Practical Cardiovascular Medicine

Автор книги: Elias B. Hanna id книги: 2263843 Оценка: 0.0 Голосов: 0 Отзывы, комментарии: 0 13323,6 руб. (121,59$) Читать книгу Купить и скачать книгу Электронная книга Жанр: Медицина Правообладатель и/или издательство: John Wiley & Sons Limited Дата добавления в каталог КнигаЛит: 12 февраля 2022, 00:32 ISBN: 9781119832720 Скачать фрагмент в формате fb2 fb2.zip Возрастное ограничение: 0+ Оглавление Отрывок из книги

Реклама. ООО «ЛитРес», ИНН: 7719571260.

Описание книги

Providing a complete but succinct overview of the information cardiologists and cardiology trainees need to have at their fingertips, Practical Cardiovascular Medicine, Second Edition is an everyday primary guide to the specialty. Provides cardiologists with a thorough and up-to-date review of cardiology, from pathophysiology to practical, evidence-based management Ably synthesizes pathophysiology fundamentals and evidence-based approaches to prepare a physician for a subspecialty career in cardiology Clinical chapters cover coronary artery disease, heart failure, arrhythmias, valvular disorders, pericardial disorders, congenital heart disease, and peripheral arterial disease Practical chapters address ECG, coronary angiography, catheterization techniques, echocardiography, hemodynamics, and electrophysiological testing Includes over 730 figures, key notes boxes, references for further study, and coverage of clinical trials Review questions help clarify topics and can be used for Board preparation – over 650 questions in all The Second Edition has been comprehensively updated with the newest data and with both the American and European guidelines. More specifically, 20 clinical chapters have been rewritten and extensively revised. Procedural chapters have been enhanced with additional concepts and illustrations, particularly the hemodynamic and catheterization chapters. Clinical questions have been revamped, new questions have been added, including a new, 259-question section at the end of the book. Practical Cardiovascular Medicine, Second Edition is an ideal reference for the resident, fellow, cardiologist, and any professional treating patients with cardiovascular disease.

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

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

4 Heart Failure

DEFINITION, TYPES, CAUSES, AND DIAGNOSIS OF HEART FAILURE. 1. DEFINITION AND TYPES OF HEART FAILURE. I. Heart failure is diagnosed clinically, not by echocardiography

A. Congestive findings

B. Low-output findings (also known as “cold” signs) correlate with a more advanced HF stage:

II. After HF is defined clinically, echocardiography is used to differentiate the three major types of HF. A. HF secondary to LV systolic dysfunction, where EF is reduced ≤40%

B. HF secondary to LV diastolic dysfunction, where EF is normal (≥50%), sometimes supranormal, and LV is generally of normal or small size

III. Two additional types of HF. A.High-output heart failure, particularly obesity, which overlaps with the obese subtype of HFpEF

B. Predominant or isolated right heart failure

2. CAUSES OF HEART FAILURE. I. Systolic HF or HF with reduced EF (HFrEF) A. CAD

B. Hypertension

C. Advanced valvular heart disease (MR, AI, AS) D. Dilated cardiomyopathy (DCM)

The worst prognosis is seen with the following three cardiomyopathies: HIV cardiomyopathy, amyloidosis, and doxorubicin- associated cardiomyopathy. 15

II. HF with preserved EF (HFpEF) A. Hypertension or obesity with or without LV hypertrophy

B. CAD (ischemia without infarction)

C. Restrictive cardiomyopathy (RCM)

D. Constrictive pericarditis

III. Right HF

3. DIAGNOSTIC TESTS. I. Echocardiography

II. BNP

III. ECG. A completely normal ECG almost excludes the diagnosis of HF, particularly systolic HF and acute HF.8

IV. Coronary angiography and other ischemic tests

V. Diastolic stress testing

VI. Endomyocardial biopsy

VII. Cardiac MRI

CHRONIC TREATMENT OF HEART FAILURE. 1. TREATMENT OF SYSTOLIC HEART FAILURE. I. Treat the underlying etiology: target BP and CAD

II. Value of revascularization in ischemic cardiomyopathy: STICH trial

III. Role of viability testing and ischemic testing

A. Definition of global and regional viability; viability tests

B. Variations in the definition of global viability

C. Limitations of viability testing

D. Role of ischemic testing; difference between ischemia and viability

E. Indications for revascularization in ischemic LV dysfunction

IV. Drugs that affect survival in EF<40%

V. Specifics of drugs that affect survival

A. ACE-I or ARB*

B. β -Blockers

C. Aldosterone receptor antagonists (spironolactone, eplerenone)

D. Angiotensin receptor-Neprilysin inhibitor (sacubitril–valsartan combination)

E. Hydralazine–nitrate combination

VI. Drugs that improve symptoms and morbidity. A. Diuretics

B. Digoxin

C. Ivabradine

D. Glifozins= Sodium-glucose cotransporter-2 (SGLT-2) inhibitors (class I recommendation in HFrEF per ESC)

VII. Devices. A. ICD

B. Biventricular (BiV) pacemaker = cardiac resynchronization therapy (CRT)

VIII. Other therapeutic measures

IX. Prognosis

2. TREATMENT OF HFPEF

A. Treatment of HTN to <130/80 (ACC guidelines) or <140/80 (ESC HTN guidelines) 176

B. Decongestion with diuretics, not nitrates

C. Rhythm control of tachyarrhythmias, especially in the chronic setting

D. Revascularization of CAD that is extensive enough to contribute to HF

E. Questionable value of heart rate reduction: β-Blockers, non-DHP calcium channel blockers, ivabradine

F. ACE-I, ARB, or sacubitril-valsartan

G. Spironolactone

ACUTE HEART FAILURE AND ACUTELY DECOMPENSATED HEART FAILURE

I. Triggers of acute decompensation

II. Profiles of acute HF: congestion without low cardiac output, congestion with low cardiac output. A. Always assess for:

B. Then classify the acute HF into the following hemodynamic profiles:

III. Treatment of acute HF: diagnosis and treatment of triggers

IV. Treatment of acute HF: diuretics, cardiorenal syndrome, aggressive decongestion, ultrafiltration

B. Acute cardiorenal syndrome

C. Importance of aggressive decongestion, even in the face of a rising creatinine

D. Continuous loop diuretic drip vs. intermittent boluses- Role of ultrafiltration

E. Diuretic resistance

V. Treatment of acute HF: vasodilators

VI. Treatment of acute HF: IV inotropic agents

VII. In-hospital and pre-discharge use of ACE-I/ARB, angiotensin-neprilysin inhibition, and β-blockers

VIII. Treatment of acute HF: O2, non-invasive ventilatory support (CPAP, BiPAP), intubation

IX. Summary: keys to the treatment of acute HF (Table 4.2)

X. Discharge

XI. Inability of severe HF to tolerate vasodilatation or hemodialysis

XII. Outpatient monitoring of HF and prevention of hospitalization

Appendix 1. Management of isolated or predominant RV failure. A. Causes of right HF (see Table 4.3) 260

B. RV morphological features; echocardiographic and hemodynamic features of RV dysfunction

C. Pathophysiology, ventricular interdependence

D. Treatment of acute RV failure (isolated or predominant RV failure)

QUESTIONS AND ANSWERS

References

BNP

Revascularization in ischemic cardiomyopathy, viability testing

Regional vs. global viability

ACE-I

ARB and other ACE-I data

β-Blockers

Aldosterone antagonists

Neprilysin antagonist, ARB

Hydralazine, nitrates

Diuretics

Digoxin

Devices

HFpEF

ADHF

Vasodilators and inotropes in acute heart failure

Prevention of HF hospitalizations

RV failure

Notes

5 Additional Heart Failure Topics

1. SPECIFIC CARDIOMYOPATHIES. I. Arrhythmia-induced cardiomyopathy

A. Tachycardia-induced cardiomyopathy

B. PVC-induced cardiomyopathy

D. LBBB-induced cardiomyopathy

II. Viral myocarditis

Diagnosis

III. Acute eosinophilic myocarditis

IV. HIV cardiomyopathy

V. Chagas disease

VI. Sarcoidosis

VII. LV non-compaction

VIII. Takotsubo and other stress-related cardiomyopathies. A. Takotsubo cardiomyopathy (TC, also called “stress-induced cardiomyopathy” or “apical ballooning syndrome”)

B. Other stress-related transient cardiomyopathies

IX. Infiltrative restrictive cardiomyopathy: Amyloidosis

A. ECG and echo features

B. Diagnosis

C. Treatment

X. Other infiltrative restrictive cardiomyopathies. A. Sarcoidosis

B. Hemochromatosis

C. Fabry disease: genetic metabolic storage disorder

2. ADVANCED HEART FAILURE: HEART TRANSPLANT AND VENTRICULAR ASSIST DEVICES (VADs) I. Stages of HF

II. Cardiac transplantation. A. Indications

B. Contraindications

C. Notes

D. Immune therapies

E. Complications

III. Left ventricular assist devices (LVADs)

A. Types of ventricular assist devices

B. Indications for LVAD and other considerations

C. Some technical aspects

D. Complications

3. PATHOPHYSIOLOGY OF HEART FAILURE AND HEMODYNAMIC ASPECTS. I. LV diastolic pressure in normal conditions and in HF (whether systolic or diastolic)

