CORONARY ARTERY DISEASE

Aleson Claire A. Llanes, MD

 CORONARY ARTERY DISEASE

 Generally used to refer to the pathologic process affecting the

coronary arteries (Atherosclerosis)
 Sometimes used synonymously with CHD or Ischemic Heart
Disease
 Coronary Heart Disease

Includes the diagnoses of:

 Angina Pectoris
 Myocardial Infarction
 Silent Myocardial Ischemia
 Cardiovascular Disease

• Pathologic process (usually atherosclerosis) affecting the entire arterial

circulation, not just the coronary arteries
• Examples are
 Stroke
 Transient Ischemic Attack
 Angina
 Myocardial Infarction
 Claudication
 Critical Limb Ischemia
 Epidemiology
 2017 Heart Disease and Stroke Statistics Update of American Heart
Association:

 16.5M persons in US has CHD, with slight male predominance (55%);

prevalence increases with age for both men and women
 Age >40years: lifetime risk: 49%males, 32% women
 At age 70yo; lifetime risk: 35% males, 24% in women.
 Sudden Cardiac Death (SCD): initial clinical coronary event in 15% of
patients with CAD.
 Epidemiology

 2009 Philippines Data*

 Cardiovascular Diseases ranked among the top 10 leading cause of morbidity and the
LEADING cause of Mortality.

 2017 Philippines data**

 Still Leading Cause of Mortality

* 2014 PHA CPG for Diagnosis and Management of Patients with CAD
**www.healthdata.org
 RISK FACTORS
 Family history of premature coronary artery disease
 Cigarette smoking: 34%
 Diabetes Mellitus: 39%
 Hypertension – predominant risk factor:77%
 Hyperlipidemia
 Sedentary Lifestyle
 Obesity
 Male >67 yrs

 -accelerate or modify a complex and chronic inflammatory process  fibrous atherosclerotic plaque
 STABLE ISCHEMIC HEART DISEASE

 Asymptomatic or present with typical angina (Definite), Atypical angina (probable) and
non-cardiac chest pain.

Traditional Clinical Classification of Chest Pain

DEFINITE angina Meets all three Characteristics:
1) Substernal chest discomfort of
characteristic quality and duration
2) Provoked by stress
3) Resolved with rest or nitroglycerin

PROBABLE angina Meets 2 of these criteria

NON-Cardiac pain Meets none or 1 of these criteria

Pathogenesis of
Stable Angina
 Pathophysiology of Angina

 It is not until atherosclerotic plaque reaches almost 40% of the plaque surface area before
compensatory mechanisms start to fail and the plague starts to impinge on the lumen
 70% or more obstructed – coronary blood flow starts to decline
 Non-atherosclerotic causes:
 Myocardial bridging
 Vasculitis
 Congenital Malformation of the Coronary Arteries
 Cardiomyopathies
 Valve Disease
 INITIAL PATIENT EVALUATION

 I. Patient’s history
 Most essential part
 Detailed description of chest pain ( 5 components)
 Quality or Character: “Tightness”, “squeezing”, “heaviness of the Chest”, “Constricting”, “Suffocating”,
“Viselike”
 Location: Substernal or near the sternum
 Duration: Brief (<10minutes or even less but unlikely to last for seconds)
 Precipitating Factors: Exertion, emotional Stress, after a heavy meal, cold weather
 Relieving factors: Rest or Sublingual nitrates

 Classification of the severity of chest pain based on Canadian CV Society Classification

 Determination of the presence of risk factors and co-morbid conditions
 CLINICAL PRESENTATION

ANGINA OTHER SYMPTOMS

 “pressure”  Shortness of breath
 “Tightness”  Nausea
 “squeezing”  Diaphoresis
 “heaviness of the Chest”  Occasional Vomiting
 “Constricting”  Lightheadedness
 “Suffocating”  Dyspnea without chest pain-anginal
 “Viselike” equivalent
 Radiation to the arm, jaw, shoulders, back
or abdomen
4 Angina Severity Classification by the
Canadian Cardiovascular Society
Class Manifestations
I No chest pain with ordinary activity or exertion; Angina with strenuous or
rapid or prolonged exertion at work or recreation
II Slight limitation of ordinary activity. Chest pain with moderate exertion like
walking or climbing stairs rapidly; walking or stair climbing after meals; in
cold or wind; under emotional stress; or during the first few hours of
awakening.
(Ex: walking more than 2 blocks or more than 2 flight of stairs at a normal
pace and in normal conditions)
III Marked limitation of ordinary physical activity. Chest pain with mild exertion
(Ex: walking 1-2 blocks on the level or 1 flight of stairs in normal conditions
and at a normal pace)

IV Inability to carry on any physical activity without discomfort; Chest pain with
no or minimal activity
 INITIAL PATIENT EVALUATION
 II. Physical Examination
 Often normal in patients with SIHD and generally not useful for confirming the diagnosis.
 Focused PE should be done to exclude other causes of Angina
 BMI, waist circumference, waist to hip ratio (WHR)- evaluate Metabolic Syndrome

