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Calcified Coronary Lesion:
Difficulties and Challenges
Zhou Yu Jie MD, PhD, FACC, FSCAI, FHRS
Beijing An Zhen Hospital, Capital Medical University, Beijing, China
Sweet dream or nightmare ?
Marker for CAD and increased mortality
JACC: CARDIOVASCULAR IMAGING. 2010 Dec;3(12). JACC: CARDIOVASCULAR IMAGING. 2012 Oct;5(10)
4,425 Suspected CAD patientsFollow-up 3 years
4,609 asymptomatic individuals Follow-up 3.1 years
Coronary Artery Calcium (CAC) in the Multi-Ethnic Study
Coylewright et al. Atherosclerosis.2011
CAC are associated with CHD events
Risk Factors ( The MESA study )
Race and gender
Age
BMI
Smoking
Family history of heart attack
Hyperlipidemia Intimal calcification
Hypertension Intimal calcification
Diabetes Medial calcification
CKD Medial calcification
Rheumatic diseases
Circulation. 2007;115:2722-2730
Inverse relationship between BMI and CAC
Atherosclerosis. 2012 March ; 221(1): 176–182.
Method :9,993 patients undergoing PCIThe degree of index lesion calcification (ILC) based on angiography
Elevated BSA is a predictor of CAC, not BMI
Coron Artery Dis 2012 Mar;23(2):113-7
Method : 3172 consecutive patients underwent CAC scores
Mechanism of CAC
Vascular calcification is an active ,regulated process
BMP-Wnt signalingBMP-Smad signaling
Major Theories of Vascular Calcification
Vascular calcification
Apoptotic bodies
CELL DEATH
LOSS OF INHIBITIONPyrophosphateMGPOPNFetuin/alpha2-HS glycoproteinOthers
Matrix Vesicles
DISTURBED Ca/Pi BALANCEHyperphosphatemiaHypercalcemia
INDUCTION OF BONE FORMATIONVascular bone and cartilage-like cells
INDUCING FACTORSPiLipidsInflammatory cytokinesOthers
BisphosphonatesOPG
Bone Remodeling
CIRCULATING NUCLEATIONAL COMPLEXES
Ca x Pi
DISTURBED Ca/Pi BALANCEHyperphosphatemiaHypercalcemia
INDUCING FACTORSPiLipidsInflammatory cytokinesOthers
Apoptotic bodies
Matrix Vesicles
INDUCTION OF BONE FORMATIONVascular bone and cartilage-like cells
DISTURBED Ca/Pi BALANCEHyperphosphatemiaHypercalcemia
INDUCING FACTORSPiLipidsInflammatory cytokinesOthers
CELL DEATH
BisphosphonatesOPG
Apoptotic bodies
Matrix Vesicles
INDUCTION OF BONE FORMATIONVascular bone and cartilage-like cells
DISTURBED Ca/Pi BALANCEHyperphosphatemiaHypercalcemia
INDUCING FACTORSPiLipidsInflammatory cytokinesOthers
CIRCULATING NUCLEATIONAL COMPLEXES
CELL DEATH
BisphosphonatesOPG
Apoptotic bodies
Matrix Vesicles
INDUCTION OF BONE FORMATIONVascular bone and cartilage-like cells
DISTURBED Ca/Pi BALANCEHyperphosphatemiaHypercalcemia
INDUCING FACTORSPiLipidsInflammatory cytokinesOthers
Bone Remodeling
CIRCULATING NUCLEATIONAL COMPLEXES
CELL DEATH
BisphosphonatesOPG
Apoptotic bodies
Matrix Vesicles
INDUCTION OF BONE FORMATIONVascular bone and cartilage-like cells
DISTURBED Ca/Pi BALANCEHyperphosphatemiaHypercalcemia
INDUCING FACTORSPiLipidsInflammatory cytokinesOthers
No effective medicine treatment
• Evidence from meta-analysesStatin and LDL-C
Statin and calcification
Coylewright et al. Atherosclerosis.2011
Statins promote CAC (VADT trail)
Saremi et al. Diabetes Care.2012;2390-2
Stent thrombosis12
Strategy of PCI in CAC
Balloon angioplastyCutting balloonRotablatorStentPost dilationLaser
Strategy for balloon angioplasty
Small size balloon preferedPressure of BC from 8 atm, slowly increase The up limit of pressure may be 16 atmFlow restricting dissection or perforation be
concerned
14
Cutting balloon for calcified lesion
• Indication for cutting balloon: Lesion relatively short (<20mm) Concentric lesions • Heavily calcified lesion not appropriate, but
sometimes brought supprise
15
Rotablator for calcified lesion
Effective device for calcified lesionDifferential tissue cutting ----selectively hard lesion, no soft tissueOptimal burr size---60%-70% of reference vessel
diameter Prevent no flow & slow flow ----nitroprusside, adenosine , etcUpper limit of rotablator: just enough for
revascularization
16
Rotational Atherectomy(RA)
JACC Cardiovasc Interv 2013 Jan;6(1):10-9
Randomized ROTAXUS Trial Outcome
Randomized ROTAXUS Trial Outcome
Death MI
TVR MACE
JACC Cardiovasc Interv 2013 Jan
CONCLUSIONS :
RA does not increase the efficacy of DES in calcified lesions
Using RA did not reduce late lumen loss of DES at 9 months
RA remains the default strategy for complex calcified lesions
Analysis of the UK central cardiac audit database
Method :221,669 PCI procedures 2152 patients (0.97%) : RA (RA+) Remainder conventional PCI : (RA-)
CONCLUSIONS :RA was undertaken in patients with higher pre-procedural risk. Medium term survival was worse among patients undergoing RA.Procedural success and complication rates seem acceptable in this context. RA remains clinically useful for patients with calcified coronary lesions.
