Ischemic heart disease (IHD) is caused by an imbalance between myocardial oxygen supply and demand. The most common cause is atherosclerosis leading to decreased blood flow. IHD presents as stable angina, acute coronary syndrome (ACS), or sudden cardiac death. ACS includes ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (UA). STEMI is diagnosed based on ECG changes and cardiac enzyme levels and requires emergency reperfusion therapy. Risk factors include age, family history, smoking, diabetes, hypertension, and dyslipidemia. Management involves antithrombotic therapy, anti-ischemic drugs, revascularization, and controlling cardiovascular risk factors
2. INTRODUCTION
Ischemic heart disease (IHD)
is a condition in which there is an inadequate supply of
blood and oxygen to a portion of the myocardium;
it typically occurs when there is an imbalance between
myocardial oxygen supply and demand
2
4. ETIOLOGY
Decreased coronary blood flow due to
mechanical obstruction: Atheroma, CA spasm,
thrombosis, embolus, coronary
arteritis(SLE,PAN)
Increased O2 requirement: thyrotoxicosis,
myocardial hypertrophy(AS,HTN)
Decreased flow of oxygenated blood to
myocardium: anemia, hypotension, CO
poisoning
N.B: Atheroma is the most common cause of
IHD 4
5. EPIDEMIOLOGY
IHD is the leading cause of morbidity and mortality in
developed countries.
The prevalence of IHD is also increasing in developing
countries
It is likely to become the most common cause of death
worldwide by 2020
Commonly affects Elderly, Men,…
Among patients with ACS, approximately 60% have UA
and 40% have MI.
Of the patients with MI two third have NSTEMI and one
third have STEMI
5
6. RISK FACTORS
Non- modifiable
-Age(men>45, female>55)
-Sex
-Family history of premature CAD
-Race
6
7. CONT’D….
Modifiable
Smoking
DM, HTN
Dyslipidemia
Hypercholesterolemia
Obesity
Type A Personality
Lack of exercise
Psychosocial stress
7
8. CONT’D….
It has four spectrums of presentation
1. Asymptomatic
2. Ischemic cardiomyopathy
3. Sudden cardiac death
4. Symptomatic phase
a) Chronic Coronary artery disease(CAD): Stable
Angina
b) Acute coronary syndrome:
ST-segement elevation MI(STEMI)
Non-ST-segement elevation MI(NSTEMI)
Unstable angina(UA )
8
9. STABLE ANGINA PECTORIS
Occurs when coronary perfusion is impaired by
fixed/stable atheroma of coronary arteries
The typical patient with angina is a man older
than 50 years or a woman older than 60 years of
age with risk factors for atherosclerosis
9
10. CLINICAL FEATURES
Presents with a chest discomfort:
usually described as heaviness, pressure, squeezing,
smothering, or choking
It is retrosternal in location with radiation to either shoulder
and to both arms (especially the ulnar surfaces of the
forearm and hand).
It can also arise in or 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
Ttypically lasts 2–5 min
typically exertional (e.g., exercise, hurrying, or sexual
activity) or emotion (e.g., stress, anger, fright, or
frustration) and are relieved by rest but they may also
10
11. CONT’D….
Anginal "equivalents“:
are symptoms of myocardial ischemia other than
These include dyspnea, nausea, fatigue, and faintness,
and
are more common in the elderly and in diabetic
Elderly could present with indigestion: dyspepsia like
presentation
Could be asymptomatic in DM
11
12. CONT’D….
The patient with angina should be questioned and
examined for peripheral arterial disease, stroke, or
transient ischemic attacks
Angina occurs more commonly in the morning due
to a diurnal increase in sympathetic tone
They can have associated symptom like shortness of
breath, dizziness, fainting, chocking sensation
12
13. SIGNS
During the attack looks anxious, dyspnea, pale, cold
sweet but normal in b/n.
