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Cover
Title Page
List of Contributors
Preface
Part I: Guidelines, Thrombolytic Therapy, Pharmacology
1. 1 Compendium of STEMI Clinical Trials
  1. Introduction
  2. References
2. 2 European Society of Cardiology and American College of Cardiology STEMI Guidelines
  1. Introduction
  2. References
3. 3 The Role of Thrombolytic Therapy in the Era of STEMI Interventions
  1. Introduction
  2. Thrombolytic Therapy: Clinical Benefit, Risks and Contraindications
  3. Primary PCI: Overview of Randomized Clinical Trials
  4. Clinical Impact of Time to Reperfusion
  5. Facilitated PCI and the Pharmacoinvasive Strategy
  6. Conclusions
  7. References
4. 4 Anticoagulants in STEMI Interventions
  1. Introduction
  2. Anticoagulants
  3. Discussion
  4. How to Choose: The Eternal Dilemma Between Bleeding and Ischemic Risk
  5. References
5. 5 New Oral and Intravenous Adenosine Diphosphate Blockers in STEMI Intervention
  1. Introduction
  2. Physiology
  3. Aspirin in STEMI
  4. ADP Blockers in ACS, PCI and STEMI Intervention
  5. Other Important Issues
  6. Future Directions
  7. Summary
  8. References
Part II: The STEMI Procedure
1. 6 The Role of Acute Circulatory Support in STEMI
  1. Introduction
  2. Intra‐Aortic Balloon Counterpulsation
  3. Impella Use in STEMI
  4. The TandemHeart Device in STEMI
  5. Venoarterial Extracorporeal Membrane Oxygenation
  6. Right Ventricular Myocardial Infarction
  7. Time for a Paradigm Shift: From Primary Reperfusion to Primary Unloading in STEMI
  8. References
2. 7 Thrombus Management for STEMI Interventions
  1. Introduction
  2. Pathophysiology of Thrombus
  3. Thrombus and STEMI
  4. Mehta Strategy
  5. Global Strategies of Thrombectomy and Recent Trials
  6. Conclusions
  7. References
3. 8 Transradial Techniques to Improve STEMI Outcomes
  1. Introduction and Historical Perspective
  2. The Transradial Approach and STEMI Interventions
  3. Rationale for Using the Transradial Route for STEMI Interventions
  4. Developing a Transradial Acute Myocardial Infarction Program
  5. Limitations
  6. Conclusions
  7. References
4. 9 Management of Cardiogenic Shock
  1. Diagnosis and Pathophysiology
  2. Incidence and Prognosis
  3. Interventional Management
  4. Treatment of Mechanical Complications
  5. Intensive Care Unit Treatment
  6. Mechanical Support
  7. Summary
  8. References
5. 10 Present Role of Thrombectomy in STEMI Interventions
  1. Rationale for Thrombectomy in Acute Myocardial Infarction
  2. Thrombectomy Devices
  3. Evidence for Manual Thrombectomy
  4. Evidence for Mechanical Thrombectomy
  5. Conclusions
  6. References
6. 11 Choice of Stent in STEMI Interventions
  1. Introduction
  2. Historical Perspective
  3. Stents in STEMI Interventions: How it all Started
  4. Re‐stenosis
  5. Great Expectations: First‐Generation Drug‐Eluting Stents in STEMI
  6. Dawn of a New Era: Second‐Generation Drug‐Eluting Stents
  7. The Emperor’s New Clothes
  8. Bioresorbable Vascular Scaffold in acute Myocardial Infarction
  9. Conclusion
  10. References
7. 12 Illustrated STEMI Procedures I – Basic STEMI Skills
  1. Introduction
  2. Case 1
  3. Case 2
  4. Case 3
  5. Case 4
  6. Case 5
8. 13 Illustrated STEMI Procedures II – Basic STEMI Skills
  1. Introduction
  2. Case 6
  3. Case 7
  4. Case 8
  5. Case 9
  6. Case 10
  7. References
9. 14 Illustrated STEMI Procedures III – Basic STEMI Skills
  1. Introduction
  2. Case 11
  3. Case 12
  4. Case 13
  5. Case 14
  6. Case 15
10. 15 Remote Ischemic Conditioning for Acute Myocardial Infarction
  1. Introduction
  2. The Concepts of Ischemic Conditioning
  3. Mechanisms of Remote Ischemic Conditioning
  4. Measuring Myocardial Injury in the Clinic
  5. Effect of Remote Ischemic Conditioning in Acute Myocardial Infarction
  6. Confounding Factors in Remote Ischemic Conditioning
  7. Alternative Methods to Achieve Cardioprotection
