ISCHEMIC HEART DISEASE

CHRISTINE JOY RAQUID, MD,FPCP

Ischemic Heart Disease (IHD)

Condition in which there is an inadequate supply of

blood and oxygen to a portion of the myocardium.

Occurs when there is an imbalance between

myocardial oxygen supply and demand.

Most common cause of myocardial ischemia is

atherosclerotic disease of an epicardial coronary
artery (or arteries).

Powerful risk factors: Obesity, insulin resistance, and

type 2 diabetes mellitus
PATHOPHYSIOLOGY: SUPPLY AND DEMAND
 PATHOPHYSIOLOGY:

▪ Blood flows through the

coronary arteries in a
phasic fashion, with the
majority occurring during
diastole.
 PATHOPHYSIOLOGY:

About 75% of (1) large epicardial arteries

the total (Resistance 1 = R1 )
coronary
resistance to
flow occurs (2) prearteriolar vessels (R2 ), and
across three
sets of arteries:

(3) arteriolar and intramyocardial

capillary vessels (R3 ).

In the absence of significant flow-limiting

atherosclerotic obstructions, R1 is trivial; the major
determinant of coronary resistance is found in R2 and
R3
 CORONARY ATHEROSCLEROSIS

Major site of
atherosclerotic Epicardial coronary arteries
disease.

Major risk factors high levels of plasma low-density lipoprotein [LDL]

for
atherosclerosis
low plasma high-density lipoprotein [HDL]
cigarette smoking
hypertension
diabetes mellitus
 CORONARY ATHEROSCLEROSIS

Predilection for atherosclerotic plaques: sites of increased

turbulence in coronary flow, such as at branch points in the
epicardial arteries.
50% limitation of the ability to increase flow to meet increased
myocardial demand.
stenosis :

80% blood flow at rest may be reduced, and further minor decreases in
the stenotic orifice area can reduce coronary flow dramatically to
stenosis: cause myocardial ischemia at rest or with minimal stress.
 CORONARY
ATHEROSCLEROSIS

Segmental atherosclerotic narrowing of epicardial coronary arteries is

caused most commonly by the formation of a plaque, which is subject to
rupture or erosion of the cap separating the plaque from the
bloodstream.

Upon exposure of the

plaque contents to blood, (1) platelets are activated and aggregate
two important and
interrelated processes
(2) the coagulation cascade is activated, leading to
are set in motion: deposition of fibrin strands.

A thrombus composed of platelet aggregates and fibrin strands

traps red blood cells and can reduce coronary blood flow, leading to
the clinical manifestations of myocardial ischemia.
 CORONARY
ATHEROSCLEROSIS

The location of the obstruction influences the quantity of

myocardium rendered ischemic and determines the
severity of the clinical manifestations.

Example: left main coronary artery and the proximal left

anterior descending coronary artery, are particularly
hazardous.

Chronic severe coronary narrowing and myocardial

ischemia frequently are accompanied by the development
of collateral vessels, especially when the narrowing
develops gradually. When well developed, such vessels can
by themselves provide sufficient blood flow to sustain the
viability of the myocardium at rest but not during
conditions of increased demand.
 CORONARY ATHEROSCLEROSIS

Formation of platelet plug

•Platelets can plug holes in small vessels

•Plug formation includes
•Adhesion
•Activation
•Aggregation
vWF binds to the platelet
receptor known as
glycoprotein Ib/Ia (Gp
Ib/Ia), which is a dimer of
Gp Ib linked to Gp Ia.

Increase in shearing force

at the surface of platelets
and endothelial cells >
trigger release of vWF from
endothelial cells.

Vessel injury > breach of

the endothelium > exposes
platelet receptors to
ligands (components of the
subendothelial matrix)
Activated dense
platelets storage
ATP, ADP, serotonin, and
exocytose: granules: Ca2+
contains

α granules: contains proteins, including a host of

growth factors

three hemostatic factors:

vWF and two clotting
factors : factor V and
fibrinogen.
also use cyclooxygenase to initiate the
breakdown of arachidonic acid to
thromboxane A2
PLATELET AGGREGATION
PLATELET AGGREGATION
 Aggregation
INHIBITORS
• Aspirin
• inhibitor of
cyclooxygenase
• inhibits clotting
by reducing the
release of
thromboxane
A2.
• Clopidogrel
• acts by
inhibiting the
P2Y12
receptors on
the platelet
surface.
 Episodic clinical syndrome is due
STABLE ANGINA PECTORIS to transient myocardial ischemia.