II. Definition of afterload

III. Cardiac output, relation to preload and afterload

IV. LV pressure–volume relationship in systolic versus diastolic failure: therapeutic implications

V. Optimal heart rate in HF

VI. Mechanisms of exercise intolerance in HF

VII. Pressure–volume (PV) loops

VIII. Additional features of HF with preserved EF

IX. High-output HF

QUESTIONS AND ANSWERS

References. Cardiomyopathies

Advanced HF

Pathophysiology of HF

Notes

6. Valvular Disorders

1. MITRAL REGURGITATION. I. Mechanisms of mitral regurgitation

II. Specifics of various causes of mitral regurgitation. A. Acute MR

B. Degenerative mitral valve disease or mitral valve prolapse (MVP)

Notes on MVP (degenerative MV disease)

C. Functional ischemic MR and functional non-ischemic MR (Figures 6.4, 6.5)

Functional MR is dynamic

D. Atrial functional MR

E. Rheumatic fever

F. Other causes of MR

Causes of transient severe MR

Important situation: severe MR with severe LV dysfunction

III. Assessment of MR severity. A. TTE (see also Chapter 32: Figures 32.24-27, and Table 32.1)

B. TEE or cardiac MRI for indeterminate MR

C. Left ventriculography

D. Right heart catheterization

E. Stress testing and BNP

IV. Natural history and pathophysiology of organic MR

V. Treatment of organic (primary) MR. A. Surgical indications in primary MR

LV function may deteriorate after mitral surgery:

B. MV repair is preferred to MV replacement in isolated posterior leaflet prolapse limited to less than half of the posterior leaflet (class I), where MV replacement is now contraindicated unless repair has been attempted (class III). It is also indicated with anterior or bileaflet prolapse, when durable repair seems probable (class I)

C. Medical therapy

VI. Treatment of secondary MR (ischemic and non-ischemic functional MR)

A. What is the primary driver of HF (MR vs. underlying LV failure)?

B. Will revascularization alone reverse MR?

C. Can MR therapy reverse the underlying tethering process?

D. Guidelines for the management of ischemic or non-ischemic functional MR

VII. Treatment of acute severe MR related to acute MI

VIII. Percutaneous mitral valve repair using the Mitraclip device (transcatheter edge-to-edge repair)

2. MITRAL STENOSIS. I. Etiology and natural history

II. Diagnosis (Table 6.1) A. Echocardiographic features (see also Chapter 32)

B. Catheterization

C. Echocardiographic Wilkins score

D. TEE

E. Stress testing and other maneuvers for MS

III. Treatment. A. Medical therapy

B. Indications for percutaneous or surgical therapy

C. Percutaneous commissurotomy (or percutaneous mitral balloon valvotomy [PMBV])

D. Surgical mitral commissurotomy

E. Mitral valve replacement; AF procedures

3. AORTIC INSUFFICIENCY. I. Etiology. A. Acute AI

B. Chronic AI

II. Pathophysiology and hemodynamics (Figure 6.16) A. Acute AI

B. Chronic compensated AI

C. Chronic decompensated AI

III. Diagnosis. A. TTE

B. TEE and cardiac MRI

C. Invasive assessment (aortic root angiography and hemodynamic measurements)

IV. Natural history and symptoms

V. Treatment. A. Medical therapy

B. Indications for surgery

C. AI and ascending aortic dilatation

D. Aortic valve repair

4. AORTIC STENOSIS. I. Etiology. A. Age-related calcific degeneration

B. Bicuspid aortic valve

II. Echo and catheterization diagnosis, pitfalls, and hemodynamics

A. Echo and Doppler features of severe AS

B. The three types of transaortic pressure gradients

C. Case of AF

III. Low-gradient AS with aortic valve area (AVA) ≤1 cm2 and low EF<50%

IV. Low-gradient AS with aortic valve area (AVA) ≤ 1 cm2 but normal EF: paradoxical low-flow/ low-gradient severe AS and normal-flow/low-gradient severe AS

V. Pressure recovery phenomenon

VI. Symptoms

VII. Natural history

VIII. AS should be differentiated from subvalvular and supravalvular AS in children or young adults

A.Subvalvular AS

B. Supravalvular AS

IX. Treatment. A. Antihypertensives

B. Indications for aortic valve replacement (AVR) (the first 4 are class I indications)

C. Ross procedure

D. Surgery for severe asymptomatic AS with normal EF

E. MR associated with severe AS

F. Percutaneous aortic valvuloplasty

G. Transcutaneous aortic valve replacement (TAVR) vs. surgical AVR

5. TRICUSPID REGURGITATION AND STENOSIS. I. Etiology of tricuspid regurgitation (TR) A. TR is often secondary to RV pressure or volume overload (functional TR, 80% of all TRs) (Figures 6.22, 6.23)

B. Primary TR

C. Isolated TR

II. Natural history of TR

III. Treatment of TR. A. Medical therapy of RV pressure or volume overload

B. Surgical indications

C. Timing of tricuspid valve surgery

IV. Tricuspid stenosis

6. PULMONIC STENOSIS AND REGURGITATION. I. Pulmonic stenosis (PS)

II. Pulmonic regurgitation (PR)

7. MIXED VALVULAR DISEASE; RADIATION HEART DISEASE. I. Mixed single-valve disease

II. Multiple valvular involvement (combined stenosis or regurgitation of two different valves)

III. Radiation heart disease

8. PROSTHETIC VALVES. I. Bioprosthesis versus mechanical prosthesis

II. Determinants of valve degeneration and valve thrombosis; anticoagulation guidelines. A. Bioprosthetic valve degeneration depends on:

B. Prosthetic valve thrombosis depends on:

Anticoagulation goals 15,17

Bridging for a planned procedure

III. Particular cases: women who wish to become pregnant and dialysis patients

IV. Echocardiographic follow-up of prosthetic valves

V. Complications

A. Degeneration

B. Prosthetic valve thromboembolism and thrombosis

C. Paraprosthetic leak

D. Endocarditis

E. Patient/prosthesis mismatch (PPM)

F. Mechanical valve obstruction

G. Differential diagnosis of a high transvalvular prosthetic gradient

9. AUSCULTATION AND SUMMARY IDEAS. I. Auscultation and other physical findings (see Table 6.5) A. MR murmur

B. MS murmur

C. AS murmur

D. AI murmur

E. TR murmur

F. HOCM murmur

G. Patent ductus arteriosus

H. Other pathological murmurs

I. Benign murmurs

J. Effects of different maneuvers on murmurs

K. Second heart sound (S2) abnormalities and splits

M. Precordial palpation of the apical impulse in the left lateral decubitus position: point of maximal impulse (PMI)

II. General ideas and workup. A. There is no role for medical therapy in symptomatic, severe valvular disorders or in valvular disorders associated with secondary LV dysfunction

B. Transesophageal echocardiography (TEE)

C. Exercise testing

D. Preoperative coronary angiography, and preoperative angiographic and hemodynamic assessment of valvular disease

E. Endocarditis prophylaxis

F. Follow-up echo

G. Surgical mortality

H. Volume and pressure overload with valvular disease

QUESTIONS AND ANSWERS

References. MR

Survival in asymptomatic severe MR

Guidelines

AF and pulmonary hypertension as indication for MV surgery

Value of early surgery

Role of symptoms and EF in determining long-term outcomes

MV repair improves early and late mortality vs replacement

MV surgery for functional MR

Mitraclip

Wilkins score and PMBV results

Reoperation with sparing, good long-term result

Radiation heart disease

Prosthetic valves

7. Hypertrophic Cardiomyopathy

I. Definition and features of HCM. A. Definition

B. Asymmetry

C. LVOT obstruction

D. Causes of MR in HOCM; mitral valve abnormalities in HOCM

E. Less common forms of HCM

II. Natural history and mortality

III. Symptoms and ECG

IV. Exam (see Table 7.1) V. Invasive hemodynamic findings

VI. Echocardiographic findings

VII. Provocative maneuvers

VIII. Genetic testing for diagnosis; screening of first-degree relatives

IX. Differential diagnosis of LVOT obstruction

X. Differential diagnosis of severe LV hypertrophy

XI. Treatment of symptoms. A. Chronic medical therapy of HOCM

B. AF

C. Acute therapy of acute HF or shock

D. AV sequential ventricular pacing

E. Invasive septal reduction

F. Activity restriction

XII. Treatment: sudden cardiac death risk assessment and ICD therapy

XIII. Athlete’s heart

QUESTIONS AND ANSWERS

References

8. Approach to Narrow and Wide QRS Complex Tachyarrhythmias

I. The unstable patient (shock, acute pulmonary edema)

II. Initial approach to any tachycardia

III. Approach to narrow QRS complex tachycardias (see Figures 8.1, 8.2)

IV. Approach to wide QRS complex tachycardias

V. Features characteristic of VT, as opposed to SVT with aberrancy. A. Four features are most helpful in differentiating VT from SVT. The presence of any one VT feature is immediately diagnostic of VT

