Manual of STEMI Interventions E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 798

Veröffentlichungsjahr: 2017

Beschreibung

Benefit from this concise yet comprehensive manual, designed to improve the practice and process of STEMI interventions

• Understand the varied pharmacological options available in managing STEMI patients, including newer anti-coagulants   
• Improve your STEMI procedure technique through expert guidance, including stent choice, and other techniques such as trans radial procedures 
• Provides an overview of STEMI networks internationally and how to set up a STEMI program
• Reviews future perspectives for STEMI and the role of telemedicine for STEMI procedures

Leseprobe

Table of Contents

Cover

Title Page

List of Contributors

Preface

Part I: Guidelines, Thrombolytic Therapy, Pharmacology

1 Compendium of STEMI Clinical Trials

Introduction

References

2 European Society of Cardiology and American College of Cardiology STEMI Guidelines

Introduction

References

3 The Role of Thrombolytic Therapy in the Era of STEMI Interventions

Introduction

Thrombolytic Therapy: Clinical Benefit, Risks and Contraindications

Primary PCI: Overview of Randomized Clinical Trials

Clinical Impact of Time to Reperfusion

Facilitated PCI and the Pharmacoinvasive Strategy

Conclusions

References

4 Anticoagulants in STEMI Interventions

Introduction

Anticoagulants

Discussion

How to Choose: The Eternal Dilemma Between Bleeding and Ischemic Risk

References

5 New Oral and Intravenous Adenosine Diphosphate Blockers in STEMI Intervention

Introduction

Physiology

Aspirin in STEMI

ADP Blockers in ACS, PCI and STEMI Intervention

Other Important Issues

Future Directions

Summary

References

Part II: The STEMI Procedure

6 The Role of Acute Circulatory Support in STEMI

Introduction

Intra‐Aortic Balloon Counterpulsation

Impella Use in STEMI

The TandemHeart Device in STEMI

Venoarterial Extracorporeal Membrane Oxygenation

Right Ventricular Myocardial Infarction

Time for a Paradigm Shift: From Primary Reperfusion to Primary Unloading in STEMI

References

7 Thrombus Management for STEMI Interventions

Introduction

Pathophysiology of Thrombus

Thrombus and STEMI

Mehta Strategy

Global Strategies of Thrombectomy and Recent Trials

Conclusions

References

8 Transradial Techniques to Improve STEMI Outcomes

Introduction and Historical Perspective

The Transradial Approach and STEMI Interventions

Rationale for Using the Transradial Route for STEMI Interventions

Developing a Transradial Acute Myocardial Infarction Program

Limitations

Conclusions

References

9 Management of Cardiogenic Shock

Diagnosis and Pathophysiology

Incidence and Prognosis

Interventional Management

Treatment of Mechanical Complications

Intensive Care Unit Treatment

Mechanical Support

Summary

References

10 Present Role of Thrombectomy in STEMI Interventions

Rationale for Thrombectomy in Acute Myocardial Infarction

Thrombectomy Devices

Evidence for Manual Thrombectomy

Evidence for Mechanical Thrombectomy

Conclusions

References

11 Choice of Stent in STEMI Interventions

Introduction

Historical Perspective

Stents in STEMI Interventions: How it all Started

Re‐stenosis

Great Expectations: First‐Generation Drug‐Eluting Stents in STEMI

Dawn of a New Era: Second‐Generation Drug‐Eluting Stents

The Emperor’s New Clothes

Bioresorbable Vascular Scaffold in acute Myocardial Infarction

Conclusion

References

12 Illustrated STEMI Procedures I – Basic STEMI Skills

Introduction

Case 1

Case 2

Case 3

Case 4

Case 5

13 Illustrated STEMI Procedures II – Basic STEMI Skills

Introduction

Case 6

Case 7

Case 8

Case 9

Case 10

References

14 Illustrated STEMI Procedures III – Basic STEMI Skills

Introduction

Case 11

Case 12

Case 13

Case 14

Case 15

15 Remote Ischemic Conditioning for Acute Myocardial Infarction

Introduction

The Concepts of Ischemic Conditioning

Mechanisms of Remote Ischemic Conditioning

Measuring Myocardial Injury in the Clinic

Effect of Remote Ischemic Conditioning in Acute Myocardial Infarction

Confounding Factors in Remote Ischemic Conditioning

Alternative Methods to Achieve Cardioprotection

Introducing Remote Ischemic Conditioning as Standard Adjuvant Therapy in STEMI

Conclusions

References

Part III: The STEMI Process

16 Reducing Door‐to‐Balloon Times

Introduction

Early Initiatives and Quality‐of‐Care Measures to Minimize Door‐to‐Balloon Time

Regional STEMI Systems to Further Reduce Door‐to‐Balloon Time

Limitations of Door‐to‐Balloon Time

Future Directions

References

17 Pre‐hospital Triage and Management

Introduction

The STEMI Receiving Center Network

Essential Roles for the Emergency Medical Services

Supplemental Roles for the Emergency Medical Services

Emergency Medical Services Transport Logistics

Quality Improvement for Emergency Medical Services: Three Key Time Intervals

Pre‐hospital Medications

STEMI Complicated by Out of Hospital Cardiac Arrest

Conclusions

References

18 Creating Networks for Optimal STEMI Management

Introduction

Transfer for PPCI Trials

Growth and Success of STEMI Systems of Care Within the United States

Organizing A System for Inter‐Hospital Transfer

Key Components of a STEMI System of Care

Challenges to Implementing and Maintaining a Regional STEMI System of Care

Conclusions

References

19 Pharmacoinvasive Management of STEMI

Introduction

Fibrinolytic Therapy

Pharmacoinvasive Therapy

Trials Comparing Routine Early PCI After Fibrinolysis With Standard Therapy and Primary PCI Alone

Current Guidelines for Pharmacoinvasive Therapy

Guideline Recommendations

Discussion

References

Part IV: Global STEMI Initiatives

20 Stent for Life

Introduction

Stent for Life Initiative

Summary

References

21 Urban Combined Pharmacoinvasive Management of STEMI Patients as Antidote to Traffic in Large Metropolitan Cities

Introduction

The Role of Coronary Thrombosis in Pathogenesis of STEMI

The Experience of Moscow

Conclusions

References

22 Lessons from the Puerto Rico Infarction National Collaborative Experience Initiative

Introduction and Background

Inspired to Make Changes

Executing the Plan

The Ultimate Goal: Total Ischemia Time

Summary

Acknowledgements

References

23 The STEMI Care Program in China

Introduction

Current Status of STEMI Reperfusion in China

China STEMI Care Program

Conclusions

References

24 STEMI INDIA

Introduction

Beginnings

Aims and Goals

Developing a STEMI System of Care: The STEMI INDIA Model

The Prototype Statewide STEMI Project: The Pilot Tamilnadu STEMI Project

Framework for a Statewide STEMI Program

Other Important Activities of STEMI INDIA

References

25 The Role of Telemedicine in STEMI Interventions

Definition of Telemedicine

Computer Power

Artificial Intelligence

Cloud Computing

Pervasive Computing, Ubiquitous Computing or the Internet of Things

Socioeconomic Disparities

Healthcare Disparities

Time as a Strong Predictor of Outcomes

LATIN, A Cloud Computing STEMI Network Supported by Artificial Intelligence

Conclusions

References

26 Innovative Telemedicine STEMI Protocols

Introduction

Methods

Results

Discussion

Conclusions

References

Part V: Future Perspectives

27 STEMI Interventions, Beyond the Culprit Lesion

Introduction

The Clinical Conundrum

Current Evidence

Special Circumstances

Conclusions

References

28 Promising Technologies for STEMI Interventions

Introduction

Endothelial Progenitor Cell Capture Stent

Potential Advantages of the EPC Capture Stent in STEMI

EPC Capture Stent in STEMI

The Combo Stent: A Combined DES and EPC Capture Stent

Bioresorbable Vascular Scaffold

Conclusions

References

Index

End User License Agreement

List of Tables

Chapter 01

Table 1.1 Which stent is most desirable for STEMI interventions?