Males constitute ~70% of all patients

Man >50 years or a woman >60 years of age

Description of chest pain: Episodes of chest discomfort, usually described as heaviness, pressure, squeezing, smothering, or choking and
only rarely as frank pain.

Localization: He or she typically places a hand over the sternum, sometimes with a clenched fist, to indicate a squeezing, central,
substernal discomfort (Levine’s sign).

Radiation: radiate to either shoulder and to both arms (especially the ulnar surfaces of the forearm and hand). It also can arise in or
HISTORY

radiate to the back, interscapular region, root of the neck, jaw, teeth, and epigastrium. Angina is rarely localized below the umbilicus or
above the mandible.
Character: Crescendo-decrescendo in nature, typically lasts 2–5 min

Exacerbating factor: episodes of angina typically are caused by exertion (e.g., exercise, hurrying, or sexual activity) or emotion (e.g.,
stress, anger, fright, or frustration) and are relieved by rest, they also may occur at rest and while the patient is recumbent (angina
decubitus)
Relieving factor: Exertional angina typically is relieved in 1–5 min by slowing or ceasing activities and even more rapidly by rest and
sublingual nitroglycerin.
 STABLE ANGINA PECTORIS

Anginal “equivalents”:

•Common in the elderly and in

diabetic patients
•Includes: dyspnea, nausea,
fatigue, and faintness
STABLE ANGINA
PECTORIS
 STABLE ANGINA PECTORIS:
PHYSICAL EXAMINATION
ASYMPTOMATIC

Search for evidence of atherosclerotic disease:

•abdominal aortic aneurysm
•carotid arterial bruits
•arterial pulses in the lower extremities
•xanthelasmas and xanthomas
•comparing the blood pressure between the arms and between the arms and the legs (anklebrachial index)

Hypertension: Examination of the fundi may reveal an increased light reflex and arteriovenous nicking

Metabolic Syndrome: protuberant abdomen

Nicotine stains on the fingertips from cigarette smoking.

Palpation may reveal cardiac enlargement and abnormal contraction of the cardiac impulse (LV dyskinesia).

Auscultation can uncover arterial bruits, a third and/or fourth heart sound, and, if acute ischemia or previous infarction has impaired papillary
muscle function, systolic murmur, MR.
 STABLE ANGINA PECTORIS:
DIAGNOSTICS

Urine: evidence of diabetes mellitus and renal disease (including

microalbuminuria) since these conditions accelerate atherosclerosis.

Lipid profile (cholesterol—total, LDL, HDL—and triglycerides),

Hemoglobin A1C

Creatinine

Hematocrit

If indicated, thyroid function test

 STABLE ANGINA PECTORIS:
DIAGNOSTICS

Chest x-ray
Cardiac enlargement, ventricular aneurysm,
or signs of heart failure.

Elevated Independent risk factor for IHD.

level of high-
sensitivity C-
reactive
protein Useful in therapeutic decision-making about
(CRP): the initiation of hypolipidemic treatment.
 STABLE ANGINA PECTORIS:
DIAGNOSTICS

•Normal

Resting ECG:
•Signs of an old myocardial infarction
•Presence of LVH is a significant indication of increased risk of adverse outcomes from IHD
•Dynamic ST-segment and T-wave changes that accompany episodes of angina pectoris and
disappear thereafter are more specific.

Stress Test: •Most widely used test for both the diagnosis of IHD and the estimation of risk and prognosis
involves recording of the 12-lead ECG before, during, and after exercise, usually on a treadmill.

Cardiac •When the resting ECG is abnormal, information gained from an exercise test can be enhanced
by stress myocardial radionuclide perfusion imaging after the intravenous administration of

Imaging: thallium-201 during exercise (or with pharmacologic) stress.