CARDIAC OTHER THINGS TO LOOK OUT FOR:

FINDINGS  Findings of Cardiomyopathy or Valvular disorders can also be present
Paradoxical splitting of  Hypertension
the second heart sound  Signs of Hyperlipidemia (Corneal arcus, periorbital xanthelasma, tendinous
Systolic murmurs xanthomas)
S3 or S4  Findings of Diabetes Mellitus
 Peripheral neuropathy
 Diabetic Retinopathy
 INITIAL PATIENT EVALUATION

 III. Resting ECG 12 leads

 It is recommended during initial evaluation and during or immediately after an episode of chest
pain suspected to indicate clinical instability.
 Baseline ECG is advised for comparison in future situations.
 A normal ECG suggests the presence of normal resting LV function and a more favorable long-
term prognosis.
 INITIAL PATIENT EVALUATION
 Most common ECG abnormalities:
 A) Non-specific ST-T wave changes with or without abnormal Q waves.
 B) ST segment depression or elevation in two contiguous leads, new T-wave inversions or
Pseudonormalization of already inverted T waves.
 C) Other abnormalities:
 LVH
 LBBB or Left anterior fascicular block
 Arrhythmias: Atrial Fibrillation or Ventricular premature beats and pre-excitation

 Although these abnormalities have low specificity and sensitivity for CAD, these findings suggest a poor
prognosis since they are often associated with multi-vessel disease and impairment of LV function.
 Yearly ECGs or more interval is considered reasonable for patients with SIHD. (RAKEL’s Textbook)
ECG CHANGES
 INITIAL PATIENT EVALUATION

 IV. LABORATORY TESTS

 Recommended that the following initial laboratory tests be performed:

Lipid profile
FBS
CBC
Creatinine level with eGFR
Biochemical markers: Trop T or I if clinical evaluation suggests an Acute
Coronary Syndrome
Thyroid Hormone levels if with clinical suspicion of thyroid disorder
Liver Function Tests early after beginning statin therapy
 INITIAL PATIENT EVALUATION

 V. CHEST XRAY (PA or Lateral Views)

 Does not provide specific information for diagnosis but is RECOMMENDED in patients with
signs or symptoms of Congestive Heart failure (CHF); aortic dissection and/or aneurysm; valvular
heart disease; pericardial disease; or pulmonary disease
 VI. Echocardiography
 Transthoracic 2d Echo and Doppler echocardiography is RECOMMENDED in the initial
evaluation of all patients for
 Exclusion of alternative causes of angina
 Identification of segmental wall motion abnormalities suggestive of CAD
 Measure LV ejection fraction (LVEF) and LV diastolic function for risk stratification purpose
 INITIAL PATIENT EVALUATION
 VI. Ambulatory ECG Monitoring/ HOLTER Monitoring
 It is RECOMMENDED in patients with suspected arrhythmia and may be recommended in
patients with suspected vasospastic angina.
 VII. Pre-test Probability (PTP) Assessment
 ACC/AHA and ESC guidelines STRONGLY RECOMMENDS estimating the PTP in patients
with suspected SIHD.
 Diamond and Forrester pre-test probability of CAD by age, sex and symptoms
DIAMOND AND FORRESTER
PRE-TEST PROBABILITY
High: >90% Pre-test
probability

Intermediate: 10-90%
probability

Low: 5-10%
probability

Very Low: <5% pre-

test probability
 Likelihood
that signs and
symptoms are
secondary to
CAD
Recommended Approach to Diagnostic Testing
based on PTP
 ESTABLISHING DIAGNOSIS

 Once Intermediate Pre-Test Probability is established, the next step is to proceed with non-
invasive stress testing for definitive diagnosis as well as risk stratification assessment.
 Stress Imaging (preferred testing) has higher sensitivity(70-90%) compared to an exercise
ECG or treadmill test (45-50%)
 ESTABLISHING DIAGNOSIS

 Stress Imaging
 RECOMMENDED as the initial diagnostic and prognostic test, if facilities, resources and local
expertise permit, for
 Patients within higher range of PTP
 Patients with LVEF <50% without typical angina
 Patients with resting ECG abnormalities
 Symptomatic patients with prior revascularization (PCI, CABG)

 1) Stress Echocardiography –performed with Exercise or Pharmacological

agents (Dobutamine or Adenosine)
 2) Stress MPI
 3) Stress CMR
 ESTABLISHING DIAGNOSIS

 Exercise ECG (Treadmill Exercise Test or TET)

