Acute coronary syndromes

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Resident
Survival
Guide

Acute Coronary Syndrome Chapters

Heart Attack Patient Information

Unstable Angina Patient Information

Overview

Classification

Unstable Angina
Non-ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction

Causes

Differential Diagnosis

Treatment

AHA/ACC Guidelines for Acute Coronary Syndrome

Guideline for Risk Stratification in ACS
Guideline for Pre-Hospital Evaluation and Care
Guidelines for Initial Management of ACS
Guidelines for Patients with Atrial Fibrillation Complicating ACS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]; Tarek Nafee, M.D. [3]; Sabawoon Mirwais, M.B.B.S, M.D.[4]

Synonyms and keywords: ACS

Overview

Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary arteries. The most common symptom prompting diagnosis of ACS is chest pain, often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST-elevation myocardial infarction (30%), non ST-elevation myocardial infarction (25%), or unstable angina (38%). These types are named according to the appearance of the electrocardiogram. There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome. ACS should be distinguished from stable angina, which is chest pain which develops during exertion and resolves at rest. New onset angina however should be considered as a part of acute coronary syndrome, since it suggests a new problem in a coronary artery.Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. Cardiac chest pain can also be precipitated by anemia, bradycardias or tachycardias.


Historical Perspective

Classification


Pathophysiology

For more information on atherosclerotic plaque, click here.

The pathophysiology of acute coronary syndromes depends on coronary atherosclerotic plaque which includes:

Initiation and Progression of Coronary Atherosclerotic Plaque

Plaque Vulnerability

The plaque vulnerability depends on the following factors:[1]

The pathogenesis of acute coronary syndrome depends on:

Following plaque rupture or endothelial erosion, the subendothelial matrix is exposed to the circulating platelets, which get activated leading to thrombus formation. Two types of thrombi can form:

  • White clots: Platelet-rich clots which partially occludes the artery
  • Red clots: Fibrin rich clots superimposed on white clots and cause total occlusion of the artery

Causes

Differentiating Xyz from other Diseases

  • Diagnosis of ACS is initiated by a clinical suspicion based on a thorough history of the patient's symptoms.
  • Subsequently, confirmatory tests should be ordered to confirm the diagnosis, identify the specific cause of ACS, or to rule out other possible differentials.
  • In some circumstances, utilizing a clinical prediction tool may be beneficial in guiding the clinician's diagnosis.
  • View the page on diagnosis using the clinical prediction rule for ACS for more detail.
  • Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows:
Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Cardiovascular Acute Coronary Syndrome + + + + + + + + + + + •Palpitations

•Sweating

Aortic Dissection + + + - + + - + •Pain maximal upon onset •Pain difficult to treat with opiates

•Weak pulse in one arm compared to other

•Syncope

•Symptoms similar to stroke

•Smoking

Brugada Syndrome No chest pain + •Syncope

•Cardiac arrest

•ST-segment elevation

•F/H of sudden cardiac death

Takotsubo carditis Sudden onset of chest pain mimicking myocardial infarction + + + + + - •Extreme emotional or physical stress•syncope

•Women>men

•ST segment elevation

•Left ventricular apical ballooning on echo

•Normal coronary arteries

Pericarditis + + + •Relieving factor: Sitting up and leaning forward

•Aggravating factor: Lying down and breathing deep

+ + + + + + + •Other causes:Malignancy, autoimmune disorders, chest trauma

•Pericardial friction rub

Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Pulmonary Pleuritis
(pleurisy) 		+ + + + •Aggravating factor: Deep breathing + + + + + + •Other causesPulmonary embolism, malignancy, autoimmune diseases
Pulmonary Embolism + •Aggravating factors: Deep breathing, coughing, eating, bending and stooping + + + •Other causes: Immobility, pregnancy, oral contraceptive pills
Pneumonia + + + + + + •Complications: Sepsis, ARDS, Lung abscess
Gastrointestinal GERD + + + •Other symptoms: Hoarseness, Dry cough at night, Sensation of lump in throat etc
Esophageal Spasms + + + + + + + • Risk factors: Anxiety or depression and drinking wine, very hot or cold foods
Esophagitis + + + + + + + • Causes: Hiatal hernia, infection, medications, radiation therapy
Gastritis + + + + + + + • Causes: H.pylori infection, bile reflux, alcohol use, alcohol use
Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Musculoskeletal Muscle sprain/Spasm + + + + • Causes: Over use, dehydration, electrolyte abnormalities
Costochondritis + + + + + + + + + + + • Risk factors: Rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome
Rib fracture/Trauma + + + + + + + + + + • Complications: Pneumothorax, hemothorax, surgical emphysema
Psychiatry Anxiety (Panic Attack) Chest tightness + + • Other symptoms: Palpitations, trembling, sweating, choking, light headed, hot or cold flashes.


