Ischemic Heart Disease (Ihd) : by Tolcha Regasa

By Tolcha Regasa 1
ISCHEMIC HEART
DISEASE(IHD)
09/22/2021
Objectives
2
 Overview of blood supply to CVS

 Define IHD
 Stable angina
 Acute coronary syndrome
 Cause acute ACS
 Pathogenesis of ACS
 Clinical features of ACS
 Diagnostic work up
 Treatment of CHD
By Tolcha Regasa 09/22/2021

3 By Tolcha Regasa 09/22/2021
• The intima, the innermost layer, overlies the muscular media demarcated by the
internal elastic lamina. The external elastic lamina separates the media from the
outer layer, the adventitia.
Atherosclerosis
6

Ischemic Heart disease.
8
 IHD is a syndrome that arises from imbalance

between oxygen demand and supply to the
myocardium.
 It is broadly divided into
-Chronic stable angina

-Acute Coronary syndrome
Acute coronary syndrome in turn is divided into
1-NSTEMI/UA
2-STEMI
The imbalance between oxygen supply and
9
demand will result in IHD
Clinical Definitions
09/22/2021 By Tolcha Regasa 10

Definition cont…..
• ACS refers to a spectrum of clinical presentations ranging from those for STEMI to
presentations found in NSTEMI or in UA

Major Risk Factors for Ischemic Heart Disease

Metabolic syndrome
Metabolic syndrome increases the risk of developing IHD and related
complications by twofold
According to a joint statement from several large organizations, including the
AHA, patients must meet at least three of the following criteria for the
diagnosis of metabolic syndrome
1. Increased waist circumference (40 inches [102 cm] or greater in men and
35 inches [89 cm] or greater in women)
2. Triglycerides of 150 mg/dL (1.70 mmol/L) or greater or active treatment to
lower triglycerides
3. Low high-density lipoprotein (HDL) cholesterol (less than 40 mg/dL [1.03
mmol/L] in men and less than 50 mg/dL [1.29 mmol/L] in women) or
active treatment to raise HDL cholesterol
4. Systolic blood pressure (BP) of 130 mm Hg or greater, diastolic BP of 85
mm Hg or greater, or active treatment with antihypertensive therapy.
5. Fasting blood glucose of 100 mg/dL (5.6 mmol/L) or greater or active
treatment
09/22/2021
for diabetes By Tolcha Regasa 13
Etiology of IHD
14
 Reduced myocardial oxygen supply

 atherosclerotic heart disease (vast majority)
 coronary vasospasm (variant angina)
 severe aortic stenosis or insufficiency
 thromboembolism
 severe anemia
 arteritis
 dissection
 congenital anomalies
Cont…
15
 increased myocardial oxygen demand

 Myocardial hypertrophy
 Severe tachycardia
 Severe hyperthyroidism
 Severe anemia

Cause of ACS
• The predominant cause of ACS in more than
90% of patients is atheromatous plaque
rupture, fissuring, or erosion of an unstable
atherosclerotic plaque that occludes less than
50% of the coronary lumen prior to the event,
rather than a more stable 70% to 90% stenosis
of the coronary artery

Cause cont’’
 Vasculitis syndrome
 Coronary embolism
 Congenital anomalies of coronary artery
 Coronary trauma or aneurysm
 Severe coronary artery spasm

 Increased blood viscosity
 Severe aortic stenosis

Pathogenesis
 >90 % plug disruption with platelets
aggregation followed by intracoronary
thrombus formation
 NSTEMI/UA-ACS Commonly due to imbalance
between oxygen supply and oxygen demand
resulting from a partially occluding thrombus
forming on a disrupted atherothrombotic
coronary plaque or on eroded coronary artery
endothelium.
Cont…
19
NSTEMI/UA-ACS may be occurred due to

(1) Dynamic obstruction (e.g., coronary spasm, as in
Prinzmetal’s variant angina [see “Prinzmetal’s Variant
Angina
(2) Severe mechanical obstruction due to progressive
coronary atherosclerosis; and
(3) Increased myocardial oxygen demand produced by
conditions such as fever, tachycardia, and
thyrotoxicosis in the presence of fixed epicardial
coronary obstruction.
20
 STEMI usually occurs when

 Coronary blood flow decreases abruptly after a
thrombotic occlusion of a coronary artery
previously affected by atherosclerosis.
 Coronary artery thrombus develops rapidly at a
site of vascular injury.