  8. Introducing Remote Ischemic Conditioning as Standard Adjuvant Therapy in STEMI
  9. Conclusions
  10. References
Part III: The STEMI Process
1. 16 Reducing Door‐to‐Balloon Times
  1. Introduction
  2. Early Initiatives and Quality‐of‐Care Measures to Minimize Door‐to‐Balloon Time
  3. Regional STEMI Systems to Further Reduce Door‐to‐Balloon Time
  4. Limitations of Door‐to‐Balloon Time
  5. Future Directions
  6. References
2. 17 Pre‐hospital Triage and Management
  1. Introduction
  2. The STEMI Receiving Center Network
  3. Essential Roles for the Emergency Medical Services
  4. Supplemental Roles for the Emergency Medical Services
  5. Emergency Medical Services Transport Logistics
  6. Quality Improvement for Emergency Medical Services: Three Key Time Intervals
  7. Pre‐hospital Medications
  8. STEMI Complicated by Out of Hospital Cardiac Arrest
  9. Conclusions
  10. References
3. 18 Creating Networks for Optimal STEMI Management
  1. Introduction
  2. Transfer for PPCI Trials
  3. Growth and Success of STEMI Systems of Care Within the United States
  4. Organizing A System for Inter‐Hospital Transfer
  5. Key Components of a STEMI System of Care
  6. Challenges to Implementing and Maintaining a Regional STEMI System of Care
  7. Conclusions
  8. References
4. 19 Pharmacoinvasive Management of STEMI
  1. Introduction
  2. Fibrinolytic Therapy
  3. Pharmacoinvasive Therapy
  4. Trials Comparing Routine Early PCI After Fibrinolysis With Standard Therapy and Primary PCI Alone
  5. Current Guidelines for Pharmacoinvasive Therapy
  6. Guideline Recommendations
  7. Discussion
  8. References
Part IV: Global STEMI Initiatives
1. 20 Stent for Life
  1. Introduction
  2. Stent for Life Initiative
  3. Summary
  4. References
2. 21 Urban Combined Pharmacoinvasive Management of STEMI Patients as Antidote to Traffic in Large Metropolitan Cities
  1. Introduction
  2. The Role of Coronary Thrombosis in Pathogenesis of STEMI
  3. The Experience of Moscow
  4. Conclusions
  5. References
3. 22 Lessons from the Puerto Rico Infarction National Collaborative Experience Initiative
  1. Introduction and Background
  2. Inspired to Make Changes
  3. Executing the Plan
  4. The Ultimate Goal: Total Ischemia Time
  5. Summary
  6. Acknowledgements
  7. References
4. 23 The STEMI Care Program in China
  1. Introduction
  2. Current Status of STEMI Reperfusion in China
  3. China STEMI Care Program
  4. Conclusions
  5. References
5. 24 STEMI INDIA
  1. Introduction
  2. Beginnings
  3. Aims and Goals
  4. Developing a STEMI System of Care: The STEMI INDIA Model
  5. The Prototype Statewide STEMI Project: The Pilot Tamilnadu STEMI Project
  6. Framework for a Statewide STEMI Program
  7. Other Important Activities of STEMI INDIA
  8. References
6. 25 The Role of Telemedicine in STEMI Interventions
  1. Definition of Telemedicine
  2. Computer Power
  3. Artificial Intelligence
  4. Cloud Computing
  5. Pervasive Computing, Ubiquitous Computing or the Internet of Things
  6. Socioeconomic Disparities
  7. Healthcare Disparities
  8. Time as a Strong Predictor of Outcomes
  9. LATIN, A Cloud Computing STEMI Network Supported by Artificial Intelligence
  10. Conclusions
  11. References
7. 26 Innovative Telemedicine STEMI Protocols
  1. Introduction
  2. Methods
  3. Results
  4. Discussion
  5. Conclusions
  6. References
Part V: Future Perspectives
1. 27 STEMI Interventions, Beyond the Culprit Lesion
  1. Introduction
  2. The Clinical Conundrum
  3. Current Evidence
  4. Special Circumstances
  5. Conclusions
  6. References
2. 28 Promising Technologies for STEMI Interventions
  1. Introduction
  2. Endothelial Progenitor Cell Capture Stent
  3. Potential Advantages of the EPC Capture Stent in STEMI
  4. EPC Capture Stent in STEMI
  5. The Combo Stent: A Combined DES and EPC Capture Stent
  6. Bioresorbable Vascular Scaffold
  7. Conclusions
  8. References
Index
End User License Agreement

List of Tables