Table 1.2 Management of no‐reflow.

Table 1.3 Is thrombectomy an available tool in STEMI?

Table 1.4 Percutaneous coronary intervention in non‐culprit vessel.

Table 1.5 Role of the intra‐aortic balloon pump and counterpulsation in STEMI intervention.

Chapter 02

Table 2.1 Classification of recommendations and levels of evidence.

Table 2.2 Recommendations for the use of glycoprotein IIb/IIIa receptor antagonists.

Table 2.3 Recommendations for the use of thienopyridines.

Table 2.4 Recommendations for the use of parenteral anticoagulants.

Table 2.5 Recommendations for triage and transfer for percutaneous coronary intervention.

Table 2.6 Recommendations for intensive glucose control in STEMI.

Table 2.7 Recommendations for thrombus aspiration during percutaneous coronary interventions (PCI) for STEMI.

Table 2.8 Recommendations for the use of stents in STEMI.

Table 2.9 Recommendation for angiography in patients with chronic kidney disease.

Table 2.10 Recommendations for the use of fractional flow reserve.

Table 2.11 Recommendations for percutaneous coronary interventions (PCI) for unprotected left main coronary artery disease.

Table 2.12 Antiplatelet therapy to support primary percutaneous coronary interventions (PCI) for STEMI.

Table 2.13 Antiplatelet and anticoagulant therapy discussed in the 2013 American Heart Association (AHA) and European Society of Cardiology (ESC) guidelines to support percutaneous coronary interventions in STEMI.

Table 2.14 Evaluation and management of patients with STEMI and out‐of‐hospital cardiac arrest.

Table 2.15 Primary percutaneous coronary interventions and STEMI.

Chapter 03

Table 3.1 Characteristics of thrombolytic therapy agents.

Table 3.2 Guidelines recommending antithrombotic therapy with thrombolytic therapy.

Chapter 04

Table 4.1 Selection of the most important studies on anticoagulants in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). The ischemic endpoint was the main ischemic endpoint at 30 days available in the study results. The bleeding endpoint was the main definition used for major/severe bleeding in each trial.

Table 4.2 Dose, contraindications, advantages and disadvantages of the main anticoagulant drugs available for STEMI patients undergoing primary percutaneous coronary intervention.

Chapter 05

Table 5.1 P2Y

12

Inhibitors.

Table 5.2 Ticlopidine and clopidogrel studies.

Table 5.3 Prasugrel studies.

Table 5.4 Ticagrelor studies.

Table 5.5 Cangrelor studies.

Chapter 07

Table 7.1 Thrombolysis in myocardial infarction (TIMI) thrombus grade.

Table 7.2 Strategy for the management of the STEMI lesion based on thrombus grade; Mehta Classification.

Table 7.3 Step by step technique for STEMI interventions.

Table 7.4 Thrombectomy devices.

Chapter 09

Table 9.1 Technical features of currently available percutaneous support devices.

Chapter 10

Table 10.1 Characteristics of the most common manual and mechanical thrombectomy devices compatible with 0.014‐inch guide wires.

Table 10.2 Randomized studies showing the effects of manual thrombus aspiration.

Table 10.3 Randomized studies showing the effects of mechanical thrombus aspiration.

Chapter 11

Table 11.1 Median rate per 1000 patient‐years of follow‐up of selected efficacy and safety outcomes and the probability that each stent type has the lowest rate from mixed treatment comparison analysis.

Chapter 15

Table 15.1 Clinical studies of remote ischemic conditioning in acute myocardial infarction.

Chapter 17

Table 17.1 Emergency medical services roles.

Table 17.2 Advantages and disadvantages of methods of interpreting pre‐hospital electrocardiogram (adapted from the American Heart Association statement,

Circulation

, 2008; 118: 1066–1079) [10].

Table 17.3 Common QRS complex ST‐elevation mimics.

Table 17.4 Three scenarios for appropriate catheterization laboratory activation involving patients with out‐of‐hospital cardiac arrest.

Table 17.5 Three emergency medical services (EMS) time intervals.

Chapter 21

Table 21.1 Main historical and demographic data in the studied groups of patients.

Table 21.2 Complications in the pre‐hospital thrombolysis group.

Table 21.3 In‐hospital clinical and angiographic data in the studied groups of patients.

Table 21.4 Frequency of ventricular fibrillation in the studied groups of patients.

Table 21.5 Long‐term clinical and angiographic data in the studied groups of patients.

Table 21.6 Long‐term changes in left ventricular ejection fraction (LVEF) in the studied groups of patients.

Chapter 23

Table 23.1 Components and aims of the China STEMI care program.

Chapter 24

Table 24.1 STEMI INDIA model; two strategies, employing a) primary percutaneous coronary intervention (PCI) for patients with short transportation times, and b) pharmacoinvasive strategy for patients with long transportation times.

Chapter 26

Table 26.1 Relevant Statistics Comparison between Developed and Developing Countries.

Chapter 27

Table 27.1 Current guidelines for the management of non‐culprit bystander coronary lesions.

Table 27.2 Prospective clinical trials of the management of non‐culprit bystander coronary lesions.

Table 27.3 Current prospective clinical trials of the management of non‐culprit bystander coronary lesions.

Chapter 28

Table 28.1 Published studies on endothelial progenitor cell capture stent in STEMI.

List of Illustrations

Chapter 02

Figure 2.1 Triage and transfer for PCI.

Chapter 03

Figure 3.1 Short‐ and long‐term clinical outcomes in patients treated with primary percutaneous coronary intervention or thrombolytic therapy.

Figure 3.2 Reperfusion therapy for patients with STEMI. * Patients with cardiogenic shock or severe heart failure initially seen at a non‐percutaneous coronary intervention (PCI)‐capable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from onset of myocardial infarction (class I, level of evidence (LOA): B). † Angiography and revascularization should not be performed within the first 2–3 hours after administration of fibrinolytic therapy. CABG, coronary artery bypass graft; cath lab, catheterization laboratory; DIDO, door in, door out; FMC, first medical contact.

Figure 3.3 Thirty‐day combined endpoint of mortality, reinfarction and ischemia with odds ratio (95% confidence interval, CI) favoring routine early percutaneous coronary intervention (PCI) following thrombolytic therapy.

Chapter 04

Figure 4.1 Different efficacy of the available anticoagulant drugs, according to the data coming from the primary percutaneous coronary intervention (PPCI) studies. The ideal agent should offer the best efficacy in reducing ischemic events, giving at the same time an optimal protection from bleeding complications. The picture shows that adding glycoprotein IIb/IIIa inhibitors to unfractionated heparin improves the antithrombotic efficacy, but at the cost of a significantly increased risk of thrombosis. Prolonging the bivalirudin infusion after PPCI would overcome this problem.