 RECOMMENDED as the initial diagnostic and prognostic test, if resources and local expertise
for a stress imaging are not available, in patients with intermediate PTP who have normal resting
ECGs and are able to exercise.
 Not a diagnostic value in the presence of significant ECG abnormalities such as LBBB, RBBB,
Intraventricular conduction defects, WPW, paced rhythm, LVH, AF, electrolyte imbalance and the
use of digitalis
 Coronary Computed Tomographic Angiography
 Alternative for Stress imaging study or TET in patients within the lower range of intermediate
PTP, nonconclusive stress study or who have contraindications to a stress study
 Not for screening test in asymptomatic individuals or those with a low probability of obstructive
CAD.
 ESTABLISHING DIAGNOSIS

 Others:
 Invasive Coronary Angiography (ICA):
 for pxs with high PTP as an initial test;
 remains the gold standard for the diagnosis of obstructive CAD
 CORONARY ANGIOGRAM

 Recommended as Initial Diagnostic and Prognostic test in:

 Patients who survived a sudden cardiac arrest or serious ventricular arrhythmia and are
now in stable condition
 Clinically stable SIHD patients who develop s/sx of HF despite medical therapy
 Patients with typical angina and reduced EF<50% and are unable to undergo stress
imaging studies due to contraindications
 Patients with severe angina (CCS III-IV) and high PTP(85%) with likelihood for CV
event, particularly if the symptoms inadequately respond to medical therapy
 Patients whose special professions (Pilots, bus drivers) require a definitive diagnosis
 ESTABLISHING DIAGNOSIS

 ICA is recommended after an initial non-invasive stress imaging or TET in:

 Patients with clinical characteristics and high PTP (>85%) of severe CAD or non-invasive stress
testing regardless of angina severity
 Patients with angina refractory to medical therapy
 Patient with mild or no angina but with high event risk profile on invasive stress testing for risk
stratification purpose
 Patients with reduced LVEF <50% with moderate risk criteria on non-invasive stress testing and
demonstrable ischemia
 Patients with inconclusive or conflicting results from multiple non-invasive test and in whom
definitive diagnosis needs to be established.
 MANAGEMENT

 GENERAL OVERVIEW OF MANAGEMENT:

 Lifestyle Modification
 Control and treatment of risk factors
 Pharmacological therapy: improve prognosis and reduce anginal symptoms
 Patient education
 Revascularization
 LIFESTYLE MODIFICATIONS
 It is STRONGLY RECOMMENDED that lifestyle modification and treatment of risk factors be
integrated into GMDT to reduce major CV events.
 Healthy diet
 ↑ polyunsaturated fatty acid (PUFA) consumption mainly from oily fish: 2-3 servings of oily fish per week
 Saturated Fatty acids <10% of total energy intake
 Limit salt intake <5g/day
 Consume 30-45g of fiber/day (wholegrain, fruits and vegetables), simple CHOs that have a high glycemic
load should be avoided in favor of carbohydrate sources that are high in fiber
 Consume 200g of vegetables per day (2-3 servings or 1-2.5 cups/day)
 Eat 200g of fruits per day (2-3 servings or 1-2.5cups/day)
 Limit consumption of alcoholic beverages to 2 glasses/day-20g in men, 1 glass/day -10g in women
 PHARMACOLOGIC TREATMENT

 It is STRONGLY RECOMMENDED that all patients, whether or not revascularization is

being considered, receive the following medications to improve prognosis, thereby
reducing the risk for MI and death:
 1) Low dose Aspirin (80-160mg/day)
 2) Clopidogrel in case of aspirin tolerance (75mg/day)
 3) Statins irrespective of LDL-cholesterol levels
 4) Beta blockers post MI
 5) ACEIs or ARBs (especially in patients with concomitant HF, HPN, or diabetes)
 Aspirin and Clopidogrel

 Antiplatelet agents decrease platelet aggregation, thereby reducing plaque progression and
preventing thrombus formation should plaque rupture or erosion occur.
 Aspirin dose: 80-160mg/day
 Acts via irreversible inhibition of COX-1 and subsequent thromboxane production
 GI side effects, bleeding, increase at higher dose
 Clopidogrel: 75mg/day
 Antagonist of the platelet ADP receptor P2Y12, thus inhibiting platelet aggregation
 Prasugrel and Ticagrelor
 New P2Y12 antagonist that achieve greater platelet inhibition than clopidogrel
 No clinical studies showing their benefit in SIHD patients
 Statins

 Should be given to all patients with SIHD irrespective of their LDL cholesterol levels.
 Reduced risk for CV events by at least 30% with statin therapy
 Lowers LDL cholesterol, with anti-inflammatory and anti-thrombotic effects contribute
further to the CV risk reduction.
 National Cholesterol Education Program guidelines: target LDL <100mg/dl
 European Atherosclerotic Society Guidelines: target LDL <70mg/dl and/or >50%
reduction if the target level cannot be reached.
 Betablockers