Chapter 01
1. Table 1.1 Which stent is most desirable for STEMI interventions?
2. Table 1.2 Management of no‐reflow.
3. Table 1.3 Is thrombectomy an available tool in STEMI?
4. Table 1.4 Percutaneous coronary intervention in non‐culprit vessel.
5. Table 1.5 Role of the intra‐aortic balloon pump and counterpulsation in STEMI intervention.
Chapter 02
1. Table 2.1 Classification of recommendations and levels of evidence.
2. Table 2.2 Recommendations for the use of glycoprotein IIb/IIIa receptor antagonists.
3. Table 2.3 Recommendations for the use of thienopyridines.
4. Table 2.4 Recommendations for the use of parenteral anticoagulants.
5. Table 2.5 Recommendations for triage and transfer for percutaneous coronary intervention.
6. Table 2.6 Recommendations for intensive glucose control in STEMI.
7. Table 2.7 Recommendations for thrombus aspiration during percutaneous coronary interventions (PCI) for STEMI.
8. Table 2.8 Recommendations for the use of stents in STEMI.
9. Table 2.9 Recommendation for angiography in patients with chronic kidney disease.
10. Table 2.10 Recommendations for the use of fractional flow reserve.
11. Table 2.11 Recommendations for percutaneous coronary interventions (PCI) for unprotected left main coronary artery disease.
12. Table 2.12 Antiplatelet therapy to support primary percutaneous coronary interventions (PCI) for STEMI.
13. 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.
14. Table 2.14 Evaluation and management of patients with STEMI and out‐of‐hospital cardiac arrest.
15. Table 2.15 Primary percutaneous coronary interventions and STEMI.
Chapter 03
1. Table 3.1 Characteristics of thrombolytic therapy agents.
2. Table 3.2 Guidelines recommending antithrombotic therapy with thrombolytic therapy.
Chapter 04
1. 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.
2. Table 4.2 Dose, contraindications, advantages and disadvantages of the main anticoagulant drugs available for STEMI patients undergoing primary percutaneous coronary intervention.
Chapter 05
1. Table 5.1 P2Y₁₂ Inhibitors.
2. Table 5.2 Ticlopidine and clopidogrel studies.
3. Table 5.3 Prasugrel studies.
4. Table 5.4 Ticagrelor studies.
5. Table 5.5 Cangrelor studies.
Chapter 07
1. Table 7.1 Thrombolysis in myocardial infarction (TIMI) thrombus grade.
2. Table 7.2 Strategy for the management of the STEMI lesion based on thrombus grade; Mehta Classification.
3. Table 7.3 Step by step technique for STEMI interventions.
4. Table 7.4 Thrombectomy devices.
Chapter 09
1. Table 9.1 Technical features of currently available percutaneous support devices.
Chapter 10
1. Table 10.1 Characteristics of the most common manual and mechanical thrombectomy devices compatible with 0.014‐inch guide wires.
2. Table 10.2 Randomized studies showing the effects of manual thrombus aspiration.
3. Table 10.3 Randomized studies showing the effects of mechanical thrombus aspiration.
Chapter 11
1. 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
1. Table 15.1 Clinical studies of remote ischemic conditioning in acute myocardial infarction.
Chapter 17
1. Table 17.1 Emergency medical services roles.
2. 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].
3. Table 17.3 Common QRS complex ST‐elevation mimics.
4. Table 17.4 Three scenarios for appropriate catheterization laboratory activation involving patients with out‐of‐hospital cardiac arrest.
5. Table 17.5 Three emergency medical services (EMS) time intervals.
Chapter 21
1. Table 21.1 Main historical and demographic data in the studied groups of patients.
2. Table 21.2 Complications in the pre‐hospital thrombolysis group.
3. Table 21.3 In‐hospital clinical and angiographic data in the studied groups of patients.
4. Table 21.4 Frequency of ventricular fibrillation in the studied groups of patients.
5. Table 21.5 Long‐term clinical and angiographic data in the studied groups of patients.
6. Table 21.6 Long‐term changes in left ventricular ejection fraction (LVEF) in the studied groups of patients.
Chapter 23
1. Table 23.1 Components and aims of the China STEMI care program.
Chapter 24
1. 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
1. Table 26.1 Relevant Statistics Comparison between Developed and Developing Countries.
Chapter 27
1. Table 27.1 Current guidelines for the management of non‐culprit bystander coronary lesions.
2. Table 27.2 Prospective clinical trials of the management of non‐culprit bystander coronary lesions.
3. Table 27.3 Current prospective clinical trials of the management of non‐culprit bystander coronary lesions.
Chapter 28
1. Table 28.1 Published studies on endothelial progenitor cell capture stent in STEMI.

List of Illustrations

Chapter 02
1. Figure 2.1 Triage and transfer for PCI.
Chapter 03
1. Figure 3.1 Short‐ and long‐term clinical outcomes in patients treated with primary percutaneous coronary intervention or thrombolytic therapy.