Figure 4.2 Anticoagulant protocol for patients undergoing primary percutaneous coronary intervention adopted by the Bristol Heart Institute, Bristol, United Kingdom.

Chapter 05

Figure 5.1 The process of coagulation viewed as four key steps. All available anticoagulant and antiplatelet agents work at one or more of the steps, as illustrated. GP, glycoprotein; LMWH, low molecular weight heparin; UFH, unfractionated heparin.

Figure 5.2 There are two primary P2Y receptors, P2Y

1

(high affinity; initiation) and P2Y

12

(low affinity; amplification and clot stabilization); P2Y

12

inhibitors include pro‐drugs (thienopyridines clopidogrel and prasugrel) and active drugs (adenosine triphosphate, ATP, analog cangrelor and cyclo‐pentyl‐triazolo‐pyrimidine, CPTP, ticagrelor). There are potential interactions between the binding of cangrelor and thienopyridines; no such interactions have been noted between cangrelor and ticagrelor. G‐protein‐coupled signaling of the P2Y receptors culminates in platelet shape change, activation and aggregation. cAMP, cyclic adenosine monophosphate; MLC, myosine light chain; PKA, protein kinase A; VASP, vasodilator‐stimulated phosphoprotein.

Chapter 06

Figure 6.1 Number of mechanical circulatory support (MCS) and intra‐aortic balloon counter pulsation (IABP) insertions. Use of short‐term (acute) circulatory support pumps is increasing. Coincident with the growth in use of durable or permanent MCS, the use of short‐term percutaneous MCS, extracorporeal membrane oxygenation (ECMO), and percutaneous cardiopulmonary support (PCPS) options have been steadily increasing since 2007.

Figure 6.2 Classification of acute circulatory support devices. a) Intra‐aortic balloon pump (IABP). b) Impella CP

®

axial flow catheter. c) Percutaneous heart pump (PHP) an investigational axial flow catheter. d) TandemHeart centrifugal flow pump. e) Venoarterial extracorporeal membrane oxygenation (VA‐ECMO).

Figure 6.3 Intra‐aortic balloon counter pulsation (IABP) augments myocardial perfusion during ischemia. During ischemia, dysregulation of microvascular autoregulation creates a hyperemic state that allows for a linear relationship between forward compression wave energy generated by an IABP (IABP‐FCW) and coronary flow (average peak velocity; APV).

Figure 6.4 Distinct hemodynamic effects of acute circulatory support devices percutaneous mechanical circulatory support systems. (a) The Impella axial flow catheters are deployed in retrograde fashion across the aortic valve and directly displace blood from the left ventricle (LV) into the proximal aorta. Immediate effects of the Impella activation include reduced LV pressure and volume as shown by pressure–volume (PV) loops. (b) The TandemHeart centrifugal flow pump displaces oxygenated blood from the left atrium (LA) to a femoral artery, thereby reducing LV preload. The net effect of immediate TandemHeart activation is a reduction in total LV volume and native LV stroke volume (width of the PV loop). (c) Venoarterial extracorporeal membrane oxygenation (VA‐ECMO) displaces venous blood from the right atrium (RA) through an extracorporeal centrifugal pump and oxygenator, then returns oxygenated blood into the femoral artery. The immediate effect of VA‐ECMO without an LV decompression mechanism is an increase in LV pressures and a reduction in LV stroke volume.

Figure 6.5 Acute right ventricular support devices.

Figure 6.6 Future directions: Primary reperfusion versus primary unloading. a) Future studies are required to test the utility of preclinical observations showing that first unloading the left ventricle, then delaying reperfusion (primary unloading) reduces infarct size compared with primary reperfusion alone. b) Representative left ventricular sections after staining with triphenyltetrazolium chloride. Infarct zones are outlined in black.

Chapter 07

Figure 7.1 Dynamic thrombus (AMI, acute myocardial infarction; RBC, red blood cells).

Figure 7.2 Primary percutaneous coronary intervention for STEMI with low thrombus burden. Lesions with low‐grade thrombus can be treated safely without the need for more complex catheters or procedures. Angiograms from a patient who presented with an acute anterior wall STEMI. The initial angiogram demonstrated a critical mid left anterior descending culprit lesion with a low‐grade 0–1 thrombus burden (a). The lesion was direct stented with a 3.5‐mm drug‐eluting stent (b), with a door‐to‐balloon time of 56 minutes. The final angiography demonstrates TIMI 3 flow (c).

Figure 7.3 Direct stenting for low grade thrombus. a) Grade 1 thrombus. b) Direct stenting with 4‐mm bare‐metal stent. c) Post stenting.

Figure 7.4 Direct stenting for low‐grade thrombus. a) Grade 1 thrombus. b) Direct stenting with 4‐mm bare‐metal stent. c) Post stenting.

Figure 7.5 Direct stenting for low‐grade thrombus. a) Grade 1 thrombus. b) Direct stenting with 4‐mm bare‐metal stent. c) Post stenting.

Figure 7.6 Primary percutaneous coronary intervention for STEMI with moderate thrombus burden. Lesions with moderate grade thrombus are best treated with aspiration thrombectomy devices, prior to definitive treatment and stenting. The angiograms show a moderate thrombus (grade 3) in a patient with ST‐elevation in leads DII‐III. The first angiogram demonstrates a discerning mid right coronary artery culprit lesion with a moderate grade thrombus (a). The lesion was treated then with an aspiration catheter (b) followed by angioplasty and stenting with a 4‐mm bare‐metal stent with a door‐to‐balloon time of 61 minutes, with good results (c).

Figure 7.7 Thrombo‐aspiration for moderate thrombus. a) Grade 2 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 3.5‐mm bare‐metal stent. e) Post stenting.

Figure 7.8 Thrombo‐aspiration for moderate thrombus. a) Grade 1–2 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 3.5‐mm bare‐metal stent. e) Post stenting.

Figure 7.9 Thrombo‐aspiration for moderate thrombus. a) Grade 2–3 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 3.5‐mm drug‐eluting stent. e) Post stenting.

Figure 7.10 Primary percutaneous coronary intervention for STEMI with large thrombus burden. Lesions with high‐grade thrombus may require some thrombectomy prior to definitive treatment and stenting. The initial angiogram on this patient, who presented with an acute inferior wall STEMI, demonstrated a large amount of thrombus (grade 3–4) (a). An AngioJet catheter (b) was initially used for rheolytic thrombectomy and after angioplasty and stenting, the final angiographic result was excellent (c).

Figure 7.11 Rheolytic thrombectomy for large thrombus. a) Grade 5 thrombus. b) Rheolytic thrombectomy performed with AngioJet. c) Post thrombectomy. d) 4‐mm bare‐metal stent. e) Post stenting.

Figure 7.12 Rheolytic thrombectomy for large thrombus. a) Large, bulky thrombus in mid left anterior descending coronary artery. b) Rheolytic thrombectomy performed with AngioJet. c) Post thrombectomy. d) Post stenting, final result.

Figure 7.13 Rheolytic thrombectomy for large thrombus. a) Grade 5 thrombus. b) Rheolytic thrombectomy performed with AngioJet. c) Post thrombectomy. d) 4.5‐mm bare‐metal stent. e) Post stenting.

Figure 7.14 Thrombo‐aspiration as default strategy. a) Grade 5 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 3.5‐mm Xience drug‐eluting stent. e) Post stenting.

