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CORONARY CIRCULATIONAND ACUTE CORONARY
SYNDROMES
LeRoy E. Rabbani, MD Director, Cardiac Inpatient ServicesDirector, Cardiac Intensive Care Unit
Professor of Clinical Medicine
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Cellular innateImmunity
Complement
Factor H tissue bindingInhibits neutrophil
migration anddegranulation
C3bBb degradation
Stimulates EC tosecrete MCP-1
Promotes monocyteadhesion and migration
Stimulates monocytephagocytosis of E-
LDL
Stimulates IL-1 receptorantagonist
Absorbs circulating LPS,platelet activatingfactors and IL-1
CRP
–
+ Binds C1q
Complementactivation and tissue
damageFoam cellformation
Mazer SP, Thromb & Thrombolysis in press
In Vitro Effectsof CRP
eNOS
NO
NFkB
IL-6
MCP-1
CRP
Tissue Factor
ET-1
ICAM-1
VCAM-1
E-selectin
Mazer SP, Thromb & Thrombolysis i n press
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Macrophage Foam CellsMatrix Metalloproteinases– Collagenase– Stromelysin– Gelatinase– Elastase
Tissue FactorCRPMyeloperoxidase
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TIMI Risk Score for UA/NSTEMI:7 Independent Predictors
1. Age ≥65 y2. ≥3 CAD risk factors (high
cholesterol, family history,hypertension, diabetes,smoking)
3. Prior coronary stenosis ≥50%4. Aspirin in last 7 days5. ≥2 anginal events ≤24 h6. ST-segment deviation7. Elevated cardiac markers
(CK-MB or troponin)Number of Predictors
0
5
10
15
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0/1 2 3 4 5 6/7
% D
eath
/ M
I / R
evas
c
TIMI = Thrombolysis in Myocardial Infarction.Antman EM, et al. JAMA. 2000;284:835-842.
ACC/AHA Guidelines Recommendations:NSTE ACS Patients at High Risk
of Death or MIAt least one of the following features must be present: Prolonged ongoing rest pain > 20 minutes
Elevated cardiac troponin (TnT or TnI > 0.1 ng/mL)
New or presumably new ST-segment depression
Sustained ventricular tachycardia
Pulmonary edema, most likely due to ischemia
New or worsening mitral regurgitation (MR) murmur
S3 or new/worsening rales
Hypotension, bradycardia, tachycardia
Age > 75 years
Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.
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Balloon
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Lateral: Circumflex / Anterior:LAD
Vessel: RCA, Circumflex
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Vessel: RCA
RCA
V1-V3: LargeR + ST
DepressionPosterior
Circumflex,Diagonal
I, aVL,V5-V6Lateral
RCAV1-V3,
V3R-V6RRight Ventr.
RCA,Circumflex
II, III,aVFInferior
LADV1-V2Septal
LADV1-V4Anteroseptal
LAD, DiagonalV1-V6,1, aVLAnterolateral
V6Lateral
V3Anterior
aVFInferior
IIIInferior
LADV3-V4AnteriorV5
LateralV2 SeptalaVL
LateralII
Inferior
VesselsLeadsLocationV4
AnteriorV1 Septal aVRI
Lateral
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Goal
“Door-to-lytic”30 minutes
“Door-to-balloon” 90 minutes
Pharmacological Reperfusion for STEMIFibrinolysis Background/Limitations
Initial occluded artery remains (TFG 0/1), in~20% of patients → 2-fold ↑ in mortality1,2
Reocclusion occurs in 5-10% of patients → 3-fold ↑ in mortality 3,4
Reinfarction occurs in ~5% of patients → 3-fold ↑ in mortality 5
1.TIMI 1, Am J Cardiol 1998;62:179 2. GUSTO I Angio, NEJM 1993;329:1615) 3.Ohman et al., Circulation1990;82:781 4. HART II, Circ 2001;104:648; PENTALYSE, EHJ 2001;22:1716 5. TIMI 2, JACC 1995;26:900; TIMI 4 &5, Am J Cardiol 1997;80:696
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Percutaneous CoronaryIntervention (PCI)
The advantages of Primary PCIHigh 85-95% infarct vessel patency rateLow rates of recurrent ischemia,reinfarction, death, and strokeAvoidance of ICHShortened LOSAbility to treat lytic-ineligible patients
Nallamothu BK, et al. Circulation. 2005;111:761-767.
Transfer for PCI in STEMI:NRMI (1999–2002), 4278 Patients
28.4>4 h
55.42–4 h
16.2<2 h
4.2<90 min
% of PatientsDoor-to-Balloon Time
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*P<.05 for all.
Bradley EH, et al. N Engl J Med. 2006;355:2308-2320.
D2B: Strategies Associated With a SignificantReduction in Door-to-Balloon Time (“Code
90”)
8.6Having staff in the ED and cath lab use andreceive real-time feedback
14.6Having an attending cardiologist always on site
19.3Expecting staff to arrive at the cath lab within20 minutes after page
15.4Having the ED activate the cath lab whilepatient is still en route
13.8Having a single call to a central pageoperator activate the cath lab
8.2Having emergency medicine physicians activatethe cath lab
Mean reduction indoor-to-balloon
time (min)*Strategy
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