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Holistic in Risk Holistic in Risk factors and factors and
Cardiovascular Cardiovascular ManagementManagement
Warong Lapanun MD.Warong Lapanun MD.
Cardiology divisionCardiology division
Bhumibol Adulyadej Bhumibol Adulyadej HospitalHospital
Emergency Medicine Lunch Symposium: 2/9/07
Atherosclerosis
Cross-section through the wall of a healthy artery with intact endothelium, intima and smooth muscle bundles (SEM)
Artery demonstrating endothelial erosion (SEM)
Intimal thickening
Extralipid pool
Fibrous scar
Atheromato us plaque
Plaque Rupture
Coronary occlusion
Plaque rupturePlaque ruptureOcclusive thrombus
Most Myocardial Infarctions Are Most Myocardial Infarctions Are CausedCaused
by Low-Grade Stenosesby Low-Grade Stenoses
Pooled data from 4 studies: Ambrose et al, 1988; Little et al, 1988; Nobuyoshi et al, 1991; Pooled data from 4 studies: Ambrose et al, 1988; Little et al, 1988; Nobuyoshi et al, 1991; and Giroud et al, 1992.and Giroud et al, 1992.(Adapted from Falk et al.)(Adapted from Falk et al.)Falk E et al, Circulation, 1995.
• Eccentric, lipid-rich
• Fragile fibrous cap
• Prior luminal obstruction < 50%
• Visible rupture and thrombus
Constantinides P. Am J Cardiol. 1990;66:37G-40G.
Features of a Ruptured Atherosclerotic Plaque
Plaque rupture triggersPlaque rupture triggers
Emotional stressEmotional stress Physical activityPhysical activity VasospasmVasospasm CathecholaminesCathecholamines
Libby P. Circulation. 1995;91:2844-2850.
Vulnerable Plaque
•Thin fibrous cap•Inflammatory cell infiltrates: proteolytic activity•Lipid-rich plaque
Lumen LipidCore
Fibrous Cap
•Thick fibrous cap•Smooth muscle cells:
more extracellular matrix•Lipid-poor plaque
Stable Plaque
Lumen LipidCore
Fibrous Cap
Vulnerable Versus Vulnerable Versus Stable Stable
Atherosclerotic PlaquesAtherosclerotic Plaques
(Adapted from Glagov et al.)(Adapted from Glagov et al.)
Coronary RemodelingCoronary RemodelingCoronary RemodelingCoronary Remodeling
NormalNormalvesselvessel
MinimalMinimalCADCAD
ProgressionProgression
Compensatory expansionmaintains constant lumen
Expansion Expansion overcome:overcome:
lumen narrowslumen narrows
SevereSevereCADCAD
ModerateModerateCADCAD
Glagov et al, Glagov et al, N Engl J MedN Engl J Med, 1987., 1987.
Atherosclerosis: Atherosclerosis: A Progressive ProcessA Progressive Process
Disease progression
PHASE I: Initiation PHASE II: Progression PHASE III: Complication
NormalFatty
StreakFibrousPlaque
Occlusive Atherosclerotic
Plaque
PlaqueRupture/Fissure &
Thrombosis
MI
Stroke
Critical Leg Ischemia
Coronary Death
UnstableAngina
Libby P. Circulation. 2001;104:365-372.
IVUS=intravascular ultrasoundNissen S, Yock P. Circulation 2001; 103: 604–616
AngiogramIVUS
Little evidence of disease
Atheroma
No evidence of disease
The IVUS technique can detect angiographically
‘silent’ atheroma
Correlation of CT angiography of the coronary arteries with intravascular ultrasound illustrates the ability of MDCT to demonstrate calcified and non-calcified coronary plaques (Becker et al., Eur J Radiol 2000)
Non-calcified, soft, lipid-rich plaque in left anterior descending artery (arrow) . The plaque was confirmed by intravascular ultrasound (Kopp et al., Radiology 2004)
Estimated 10-Year CHD Risk in 55-Year-Old Adults According to Levels of Various Risk Factors : Framingham Heart Study
AA B B C C D D
Blood Pressure (mm Hg)Blood Pressure (mm Hg) 120/80120/80 140/90140/90 140/90140/90 140/90140/90
Total Cholesterol (mg/dL)Total Cholesterol (mg/dL) 200 200 240 240 240 240 240 240
HDL Cholesterol (mg/dL)HDL Cholesterol (mg/dL) 50 50 50 50 40 40 40 40
DiabetesDiabetes No No No No Yes Yes Yes Yes
CigarettesCigarettes No No No No No No Yes Yes
Source: Circulation 1998;97:1837-1847.
