Download Sudden cardiac death and variant angina

REVIEW
Sudden cardiac death
and variant angina
R4 최은용 / Pf. 김원
Sudden Cardiac Death is one of the
Leading Causes of Death in the U.S.
300,000
250,000
200,000
150,000
100,000
50,000
0
AIDS
Breast Cancer
Lung Cancer
Stroke
Source: Statistical Abstract of the U.S. 1998, Hoover’s Business Press, 118th Edition
SCA
SCD definition
• Sudden cardiac death (SCD)
natural death due to cardiac causes
time and mode of death are unexpected
1 h or less, unwitnessed deaths(death within 24h)
-2/3 of SCDs heart disease
- Incidence : 400,000 - 500,000/year in U.S.
Only 2% - 15% reach the hospital
Half of these die before discharge
High recurrence rate
may be reversible
cardiovascular collapse, cardiac arrest, and death
Incidence of SCD
Incidence
Events per Year
Adult population
CAD
History of a
coronary event
Heart failure
MADITII
Resuscitation
SCD-HeFT
AVID,CIDS,CASH
Resuscitation
with previous MI
MADJTI,MUSTT
0
1
2
5
10
PERCENT
20
50
0
100000
200000
300000
ABSOLUTE NUMBER
Sudden cardiac
death in Hispanic Americans and African Americans. Am J Public Health 87:1461, 1997.)
Myerburg et al., Circulation
1992
Age related risk of SCD
Modified from Myerburg and Castellanos 2008
Time-dependent risk of SCD
after MI
Sudden cardiac death: Structure, function, and time-dependence of risk. Circulation 85[Suppl I]:I2, 1992
Etiology
Sudden cardiac death
• Causes
– 80-90% are tachyarrhythmias
– Only 10-20% are due to an acute myocardial
infarction or to bradyarrhythmias
Underlying Arrhythmia of Sudden Death
Holter recordings
from 157 cases with
fatal arrhythmias
Bradyarrhythmias
17%
Primary VF
9%
Torsade 13%
de Pointes
Bayes de Luna et al. Am Heart J 1989
VT VF
62%
Coronary artery Abonormalities
Atherosclerotic Coronary Artery Disease
• Cronary artery abnormality : 80% of SCDs in Western countries
nonischemic cardiomyopathies 10% to 15%
• Atherosclerotic Coronary Artery Disease
electrophysiologic alterations that result from the myocardial impact
of an ischemic burden
-modulation by hemodynamic, autonomic, genetic
-short-term risk of life-threatening events: acute ischemia
- longer term risk : transient ischemia, myocardial scarring, remodeling, ischemic
cardiomyopathy, and heart failure.
Pathophysiology of ventricular tachyarrhythmias
in coronary heart disease
Modified from Myerburg RJ: Implantable cardioverter-defibrillators after
myocardial infarction. N Engl J Med 359:2245, 2008.)
Pathology
• CHD as the major structural etiologic factor
•
More than 80% of SCD
• combination atherosclerosis of CA and unstable coronary artery
lesions
• 70–75% male SCD healed MIs, Only 20–30% recent acute Mis
• transient ischemia  mechanism of onset, electrophysic alterance
regional or global left ventricular (LV) hypertrophy often coexists
with prior MIs
Nonatherosclerotic Coronary
Artery Abnormalities
•
•
•
•
•
•
•
Congenital lesions, coronary artery embolism
Anomalous Origin of Coronary Arteries
Coronary Arteritis
Kawasaki disease
Polyarteritis nodosa
Mechanical Obstruction to Coronary Arteries
Deep myocardial bridges
• Coronary Artery Spasm
serious arrhythmias and SCD
concomitant CAD
: Painless myocardial ischemia
Prediction and Prevention of
Cardiac Arrest and Sudden
Cardiac Death
• High risk subgroups provide more focused
• Effective prevention of underlying diseases
• Classified as primary and secondary: multiple ICD trial
primary prevention
secondary prevention
Risk of sudden death by decile
of multivariate risk
.
J Am Coll Cardiol 5[Suppl 6]:141B, 1985.