 STABLE ANGINA PECTORIS:
DIAGNOSTICS

Echocardiography

Cardiac magnetic
resonance (CMR)
Stress (exercise or stress testing is
dobutamine) also evolving as an
Assess LV function in
echocardiography may alternative to
cause the emergence of
patients with chronic
Assess both global and regions of akinesis or radionuclide, PET,
stable angina and patients dyskinesis that are not or
regional wall motion
with a history of a prior present at rest.
myocardial infarction,
abnormalities of the left echocardiographic
ventricle that are transient Stress echocardiography,
pathologic Q waves, or
when due to ischemia. like stress myocardial
stress imaging.
clinical evidence of heart
failure. perfusion imaging, is more
sensitive than exercise
electrocardiography in the
diagnosis of IHD.
 STABLE ANGINA PECTORIS:
DIAGNOSTICS

Computed Detecting coronary calcium

Tomography (CT)
applications that
achieve rapid Diagnostic accuracy of this imaging
acquisition of method is high (sensitivity, 90–94%;
images (electron specificity, 95–97%
beam [EBCT] and Role management of patients with IHD
multidetector has not been clarified.
[MDCT] detection).
 CORONARY ARTERIOGRAPHY INDICATIONS:

Patients with chronic stable angina pectoris who are severely symptomatic despite medical therapy and are being
considered for revascularization, i.e., a percutaneous coronary intervention (PCI) or coronary artery bypass grafting
(CABG).

Patients with troublesome symptoms that present diagnostic difficulties in whom there is a need to confirm or rule out
the diagnosis of IHD.

Patients with known or possible angina pectoris who have survived cardiac arrest.

Patients with angina or evidence of ischemia on noninvasive testing with clinical or laboratory evidence of ventricular
dysfunction.

Patients judged to be at high risk of sustaining coronary events based on signs of severe ischemia on noninvasive
testing, regardless of the presence or severity of symptoms.
 CORONARY ARTERIOGRAPHY INDICATIONS:

Patients with chest discomfort suggestive of angina pectoris but a negative or nondiagnostic stress test who require a definitive diagnosis for
guiding medical management, alleviating psychological stress, career or family planning, or insurance purposes.

Patients who have been admitted repeatedly to the hospital for a suspected acute coronary syndrome, but in whom this diagnosis has not
been established and in whom the presence or absence of CAD should be determined.

Patients with careers that involve the safety of others (e.g., pilots, firefighters, police) who have questionable symptoms or suspicious or
positive noninvasive tests and in whom there are reasonable doubts about the state of the coronary arteries.

Patients with aortic stenosis or hypertrophic cardiomyopathy and angina in whom the chest pain could be due to IHD.

Male patients >45 years and females >55 years who are to undergo a cardiac operation such as valve replacement or repair and who may or
may not have clinical evidence of myocardial ischemia.

Patients after myocardial infarction, especially those who are at high risk after myocardial infarction because of the recurrence of angina or
the presence of heart failure, frequent ventricular premature contractions, or signs of ischemia on the stress test.

Patients with angina pectoris, regardless of severity, in whom noninvasive testing indicates a high risk of coronary events (poor exercise
performance or severe ischemia).

Patients in whom coronary spasm or another nonatherosclerotic cause of myocardial ischemia (e.g., coronary artery anomaly, Kawasaki
disease) is suspected.
 TREATMENT:

The Explanation of the problem and reassurance about the ability to formulate a
management treatment plan.
plan should Identification and treatment of aggravating conditions
include the
following Recommendations for adaptation of activity as needed.
components:
Treatment of risk factors that will decrease the occurrence of adverse
coronary outcomes
Drug therapy for angina

Consideration of revascularization
 TREATMENT:

Obesity

•Diet low in saturated and trans-unsaturated fatty acids and a reduced caloric
•Weight loss and regular exercise in patients with the metabolic syndrome or overt diabetes mellitus.

Cigarette smoking cessation.

Hypertension

•LVH that results from sustained hypertension aggravates ischemia.

Diabetes mellitus

•Accelerates coronary and peripheral atherosclerosis.

