www.metcardio.org use of troponins in the diagnosis and management of peri-procedural myocardial...
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Use of troponins in the Use of troponins in the diagnosis and management diagnosis and management
of peri-procedural of peri-procedural myocardial infarctionmyocardial infarction
Giuseppe Biondi ZoccaiGiuseppe Biondi Zoccai
Division of Cardiology, University of Modena and Reggio Emilia
Meta-analysis and Evidence-based medicine Training in Cardiology (METCARDIO), Ospedaletti, Italy
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LEARNING MILESTONES
• Scope of the problem
• Diagnosis of peri-procedural infarction
• Management of peri-procedural infarction
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LEARNING MILESTONES
• Scope of the problem
• Diagnosis of peri-procedural infarction
• Management of peri-procedural infarction
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BASICS OF PERI-PCI MI
Herrmann et al, Eur Heart J 2005
Item Comment
Definition and diagnosis
Cardiac serum marker elevation above the ULN after PCI related presumably to myocardial necrosis (ideally, rise and fall pattern on serial blood sampling; spot check at 24 (–48) h after PCI may be permissible)
Incidence On average, 25-30% of all coronary procedures (range 0-70%)
Risk factors Patient-related: diffuse, multivessel CAD, age, UAP, (hs)CRP; lesion-related: complex, de novo lesions,especially SVG lesions; procedure-related: new device use, procedural complications
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BASICS OF PERI-PCI MI
Herrmann et al, Eur Heart J 2005
Item Comment
Pathophysiology Blood flow impairment on epicardial level (proximal type, type I) or, in the majority of cases, on microcirculatory level (distal type, type II)
Presentation Mainly clinically silent, in some cases CP, arrhythmias, hypotension
Prognosis Increased risk of cardiac mortality Prevention and treatment
Acute: supportive, symptomatic therapy per MI recommendations; chronic: CAD/CHF managementMechanical: distal filter/balloon occlusion systems, pre-conditioning; pharmacological: antiplatelet agents,statins, IC non-selective beta-blocker
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TYPES OF PERI-PCI MI
Herrmann et al, Eur Heart J 2005
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MECHANISMS OF PERI-PCI MI
Zimarino et al, Atherosclerosis 2011
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MECHANISMS OF PERI-PCI MI
Side-branch closure
Thrombo-embolism
Dissection
Microvascular impairment
Prolonged occlusion
Spasm
Zimarino et al, Atherosclerosis 2011
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TOOLS TO RECOGNIZE PERI-PCI MI
EKG
MRI
Echo
Nuclear scan
ALT/AST
CK
CK-MB activity
CK-MB mass
Troponin
HS troponin
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WHY I HATE TROPONINS
Hickman et al, Clin Chim Acta 2010
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WHY I HATE TROPONINS
Hickman et al, Clin Chim Acta 2010
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WHY I HATE TROPONINS
Hickman et al, Clin Chim Acta 2010
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WHY I HATE TROPONINS
Hickman et al, Clin Chim Acta 2010
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(SOME) MECHANISMS OF TROPONIN RELEASE
Kociol et al, JACC 2010
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EVOLUTION OF TROPONIN
Mahajan et al, Circulation 2011
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HS TROPONIN T ASSAYS
Twerenbold et al, Swiss Med Wkly 2011
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HS TROPONIN T ASSAYS
Twerenbold et al, Swiss Med Wkly 2011
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STANDARD VS HIGH-SENSITIVITY TROPONIN
ASSAYS
Twerenbold et al, Swiss Med Wkly 2011
Standard cTnT
cTnI (Siemens)
cTnI (Abbott)
cTnT (Roche)cTnI (Roche)
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COMPREHENSIVE TROPONIN ASSESSMENT IN ACS
Ndrepepa et al, Clin Chim Acta 2011
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COMPREHENSIVE TROPONIN ASSESSMENT IN ACS
Ndrepepa et al, Clin Chim Acta 2011
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COMPREHENSIVE TROPONIN ASSESSMENT IN ACS
Ndrepepa et al, Clin Chim Acta 2011
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HS TROPONIN IN STABLE CAD
Ndrepepa al, Am J Cardiol 2011
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USEFULNESS AT ADMISSION
Celik et al, Clin Res Cardiol 2011
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USEFULNESS AT ADMISSION
Celik et al, Clin Res Cardiol 2011
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IMPACT ON OUTCOMES
Brener et al, Eur Heart J 2002
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ANY SYNTHESIS POSSIBLE?CK-MB mass Standard
troponinHS troponin MRI
Cutoff: normal vs. pathologic
Well-defined Well-defined Evolving Evolving
Sensitivity Low High Very high High
Localization No No No Yes
Time pattern of rise and fall
Well-defined Well-defined Evolving Well-defined
Method of standardization
High High High Evolving
Relation with prognosis
Well-defined Controversial Evolving Evolving
Fulfills universal definition of MI
Yes Yes Yes No
Schoenhagen et al, JACCInt 2010