Cont…
21
 This injury is produced or facilitated by factors

such as cigarette smoking, hypertension, and lipid
accumulation. In most cases, STEMI occurs when
the surface of an atherosclerotic plaque becomes
disrupted (exposing its contents to the blood) and
conditions (local or systemic) favor
thrombogenesis.

Mechanism of coronary thrombus formation

Consequences of coronary thrombosis

Mechanism of cell death in MI

Clinical spectrum of IHD
Chronic coronary artery disease(CAD)
Acute Coronary syndromes (ACS)

 STEMI
 NSTEMI/UA

Stable angina/Angina pectoris
Angina is a clinical usually crescendo-
syndrome characterized decrescendo in nature,
by discomfort in the typically lasts 2 to 5
chest, jaw, shoulder, min, and can radiate to
back, or arm. either shoulder and to
It is typically aggravated both arms (especially
by exertion or emotional the ulnar surfaces of the
stress and relieved by forearm and hand).
nitroglycerin

Clinical classification of chest pain

Diagnostic work up…
Anginal equivalents
P/E- often normal Funduscopy

 Echo
Look for evidence of other  Stress test –ECG/imaging 
intermediate likelihood
atherosclerotic diseases  -risk estimation and
Look for risk factors prognosis
 Asses for risk factors

 Rest ECG-≤50% normal
 CxR

ACS diseases
NSTEMI
Unstable Angina
UA is
 ischemic discomfort with at least one of three features:
(1) it occurs at rest (or with minimal exertion), usually lasting >10
minutes;
(2)
 it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
(3) it occurs with a crescendo pattern (i.e., distinctly more severe,
prolonged, or frequent than previously).

points to think about!
About 6million persons/yr present to ED with a

complaint of chest pain or other symptoms suggestive
of ACS.
ACS is established in 20 to 25% of such patients.
The first step in evaluating ACS patients is to
determine the likelihood that CAD is the cause of the
presenting symptoms.
High likelihood: prior Hx of typical Acs, prior hx of
typical stable angina, hx of established CAD by angio,
prior MI, CHF, new ECG changes, or elevated CBM

Risk Stratifications Tools for Acute Coronary Syndrome

Killip classification of STEMI
 Killip class I -no signs of pulmonary or venous congestion
 Killip class II -moderate heart failure as evidenced by rales at
the lung bases, S3 gallop, tachypnea, or signs of failure of the

right side of the heart, including venous and hepatic congestion
 Killip III -severe heart failure, pulmonary edema;
 Killip class IV - shock with systolic pressure <90 mmHg and
evidence of peripheral vasoconstriction, peripheral cyanosis,

mental confusion, and oliguria

Clinical manifestation
36
 Chest pain is the usual presentation ( heavy,

squeezing, and crushing)
 Usually preceded by precipitants
 Occasionally it is described as stabbing or burning
 Patient often diaphoretic.
 The pain usually involves the central portion of the
chest /epigastrium and often radiates to the Lt.arm.
Less commonly radiates to abdomen, back, lower
jaw,
Cont…
37
 Anginal equivalents are atypical chest pain

syndromes in elderly individuals and diabetic
patient. It includes dyspnea, syncope, faintness,
epigastric discomfort etc.
 The index of suspicion of ACS must be high in
patients with diabetes.

Signs and symptoms

Work up for diagnosis

Lab work
40
 CBC
 EKG
 Cardiac Biomarkers
Troponin T and I
CKMB

ECGs

Cardiac biomarkers

Diagnosis of acute coronary syndrome.
43
-Unstable angina (UA) is a diagnosis by criteria

STEMI
Is diagnosed when there is evidence of ST segment
elevation on the ECG.

Differential Diagnosis
47
Differential diagnosis of ACS are all cause of an acute

chest pain which includes,
 Aortic dissection
 Acute pericarditis
 Pulmonary thromboembolism
 Pneumothorax
 Acute myocarditis
 Pneumonia
 Costochondritis , PUD, GERD and etc.