CHD MortalityCHD Mortality
0 2 4 6 8 10 12
0
5
10
15
20
RR (95% CI), 3.77 (1.74-8.17)
Follow-up, Y
Cu
mu
lati
ve H
azar
d (
%)
Yes
No
866
288
852
279
834
234
292
100
The Kuopio Ischaemic Heart Disease Risk Factor StudyThe Kuopio Ischaemic Heart Disease Risk Factor Study
Unadjusted Kaplan-Meier Curve
No. at RiskMetabolic Syndrome
YesMetabolic Syndrome:
0 2 4 6 8 10 12
0
5
10
15
20
RR (95% CI), 3.55 (1.96-6.43)
Follow-up, Y
866
288
852
279
834
234
292
100
0 2 4 6 8 10 12
0
5
10
15
20
RR (95% CI), 2.43 (1.64-3.61)
Follow-up, Y
866
288
852
279
834
234
292
100
CVD MortalityCVD Mortality All Cause All Cause MortalityMortality
Lakka H-M, et al. JAMA. 2002;288:2709-2716.
No
The INTERHEART StudyThe INTERHEART StudyMetabolic risk factors and their influence Metabolic risk factors and their influence
on theon the occurrence of AMI occurrence of AMI
Feb. 1999 to Mar 2003, 15,000 cases Feb. 1999 to Mar 2003, 15,000 cases of AMI were compared with 15,000 of AMI were compared with 15,000 controls in 52 countriescontrols in 52 countries
The prevalence of modifiable RF, The prevalence of modifiable RF, calculation of the population calculation of the population attributable risk (PAR)attributable risk (PAR)
Frequency of RF in total pop. – Frequency of RF in Frequency of RF in total pop. – Frequency of RF in those those withoutwithout MI MI
Frequency of RF in total pop.Frequency of RF in total pop.
Yusuf S et al. Lancet 2004, 364;937-962
The INTERHEART StudyThe INTERHEART StudyPopulation Attributable Risk Population Attributable Risk (cumulated men& women)(cumulated men& women)
SmokingSmoking DMDM Abdo ObesityAbdo Obesity Abn LipidsAbn Lipids
PAR in%PAR in%
Western EuropeWestern Europe 29.329.3 15.015.0 63.4 63.4 44.644.6
Central Eastern EuCentral Eastern Eu 30.230.2 9.19.1 28.0 28.0 35.035.0
Middle EastMiddle East 45.545.5 15.515.5 25.9 25.9 70.570.5
AfricaAfrica 38.938.9 16.716.7 58.4 58.4 74.174.1
South AsiaSouth Asia 37.437.4 11.811.8 37.7 37.7 58.758.7
South East Asia+ JapanSouth East Asia+ Japan 36.736.7 21.021.0 58.0 58.067.767.7
Australia+NZAustralia+NZ 44.844.8 7.2 61.37.2 61.3 43.443.4
South AmericaSouth America 38.338.3 17.717.7 45.5 45.5 47.647.6
North AmericaNorth America 26.126.1 13.013.0 59.5 59.5 50.550.5
All 52 countriesAll 52 countries 36.436.4 12.312.3 33.7 33.7 64.164.1
Yusuf S et al. Lancet 2004, 364;937-962
INTERHEART: Risk of AMIINTERHEART: Risk of AMIAssociated With Risk FactorsAssociated With Risk Factors
Risk FactorRisk Factor Control(%) Case AMI(%)Control(%) Case AMI(%) OROR
( adj.for age,sex, smoking)( adj.for age,sex, smoking)
Lipid(ApoB/ApoA-1)Lipid(ApoB/ApoA-1) 20.020.0 33.533.5 3.873.87
Current smokingCurrent smoking 26.826.8 45.245.2 2.952.95
DMDM 7.57.5 18.418.4 3.083.08
HTHT 21.921.9 39.039.0 2.482.48
Abdo. ObesityAbdo. Obesity 33.333.3 46.346.3 2.222.22
PsychosocialPsychosocial 2.512.51
Veg.& Fruit dailyVeg.& Fruit daily 42.442.4 35.835.8 0.700.70
ExerciseExercise 19.319.3 14.314.3 0.720.72
Alcohol intakeAlcohol intake 24.524.5 24.024.0 0.790.79
Yusuf S et al. Lancet 2004, 364;937-962
Discharge DxDischarge Dx
GenderGender
Risk factorsRisk factors
Prevalence of RF according to Prevalence of RF according to gendergender
Relationship Between Changes Relationship Between Changes in LDL-C and HDL-C Levels in LDL-C and HDL-C Levels
and CHD Riskand CHD Risk
Third Report of the NCEP Expert Panel. NIH Publication No. 01-3670 2001. http://hin.nhlbi.nih.gov/ncep_slds/menu.htm
1% decreasein LDL-C reduces
CHD risk by1%
1% increasein HDL-C reduces
CHD risk by3%
Mean CHD CHD
No. No. Person- cholesterol Incidence Mortality
Intervention trials treated years reduction (%) (% change) (% change)
Surgery 1 421 4,084 22 -43 -30
Sequestrants 3 1,992 14,491 9 -21 -32
Diet 6 1,200 6,356 11 -24 -21
Statins 12 17,405 89,123 20 -30 -29
Source: This table is adapted from the meta-analysis of Gordon, 2000.
