Жанры Авторы Контакты О сайте

Книжные новинки Популярные книги

Главная Авторы Elias B. Hanna Practical Cardiovascular Medicine

Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 1

Оглавление

Предыдущая Следующая

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 ...247

Оглавление

Practical Cardiovascular Medicine

Купить и скачать книгу Вернуться на страницу книги Practical Cardiovascular Medicine

Оглавление

Страница 1 Table of Contents List of Tables List of Illustrations Guide Pages Practical Cardiovascular Medicine Страница 8Страница 9 Preface Abbreviations About the Companion Website Страница 13 1
Non-ST-Segment Elevation Acute Coronary Syndrome I. Definition, types of myocardial infarction, and pitfalls A .Type 1 MI (spontaneous MI) = True acute coronary syndrome (ACS) B. Type 2 MI (secondary MI) with or without underlying CAD C. Non-ischemic myocardial injury (also called “non-MI troponin elevation”) D .Coronary vasospasm and microvascular dysfunction E. MI with non-obstructed coronary arteries (MINOCA) F. Unstable angina G. Additional notes: definition of reinfarction, type 3 MI, post-PCI MI (type 4 MI), and post-CABG MI (type 5 MI) Additional note: importance of LVEDP II. Clinical features, ECG, cardiac biomarkers, and echocardiography in ACS A. Assess the clinical features of chest pain (Table 1.2) B. ECG C. Cardiac Troponin I or T D. Echocardiography and acute resting nuclear scan III. Initial approach to acute chest pain presentations and the use of conventional and high-sensitivity troponins A. Assess for other serious causes of chest pain at least clinically, by chest X-ray and by ECG (always think of pulmonary embolism, aortic dissection, and pericarditis). B. Use conventional troponin and hs-troponin for MI rule-in and rule-out C. Stratification of patients who rule in for MI IV. Management of NSTEMI A. Initial invasive strategy B. Antiplatelet therapy (Figure 1.4) (see Appendix 4 for a detailed discussion) C. Anticoagulant therapy (see Appendix 4 for a detailed discussion) D. Anti-ischemic therapy and other therapies V. General procedural management after coronary angiography: PCI, CABG, or medical therapy only A. CABG indications B. PCI indications C. Among patients with high-risk ACS managed invasively, ~25–30% do not undergo any revascularization after coronary angiography VI. Discharge medications in NSTEMI A. Antiplatelet and anticoagulant therapy B. Other therapies VII. Prognosis (Table 1.5) Appendix 1. Complex angiographic disease- Moderate disease progression A. Complex angiographic plaque B. Extent of CAD in patients with NSTE-ACS (Table 1.6) C. Moderate CAD-Risk of progression of moderate CAD in NSTEMI and in stable CAD Appendix 2. Women and ACS, elderly patients and ACS, CKD A. Women and ACS B. Elderly patients and ACS C. CKD Appendix 3. Bleeding, transfusion, patients on chronic warfarin or NOAC, gastrointestinal bleed A. The negative impact of bleeding B. Transfusion in ACS C. Patients on chronic anticoagulation who present with ACS D. Gastrointestinal (GI) bleed in patients receiving aspirin and clopidogrel after stent placement E. Management of elevated troponin in a patient with GI bleed Appendix 4. Antiplatelet and anticoagulant therapy A. Antiplatelet therapy (Table 1.7) B. Clopidogrel resistance is seen in ~30% of patients C. Anticoagulant therapy (Table 1.8) Appendix 5. Difference between plaque rupture and plaque erosion Appendix 6. Spontaneous coronary artery dissection Appendix 7. Harmful effects of NSAIDs and cyclooxygenase-2 inhibitors in CAD Appendix 8. Additional ideas on the physiology of hs-troponin-Role of hs-troponin in primary prevention QUESTIONS AND ANSWERS References Definition of MI, type 1 and type 2 MI Vasospasm MINOCA diagnosis and prognosis Hs-troponin and prognosis Peri-PCI MI Zero flow LVEDP Clinical approach ECG Undetectable hs-troponin and hs-troponin algorithms (+references 28-30 and 45) Invasive strategy vs conservative strategy Timing of initial invasive strategy Initial medical therapy CABG vs PCI Multivessel PCI Bad outcomes of patients with significant CAD who are not revascularized (in addition to reference 25) Duration of dual antiplatelet therapy after ACS and DES 1 to 3 months DAPT after DES: Dual antiplatelet therapy and anticoagulation Other discharge medications Prognosis Complex plaques and CAD progression Women and ACS Elderly and ACS CKD Bleeding Transfusion in ACS GI bleed Antiplatelet and anticoagulant therapies in ACS Plaque erosion Spontaneous coronary artery dissection Physiology of hs-troponin Notes 2 ST-Segment Elevation Myocardial Infarction 1. DEFINITION, REPERFUSION, AND GENERAL MANAGEMENT I. Definition II. Timing of reperfusion III. ECG phases of STEMI (Figure 2.1) IV. STEMI diagnostic tips and clinical vignettes 1. A patient presents with one episode of chest pain that lasted 10 minutes. He does not have any pain currently. He reports a prior history of a large MI 2 years previously. His ECG shows 1.5 mm ST elevation in the anterior leads with Q waves and T-wave inversion. Should he undergo emergent reperfusion? 