TREATMENT OF IHD

Desired Outcomes
• Short-term goals are:
– (a) early restoration of blood flow;
– (b) prevention of death and other MI complications;
– (c) prevention of coronary artery re-occlusion;
– (d) relief of ischemic chest discomfort; and
– (e) resolution of ST-segment and T-wave changes on the ECG.
• Long-term goal are:
– control of CV risk factors,
– prevention of additional CV events, including
• reinfarction,
• stroke, and
• HF, and
– improvement in quality of life.
Myocardial Ischemia
Rationale for treatment of myocardial ischemia:
Treatment of myocardial ischemia and the

resulting angina can involve two strategies:
1. Increase coronary blood flow by dilating
coronary arteries.
2. Reduce cardiac workload by reducing heart
rate and/or force of contraction

Myocardial Ischemia
Treatment of myocardial ischemia:

The treatment regimen may include :
1. nonpharmacologic treatment
2. pharmacologic therapies.
Nonpharmacologic treatment
• Pacing of physical activity.

• Avoidance of stress (emotional, physiologic,
cold).
• Reduction of risk factors for ischemic heart
disease, (hyperlipidemia, obesity, hypertension,
diabetes, smoking, etc.)
Pharmacologic treatment
Organic Nitrates
Mechanism of action:
• Dilate coronary arteries and increase myocardial blood flow.
• Dilate peripheral arteries and reduce afterload.
• Dilate peripheral veins and reduce preload.

Examples
Amyl nitrate, nitroglycerine, isosorbide dinitrite
Route of administration : Inhalation, sublingual, oral, transdermal, intravenous

Long-acting forms such as isosorbide dinitrite used for prophylaxis of angina
Short-acting forms such as sublingual nitroglycerin may be used during angina

attacks
Major adverse effects :include headache, hypotension. Tolerance may develop

rapidly.
β-Adrenergic blockers
Block myocardial β-adrenergic receptors.
Reduce heart rate and cardiac output (reduced myocardial
workload and oxygen demand).
Examples of β-Adrenergic Receptor Antagonists :
May be selective β1 (atenolol), or
nonselective β1 and β2 blockers (propranolol)
Major adverse effects :
include bradycardia, reduced cardiac output, pacemaker
depression and bronchoconstriction with nonspecific drugs
Calcium channel blockers

• Block calcium channels in vascular smooth muscle.
• Dilate coronary arteries and increase myocardial blood
flow.
Examples: Dihydropyridines (nifedipine), verapamil,
• Dilate peripheral arteries and reduce afterload.
diltiazem
Dihydropyridines have greater specificity for relaxing
vascular smooth muscle
Verapmail and diltiazem have greater effects on cardiac
pacemaker tissues
Major adverse effects include headache, hypotension, reflex

Afterload :The force that the contracting heart must
tachycardia; risk of
09/22/2021generate to eject blood. Affected by peripheral vascular
By Tolcha Regasa 54
resistance and arterial pressure.
Aspirin
• Prevent platelet aggregation.

• Use for prophylaxis of blood clots particularly in
unstable angina.

Surgical treatment
Coronary angioplasty
• Uses a balloon catheter to open occluded blood vessels
• Usually performed under local anesthetic
• 5% mortality, high rate of vessel re-occlusion
• Use of metal “stents” in opened vessel reduces rate of
occlusion
Coronary artery bypass graft

• Revascularization procedure in which a blood vessel is
taken from elsewhere in the body and surgically sutured
around a blocked coronary artery
• May involve multiple (one to five) blood vessels
• Re-occlusion of transplanted vessel is possible
General Approach
• For all STE MI and high- and intermediate-risk