CHD Outcomes in Clinical CHD Outcomes in Clinical Trials of Trials of
LDL Cholesterol-Lowering LDL Cholesterol-Lowering TherapyTherapy
% LDL-C Reduction
10
0
20
40
70% R
edu
ctio
n I
n R
isk
Of
No
nfa
tal
MI
Or
CH
D
Pravastatin
LRC-CPPTWOSCOPS
CARE
POSCH 4S (Simvastatin)
13 26 35 60
% LDL-C Reduction
10
0
20
40
70% R
edu
ctio
n I
n R
isk
Of
No
nfa
tal
MI
Or
CH
D(4
.5 y
)
LRC-CPPT (P>.05)
WOSCOPSCARE
POSCH (P>.05)
4S (Simvastatin)
13 26 35 60
*
Relation Between LDL-CholesterolRelation Between LDL-CholesterolReduction And Risk Of Cardiovascular Reduction And Risk Of Cardiovascular
EventsEvents
• When outcomes at 4.5 y are considered, beneficial effects of statins occurred more rapidly
• These effects may not be entirely cholesterol dependent; *difference possibly due to pleiotropic effects
Reproduced from Liao and Laufs. Annu Rev Pharmacol Toxicol. 2005;45:89, with permission fromAnnual Reviews. www.annualreviews.org.
Liao. Am J Cardiol. 2005;96(suppl):24F.
Vessel Wall And Endothelial CellVessel Wall And Endothelial CellMembrane Changes With Membrane Changes With
AtherogenesisAtherogenesis
Reproduced from Mason et al. Circulation. 2004;109(suppl II):II-34, with permission.
Mason et al. Am J Cardiol. 2005;96(suppl):11F.
Role Of Statins In ACS: Non-Role Of Statins In ACS: Non-Lipid Effects ( Pleiotropic Lipid Effects ( Pleiotropic effects)effects)
ADP = adenosine diphosphate; CD40-L = CD40 ligand; IFN = interferon; IL = interleukin;vWF = von Willebrand factor.
Reproduced from Ray and Cannon. J Thromb Thrombolysis. 2004;18:89, with permission.
Cannon and Ray. Am J Cardiol. 2005;96:54F.
Clinical Events Correlate Clinical Events Correlate Directly WithDirectly With
On-Treatment LDL-Cholesterol On-Treatment LDL-Cholesterol LevelsLevels
P = placebo; S = statin.Reproduced from O'Keefe et al. J Am Coll Cardiol. 2004;43:2142, with permission.
CHD Events(%)
10
9
8
7
6
5
4
3
2
1
0
-1
55 75 95 115 135 155 175 195
LDL Cholesterol (mg/dL)
y = 0.0599x - 3.3952
R2 = 0.9305
P=.0019
AFCAPS-S
WOSCOPS-S
ASCOT-S
ASCOT-P
AFCAPS-P
WOSCOPS-P
Primary prevention: 4-5 yr duration
ASCOT-LLA: Nonfatal MI And ASCOT-LLA: Nonfatal MI And Fatal CADFatal CAD
Primary End PointPrimary End Point
Adapted from Sever et al. Lancet. 2003;361:1149, with permission.
Sever et al. Am J Cardiol. 2005;96(suppl):39F.