 30% risk reduction for CV death and MI in post-MI patients with or without Heart failure
 Current concensus is that beta blockers may still be protective in patients with SIHD.
 Choice with predominantly beta blockade:
 Metoprolol
 Bisoprolol
 Atenolol
 Nevibolol
 Carvidelol – non selective Beta-alpha 1 blocker
 ACE Inhibitors

 Are recommended for specific subgroup of patients with SIHD

 Co-existing Heart Failure or Asymptomatic LV dysfunction (LVEF <40%)
 Hypertension
 Diabetes
 Potential beneficial mechanisms of ACEIs include:
 Regression in LVH and vascular hypertrophy
 Prevention of atherosclerosis progression
 Prevention of plaque rupture and thrombosis
 Favorable influence in coronary endothelial vasomotor function
 ACE Inhibitors

 In patients with stable CAD+HPN, a combination therapy consisting of and ACEI and a
dihydropyridine CCB like PERINDOPRIL/AMLODIPINE (ASCOT trial) and
Benazepril/Amlodipine (ACCOMPLISH trial) is preferred.
 In HOPE trial and EUROPA trial, ACEI showed relative risk reduction of 22% and 20%
respectively.
 Ramipril and Perindopril are tissue ACEIs that are lipophilic and have high-enzyme
binding capabilities. It allows greater penetrance into the atherosclerotic plaque
 ARBs may be an alternative to ACEIs when the latter are not tolerated
 NO studies show that clinical benefit of ARBs in patients with stable CAD
 Pharmacologic Therapy
to Reduce Angina
 It is RECOMMENDED
 First-line: control heart rate and symptoms
 Beta blocker- control HR, contractility and AV conduction and ectopic activity
 Increase perfusion of ischemic areas by prolonging diastole and increasing vascular resistance in non-ischemic areas
 METOPROLOL 50-100mg BID-QID
 METOPROLOL XL 50-200MG OD
 CARVIDELOL 3.125MG-50MG BID
 ATENOLOL 50-100MG OD
 BISOPROLOL 5-20MG OD
 Pharmacologic Therapy
to Reduce Angina
 Calcium channel blockers (DHP and non-DHPs) – vasodilation and reduce PVR
 Non DHPs: Verapamil 80-20MG TID-QID OR Diltiazem 30-90mg TID-QID
 DHP: Amlodipine 2.5mg -10mg OD, Felodipine 2.5mg-10mg OD

 Avoid Non DHPs + Betablockers due to risk of heart block, symptomatic bradycardia and
Heart Failure
 Pharmacologic Therapy
to Reduce Angina
 Second line treatment:
 Long-acting nitrate: coronary arteriolar/venous vasodilator
 ISDN 5mg SL
 ISDN 10-49mg BID-TID
 ISMN 30-240mg OD
 Nitroglycerin 0.3-0.5mg SL as needed up to 3 doses, 5 minutes apart
 Nitroglycerin transdermal patch 0.2-0.8mg/h OD(remove at bedtime for 12-
14hours) to avoid nitrate tolerance
 Pharmacologic Therapy
to Reduce Angina
 Ivabradine 7.5mg BID – selective sinus node inhibitor chronotropic effect
 Nicorandil 10-20mg OD –dilates epicardial coronary arteries
 Trimetazidine 35mg BID- reduces fatty acid oxidation and stimulates glucose
oxidation, thus, improving cardiac performance; non-hemodynamic anti-ischemic
action
 Ranolazine 500-1000mg BID – Inhibits late inward Na current leading to a shift
in myocardial substrate uptake from fatty acid to glucose.
 Revascularization Therapy

 Percutaneous Coronary Intervention (PCI)

 Balloon Dilatation with Coronary Stenting
 INDICATION: Persistent or symptom-limiting angina pectoris despite medical TX
 Patients with drug eluting stent will need:
 Dual antiplatelets for 1 year (Aspirin +ADP P2Y12-Inhibitor, then
 Single platelte indefinitely usually Aspirin

 Coronary Artery Bypass Graft (CABG) Surgery

 Recommended for 2- or 3-vessel CAD or multivessel CAD and Diabetes
 NONCONVENTIONAL TREATMENT

 Chelation therapy, Vitamin C and E supplementation, Coenzyme Q, acupuncture,

Hormonal replacement in postmenopausal women and herbal medicine---for the purpose
of improving CV outcomes IS NOT RECOMMENDED due to lack of supportive
evidence
 Vaccination

 Influenza Vaccination
 Yearly vaccination is required
 Data suggest that Influenza virus may precipitate plaque rupture and
vaccination against this virus can prevent onset of ACS and death
 FOLLOW UP TESTS

