJ, Moss AJ. Decreased heart rate
variability and its association with increased mortality after acute
myocardial infarction. Am J Cardiol. 1987;59:256–262.
42. Carlson MD, Smith ML, Thames MS. Autonomic influences on
arrhythmia development. Prog Cardiol. 1992;51:59–72.
43. Corr PB, Gills GA. Autonomic neural influences on the
dysrhythmias resulting from myocardial infarction. Circ Res.
1978;43:1.
44. Nordrehaug JE, Johannessen KA, von der Lippe G. Serum
potassium as an independent risk factor of ventricular
arrhythmias in AMI. Circulation. 1985;71:645–649.
45. Carmeliet E. Cardiac ionic currents and acute ischemia: from
channels to arrhythmias. Physiol Rev. 1999;79:917–1017.
46. Echt DS, Liebson PR, Mitchell LB, et al. and the CAST
Investigators. Mortality and morbidity in patients receiving
encainide, flecainide, or placebo: the Cardiac Arrhythmia
Suppression Trial. N Engl J Med. 1991;324:781–788.
47. Weinberg B, Zipes D. Strategies to manage the post-MI patient
with ventricular arrhythmias. Clin Cardiol. 1989;12(supplII):86.
48. Lown B, Fakhro A, Hood WB, et al. The coronary care unit: new
perspectives and directions. JAMA. 1981;199:188.
49. Lee KJ, Wellens HJJ, Dorsnar E, et al. Observations on patients
with primary ventricular fibrillation complicating acute
myocardial infarction. Circulation. 1975;52:755.
50. El-Sherif N, Myerburg RJ, Scherlag BJ, et al. Electrocardiographic
antecedents of primary ventricular fibrillation: value of R-on-T
phenomenon in myocardial infarction. Br Heart J. 1976;38:415.
51. Lawrie DM, Higgins MR, Godman MJ, et al. Ventricular
fibrillation complicating acute myocardial infarction. Lancet.
1968;2:523.
52. Bennett MA, Pentecost BL. Warning of cardiac arrest due to
ventricular fibrillation and tachycardia. Lancet. 1972;1:1351.
53. Roberts R, Ambos HD, Loh CW, et al. Initiation of repetitive
ventricular depolarization by relatively late premature complexes
in patients with acute myocardial infarction. Am J Cardiol.
1978;41:678.
54. Wellens JJ, Frits WM, Liew KI. The value of the
electrocardiogram in the differential diagnosis of a tachycardia
with a widened QRS complex. Am J Med. 1978;64:27–33.
55. Brugada P, Brugada J, Mont L, et al. A new approach to the
differential diagnosis of a regular tachycardia with a wide QRS
complex. Circulation. 1991;83:1649–1659.
56. Kleinman RB, Miller JM, Buxton AE, et al. Prognosis following
sustained ventricular tachycardia occurring early after
myocardial infarction. Am J Cardiol. 1988;62:528.
57. El-Sherif N, Gough WB, Restivo M. Reentrant ventricular
arrhythmias in the late myocardial infarction period: mechanism
by which a short-long-short cardiac sequence facilitates the
induction of reentry. Circulation. 1991;83:268.
58. Bigger JT Jr, Weid FM, Rolnitzky LM. Prevalence, characteristics
and significance of ventricular tachycardia (three or more
complexes) detected with ambulatory electrocardiographic
recording in the late hospital phase of acute myocardial
infarction. Am J Cardiol. 1981;48:815.
59. Restivo M, Gough WB, El-Sherif N. Ventricular arrhythmias in
the subacute myocardial infarction period: High-resolution
activation and refractory patterns of reentrant rhythms. Circ Res.
1990;66:1310–1327.
60. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA
Guideline for the management of ST-elevation myocardial
infarction: executive summary: a report of the ACCF/AHA
Task Force on Practice Guidelines. Circulation.
2013;127(4):529–555.
61. Wolfe CL, Nibley C, Bhandari A. Polymorphous ventricular
tachycardia associated with acute myocardial infarction.
Circulation. 1991;84:1543–1551.
62. Birbnaum Y, Sclarovsky S, Ben-Ami R, et al. Polymorphous
ventricular tachycardia early after acute myocardial infarction.
Am J Cardiol. 1993;71:745–748.
63. Bezzina CR, et al. Genome-wide association study identifies a
susceptibility locus at 21q21 for ventricular fibrillation in acute
myocardial infarction. Nat Genet. 2010;42:688–691.