B. Other features (again, the presence of any one feature is suggestive of VT)

VI. Features characteristic of SVT with pre-excitation

VII. Role of adenosine in establishing a diagnosis

VIII. Differential diagnosis of a wide complex tachycardia on a one-lead telemetry or Holter monitor strip

IX. Various notes. A. Retrograde P wave

B. Ashman’s phenomenon

C. How the tachycardia starts

D. How the tachycardia ends

E. Role of physical exam in the differential diagnosis of wide complex tachycardia

X. General management of SVT. A. Management of AF or atrial flutter (Table 8.2)

B. AVNRT, AVRT

C. Focal atrial tachycardia (Table 8.3)

XI. Non-tachycardic wide complex rhythms (see Figures 8.15, 8.16, 8.17) XII. Practice ECGs of wide complex tachycardias

Further reading

9 Ventricular Arrhythmias: Types and Management, Sudden Cardiac Death

I. Premature ventricular complexes

How to differentiate PVC from PAC with aberrancy

II. Ventricular tachycardia (VT) A. Types (Figure 9.3)

B. Causes of sustained VT

C. Causes and prognosis of non-sustained VT

D. Acute management of sustained VT

E. Chronic management of sustained VT

F. NSVT management

G. Accelerated idioventricular rhythm (AIVR)

H. Workup of VT occurring without obvious heart disease on echo and coronary angiography (see Sections VI-VIII)

III. Polymorphic ventricular tachycardia. A. Morphology and types

B. Treatment

Long-term treatment:

IV. Congenital long QT syndrome (LQT) A. Types

B. Problems with the definition of long QT and with the diagnosis

C. Epidemiology and risk of sudden death

D. Genetic testing

E. Therapy

V. Indications for ICD implantation. A. Secondary prevention

B. Primary prevention means ICD implantation in a patient without a history of sustained VT or sudden death

C. Syncope of undetermined origin with inducible, hemodynamically significant, sustained VT or VF on EP study (performed as part of syncope evaluation) (class I recommendation) D. Dilated cardiomyopathy with syncope of unknown origin (class IIa) E. Hypertrophic cardiomyopathy

Note: Wearable, external cardioverter defibrillator (Lifevest)

VI. VT with no obvious heart disease: VT related to subtle, overlooked cardiomyopathy. A. Arrhythmogenic right ventricular dysplasia or cardiomyopathy (ARVD/ARVC)

ECG features of the localized RV delay 50

Echo features of ARVD51

Diagnosis of ARVD51

Treatment of ARVD

B. Cardiac sarcoidosis

C. Mitral valve prolapse

VII. VT with no obvious heart disease: VT related to electrical disorders and channelopathies

A. Brugada syndrome

B. Idiopathic catecholaminergic polymorphic VT

C. WPW

D. Congenital long QT syndrome (see Section IV) E. Congenital short QT syndrome

F. Malignant early repolarization and idiopathic VF

VIII. VT with no obvious heart disease: idiopathic outflow tract PVC or VT and idiopathic left fascicular PVC or VT

IX. Sudden cardiac death and athlete’s ECG screening. A. The mechanism of sudden cardiac death (SCD) is usually VT/VF

B. Athlete preparticipation ECG analysis

C. Clinical red flags- Cases of bicuspid aortic stenosis and pulmonic stenosis- Myocarditis

D. Work-up of SCD survivors

E. Athletic activity in patients with ICD

QUESTIONS AND ANSWERS

References

Notes

10 Atrial Fibrillation

I. Predisposing factors (see Table 10.1)

II. Types of AF

III. General therapy of AF

A. Anticoagulation

B. Rate control

C. Rhythm control

IV. Management of a patient who presents with acute, symptomatic AF

V. Peri-cardioversion anticoagulation management

VI. Antiarrhythmic management after the acute presentation

VII. Decisions about long-term anticoagulation, role of clopidogrel, role of triple therapy. A. Long-term anticoagulation

B. Bleeding risk

C. Anticoagulation in acute TIA or stroke, and after intracranial bleed

D. Therapy in patients with AF and CAD- Question of triple combination of aspirin, clopidogrel and oral anticoagulation

E. Role of clopidogrel

VIII. Special situation: atrial fibrillation and heart failure. Optimal heart rate in heart failure. A. General management

B. Rate control in HF (Table 10.7)

C. Effect of AF on EF and value of AF ablation in HF

IX. Special situation: atrial fibrillation with borderline blood pressure or non-AF-related hypotension

X. AF burden as a correlate and a driver of HF progression

Appendix 1. Optimal heart rate and AF rate for optimal cardiac output

Appendix 2. Antiarrhythmic drug therapy

A. Class III agents

B.Class Ic agents (propafenone, flecainide)

C. Side effects

Appendix 3. Catheter ablation of atrial fibrillation, surgical ablation, AV nodal ablation

Appendix 4. INR follow-up in patients receiving warfarin-Non-vitamin K oral anticoagulants

Appendix 5. Bridging anticoagulation in patients undergoing procedures

Appendix 6. Management of elevated INR values

Appendix 7. Left atrial appendage surgical and percutaneous closure

Appendix 8. A common situation: AF and symptomatic pauses or bradycardia

Appendix 9. DC cardioversion in patients with a slow ventricular response

Appendix 10. AF occurring post-cardiac surgery and AF related to acute transient triggers

Appendix 11. Brief asymptomatic runs of AF on device interrogation and association with stroke. Role of rhythm monitoring after cryptogenic stroke

QUESTIONS AND ANSWERS

References

11 Atrial Flutter and Atrial Tachycardia

I. Atrial flutter. A. Definition

B. Electrophysiological features

C. Underlying pathology and anatomical substrate

D. ECG

E. Management of atrial flutter. 1. Acute treatment

2. Chronic treatment

3. The association between Aflutter and AF

II. Focal atrial tachycardia. A. Electrophysiological mechanisms

B. Site of origin

C. Natural history

D. ECG

Difference between Aflutter and AT

E. Treatment. 1. Acute treatment

2. Long-term therapy

III. Multifocal atrial tachycardia (MAT) (or chaotic atrial tachycardia)

IV. Ectopic atrial rhythm

QUESTIONS AND ANSWERS

References

Further reading

12 Atrioventricular Nodal Reentrant Tachycardia, Atrioventricular Reciprocating Tachycardia, Wolff–Parkinson–White Syndrome, and Junctional Rhythms

I. Inappropriate Sinus tachycardia (IST) and postural orthostatic tachycardia syndrome (POTS)

II. Atrioventricular nodal reentrant tachycardia (AVNRT) A. Mechanism (see Figure 12.1)

B. ECG

C. Treatment. 1. Acute therapy

2. Long-term treatment is required in case of frequent recurrences of sustained episodes

D. Termination

III. Atrioventricular reciprocating tachycardia (AVRT) and Wolff–Parkinson–White (WPW) syndrome. A. Pathophysiology

B. Baseline ECG is not affected by a concealed accessory pathway. C. Baseline ECG is affected by a manifest accessory pathway (pre-excitation or WPW pattern) (see Figures 12.8, 12.9, 12.10)

D. Localization of the accessory pathway according to the baseline ECG

E. Types of tachyarrhythmias: mechanisms and initiation. 1. Concealed accessory pathway (see Figure 12.11 )

2. Manifest accessory pathway (see Figure 12.12 )

F. More electrophysiological mechanisms

G. Treatment. 1. Acute treatment

2. Chronic preventive treatment

3. Asymptomatic pre-excitation/WPW diagnosed on a resting ECG

H. Additional WPW examples (Figures 12.18–12.21) IV. Junctional escape rhythm and accelerated junctional rhythm (or non-paroxysmal junctional tachycardia) A. Junctional escape beats or rhythm