Aggressive control of the dyslipidemia

•HMG-CoA reductase inhibitors (statins) are required and can lower LDL cholesterol (25–50%), raise HDL cholesterol
(5–9%), and lower triglycerides (5–30%).
 TREATMENT: DRUG THERAPY

NITRATES

MOA: systemic venodilation with concomitant

reduction in LV end-diastolic volume and pressure,

reducing myocardial wall tension and oxygen

requirements; dilation of epicardial coronary vessels;
and increased blood flow in collateral vessels
 TREATMENT: DRUG THERAPY

Adrenergic Reduce myocardial oxygen demand by inhibiting the increases

Blockers : in heart rate, arterial pressure, and myocardial contractility
caused by adrenergic activation.

Reduce mortality and reinfarction rates in patients after

myocardial infarction and are moderately effective
antihypertensive agents.

Relative contraindications include asthma and reversible

airway obstruction in patients with chronic lung disease,
atrioventricular conduction disturbances, severe bradycardia,
Raynaud’s phenomenon, and a history of mental depression
 TREATMENT: DRUG THERAPY

Coronary vasodilators that produce variable and dose dependent reductions in myocardial
Calcium oxygen demand, contractility, and arterial pressure.

channel Indicated when beta blockers are contraindicated, poorly tolerated, or ineffective.

blockers: Verapamil ordinarily should not be combined with beta blockers because of the combined
adverse effects on heart rate and contractility.
Diltiazem can be combined with beta blockers in patients with normal ventricular function
and no conduction disturbances.
Amlodipine and beta blockers have complementary actions on coronary blood supply and
myocardial oxygen demands.

Amlodipine and the other second-generation dihydropyridine calcium antagonists

(nicardipine, isradipine, long-acting nifedipine, and felodipine) are potent vasodilators and are
useful in the simultaneous treatment of angina and hypertension.

Short-acting dihydropyridines should be avoided because of the risk of precipitating

infarction, particularly in the absence of concomitant beta blocker therapy
TREATMENT: DRUG THERAPY
 TREATMENT: DRUG THERAPY

Antiplatelet Drugs

• Aspirin
• Irreversible inhibitor of platelet cyclooxygenase and thereby interferes with platelet activation.
• 75–325 mg orally per day
• Dose-dependent increase in bleeding when aspirin is used chronically. It is preferable to use an
enteric-coated formulation in the range of 81–162 mg/d.
• Clopidogrel
• 300–600 mg loading and 75 mg/d
• oral agent that blocks P2Y12 ADP receptor–mediated platelet aggregation.
• Benefits similar to those of aspirin.
• Clopidogrel combined with aspirin
• Reduces death and coronary ischemic events in patients with an acute coronary syndrome and also
reduces the risk of thrombus formation in patients undergoing implantation of a stent in a coronary
artery.
• Prasugrel and Ticagrelor
• Alternative antiplatelet agents that block the P2Y12 platelet receptor
• More effective than clopidogrel for prevention of ischemic events after placement of a stent for an
acute coronary syndrome, but are associated with an increased risk of bleeding
 TREATMENT: DRUG THERAPY

ACE IHD patients at increased risk, especially if diabetes

inhibitors mellitus or left ventricle dysfunction is present, and
those who have not achieved adequate control of
blood pressure and LDL cholesterol on beta blockers
and statins.
Routine administration of ACE inhibitors to IHD
patients who have normal LV function and have
achieved blood pressure and LDL goals on other
therapies does not reduce the incidence of events
and therefore is not cost-effective.
 CORONARY REVASCULARIZATION

PERCUTANEOUS CORONARY INTERVENTION

• Indications and Patient Selection

• Most common clinical indication for PCI is symptom-limiting angina pectoris,
despite medical therapy, accompanied by evidence of ischemia during a stress test
• PCI is more effective than medical therapy for the relief of angina.
• PCI improves outcomes in patients with unstable angina or when used early in the
course of myocardial infarction with and without cardiogenic shock.
• PCI can be used to treat stenoses in native coronary arteries as well as in bypass
grafts in patients who have recurrent angina after CABG.
• For stable exertional angina does not reduce the occurrence of death or myocardial
infarction compared to optimum medical therapy.