64. Behar S, Goldbourt U, Peicher-Reiss H, et al. Prognosis of acute
myocardial infarction complicated by primary ventricular
fibrillation. Principal investigators of the SPRINT study. Am J
Cardiol. 1990;66:1208–1211.
65. Norris RM, Singh BN. Arrhythmias in acute myocardial
infarction. In: Norris RM, ed. Myocardial Infarction. Edinburgh:
Churchill Livingstone; 1982:55–86.
66. Gorgels AOM, Vos MA, Letsch IS, et al. Usefulness of the
accelerated idioventricular rhythm as a marker for myocardial
necrosis and reperfusion during thrombolytic therapy in acute
myocardial infarction. Am J Cardiol. 1988;61:231.
67. Kaplinsky E, Ogawa S, Michelson EL, et al. Instantaneous and
delayed ventricular arrhythmias after reperfusion of acutely
ischemic myocardium: evidence for multiple mechanisms.
Circulation. 1981;63:333–340.
68. Ferrier GR, Moffat MP, Kukas K. Possible mechanisms of
ventricular arrhythmias elicted by ischemia followed by
reperfusion: studies on isolated canine ventricular tissue. Circ
Res. 1985;65:184–194.
69. Lichstein E, Ribas-Meneclier C, Gupta PK, et al. Incidence
and description of accelerated ventricular rhythm
complicating acute myocardial infarction. Am J Med.
1975;58:192.
70. De Soyza N, Bissett BK, Kane J, et al. Association with
accelerated idioventricular rhythm and paroxysmal ventricular
tachycardia in acute myocardial infarction. Am J Cardiol.
1974;34:667.
71. ACC/AHA/ESC 2006 guidelines for management of patients
with ventricular arrhythmias and the prevention of sudden
cardiac death: a report of the American College of Cardiology/
American Heart Association Task Force and the European
Society of Cardiology Committee for Practice Guidelines. J Am
Coll Cardiol. 2006;48:e247–e346.
72. Dunn HM, McComb JM, Kinney CD, et al. Prophylactic
lidocaine in the early phase of suspected myocardial infarction.
Am Heart J. 1983;110:353.
73. Wyse DG, Kellen J, Rademaker AW. Prophylactic versus selective
lidocaine for early ventricular arrhythmias of myocardial
infarction. J Am Coll Cardiol. 1998;12:507.
74. Hine LK, Laird N, Hewitt P, et al. Meta-analytic evidence against
prophylactic use of lidocaine in the coronary care unit. Clin
Pharmacol Ther. 1986;40:71.
75. Russo AM, Beauregard LAM, Waxman HL. Oral amiodarone
loading for the rapid treatment of frequent, refractory, sustained
ventricular arrhythmias associated with coronary artery disease.
Am J Cardiol. 1993;72:1395–1399.
CHAPTER 16 Supraventricular and Ventricular Arrhythmias 173.e3
https://t.me/medicina_free
76. Evans SJ, Myers M, Zaher C, et al. High dose oral amiodarone
loading: electrophysiologic effects and clinical tolerance. J Am
Coll Cardiol. 1992;19:169–173.
77. Kalbfleisch SJ, Williamson B, Ching Man K, et al. Prospective,
randomized comparison of conventional and high dose loading
regimens of amiodarone in the treatment of ventricular
tachycardia. J Am Coll Cardiol. 1993;2:1723–1729.
78. Scheinman MM, Levine JH, Cannom DS, et al. Dose-ranging
study of intravenous amiodarone in patients with lifethreatening ventricular tachyarrhythmias. The Intravenous
Amiodarone Multicenter Investigators Group. Circulation.
1995;92:3264–3272.
79. Lee TH, Goldman L. The coronary care unit turns 25: historical
trends and future directions. Ann Intern Med. 1988;108:887.
80. Bigger JT Jr. Prophylactic use of implanted cardiac defibrillators
in patients at high risk for ventricular arrhythmias after
coronary-artery bypass graft surgery. Coronary Artery Bypass
Graft (CABG) Patch Trial Investigators. N Engl J Med.
1997;337:1569–1575.
81. Hohnloser SH, Kuck KH, Dorian P, et al. Prophylactic use of an
implantable cardioverter-defibrillator after acute myocardial
infarction. N Engl J Med. 2004;351:2481–2488.