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LEARNING MILESTONES
• Scope of the problem
• Diagnosis of peri-procedural infarction
• Management of peri-procedural infarction
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UNIVERSAL DEFINITION OF MI
Thygesen et al, Eur Heart J 2007
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UNIVERSAL DEFINITION OF MI
Thygesen et al, Eur Heart J 2007
www.metcardio.orgTesta et al, QJM 2009
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IMPACT OF TROPONIN ON MACE
Testa et al, QJM 2009
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BIAS OF REGISTRIES VS RCT
Tzoulaki et al, BMJ 2011
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CK-MB BESTS TROPONIN
Lim et al, JACC 2011
G1: no necrosis
G2: Peri-PCI myocardial injury (PMI)
G3: Peri-PCI MI
LGE: MRI late gadolinium enhancement
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CK-MB BESTS TROPONIN
Lim et al, JACC 2011
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CK-MB BESTS TROPONIN
Lim et al, JACC 2011
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PERI-PCI MI AND SYNTAX SCORE
van Gaal et al, Int J Cardiol 2009
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PERI-PCI MI AND LESION TYPE
van Gaal et al, Int J Cardiol 2009
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OTHER CAUSES OF TROPONIN
Thygesen et al, Eur Heart J 2007
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PERI-PCI INCREASE >ULN
Wiseth et al, EuroIntervention 2006
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REVISED ACADEMIC RESEARCH CONSORTIUM CRITERIA
Vranckx et al, EuroIntervention 2010
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REVISED ACADEMIC RESEARCH CONSORTIUM CRITERIA
Vranckx et al, EuroIntervention 2010
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LEARNING MILESTONES
• Scope of the problem
• Diagnosis of peri-procedural infarction
• Management of peri-procedural infarction
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WHAT SHOULD YOU DO IF• A patient has an increased post-PCI level
of cTn or CKMB:
– If not an MI (cTn>3 x ULN but CKMB < 3 x ULN):
• Reassess Hx/PE, EKG, angio and procedural features to define individual risk
• Maximize medical Rx• Proceed with discharge and set up follow-up
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WHAT SHOULD YOU DO IF• If a patient has an increased post-PCI level of
cTn or CKMB:
– It qualifies as MI (CKMB>3 x ULN):• Reassess Hx/PE, EKG, angio and procedural features to
define individual risk• Enforce continuous EKG monitoring• Assess whether repeat cath is required• Continue blood draws for CKMB curve• Maximize medical Rx• Do not discharge until CK-MB below ULN• Then, proceed with discharge and set up follow-up
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HOW CAN YOU MAXIMIZE MEDICAL RX AFTER PCI
Biondi-Zoccai et al, Int J Cardiol 2011
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HOW CAN YOU MAXIMIZE MEDICAL RX AFTER PCI
Biondi-Zoccai et al, Int J Cardiol 2011
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HOW CAN YOU MAXIMIZE MEDICAL RX AFTER PCI
Biondi-Zoccai et al, Int J Cardiol 2011
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MCQ1. Come si definisce l’infarto miocardico periprocedurale nei pazienti sottoposti ad angioplastica coronarica?
A. Rialzo di oltre 2 volte il 99° percentile del limite superiore di riferimento
B. Rialzo di oltre 5 volte il 99° percentile del limite superiore di riferimento
C. Rialzo di oltre 1 volta il 99° percentile del limite superiore di riferimento
D. Rialzo di oltre 3 volte il 99° percentile del limite superiore di riferimento
E. Rialzo di oltre 10 volte il 99° percentile del limite superiore di riferimento
2. L’impatto prognostico del rialzo periprocedural dei marker miocardici nei pazienti sottoposti ad angioplastica coronarica è stato:
A. Dimostrato in alcuni studi, ma non dopo aggiustamento multivariabile in altri
B. Dimostrato in alcuni pazienti, ma non in quelli a basso rischio
C. Dimostrato in alcuni pazienti, ma non in quelli ad alto rischio
D. Dimostrato in tutti i pazienti e in tutti gli studi
E. Negato incontrovertibilmente
3. L’utilità di monitorare la troponina nei pazienti sottoposti ad angioplastica coronarica risiede nella sua capacità di:
A. Identificare i pazienti con quadro angiografico a maggior rischio di infarto o morte
B. Identificare i pazienti che necessitano di procedura complessa a maggior rischio di infarto o morte
C. Identificare i pazienti che manifestano complicanze inattese precoci successivamente alla procedura
D. Identificare i pazienti con aumentato rischio di eventi a partire da 1 mese dopo l’angioplastica
E. Identificare i pazienti con aumentato rischio di eventi a partire da 1 anno dopo l’angioplastica
4. I meccanismi più frequenti di infarto peri-procedurale sono:
A. La trombosi intrastent e l’occlusione di branche laterali
B. Lo spasmo occlusivo e la trombosi intrastent
C. L’occlusione di branche laterali e l’embolizzazione di materiale atero-trombotico
D. L’embolizzazione di materiale atero-trombotico e la trombosi intrastent
E. Lo spasmo occlusivo e l’occlusione di branche laterali
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Thank you for your attention
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