The following table summarizes the significant history, and diagnostic test findings that will help differentiate the acute coronary syndromes from one another, as well as from other coronary artery diseases:

Acute Coronary Syndromes History and Symptoms Pathology Diagnostic tests Treatment Complications Prognosis
Chest pain Duration of Chest pain Coronary Artery Plaque Cardiac Biomarkers
(e.g.CK-MB, Troponins) 		EKG Findings Medical Therapy Reperfusion
(e.g. PCI, CABG, or Medical)
At Rest Exertion
Unstable Angina + + <30 minutes Partial occlusion Erosion

or

Rupture

(39%)

Normal •Normal EKG findings (some cases)


•Flipped or inverted T waves


•ST segment depression


•Non-specific ST-T changes

+ •Arrhythmias

•Congestive heart failure

•Hypotension

•New mitral regurgitation

•MI

•Sudden death

•1 year mortality rate is 1.7%
NSTEMI + + >30 minutes Partial or complete occlusion Rupture

(56%)

or

Erosion

Elevated •No EKG findings (some cases)


•Flipped or inverted T waves


•ST segment depression


•Non-specific ST-T changes

•New left bundle branch block

+ + •Arrhythmias

•Congestive heart failure

•Hypotension

•New mitral regurgitation

•Ventricular aneurysms

•Sudden death

•1 year mortality rate is 24.4%

•30 day mortality rate is about 2%

STEMI + + >30 minutes Complete occlusion Rupture

(50%-75%) or

Erosion

Elevated •ST elevation in at least 2

contiguous leads in V2-V3


•ST depression in at least

two precordial leads V1-V4


•ST depression in several

leads plus ST elevation in

lead aVR (suggestive of occlusion of the left main or proximal LAD artery)


+ + •Reinfarction

•Arrhythmias

•Left ventricular aneurysm

•Pseudoaneurysm

•rupture of papillary muscle,

interventricular septum and LV free wall

•Sudden death

•30 day mortality rate is

1.1% in <45 yrs and 20.4% in >75 yrs patients

Other Coronary Artery Diseases
Chronic stable angina - + ≤ 5 minutes Severely narrowed

coronary vessels

Stable plaque Normal •Normal EKG in 50% of cases

•Down sloping, up sloping or

horizontal ST segment depression

•T wave inversion

+ •Heart failure •Estimated annual mortality rate is 0.9%-1.4%

•Annual incidence of non-fatal MI between 0.5%-2.6%

•1 year mortality rate is 1.3%

Prinzmetal's angina •Occur at rest

(Mid night to early morning)

•Not associated with exertion

5-30 minutes Coronary artery vasospasm - Normal •Transient ST segment elevation + •Arrhythmias

•MI

•5 year survival is excellent (90%-95%)


Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain


Cardiac Pulmonary Vascular Gastrointestinal Orthopedic Other
Myopericarditis

Cardiomyopathiesa

Pulmonary embolism Aortic dissection Esophagitis, reflex or spasm Musculoskeletal disorders Anxiety disorders
Tachyarrhythmias (Tension)-Pneumothorax Symptomatic aortic aneurysm Peptic ulcer, gastritis Chest trauma Herpes zoster
Acute heart failure Bronchitis, pneumonia Stroke Pancreatitis Muscle injury/inflammation Anemia
Hypertensive emergencies Pleuritis Cholecystitis Costochondritis
Aortic valve stenosis Cervical spine pathologies
Tako-Tsubo cardiomyopathy
Coronary spasm
Cardiac trauma
Bold = Common and/or important differential diagnoses

aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort



Epidemiology and Demographics

Risk Factors

Common risk factors in the development of acute coronary syndrome are:[2]

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies


=


Diagnosis

Diagnostic Study of Choice History and Symptoms Physical Examination Laboratory Findings Electrocardiogram X-ray Echocardiography or Ultrasound CT scan MRI Other Imaging Findings Other Diagnostic Studies

  • Diagnosis of acute coronary syndrome needs a combination of:
    • careful history
    • physical examination
    • Electrocardiography (ECG)
    • serum markers of myocardial injury
  • According to the 2014 ACC/AHA guidelines for managing Non-ST-elevation ACS, clinical assessment and initial evaluation of patients with suspected ACS should include risk stratification based on the likelihood of ACS as well as adverse clinical outcomes. These assessments would help for the decision on the need for hospitalization and guide in choosing appropriate treatment strategies.
  • In all patients with suspected ACS these two questions should be answered:
    • 1) What is the likelihood that this patient is having ACS?
      • The likelihood that symptoms and signs represent an ACS can be assessed according to the table below.