82. Steinbeck G, Andresen D, Seidl K, et al. Defibrillator
implantation early after myocardial infarction. N Engl J Med.
2009;361:1427–1436.
83. Russo AM, Stainback RF, Bailey SR, et al. ACCF/HRS/AHA/ASE/
HFSA/SCAI/SCCT/SCMR 2013 Appropriate Use Criteria for
Implantable Cardioverter-Defibrillators and Cardiac
Resynchronization Therapy: a report of the American College of
Cardiology Foundation Appropriate Use Criteria Task Force,
Heart Rhythm Society, American Heart Association, American
Society of Echocardiography, Heart Failure Society of America,
Society for Cardiovascular Angiography and Interventions,
Society of Cardiovascular Computed Tomography, and Society
for Cardiovascular Magnetic Resonance. J Am Coll Cardiol.
2016;61(12):1318–1368.
84. Buxton AE, Kerry LL, Fisher JD, et al; for the Multicenter
Unsustained Tachycardia Trial Investigators. A Randomized
Study of the Prevention of Sudden Death in Patients with
Coronary Artery Disease. N Engl J Med. 1999;341:1882–1890.
17
https://t.me/medicina_free
Conduction Disturbances in Acute
Myocardial Infarction
David L. Brown
OUTLINE
Anatomy, 174
Incidence, 174
Specific Conduction Abnormalities, 175
Sinoatrial Node, 175
Sinus Bradycardia, 175
Sinoatrial Block and Sinus Arrest, 175
Atrioventricular Node, 175
Infranodal Conduction Abnormalities, 175
Inferior Wall Versus Anterior Wall Myocardial
Infarction, 176
Mortality, 176
Management, 177
Temporary Transvenous Pacing, 177
Guidelines for Permanent Pacemaker
Placement, 177
Infarction or ischemia of myocardial conduction tissue and/or
autonomic imbalance that results in altered conduction through
the heart can dramatically alter the presentation, management,
and outcomes of patients presenting with an acute myocardial
infarction (MI). Immediate recognition of conduction disturbances in the acute phase of MI is of prognostic and therapeutic
significance. The nature of any conduction disturbance not only
gives clues to the location of the infarct, but also aids in prioritizing the management of MI, including, but not limited to, the
potential need for temporary pacemaker support.
ANATOMY
The sinus node, sinoatrial conduction system, atrioventricular
(AV) node, bundle of His, right bundle, left bundle dividing into
anterior and posterior fascicles and myocardial Purkinje fibers
form the cardiac conduction system (Fig. 17.1). The bundle of
His divides into the right and left bundle branches after leaving
the AV node. The right bundle traverses the right side of the
interventricular septum without giving off branches for most
of its course. Ultimately, it branches near the base of the right
anterior papillary muscle with fascicles supplying the septal and
free wall of the right ventricle. The left bundle divides into several
discrete branches after penetrating the membranous septum
under the aortic valve. The anterior fascicle crosses the left
ventricular outflow tract and terminates in the Purkinje system
of the anterolateral wall of the left ventricle. The posterior fascicle
courses inferiorly and posteriorly. The septum is activated earliest
in all hearts by either a discrete septal fascicle or branches of
the posterior fascicle.
1–4
The sinoatrial node is supplied by the atrial branch of the
proximal right coronary artery (RCA) in 55% of cases and by
the proximal left circumflex coronary artery (LCX) in 45% of
cases.5 The RCA perfuses the AV node and the proximal portion
of the His bundle in 90% of patients with perfusion originating
from the LCX in the remaining 10%. The septal branches of the
left anterior descending coronary artery (LAD) supply the distal
part of the His bundle, the right bundle branch, and the anterior
fascicle of the left bundle branch. The proximal portion of
posterior fascicle of the left bundle is supplied by the AV nodal
artery or by septal branches of the LAD. The distal portion is
supplied by septal branches from the LAD coronary artery
and RCA.