Figure 7.15 Thrombo‐aspiration as default strategy. a) Grade 5 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 4‐mm bare‐metal stent. e) Post stenting.

Figure 7.16 Thrombo‐aspiration as default strategy. a) Grade 5 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 4‐mm bare‐metal stent. e) Post stenting.

Figure 7.17 Thrombo‐aspiration as default strategy. a) Grade 5 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 4‐mm bare‐metal stent. e) Post stenting.

Figure 7.18 Thrombo‐aspiration as default strategy. a) Grade 5 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 4‐mm bare‐metal stent. e) Post stenting.

Figure 7.19 Thrombo‐aspiration as default strategy. a) Grade 5 thrombus. b) Thrombo‐aspiration performed by Export Catheter. c) Post thrombectomy. d) 4‐mm Xience V drug‐eluting stent. e) Post stenting.

Figure 7.20 Thrombus management strategy (DAPT, dual antiplatelet therapy; i/c, intracoronary; TIMI, thrombolysis in myocardial infarction; UFH, unfractionated heparin).

Chapter 08

Figure 8.1 a) An example of a complex radio‐brachial loop. b) A guide catheter being negotiated through the loop. c) The catheter is traversing beyond the loop.

Figure 8.2 An example of left circumflex artery stenting in acute myocardial infarction through the arteria lusoria.

Figure 8.3 a) Contrast injection revealed very small caliber of radial artery. b) Smooth passage of a 6 Fr guide catheter using balloon‐assisted tracking (arrow).

Figure 8.4 a) In vitro demonstration of modified sheathless technique (arrow). b) A 7 Fr extra backup (EBU) guide catheter is tracked over a long (125‐cm) 5 Fr multipurpose (MP) diagnostic catheter and a standard 0.035‐inch (260‐cm) guide wire (arrow). c) Left main coronary artery bifurcation lesion is profiled. d) Optimal end result is obtained.

Chapter 09

Figure 9.1 Current concept of CS pathophysiology. The classic shock spiral (black) and the parameters influencing the spiral by inflammation and bleeding/transfusion (blue) are shown. Treatment options such as: 1) revascularization; 2) mechanical support by left ventricular assist devices (LVAD) or extracorporeal life support systems (ECLS); and 3) inotropes or vasopressors to reverse the shock spiral are shown in green (LVEDP, left ventricular end‐diastolic pressure; PCWP, pulmonary capillary wedge pressure).

Figure 9.2 Treatment algorithm for patients with cardiogenic shock complicating acute myocardial infarction. Class of recommendation and level of evidence according to American College of Cardiology/ American Heart Association guidelines is provided if available (IABP, intra‐aortic balloon pump) [12].

Figure 9.3 Current percutaneous mechanical support devices for cardiogenic shock: (left to right) intra‐aortic balloon pump (IABP); Impella

®

2.5, 3.5 or 5.0; TandemHeart™; extracorporeal life support system (ECMO) extracorporeal membrane oxygenation (ECMO); iVAC 2 L

®

.

Chapter 10

Figure 10.1 Manual thrombectomy devices: a) Export catheter. b) Diver CE catheter. c) Pronto catheter. d) QuickCat catheter. e) Fetch catheter. f) Thrombuster. g) Hunter catheter. h) Vmax catheter.

Figure 10.2 Mechanical thrombectomy devices: a) Angiojet system. b) X‐sizer system. c) Rinspirator system. d) Rescue. e) TVAC system.

Chapter 11

Figure 11.1 Definite or probable late stent‐thrombosis after primary percutaneous coronary intervention with either bare‐metal or drug‐eluting stents in major clinical trials. Stent thrombosis rates were at 5 years for the PASSION trial, at 3 years for MISSION!, 4 years in TYPHOON, 3 years in DEDICATION, and 3 years in HORIZONS‐AMI [5].

Figure 11.2 Kaplan–Meier estimates of cumulative stent thrombosis rates After primary percutaneous coronary intervention bare‐metal (BMS) or drug‐eluting stents (DES) for STEMI in the DES Era. A cumulative frequency of ST B landmark analysis showing the cumulative frequency of very late stent thrombosis (> 1 year) comparing BMS and DES.

Figure 11.3 Landmark analysis of definite stent thrombosis up to 3 years in the Swedish Coronary Angiography and Angioplasty Register.

Figure 11.4 Network meta‐analysis of bare‐metal compared with drug‐eluting stents.

Figure 11.5 Pooled odds ratio (OR) of outcomes of all the randomized trials in the network meta‐analysis (BMS, bare‐metal stent; CI, confidence interval; DES, drug‐eluting stent) [49].

Chapter 15

Figure 15.1 Chain of efforts during treatment of acute ST‐elevation myocardial infarction to secure infarct reduction and optimal outcome. PPCI, primary percutaneous coronary intervention.

Figure 15.2 Reperfusion injury adds to the injury developed during initial ischemia. Protective procedures, such as drugs (e.g. cyclosporine, glucagon‐like peptin 1 analogs and beta blockers), mild hypothermia and remote conditioning can modify the extent of reperfusion injury, when applied before onset of reperfusion.

Figure 15.3 Simplified schematic presentation of the cytosol pathways that converge to prevent mitochondrial permeability transition pore (MPTP) opening in cardioprotection. eNOS/PGK: the nitric oxide dependent G‐protein coupled receptor‐eNOS‐protein kinase G pathway; RISK: the reperfusion‐injury salvage kinase pathway based on protein kinase B; PI3K‐Akt and glycogen synthase kinase 3β; and SAFE: the survivor activating factor enhancement signaling pathway involving the JAK‐STAT system and TNF‐alpha receptors. eNOS, endothelial nitric oxide synthase; ERK, extracellular regulated kinase; GFR, growth factor receptor (insulin‐like growth factor‐1 and fibroblast growth factor‐2); GPCR, G‐protein‐coupled receptor; GSK3‐β: glycogen synthase kinase 3β.

Figure 15.4 Cumulative incidence (%) of major adverse cardiovascular events (MACCE) by year since randomization (per‐protocol analysis)

P

 = 0.010.PPCI, primary percutaneous coronary intervention; RIC, remote ischemic conditioning.

Figure 15.5 Short axis cardiac magnetic resonance images and corresponding pathology four days after ischemia/reperfusion injury in a porcine heart. Pathology shows intramural hemorrhage in the anteroseptal myocardium (a), which corresponds to a hypointense region on a T2‐weighted area‐at‐risk (b). On the T1‐weighted image, intramyocardial hemorrhage is depicted by a hyper‐intense region (c). The late gadolinium image, which reflects the final infarct size, shows that microvascular obstruction is present within the infarct core (d).

Chapter 17

Figure 17.1 STEMI network: four express lanes . EMS, emergency medical services; FMC, first medical contact; PPCI, primary percutaneous coronary intervention.

Chapter 18

Figure 18.1 Relative risks for the composite of death, reinfarction, and stroke (a) and Death (b) with thrombolysis and transfer for primary percutaneous cardiopulmonary support in individual trials and the combined analysis.

Figure 18.2 (a) Map of Minnesota with the percutaneous coronary intervention (PCI) center (Abbott Northwestern Hospital) in Minneapolis, zone 1 hospitals (≤ 60 miles from PCI hospital, and zone 2 hospitals (60–210 miles from PCI hospital. UFH, unfractionated heparin. (b) Map of Los Angeles County STEMI system of care. (c) Map of North Carolina state‐wide Reperfusion of Acute Myocardial Infarction in Carolina Emergency Departments (RACE) STEMI system of care.