NSTE ACS patients need,
– admission to hospital,
– oxygen administration(if S02 less than 90%),
– continuous ECG monitoring for arrhythmias and
ischemia,
– frequent measurement of vital signs,
– Bed rest for 12 hours in hemodynamically stable
patients,
– avoidance of the Valsalva maneuver (prescribe stool
softeners routinely), and
– pain relief.
Pharmacologic Interventions STEMI
1. INO2, SL NTG, morphine
2. Fibrinolytics
3. Unfractionated heparin
4. Enoxaparin /bivaluridin/fondaparinax
5. Dual platelet inhibition
6. Statin
7. Beta blocker
8. ACE inhibition for LV dysfunction
9. Consideration of minerocorticoid receptor
antagonism for LV dysfunction, e.g. EF < 40%
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Treatment
• Fibrinolytic Therapy for STE MI: The survival benefit
of fibrinolysis is highest with early administration and
diminishes after 12 hours.
• Fibrinolytic therapy is preferred over primary PCI in
patients presenting,
– within 3 hours of symptom onset
– where there is a delay in “door-to-primary PCI” less than
90 minutes.
• Fibrinolytic therapy is not indicated in
– any patient with NSTE ACS because increased
mortality has been reported with fibrinolytics
compared with controls in clinical trials.
Nonpharmacologic Therapy
Primary PCI for STE MIs
• Results from a meta-analysis of trials comparing
fibrinolysis with primary PCI indicate a lower
mortality rate with primary PCI.
• The reason is that
– more than 90% of occluded infarct-related coronary
arteries are opened with primary PCI
– fewer than 60% of coronary arteries opened with
currently available fibrinolytics.
– intracranial hemorrhage (ICH) and major bleeding risks
from primary PCI is low
Huynh T, Perron S, O’Loughlin J, et al. Comparison of primary PCI and fibrinolytic therapy in
STSE MI: meta-analyses of RCT and observational studies. Circulation 2009;119:3101–3109.
Dual anti platelet therapy
• Because of increased bleeding risk in patients
receiving ASA plus a P2Y12 inhibitor compared
with ASA alone,
– low-dose ASA (81 mg daily) is preferred following
– ASA dose of 162 to 325 mg,
• Although not FDA approved, a clopidogrel
loading dose of 600 mg is recommended
– over administration of 300 mg for patients
undergoing PCI.

ACS
PT in
A
6D
201
A
AH
From
Clopidogerel and omeprazole
• The production of clopidogrel’s active metabolite
and consequently its antiplatelet effect is reduced
by,
– moderate and strong inhibitors of CYP2C19
• A genetic variations in the gene coding for CYP2C19
– significantly modulate the antiplatelet effects of
clopidogrel.
– Hence, ticagrelor or prasugrel may be considered.
• meta-analysis of, concomitant clopidogrel-PPI
therapy following
– PCI appears to be significantly associated with adverse
Michael A.cardiovascular events. of clopidogerel and PPI Academy of Managed Care
Serbin et al. A Meta-analysis
Pharmacy.
09/22/2021
2016;22(8):939-47 By Tolcha Regasa 64
Anticoagulants (1)
For patients undergoing primary PCI, either
– UFH or
– bivalirudin is preferred,
• There is no formal recommendation by the ACCF-AHA regarding the
use of enoxaparin in STEMI.
• The ESC provides a class IIb recommendation for its use during PCI,
stating that it may be preferred over UFH.
whereas for fibrinolysis,
– UFH,
– enoxaparin, or
– fondaparinux may be administered.
• The use of enoxaparin has been more extensively studied and proven
in conjunction with fibrinolysis,
– and it therefore carries a class I recommendation from both ACC/AHA and
ESC guidelines for up to 8 days in patients with STEMI treated medically.
Anticoagulants (2)
Unfractionated heparin dosing,
• UFH has a pharmacokinetic profile with large
inter individual variability and a narrow
therapeutic window.
– Weight-adjusted i.v. administration with an initial
bolus of 60–70 IU/kg up to a maximum of 5000 IU,
• Followed by an infusion of 12-15IU/kg/h up to
a maximum of 1000 IU/h, is recommended.

B.B indication
• β-Blockers should be continued for,
– at least 3 years in patients with normal LV
function and
– indefinitely in patients with LV systolic dysfunction
and an LVEF less than or equal to 40% (0.40).
• IV BB, should be limited to patients who
present with
– hypertension (HTN) and/or
– have ongoing signs of myocardial ischemia and
– do not demonstrate any signs or symptoms of
acute HF.
B.B contraindication
• A registry study of 21 822 NSTEMI,
– patients with pulmonary edema and at risk of
developing cardiogenic shock
• (i.e. age >70 years, heart rate >110 beats/min,
• systolic blood pressure <120 mmHg)
– the observed shock or death rate was significantly increased in
patients receiving beta-blockers within 24 h of hospital
admission.
– Beta-blockers should not be administered in
patients
• coronary vasospasm or
• cocaine use
ESC 2015 ACS management guideline
RAAS system blockers
• ACE inhibitor or ARB,
– Should be initiated within the first 24 hours of
patients presenting with ACS,
• who have pulmonary congestion,
• HF,
• STEMI with anterior location, or
• Left ventricular ejection fraction (LVEF) < 40% in the
– absence of contraindications to therapy (strength
of recommendation A).