B. Accelerated junctional rhythm

QUESTIONS AND ANSWERS

Further reading

IST

AVNRT and AVRT pictures and mechanisms

Effect of pacing on AVNRT vs. AVRT

Prognosis of WPW

Assessment of asymptomatic WPW

13 Bradyarrhythmias

I. AV block. A. Types of AV block

B. Causes of a pause on the rhythm strip

C. Location of the AV block

D. Causes

E. Treatment

F. Other ECG examples of AV block (see Figures 13.16–13.19)

II. Sinus node dysfunction. A. Types

B. Causes

C. Treatment

Important clinical tips

III. Bundle branch blocks, bifascicular and trifascicular block. A. Definitions

B. Causes and prognosis- Consider the following 3 ideas:

C. Work-up

D. Treatment

E. Tachycardia or acceleration-dependent bundle branch block

F. Bradycardia or deceleration-dependent bundle branch block and AV block

G. Alternating bundle branch block

QUESTIONS AND ANSWERS

References

14 Permanent Pacemaker and Implantable Cardioverter Defibrillator

I. Indications for permanent pacemaker implantation1

II. Types of cardiac rhythm devices

A. VVI = ventricular demand pacing

B. DDD = AAI + VAT + VVI

C. Biventricular pacemaker

D. Implantable cardioverter defibrillator (ICD)

III. Pacemaker intervals. A. VVI

B. DDD pacemaker’s four basic intervals (Figure 14.7)

C. Two other intervals are derived from the four basic intervals

D. Upper rate behavior (see Figures 14.8, 14.9)

E. Prevention of crosstalk4,6. Atrial-initiated ventricular blanking period

Ventricular-initiated atrial refractory period

F. Upper rate intervals (see Figure 14.10)

G. Magnet mode

IV. Leads (see Figure 14.11)

V. Systematic PM/ICD interrogation using the programmer. A. Summary screen

B. Lead impedance

C. Capture testing

D. Sensing assessment

VI. Pacemaker troubleshooting. A. Undersensing or failure to sense

B. Oversensing

C. Failure to capture

D. Manifestations of lead fracture and insulation defect

E. Absence of a pacemaker spike (or spikes) when there should be one

F. Pacemaker syndrome

G. Pacemaker-mediated tachycardia (PMT) (see Figure 14.14)

H. Differential diagnosis of a tachycardia occurring in a patient who has a DDD PM

PM and ICD magnet effect

I. Fusion and pseudofusion

J. Diaphragmatic stimulation

VII. Perioperative management of PM and ICD (during any surgery)

VIII. Differential diagnosis and management of the patient who presents with ICD shock(s)

IX. Evidence and guidelines supporting various pacing devices. A. DDD or AAI vs. VVI pacing

B. Mechanism of action of biventricular pacing (cardiac resynchronization therapy), evidence supporting its use, and clinical subsets

(a) QRS < 130 ms and QRS 130–150 ms

(b) RBBB and non-specific intraventricular conduction delay

(d) Paced ventricular rhythm

(e) Wide QRS and severe functional MR

(f) RV failure

C. Response to CRT and LV lead position

D. Optimization of AV delay in patients with CRT

E. Echocardiographic dyssynchrony parameters

F. Importance of the change of QRS width after CRT

G. Arrhythmic death in patients with ICD

H. His bundle pacing

Appendix. Cases of PM troubleshooting

QUESTIONS AND ANSWERS

References

Note

15 Basic Electrophysiologic Study

I. General concepts; intracardiac electrograms

II. AV conduction abnormalities

III. Sinus node assessment

IV. Ventricular vs. supraventricular tachycardia

V. Dual AV nodal pathways

VI. AVNRT

VII. Accessory pathway, orthodromic AVRT, antidromic AVRT

VIII. Atrial flutter

IX. Inducible VT

X. Mapping for ablation

Pacing for the differential diagnosis of SVT

Activation mapping

Entrainment mapping and post-pacing interval (see Figures 15.17, 15.18)

Pace mapping

Fractionated electrogram mapping

XI. EP electro-anatomical mapping

Further reading

16 Action Potential Features and Propagation: Mechanisms of Arrhythmias, Antiarrhythmic Drugs

I. Action potential (see Figures 16.1, 16.2) II. Action potential propagation and mechanisms of arrhythmias

III. General mechanism of action of antiarrhythmic agents

IV. Modulated receptor hypothesis and use dependence

V. Concept of concealed conduction

VI. Specific examples of drugs (see also Chapter 10) A. Class I

B. Class III (amiodarone, dronedarone, sotalol, ibutilide, dofetilide)

VII. Amiodarone toxicity. Thyroid toxicity

Lung toxicity

VIII. Effect on pacing thresholds and defibrillation thresholds

Further reading

17. Pericardial Disorders

1. ACUTE PERICARDITIS. I. Causes of acute pericarditis

II. History and physical findings. A. Chest pain

B. Friction rub

III. ECG findings

A. Diffuse concave ST elevation in all leads except aVR and V1

B. PR depression

C. Low QRS voltage and QRS alternans

IV. Echocardiography

V. Myopericarditis and perimyocarditis

VI. Treatment

A. Initial therapy

B. Recurrent pericarditis

2. TAMPONADE. I. Definition

II. Pathophysiology and hemodynamics

III. Diagnosis: tamponade is a clinical diagnosis, not an echocardiographic diagnosis

IV. Echocardiographic findings supporting the hemodynamic compromise of tamponade

V. Role of hemodynamic evaluation

VI. Special circumstances: low-pressure tamponade, tamponade with absent pulsus paradoxus, regional tamponade. A. Low-pressure tamponade

B. Underlying RV or LV failure and causes of absent pulsus paradoxus (and of attenuated septal and E variations)

C. Regional tamponade

D. COPD and other causes of pulsus paradoxus and RV–LV respiratory discordance

VII. Effusive–constrictive pericarditis

VIII. Treatment of tamponade

3. PERICARDIAL EFFUSION

I. Causes of a pericardial effusion with or without tamponade

II. Management of asymptomatic effusions and role of pericardiocentesis. A. General approach to a large asymptomatic effusion (Figure 17.4)

B. Pericardiocentesis and open pericardiotomy (pericardial window)

III. Note on postoperative pericardial effusions (after cardiac surgery)

Management

IV. Note on uremic pericardial effusion

4. CONSTRICTIVE PERICARDITIS

I. Causes

II. Pathophysiology and hemodynamics

III. Hemodynamic findings in constrictive pericarditis and differential diagnosis of constrictive pericarditis: restrictive cardiomyopathy, decompensated RV failure, COPD (Table 17.1)

B. Severe ventricular failure (particularly RV failure)

C. COPD and other causes of RV–LV respiratory discordance

IV. Practical performance of a hemodynamic study when constrictive pericarditis is suspected (see Table 17.2)

V. Echocardiographic features of constrictive pericarditis, and differentiation between constrictive pericarditis and restrictive cardiomyopathy (see Table 17.3)

VI. Physical exam, ECG findings, BNP, pericardial thickness (CT/MRI) A. Physical exam

B. ECG

C. BNP

D. Pericardial thickness

E. Endomyocardial biopsy

VII. Transient constrictive pericarditis

VIII. Treatment. A. Survival and symptomatic improvement after pericardiectomy

B. Persistent diastolic dysfunction

C. Systolic function

Summary

IX. Hemodynamic case analysis (Figure 17.13)

QUESTIONS AND ANSWERS

References. Acute pericarditis

Tamponade

Pericardial effusion

Constrictive pericarditis

Further reading

Chapter 18. Congenital Heart Disease

1. ACYANOTIC CONGENITAL HEART DISEASE. I. Atrial septal defect (ASD) A. Embryology (see Figure 18.1)

C. Consequences

D. Diagnosis

E. Treatment

II. Patent foramen ovale (PFO)

Treatment of a cryptogenic stroke presumably due to PFO

III. Ventricular septal defect (VSD) A. Types (see Figure 18.7)

B. Consequences and associations

C. Exam and natural history

D. Diagnosis, location, and shunt fraction Qp/Qs are established by TTE

E. Treatment

IV. Patent ductus arteriosus (PDA) A. Definition and consequences

B. Severity and presentation

C. Diagnosis

D. Treatment

V. Coarctation of the aorta

A. Diagnosis

B. Treatment

C. Long-term sequelae

VI. Other anomalies

A. Sinus of Valsalva aneurysm

B. Scimitar syndrome

C. Persistent left SVC

2. CYANOTIC CONGENITAL HEART DISEASE. I. Pulmonary hypertension secondary to shunt. A. Definition and mechanisms

B. Clinical presentation of Eisenmenger syndrome

C. Treatment

II. Tetralogy of Fallot. A. Pathology and consequences

B. Treatment

III. Ebstein anomaly

A. Natural history and exam

B. ECG and CXR

C. Treatment

3. MORE COMPLEX CYANOTIC CONGENITAL HEART DISEASE AND SHUNT PROCEDURES. I. Functionally single ventricle and Fontan procedure. A. Fontan procedure

B. Indications for Fontan

C. Variations of Fontan: the three surgeries required in single-ventricle syndromes

D. Exam and long-term complications

II. Transposition of great arteries (TGA) A. D-TGA

B. L-TGA

III. Other anomalies. A. Truncus arteriosus

B. Total anomalous pulmonary venous return

QUESTIONS AND ANSWERS

References

19. Peripheral Arterial Disease

1. LOWER EXTREMITY PERIPHERAL ARTERIAL DISEASE

I. Clinical tips

II. Clinical classification of PAD – Critical limb ischemia, acute limb ischemia, atheroembolization

A. Rutherford classification

B. Critical limb ischemia (CLI)

C. Acute limb ischemia (ALI) and acute compartment syndrome

D. Atheroembolization

III. Diagnosis of PAD. A. Ankle–brachial index (ABI)

Note: normal or elevated ABI in patients with CLI

Note: use of the higher ankle pressure (the higher of the AT and PT pressures) vs. the lower pressure in ABI calculation

B. Ultrasound and Doppler study

C. Segmental pressures and pulse volume recordings

D. CT angiography (CTA)

IV. Medical therapy of PAD

V. Revascularization for PAD. A. Indications

B. Revascularization modalities: surgical bypass vs. percutaneous therapy

VI. Notes on the technical aspects of surgical and percutaneous therapies. A. Technical aspects of surgical therapy. 1. Aortobifemoral grafting, femorofemoral and axillofemoral grafting