CORONARY ARTERY BYPASS GRAFTING

ACUTE CORONARY SYNDROME:
UNSTABLE ANGINA
NSTEMI
STEMI
CHRISTINE JOY RAQUID, MD,FPCP
Acute Coronary Syndrome
 Non ST Elevation (NSTE-ACS):

▪ Imbalance between myocardial oxygen supply and demand

▪ plaque rupture: most common etiology of coronary thrombosis
▪ “vulnerable plaques”
▪ Responsible for ischemia may show an eccentric stenosis with scalloped or
overhanging edges and a narrow neck on coronary angiography.
▪ Composed of a lipid-rich core with a thin fibrous cap.
▪ four processes that lead to thrombus formation :
▪ (1) disruption of an unstable coronary plaque due to plaque rupture, erosion,
or a calcified protruding nodule that leads to intracoronary thrombus
formation) and an inflammatory response;
▪ (2) coronary arterial vasoconstriction;
▪ (3) gradual intraluminal narrowing; and
▪ (4) increased myocardial oxygen demand produced by conditions such as
fever, tachycardia, and thyrotoxicosis in the presence of fixed epicardial
coronary obstruction.
 Non ST Elevation (NSTE-ACS):

▪ Angiography:
▪ ~10% have stenosis of the left main coronary artery,
▪ 35% have three-vessel CAD,
▪ 20% have two-vessel disease,
▪ 20% have single-vessel disease, and
▪ 15% have no apparent critical epicardial coronary artery stenosis;
some of the latter may have obstruction of the coronary
microcirculation and/or spasm of the epicardial vessels.
▪
 Non ST Elevation (NSTE-ACS):

Diagnosis: based
largely on the clinical
presentation
Non ST Elevation (NSTE-ACS) HISTORY and PE:

▪ Typically, chest discomfort is severe and has at least one of three

features:
▪ (1) Occurrence at rest (or with minimal exertion), lasting >10 min.
▪ (2) Relatively recent onset (i.e., within the prior 2 weeks).
▪ (3) Crescendo pattern, i.e., distinctly more severe, prolonged, or frequent than
previous episodes.
▪ Location: substernal region and radiates to the left arm, left shoulder,
and/or superiorly to the neck and jaw.
▪ Anginal equivalents ( women, elderly, with DM): dyspnea, epigastric
discomfort, nausea, or weakness
▪ Large area of myocardial ischemia or a large NSTEMI: Diaphoresis; pale,
cool skin; sinus tachycardia; a third and/or fourth heart sound; basilar
rales; and, sometimes, hypotension.
 Non ST Elevation (NSTE-ACS) ECG :

▪ Electrocardiogram
▪ 1/3 : New ST-segment depression
▪ Transient but may persist for several days
following NSTEMI.
▪ T-wave changes:
▪ more common but are less specific signs
of ischemia, unless they are new and deep
T-wave inversions (≥0.3 mV)
Non ST Elevation (NSTE-ACS) ECG :
 Non ST Elevation (NSTE-ACS) BIOMARKERS:

▪ Cardiac Biomarkers Patients with

NSTEMI have
▪ Cardiac troponin (cTn) I or T
▪ Elevated, biomarkers of necrosis
▪ Specific, sensitive, and the preferred
markers of myocardial necrosis. The
▪ MB isoform of creatine kinase (CK-MB)
▪ Less sensitive alternative.
 Non ST Elevation (NSTE-ACS) Diagnostics:

▪ 3 major noninvasive tools are used in the evaluation of NSTEMI-ACS:

1. ECG
2. Cardiac biomarkers
3. Stress test
▪ Equivocal cases, coronary computed tomographic angiography (CCTA) can be done.