INCIDENCE
The overall incidence of new conduction disturbances, including
bundle branch and fascicular block, during acute MI is difficult
to accurately determine because these abnormalities may often
be chronic and unrelated to the acute presentation. The National
Registry of Myocardial Infarction 2 (NRMI-2) evaluated the
incidence of bundle branch block in 297,832 patients admitted
to a hospital in the United States with an acute MI between 1994
and 1997: 6.7% of patients had a left bundle branch block (LBBB)
and 6.2% had a right bundle branch block (RBBB) on the initial
electrocardiogram (ECG).6 A similar rate of LBBB (9%) was
noted in a prospective analysis of over 88,000 acute MI patients
in Sweden.7 Since both series only assessed the presence of a
bundle branch block (BBB) on the initial ECG, these data provide
no information on the incidence of new conduction disease in
174
CHAPTER 17 Conduction Disturbances in Acute Myocardial Infarction 175
e
Right bundl
https://t.me/medicina_free
with STEMI, 33% with non-ST elevation MI [NSTEMI]) at 126
hospitals in 14 countries.14 Second-degree Mobitz II or thirddegree AV block occurred in 2.9% of patients (5% of STEMI
patients, 1.9% of NSTEMI patients). AV block was noted on
SA node
Internodal
tracts
AV node
Bundle
of His
e
branch
Fig. 17.1 Cardiac conduction system. AV, Atrioventricular; SA,
sinoatrial.
Bachmann’s
bundle
Left bundl
branch
Posterior
fascicle
Anterior
fascicle
presentation in about half the patients and developed following
admission in the other half. The RCA was the culprit vessel in
65% of patients with AV block and 31% of patients without AV
block. A total of 35% of patients with AV block underwent
temporary pacemaker placement and 5.9% required a permanent
pacemaker.
Most reports that have assessed the incidence and prognostic
significance of high-degree AV block after MI have not distinguished between STEMI and NSTEMI. In the Second Prevention
Reinfarction Israeli Nifedipine Trial (SPRINT) of 610 patients
with a first NSTEMI,20 second- or third-degree AV block developed
in 7% of patients. In the GRACE registry, 5% of STEMI patients
developed Mobitz II second- or third-degree AV block compared
to 1.9% of NSTEMI patients.
14
acute MI. The development of BBB complicating acute MI after
initial presentation appears to be rare, with only 0.73% and
0.15% of patients developing RBBB and LBBB, respectively, in
the first 60 minutes after presentation.8 However, this is likely
an underestimate, as many patients probably develop an acute
BBB prior to presenting to the hospital.
The largest experience with high-degree AV block in the
fibrinolytic era comes from a review of almost 76,000 patients
with ST-elevation MI (STEMI) enrolled in four large randomized trials.9 The overall incidence of high-degree AV block was
6.9%: 9.8% associated with an inferior MI and 3.2% with an
anterior MI.
In the thrombolytic era, the incidence of complete block
has been reported in 3.2% of patients, 5.9% of patients with
RCA occlusion, and 1.5% of patients with other infarct-related
arteries.
10–14
These generally develop within the first 2 days.
The incidence of complete heart block (CHB) in acute MI was
about 4% to 5%,
occurring in 7% to 10% of patients.
15–19
with CHB or second-degree AV block
9,18
Since the widespread
use of primary PCI, the incidence of AV block appears to have
declined. Among 2073 STEMI patients treated with primary PCI
in the Danish National Patient Registry, only 3.2% presented
with second- or third-degree AV block or developed it during
hospitalization.
10
Among 6662 STEMI patients enrolled in a French prospective
registry between 2006 and 2013,11 of whom 74% of patients
underwent primary PCI and 90% had PCI at some point in the
index hospitalization, 3.5% of patients developed Mobitz II or
third-degree AV block—2.2% on admission and 1.3% later in
the hospitalization. AV block was more common among those
with RCA occlusion (5.9%) than those with other infarct-related
arteries (1.5%). Rates of AV block developing during hospitalization were lower in patients who received primary PCI (1.2%) or
thrombolysis (0.5%) than those with no reperfusion treatment
(2.6%).
The Global Registry of Acute Coronary Events (GRACE)
enrolled 59,229 patients with acute coronary syndromes (37%
SPECIFIC CONDUCTION ABNORMALITIES
Sinoatrial Node
Sinus Bradycardia. Sinus bradycardia is the most common
arrhythmia in inferior MI and three times more common in
inferoposterior than anterolateral MI.21 Potential mechanisms
include infarction or ischemia of the sinus node or the surrounding atrium, increased vagal tone (most commonly), and
the Bezold-Jarisch reflex. The Bezold-Jarisch reflex consists of
vasodilation and bradycardia, resulting in hypotension triggered
by stimulation of cardiac inhibitory receptors during myocardial
ischemia.