2
0
1
4
3
Years
0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5
CumulativeIncidence
(%)
Placebo
Atorvastatin 10 mg
Number of Events
36% Reduction
HR = 0.64 (0.50-0.83)P=.0005
Number of Events
154
100
N=10,305
Effects of Lipid-Lowering Effects of Lipid-Lowering Therapy on CHD Events in Therapy on CHD Events in
Statin TrialsStatin Trials
25
20
15
10
5
0
Pat
ien
ts w
ith
CH
D e
ven
t (%
)
90 110 130 150 170 190 210
S = statin-treated P = placebo-treated
*Extrapolated to 5 y
4S-P
CARE-P
LIPID-P4S-S
WOSCOPS-SWOSCOPS-P
AFCAPS-PAFCAPS-S
LIPID-S
CARE-S
Primary prevention
Simvastatin
Pravastatin
Lovastatin
Modified from Kastelein JJP. Atherosclerosis. 1999;143(suppl 1): S17-S21.
HPS-S
HPS-P
Atorvastatin
ASCOT-S*ASCOT-P*
Secondary prevention
LDL-C (mg/dL)
PROVE IT-TIMI 22: A Major PROVE IT-TIMI 22: A Major CardiovascularCardiovascular
Event Or Death From Any CauseEvent Or Death From Any Cause Primary End PointPrimary End Point
Adapted from Cannon et al. N Engl J Med. 2004;350:1495, with permission.
Ray and Cannon. Am J Cardiol. 2005;96(suppl):54F.
15
0
10
30
25
5
20
Months Of Follow-Up
0 3 9 15 216 12 18 24 27 30
Death Or MajorCardiovascular
Event (%)
Pravastatin 40 mg
Atorvastatin 80 mg
P=.005 OverallP=.03
n= 4,162 with CHD
PROVE IT-TIMI 22: Effect Of PROVE IT-TIMI 22: Effect Of DifferentDifferent
Statin Regimens On LDL Cholesterol Statin Regimens On LDL Cholesterol And CRPAnd CRP
BiologicalBiological StatinStatinResponseResponse RegimenRegimen BaselineBaseline 30 Days30 Days 4 Months4 Months
LDL mg/dL (mean)LDL mg/dL (mean) Pravastatin 40 mgPravastatin 40 mg 106106 8888 9797Atorvastatin 80 mgAtorvastatin 80 mg 106106 6060 6767PP value value NSNS <.001<.001 <.001<.001
CRP mg/L (median)CRP mg/L (median) Pravastatin 40 mgPravastatin 40 mg11.911.9 2.32.32.12.1Atorvastatin 80 mgAtorvastatin 80 mg 12.212.2 1.61.6 1.31.3PP value value NSNS <.001<.001 <.001<.001
Cannon et al. N Engl J Med. 2004;350:1495.
Ridker et al. N Engl J Med. 2005;352:20.
Reproduced from Ray and Cannon. Am J Cardiol. 2005;96(suppl):54F, with permission.
PROVE IT-TIMI 22: A Major PROVE IT-TIMI 22: A Major CardiovascularCardiovascular
Event Or Death From Any Cause At Event Or Death From Any Cause At DifferentDifferent
Censoring TimesCensoring Times
Reproduced from Cannon et al. N Engl J Med. 2004;350:1495, with permission.
Ray and Cannon. Am J Cardiol. 2005;96(suppl):54F.
Censoring Time Hazard Ratio (95% CI)Risk
Reduction (%)
Event Rate (%)
Atorvastatin Pravastatin
30 days
90 days
180 days
End of follow-up
17 1.9 2.2
18 6.3 7.7
14 12.2 14.1
16 22.4 26.3
0.50 0.75 1.0
High-DoseAtorvastatin
Better
Standard-DosePravastatin
Better
1.501.25
NCEP-ATP NCEP-ATP IIIIII
National Cholesterol National Cholesterol Education Program Education Program
Adult Treatment Panel IIIAdult Treatment Panel III
Evolution of Lipid Evolution of Lipid Management GuidelinesManagement Guidelines
ATP I (1988) ATP II (1993) ATP III (2001)
Diet; low-dose,nonstatin
monotherapy
High-dose statin, combination therapy
Low- to moderate-dose statin monotherapy
Increasing aggressiveness of cholesterol-lowering therapy
The National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP)
Update to ATP III:Update to ATP III:Risk Categories, LDL-C GoalsRisk Categories, LDL-C Goals
Risk CategoryRisk Category LDL-C GoalLDL-C Goal
(mg/dL)(mg/dL)Initial Initial TLCTLC
(mg/dl)(mg/dl)
Consider drugConsider drug
(mg/dl)(mg/dl)
High risk:High risk:
CHD or CHD risk CHD or CHD risk equivalents equivalents
(10-year risk >20%)(10-year risk >20%)
<100<100
(optional (optional <70)<70)
>>100100 >>100100
(optional (optional <100)<100)
Moderately high risk:Moderately high risk:
2+ risk factors 2+ risk factors
(10-year risk 10-20%)(10-year risk 10-20%)
<130<130 >>130130 >> 130 130
(optional 100-(optional 100-129)129)
Moderate risk: Moderate risk:
2+ risk factors 2+ risk factors (10-year risk (10-year risk 10%)10%)
<130<130 >>130130 >160>160
Lower risk:Lower risk:
0–1 risk factor0–1 risk factor<160<160 >>160160 >>190190
(optional 160-(optional 160-189)189)Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult
Treatment Panel III Guidelines: Circulation. 2004;110:227-239.