"The likelihood that Signs and symptoms reflect an underlying ACS"

Feature High

(Any of the Following)

Intermediate

(Absence of High-Likelihood Features and Presence of Any of the Following)

Low

(Absence of High- or Intermediate-Likelihood Features but May Have the Following)

History
  • Chest or left arm pain or discomfort as chief symptom
  • Known history of CAD, including MI
  • Chest or left arm pain or discomfort as chief symptoms
  • Age older than 70 yr, male gender
  • Probable ischemic symptoms in absence of any of the intermediate likelihood characteristics
  • Recent cocaine use
Physical examination
  • Transient MR murmur
  • Hypotension
  • Diaphoresis
  • Pulmonary edema or rales
  • Extracardiac vascular disease
  • Chest discomfort reproduced by palpation
ECG
  • New, or presumably new, transient ST-segment deviation (1 mm or more)

or

  • T-wave inversion in multiple precordial leads
  • Fixed Q waves
  • ST depression 0.5 to 1 mm

or

  • T-wave inversion more than 1 mm
  • T-wave flattening or inversion less than 1 mm in leads with dominant R waves
  • Normal ECG
Cardiac markers
  • Elevated cardiac TnI, TnT, or CK-MB levels
  • Normal
  • Normal
    • 2) What is the likelihood of adverse clinical outcome(s) in this patient?
      • Several risk assessment scores and clinical prediction algorithms have been used to identify patients who are at high risk of developing adverse outcomes.
      • These risk scores and algorithms use an integration of clinical history, physical examination findings, ECG, and cardiac troponins.
      • The most common risk assessment tools include:
        • TIMI (Thrombolysis In Myocardial Infarction) risk score
        • PURSUIT (Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) risk score
        • GRACE (Global Registry of Acute Coronary Events) risk score
        • NCDR-ACTION (National Cardiovascular Data Registry-Acute Coronary Treatment and Intervention Outcomes Network) registry (https://www.ncdr.com/webncdr/action/).
      • The following risk scores have been designed to specifically assess patients presenting to the ED with chest pain:
        • Sanchis score
        • Vancouver rule
        • Heart (History, ECG, Age, Risk Factors, and Troponin) score
        • HEARTS3 score
        • Hess prediction rule


Symptoms

The symptoms of acute coronary syndrome include:

  • Chest discomfort described as:
    • pain
    • pressure
    • tightness
    • burning.
  • In contrast to the pain described in stable angina as deep, poorly localized retrosternal chest discomfort that is reproducible with activity or emotional stress and relieved promptly (within less than 5 minutes) by rest and/or short-acting nitroglycerin, ACS patients tend to experience the episodes that are more severe and prolonged, may occur at rest, or may be precipitated by less exertion than the patient's previous experiences.
  • Pain frequently radiates to the left arm, left shoulder, back, jaw, neck, or epigastric region
  • Some patients may not have chest pain and present with other symptoms, known as "anginal equivalents", including:
  • Syncope may be a rare presentation of ACS.

The following features are usually in favor of the non-ischemic nature of pain:

  • Pleuritic pain: sharp or stabbing pain increased in intensity by respiration or cough
  • Pain reproduced with movement or palpation
  • Pain which can be localized by the tip of 1 finger
  • Brief episodes of pain (lasting a few seconds)
  • Pain with maximal intensity at onset
  • Primary or the only location of pain in the middle or lower abdomen
  • Pain radiating to lower extremities


Treatment

Medical Therapy

  • The management of non-ST-elevation (NSTE) acute coronary syndrome (ACS) is presented here.
  • For more information on the management of ST-elevation myocardial infarction, click here.
  • Standard Medical Therapies in NSTE-ACS include the following:

Oxygen

(Class I, Level of Evidence: C)