Stimulation of these inhibitory cardiac receptors increases
parasympathetic activity and inhibits sympathetic activity.
Paradoxically, reperfusion can also trigger this reflex.
Sinoatrial Block and Sinus Arrest. Grade 2 or complete
sinoatrial block suggests a proximal occlusion of the RCA or
LCX and is often accompanied by atrial infarction. This is a sign
of a large MI, potentially involving the right ventricle.
22
23
ATRIOVENTRICULAR NODE
Prolongation of the PR interval (first-degree block) can arise in
the AV node, the bundle of His, or the bundle branches. When
the block is at the level of the AV node, it is caused by occlusion
of the artery supplying the AV node (RCA or LCX). First-degree
AV block from RCA occlusion is usually transient, resolving in
5 to 7 days with no treatment indicated. The mechanism of
Wenckebach second-degree AV block (Mobitz type I) is similar
to first-degree AV block. It is also transient and requires no
specific treatment.
Infranodal Conduction Abnormalities
The various forms of conduction abnormalities known to occur
below the AV node include Mobitz II second-degree AV block,
2 : 1 AV block, RBBB with or without left anterior fascicular
block (LAFB) or left posterior fascicular block (LPFB), and LBBB.
176 PART III Coronary Artery Disease
https://t.me/medicina_free
RBBB is much more common than complete LBBB owing to
the dual blood supply of various fascicles of the left bundle and
a wide area of distribution within the myocardium. The clinical
prognosis is worse when an MI results in RBBB with LAFB due
to the large amount of myocardium involved.
6
Complete heart block 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-degree to seconddegree to third-degree block (Fig. 17.2). It often results in
asymptomatic bradycardia (40 to 60 beats/min) and is usually
transient, resolving within 5 to 7 days. LBBB occurs as a form
of aberration during bradycardia—either sinus bradycardia or
AV block with a junctional escape mechanism. Complete heart
block 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 LAFB or LPFB (bifascicular
or trifascicular block; Fig. 17.3).24 The escape rhythm is wide
and unstable, and the event is associated with a high mortality
from 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.
Inferior Wall Versus Anterior Wall
Myocardial Infarction
High-degree (second- or third-degree) AV block associated
with inferior wall MI is located above the His bundle in 90% of
patients.25 For this reason, complete heart block often results in
only a modest and usually transient bradycardia with junctional
or escape rhythm rates greater than 40 beats/min (Fig. 17.4). It
is common, however, for the junctional pacemaker that controls
the ventricles to accelerate to greater than 60 beats/min. The
QRS is narrow in this setting and the risk of mortality is low.
High-degree AV block associated with anterior MI is more
often located below the AV node (more frequently within the
His bundle or proximal bundle branches).26 It is usually symptomatic and was historically associated with a mortality rate
approaching 80% largely because of greater infarct size. Mortality
rates may be lower in the current era because of improvements
in the management of congestive heart failure and cardiogenic
shock, but the risk remains substantial.
MORTALITY
High-degree AV block is associated with increased mortality in
patients with inferior or anterior MI. Most of the increased risk
is within the first 30 days.27 High-degree AV block in patients
with an anterior wall MI is associated with a greater increase in
in-hospital and 30-day mortality than seen with an inferior wall
MI, probably because of more extensive myocardial involvement
and a higher incidence of hemodynamic complications.
The presence of a fascicular or bundle branch block during
an acute MI is associated with increased in-hospital and long-term
9
II
Fig. 17.2 Mobitz type I atrioventricular block and inferior myocardial infarction. (Courtesy Ary
Goldberger, MD.)
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Fig. 17.3 12-Lead electrocardiogram from a patient with a history of an anteroseptal myocardial
infarction (Q waves seen in leads V
anterior fascicular block.
to V3) shows a typical right bundle branch block and left
1
CHAPTER 17 Conduction Disturbances in Acute Myocardial Infarction 177
https://t.me/medicina_free
PP PPP
Fig. 17.4 Sinus rhythm with high-grade atrioventricular block. (Courtesy Ary Goldberger, MD.)
mortality. However, since it is usually impossible to know if
these findings are chronic or acute, the increased mortality may
represent increased comorbidity in the former and a larger infarct
in the latter. Among 26,000 patients treated with thrombolytic
therapy in the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)-1 trial, in-hospital mortality was higher
in patients with a BBB on initial ECG (18% vs. 11%). In addition,
patients with a BBB were more likely to develop cardiogenic
shock (19% vs. 11%), AV block or asystole (30% vs. 9%), and
to require a pacemaker (18% vs. 11%). In the primary PCI era,
RBBB or LBBB on baseline ECG remains associated with increased
in-hospital and long-term mortality.