2. Femoropopliteal or femorotibial bypass

B. Technical aspects of percutaneous revascularization

1. Iliac level

2. SFA and popliteal level

3. Infrapopliteal level

C. Special case of the common femoral artery (CFA)

VII. Management of acute limb ischemia

VIII. Management of lower extremity ulcers (Table 19.6)

2. CAROTID DISEASE

I. Assessment of carotid stenosis

II. Medical therapy of carotid stenosis

III. Revascularization of asymptomatic carotid stenosis

IV. Revascularization of symptomatic carotid stenosis

V. Main risks of CEA and carotid stenting

VI. CEA versus carotid stenting

VII. Carotid disease in a patient undergoing CABG

VIII. Subtotal and total carotid occlusions

3. RENAL ARTERY STENOSIS. I. Forms of renal artery stenosis

II. Screening and indications to revascularize renal artery stenosis

III. Notes. A. Benefit of percutaneous intervention in FMD vs. atherosclerotic RAS

B. ASTRAL and CORAL trials

C. Role of ACE inhibitors or ARBs

QUESTIONS AND ANSWERS

References. Lower extremity peripheral arterial disease

Carotid disease

Renal artery stenosis

20 Aortic Diseases

I. Aortic dissection. A. Two types of aortic dissection

B. Causes

C. Mechanisms of acute and chronic aortic dissection

D. Other acute aortic syndromes: intramural hematoma and penetrating atherosclerotic ulcer

E. Clinical suspicion

F. Diagnosis

G. Complications

H. Treatment. 1. Administer IV β -blockers to decrease the aortic wall stress dP/dt

2. Type A aortic dissection

3. Type B aortic dissection

6. Chronic dissection (= dissection that occurred >2 weeks prior)

I. Notes on surgical techniques. 1. Ascending aortic dissection

2. Dissection extending into the aortic arch with malperfusion

3. Acute type B aortic dissection that requires therapy (peripheral ischemia)

II. Thoracic aortic aneurysm

A. Ascending thoracic aortic aneurysm (TAA)

1. Diagnosis

2. Prognosis and surgical indications

3. Surgical treatment

4. Perioperative complications

5. Surveillance schedule when surgery is not indicated

B. Descending TAA

C. Aortic arch aneurysm

D. Traumatic transection of the aorta

E. Medical therapy of TAA

III. Abdominal aortic aneurysm

A. Diagnosis

B. Surgical treatment of AAA, iliac aneurysm, popliteal aneurysm

C. Percutaneous endovascular aortic repair (EVAR)

D. Surveillance for smaller aneurysms (3.0–5.5 cm)

References

21. Pulmonary Embolism and Deep Vein Thrombosis

1. PULMONARY EMBOLISM. I. Presentation of pulmonary embolism (PE) and risk factors. A. Signs and symptoms

B. Risk factors (see Table 21.1)

II. Probability of PE

III. Initial workup

A. ECG

B. Arterial blood gas

C. Chest X-ray

D. D-dimer

IV. Specific PE workup

V. Submassive or intermediate-high risk PE, pulmonary hypertension, and thrombolysis

VI. PE and chronic pulmonary hypertension

VII. Acute treatment of PE. A. Initial anticoagulation

B. Initial outpatient treatment of acute PE

C. Indications for thrombolysis and thrombectomy

D. IVC filter

VIII. Duration of anticoagulation

IX. Thrombophilias

X. PE prognosis and long-term follow-up

2. DEEP VEIN THROMBOSIS. I. Types

II. Diagnosis

III. Treatment

3. IMMUNE HEPARIN-INDUCED THROMBOCYTOPENIA

I. Incidence

II. Diagnosis

III. Treatment

Note: Anticoagulant therapies in a patient with a prior history of HIT

QUESTIONS AND ANSWERS

References

22 Shock and Fluid Responsiveness

1. SHOCK

I. Shock definition and mechanisms

II. Goals of shock treatment

Note on SvO2 and cardiac power output

III. Immediate management of any shock

A. Intravenous fluid boluses

B. If the patient remains hypotensive despite the quick initial 1–2 L of intravenous fluids or if signs of fluid repletion develop (elevated JVP, pulmonary edema, decreased O2 saturation)

C. In the context of septic shock, if low perfusion signs persist despite achieving the target systemic pressure and despite a presumably normal volume status

D. Provide adequate oxygenation (arterial O2 saturation >90–95%), and adequate hemoglobin level

E. Perform a quick workup in parallel to the previous steps

F. Start empiric broad-spectrum, one or several antibiotics whenever there is any suspicion of sepsis (start the antibiotics within 1 hour of this suspicion)

G. Administer stress doses of steroids for a shock that persists several hours despite high doses of at least one vasopressor, or for the patient who uses steroids chronically. IV. Sepsis and septic shock

Pitfalls:

V. Cardiogenic shock

2. FLUID RESPONSIVENESS

Appendix. Hemodynamic equations, transfusion, and miscellaneous concepts. A. Hemodynamic variables and equations

B. Peripheral edema that occurs after resuscitation means hypervolemia and signals the need to back off fluid resuscitation

C. SvO2 vs. ScvO2

D. Colloid fluids (Dextran, Hetastarch)

E. Types of crystalloid fluids

F. Corticosteroids in septic shock

G. Intensive insulin therapy

H. Note about inotropes and vasopressors

I. Indications for transfusion

QUESTIONS AND ANSWERS

References

Note

23 Hypertension

1. HYPERTENSION. I. Definition

II. ACC and ESC targets of therapy and rationale. A. Targets of therapy

B. Rationale for the guidelines (SPRINT trial is the driver of ACC guidelines)

III. Treatment of hypertension: timing, first-line drugs, compelling indications for specific drugs. A. BP 130-159/80-99

B. BP ≥ 160/100 mmHg on two readings

C. How and what to start

D. First-line drugs

E. Follow-up

F. Compelling indications for specific antihypertensive drugs

IV. Resistant hypertension

A. Causes34-36

B. If HTN is truly resistant, second-line drugs may be added

C. Consider the mechanism of the resistant HTN, and try to treat it accordingly35 (volume, vascular tone, catecholamine tone)

V. Secondary hypertension

VI. Peripheral vs. central aortic pressure: therapeutic implications

VII. First-line antihypertensive drugs. A. ACE-Is and ARBs. 1. Mechanism of benefit in CKD

2. Contraindications and monitoring

3. Differences between ACE-I and ARB

4. The combination of ACE-I and ARB should be avoided1,2,16

B. CCBs. 1. Types of CCBs and mechanisms of action

2. Contraindications

3. Other side effects

C. Diuretics (thiazide diuretics, loop diuretics, aldosterone antagonists) 1. Thiazide diuretics (hydrochlorothiazide, chlorthalidone)

2. Loop diuretics (furosemide, bumetanide, torsemide)

3. Aldosterone receptor antagonists (spironolactone 25-50 mg/d, eplerenone)

VIII. Second-line antihypertensive drugs. A. β-Blockers

B. α1-Blockers

C. Clonidine (centrally acting sympathomimetic, alpha-2 receptor agonist)

D. Hydralazine

E. Direct renin inhibitor

IX. Orthostatic hypotension and extremely labile HTN. A. Orthostatic hypotension

B. Extremely labile HTN

C. Treatment of patients with extreme BP lability75,76

2. ACUTE SEVERE HYPERTENSION: HYPERTENSIVE EMERGENCIES AND URGENCIES. I. Definitions. A. Malignant HTN = hypertensive emergency

B. Hypertensive urgency

C. Causes of acute severe HTN

II. Treatment of hypertensive emergencies. A. Guidelines of treatment

B. Intravenous drugs

III. Treatment of hypertensive urgencies

IV. Specific situations (see Table 23.5)

QUESTIONS AND ANSWERS

References

24 Dyslipidemia

I. Indications for therapy

II. Notes on LDL, HDL, and triglycerides. A. LDL

B. Non-HDL cholesterol

C. HDL

D. Triglycerides (TGs)

III. Drugs: LDL-lowering drugs. A. Statins

B. Ezetimibe

C. Anti-PCSK9 antibodies (alirocumab, evolocumab)

D. Bile acid sequestrants (cholestyramine, colestipol)

E. Nutrients high in phytosterols (plant sterols)

IV. Drugs: TG/HDL-treating drugs and lifestyle modification. A. Niacin

B. Fibrates

C. Omega-3 fatty acids

D. Tight glycemic control

E. Lifestyle modification

V. Metabolic syndrome. A. Diagnosis

B. Treatment

VI. Diabetes and cardioprotective diabetic drugs. A. Statin therapy

B. SGLT-2 inhibitors (gliflozins) and GLP-1 receptor agonists (“-glutides”) are recommended after initial metformin therapy

VII. Elevated hs-CRP (high-sensitivity C-reactive protein test) ≥2 mg/l

VIII. Chronic kidney disease (CKD)

IX. Causes of dyslipidemia to consider. A. Markedly elevated LDL (>190 mg/dl) suggests familial hypercholesterolemia

B. Markedly elevated TG level (>500 mg/dl) suggests familial hypertriglyceridemia. C. Consider secondary causes of dyslipidemia in the proper setting