risk factors for atherosclerosis, such as xanthelasmas,
xanthomas and hypertension
evidence of atherosclerotic disease at other sites: carotid
bruits, PAD
ischemia can cause transient LV failure with the
appearance of a third and/or fourth heart sound, a
dyskinetic cardiac apex, mitral regurgitation, and even
pulmonary edema
13
14. INVESTIGATIONS
STRESS ECG:
ST segment depression with or with out T wave
inversion
RESTING ECG: normal or evidence of old infarct
Coronary angiography
FBS,
lipid profile,
RFT,
serum electrolyte,
U/A,
Hgb 14
15. MANAGMENT OF ANGINA
1. explanation of the problem and reassurance about the
ability to formulate a treatment plan
2. identification and treatment of aggravating conditions
3. recommendations for adaptation of activity as needed
4. treatment of risk factors that will decrease the
occurrence of adverse coronary outcomes
5. drug therapy for angina: CCB, Nitrates, B-blockers
6. Preventive therapies: antiplatlates
7. consideration of revascularization
15
16. CONT’D….
Mnemonic to remember the mx of SA
A. Antiplatlates
B. B-blockers, BP control
C. Cigarate smocking cessation, Cholesterol
control, CCB with indication
D. Diabetes control, Dietary modification
E. Education, Exercise
F. Follow up
16
17. ACUTE CORONARY SYNDROM
is a group of clinical entities characterized by severe,
acute myocardial ischemia or infarction resulting from
thrombotic occlusion of coronary arteries.
is a medical emergency and should be managed in the
ICU.
17
18. It comprises
1. ST segment elevation MI(STEMI)
2. Non-ST segment elevation MI
3. Unstable angina(UA)
18
20. DIAGNOSTIC CRITERIA FOR ACUTE MYOCARDIAL
INFARCTION
Typical rise and gradual fall (troponin) or more
rapid rise and fall (CK-MB) of biochemical
markers of myocardial necrosis with at least one
of the following:
a) Ischemic symptoms
b) Development of pathologic Q waves on the
ECG
c) ECG changes indicative of ischemia (ST
segment elevation or depression)
d) Coronary artery intervention (eg, angioplasty)
e) Imaging evidence of new loss of myocardium
or new regional wall motion abnormality
Pathologic findings of an acute MI
20
21. CONT’D….
UA is considered to be present in patients with
ischemic symptoms suggestive of an ACS and no
elevation in troponins or CK-MB, with or without
ECG changes indicative of ischemia (ex. ST
segment depression or transient elevation or
new T wave inversion)
21
22. UA/NSTEMI
UA is defined as angina pectoris or equivalent
ischemic discomfort with at least one of three
features:
1. It occurs at rest (or with minimal exertion), usually
lasting >10 min
2. It is severe and of new onset (i.e., within the prior
4–6 weeks)
3. It occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than
previously)
No elevation of cardiac markers
With or without ECG changes indicative of ischemia
22
23. CONT’D…
NSTEMI is defined
with the clinical features of UA
evidence of myocardial necrosis, as reflected in
elevated cardiac biomarkers
Persistent ST segment/ T-wave changes
23
24. PATHOPHYSIOLOGY
UA/NSTEMI is most commonly caused by a reduction in
oxygen supply and/or by an increase in myocardial
oxygen demand superimposed on an atherosclerotic
coronary plaque, with varying degrees of obstruction
1. Plaque rapture or erosion with superimposed
nonocclusive thrombus(the most common cause)
2. Dynamic obstruction
3. Progressive mechanical obstruction (e.g., rapidly
advancing coronary atherosclerosis)
4. Secondary UA related to increased myocardial oxygen
demand and/or decreased supply (e.g., tachycardia,
anemia)
More than one pathogenetic mechanism can work at a time
24
25. CLINICAL FEATURES
The clinical hallmark of UA/NSTEMI is chest pain
Anginal "equivalents’’
The examination resembles that in patients with stable
angina and may be unremarkable
If the patient has a large area of myocardial ischemia or
a large NSTEMI, the physical findings can include:
diaphoresis, pale cool skin,
sinus tachycardia, a third and/or fourth heart sound,
basilar rales, and sometimes hypotension, resembling
the findings of large STEMI
25
26. INVESTIGATIONS
ECG:
UA: Transient ST/T wave changes if at all
NSTEMI:ST segment depression, T wave changes
Cardiac enzymes: troponin and CK elevated in NSTEMI
CBC,RFT,blood glucose,lipid profile,serum electrolyte
CXR:pulmonary edema
Stress test
ECHO
Angiography
26
28. CONT’D….
ANTITHROMBOTIC THERAPY
Aspirin loading162 to 325 mg. and maintenance 75 mg
po per day. The first tablet should be chewed to establish
a high blood level quickly
Clopidogrel given in combination with aspirin leads to
significant benefits in patients with non-ST elevation ACS
A glycoprotein IIb/IIIa inhibitor should be given, in
addition to ASA, clopidogrel, and heparin, when there is
continuing ischemia, an elevated serum troponin or
other high-risk features and the patient is scheduled for
angiography
In patients with a non-ST elevation ACS, anticoagulant
therapy should be added to antiplatelet therapy
Thrombolytic therapy should not be administered to
patients with UA or NSTEMI
28
31. ADDITIONAL TREATEMENTS
ACEIs: for patients with diabetes, heart failure, a left ventricular
ejection fraction <40 percent, and hypertension. ACE inhibitors are
started in-hospital but not necessarily in the first 24 hours
ARBs
Statins: atrovastatin at a dose of 80mg/day for all patients irrespective of lipide
profile
Aldosterone antagonist
Are receiving an ACE inhibitor
Have an LVEF 40 percent
Have either symptomatic heart failure or diabetes
Have a creatinine clearance >30 ml/min
Have a serum potassium <=5.0 meq/L
31
33. CLINICAL PRESENTATION
Anginal pain:
Quality: heavy, squeezing, and crushing, although
occasionally it is described as stabbing or burning
Site: typically the pain involves the central portion of the
chest and/or the epigastrium, and on occasion it
to the arms, abdomen(above umbilicus), back, lower
precipitating factors: vigorous physical exercise,
emotional stress, or a medical or surgical illness-up to
pts
onset the time of onset of STEMI has a pronounced
circadian periodicity, with peak incidence of events
between 6 am and noon due to:
• Increase in cathecolamine and cortisol level
• increases in platelet aggregability
Relieving factor: pain may commence when the patient
at rest, but when it begins during a period of exertion, it
does not usually subside with cessation of activity, in
33
34. CONT’D
Duration: the pain is prolonged, usually lasting for more than 30
minutes and frequently for a number of hours
Severity: the pain of STEMI varies in intensity; in most
patients, it is severe and in some instances intolerable
Associated symptoms: it is often accompanied by weakness,
sweating, nausea, vomiting, anxiety, and a sense of impending
doom
34
35. CONT’D……
Atypical presentations of STEMI include the following:
Heart failure (i.e., dyspnea without pain beginning de novo or
worsening of established failure)
Classic angina pectoris without a particularly severe or prolonged
episode
Atypical location of the pain
Central nervous system manifestations, resembling those of stroke,
secondary to a sharp reduction in cardiac output in a patient with
cerebral arteriosclerosis
Apprehension and nervousness,Sudden mania or psychosis
Ssyncope
Ooverwhelming weakness
Acute indigestion
Peripheral embolization
35
36. CONT’D…
Silent STEMI: occurs more commonly in patients
without antecedent angina pectoris and in
patients with diabetes and hypertension
The prognoses of patients with silent and
symptomatic presentations of STEMI appear
quite similar
36
37. SIGNS
General appearance: anxious,restless and may be in cardiopulmonary distress
Vital signs:
o PR: the heart rate can vary from a marked bradycardia to a rapid
regular or irregular tachycardia
o BP: it is determined by the degree of infarction,site of infarction and the +/- of
hypertension prior to infarction.
o T0 : febrile(38.3° to 38.9° C (101° to 102° F)
most patients with extensive STEMI develop fever,
a nonspecific response to tissue necrosis, within 24 to 48 hours of
the onset of infarction.