▪ Goals are to:

▪ Recognize or exclude myocardial infarction (MI) using cardiac biomarkers,
preferably cTn.
▪ Detect rest ischemia (using serial or continuous ECGs).
▪ Detect significant coronary obstruction at rest with CCTA and/ or myocardial
ischemia using stress testing.
 Non ST Elevation (NSTE-ACS) Diagnostics:

Patients with a low likelihood of ischemia

Clinical monitoring for recurrent ischemic discomfort and continuous monitoring of ECGs and cardiac markers

ECG and Cardiac Biomarkers obtained at baseline and at 4–6 h and 12 h after presentation
New elevations in cardiac markers or ST-T- Patients who remain pain-free with negative
wave changes on the ECG are noted markers

•Patient should be admitted to the hospital. • Stress testing to determine the presence of ischemia or
CCTA to detect coronary luminal obstruction
 Non ST Elevation (NSTE-ACS):

Diagnosis: based
largely on the clinical
presentation
Non ST Elevation (NSTE-ACS)
RISK STRATIFICATION :
 Non ST Elevation (NSTE-ACS)
TREATMENT:

▪ Admitted at CCU
▪ Bed rest
▪ Continuous ECG monitoring for ST-segment deviation and cardiac arrhythmias
▪ Ambulation is permitted if the patient shows no recurrence of ischemia
(symptoms or ECG changes) and does not develop an elevation of a biomarker
of necrosis for 12–24 h.
▪ Medical therapy consists
▪ Acute phase focused on the clinical symptoms and stabilization of the culprit
lesion.
▪ Long-term phase that involves therapies directed at the prevention of disease
progression and future plaque rupture/erosion.
Non ST Elevation (NSTE-ACS)
TREATMENT:
Non ST Elevation (NSTE-ACS)
TREATMENT:
Non ST Elevation (NSTE-ACS)
TREATMENT:
 INVASIVE VS.
CONSERVATIVE STRATEGY

▪ Invasive strategy, following

initiation of anti-ischemic and
antithrombotic agents,
▪ High-risk patients
▪ Coronary arteriography is carried out
within ~48 h of presentation
▪ Followed by coronary
revascularization (PCI or coronary
artery bypass grafting).
▪ Low risk patients
▪ Outcomes from an invasive strategy
are similar to those obtained from a
conservative strategy.
ST-Segment Elevation Myocardial Infarction
(STEMI)
 ST-Segment Elevation Myocardial Infarction
(STEMI)

Most common diagnosis in hospitalized patients in industrialized countries.

Half of deaths occur before reaching the hospital.
12-lead
electrocardiogram Pivotal diagnostic and triage tool because it is at the center of the
(ECG) decision pathway for management.
Permits distinction of those patients presenting with ST-segment
elevation from those presenting without ST-segment elevation.
Serum cardiac
biomarkers Obtained Distinguish unstable angina (UA) from non-ST-segment
to: elevation myocardial infarction (NSTEMI).
Assess the magnitude of an ST-segment elevation myocardial
infarction (STEMI).
ST-Segment Elevation Myocardial Infarction
(STEMI)

Source: https://ecgwaves.com/topic/stemi-st-
elevation-myocardial-infarction-criteria-ecg/
 PATHOPHYSIOLOGY: ROLE
OF ACUTE PLAQUE
RUPTURE

STEMI occurs when coronary blood flow

decreases abruptly after a thrombotic
occlusion of a coronary artery previously
affected by atherosclerosis.

Slowly developing, high-grade coronary

artery stenoses do not typically precipitate
STEMI because of the development of a
rich collateral network over time.

This injury is produced or facilitated by

factors such as cigarette smoking,
hypertension, and lipid accumulation.
ST-Segment Elevation Myocardial Infarction
(STEMI)
 PATHOPHYSIOLOGY: ROLE OF ACUTE PLAQUE
RUPTURE

STEMI occurs when the surface of an atherosclerotic plaque

becomes disrupted (exposing its contents to the blood) and
conditions (local or systemic) favor thrombogenesis.
A mural thrombus forms at the site of plaque disruption, and the
involved coronary artery becomes occluded.

Histologic studies indicate that the coronary plaques prone to

disruption are those with a RICH LIPID CORE AND A THIN
FIBROUS CAP.
 PATHOPHYSIOLOGY: ROLE OF ACUTE PLAQUE
RUPTURE

After an initial platelet monolayer forms at the site of the disrupted plaque, various agonists (collagen, ADP,
epinephrine, serotonin) promote platelet activation.