Am J Cardiol. 2004;93: 154-8
HDLHDL
LDLLDL
TGTG
Total Total cholchol
Cardiac Cardiac Emergency Emergency
Cardiac EmergencyCardiac Emergency
Acute coronary syndromeAcute coronary syndrome ArrhythmiaArrhythmia Hypertensive emergencyHypertensive emergency Aortic dissectionAortic dissection Cardiac tamponadeCardiac tamponade
P : P : PPrecipitatingrecipitating, Position , Position Q : Quality and Quantity Q : Quality and Quantity R : Region, Radiate, Refer R : Region, Radiate, Refer S : S : Symptom associatedSymptom associated T : Timing T : Timing, Terminating, Terminating
Taking Hx of obscure pai Taking Hx of obscure painn
Acute myocardial infarctionAcute myocardial infarction Acute aortic dissectionAcute aortic dissection Acute pulmonary embolismAcute pulmonary embolism Tension pneumothoraxTension pneumothorax
Killer chest painKiller chest pain
Characteristics of Typical Characteristics of Typical and Atypical angina pectoris and Atypical angina pectoris
(1)(1) TypicalTypical
SubsternalSubsternal Burning, heavy, or squeezing Burning, heavy, or squeezing
feelingfeeling Precipitated by exertion or emotionPrecipitated by exertion or emotion Promptly relieved by rest of NTG Promptly relieved by rest of NTG
Angina chest pain Angina chest pain
DDx of AMI DDx of AMI
Aortic dissectionAortic dissection Acute pericarditisAcute pericarditis Acute pulmonary embolismAcute pulmonary embolism Intercostal neuralgiaIntercostal neuralgia CostochondritisCostochondritis Abdominal visceral disordersAbdominal visceral disorders
PU, Pancreatitis, biliary colicPU, Pancreatitis, biliary colic
Atypical symptomsAtypical symptoms
ElderlyElderly WomenWomen DiabetesDiabetes Post operationPost operation
Angina Angina equivalentequivalent
AMI Definition
• Chest pain• ECG
• Troponin
positive
STEMI
Blood flow
Chest discomfort PMVT, VF
SuddenDeath
M. Ischemia
Heart failure
Cardiogenic shockElevated
+CK,Trop-T
M.stunning
Consequences after acute coronary artery occlusion
NSTEMI ,UA
Cardiovascular Research & Prevention Center, Bhumibol Adulyadej hospital
Wave Front TheoryWave Front TheoryLAD occlusion
False +ve TroponinFalse +ve Troponin
CardioversionCardioversion Pulmonary embolismPulmonary embolism TachycardiaTachycardia Decompensated heart failureDecompensated heart failure SepsisSepsis
TIMI Risk Score for STEMITIMI Risk Score for STEMI( Total points 0-14 )( Total points 0-14 )
HistoricalHistorical PointsPoints Age Age >> 75 75 3 3
65-7465-74 2 2DM or HT or DM or HT or 1 1AnginaAngina
Exam.Exam.SBP<100SBP<100 3 3HR >100HR >100 2 2Killip II-IVKillip II-IV 2 2Wt< 67kg( 150 lb)Wt< 67kg( 150 lb) 1 1
PresentationPresentationAnt. STE or LBBBAnt. STE or LBBB 1 1Time to Rx > 4 hrTime to Rx > 4 hr 1 1
Risk ScoreRisk Score 30-d MR(%)30-d MR(%)00 0.8 0.811 1.6 1.622 2.2 2.233 4.4 4.444 7.3 7.355 12 1266 16 1677 23 2388 27 27
>8>8 36 36
Morrow et al. Circulaion 2000
- Acute antero lateral MI - Acute antero lateral MI
Time From Onset of Symp Time From Onset of Symptomstoms
Select a reperfusion strategy
<12 hours
>12 hours
•How is “onset of symptoms”defined?