28–30
A post-hoc analysis of
over 17,000 patients demonstrated that after adjustment for
baseline characteristics, 30-day mortality was significantly
increased only in patients with an RBBB at baseline and an
anterior MI and in patients with a new LBBB or new RBBB with
an anterior MI.
8
MANAGEMENT
Patients with AV block may by asymptomatic or symptomatic.
Even if asymptomatic, AV block associated with bradycardia
may cause hypotension, reduced coronary perfusion pressure, and recurrent ischemia. In symptomatic patients, the
most common therapies are atropine or transvenous right
ventricular pacing. Transcutaneous pacing is painful and unreliable; thus, it should be avoided except when no alternatives
exist.
Symptomatic bradyarrhythmias in the setting of an inferior
MI may respond to atropine when they occur early in the course
while those that occur more than 24 hours after presentation
often do not. Atropine is administered intravenously in 0.5- or
1-mg doses to a maximum of 3 mg. Ventricular fibrillation has
been described after atropine administration in the setting of
BBB or Mobitz type II AV block. Refractory hypotension in
an inferior MI after treatment of bradycardia with atropine
should raise suspicion for volume depletion or right ventricular
infarction.
Patients with two or more of the following new findings are
at 25% to 36% risk of progression to complete heart block: PR
prolongation, second-degree AV block, left anterior or posterior
fascicular block, LBBB, and RBBB.
31
Temporary Transvenous Pacing
The purpose of temporary transvenous pacemaker insertion is
to maintain circulatory integrity by providing for standby pacing
should sudden complete heart block ensue, to increase heart
rate during periods of symptomatic bradycardia and occasionally
to control sustained supraventricular or ventricular tachycardia.32
Whether ventricular or AV sequential pacing should be used
depends on hemodynamic considerations. An infarcted, preloaddependent right ventricle may require atrial filling achieved by
AV synchronous pacing to maximize stroke volume and reverse
shock. Performance of AV temporary pacing requires additional
experience and can be considerably more difficult from a technical
standpoint. Because temporary pacemakers are manufactured
by many different vendors, physicians credentialed to insert
temporary pacemakers should be familiar with the insertion
equipment, leads, and external generators used in their own
hospitals.
First-degree AV block does not require treatment. High-grade
AV block with inferior STEMI usually is transient and associated
with a narrow complex/junctional escape rhythm that can be
managed conservatively. Prophylactic placement of a temporary
pacing system is recommended for high-grade AV block and/or
new bundle-branch (especially LBBB) or bifascicular block in
patients with anterior MI.33 Pacing can be considered in symptomatic bradycardia of any etiology if associated with hypotension
and atropine administration is unsuccessful, Mobitz type II
second-degree AV block, and bradycardia-induced tachyarrhythmias, such as torsades de pointes.
Guidelines for Permanent Pacemaker Placement
The American College of Cardiology/American Heart Association/
Heart Rhythm Society (ACC/AHA/HRS) class I indications for
placement of a permanent pacemaker after an acute MI are
described in Box 17.1.34 Indications for permanent pacing after
STEMI in patients experiencing AV block are related in large
measure to the presence of intraventricular conduction defects.
In contrast to some other indications for permanent pacing, the
criteria for patients with STEMI and AV block do not depend
on the presence of symptoms. The requirement for temporary
pacing in STEMI does not by itself constitute an indication for
permanent pacing.
178 PART III Coronary Artery Disease
https://t.me/medicina_free
BOX 17.1 Permanent Pacing for
Bradycardia or Conduction Blocks Associated
With ST Segment Elevation Myocardial
Infarction (STEMI)
Class I
1.
Permanent ventricular pacing is indicated for persistent second-degree AV
block in the His-Purkinje system with alternating bundle branch block or
third-degree AV block within or below the His-Purkinje system after STEMI
(level of evidence: B).
2.
Permanent ventricular pacing is indicated for transient advanced second- or
third-degree infranodal AV block and associated bundle branch block. If the
site of block is uncertain, an electrophysiologic study may be necessary
(level of evidence: B).
3.