After agonist stimulation of platelets, thromboxane A2 (a potent local vasoconstrictor) is released, further
platelet activation occurs, and potential resistance to fibrinolysis develops. In addition to the generation of
thromboxane A2 , activation of platelets by agonists promotes a conformational change in the glycoprotein
IIb/IIIa receptor.
Once converted to its functional state, this receptor develops a high affinity for soluble adhesive proteins
(i.e., integrins) such as fibrinogen. Since fibrinogen is a multivalent molecule, it can bind to two different
platelets simultaneously, resulting in platelet cross-linking and aggregation.

The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of
the disrupted plaque. Factors VII and X are activated, ultimately leading to the conversion of prothrombin to
thrombin, which then converts fibrinogen to fibrin
 ST-Segment Elevation Myocardial Infarction
(STEMI): HISTORY
Description: deep and visceral; adjectives commonly used to describe it are heavy, squeezing, crushing and stabbing
Pain is the
most Substernal chest pain persisting for >30 min and diaphoresis strongly suggests STEMI.
common
presenting Commence when the patient is at rest and usually more severe, and lasts longer.

complaint When it begins during a period of exertion, it does not usually subside with cessation of activity, in contrast to angina
pectoris precipitating factor vigorous physical exercise, emotional stress, or a medical or surgical illness.

Commence at any time of the day or night, circadian variations have been reported such that clusters are seen in the
morning within a few hours of awakening.

Location: central portion of the chest and/or the Frequent location of the pain beneath the xiphoid and epigastrium is
responsible for the common mistaken impression of indigestion.
epigastrium

Radiation: Arms
Occipital area but not below the umbilicus.

Associated Weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom.

symptoms:
 ST-Segment Elevation Myocardial Infarction
(STEMI): PHYSICAL EXAMINATION
Most anxious and restless, attempting unsuccessfully to relieve the pain by moving about in bed, altering their
position, and stretching.

Pallor associated with perspiration and coolness of the extremities, diaphoresis

Normal pulse rate ¼: anterior infarction have manifestations of sympathetic nervous system hyperactivity
and blood pressure (tachycardia and/or hypertension)
within the first hour of
STEMI, ½: inferior infarction show evidence of parasympathetic hyperactivity (bradycardia and/or
hypotension)
Precordium is usually quiet

Apical impulse may Anterior wall infarction, an abnormal systolic pulsation caused by dyskinetic bulging of infarcted
be difficult to palpate. myocardium may develop in the periapical area within the first days of the illness and then may
resolve.
 ST-Segment Elevation Myocardial Infarction
(STEMI): PHYSICAL EXAMINATION
Ventricular
dysfunction: fourth and third heart sounds, decreased intensity of the first
heart sound, and paradoxical splitting of the second heart.
Transient midsystolic
or late systolic apical Due to dysfunction of the mitral valve.
systolic murmur
Pericardial friction rub may be heard in patients with transmural STEMI at some time in the course of the
illness.

Temperature
Elevated at 38C maybe observed during first week of MI.

Arterial pressure
Variable; in most patients with transmural infarction, systolic
pressure declines by ~10–15 mmHg from the preinfarction state.
 ST-Segment Elevation Myocardial Infarction
(STEMI): DIAGNOSTICS

LABORATORY FINDINGS

STEMI progresses (1) acute (first few hours–7 days)

through the
following
temporal stages:
(2) healing (7–28 days)

(3) healed (≥29 days)

Laboratory tests (1) ECG

of value in
confirming the (2) serum cardiac biomarkers
diagnosis:
(3) cardiac imaging
(4) nonspecific indices of tissue necrosis and inflammation
ST-Segment Elevation Myocardial Infarction
(STEMI): ECG
 ST-Segment Elevation
Myocardial Infarction
(STEMI): ECG

Source: https://ecgwaves.com/topic/stemi-st-
elevation-myocardial-infarction-criteria-ecg/
 ST-Segment
Elevation
Myocardial
Infarction
(STEMI): ECG
ST-Segment Elevation Myocardial Infarction
(STEMI):Myocardial
ST-Segment Elevation ECG Infarction
(STEMI): ECG
ST-Segment Elevation Myocardial Infarction
(STEMI): Cardiac Biomarker
 ST-Segment Elevation Myocardial Infarction
(STEMI): Cardiac Imaging

2dechocardiogram:
Detect abnormalities of wall motion

Several
radionuclide Available for evaluating patients with suspected
imaging techniques STEMI.