2. 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.
3. 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
1. 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.
2. Figure 4.2 Anticoagulant protocol for patients undergoing primary percutaneous coronary intervention adopted by the Bristol Heart Institute, Bristol, United Kingdom.
Chapter 05
1. 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.
2. Figure 5.2 There are two primary P2Y receptors, P2Y₁ (high affinity; initiation) and P2Y₁₂ (low affinity; amplification and clot stabilization); P2Y₁₂ 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
1. 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.
2. 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).
3. 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).
4. 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.
5. Figure 6.5 Acute right ventricular support devices.
6. 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
1. Figure 7.1 Dynamic thrombus (AMI, acute myocardial infarction; RBC, red blood cells).
2. 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).
3. 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.
4. 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.
5. 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.
6. 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).
7. 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.
8. 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.
9. 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.
10. 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).
11. 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.
12. 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.
13. 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.
14. 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.
15. 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.
16. 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.
17. 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.
18. 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.
19. 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.
20. Figure 7.20 Thrombus management strategy (DAPT, dual antiplatelet therapy; i/c, intracoronary; TIMI, thrombolysis in myocardial infarction; UFH, unfractionated heparin).
Chapter 08
1. 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.
2. Figure 8.2 An example of left circumflex artery stenting in acute myocardial infarction through the arteria lusoria.
3. 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).
4. 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
1. 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).
2. 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].
3. 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
1. 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.
2. Figure 10.2 Mechanical thrombectomy devices: a) Angiojet system. b) X‐sizer system. c) Rinspirator system. d) Rescue. e) TVAC system.
Chapter 11
1. 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].
2. 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.
3. Figure 11.3 Landmark analysis of definite stent thrombosis up to 3 years in the Swedish Coronary Angiography and Angioplasty Register.
4. Figure 11.4 Network meta‐analysis of bare‐metal compared with drug‐eluting stents.
5. 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
1. 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.
2. 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.
3. 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.
4. 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.
5. 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
1. Figure 17.1 STEMI network: four express lanes . EMS, emergency medical services; FMC, first medical contact; PPCI, primary percutaneous coronary intervention.
Chapter 18
1. 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.
2. 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.
3. Figure 18.3 US STEMI systems of care from the Mission: Lifeline coverage Map.
4. 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.
5. Figure 18.5 Example protocol from Minneapolis Heart Institute’s Level 1 STEMI protocol.
6. Figure 18.6 Sample patient transfer datasheet from Minneapolis Heart Institute’s Level 1 STEMI protocol; reproduced with permission.
Chapter 19
1. 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.
2. 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.
3. 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
1. 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.
2. Figure 22.2 Data collection sheet designed for the Puerto Rico Infarction National Collaborative Experience participating centers.
3. 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”.
4. 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.
5. Figure 22.5 Schematic representation of integration in a ST‐segment elevation myocardial infarction percutaneous coronary intervention system of care.
6. 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
1. Figure 23.1 Regional network of STEMI care.
Chapter 24
1. Figure 24.1 ST‐elevation myocardial infarction cluster; hub and spoke model. EKG, electrocardiogram; PCI, percutaneous coronary intervention.
Chapter 25
1. Figure 25.1 Cloud computing: Applications, hardware and systems software located in datacenters delivered as services over the internet.
2. Figure 25.2 An integrated telemedicine platform.
Chapter 26
1. Figure 26.1 Roles of the ambulance in ST‐elevation myocardial infarction interventions.
2. 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.
3. Figure 26.3 Enhancement of thrombolysis and pharmacoinvasive management with telemedicine. Cath, catherization; CVL, central venous line; PCI, percutaneous coronary intervention; TM, telemedicine.
4. 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].
5. Figure 26.5 The Lumen Americas Telemedicine Infarct Network hub and spokes model. PCI, percutaneous coronary intervention.
6. Figure 26.6 Comparison of three methods of pre‐hospital diagnosis and triage.
7. 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
1. 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.
2. 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).
3. 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
1. Figure 28.1 Genous™ endothelial progenitor cell capture (EPC) stent.
2. Figure 28.2 Combo™ bioengineered sirolimus‐eluting stent.
3. Figure 28.3 ABSORB bioresorbable vascular scaffold.