 It is RECOMMENDED that follow-up tests should be done in patients with worsening

angina or development of co-morbid conditions despite GDMT with or without
revascularization.
 It is NOT RECOMMENDED to do annual or repeat tests at regular intervals in patients
without worsening of angina or change in clinical status.
 FOLLOW UP TESTS
 CXR PA for patients with new or worsening heart failure symptoms
 2d ECHO for assessment of LV Ejection Fraction and segmental wall motion in patients with
new or worsening angina or HF symptoms
 2D ECHO for evidence of new or worsening valvular heart disease by clinical evaluation
 Stress imaging studies in patients with or without prior revascularization who have a worsening
of angina or significant change in symptoms or clinical status
 TET, if stress imaging studies are not available, in patients who have a worsening of angina or
significant change in clinical status; patients should have normal resting ECGs and are able to
exercise
 ICA in patients with intermediate to high risk results on stress imaging or TET, and those with
limiting angina or marked limitation of physical activity depsite GDMT with or without
revascularization
 SPECIAL CONSIDERATIONS

 Angina with Normal Coronary arteries

 Microvascular Angina
 ECGs and Stress results are indicative of ISCHEMIA but ICA does not show fixed
or dynamic obstructions in the epicardial coronary arteries
 Pathophysiology: REDUCED CORONARY FLOW RESERVE resulting in
impaired diastolic function
 Treatment: Aspirin, statins, beta blockers (1st line), ACEI, long acting nitrates and
CCBs(less established)
 SPECIAL CONSIDERATIONS
 Vasospastic Angina or Prinzmetal’s Angina or Variant Angina
 Presents as angina at rest occurring at night and in the early morning hours, and
usually relieved by nitrates within minutes.
 ECG: ST elevation, but occasionally is associated with ST depression.
 Demonstration of spontaneous focal or diffuse spasm (lumen reductions from 75-
99%) in normal coronary arteries at the time of rest angina and ST elevation
makes the diagnosis highly likely
 Treatment: CCBs, long acting nitrates;
 Betablockers are contraindicated; might produce vasospasm
 SPECIAL CONSIDERATIONS

 Refractory Angina
 Defined as a clinically established CAD which cannot be adequately controlled by a combination
of medical therapy and revascularization
 Asymptomatic Patient at risk for CAD
 Measurement of risk factors and non-invasive stress tests MAY BE RECOMMENDED as
screening investigations for the purpose of risk stratification and management principles, as has
been described for symptomatic patients.
 ACUTE CORONARY SYNDROME

 Results of sudden atheromatous plaque rupture.

 2 presentations of ACS
 Unstable Angina/Non-STEACS
 STEMI
 UNSTABLE ANGINA

 Patients with Unstable angina or Non-STEMI experience a partial occlusion to coronary

flow as a result of plaque rupture and thrombus formation, microembolization or the
release of vasoactive substances leading to localized spasm.
 Defined as:
 CLASS IV rest angina of at least 20minutes in duration occurring at rest (within 1 week of
presentation)
 New onset Class III angina occurring within 2 months of presentation
 Previously diagnosed chronic angina increased by more or equal 1 class in severity in the 2
months before presentation
 NON-ST Elevation Myocardial Infarction
(NSTEMI)
 Prolonged rest angina (generally more than 30 minutes to 1hour)typically leads to
myocardial necrosis and NSTEMI
 These patients are generally at HIGH risk for developing STEMI and sudden
death at a rate of 7.3% to 18.5%, depending on the severity of their symptoms,
with postinfarction angina carrying the highest risk
 ECG Findings

 Ischemia: ST depression in contiguous leads

 T wave inversion
 Pseudonormalization of T waves
 Silent ECG – advise to repeat ECG for comparison to detect subtle changes
ST SEGMENT DEPRESSION IN II, III, PSEUDONORMALIZATION OF T WAVES
AVF IN II, III, AVF, INFERIOR LEADS
2014 PHA CPG for the DIAGNOSIS and
MANAGEMENT of Patients with Non-ST Elevation
Acute Coronary Syndrome
Aleson Claire A. Llanes
 Statement 1: Diagnosis and Risk
Assessment
 Chest Pain or severe epigastric pain, non-traumatic in origin, with
component typical of Myocardial ischemia or Myocardial Infarction (MI).
Central or substernal compression or crushing chest pain pressure,
tightness, heaviness, cramping, burning, aching sensation
It is RECOMMENDED that patients
with the following symptoms and signs
 Unexplained indigestion, belching, epigastric pain
undergo immediate assessment for the  Radiating pain in neck, jaw, shoulders, back, or one of both arms
diagnosis of Acute Coronary Syndome  Unexplained syncope
 Palpitations
 Dyspnea
 Nausea and/or vomiting
 Diaphoresis
 Traditional Characteristic of ACS

 Prolonged anginal pain (>20minutes) at rest

 New-onset severe angina
 Crescendo or accelerated angina
 Post-MI angina
 Post revascularization ANGINA
 Post CABG Angina
 Statement 2: Electrocardiogram