Figure 18.3 US STEMI systems of care from the Mission: Lifeline coverage Map.

Figure 18.4 Trends in US STEMI Care 2003–2011. Increasing PCI to 80% with decreasing mortality.PCI, percutaneous coronary intervention; ST‐segment elevation myocardial infarction.

Figure 18.5 Example protocol from Minneapolis Heart Institute’s Level 1 STEMI protocol.

Figure 18.6 Sample patient transfer datasheet from Minneapolis Heart Institute’s Level 1 STEMI protocol; reproduced with permission.

Chapter 19

Figure 19.1 Reperfusion therapy for STEMI . CABG, coronary artery bypass graft; DIDO, door in, door out; FMC, first medical contact; PPCI, primary percutaneous coronary intervention.

Figure 19.2 Pre‐hospital and in‐hospital management, and reperfusion strategies within 24 hours of first medical contact [24]. PPCI, primary percutaneous coronary intervention.

Figure 19.3 Components of delay in STEMI and ideal time intervals for intervention. EMS, emergency medical services; PPCI, primary percutaneous coronary intervention.

Chapter 22

Figure 22.1 Map of Puerto Rico; stars represent Puerto Rico Infarction National Collaborative Experience ST‐segment elevation myocardial infarction percutaneous coronary intervention centers, surrounded by bigger circles representing an approximate 1‐hour driving time radius. The smaller circle represents the denser San Juan metro area.

Figure 22.2 Data collection sheet designed for the Puerto Rico Infarction National Collaborative Experience participating centers.

Figure 22.3 Example of a ST‐segment elevation myocardial infarction to percutaneous coronary intervention time interval form implemented as a tool to deliver focused feedback on case reviews to “interval owners”.

Figure 22.4 Reperfusion performance measures of median door‐to‐balloon times and percentage with door‐to‐balloon time of less than 90 minutes in one Puerto Rico Infarction National Collaborative Experience institution over an 8‐year period.

Figure 22.5 Schematic representation of integration in a ST‐segment elevation myocardial infarction percutaneous coronary intervention system of care.

Figure 22.6 Two‐tiered process for pre‐hospital diagnosis and ST‐elevation myocardial infarction (STEMI)‐alert hospital activation in the Puerto Rico Infarction National Collaborative Experience initiative. CCL, cardiac catheterization laboratory; ED, emergency department; EKG, electrocardiogram; EMS, emergency medical services; PCI, percutaneous coronary intervention.

Chapter 23

Figure 23.1 Regional network of STEMI care.

Chapter 24

Figure 24.1 ST‐elevation myocardial infarction cluster; hub and spoke model. EKG, electrocardiogram; PCI, percutaneous coronary intervention.

Chapter 25

Figure 25.1 Cloud computing: Applications, hardware and systems software located in datacenters delivered as services over the internet.

Figure 25.2 An integrated telemedicine platform.

Chapter 26

Figure 26.1 Roles of the ambulance in ST‐elevation myocardial infarction interventions.

Figure 26.2 Roles of telemedicine (TM) in ST‐elevation myocardial infarction (STEMI) intervention. cath, catherization; D2B, door‐to‐balloon; D2N, door‐to‐needle; EKG, electrocardiogram; PCI, percutaneous coronary intervention.

Figure 26.3 Enhancement of thrombolysis and pharmacoinvasive management with telemedicine. Cath, catherization; CVL, central venous line; PCI, percutaneous coronary intervention; TM, telemedicine.

Figure 26.4 Comprehensive acute myocardial infarction management with telemedicine. CATH LAB, catheterization laboratory; CI, contraindication; D2B, door‐to‐balloon; D2N, door‐to‐needle; EKG, electrocardiogram; PCI, percutaneous coronary intervention; Sx, symptoms; TH, thrombolysis; TM, telemedicine; * [15,32].

Figure 26.5 The Lumen Americas Telemedicine Infarct Network hub and spokes model. PCI, percutaneous coronary intervention.

Figure 26.6 Comparison of three methods of pre‐hospital diagnosis and triage.

Figure 26.7 ITMS Telemedicine ST‐elevation myocardial infarction (STEMI) diagnosis and triage. ACS, acute coronary syndrome; Cath Lab, catheterization laboratory; EKG, electrocardiogram; PCI, percutaneous coronary intervention; PIT, Platform Integrated Telemedicine; TH, thrombolysis.

Chapter 27

Figure 27.1 Staged percutaneous coronary intervention (PCI) following culprit vessel intervention. The patient presented with posterior ST‐elevation myocardial infarction. The patient proceeded to primary percutaneous coronary intervention and the culprit vessel was identified as the left anterior descending artery (arrow, a). This was treated successfully with the implantation of a 3.0 × 18 mm drug‐eluting stent (b), with an excellent final result (c). The patient was hemodynamically stable and the critical bystander lesion in the right coronary artery (d) was successfully treated as a staged procedure 6 weeks after the index procedure with the implantation of a 3.0 × 23 mm drug‐eluting stent (e), with an excellent final angiographic result (f). By current evidence, the lesions in the right coronary artery could have been treated during the index procedure or admission.

Figure 27.2 Multivessel percutaneous coronary intervention (PCI) in the setting of acute myocardial infarction with cardiogenic shock. The patient presented with an inferoposterior ST‐elevation myocardial infarction and proceeded to emergency primary percutaneous coronary intervention. The culprit circumflex artery (arrow, a) was successfully treated with implantation of a 2.75 × 28 mm drug‐eluting stent (b), with a good final angiographic result (c). In view of the hazy appearance of the critical mid left anterior descending artery lesion (arrow, d), this was treated at the index procedure with implantation of a 3.5 × 28 mm drug‐eluting stent (e), with an excellent final angiographic result (f).

Figure 27.3 Multivessel percutaneous coronary intervention (PCI) following culprit vessel intervention due to unstable features of bystander disease. The patient presented as an emergency with anterior ST‐elevation myocardial infarction with cardiogenic shock. Angiography revealed the left anterior descending artery to the culprit vessel (arrow, a), with a critical circumflex lesion (arrow, a). The patient proceeded to primary percutaneous coronary intervention of the left anterior descending artery with successful implantation of a 3.5 × 23 mm drug‐eluting stent (DES, b) with an excellent result (c). The right coronary artery was noted to have mild atheroma only (d). In view of continuing hemodynamic instability, an intra‐aortic balloon pump (IABP) was inserted (arrows, e), and the critical bystander disease (arrow, c) was treated (f) with implantation of a 3.0 × 38 mm DES with final kissing balloon post‐dilatation (g) with an excellent final angiographic result (h).

Chapter 28

Figure 28.1 Genous™ endothelial progenitor cell capture (EPC) stent.

Figure 28.2 Combo™ bioengineered sirolimus‐eluting stent.

Figure 28.3 ABSORB bioresorbable vascular scaffold.