Used less often because they are more cumbersome

and lack sensitivity and specificity in many clinical
circumstances.
 ST-Segment Elevation Myocardial Infarction (STEMI):
MANAGEMENT IN THE EMERGENCY DEPARTMENT

Control of cardiac discomfort

ER
GOAL: Rapid identification of patients who are
candidates for urgent reperfusion therapy
Triage of lower-risk patients to the appropriate
location in the hospital
Avoidance of inappropriate discharge of patients
with STEMI.
 ST-Segment Elevation Myocardial Infarction (STEMI):
MANAGEMENT IN THE EMERGENCY DEPARTMENT

Sublingual nitroglycerin up to three doses of 0.4 mg

NITRATES should be administered at about 5-min intervals.
CONTROL OF CHEST

Given sublingual nitroglycerin but return of chest

discomfort use of intravenous nitroglycerin.
DISCOMFORT

Administered by repetitive (every 5 min) intravenous

Morphine injection of small doses (2–4 mg), rather than by the
subcutaneous administration of a larger quantity,
because absorption may be unpredictable by the
latter route.
Metoprolol, 5 mg every 2–5 min for a total of three
Intravenous beta doses, provided the patient has a heart rate >60
beats/min, systolic pressure >100 mmHg, a PR
blockers interval 0.24 s, second- or third-degree heart block,
active asthma, or reactive airway disease).

Calcium antagonists are of little value in the acute

setting.
 ST-Segment Elevation Myocardial Infarction (STEMI):
MANAGEMENT IN THE EMERGENCY DEPARTMENT

While the central zone of the infarct contains necrotic tissue that is irretrievably lost, the
LIMITATION OF INFARCT

fate of the surrounding ischemic myocardium (ischemic penumbra) may be improved by

timely restoration of coronary perfusion, reduction of myocardial O2 demands, prevention
of the accumulation of noxious metabolites, and blunting of the impact of mediators of
reperfusion injury.

Up to one-third of patients with STEMI may achieve spontaneous reperfusion of the infarct-
SIZE

related coronary artery within 24 h and experience improved healing of infarcted tissue.

Reperfusion, either pharmacologically (by fibrinolysis) or by PCI, accelerates the opening of

infarct-related arteries

Timely restoration of flow in the epicardial infarct–related artery combined with improved
perfusion of the downstream zone of infarcted myocardium results in a limitation of infarct
size.
 ST-Segment Elevation Myocardial Infarction
(STEMI): MANAGEMENT

Reperfusion — PERCUTANEOUS CORONARY INTERVENTION — If high-quality

Prompt PCI is available, multiple randomized trials have shown
restoration of enhanced survival and a lower rate of intracranial
myocardial hemorrhage and recurrent MI compared to fibrinolysis
blood flow is
essential to
optimize FIBRINOLYSIS - For patients with STEMI in whom fibrinolysis
myocardial is chosen as the reperfusion strategy (ie, when primary
salvage and percutaneous coronary intervention is not available),
to reduce treatment should be given as soon as possible after the
mortality . diagnosis.
FOR VIDEO: https://ecgwaves.com/topic/stemi-st-elevation-myocardial-infarction-criteria-ecg/
 ST-Segment
Elevation
Myocardial
Infarction (STEMI):
MANAGEMENT
 ST-Segment
Elevation
Myocardial
Infarction (STEMI):
MANAGEMENT
ST-Segment Elevation Myocardial Infarction
(STEMI): MANAGEMENT
 ST-Segment Elevation Myocardial Infarction
(STEMI): MANAGEMENT

Bypass Infrequently performed in patients with STEMI.

surgery -
Coronary
artery
bypass Main indications are for emergent or urgent CABG
graft related to failure of fibrinolysis or PCI, or
surgery hemodynamically important mechanical complications.
(CABG)
ST-Segment Elevation Myocardial Infarction
(STEMI): COMPLICATIONS

Source:
https://ecgwaves
.com/topic/stem
i-st-elevation-
myocardial-
infarction-
criteria-ecg/
THANK YOU