RAAS system blockers
• EPHESUS (Eplerenone Post-Acute Myocardial Infarction
Heart Failure Efficacy and Survival Study) found that
– eplerenone reduced morbidity and mortality rates for
patients with MI complicated by
• LV dysfunction and
• either CHF or diabetes mellitus.
• Long-term administration of eplerenone is indicated for
selected patients,
– in the absence of severe renal dysfunction or hyperkalemia.
Pitt B, et al; Eplerenone, a selective aldosterone blocker, in patients with left ventricular
dysfunction after myocardial infarction N Engl J Med.2003

Statin in ACS
• It is recommended to initiate or continue statin
therapy in all patients presenting with ACS and
no contraindications to its use
– (strength of recommendation A).
• High-intensity statin therapy following an ACS
– confer an absolute risk reduction of 3.9% as
compared with a moderate intensity statin,
• for the composite endpoint of death from any cause,
• recurrent MI,
• UA requiring rehospitalization,
• revascularization, and stroke
– (level of evidence 1).
Jennifer N. et al. CLINICAL REVIEW, Diagnosis and Management of Acute Coronary
Syndrome: An Evidence-Based Update
09/22/2021 By 2015
Tolcha Regasa 71
Statin in ACS
• Following ACS even in patients with baseline LDL

levels of <70 mg/dL.
• ACC and AHA Guidelines on treatment of
cholesterol recommend
– high intensity statins (ie, atorvastatin >=40 mg daily or
rosuvastatin >=20 mg daily)
– for high-risk patients, which include patients who have
an ACS event.
• Lower-dose statins can be considered if patients
are75 years old or if patients cannot tolerate high-
intensity statins (strength of recommendation A).
Jennifer Net al. CLINICAL REVIEW, Diagnosis and Management of Acute Coronary
Syndrome: An Evidence-Based Update
09/22/2021 By 2015
Tolcha Regasa 72
2016 ACC Expert Consensus Decision Pathway on the Role of Non-Statin Therapies for LDL-
Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk
a: Early hospital care consists of oxygen for
oxygen saturation
<90%, SL nitroglycerin, IV nitroglycerin, IV
morphine, β-blocker, ACE inhibitor or ARB,
aldosterone antagonist,
stool softener, and statin.
b: standard indications, dosing, and
contraindications.
c: For at least 48 hours.
d: For the duration of the hospitalization, up to
8 days.

Primary PCI
• Early reperfusion therapy with primary PCI of the infarct artery within 90 minutes
from time of hospital presentation is the reperfusion treatment of choice for patients
with STEMI who present within 12 hours of symptom onset
• Current guidelines indicate that the time from first medical contact to device should
be less than or equal to 90 minutes, with every effort made to ensure the time to
reperfusion is as short as possible
• PCI during hospitalization for STEMI may also be appropriate in other patients
following STE MI
- those in whom fibrinolysis is not successful
- those presenting later in cardiogenic shock
- those with life-threatening ventricular arrhythmias, and those with persistent rest
ischemia or signs of ischemia on stress
09/22/2021 By Tolchatesting
Regasa following M 78
PCI
• All patients undergoing PCI should receive low-
dose aspirin (ASA) therapy indefinitely.
• A P2Y12 inhibitor antiplatelet (clopidogrel,
prasugrel, or ticagrelor) should be administered
concomitantly with ASA for at least 12 months
following PCI for a patient with ACS
• Read bout use of dual antiplatelet therapy in bare
metal stent vs drug-eluting stent ( duration of
therapy, importance of stent)