• profiling for risk of developing CHD and risk factor control
• long-term risk factors :
age, cigarette smoking, elevated serum cholesterol, diabetes mellitus, elevated blood
pressure, LV hypertrophy, and nonspecific electrocardiographic abnormalities,
elevated CRP
not sufficiently or specifically enough to warrant therapies targeted
to potentially fatal arrhythmias
Primary prevention
• After coronary artery disease  additional strategies for risk profiling
• initial 6–18 months after the event and then plateaus
 nonsudden, diluting the potential benefit of strategies targeted
specifically to SCD. Erly after MI ICD ?
Primary prevention
• Subgroups at high absolute risk of SCD post MI
acute phase: 48 h, risk ~ 15%, not at risk for recurrent cardiac
arrest
convalescent phase : 3 days to ~6 weeks, episode of sustained VT
or VF(large infarct), motality >25% at 12 months, ½ SCD 
Aggressive intervention
chronic phase: : predicted by a number of factors
-extent of myocardial damage
-EF and/or HF EF <40%.
-VT or VF during EPS , EF <35 or 40% strong predictor of SCD
risk.
implantable cardioverter defibrillators (ICDs)
Secondary prevention
• Surviving victims of a cardiac arrest
Not acute MI or a transient risk of SCD (e.g., drug exposures,
correctable electrolyte imbalances)
Multivessel CAD and DCMP (↓ EF )1- to 2-year risk of
recurrence SCD or cardiac a rrest 30%
life-threatening arrhythmias with long QT syndromes or
right ventricular dysplasia
Clinical Characteristics of
Cardiac Arrest Prodrome, Onset,
Arrest, Death
• Prodrome: angina, dyspnea, palpitations, easy fatigability,
not specific for predicting SCD
• HR ↑and for advanced grades of PVCs to evolvenonsustained or
sustained VT VF
• Prognosis: pulseless VT>VF >asystole, PEA
primary and secondary cardiac arrests( ddx by
hemodynamic instability):90%vs 70%
Treatment: Cardiac Arrest
(1) initial evaluation and basic life support
(2) public access defibrillation (when available)
(3) advanced life support
(4) postresuscitation care
(5) long-term management
ADVANCED CARDIAC LIFE
SUPPORT (ACLS)
(1) defibrillation/cardioversion and/or pacing, (2) intubation with an
endotracheal tube, and (3) insertion of an intravenous line
Defibrillation
Immediate defibrillation should precede intubation and insertion of an
intravenous line
VF or VT 300 J monophasic or 120–150 J with a biphasic
maximum of 360 J monophasic (200 J biphasic)
Epi: 1 mg failed defibrillation: 3–5 min
Vasopressin : a single 40-unit dose given IV
Acidosis (not correted with defibrilation and intubation )
NaHCO3: 1 meq/kg initially and an additional 50% of the dose
repeated every 10–15 min; not be used routinely
antiarrhythmic therapy
- amiodarone (150 mg over 10 min, followed by 1 mg/min for up to 6
h and 0.5 mg/min thereafter)
- lidocaine; VF in the early phase of an acute coronary syndrome,
amiodarone unsuccessful:
a bolus of 1 mg/kg , repeated in 2 min
POSTRESUSCITATION CARE
• Hypothermia to reduce metabolic demands and cerebral edema
• outcome noncardiac diseases is poor, survival rate of <10%
sepsis, cancer,
CRF, pnuemonia
vs
transient airway obstruction, electrolyte
disturbances, proarrhythmic effects of drugs, and
severe metabolic abnormalities
LONG-TERM MANAGEMENT AFTER
SURVIVAL OF OUT-OF-HOSPITAL
CARDIAC ARREST
• without irreversible damage to the CNS and hemodynamic
stability: diagnostic testing
 therapeutic interventions (cardiac arrest is followed by a 10–25%
mortality rate during the first 2 years after the event)
• significant survival benefits ICD: motality 20–35% reduction over
2–5 yr
not associated with an ACS
MI with an ejection fraction less than 30–35%
HCMP, DCMP, rare inherited disorders
(e.g., right ventricular dysplasia, long QT syndrome, Brugada syndrome,
catecholaminergic polymorphic VT, and so-called idiopathic VF
Prevention of SCD in High-Risk
Individuals Without Prior Cardiac
Arrest