Int J Cardiol. 2014 Jan 1;170(3):381-7
Rotational atherectomy for LM in octogenarians 42 patients ≥80 years had undergone stenting for calcified LMCA
disease Procedural success is good (92.3% vs. 96.6%) RA appeared to be a safe and effective strategy for the treatment of
LMCA disease in octogenarians who were refused for surgery
Int J Cardiol 2013 Apr;26(2):173-82
Rotablator for failed angioplasty • An 84 year man• Previous failed angioplasty due to balloon rupture• CAG showing severe CCL21
PCI for LADPCI for LAD- - Rotablator 22
Stent deployment23
Rotational Atherectomy and IVUS
a
b
Pre
Post RA1.75 mm
burr
Post 1.75 mm burr RA
Pre
DES for calcified lesion
DES use was associated with a significantly lower risk in repeat revascularization (HR = 0.57; 95% CI 0.40–0.82; P = 0.002) compared to BMS group in CCL
TAXUS-IV sub study : 9-month angiographic follow-up, DES significantly reduced the amount of late loss compared with the BMS (0.26 +/- 0.56 vs 0.51 +/- 0.48 mm, p = 0.015) in the calcific lesions
25
Sripal Bangalore, CCI 77:22–28 (2011)Moussa I, Am J Cardiol. 2005 Nov 1;96(9):1242-7
Post dilation for calified lesion
Post dialation last straw for calified lesion Non compliant, high pressure balloon first
choiceBe careful coronary perforation or serious
dissection
26
Postdilation in severe CCL27
Clinical presentationClinical presentation
33
Diagnosis: UAP Diagnosis: UAP
Prior MIPrior MI
HypertensionHypertension
11Progressive deterioration of chest pain for 3 Progressive deterioration of chest pain for 3
years (CCS II), presented with unstable years (CCS II), presented with unstable
episodes in last 2 weeks (CCS III)episodes in last 2 weeks (CCS III)
22With a history of HBP, prior inferior and With a history of HBP, prior inferior and
anterior myocardial infarctionanterior myocardial infarction
Male, 84-year-oldMale, 84-year-old
TnI levels of 0.01 ng/mL (normal
range,
<0.05 ng/mL), Cre 76umol/L, ALT
23U/L,
AST 34U/L
A 2-dimensional echocardiogram
demonstrated decreased left
ventricular
function, with an ejection fraction of
41%
Laboratory tests
Electrocardiogram
Coronary Angiography
Coronary Angiography
The patient refused the surgical solution and medical conservative therapy
After discussion the decision was made to perform sequential PCI: RCA CTO first, then unprotected LM lesions
Treatment strategy
PCI for RCA
GC: JR 4.0, GW: Pilot 50Predilation BC: Sprinter 1.5 x 15mm and 2.0 x20mm
Final result-RCA
DES implantation: Firebird2 2.75x33mm for d-RCA and Partner 3.0x36mm for p-RCA
PCI for LMPCI for LM1 week later
GC: EBU 3.5, GW: BMW (to LAD) and Runthrough NS (to LCX)
Pre-PCI IVUSPre-PCI IVUS
PCI for LMPCI for LM-Predilation-Predilation
Predilation BC: Sprinter 2.5 x 15mm, 12-20atm
PCI for LMPCI for LM--11stst Stent Implantation Stent Implantation
DES implantation : Firebird2 2.75x23mm for m-LAD (12atm)
PCI for LMPCI for LM-2-2ndnd Stent Stent MigrationMigration
LM/p-LAD Stent Migration (Cypher 3.5x33mm), exchange to 8F sheath
PCI for LMPCI for LM-Retrieving Stent-Retrieving Stent
Migrated stent was retrieved successfully assisted with Sprinter 1.5x15mm
Migrated stent
PCI for LMPCI for LM -Continue with Mini-Crush -Continue with Mini-Crush
Continue with 7F EBU 3.5; Mini-Crush technique was usedFirebird2 3.5x33mm for LM/p-LAD and Firebird2 3.0x18mm for LCX
PCI for LMPCI for LM-Postdilation-Postdilation
Postdilatation with Avita HP 3.5x15mm (14-20atm for LM/p-LAD stent)
PCI for LMPCI for LM--1st Final Final KissingKissing
1st final kissing with Avita HP 3.5x15mm (LAD) and Sprinter 3.0x12mm (LCX)
2nd IVUS test LAD ostia stent expansion unacceptable
PCI for LMPCI for LM--Re-postdilatation
Re-postdilatation with Avita HP 3.5x15mm (18-24atm for LM/p-LAD stent)
PCI for LMPCI for LM--2st Final KissingFinal Kissing
2nd final kissingAvita HP3.5x15mm (LAD) and Sprinter3.0x12mm (LCX)
Final result
Final IVUS test-acceptable