Fibrinolytics Therapy
• Administration of a fibrinolytic agent is indicated in patients with STEMI who present to the
hospital within 12 hours of the onset of chest discomfort, who are initially seen at a non-PCI-
capable hospital and who have an anticipated time from first medical contact-to-device
greater than 120 minutes if transferred to a PCI capable hospital
• The reduction in mortality with fibrinolysis is greatest with early administration and
diminishes after 12 hours
• Because administration of fibrinolytics result in clot lysis, patients who are at high risk of
major bleeding (including ICH) presenting with an absolute contraindication should not
receive fibrinolytic therapy; primary PCI is preferred
• Fibrinolytic therapy is not indicated and should not be used in patients with NSTE-ACS
because increased mortality has been reported with these agents compared with controls in
clinical trials

Fibrinolytic Therapy

Indications and Contraindications to Fibrinolytic Therapy Per
ACC/AHA Guidelines for Management of Patients with ST-
Segment Elevation Myocardial Infarction

Early Invasive Therapy for
NSTE-ACS
• Clinical practice guidelines recommend coronary angiography followed by
either PCI or coronary artery bypass graft (CABG) surgery revascularization
as an early treatment (early invasive strategy) for patients with NSTE-ACS at
an elevated risk for death or MI, including those with a high risk score
• or patients with refractory angina, hemodynamic instability or electrical

instability
• An early invasive approach results in a long-term reduction in the rates of CV

death or MI, with the largest absolute effect seen in higher risk patients

Treatment…
• All patients undergoing PCI should receive ASA therapy

indefinitely.
• A P2Y12 inhibitor antiplatelet (clopidogrel, prasugrel, or

ticagrelor) should be administered concomitantly with ASA
for at least 12 months following PCI for a patient with ACS

Ischemia-Guided Therapy for
NSTE-ACS
• For patients with NSTE-ACS, an initial ischemia-guided strategy is
recommended for patients with a low risk score, normal ECGs, and negative
troponin tests who are without recurrence of chest discomfort
• Stress test
- recurrent ischemia: angiography and then PCI
- Low risk: optimal medical therapy
• Patients with NSTE-ACS at low risk for recurrent CHD events following stress
testing should be given ASA indefinitely and either clopidogrel or ticagrelor for
up to 12 months following hospital discharge in addition to other secondary
preventative pharmacotherapy

Early pharmacologic therapy
All patients should receive anti-
ischemic and analgesic
medications early in care.
“MONA” plus β-blocker

Antiplatelet Management Strategies in ACS

GP IIb/IIIa Inhibitor Dosing in ACS with or Without PCI

Anticoagulant Management Strategies in ACS

Long-term therapy
Dual antiplatelet therapy
Beta-blocker
ACEI/ARB
MRA
Lipid management: high intensity statins

Process of Care Quality Performance
Measures for Myocardial Infarction

Summary of IHD
94
-Management of NSTEMI/UA is similar to

management of STEMI except that patients with
STEMI need a thrombolytics if they present in a
specific time window.

Management of STEMI in
95
summary
 ASA 160-325 mg chewed followed by maintenance ASA at a dose of 75-162mg
 The P2y12 receptor inhibitors like clopidogrel should be added to ASA .
prasugrel and Ticagrelor are more effective but bleeding
 Oxygen ( 2-4litres/m) in those who need it
 Sublingual nitroglycerin 0.4mg every 5 min for up to 3 doses, if no response, IV
 Morphine IV 2-4mg every 5 minutes
 IV B-blockers
A commonly employed regimen is metoprolol, 5 mg every 2–5 min for a total of
three doses, provided the patient has a heart rate >60 beats/min, systolic pressure
>100 mmHg, a PR interval <0.24 s, and rales that are no higher than 10 cm up
from the diaphragm. Fifteen minutes after the last intravenous dose, an oral
regimen is initiated of 50 mg every 6 h for 48 h, followed by 100 mg every 12 h.