X. Side effects of specific drugs: muscle and liver intolerance with statins, fibrates, and niacin

A. Statins

B. PCSK9 inhibitors

C. Niacin (nicotinic acid)

D. Fibrates

E. Cholestyramine

XI. Aspirin is ineffective in primary prevention

QUESTIONS AND ANSWERS

References

25 Pulmonary Hypertension

I. Definition

II. Categories of PH

A. PH secondary to left heart disease (also called pulmonary venous hypertension or postcapillary PH)

B. Precapillary PH

III. Two tips in the evaluation of PH

IV. Hypoxemia in patients with PH

V. Diagnosis: echocardiography; right and left heart catheterization. A. Echocardiography

B. Catheterization

C. Other tests

VI. Treatment. A. PH secondary to left heart failure, pulmonary thromboembolic disease, or lung disease: treat the underlying cause

B. Pulmonary arterial hypertension

QUESTIONS AND ANSWERS

References

26 Syncope

I. Neurally mediated syncope (reflex syncope)

A. Vasovagal syncope (neurocardiogenic syncope)

B. Situational syncope

C. Carotid sinus hypersensitivity

D. Post-exertional syncope

II. Orthostatic hypotension and postural orthostatic tachycardia syndrome. A. Orthostatic hypotension

B. Postural orthostatic tachycardia syndrome (POTS)

III. Cardiac syncope

IV. Other causes of syncope

V. Syncope mimic: seizure (see Table 26.1)

VI. Clinical clues (see Table 26.2)

VII. Diagnostic evaluation of syncope (Figure 26.1)

A. Basic initial strategy

B. If the heart is normal clinically and by ECG

C. If the patient has signs or symptoms of heart disease

D. If no heart disease is suggested by ECG and echocardiography

E. If heart disease is diagnosed by echocardiography or if significant ECG abnormalities are found

F. Heart disease with LV dysfunction and EF ≤ 35%

G. Note on LBBB and RBBB

VIII. Tilt table testing (see Table 26.4)10,40

IX. Indications for hospitalization

X. Treatment of vasovagal syncope, orthostatic hypotension, and POTS. A. Treatment of vasovagal syncope

B. Carotid sinus hypersensitivity

C. Orthostatic hypotension and POTS

D. Syncope and driving

QUESTIONS AND ANSWERS

References

27 Chest Pain, Dyspnea, Palpitations

1. CHEST PAIN. I. Causes (see Table 27.1)

II. Features. A. Angina and acute coronary syndrome

B. Aortic dissection

C. Pulmonary embolism (PE) 1. Clinical features

2. The clinical probability of PE is assessed using the Wells criteria, which essentially give weight to three features

3. Initial workup

D. Acute pericarditis

E. Pneumonia, pleural effusion, pneumothorax

III. Management of chronic chest pain

IV. Management of acute chest pain. A. ECG

B. CXR, cardiac troponin (sensitive or highly sensitive assay), ± bedside echo during active pain

C. If any clinical, X-ray, or ECG feature suggests aortic dissection, PE, pericarditis, or a pulmonary cause of chest pain, proceed to the appropriate workup and therapy. Avoid anticoagulation if the clinical or radiographic likelihood of aortic dissection is more than low. Before starting anticoagulation, verify the lack of mediastinal enlargement on CXR

D. In the absence of aortic dissection, PE, pericarditis, or pulmonary features, use conventional troponin or hs-troponin for MI rule-in and rule-out. A single undetectable or very low hs-troponin (eg, <0.005 ng/ml) is associated with <0.5% risk of acute MI and nearly 0% risk of cardiac death at 30 days. This risk is further reduced in patients whose ECG is not suggestive of ischemia. Therefore, home discharge is safe in those patients

2. ACUTE DYSPNEA. I. Causes (see Table 27.2)

II. Notes. A. Differential diagnosis of shock + respiratory distress

B. Wheezing

C. Pulmonary shunt and pulmonary shunt effect

D. Cyanosis

III. Management

A. Quick and specific therapies are instituted

B. Intubation and non-invasive ventilation

3. PALPITATIONS. I. Causes. A. Benign premature beats: 20–30% of palpitations are secondary to PACs or PVCs. B. Sustained cardiac arrhythmia, consisting of one of the following (10–20% of palpitations):

II. Diagnosis. A. The diagnosis mainly relies on the history and examination (see Table 27.3) B. Workup of palpitations (see Table 27.4)

References

28 Infective Endocarditis and Cardiac Rhythm Device Infections

1. INFECTIVE ENDOCARDITIS. I. Clinical diagnosis

II. Echocardiography: timing and indications

III. Organisms

IV. Morphology

V. Anatomical complications

VI. Indications for valvular surgery and special situations. A. Indications for valvular surgery in left-sided endocarditis

B. Case of a large vegetation >1 cm or prior embolization

C. Types of valvular surgery

D. Indications for tricuspid valve surgery

E. Role of partial oral antibiotic treatment

2. CARDIAC RHYTHM DEVICE INFECTIONS. I. Organisms and mechanisms of infection

II. Diagnosis. A. Clinical

B. Echocardiography

III. Diagnosis in patients with bacteremia but no local or TEE signs of infection

IV. Management

References. Infective endocarditis

Cardiac rhythm device infections

29 Preoperative Cardiac Evaluation

I. Steps in preoperative evaluation. A. First step: if the surgery is emergent, no cardiac workup is performed preoperatively

B. Second step: if the surgery is not emergent, evaluate for active cardiac conditions

C. Third step: in the absence of active cardiac conditions, look for clinical risk factors, and use the revised cardiac risk index or Lee index

II. Surgical risk: surgery’s risk and patient’s risk. A. Classification of the surgery’s risk

B. Classification of the patient’s overall risk (integrates the surgery’s risk with the patient’s risk factors)

C. Risk of MACE according to stress testing results

III. CARP and DECREASE V trials

Caveats

IV. Only the highest-risk coronary patients require revascularization preoperatively

V. Preoperative percutaneous revascularization

VI. Surgery that needs to be performed soon after stent placement

VII. Preoperative β-blocker therapy

VIII. Other interventions that improve outcomes. A. Statin therapy

B.Aspirin

C. Optimize the volume status of patients with HF

IX. Severe valvular disease

X. Perioperative hypertension

XI. Preoperative management of patients with pacemakers or ICDs

QUESTIONS AND ANSWERS

References

30 Miscellaneous Cardiac Topics: Cardiac Masses and Tumors, Pregnancy, HIV and Heart Disease, Cocaine and the Heart, Chemotherapy and Heart Disease, Chest X-Ray

1. CARDIAC MASSES. I. Differential diagnosis of a cardiac mass

II. Cardiac tumors; focus on atrial myxoma. A. General features

B. Clinical presentation and diagnosis of myxoma

C. Treatment

2. PREGNANCY AND HEART DISEASE

I. High-risk cardiac conditions during which pregnancy is better avoided9. A. Eisenmenger syndrome, or primary or secondary severe pulmonary hypertension

B. Severe AS, even if asymptomatic

C. Severe MS, even if asymptomatic

D. Any cardiomyopathy or valvular disease with EF < 30% or NYHA III/IV

E. Aortic root dilatation ≥ 45 mm. F. Complex cyanotic congenital heart disease (tetralogy of Fallot, Ebstein, Fontan circulation)

II. Cardiac conditions that are usually well tolerated during pregnancy, but in which careful cardiac evaluation and clinical and echo follow-up are warranted9

III. Cardiac indications for cesarean section

IV. Mechanical prosthetic valves in pregnancy: anticoagulation management

V. Peripartum cardiomyopathy (PPCM)

A. Prognosis, LV recovery

B. Treatment

VI. Cardiovascular drugs during pregnancy (see Table 30.2)

VII. Arrhythmias during pregnancy

VIII. MI and pregnancy

IX. Hypertension and pregnancy. A. Types

B. Treatment

C.Pre-eclampsia and HF

3. HIV AND HEART DISEASE. I. Pericardial disease

II. HIV cardiomyopathy

III. Pulmonary hypertension (PH)

IV. CAD

4. COCAINE AND THE HEART. I. Myocardial ischemia. A. Causes

B. Presentation

C. Diagnosis

D. Treatment of cocaine-related MI or ischemia. 1. Medical therapy

2. Role of invasive management and thrombolysis

3. Role of stress testing

II. Other cardiac complications of cocaine

5. CHEMOTHERAPY AND HEART DISEASE. I. Cardiomyopathy. A. Anthracyclines

B. Cyclophosphamide

C. Trastuzumab (Her-2 receptor antagonist used in breast cancer)

D.Tyrosine kinase antibodies and inhibitors

E. Immune checkpoint inhibitors

II. Myocardial ischemia

III. Atrial fibrillation

6. CHEST X-RAY. I. Chest X-ray in heart failure (see Figures 30.2, 30.3)

A. Early signs of LV failure

B. At a later stage, interstitial pulmonary edema occurs and manifests as:

II. Various forms of cardiomegaly (see Figure 30.4) A. False impression of cardiomegaly

B. Enlarged RV

C. Enlarged LV

III. Left atrial enlargement; aortic dilatation

IV. Lateral chest X-ray

V. Chest X-ray in congenital heart disease

QUESTIONS AND ANSWERS

References

31. Electrocardiography

I. Overview of ECG leads and QRS morphology

II. Stepwise approach to ECG interpretation

III. Rhythm and rate. A. Look at the rhythm strip and survey for the following:

B. Calculate the ventricular rate

C. The rhythm is sinus if P wave is upright in leads I, II, and aVF and inverted in lead aVR, corresponding to a P-wave axis of 0–75°