• Post-MI patients
30 days or more after the MI
EFs <35%
- Markers of risk such as ambient ventricular arrhythmias, inducible
ventricular tachyarrhythmias in EPS
Hx of heart failure
very low EFs (e.g., <20%) may receive less benefit
Prinzmetal’ s variant angina
− Spontaneous angina with ST elevation
− First described in 1930s (not by Prinzmetal first)
− Transient, abrupt reduction in luminal diameter without preceding
increased demand
− Normal or diseased vessel, usually within 1cm of plaque
− Reversed by nitroglycerin or calcium channel blocker
Clinical characteristics
− Younger, Associated with migraine, Raynaud’s, cocaine, cigarettes,
thyroid disease
− Can be precipitated by exercise, hyperventilation
− Circadian: midnight to early morning
− Arrhythmias: VT, block
− MI: usually with underlying diseased vessel
− Silent ischemia
− Small elevations of troponin
Pathogenesis
− Autonomic nervous system:
Precipitated by acetylcholine / methacholine,
Prevented by atropine and alpha blockers
− Endothelial dysfunction: increased endothelin release and activity,
relation to low estradiol levels
May lead to vessel damage, stasis, thrombosis
− hypercontractility of vascular smooth muscle due to vasoconstrictor
mitogens, leukotrienes, or serotonin.
Diagnosis
− ECG: ST elevation with chest discomfort -> baseline with resolution
61% have normal ECGs on ED arrival
− Exercise stress myocardiac cintigraphy : limited sensitivity
− Dobutamine echo: may provoke vasospasm, limited sensitivity
−
Hyperventilation with ECG changes (6 minutes): 62% sensitive
Angiography (Class Iia indication):
− usually RCA
− multivessel: migratory, sequential at 2 different sites, or
simultaneous
Ergonovine:
− 50 -> 400 micrograms until max dose or positive result (normal
arteries will respond diffusely with >400)
−
−
4 /1000 refractory spasm or VF (only used in those with nl vessels)
stress echo: compares well with angiography as gold standard
(93% sens / 91% spec)
Treatment
− Nitrates and calcium channel : treat acute episodes and to abolish
recurrent episodes of PVA
− Avoid nonselective beta blockers
− Aspirin : result of the exquisite sensitivity of coronary tone to modest
changes in the synthesis of prostacyclin
− Coronary revascularization : helpful discrete, proximal fixed
obstructive lesions
Prognosis
− Many acute, active phase, with frequent episodes during the first 6
months
− Long-term survival at 5 years: 90–95%
− Nonfatal MI : ~20% by 5 years
− Develop serious arrhythmias during spontaneous episodes of pain
higher risk for SCD
− Condition stabilizes, and there is a tendency for symptoms and
cardiac events to diminish over time
Variant angina and VT
Am J Cardilol 1996:88355-360
Circulation 1979,60:1343`13
Indian Heart J. 2009; 61:389-391
ECG
• variant angina: ST elevation
ddx : ST segment depression( subendocardial may occur with
spasm of smaller epicardial vessels
• ECG changes during spontaneous episodes of variant angina by
Chierchia and colleagues (1980)
peaking of the T waves ST segment elevation, with T wave
inversion Over the following days the inverted T waves will
progressively become less deep normal morphology
T wave is inverted, the T wave will rapidly become upright and
recommence the sequence with peaking of the T wave.
• "pseudonormalization."
(1) transient Q waves; (2) increasing R wave voltage; and (3) ST
segment alterans
• Ambulatory ECG studies: ddx exertional angina:
(1) an absence of a precipitating tachycardia prior to the ischemic
changes; and (2) a circadian pattern of disease activity with most
ischemic episodes occurring in the early morning, even though they
may be asymptomatic (silent ischemia)
• exercise stress testing would usually be negative30 to 60 percent
of patients.
(1) coexistent atherosclerotic coronary artery disease
(2) an increased sensitivity to catecholamines during the hot phase
of the disorder.