Guide

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Manual of STEMI Interventions

Edited by Sameer Mehta MD FACC MBA

University of Miami Miller School of Medicine, and Lumen Foundation, Miami, FL, USA

This edition first published 2017 © 2017 by John Wiley & Sons Ltd

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Names: Mehta, Sameer, editor.Title: Manual of STEMI interventions / edited by Sameer Mehta.Description: Hoboken, NJ : Wiley, 2017. | Includes index. |Identifiers: LCCN 2017014480 (print) | LCCN 2017015848 (ebook) | ISBN 9781119095439 (pdf) | ISBN 9781119095422 (epub) | ISBN 9781119095415 (cloth)Subjects: | MESH: Myocardial Infarction–therapy | Anticoagulants–therapeutic use | StentsClassification: LCC RC685.I6 (ebook) | LCC RC685.I6 (print) | NLM WG 310 | DDC 616.1/23706–dc23LC record available at https://lccn.loc.gov/2017014480

Cover design: WileyCover images: (From left to right) © Feverpitched/Gettyimages; © Ryan McVay/Gettyimages; © Nils Versemann/Shutterstock; © kupicoo/Gettyimages

List of Contributors

Thomas Alexander MDKovai Medical Center and Hospital, Coimbatore, India

Laura Álvarez MDLumen Foundation, Miami, FL, USA

Juanita Gonzalez Arango MDLumen Foundation, Miami, FL, USA

Miguel Vega Arango MDLumen Foundation, Miami, FL, USA

Yousef Bader MDCardiovascular Center, Tufts Medical Center, Boston, MA, USA

Andreas Baumbach MDBristol Heart Institute, Bristol, UK

Neeraj Bhalla MDDepartment at BLK Super Speciality Hospital, New Delhi

Freddy Bojanini MDLumen Foundation, Miami, FL, USA

Roberto Vieira Botelho MD PhDEurolatino Medical Research, Lumen Foundation, Miami, FL, USA

Estefania Calle Botero MDLumen Foundation, Miami, FL, USA

Hans Erik Bøtker MD PhD FACC FESCDepartment of Cardiology, Aarhus University Hospital Skejby, Aarhus, Denmark

Miguel A. Campos‐Esteve MD FACCCardiac Catheterization Laboratories, Pavia Hospital Santurce, San Juan, Puerto Rico, USA

Antonio Colombo MDInterventional Cardiology Unit, San Raffaele Scientific Institute, Milan, Italy; Interventional Cardiology Unit, EMO‐GVM Centro Cuore Columbus, Milan, Italy

Juan Corral MDLumen Foundation, Miami, FL, USA

Suzanne de Waha MDUniversity Heart Center Luebeck, University Hospital Schleswig‐Holstein, Luebeck, Germany

Landy Luna Diaz MDLumen Foundation, Miami, FL, USA

Daniela Parra Dunoyer MDLumen Foundation, Miami, FL, USA

Jose Escabi‐Mendoza MD FACCCardiac Care Unit and Chest Pain Center, VA Caribbean Healthcare System, San Juan, Puerto Rico, USA

Denis Fabiano de Souza RNResearch Nurse, Eurolatino Medical Research, USA

James J. Ferguson III MDSt Luke’s Episcopal Hospital,Texas, USA

Wladimir Fernandes de Rezende MBADax Tecnologia da Informação, Brasilão

Francisco Fernandéz MBACIO ITMS do Brasil

Alexandra Ferré MDLumen Foundation, Miami, FL, USA

Francesco Giannini MDInterventional Cardiology Unit, San Raffaele Scientific Institute, Milan, Italy

Juliana Giraldo MDLumen Foundation, Miami, FL, USA

Cindy L. Grines MDDetroit Medical Center, Heart Hospital, Detroit, MI, USA

Timothy D. Henry MDCedars‐Sinai Heart Institute, Los Angeles, CA, USA

Gerd Heusch MD FACC FESC FRCPInstitute for Pathophysiology, West German Heart and Vascular Centre Essen, University of Essen Medical School, Essen, Germany

David Hildebrandt RNCedars‐Sinai Heart Institute, Los Angeles, CA, USA

Yong Huo MDPeking University First Hospital, Beijing, China

David G. Iosseliani MD FACC FESCMoscow City Center of Interventional Cardioangiology, Moscow, Russian Federation

Thomas W. Johnson BSc MBBS MD FRCPBristol Heart Institute, Bristol, UK

Navin K. Kapur MDCardiovascular Center, Tufts Medical Center, Boston, MA, USA

Sasko Kedev MD PhD FESC FACCMedical Faculty, Ss Cyril and Methodius University, and Director, University Clinic of Cardiology, Skopje, Macedonia

Julius Cezar Q. Ladeira DDS MScITMS do Brasil

David C. Lange MDCedars‐Sinai Heart Institute, Los Angeles, CA, USA

Fernando Lapetina‐Irizarry MD FACCCardiology Department, Pavia Hospital Santurce, San Juan, Puerto Rico, USA

David M. Larson MDMinneapolis Heart Institute, Minneapolis, MN, USA

Azeem Latib MDSan Raffaele Scientific Institute, Milan, Italy; Interventional Cardiology Unit, EMO‐GVM Centro Cuore Columbus, Milan, Italy

Michel Le May MDDirector of the Coronary Care Unit, and Director of the University of Ottawa Heart Institute Regional STEMI Program, Ontario, Canada

Joshua PY Loh MDConsultant at the National University Heart Centre, Singapore, and an Assistant Professor at the Yong Loo Lin School of Medicine, Singapore

Cindy Manotas MDLumen Foundation, Miami, FL, USA

Sameer Mehta MD FACC MBAUniversity of Miami Miller School of Medicine, and Lumen Foundation, Miami, FL, USA

Nestor Mercado MDDetroit Medical Center, Heart Hospital, Detroit, MI, USA

Isaac Yepes Moreno MDLumen Foundation, Miami, FL, USA

Sebastián Moreno MDLumen Foundation, Miami, FL, USA

Ajit S. Mullasari MDMadras Medical Mission, Chennai, India

Daniella Nacad MDLumen Foundation, Miami, FL, USA

Estefania Oliveros MDLumen Foundation, Miami, FL, USA

Samir Pancholy MD FACC FSCAIWright Center for Graduate Medical Education, Commonwealth Medical College, Scranton, PA, USA

Tejas Patel MD DM FACC FESC FSCAIApex Heart Institute, Ahmedabad, Gujarat, India

Marco Perin MDLumen Foundation, Miami, FL, USA

Carlos Otávio Lara Pinheiro BScDax Tecnologia da Informação, Brasilão

Maria Teresa Bedoya Reina MDLumen Foundation, Miami, FL, USA

Sergio Reyes MDLumen Foundation, Miami, FL, USA

Olga Reynbakh MDLumen Foundation, Miami, FL, USA

Daniel Rodriguez MDLumen Foundation, Miami, FL, USA

Orlando Rodríguez‐Vilá MD MMS FACC FSCAICardiac Catheterization Laboratories, and Associate Chief of Medicine, VA Caribbean Healthcare System, San Juan, Puerto Rico, USA

Ivan Rokos MDUCLA, California, USA

Neil Ruparelia PhD MRCPSan Raffaele Scientific Institute, Milan, Italy; Imperial College, London, UK; EMO‐GVM Centro Cuore Columbus, Milan, Italy

Roopa Salwan MDCardiology and Interventional Cardiology, Max Super Speciality Hospital‐Saket, Delhi, India

Márcio Sanches MDITMS do Brasil

Theodore L. Schreiber MDDetroit Medical Center, Heart Hospital, Detroit, MI, USA

Michael Schweitzer MDLumen Foundation, Miami, FL, USA

Sanjay Shah MD DMApex Heart Institute, Ahmedabad, Gujarat, India

Holger Thiele MDUniversity Heart Center Luebeck, University Hospital Schleswig‐Holstein, Luebeck, Germany