IV. QRS axis in the limb leads and normal QRS progression in the precordial leads. A. Determine the frontal QRS axis by looking at the net QRS voltage (upward minus downward deflection) in leads I, II, and aVF (see Figure 31.16)

B. Look at the normal QRS progression across V1–V6

V. P wave: analyze P wave in leads II and V1 for atrial enlargement, and analyze PR interval (see Figures 31.18, 31.19) A. Lead V1 (and/or V2)

B. Lead II (and I, III)

C. Normal PR interval

VI. Height of QRS: LVH, RVH

A. Look for LVH (see Figure 31.20)

B. Look for RVH (Figure 31.21)

RVH differential diagnosis and coexisting patterns

C. Biventricular enlargement

VII. Width of QRS. Conduction abnormalities: bundle brunch blocks

A. RBBB

B. LBBB

VIII. Conduction abnormalities: fascicular blocks

A. Left anterior fascicular block (LAFB)

B. LPFB

C. Bifascicular and trifascicular blocks

D. Wide QRS 110–119 ms or ≥ 120 ms that does not fulfill the typical LBBB or RBBB morphology

IX. Low QRS voltage and electrical alternans

A. Differential diagnosis of small QRS voltage

B. High QRS voltage in the precordial leads with low QRS voltage in the limb leads is relatively specific for a dilated LV with low EF. C. Electrical alternans is an every-other-beat alternation of two different but equally wide and equidistant QRS complexes

X. Assessment of ischemia and infarction: Q waves

XI. Assessment of ischemia: ST-segment depression and T-wave inversion

A. Secondary ST-segment and/or T-wave abnormalities

B. Ischemic ST-segment depression and/or T-wave inversion

Note: T-wave inversion and Wellens syndrome

C. Frequently missed diagnoses manifesting as ST-segment depression or T-wave inversion. 1. True posterior ST-segment elevation myocardial infarction (STEMI)

2. Acute pulmonary embolism

3. ST-segment depression reciprocal to a subtle ST-segment elevation

4. Hypokalemia and digitalis effect

5. Memory T waves

D. Diffuse (global) T-wave inversion

E. Other causes of T-wave inversion or ST-segment depression

XII. Assessment of ischemia: differential diagnosis of ST-segment elevation

A. STEMI (acute subepicardial injury pattern)

B. Early repolarization

C. Pericarditis (Figure 31.53)

D. Left ventricular hypertrophy (LVH) and left bundle branch block (LBBB) (see Figures 31.54, 31.55, 31.56)

E. Pre-excitation (Figure 31.57)

F. Hyperkalemia (Figure 31.58)

G. Other causes of ST-segment elevation

XIII. Assessment of ischemia: large or tall T wave. A. Differential diagnosis of a tall upright T wave

B. deWinter complex, ”shark fin” pattern, and spiked helmet sign

XIV. QT analysis and U wave. A. QT interval measurement

B. U wave

C. Differential diagnosis of a prolonged QTc (Figures 31.64, 31.65)

D. Differential diagnosis of an abnormal U wave

XV. Electrolyte abnormalities, digitalis effect and digitalis toxicity, hypothermia, PE, poor precordial R-wave progression. A. Electrolyte abnormalities

B. Digitalis effect and digitalis toxicity (Figure 31.71)

C. Hypothermia (see Figure 31.72)

D. Pulmonary embolism (see Figure 31.73, Table 31.1) E. Poor precordial R-wave progression in COPD and anterior MI (see Figures 31.74, 31.75) F. ASD and Ebstein anomaly

XVI. Approach to tachyarrhythmias

A. Approach to narrow QRS-complex tachycardias (Figures 31.76–31.79)

B. Approach to wide QRS-complex tachycardias

XVII. Approach to bradyarrhythmias: AV block

XVIII. Abnormal automatic rhythms that are not tachycardic

XIX. Electrode misplacement

Appendix 1. Supplement on STEMI and Q‐wave MI: phases and localization. A. Electrophysiology of the ST-segment changes

B. Phases of STEMI (see Figures 31.96, 31.97)

C. Localization of STEMI. 1. MI territories

2. Reciprocal changes

3. Exact location and extent (see Tables 31.3, 31.4; Figures 31.98, 31.99)

4. Conduction blocks and diagnostic dilemmas in LBBB and RBBB

Appendix 2. Spread of electrical depolarization in various disease states using vector illustration (Figures 31.100â€“31.103)

QUESTIONS AND ANSWERS

References

ST-segment depression and T-wave inversion

ST-segment elevation

Large or tall T wave

Q waves and their regression

Further reading

Poor precordial R-wave progression

Anatomical LA enlargement mimicking RA enlargement

LAFB

Long QT Hodges formula

U wave is T2 wave in hypokalemia and LQT

Localization of anterior MI

Inferior STEMI RCA vs. LCx

32 Echocardiography

1. GENERAL ECHOCARDIOGRAPHY. I. The five major echocardiographic views and the myocardial wall segments

II. Global echo assessment of cardiac function and structure. A. Global assessment of myocardial function

1. Overall assessment of LV function

B. Paradoxical septal motion

C. Valvular structure assessment

2. Aortic valve

III. Doppler and assessment of valvular regurgitation and stenosis. A. Types

B. Routine Doppler interrogations

C. Routine Doppler calculations. 1. Volume and flow calculations

2. Aortic valve area (AVA) calculation using the continuity equation

3. Calculation of the systolic PA pressure using the TR jet

4. Assessment of RA pressure

IV. Summary of features characterizing severe valvular regurgitation and stenosis (see Tables 32.1, 32.2)

V. M-mode echocardiography

VI. Pericardial effusion. A. Size (see Figures 32.44, 32.45)

B. IVC plethora

C. Pre-tamponade echocardiographic signs (see Figure 32.46)

VII. Echocardiographic determination of LV filling pressure and diastolic function. A. Main parameters

B. Other parameters that correlate with left-sided filling pressure

C. Putting it all together (Figures 32.47, 32.48)

D. Assess the volume status and cardiac output of critically ill patients

VIII. Additional echocardiographic hemodynamics

A. Proximal isovelocity surface area (PISA) of MR (Figure 32.49)

B. Other modality of regurgitant volume calculation

C. Pitfalls in MS assessment, pitfalls in mitral valve area calculation using pressure half-time, and various methods of mitral valve area calculation (Figures 32.50, 32.51)

D. Pitfalls in PHT use for AI assessment (Figure 32.52)

E. Correlation between hepatic venous Doppler and RA pressure. Correlation between pulmonary venous Doppler and LA pressure (Figure 32.53)

F. Systolic PA pressure

G. Diastolic PA pressure

H. Other modality of PA pressure assessment

I. Calculation of LVEDP from AI Doppler flow

J. Calculation of LA pressure from MR Doppler flow in patients with any degree of MR

K. Calculation of the peak LV systolic pressure in patients with AS

L. Calculation of Qp/Qs ratio in the case of a shunt

IX. Prosthetic valves. A. Differentiate a biprosthetic valve from a mechanical valve (see Figures 32.54, 32.55, 32.56)

B. Prosthetic valve gradients

C. Prosthetic and periprosthetic valvular regurgitation

X. Brief note on Doppler physics and echo artifacts. A. Doppler physics

B. Artifacts

2. TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) VIEWS

A. First step: mitral valve and left-sided chambers (see Figures 32.61–32.68)

B. Second step: aortic valve evaluation (see Figure 32.69)

C. Third step: left atrial appendage (Figure 32.70)

D. Fourth step: right-sided structures (see Figures 32.71, 32.72)

E. Fifth step: interatrial septum (see Figures 32.73–32.76)

F. Sixth step: structures at the base of the heart (see Figures 32.77, 32.78)

G. Seventh step: transgastric views (see Figures 32.79–32.82)

H. Eighth step: aorta (a) Ascending aorta

(b) Descending aorta

I. Advantages and indications of TEE

L. What is spontaneous echo contrast (SEC)?

M. Three-dimensional TEE of the mitral valve (see Figure 32.83)

Appendix. Note on LV mechanics and myocardial tissue strain

Further reading

33 Stress Testing, Nuclear Imaging, Coronary CT Angiography, Cardiac MRI, Cardiopulmonary Exercise Testing

I. Indications for stress testing

A. Stable chest pain presentation

B. Acute chest pain presentation, with non-ischemic ECG and negative troponin 3 hours after symptom onset, and with no typical exertional angina at low levels of exertion. C. Recent STEMI that was not urgently reperfused with PCI, whether thrombolysis was acutely administered or not