 It is STRONGLY RECOMMENDED that a 12 lead ECG be obtained immediately within

10 minutes of emergency room (ER) presentation in patients with ongoing chest
discomfort.
 If initial ECG is normal, but the patient remains symptomatic, and there is a high clinical
suspicion for ACS, serial ECGs initially at 15-30 minute intervals should be performed to
detect the potential for development of ST segment elevation or depression.
 ECGs may be repeated after 3 hours, 6-9 hours and 24hours after the initial event. It should
be done anytime during recurrence of symptoms and prior to discharge.
 ECG FINDINGS

 New horizontal or down-sloping ST depression of at least 0.5mV in two contiguous leads

 And/or T-wave inversion of at least 0.1mV in two contiguous leads, and/or T-wave
inversion of at least 0.1mV in two contiguous leads with prominent R wave or R/S ration
greater than 1.
 Pseudo-normalization of previously inverted T waves during symptomatic episodes may
also indicate acute ischemia.
Statement 3: BIOMARKERS

 It is RECOMMENDED that quantitative Troponin be measured in all patients with chest

discomfort consistent with ACS. IN patients with initially negative cardiac markers , a
repeat determination within 3 hours of presentation increases the sensitivity for MI
diagnosis to almost 100%.
 It is NOT RECOMMENDED to request for total creatinine kinase (CK) (without MB
isotype), SGOT, Beta hydroxybutyrate dehydrogenase, and/or lactate dehydrogenase as
markers for the detection of cardiac injury
Statement 3: BIOMARKERS

 High sensivity troponin I or T (cTNI or cTNT) are the preferred markers of myocardial
injury because they are more sensitive than the traditional cardiac enzymes such as CK or
its isoenzyme MB(CKMB). Additionally, troponins are the best biomarker to predict
short-term (less than 30 days) outcome with respect to MI and death
Statement 4: NON-INVASIVE IMAGING

 It is RECOMMENDED than an 2D ECHOCARDIOGRAM be done in all patients

suspected to have ACS for evaluation of global and regional LV function, for ruling in or
out Differential diagnoses and for prognostic information.
 It MAY BE RECOMMENDED to perform coronary CT Angiography to exclude ACS in
those with non-dianostic ECG and TROPONIN, and have a low to intermediate likelihood
of CAD
Statement 5: Stress Testing

 It is NOT RECOMMENDED to perform stress test in patients with active chest pain.
 It MAY BE RECOMMENDED to perform stress testing in those with non-diagnostic
ECG, normal cardiac biomarkers and no active chest pain for more than 12 hours. These
tests may be done predischarge or on OUT-PATIENT basis
Statement 6: RISK SCORING

 It is RECOMMENDED for patients who present with chest discomfort or other ischemic
symptoms to undergo early risk stratification for risk of CV events (eg death or MI) based
on an integration of the patient’s history, physical examination, ECG findings and result of
cardiac biomarkers.
 It is STRONGLY RECOMMENDED that all patients presenting with chest pain
syndrome also undergo risk assessment for bleeding.
 RISK SCORING

 TIMI risk score (7 variables)

 Increasing risk score, the composite end points of all cause mortality, new or recurrent MI, or
severe recurrent ischemia prompting revascularization within 14 days increases
 GRACE Risk model (8 variables)
 Predicts cumulative risk of death and MI during a patient’s admission, discharge and until 6
months after discharge
 Better than TIMI score to predict risk of death or MI or any cardiac events at 1 year from
admission among NSTEMI patients.
 RISK SCORING

 HEART Score model (5 variables)

 It is used at the ER for patients presenting with chest pain, whether to decide if it is of
cardiac origin or other wise.
 TIMI and GRACE scores will apply only to patients who had already been classified
to have ACS
 SCORING:
 0-3: patient may be discharged
 4-6: warrants further workup/admission for observation
 7-10: ICCU admission and/or early invasive strategy
 RISK SCORING

 Bleeding Risk (CRUSADE score): 8 variables

 Predictors:
 Baseline hematocrit less than 3%
 Creatinine cleance
 Heart Rate
 Female sex
 Signs of congestive heart failure
 Systolic blood pressure
 Diabetes Mellitus
 Prior vascular disease
 STATEMENT 7: HOSPITAL CARE

 General recommendations:
 Patients who are admitted with the diagnosis of NSTE-ACS and are stable hemodynamically
should be admitted to a unit for bed rest, with continuous ECG monitoring for ischemic and
arrhythmia detection.
 Suppplemental Oxygen should be administered to patients with UA/NSTEMI for patients with
cyanosis or respiratory distress. Finger pulse oximetry or ABG determination should be
administered to confirm adequate arterial O2 saturation(O2 sat >90%) and continued need for
supplemental oxygen in the presence of hypoxemia.
 MEDICATIONS