•Why the division between <12 and > 12 hours?
Select a Reperfusion Stra Select a Reperfusion Strategytegy
Thrombolytic Rx selected:
( no contraindication)
•Front-loaded alteplase or
•Streptokinase or
•Reteplase
Goal: Door-to-drug<30 min
Primary PTCA selected: Goal
•Door-to-Balloon < 90 min
Contraindication to thrombolyticRX
Or
Eqivalent alternative
- Extensive antero lateral isch - Extensive antero lateral ischemiaemia
Effect of thrombolytic on mortality Effect of thrombolytic on mortality according to admission ECGaccording to admission ECG
49
37
8
-14-20
-10
0
10
20
30
40
50
60
BBB Ant.ST ele. Inf.ST ele ST depress.
Liv
e sa
ve p
er t
ho
usa
nd
FTT Collaborative group: Lancet 1994; 343
Applicability and Efficacy ofApplicability and Efficacy of Lysis vs PCI Lysis vs PCI
0%
50%
100%
100%
50%
0%
Fribrinolysis Primary angioplsty
Availability Availability10%
<50% Treated
> 90% TIMI 3
> 90% Treated
Reocclusion
Stroke54% TIMI 3
5%
0.1%
10% Reocclusion
1% Stroke
25% Reocclusion
Total ischemic timeTotal ischemic time
A B C
ER
Rx<30min (lytic)
<90 min (PCI)
CP reperfuse
microvascular
epicardial
การคั�ดกรองการคั�ดกรอง
Fast Track MI
EKG ด�วนแพทย์�ด�ใน 10 นาท� ST elevation ตาม staff cardio ท�นท�No ST elevation ………………. MD.
1
3.7 4
6.4
14.1
0
2
4
6
8
10
12
14
16
<60 61-75 76-90 >91 PTCA notperformed
Time to PTCA (minutes)
30
-day m
ort
ality
(%
)
Relationship between 30-day Relationship between 30-day mortality and Door to Balloon mortality and Door to Balloon
time( N=522 )time( N=522 )
Berger et al. Circulation 1999;100:14-20
P=0.001
PCI vs Fibrinolysis with fibrin-PCI vs Fibrinolysis with fibrin-specific agentsspecific agents
Fribrinolysis is generally Fribrinolysis is generally preferred ifpreferred if
Early presentation Early presentation << 3 hr from 3 hr from symptom onset and delay to invasive symptom onset and delay to invasive strategystrategy
Invasive strategy is not an optionInvasive strategy is not an option Cath-lab occupied/not availableCath-lab occupied/not available Vascular access difficultiesVascular access difficulties Lack of access to a skilled PCI labLack of access to a skilled PCI lab
Delay to invasive strategyDelay to invasive strategy Prolonged transportProlonged transport (D-to-B) - (D-to-N) > 1 hr(D-to-B) - (D-to-N) > 1 hr Contact-to-B or D-to-B > 90 minContact-to-B or D-to-B > 90 min
Invasive Strategy is generally Invasive Strategy is generally preferred ifpreferred if
Skilled PCI lab available with Skilled PCI lab available with surgical backupsurgical backup (D-to-B) - (D-to-N) < 1 hr(D-to-B) - (D-to-N) < 1 hr Contact-to-B or D-to-B < 90 minContact-to-B or D-to-B < 90 min
Contraindications to fribrinolysis Contraindications to fribrinolysis including increased risk of bleeding including increased risk of bleeding of ICHof ICH
Late presentationLate presentation The symptom onset was >3 hr agoThe symptom onset was >3 hr ago
Assessment of Reperfusion Assessment of Reperfusion Option for Patients withOption for Patients with STEMISTEMI
Step 1: Assess Time and RiskStep 1: Assess Time and Risk Time since onset of symptomsTime since onset of symptoms Risk of STEMIRisk of STEMI Risk of fibrinolysisRisk of fibrinolysis Time required for transport to a skilled PCI labTime required for transport to a skilled PCI lab
Step 2 : Determine of Fibrinolysis or an Step 2 : Determine of Fibrinolysis or an Invasive Strategy is preferredInvasive Strategy is preferred If presentation in < 3 hr and there is no delay If presentation in < 3 hr and there is no delay
to an invasive strategy, there is no preference to an invasive strategy, there is no preference for either strategyfor either strategy