D. Known CAD of borderline significance on the coronary angiogram (45–70% stenosis)

II. Contraindications to all stress testing modalities

III. Stress testing modalities

IV. Diagnostic yields and pitfalls of stress ECG and stress imaging. A. Diagnostic yield of exercise stress ECG

B. Positive stress ECG

C. High-risk positive stress ECG (see Table 33.3)

D. Limitations of DTS and exercise stress ECG: value of stress imaging

E. Stress echocardiography

F. Nuclear myocardial perfusion imaging (MPI), using single photon emission computed tomography (SPECT) (see also Appendices 1 and 2)

G. Use of antianginal agents before stress testing

V. Mechanisms of various stress modalities

VI. Nuclear stress imaging (see Figures 33.3, 33.4, 33.5)

A-SPECT

B-PET

VII. Coronary CT angiography and coronary calcium scoring. A. Role and indications of coronary CT angiography (see Figures 33.6, 33.7, 33.8, 33.9)

B. Role of CT imaging for coronary calcium scoring

C. Brief CTA technique

D. CTA Artifacts

VIII.Cardiac MRI: summary of applications and findings

IX.Cardiopulmonary exercise testing (CPET)

References

Low-risk DTS/exercise test

ST changes in women

Strongly positive stress ECG

Nuclear myocardial perfusion imaging in multivessel disease:

TID

Fixed defects

Attenuation artifacts

34. Angiographic Views: Coronary Arteries and Grafts, Left Ventricle, Aorta, Coronary Anomalies, Peripheral Arteries, Carotid Arteries

I. Right coronary artery. A. Course

B. Branches (proximally to distally) (Figure 34.1)

C. Segments of the RCA

II. Left coronary artery. A. Left main (LM) branches into the left anterior descending and left circumflex arteries. B. Left anterior descending artery (LAD) (see Figure 34.2)

C. Left circumflex coronary artery (LCx) (see Figure 34.2)

D. Ramus intermedius (RI) branch

In ACS, the unstable ruptured lesion is identified as

Lesion haziness may signify (Figure 34.3):

III. Coronary angiography views. Recognize the angle of a view: LAO vs. RAO, cranial vs. caudal. A. Differentiate left anterior oblique (LAO) from right anterior oblique (RAO) views

B. Differentiate cranial from caudal views

IV. Coronary angiography views. General ideas: cranial vs. caudal views

V. Coronary angiography views. General ideas: foreshortening and identifying branches. A. Foreshortening

B. Arteries running on the border of the heart shadow

VI. Left coronary views (see Figure 34.8) A. RAO caudal (15° RAO, 25° caudal)

B. LAO caudal (40° LAO, 30° caudal)

C. AP cranial or shallow RAO cranial (5° RAO, 35° cranial) (shallow RAO moves the left main away from the spine)

D. LAO cranial (40° LAO, 30° cranial)

E. RAO cranial (30° RAO, 30° cranial)

F. Other views: 90° left lateral, LAO straight, RAO straight

G. Views useful for left main assessment

H. A minimum of two views is required for left coronary assessment

VII. Right coronary views. A. LAO straight

B. LAO cranial (30° LAO, 15° cranial)

C. AP cranial (30° cranial)

D. RAO straight (30° RAO)

E. Routine RCA views

VIII. Improve the angiographic view in case of vessel overlap or foreshortening: effects of changing the angulation, effects of respiration, and vertical vs. horizontal heart. A. LCx moves with the image intensifier

B. Effects of respiration

C. Vertical vs. horizontal heart

IX. Saphenous venous graft views

X. LIMA-to-LAD or LIMA-to-diagonal views

XI. Left ventriculography. A. RAO, LAO, and LAO cranial views

B. Mitral valve

C. Assessment of mitral regurgitation

XII. Aortography for assessment of aortic insufficiency

XIII. Coronary anomalies

A. Anomalous LM or RCA origin and course

B. Coronary artery fistula

C. Anomalous coronary artery originating from the pulmonary artery

XIV. Lower extremity angiography. A. Anatomical tips (see Figures 34.53, 34.54, 34.55) B. Technical tips

C. Angiographic tips

XV. Carotid angiography. A. Anatomical and technical tips

B. Angiographic tips

QUESTIONS AND ANSWERS

Further reading

OCT

38 Percutaneous Coronary Interventions and Complications, Intra-Aortic Balloon Pump, Ventricular Assist Devices, and Fractional Flow Reserve

I. Major coronary interventional devices. A. Balloon angioplasty. 1. Mechanisms of action

2. Pitfalls

3. Compliant vs. non-compliant balloons

5. Cases where plain balloon angioplasty is sometimes performed, without stenting

B. Bare-metal stents (BMSs)

C. Drug-eluting stents (DESs)

D. Rotational atherectomy (Rotablator) and orbital atherectomy

E. Aspiration thrombectomy and distal embolic protection

II. Stent thrombosis, restenosis, and neoatherosclerosis. A. Thrombosis

B. Restenosis. 1. Mechanisms

2. Neointimal hyperplasia

3. Patterns of restenosis

4. Clinical presentation

5. Treatment

C. Neoatherosclerosis

D. Mechanisms of recurrent target vessel disease after stenting (Table 38.2)

III. Peri-PCI antithrombotic therapy (see Table 38.3)

IV. Complex lesion subsets. A. Multivessel PCI

B. Long lesions and diffuse disease (multiple lesions in series)

C. Bifurcation lesions

D. Chronic total occlusion (CTO)

V. Sheath management

VI. Post-PCI mortality and coronary complications. A. Mortality

B. Coronary dissection

1. Angiographic types of coronary dissection

2. Treatment

C. Periprocedural MI

D. Coronary perforation. 1. Causes of coronary perforation

2. Classification and management of coronary perforations

VII. Femoral access complications

A. Groin hematoma

B. Retroperitoneal hematoma (~0.7% of PCIs)

C. Femoral pseudoaneurysm

D. Arteriovenous fistula

E. Limb ischemia

VIII. Renal, stroke, and atheroembolic complications. A. Contrast nephropathy (increase in creatinine >0.5 mg/dl or> 25%)

B. Stroke

C. Cholesterol atheroembolization

IX. Intra-aortic balloon pump (IABP) or intra-aortic balloon counterpulsation. A. Overview of IABP

B. Effect of IABP on coronary flow

C. Triggering and timing

D. Troubleshooting and lack of appropriate augmentation (Table 38.4)

E. Indications for IABP

F. Contraindications

G. Care and follow-up

X. Percutaneous LV assist device: Impella and TandemHeart. A. Impella or transvalvular LV assist device

B. TandemHeart LV assist device

XI. Extracorporeal membrane oxygenation (ECMO)

XII. Fractional flow reserve (FFR) A. FFR concept and application

B.Instantaneous wave-free ratio (iFR)

C. Special situation: serial stenoses (Figure 38.14)

D. Special situation: diffuse disease

E. Special situation: ostial disease

F. Artery supplying an old infarcted myocardium: value of FFR in assessing residual ischemia and viability

G. FFR vs. nuclear perfusion imaging in multivessel disease

H. Left main disease: FFR and IVUS

QUESTIONS AND ANSWERS

Suggested readings:

III. Heart failure and cardiomyopathies

Suggested readings:

V. Arrhythmias

Suggested readings:

VI. Congenital heart disease

Suggested readings:

VII. Peripheral arterial disease- Pulmonary embolism-Pulmonary hypertension

Reference:

Suggested readings:

VIII. Hypertension and syncope

IX. Pregnancy-Chemotherapy and heart disease- Miscellaneous

Suggested readings:

X. ECG

XI. Echocardiography

XII. Additional hemodynamics

XIII. Percutaneous coronary intervention and shock

Suggested readings:

Reference:

Suggested readings:

XIV. Radiation in the cardiac catheterization laboratory

Index

WILEY END USER LICENSE AGREEMENT

Отрывок из книги

Second Edition

Elias B. Hanna, MD, FACC

.....

Ticagrelor directly binds to the P2Y12 ADP receptor and reversibly inhibits it (the effect clears as the drug clears from plasma). Despite being a reversible ADP antagonist, the very potent ADP blockade and the long half-life translate into an antiplatelet effect that lasts 3–4 days (half-life ~15 h). Since it directly acts on its receptor, the response to ticagrelor is consistent and potent (~75% platelet inhibition), including in clopidogrel non-responders.

Cangrelor is an intravenous ADP receptor antagonist that directly and reversibly binds to the ADP receptor. It inhibits 90% of the platelet aggregation. In contrast to ticagrelor, it has a short half-life of 5 min, which, in addition to the reversible receptor binding, leads to a very quick onset and offset of action.

.....

Добавить отзыв

Отзывы и комментарии читателей

Нет рецензий. Будьте первым, кто напишет рецензию на книгу Practical Cardiovascular Medicine

Подняться наверх

Practical Cardiovascular Medicine

Описание книги

Оглавление

Elias B. Hanna. Practical Cardiovascular Medicine

Отрывок из книги

Добавление нового отзыва

Отзывы и комментарии читателей