 STATEMENT 8: NITRATES
 It is RECOMMENDED that nitrates (SL tablet or spray), followed by IV administration, be
administered for the immediate relief of ischemic and associated symptoms.
 It is NOT RECOMMENDED to administer nitroglycerine (NTG) or other nitrates within 24
hours of sildenafil use or within 48 hours of tadalafil use. The suitable time for nitrate
administration after vardenafil use is not determined.
 Contraindications:
 BP <90mmHg or greater than or equal to 30mmHg below baseline
 Severe bradycardia (<50bpm)
 Tachycardia (>100bpm)
 Tright ventricular infarction
 MEDICATIONS

 STATEMENT 9: BETA BLOCKERS

 It is RECOMMENDED to initiate a beta blocker by oral route for all patients within the first 24
hours unless contraindications are present. Use of IV betablockers should be considered with
caution
 NEVIBOLOL, bisopolol –excreted in the kidney
 Carvidelol and metoprolol- liver; safe in pxs with renal failure
 MEDICATIONS

 STATEMENT 10: CALCIUM CHANNEL BLOCKERS

 It MAY BE RECOMMENDED to use oral long-acting calcium antagonist for recurrent
ischemia in the absence of contraindications and when beta blocker and nitrates are maximally
used.
 Symptom control
 STATEMENT 11: ACE INHIBITORS or Angiotensin Receptor Blockers (ARBs)
 It is STRONGLY RECOMMENDED that an ACEI should be administered within 24 hours of
admission to NSTE-ACS patients with pulmonary congestion, with LVEF
 Start at low-dose, short acting agent (CAPTOPRIL) 6.125mg TID up to maximum dose of
50mg TID or RAMIPRIL
 MEDICATIONS

 ACE INHIBITORS or Angiotensin Receptor Blockers (ARBs)

 It is STRONGLY RECOMMENDED that an ACEI should be administered within 24 hours of
admission to NSTE-ACS patients with pulmonary congestion, with LVEF <40% in the absence of
hypotension and other contraindications
 Start at low-dose, short acting agent (CAPTOPRIL) 6.125mg TID up to maximum dose of
50mg TID or RAMIPRIL
 ARBS should be considered who are intolerant to ACEI and/ or who have HF or MI with LVEF
less than 40%.
 MEDICATIONS

 STATEMENT 12: MORPHINE SULFATE

 It is RECOMMENDED that Morphine sulfate be administered IV when symptoms are not
immediately relieved with NTG, or when acute pulmonary congestion and/or severe agitation is
present.
 DOSAGE: Morphine Sulfate 1-5mg IV
 May be administered along intravenous NTG, with careful BP monitoring
 Antidote: Naloxone 0.4-2mg IV
 MEDICATIONS

 STATEMENT 13: ASPIRIN

 It is STRONGLY RECOMMENDED that non-enteric coated ASPIRIN be
chewed by patients ASAP at initial presentation at an initial dose of 160-320mg
followed by 80-160mg daily indefinitely.
 MEDICATIONS

 STATEMENT 14: P2Y12 inhibitors

 It is STRONGLY RECOMMENDED to start a P2Y12 inhibitor (TICAGRELOR,
PRASUGREL, OR CLOPIDOGREL) in addition to aspirin for a period of 12 months unless
there are contraindications such as excessive risk for bleeding.
 Discontinue ticagrelor/clopidogrel at least 5 days before elective CABG, 7 days for prasugrel
 Dosage forms:
 Ticagrelor 180mg LD then 90mg OD (favorable outcomes)
 Prasugrel 60mg LD then 10mg OD
 Increased risk of bleeding >75yo

 Clopidogrel 300mg LD then 75mg OD

 MEDICATIONS

 STATEMENT 15: ANTICOAGULANTS

 It is STRONGLY RECOMMENDED to start unfractionated heparin (UFH), enoxaparin or
fondaparinux in addition to antiplatelet therapy.
 Unfractionated Heparin should be given for 48hours
 Enoxaparin or Fondaparinux should be given for 5-8 days or the whole duration of hospital
stay if admitted less than 5 days.
 Enoxaparin should be discontinued 12-24h before CABG
 Fondaparinux should be discontinued 24 hours before CABG
 MEDICATIONS
 STATEMENT 16: GP Iib/IIIa Inhibitors (tirofaban, abciximab, and eptifibatide)
 It MAY BE RECOMMENDED to give tirofaban in high risk patients undergoing either a
conservative or invasive strategy.
 PRISM and PRISM plus studies, showed that tirofaban, when given alone or in combination
with heparin, reduced the likelihood of death, MI, and refractory ischemia especially in diabetics
 MEDICATIONS