Absolute Contraindication Absolute Contraindication for thrombolytic Rxfor thrombolytic Rx
A: Aortic dissectionA: Aortic dissection
B: BleedingB: Bleeding ( active in 2-4 wk or bleeding ( active in 2-4 wk or bleeding diathesis) diathesis)
C: CranialC: Cranial : : Any prior ICH, Any prior ICH, 3 mo of ischemic stroke or closed head 3 mo of ischemic stroke or closed head
trauma,trauma, Intracranial neoplasm Intracranial neoplasm
D: Drug allergyD: Drug allergy
60 yo man, smoker, 1hr severe CP, BP 100/60
58 yo lady, DM HT, syncope, sweating, CP 2/10, BP 80/60
V4R
68 yo man, 3 hrs 8/10 CP, BP 100/60
Algorithm for ECG identification of the Algorithm for ECG identification of the IRA in Anterior MIIRA in Anterior MI
STE in VSTE in V11, V, V22 and V and V33
STE in V1 (>2.5 mm) and AVL or RBBB
with Q wave or both
ST depression (<1 mm) in II, III, and AVF
STE in II, III, and AVF
Wrap around
A 63 yo lady, 3 hrs 7/10 CP
Given Metalalyse + Clexane , continuing chest pain, VF x II in cath lab
AMI in LBBBAMI in LBBB Q wave : not be usedQ wave : not be used Indicator : Primary ST changeIndicator : Primary ST change
ST deviation in the same( concordant) ST deviation in the same( concordant) direction as the major QRS vectordirection as the major QRS vector
Concordant ST changesConcordant ST changes elevation elevation >> 1 mm 1 mm concordant with QRS concordant with QRS ST depression ST depression >> 1 mm 1 mm in leads V1, V2, or in leads V1, V2, or
V3V3 Extremely discordantExtremely discordant
ST elevation ST elevation > 5 mm> 5 mm discordant with QRS discordant with QRS
ST elevation without ST elevation without infarctioninfarction
LVHLVH LBBBLBBB Benign early repolarizationBenign early repolarization Brugada’s syndromeBrugada’s syndrome LV aneurysmLV aneurysm Acute pericarditisAcute pericarditis Myocarditis Myocarditis Ventricular pace rhythmVentricular pace rhythm
ED :55 yo man, 3 hrs Lt. CP 5/10, less with sits forward
GP: 34 yo athlete, anterior CP 3/10, pt. of tenderness
Fish hook
60-yo man severe headache and 60-yo man severe headache and collapsedcollapsed
Conditions Associated Conditions Associated with TDPwith TDP
E’lyte abnormalityE’lyte abnormality KK++, Mg, Mg++++, Ca , Ca ++++
Drug-relatedDrug-related AntiarrhythmicAntiarrhythmic
IA, IC, IIIIA, IC, III Psychotropic Psychotropic
agentsagents OrganophosphatOrganophosphat
ee Liquid protein diet Liquid protein diet
Cardiac disease• IHD, myocarditis• Bradycardia
CNS disease• Intracranial lesion• SAH
Congenital LQTS
Tachycardia with pulseTachycardia with pulse
Stable or unstableStable or unstable Unstable ( rate usually Unstable ( rate usually
>150/min)>150/min) Altered mental statusAltered mental status Chest painChest pain Hypotension Hypotension Signs of shockSigns of shock
If Unstable If Unstable Cardioversion Cardioversion
CardioversionCardioversion
AF : 100,200,300,360 JAF : 100,200,300,360 J Stable MMVT:100,200,300,360 JStable MMVT:100,200,300,360 J SVT or A SVT or A
flutter:50,100,200,300,360 Jflutter:50,100,200,300,360 J PMVT: Rx as VFPMVT: Rx as VF
Synchronized mode?
Stable tachycardiaStable tachycardia
Narrow QRS
•SVTSVT
•Vagal ma.
•Adenosine
6/12/12 mg IV
RegularRegular IrregularIrregular RegularRegular IrregularIrregular
Wide QRS
•AF, Aflutter, AF, Aflutter, MAT:MAT: Diltriazem, B-blocker
•MMVTMMVT
•Amiodarone 150 mg iv in 10 min repeat as needed
•Cardioversion
•AF with WPWAF with WPW: Amiodarone 150 mg iv
•TDP: MgSO4 1-2 g iv
Treat possible contributing factors: 6H-5T
SVT after Rx with Adenosine SVT after Rx with Adenosine 6mg IV6mg IV
AF with WPW: How to AF with WPW: How to Rx? Rx?
Unstable : Cardioversion 100 J
Stable : Amiodarone 150 mg IV
34-yo lady, gen. edema 3 mo.34-yo lady, gen. edema 3 mo.