Anti-Ischemic and Analgesic Medications

1) Nitrates
2) Analgesic therapy
3) Beta Blockers
4) Calcium Channel Blockers
Recommendations for Calcium Channel Blockers in Non-ST-elevation Acute Coronary Syndromes
Recommendations Class

of Recommendations

Level

of Evidence

In patients with NSTE-ACS, continuing or frequently recurring ischemia, and a contraindication to beta-blockers, a nondihydropyridine calcium channel blocker (CCB) (eg, verapamil or diltiazem) should be given as initial therapy in the absence of clinically significant LV dysfunction, increased risk for cardiogenic shock, PR interval greater than 0.24 second, or second- or third-degree atrioventricular block without a cardiac pacemaker. I B
Oral nondihydropyridine calcium antagonists are recommended in patients with NSTE-ACS who have recurrent ischemia in the absence of contraindications, after appropriate use of beta blockers and nitrates. I C
CCBs† are recommended for ischemic symptoms when beta blockers are not successful, are contraindicated, or cause unacceptable side effects. I C
Long-acting CCBs and nitrates are recommended in patients with coronary artery spasm. I C
Immediate-release nifedipine should not be administered to patients with NSTE-ACS in the absence of beta-blocker therapy. III: Harm B
† Short-acting dihydropyridine calcium channel blockers should be avoided.
5) Other Anti-Ischemic Interventions

Lipid-lowering therapy

In the absence of contraindications, high-intensity statin therapy should be initiated or continued in all patients with NSTE-ACS, I, regardless of baseline LDL cholesterol levels. (Class I, Level of Evidence: A).

Inhibitors of the Renin-Angiotensin-Aldosterone System

Recommendations for Inhibitors of the Renin-Angiotensin-Aldosterone System in Non-ST-elevation Acute Coronary Syndromes in Non-ST-elevation Acute Coronary Syndromes
Recommendations Class of Recommendation Level of Evidence
ACE inhibitors should be started and continued indefinitely in:
  • all patients with LVEF less than 0.40
  • those with hypertension, diabetes mellitus, or stable CKD

, unless contraindicated.

I A
ARBs are recommended in patients with HF or MI with LVEF less than 0.40 who are ACE inhibitor intolerant. I A
Aldosterone blockade is recommended in:
  • patients post–MI without significant renal dysfunction (creatinine >2.5 mg/dL in men or >2.0 mg/dL in women) or hyperkalemia (K+ >5.0 mEq/L) who are receiving therapeutic doses of ACE inhibitor and beta blocker and have a LVEF 0.40 or less, diabetes mellitus, or HF.
 I A
ARBs are reasonable in other patients with cardiac or other vascular disease who are ACE inhibitor intolerant. IIa B
ACE inhibitors may be reasonable in all other patients with cardiac or other vascular disease. IIb B

Initial Antiplatelet/Anticoagulant Therapy in Patients With Definite or Likely NSTE-ACS

Summary of Recommendations for Initial Antiplatelet/Anticoagulant Therapy in Patients With Definite or Likely NSTE-ACS and PCI
Recommendations Special considerations Class of Recommendations Level of Evidence
Aspirin
Non–enteric-coated aspirin to all patients promptly after presentation 162 mg-325 mg I A
Aspirin maintenance dose continued indefinitely 81 mg/d-325 mg/d I A
P2Y12 inhibitors
Clopidogrel loading dose followed by daily maintenance dose in patients unable to take aspirin 75 mg I B
P2Y12 inhibitor, in addition to aspirin, for up to 12 mo for patients treated initially with either an early invasive or initial ischemia-guided strategy: I B
P2Y12 inhibitor therapy (clopidogrel, prasugrel, or ticagrelor) continued for at least 12 mo in post–PCI patients treated with coronary stents N/A I B
Ticagrelor in preference to clopidogrel for patients treated with an early invasive or ischemia-guided strategy N/A IIa B
GP IIb/IIIa inhibitors
GP IIb/IIIa inhibitor in patients treated with an early invasive strategy and DAPT with intermediate/high-risk features (eg, positive troponin) Preferred options are eptifibatide or tirofiban IIb B
Parenteral anticoagulant and fibrinolytic therapy
SC enoxaparin for duration of hospitalization or until PCI is performed
  • 1 mg/kg SC every 12 h (reduce dose to 1 mg/kg/d SC in patients with CrCl<30 mL/min)
  • Initial 30 mg IV loading dose in selected patients
 I A
Bivalirudin until diagnostic angiography or PCI is performed in patients with early invasive strategy only I B
SC fondaparinux for the duration of hospitalization or until PCI is performed 2.5 mg SC daily I B
Administer additional anticoagulant with anti-IIa activity if PCI is performed while patient is on fondaparinux N/A I B
IV UFH for 48 h or until PCI is performed
  • Initial loading dose 60 IU/kg (max 4000 IU) with initial infusion 12 IU/kg/h (max 1000 IU/ h)
  • Adjusted to therapeutic aPTT range
 I B
IV fibrinolytic treatment not recommended in patients with NSTE-ACS N/A III: Harm A