 STATEMENT 17: FIBRINOLYTIC THERAPY

 It is NOT RECOMMENDED to use IV fibrinolytic therapy in patients with UA or in patients
without acute ST segment elevation, a true posterior MI, or a presumed new LBBB.
 OTHER INTERVENTIONS
 STATEMENT 18: Conservative (MEDICAL) versus Early Invasive (Coronary Angiography and
Revascularization)
 It is RECOMMENDED that an early invasive strategy ( as early as possible up to 72
hours) followed by revascularization (PCI or CABG) can be used in patients with any
of the following high-risk indicators:
 Recurrent angina/ischemia at rest or with low-level activities despite intensive
anti-ischemic therapy
 Elevated cardiac biomarkers (Trop T or Trop I); or new or presumably new ST-
segment depression
 OTHER INTERVENTIONS
 Signs or symptoms of HF, or new or worsening mitral regurgitation
 High risk findings from non-invasive testing
 Hemodynamic instability
 Sustained ventricular tachycardia
 PCI within 6 months
 Prior CABG
 High-risk score (using GRACE) and
 Reduced LV systolic function (LVEF <40%
 OTHER INTERVENTIONS

 STATEMENT 19: CORONARY ANGIOGRAPHY

 It is NOT RECOMMENDED in patients with extensive co-morbidities (eg liver or pulmonary
failure, cancer) in whom the risks or revascularization are not likely to outweigh the benefits; in
patients with acute chest pain and a low likelihood of ACS; or in patients who will not consent to
revascularization regardless of the findings.
 STATEMENT 20: REVASCULARIZATION BY PCI
 PCI is RECOMMENDED for NSTE-ACS patients with 1- or 2-vessel CAD, with or without
significant proximal LAD CAD, but with a large area of viable myocardium and high-risk criteria
on non-invasive testing.
 OTHER INTERVENTIONS

 STATEMENT 21: REVASCULARIZATION BY CABG SURGERY

 CABG IS RECOMMENDED for patients with significant left main disease, and is preferred
revascularization strategy for patients with multi-vessel coronary disease; vessels with lesions not
favorable for PCI; depressed systolic function (LVEF lower than 50%); and diabetes.
 STATEMENT 22:
HOSPITAL TRANSFER FOR REVASCULARIZATION

 In patients initially admitted in hospitals without catheterization facilities and with at least
one major high-risk feature as mentioned above, or a high GRACE risk score of over 140,
transfer to hospital with catheterization facilities is RECOMMENDED.
 STATEMENT 23: HOSPITAL DISCHARGE AND
LONG-TERM MANAGEMENT

 It is RECOMMENDED that the following specific instructions should be given upon

hospital discharge and long-term management,
 Lifestyle modification that includes smoking cessation, achievement or maintenance of
optimal weight (BMI of 18.5-24.9 kg/m2), exercise, and diet
 Consider referral of patients who are smokers to smoking cessation program or clinic
and/or outpatient cardiac rehabilitation program, and:
 Continued education about long term follow-up, adherence to medications. Any recurrence
or change in sympoms should be communicated to the health care team.
 STATEMENT 24: DRUG/MEDICATION
MANAGEMENT

 It is STRONGLY RECOMMENDED to maintain patients who were treated medically

with aspirin indefinitely, and ticagrelor 90mg twice daily or clopidogrel 75mg daily for 12
months
 It is STRONGLY RECOMMENDED to maintain patients who underwent stenting, with
aspirin indefinitely, plus TICAGRELOR 90mg BID or CLOPIDOGREL 75M OD, for
12 months in patients with drug-eluting stents, and 6 months in patients with bare-metal
stents
 It is STRONGLY RECOMMENDED that BETABLOCKERS be continued indefinitely
for all NSTE ACS patients unless contraindicated. IN those with moderate to sever e
systolic dysfunction, the dosing regimen must be titrated slowly.
 DRUG/MEDICATION MANAGEMENT

 It is to STRONGLY RECOMMENDED to continue ACE Inhibition indefinitely in all

NSTE-ACS patients who have a LVEF <40%, hypertension, DM, HF. In the absence of
these aggravating factors, use ACEIs may still be recommended. An ARB may be
prescribed if an ACEI cannot be tolerated.
 It is RECOMMENDED to continue nitrates for ischemic relief
 It is RECOMMENDED to continue CCBs as add on therapy to beta blockers or if the
latter are not tolerated for ischemic control.
 STATEMENT 25: CONTROL OF RISK
FACTORS
 It is RECOMMENDED to obtain a fasting LIPID test within 24 hours of admission.
Regardless of levels, it is STRONLY RECOMMENDED to start on statins in all NSTE-
ACS patients. The goals of lipid management in secondary prevention follow those of
SIHD.
 It is RECOMMENDED that Hypertension be controlled to a BP of less than
140/90mmHg
 Tight control of Hyperglycemia in Diabetes IS RECOMMENDED. The goal is a HBA1c
of less than 7%.
 STATEMENT 26: CARDIAC
REHABILITATION
 It is STRONGLY RECOMMENDED that patients with multiple risk factors and those
who require monitoring during exercise be enrolled in a cardiac rehabilitation program if
available.
Sources:

• 2014 PHA Clinical Practice Guidelines for the Diagnosis and Management of
Patients with CAD
• Rakel’s Texbook of Family Medicine 9th Edition c. 2016