Cardiac tamponadeCardiac tamponade
PericardiocentesisPericardiocentesis
HemopericardiumHemopericardium
23-y-old man with fever 7 day and chest 23-y-old man with fever 7 day and chest painpain
Pericardial fluidPericardial fluid
Hypertensive crisisHypertensive crisis Definition
Severe elevation in BP ( >220/120 mmHg) Sub classified into emergency and urgency
Hypertensive emergency Require an immediate reduction in BP ( 1
hr ) Rx IV therapy and in ICU
Hypertensive urgency No evidence of progressive end-organ injury Require only gradual reduction in BP in 24-
48 hr
Wong, T. Y. et al. N Engl J Med 2004;351:2310-2317
Examples of Mild Hypertensive Retinopathy
AV nicking
Focal narrowing
AV nicking
Copper wiring
Accelerated-malignant Accelerated-malignant HTHT
Fundoscopic changes Retinal hemorrhages Exudates Papilledema
HT and autoregulation of HT and autoregulation of CBFCBF
CBF : cerebral perfusion CBF : cerebral perfusion pressure ( CPP)pressure ( CPP)
CPP= MAP - ICPCPP= MAP - ICP
MAP = DBP + 1/3 Pulse MAP = DBP + 1/3 Pulse pressurepressure
Cerebral AutoregulationCerebral Autoregulation
Mean arterial pressure (mmHg)
Cer
ebra
l b
loo
d f
low
(ml/
100
gm
per
min
)
50
100
150
200150100500
Normotensive
Hypertensive
Strandgaard S,et al; Br Med J 1:507,1973
Goal of Rx in HT Goal of Rx in HT emergencyemergency
Reduce mean arterial BP no > 25% Within minutes to 1 hours
Toward 160/110 mmHg within 2- 6 hours
Toward normal BP in 24- 48 hours
JNC VII. JAMA 2003;289:2560-2572
Pitfalls in the Rx Pitfalls in the Rx
Excessive falls in BP should be Excessive falls in BP should be avoidedavoided ischemia : Renal, cerebral, cardiacischemia : Renal, cerebral, cardiac SL/ short acting Nifedipine: not SL/ short acting Nifedipine: not
recommendedrecommended Three exceptionsThree exceptions
Ischemic strokeIschemic stroke Aortic dissection Aortic dissection SBP should < 100 SBP should < 100
mmHg (+/-)mmHg (+/-) Lower BP for thrombolytic Rx ( Stroke )Lower BP for thrombolytic Rx ( Stroke )
Acute ischemic stroke Acute ischemic stroke and BP and BP
SBP>220 mmHg or DBP 120-140 SBP>220 mmHg or DBP 120-140 mmHgmmHg Caution reduction of BP 10%-15%Caution reduction of BP 10%-15% Carefully monitoring Neuro signs /BPCarefully monitoring Neuro signs /BP
DBP> 140 mmHgDBP> 140 mmHg IV infusion of Na nitroprusside IV infusion of Na nitroprusside Reduce BP 10%-15%Reduce BP 10%-15%
Lytic Rx within first 3 hrsLytic Rx within first 3 hrs >185/110 mmHg : contraindication>185/110 mmHg : contraindication BP BP >> 180/105 mmHg : 180/105 mmHg : iv anti HTiv anti HT
American Stroke Association. Stroke 2003;34
Acute aortic dissectionAcute aortic dissection
Suspected diagnosisSuspected diagnosis BP to the lowest tolerate level in 15-30 minBP to the lowest tolerate level in 15-30 min
Initial Rx : IV NaNTP and IV Beta-blockerInitial Rx : IV NaNTP and IV Beta-blocker Contraindication : hydralazine, nifedipineContraindication : hydralazine, nifedipine
Stimulation of sympathetic activityStimulation of sympathetic activity Increase shear stress on the aortic wallIncrease shear stress on the aortic wall
Approach to HT Approach to HT crisiscrisisBP > 220/120 mmHg
Headache
No neurosign
No target organ damage
Urgency
Identify the cause and Rx the cause ( panic, anxiety) Otherwise use
oral anti HTagent
Neurosign( encep., stroke)Neurosign( encep., stroke)
Retinopathy gr III, IVRetinopathy gr III, IV
severe chest pain ( IHD, disssevere chest pain ( IHD, dissecting aneu)ecting aneu)
Pulmonary edemaPulmonary edema
Cathecholamine excessCathecholamine excess
ARFARF
Emergency
IV therapy Recheck in 6-24 hr
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