Maria Botero Urrea MDLumen Foundation, Miami, FL, USA

Alicia Henao Velasquez MDLumen Foundation, Miami, FL, USA

Vincenzo Vizzi MDBristol Heart Institute, Bristol, United Kingdom

Tracy Zhang BSLumen Foundation, Miami, FL, USA

Yan Zhang MDPeking University First Hospital, Beijing, China

Preface

Fifteen years ago, I performed my first door‐to‐balloon STEMI intervention. The beauty of that procedure, as well as of more than 2000 since then, has remained pristine. Almost every procedure has either saved a life or preserved left ventricular function. Often, both. In a front page article on June 21st, 2015, the New York Times reported that cardiovascular disease is no longer the #1 killer in the Unites States on a count of the strides made with STEMI interventions. This is amazing progress whose implementation has been seismic – in our massive country, from less than 4% of primary PCI being performed in 1999, we now have a STEMI nation. As a result, almost every patient can now receive a quality primary percutaneous coronary intervention (PPCI) anytime and anywhere. I believe that achieving a nationwide capability to perform PPCI is one of the biggest success stories in modern medicine.

Progress in PPCI has also occurred worldwide. At the 2016 Lumen Global STEMI meeting in Kuala Lumpur, Malaysia, 15 developing countries representing 3.8 billion populations, presented their STEMI programs. Universally, they reported improvements in both the STEMI process and procedure and major reduction in cardiovascular mortality. I have been humbled to have contributed to these developments. Until this date, I believe, I am the world’s sole STEMI‐only performing cardiologist. This was a massive individual undertaking that required enormous personal and financial sacrifices, recalibration of lifestyle and brutal hard work. It was through sleeping in the trenches of STEMI interventions that I mastered the procedural techniques. In particular, this included a kaleidoscopic appreciation of thrombus – its dynamic nature, its varied morphology and its diverse presentation based upon the duration of chest pain. Slowly and methodically, my observations about thrombus in STEMI lesions led to formulation of a Selective Strategy of Thrombus Management, based on thrombus grade. I have adopted this methodology in my last consecutive 1000 procedures and have found it to be universally applicable. These techniques are described in detail in this textbook.

Allow me to dwell a little further in my personal journey. In 2002, when I took an unprecedented decision to devote an entire career to STEMI Interventions, I followed the fantastic dictum of Mahatma Gandhi, “In matters of conscience, the opinion of the majority does not count”. I followed this call to conscience and abandoned a thriving interventional cardiology practice. I began a STEMI‐only meeting and wrote an entire textbook on STEMI interventions. This fundamental trust in STEMI interventions has now led to my helping to create STEMI networks and educational, research, and training endeavors in 27 countries. I have also begun to use telemedicine to provide access for millions of patients to PPCI, and in creating a public campaign for reducing gender disparities. In pursuing this crusade, I attribute much of this success to the magnificent procedure of PPCI and its fantastic ability to predictably and safely save lives. I was simply fortunate in recognizing these attributes ahead of others!

This textbook, my sixth on the subject of PPCI, is an earnest effort to incorporate the most important lessons that I have learned, and to amalgamate them with current scientific data, guidelines and recommendations from the American College of Cardiology and the European Society of Cardiology. For ease of understanding, the textbook is divided into five parts – Guidelines, Thrombolytic Therapy, Physiology; the STEMI Procedure; the STEMI Process; Global STEMI Initiatives and Future Perspectives. I hope that this structure will comprehensively and seamlessly cover the critical areas. As in previous texts, the chapters on collating the illustrative cases was the hardest and it took months to select cases, to digitize the cineangiographic pictures, obtain pre‐ and post‐procedure electrocardiograms and do so from five different hospitals where these I performed these procedures.

World experts have contributed to several chapters and I am deeply gratefully to these brilliant cardiologists for their work and for their support.

Most of my work in STEMI Interventions, beyond composing this textbook, would not be possible without the supreme sacrifices of my immediate family, to whom this work is dedicated – to my wife Shoba, and to our children Aditya and Kabir.

Part IGuidelines, Thrombolytic Therapy, Pharmacology

1Compendium of STEMI Clinical Trials

Juanita Gonzalez Arango MD, Miguel Vega Arango MD, Estefania Calle Botero MD, Isaac Yepes Moreno MD, Maria Botero Urrea MD, Alicia Henao Velasquez MD, Daniel Rodriguez MD, Daniela Parra Dunoyer MD, Maria Teresa Bedoya Reina MD, Sameer Mehta MD

Introduction

As we constructed our fourth textbook of interventions for ST‐elevation myocardial infarction (STEMI), the need for including a chapter on clinical trials was paramount. To provide a complete compendium of relevant STEMI guidelines and clinical trials, two distinct chapters have been created. We recognize that this information is easily obtained from searching the internet; however, we deemed it important to present in this book the most up‐to‐date guidelines and clinical trials. In this chapter, we have divided the trials into stents (Table 1.1), no‐reflow (Table 1.2), thrombectomy (Table 1.3), percutaneous coronary interventions for non‐culprit lesions (Table 1.4), and the role of left ventricular support devices (Table 1.5). In Chapter 2, we have separated out those guidelines from the American College of Cardiology and the European Society of Cardiology. These topics are discussed further in various chapters of the textbook. However, we firmly believe that a compendium of guidelines and clinical trials will provide a useful summary of these STEMI‐related studies.

Table 1.1 Which stent is most desirable for STEMI interventions?

Study Title

Hypothesis

Cohort

Principal Findings

Conclusion

COBALT: long‐term clinical outcome of thin‐strut CoCr stents in the DES era [1].

To assess characteristics and outcomes of patients treated with 2 different new‐generation CoCr BMS, the MULTI‐LINK VISION

®

and PRO‐Kinetic Energy

®

stents.

1176 patients: MLV (

n

 = 438); PRO‐Kinetic (

n

 = 738).

TLR and TVR were lower in the MLV group. Death, MI, ARC and definite stent thrombosis were similar.

The use of last‐generation thin‐strut BMS in selected patients is associated with acceptable clinical outcome, with similar clinical results for both the MLV and PRO‐Kinetic stents.

Comparison of newer‐generation DES with BMS in patients with acute STEMI [2].

Efficacy and safety of newer‐generation DES compared with BMS in patients with STEMI.

2665 STEMI patients: 1326 received a newer‐generation DES (EES or biolimus A9 eluting stent) and 1329 received BMS.

Newer‐generation DES substantially reduced the risk of repeat TVR, target‐vessel infarction, definite stent thrombosis compared with BMS at 1 year.

Newer‐generation DES improves safety and efficacy compared with BMS throughout 1st year.

Meta‐analysis of long‐term outcomes for DES compared with BMS in PCI for STEMI [3].

Available literature examining the outcomes of DES and BMS in PPCI after > 3 years of follow‐up.

8 RCTs and 5 observational studies. 5797 patients in whom 1st‐generation DES (SES or PES) were compared with BMS control arms.

Patients with DES had lower risk of TLR, TVR, and MACE. Incidence of stent thrombosis equal between groups. No difference in mortality or recurrent MI. Those receiving DES had lower mortality.

DES use resulted in decreased repeat revascularization with no increase in stent thrombosis, mortality, or recurrent MI.

Outcomes with various DES or BMS in patients with STEMI [4].