2. A patient presents with ongoing chest pain for the last 8 hours. His ECG shows inferior ST elevation of 1 mm with deep Q waves. Should he undergo emergent reperfusion? 3. A patient presents with intermittent chest pain for the last 3 days. He had an episode of pain 2 hours previously but is currently free of any pain. His ECG shows anterolateral ST elevation. Should he undergo emergent reperfusion? 4. A patient presents with chest pain that started 4 hours previously and inferior ST elevation. His pain has just resolved with aspirin and nitroglycerin, but ST elevation is persistent. Should he undergo emergent reperfusion? 5. A patient presents with chest pain that started 4 hours previously and inferior ST elevation. Both his pain and ST elevation resolve after aspirin and nitroglycerin administration. Should he undergo emergent reperfusion? 6. A patient presents with chest pain that lasted 2–3 hours earlier today and has now resolved. His ECG shows subtle ST elevation (<1 mm) in leads II, aVF, V₅, and V₆ (Figure 2.2). Should he undergo emergent reperfusion? 7. A patient presents with chest pain that has lasted 2–3 hours earlier today and has now resolved. His ECG shows inferior Q waves and T-wave inversion, without any significant ST elevation. Should he undergo emergent reperfusion? V. Specific case of new or presumably new LBBB VI. Reperfusion strategies: fibrinolytics, primary PCI, and combined fibrinolytics–PCI A. Fibrinolytics (also called thrombolytics): mortality benefit B. Fibrinolytics: limitations, contraindications, definition of successful response, and definition of TIMI flow (Table 2.1)^1,10,20,21 C. Fibrinolytics: various agents D. Primary PCI is superior to fibrinolytic therapy; importance of time of presentation, door-to-balloon time, and PCI delay E. Combination of PCI and fibrinolytic therapy F. Putting it all together: management of patients presenting to non-PCI-capable hospitals VII. Coronary angiography and PCI later than 24 hours after presentation-role of stress testing VIII. Angiographic findings, PCI, and cellular reperfusion; multivessel disease in STEMI A. PCI: microvascular and cellular reperfusion B. Multivessel disease in STEMI IX. Antithrombotic therapies in STEMI A. Antithrombotic therapies in conjunction with primary PCI B. Antithrombotic therapies in patients treated with fibrinolytics (started upon presentation) X. Other acute therapies XI. Risk stratification A. Killip classification uses clinical features upon presentation to assess STEMI prognosis. B. TIMI risk score for STEMI XII. LV remodeling and infarct expansion after MI (see Figure 2.5) XIII. Discharge, EF improvement, ICD A. Discharge medications C. ICD 2. STEMI COMPLICATIONS I. Cardiogenic shock A. Differential diagnosis (see Table 2.4) B. Pathophysiology of LV-related cardiogenic shock and failure in acute MI C. Management of LV-related cardiogenic shock D. Management of severe acute left heart failure without shock E. RV-related cardiogenic shock: characteristics and management II. Mechanical complications A. Severe mitral regurgitation (MR) D. Clinical manifestations E. Diagnosis F. Treatment G. Another mechanical complication: dynamic left ventricular outflow tract obstruction III. Recurrent infarction and ischemia IV. Tachyarrhythmias A. Ventricular tachyarrhythmias: VF and sudden death B. Ventricular tachyarrhythmias: VF C. Ventricular tachyarrhythmias: sustained VT D. Ventricular tachyarrhythmias: non-sustained VT (NSVT) F. Acute therapy of sustained VT/VF G. Atrial fibrillation, atrial flutter H. Accelerated junctional rhythm (also called non-paroxysmal junctional tachycardia) V. Bradyarrhythmias, bundle branch blocks, fascicular blocks A. Inferior MI B. Anterior MI C. Bundle branch and fascicular blocks VI. LV aneurysm and LV pseudoaneurysm A. LV aneurysm B. LV pseudoaneurysm VII. Pericardial complications A. Acute post-infarction pericarditis B. Pericardial effusion C. Dressler