Cont…
96
 For patients who present in less than 12 hrs of symptom onset,

IV thrombolytics should be given. Ideally the first 3hrs is
ideal ( reteplase,alteplase,tenecteplase,urokinase,streptokinase
etc )
 PCI should be done in patients who present with heart failure
and cardiogenic shock.
 Glycoprotein IIb/IIIa receptor inhibitors like absciximab
appear useful for preventing thrombotic complications in
patients with STEMI undergoing PCI.
 UFH at a dose of an initial bolus of 60 U/kg (maximum 4000
U) followed by an initial infusion of 12 U/kg per hour
(maximum 1000 U/h). The activated partial thromboplastin
time during maintenance therapy should be 1.5–2 times the
Cont…
97
 Alternatives to UFH for anticoagulation of patients with STEMI

are the low-molecular-weight heparin (LMWH) preparations, a
synthetic version of the critical pentasaccharide sequence
(fondaparinux), and the direct antithrombin bivalirudin.
 ACEI/ARBs
The maximum benefit is seen in high-risk patients (those who are

elderly or who have an anterior infarction, a prior infarction,
and/or globally depressed LV function), but evidence suggests that
a short-term benefit occurs when ACE inhibitors are prescribed
unselectively to all hemodynamically stable patients with STEMI
(i.e., those with a systolic pressure >100 mmHg).

Cont…
98
 Long-term aldosterone blockade like spirinolactone

should be prescribed for STEMI patients without
significant renal dysfunction (creatinine ≥2.5
mg/dL in men and ≥2.0 mg/dL in women) or
hyperkalemia (potassium ≥5.0 mEq/L) who are
already receiving therapeutic doses of an ACE
inhibitor, have an LV ejection fraction ≤40%, and
have either symptomatic heart failure or diabetes
mellitus.

Complications
• The most serious complication of MI,
– is cardiogenic shock, (5% to 6% ).
• Mortality approaching 60%.
• Other complications are,
– HF, valvular dysfunction,
– bradycardia, heart block,
– stroke secondary to left ventricular thrombus embolization,
– ventricular septal rupture,
– left ventricular aneurysm formation, and
– ventricular and atrial tachyarrhythmias.
• ¼ of MI patients die, from ventricular fibrillation,
– prior to reaching the hospital.
Generally complications of MI are
 Arrhythmias – PVCs, VTs/Vf, SVT,…
 Pump failure- LV dysfunction, Cardiogenic shock, Rt
ventricular infarction( RVI)
 Others – recurrent chest discomfort,
pericarditis, thromboembolism, LV aneurysm

Reference
1. Eric R. Bates et al. 2016 ACC/AHA Guideline Focused
Update on Duration of Dual Antiplatelet Therapy in
Patients With Coronary Artery Disease.
2. Joseph Dipiro 10th edition, pharmacotherapy a
pathophysiologic approach.
3. 2015 ESC Guidelines for the management of acute
coronary syndromes in patients presenting without
persistent ST-segment elevation.
4. ACC and AHA 2013 guideline for ACS management
5. HIGHLIGHTS OF PRESCRIBING INFORMATION for
clopidogerel 2016 up todate.
THANK YOU!!!!!!!

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By Tolcha Regasa 1

 Overview of blood supply to CVS

 Clinical features of ACS

By Tolcha Regasa 09/22/2021

By Tolcha Regasa 09/22/2021

 IHD is a syndrome that arises from imbalance

-Chronic stable angina

09/22/2021 By Tolcha Regasa 10

09/22/2021 By Tolcha Regasa 11

09/22/2021 By Tolcha Regasa 12

 Reduced myocardial oxygen supply

 increased myocardial oxygen demand

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 Severe coronary artery spasm

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NSTEMI/UA-ACS may be occurred due to

 STEMI usually occurs when

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 This injury is produced or facilitated by factors

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Acute Coronary syndromes (ACS)

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P/E- often normal Funduscopy

 Asses for risk factors

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About 6million persons/yr present to ED with a

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 Killip class II -moderate heart failure as evidenced by rales at

the lung bases, S3 gallop, tachypnea, or signs of failure of the

 Killip class IV - shock with systolic pressure <90 mmHg and

evidence of peripheral vasoconstriction, peripheral cyanosis,

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 Chest pain is the usual presentation ( heavy,

 Anginal equivalents are atypical chest pain

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-Unstable angina (UA) is a diagnosis by criteria

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Differential diagnosis of ACS are all cause of an acute

 Costochondritis , PUD, GERD and etc.

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Rationale for treatment of myocardial ischemia:

Treatment of myocardial ischemia and the

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Treatment of myocardial ischemia:

• Pacing of physical activity.

• Dilate peripheral arteries and reduce afterload.

• Dilate peripheral veins and reduce preload.

Amyl nitrate, nitroglycerine, isosorbide dinitrite