Permanent ventricular pacing is indicated for persistent and symptomatic
second- or third-degree AV block (level of evidence: C).
Class IIb
1.
Permanent ventricular pacing may be considered for persistent second- or
third-degree AV block at the AV node level, even in the absence of symptoms
(level of evidence: B).
Class III
1.
Permanent ventricular pacing is not indicated for transient AV block in the
absence of intraventricular conduction defects (level of evidence: B).
2.
Permanent ventricular pacing is not indicated for transient AV block in the
presence of isolated left anterior fascicular block (level of evidence: B).
3.
Permanent ventricular pacing is not indicated for new bundle branch block
or fascicular block in the absence of AV block (level of evidence: B).
4.
Permanent ventricular pacing is not recommended for persistent first-degree
AV block in the presence of bundle branch block that is old or of indeterminate
age (level of evidence: B).
34
Acknowledgment
I acknowledge the contribution of the late Mark Josephson, MD,
to this chapter in prior editions.
The full reference list for this chapter is available at
ExpertConsult.com.
Full guidelines are accessible in the Appendix at ExpertConsult.com.
AV, Atrioventricular.
CHAPTER 17 Conduction Disturbances in Acute Myocardial Infarction 178.e1
https://t.me/medicina_free
REFERENCES
1. Rosenbaum M, Elizari MV, Lazzari JO. The Hemiblocks. Tampa
Tracings, Tampa, 1970.
2. Uhley HN. Some controversy regarding the peripheral
distribution of the conduction system. Am J Cardiol.
1972;30:919.
3. Hecht HH, Kossmann CE, Childers RW, et al. Atrioventricular
and intraventricular conduction. Revised nomenclature and
concepts. Am J Cardiol. 1973;31:232.
4. Demoulin JC, Kulbertus HE. Histopathological examination of
concept of left hemiblock. Br Heart J. 1972;34:807.
5. James TN. Arrhythmias and conduction disturbances in acute
myocardial infarction. Am Heart J. 1962;64:416–426.
6. Go AS, Barron HV, Rundle AC, et al. Bundle-branch block and
in-hospital mortality in acute myocardial infarction. National
Registry of Myocardial Infarction 2 Investigators. Ann Intern
Med. 1998;129:690.
7. Stenestrand U, Tabrizi F, Lindbäck J, et al. Comorbidity and
myocardial dysfunction are the main explanations for the higher
1-year mortality in acute myocardial infarction with left
bundle-branch block. Circulation. 2004;110:1896.
8. Wong CK, Stewart RA, Gao W, et al. Prognostic differences
between different types of bundle branch block during the early
phase of acute myocardial infarction: insights from the Hirulog
and Early Reperfusion or Occlusion (HERO)-2 trial. Eur Heart J.
2006;27:21.
9. Meine TJ, Al-Khatib SM, Alexander JH, et al. Incidence,
predictors, and outcomes of high-degree atrioventricular block
complicating acute myocardial infarction treated with
thrombolytic therapy. Am Heart J. 2005;149:670.
10. Gang UJ, Hvelplund A, Pedersen S, et al. High-degree
atrioventricular block complicating ST-segment elevation
myocardial infarction in the era of primary percutaneous
coronary intervention. Europace. 2012;14:1639.
11. Auffret V, Loirat A, Leurent G, et al. High-degree atrioventricular
block complicating ST segment elevation myocardial infarction
in the contemporary era. Heart. 2016;102:40.
12. Kim HL, Kim SH, Seo JB, et al. Influence of second- and
third-degree heart block on 30-day outcome following acute
myocardial infarction in the drug-eluting stent era. Am J Cardiol.
2014;114:1658.
13. Harikrishnan P, Gupta T, Palaniswamy C, et al. Complete heart
block complicating ST-segment elevation myocardial infarction.
JACCEP. 2015;1:529.
14. Singh SM, FitzGerald G, Yan AT, et al. High-grade
atrioventricular block in acute coronary syndromes: insights
from the Global Registry of Acute Coronary Events. Eur Heart J.
2015;36:976.
15. Harpaz D, Behar S, Gottlieb S, et al. Complete atrioventricular
block complicating acute myocardial infarction in the
thrombolytic era. SPRINT Study Group and the Israeli
Thrombolytic Survey Group. Secondary Prevention Reinfarction
Israeli Nifedipine Trial. J Am Coll Cardiol. 1999;34:1721.
