impact of primary coronary angioplasty delay on myocardial salvage, infarct size and microvascular...

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Francone M, Bucciarelli-Ducci C* , Carbone I, Canali E, Scardala R, Calabrese F, Sardella G, Mancone M, Catalano C, Fedele F, Passariello R, Bogaert J** and Agati L Impact Of Primary Coronary Angioplasty Delay On Myocardial Salvage, Infarct Size And Microvascular Damage in Patients with ST-Elevation Myocardial Infarction: Insight From Cardiovascular Magnetic Resonance *Royal Brompton Hospital, National Heart and Lung Institute, *Royal Brompton Hospital, National Heart and Lung Institute, Imperial College Imperial College London, United Kingdom London, United Kingdom **Leuven University, Belgium **Leuven University, Belgium Umberto I Hospital, University “La Sapienza”, Rome, Italy Umberto I Hospital, University “La Sapienza”, Rome, Italy

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Impact Of Primary Coronary Angioplasty Delay On Myocardial Salvage, Infarct Size And Microvascular Damage in Patients with ST-Elevation Myocardial Infarction: Insight From Cardiovascular Magnetic Resonance. - PowerPoint PPT Presentation

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  • Francone M, Bucciarelli-Ducci C*, Carbone I, Canali E, Scardala R, Calabrese F, Sardella G, Mancone M, Catalano C, Fedele F, Passariello R, Bogaert J** and Agati LImpact Of Primary Coronary Angioplasty Delay On Myocardial Salvage, Infarct Size And Microvascular Damage in Patients with ST-Elevation Myocardial Infarction: Insight From Cardiovascular Magnetic Resonance*Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, United Kingdom**Leuven University, BelgiumUmberto I Hospital, University La Sapienza, Rome, Italy

  • Time is muscleDe Luca, Circulation 2004Background

  • ChallengesBackgroundWhat happens to the muscle?How to recognize salvageable myocardium?How much salvageable myocardium is there?

  • BackgroundMICROVASCULAR DAMAGEMYOCARDIAL NECROSISMYOCARDIUM AT RISK

  • Aims of the Study To investigate the correlation between the extent and the nature of myocardial damage in relation to different time-to-reperfusion intervals To investigate the relationship between time-to-reperfusion intervals, myocardial damage and subsequent LV remodeling

  • Study Protocoln=70 STEMI, primary PCI

  • CMR Protocol Cine 6 months32 days

  • CMR Protocol 32 daysincreased signal intensity (myocardial edema)Myocardium at riskincreased signal intensity reduced signal intensity Infarct SizeMicrovascular Obstruction

  • Results: Myocardium at RiskMyocardial Edema(% LV)Time to reperfusion (min)p=0.37

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  • Results: Infarct SizeInfarct Size(% LV)Time to reperfusion (min)p=0.005

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  • Myocardium at Risk Infarct sizeTime to reperfusion (min)

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  • Myocardial SalvageMyocardial Salvage(%)Time to reperfusion (min)p=0.003

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  • Microvascular ObstructionMVO(% LV)Time to reperfusion (min)p=0.04

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  • EDV: Baseline90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)EDV(ml)p=0.03

  • EDV: Baseline vs 6 Months90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)EDV(ml)

  • ESV: Baseline90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)ESV(ml)p=0.02

  • ESV: Baseline vs 6 Months90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)ESV(ml)

  • EF: Baseline90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)EF(%)p=0.06

  • EF: Baseline vs 6 Months90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)EF(%)

  • LAD Infarctions90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)* MVOMyocardiumat RiskInfarctSize

  • Non-LAD Infarctions90 min>90-150 min>150-360 min>360 min Time to reperfusion (min)* MVOMyocardiumat RiskInfarctSize

  • Conclusions-1First in-vivo, clinical, non invasive evaluation of the consequences of early and delayed coronary reperfusion on myocardial damage

  • Conclusions-2 Time is muscleLonger time-to-reperfusion(>360min)Myocardial salvage, infarct size and MVO by CMRsurrogate endpoints for clinical trials assessing the efficacy of reperfusion strategies

    Dear Chairmen and colleagues. I would like to thank AHA for this opportunity and for the privilege of being here today. **TIME IS MUSCLE. Virtually every min of delay in revascularizing patients with STEMI (either with thrombolitic therapy or primary PCI) does affect the patients prognosis. In fact, the 1-year mortality is increased by 7.5% for each 30-minute delay.

    Time is muscle, but what happens to the muscle??*TIME IS MUSCLE. Virtually every min of delay in revascularizing patients with STEMI (either with thrombolitic therapy or primary PCI) does affect the patients prognosis. In fact, the 1-year mortality is increased by 7.5% for each 30-minute delay.

    Time is muscle, but what happens to the muscle??*Cardiac MRI can provide an in-vivo myocardial tissue characterization with a range of sequences that can identify irreversible myocardial Tehre is a strong evidence that CMR in vivo

    And, in particular, can identify the presence and extent of myocardial necrosis (with a T1w sequence with contrast), and myocardium at risk (using a T2w sequence). But also detect microvascular damage. All these applications have been validated histologically but the one use in clinical practice is primarly infarct imaging. *The aim of our study was to We studied 70 patients with STEMI successfully treated with primary PCI within 12 hours of the onset of symptoms.

    Patients were divided into 4 time-to-reperfusion quartiles. Time-to-reperfusion was defined as the time interval between symptoms and balloon inflation.

    Single center, high volume**CONSIDERARE METTERE CINE Aggiungere Follow-up**Increased signal intensity on T2w images was observed in 62/70 patients (89%). Mean size 168 gr. (16, 15, 15, 19%). *Infarcted region was visualized in all patients in correspondance of the territory of distribution of the IRA. Mean size 12 8 % (8, 11, 12, 18%).

    Infarct size significantly increased over time across the 4 groups (One-way analysis of variance by the use of linear trend analysis). A post-doc analysis with Bonferroni correction used for differences between groups. *How much of the initial myocardium at risk was actually salvagable?To answer this question, what we have to do is is a simple substraction of the infarct size from the initial area at risk. *Salvagable myocardium (edematous but not necrotic myocardium) was significantly reduced over time. (8.5, 3.2, 2.4, 2.1%).

    Please note that myocardial salvage is markedly decreased when reperfusion occurred after 90 min. *Mean size of MVO was 2.1 3.4%(0.5, 1.5, 3.7, 6.6%)Large EDV and ESV and reduced EF only in group IV.

    ANIMATION*Large EDV and ESV and reduced EF only in group IV.

    ANIMATION*Large EDV and ESV and reduced EF only in group IV.

    ANIMATION*Large EDV and ESV and reduced EF only in group IV.

    ANIMATION*Large EDV and ESV and reduced EF only in group IV.

    ANIMATION*Large EDV and ESV and reduced EF only in group IV.

    ANIMATION****

    *