Ischemia-Guided Strategy Versus Early Invasive Strategies

 
 
 
 
NSTE-ACS (Definite or Likely)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ischemia-guided strategy
 
Early invasive strategy
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Initiate DAPT and Anticoagilant Therapy:

1. ASA 2. P2Y12 inhibitor (in addition to ASA):

  • Clopidogrel
  • Ticagrelor

3. Anticoagulant

  • UFH
  • Enoxaparin
  • Fondaparinux
 
Initiate DAPT and Anticoagilant Therapy:

1. ASA 2. P2Y12 inhibitor (in addition to ASA):

  • Clopidogrel
  • Ticagrelor

3. Anticoagulant

  • UFH
  • Enoxaparin
  • Fondaparinux
  • Bivalirudin

4. Can consider GPI in addition to ASA and P2Y12 inhibitor in high-risk (e.g., troponin positive) patients

  • Eptifibatide
  • Tirofiban
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Therapy effective
 
Therapy Ineffective: If the patient has ANY of the following findings, pharmacologic therapy is considered ineffective:

❑ Refractory angina, OR
❑ Angina at rest or with minimal activity, OR
❑ Objective evidence of ischemia (dynamic ECG changes or myocardial perfusion defect) by non-invasive testing, OR

❑ Presence of high prognostic risk (either high TIMI risk score > 1 or high GRACE score > 109)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PCI with stenting: Initiate/continue antiplatelet and anticoagulant therapy

1. ASA 2. P2Y12 inhibitor (in addition to ASA):

  • Clopidogrel
  • Prasugrel
  • Ticagrelor

3. GPI (if not treated with bivalirudin at the time of PCI):

  • High-risk features, not adequately pretreated with clopidogrel

High-risk features, adequately treated with clopidogrel 4. Anticoagulant: Enoxaparin bivalirudin Fondaparinux as the sole anticoagulant

UFH
 
CABG: Initiate/continue ASA therapy and discontinue P2Y12 and/or GPI therapy

1. ASA 2. Discontinue clopidogrel/ticagrelor 5d before, and prasugrel at least 7d before elective CABG 3. Dicontinue clpidogrel/ticagrelor up to 24h before urgent CABG May perform CABG<5d after clopidogrel/ticagrelor and <7d after prasugrel discontinued

4. Discontinue eptifbatide/tifofiban at least 2-4 h before and abciximab >=12h before CABG
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Late hospitalization/post-hospital care:

1. ASA indefinitely 2. P2Y12 inhibitor (clopidogrel or ticagrelor), in addition to ASA, up to 12 mo if medically created

3. P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), in addition to ASA, up to 12 mo if treated with coronary stenting
 
 
 
 
 
 
 
 
 
 
 

Surgery

Primary Prevention

Secondary Prevention

Coronary Angiography

Coronary angiography within 12 hours likely benefits high risk (elevated cardiac biomarkers at baseline or diabetes or a GRACE score more than 140) patients.

Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes

Recommendations Class

of Recommendations

Level

of Evidence

Early initiation of beta-blocker treatment is recommended

in patients with ongoing ischemic symptoms and without contraindications.

I B
It is recommended to continue chronic beta-blocker therapy,

unless the patient is in Killip class III or higher.

I B
Sublingual or i.v. nitrates are recommended to relieve angina;a intravenous treatment is recommended

in patients with recurrent angina, uncontrolled hypertension or signs of heart failure.

I C
In patients with suspected/confirmed vasospastic angina, calcium channel blockers and

nitrates should be considered and beta-blockers avoided.

IIa B
aShould not be administered in patients with recent intake of sildenafil or vardenafil (< 24 h) or tadalafil (< 48 h).

Prevention

Primary Prevention

The primary prevention strategies include:

  • Dietary modifications:
  • Physical exercise
  • 30 minutes of moderate exercise

Secondary Prevention

The secondary prevention strategies include:

References

  1. ↑ Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC; et al. (1999). "Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques". Circulation. 99 (19): 2503–9. PMID 10330380.
  2. ↑ Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ, Chesebro J (1988). "Insights into the pathogenesis of acute ischemic syndromes". Circulation. 77 (6): 1213–20. PMID 3286036.

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