Efficacy (TVR) and safety (death, MI, and stent thrombosis) outcomes at the longest reported follow‐up times with DES compared with BMS.

28 randomized clinical trials; 34,068 patients comparing any DES against each other or BMS.

No increase in the risk of death, MI, or stent thrombosis with any DES compared with BMS. EES was associated with a statistically significant reduction in the rate of stent thrombosis when compared with SES, PES, and even BMS.

DES versus BMS was associated with substantial decrease in the risk of TVR. EES had substantial reduction in the risk of stent thrombosis with no increase in very late stent thrombosis.

Benefits of DES compared with BMS in STEMI: 4‐year results of PES or SES vs. BMS in primary angioplasty (PASEO) randomized trial [5].

To evaluate the short and long‐term benefits of SES and PES vs. BMS in patients undergoing primary angioplasty.

270 patients with STEMI were randomized to BMS (

n

 = 90), PES (

n

 = 90), or SES (

n

 = 90).

PES and SES were associated with significant reduction in TLR at 1year. No difference was observed in terms of death and reinfarction.

SES and PES are safe and associated with significant benefits in terms of TLR up to 4 years of follow‐up, compared with BMS.

PPCI for AMI: long‐term outcome after BMS and DES Implantation [6].

To investigate the long‐term outcomes of unselected patients undergoing PPCI with BMS and DES.

1738 patients undergoing PPCI for a new lesion. 3 cohorts of BMS (

n

 = 531), SES (

n

 = 185) or PES (

n

 = 1022).

No differences in all‐cause mortality or repeat revascularization between DES and BMS. SES was associated with lower rates of all‐cause death, nonfatal MI, or TVR compared with PES. Very late stent thrombosis only occurred in the DES groups.

DES are not associated with an increase in adverse events compared with BMS when used for PPCI, neither DES reduced repeat revascularizations.

Safety and efficacy outcomes of first‐ and second‐generation durable polymer DES and biodegradable polymer BES in clinical practice: comprehensive network meta‐analysis [7].

To investigate the safety and efficacy of durable polymer DES and biodegradable polymer BES.

60 randomized controlled trials were compared, which involved 63,242 patients treated with DES.

At 1year, there were no differences in mortality. Resolute and EZES, EES and SES were associated with reduced odds of MI compared with PES. Compared with EES, BP‐BES were associated with increased odds of MI, while EZES and PES were associated with increased odds of ST. EES and EZES offering the highest safety profiles.

The newer durable polymer EES and EZES and the BP‐BES maintain the efficacy of SES. EES and EZES are the safest stents to date.

EXAMINATION trial (EES Versus BMS in STEMI): 2‐year results from a multicenter randomized controlled trial [8].

To evaluate the outcomes of the population included in the EXAMINATION trial.

1498 patients were randomized to receive EES (

n

 = 751) or BMS (

n

 = 747).

Rate of TLR, definite or probable stent thrombosis was significantly lower in EES group than in BMS group.

Both rates of TLR and stent thrombosis were reduced in recipients of EES.

2‐year outcomes after first‐ or second‐generation DES or BMS implantation in patients undergoing PCI. A pre‐specified analysis from the PRODIGY study [9].

To assess device‐specific outcomes with respect to the occurrence of MACE, after implantation of BMS, ZESS, PES, or EES in patients undergoing PCI.

2013 randomized patients undergoing CA in a 1:1:1:1 fashion to BMS, ZESS, PES, or EES implantation.

MACE rate was lowest in EES, highest in BMS, and intermediate in PES and ZESS. The 2‐year incidence of stent thrombosis in the EES group was similar to that in ZESS group, but lower compared with PES and BMS groups.

MACE rate was lowest for EES, highest for BMS, and intermediate for PES and ZESS groups. EES outperformed BMS with safety endpoints and stent thrombosis.

New DES for STEMI: A new paradigm for safety [10].

To compare the long‐term safety of new‐generation DES with early‐generation DES and BMS for STEMI.

3464 STEMI patients were treated with BMS (

n

 = 1187), early‐generation DES (

n

 = 1,525), or new‐generation DES (

n

 = 752).

At 2 years, new‐generation DES had lower mortality, similar reinfarction, and fewer stent thromboses compared with BMS; and similar mortality, similar reinfarction, and trends for fewer stent thromboses compared with early‐generation DES.

New‐generation DES in STEMI patients have fewer stent thromboses compared with BMS and trends for fewer stent thromboses compared with early‐generation DES.

Safety and effectiveness of DES in patients with STEMI undergoing primary angioplasty [11].

To confirm the safety and effectiveness of DES in patients with STEMI.

370 patients (120 in DES group and 250 in BMS group) with STEMI treated with primary PCI. Patients were retrospectively followed for the occurrence of MACE.

There was no difference in rate of stent thrombosis in the BMS group. Incidence of MACE was lower in the DES group principally due to the lower rate of TVR.

Use of DES in the PPCI for STEMI was safe and improved the 3‐year clinical outcome compared with BMS, reducing the need of TVR.

Outcomes with DES vs. BMS in acute STEMI results from the Strategic Transcatheter Evaluation of New Therapies Group [12].

To evaluate the outcomes with DES compared with BMS in patients undergoing PPCI for STEMI.

Patients with STEMI treated with either a DES (1292 patients) or BMS (548 patients). Of those treated with DES, 46% were treated with SES and 54% with PES.

There were no differences between DES and BMS in death, reinfarction, or MACE. DES had lower rates of stent thrombosis and lower rates of TVR. There was a mild increase in stent thrombosis with DES versus BMS from 1–2 years.

DES used with PPCI for STEMI is more effective than BMS in reducing TVR and is safe for up to 2 years.

Clinical outcomes with BP‐BES vs. DP‐DES and BMS: evidence from a comprehensive network meta‐analysis [13].

Safety and efficacy of BP‐BES versus DP‐DES and BMS.

Data from 89 trials including 85,490 patients. 1‐year follow‐up.

BP‐BES was associated with lower rates of cardiac death/MI and TVR than BMS and lower rates of TVR than fast‐release Z‐ES. BP‐BES had similar rates of cardiac death, MI, and TVR compared with other second‐generation DP‐DES but higher rates of 1‐year stent thrombosis than CoCr EES. BP‐BES was associated with improved late outcomes compared with BMS and PES, with different outcomes compared with other DP‐DES, although higher rates of definite stent thrombosis compared with CoCr EES.

BP‐BES was associated with superior clinical outcomes compared with BMS and first‐generation DES and similar rates of cardiac death/MI, MI, and TVR compared with second‐generation DP‐DES but higher rates of definite stent thrombosis than CoCr EES.

DES vs. BMS in primary angioplasty. A pooled patient‐level meta‐analysis of randomized trials [14].

Evaluated the risks and benefits of DES compared with BMS in patients undergoing PPCI for STEMI.

6298 patients were randomized; 3980 assigned to DES and 2318 assigned to BMS.

DES implantation reduced the occurrence of TVR with no difference in mortality, reinfarction, and stent thrombosis. DES implantation was associated with an increased risk of very late stent thrombosis and reinfarction.

SES and PES compared with BMS are associated with TVR reduction at long‐term follow‐up. The incidence of very late reinfarction and stent thrombosis was increased with DES.

First results of the DEB‐AMI trial. A multicenter randomized comparison of DEB plus BMS vs. BMS vs. DES in PPCI, With 6‐month angiographic, intravenous, functional, and clinical outcomes [15].

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