syndrome or post-cardiac injury syndrome VIII. LV thrombus and thromboembolic complications IX. Early and late mortality after STEMI Appendix 1. Out-of-hospital cardiac arrest: role of early coronary angiography and therapeutic hypothermia A. Decision to perform immediate coronary angiography and role of post-resuscitation ECG B. Role of post-resuscitation echocardiography C. Role of extra-corporeal membrane oxygenation (ECMO) in ongoing VF arrest D. No role for thrombolysis during the resuscitation of cardiac arrest E. Mild therapeutic hypothermia F. Hemodynamic status post cardiac arrest QUESTIONS AND ANSWERS References PCI vs. thrombolysis, DTB time Combined PCI–thrombolysis. Management in non-PCI hospitals with expected PCI delays OAT and late presenters PCI flow Multivessel CAD, PCI, and CABG in STEMI Antithrombotics Other acute therapies Early discharge Prognosis ICD Shock (+ SHOCK trial and CULPRIT-SHOCK trial, references 69 and 73) RV shock (+ reference 89 above) Mechanical complications Arrhythmias VF VT AF AV block Aneurysm and pseudo-aneurysm Post-MI pericarditis LV thrombus Prognosis Cardiac arrest Note 3 Stable Ischemic Heart Disease and Approach to Chronic Chest Pain I. Causes of angina and pathophysiology of coronary flow A. Angina caused by fixed coronary obstruction B. Vasospastic angina (Prinzmetal angina) or dynamic coronary obstruction C. Angina secondary to severely increased demands Note on coronary flow physiology II. Diagnostic approach A. Clinical features of typical angina B. Pre-test clinical probability of significant CAD C. Pre-test probability of high-risk CAD (multivessel, extensive CAD) D. Testing modalities (diagnostic and prognostic purposes): E. Risk stratification with stress testing Warranty periods F. Putting it together: diagnostic approach and management of chronic chest pain (Figure 3.2) III. Silent myocardial ischemia. Is there a role for screening asymptomatic patients and post-PCI patients? IV. Medical therapy: antiplatelet therapy V. Medical therapy: antianginal therapy and risk factor control A. β-Blockers Notes B. Nitrates C. Calcium channel blockers (CCBs) D. Choice of antianginal drugs E. Ranolazine F. Control of risk factors VI. Indications for revascularization VII. CABG and CABG vs. medical therapy VIII. PCI and PCI vs medical therapy In sum, ISCHEMIA trial shifts 2 paradigms in stable CAD: IX. PCI vs. CABG in multivessel and left main disease X. High-surgical-risk patients XI. Role of complete functional revascularization XII. Hybrid CABG–PCI XIII. Enhanced external counterpulsation (EECP) XIV. Mortality in CAD (Table 3.5) Appendix 1. Notes on various surgical grafts A. SVG 1. General SVG outcomes 2. Factors determining SVG patency 3. Treatment of SVG failure B. LIMA C. Other arterial grafts D. Grafts with multiple distal anastomoses (see Chapter 34, Figure 34.41) E. Off-pump CABG Appendix 2. Coronary vasospasm (variant angina, Prinzmetal angina) A. Underlying CAD: patterns of vasospasm B. ECG, arrhythmias, and clinical manifestations C. Diagnosis of vasospasm D. Frequency of vasospasm in patients with exertional chest pain and no significant CAD E. Treatment and prognosis of macrovascular vasospasm Appendix 3. Microvascular endothelial dysfunction Appendix 4. Women with chest pain and normal coronary arteries Appendix 5. Diagnostic strategy for ischemia with non-obstructed coronary arteries (INOCA) Appendix 6. Myocardial bridging Appendix 7. Coronary collaterals, chronic total occlusion Appendix 8. Hibernation, stunning, ischemic preconditioning QUESTIONS AND ANSWERS References Revascularization (+ISCHEMIA references 19,20) PCI vs. medical therapy (+ISCHEMIA references 19,20; FAME 2 references 28,65) CABG vs. PCI Complete vs. incomplete revascularization Mortality Left main and CABG Bypass grafts Coronary spasm Microvascular dysfunction Myocardial bridging Collaterals Notes Страница 246{buyButton}

Подняться наверх

Популярные жанры Детективы Классика Искусство Психология Наука и образование Фантастика Фэнтези

Книжные новинки Популярные книги Жанры Авторы Контакты О сайте

© КнигаЛит.ру 2015 - 2024. Рейтинг книг, рецензии и отзывы о бумажных и электронных книгах, сравнение цен на книги в магазинах.

На нашем сайте вы можете скачать бесплатно и читать бесплатно онлайн фрагмент интересующего вас произведения, заказать и купить бумажную книгу с доставкой в книжных интернет-магазинах, или электронную книгу в одном из популярных форматов для чтения на ридере, мобильном устройстве и ПК. Подробнее о сайте.