16. GISSI-2: a factorial randomised trial of alteplase versus
streptokinase and heparin versus no heparin among 12,490
patients with acute myocardial infarction. Gruppo Italiano per lo
Studio della Sopravvivenza nell’Infarto Miocardico. Lancet.
1990;336:65.
17. Grines CL, Browne KF, Marco J, et al. A comparison of
immediate angioplasty with thrombolytic therapy for acute
myocardial infarction. The Primary Angioplasty in Myocardial
Infarction Study Group. N Engl J Med. 1993;328:673.
18. GUSTO investigators. An international randomized trial
comparing four thrombolytic strategies for acute myocardial
infarction. N Engl J Med. 1993;329:673.
19. Archbold RA, Sayer JW, Ray S, et al. Frequency and prognostic
implications of conduction defects in acute myocardial
infarction since the introduction of thrombolytic therapy. Eur
Heart J. 1998;19:893.
20. Haim M, Hod H, Kaplinsky E, et al. Frequency and prognostic
significance of high-degree atrioventricular block in patients
with a first non-Q-wave acute myocardial infarction. The
SPRINT Study Group. Second Prevention Reinfarction
Israeli Nifedipine Trial. Am J Cardiol. 1997;79:674.
21. Zipes DP. The clinical significance of bradycardic rhythms
in acute myocardial infarction. Am J Cardiol. 1969;24:
814–825.
22. Mark AL. The Bezold-Jarisch reflex revisited: clinical
implications of inhibitory reflexes originating in the heart. J Am
Coll Cardiol. 1983;1:90–102.
23. Wellens HJ. The ECG in Emergency Decision Making. 2nd ed.
Philadelphia: Saunders; 2005.
24. Hindman MC, Wagner GS, JaRo M, et al. The clinical
significance of bundle branch block complicating acute
myocardial infarction, 1: clinical characteristics, hospital
mortality, and one-year follow-up. Circulation. 1978;58:
679–688.
25. Feigl D, Ashkenazy J, Kishon Y. Early and late atrioventricular
block in acute inferior myocardial infarction. J Am Coll Cardiol.
1984;4:35–38.
26. Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in
acute myocardial infarction. N Engl J Med. 2003;348:933–940.
27. Aplin M, Engstrom T, Vejlstrup NG, et al. Prognostic importance
of complete atrioventricular block complicating acute
myocardial infarction. Am J Cardiol. 2003;92:853–856.
28. Melgarejo-Moreno A, Galcerá-Tomás J, Consuegra-Sánchez L,
et al. Relation of new permanent right or left bundle branch
block on short- and long-term mortality in acute myocardial
infarction bundle branch block and myocardial infarction. Am J
Cardiol. 2015;116:1003.
29. Widimsky P, Rohác F, Stásek J, et al. Primary angioplasty in acute
myocardial infarction with right bundle branch block: Should
new onset right bundle branch block be added to future
guidelines as an indication for reperfusion therapy? Eur Heart J.
2012;33:86.
30. Vivas D, Pérez-Vizcayno MJ, Hernández-Antolín R, et al.
Prognostic implications of bundle branch block in patients
undergoing primary coronary angioplasty in the stent era. Am J
Cardiol. 2010;105:1276.
31. Lamas GA, Muller JE, Turi ZG, et al. A simplified method to
predict occurrence of complete heart block during acute
myocardial infarction. Am J Cardiol. 1986;57:1213–1219.
32. Francis GS, Williams SV, Achord JL, et al. Clinical competence
in insertion of a temporary transvenous ventricular pacemaker:
a statement for physicians from the ACP/ACC/AHA Task Force
on Clinical Privileges in Cardiology. Circulation. 1994;89:
1913–1916.
33. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA
guideline for the management of ST-elevation myocardial
infarction: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice
178.e2 PART III Coronary Artery Disease
https://t.me/medicina_free
Guidelines. J Am Coll Cardiol. 2013;61:e78–e140. doi:10.1016/j.
jacc.2012.11.019.
34. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS
2008 guidelines for device-based therapy of cardiac rhythm
abnormalities: a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines
(Writing Committee to Revise the ACC/AHA/NASPE 2002
Guideline Update for Implantation of Cardiac Pacemakers
and Antiarrhythmia Devices). Circulation. 2008;117:
e350–e408.
Соседние файлы в папке Библиотека им академика М.И. Перельмана