Body temperature often begins to rise within 4 to 8 hours after the
onset of infarction
Fever usually resolves by the fourth or fifth day after infarction
o RR: tachypnea due to pulmonary congestion or anxiety 37
38. CONT’D……
Chest: Rales, wheeze, bilateral effusion
JVP increased In RV anterior wall MI
Arterial pulse character: a small pulse suggests a reduced stroke
volume, whereas a sharp, brief upstroke is often observed in
patients with mitral regurgitation or ruptured ventricular septum with
a left-to-right shunt. Pulsus alternans reflects severe left ventricular
dysfunction
Precordium: the precordium is usually quiet, and the apical impulse
may be difficult to palpate. In patients with transmural infarction systolic
and presystolic pulsations may be felt.On auscultation one may hear S3 and S4
heart sounds and murmur of MR and friction rub
Abdomen: hepatic congestion
IS: in the presence of cardiogenic shock the skin is cool and clammy, with
a bluish or mottled color over the extremities, and there is marked
facial pallor with severe cyanosis of the lips and nailbeds
MSS: Edema
CNS: include funduscopic examination
38
39. KILLIP CLASSIFICATION OF AMI
Class I - no evidence of HF
Class II - findings consistent with mild to
moderate HF (S3, rales , or jugular venous
distension)
Class III - overt pulmonary edema
Class IV - cardiogenic shock
39
40. INVESTIGATIONS
ECG
Typical ST segment elevation persists for hrs and
is followed by inversion of T waves during first few days
and by development of pathologic Q waves
40
43. CONT’D….
Cardiac enzymes: troponin, creatin kinase(CK),
myoglobin, LDH
Cardiac troponin(I and T)
Normally not found in serum
More sensitive and specific than ck and
myoglobin
Start to raise at 3-12 hrs., peak at 18-48hrs and
return to baseline over 5-14 days
Serial measurement is required
Elevated if it is >=0.01ng/ml(20times normal)
43
44. CONT’D….
CK- has limited value b/c:
It disappear early( after 48-72hrs)
can be released by other tissues
Need more tissue injury for detection
Myoglobin
Highly sensitive
Nonspecific b/c it can be released by sk. Mm
damage
44
47. CONT’D….
Echo: Ejection Fraction, wall motion abnormality,
pericardial effusion, valve morphology
BNP: not recommended for DX rather risk stratification
and prognosis
Angiography
CBC: leukocytosis, to rule out anemia
Other: RFT, FBS, Lipid profile, Serum electrolyte U/A,
47
48. RISK STRATIFICATION
This determine
-Patient outcomes
-The risk of recurrence and
-The effectiveness of specific treatments
30 days risk of death ranges from 1-10%
Global risk is assessed by scoring system
such as TIMI trial which involves 7
independent risk factors
48
51. GOALS OF THERAPY IN STEMI
Relief of ischemic pain
Assessment of the hemodynamic state and correction of
abnormalities that are present
Initiation of reperfusion therapy with primary percutaneous coronary
intervention (PCI) or fibrinolysis
Antithrombotic therapy to prevent rethrombosis or subtotal stenosis
at the site of an ulcerated plaque
Antiplatelet therapy to reduce the risk of recurrent coronary artery
thrombosis or, with PCI, coronary artery stent thrombosis
Prevention of left ventricular remodeling with an angiotensin
converting enzyme (ACE) inhibitor
Prevention of recurrent ischemia and life-threatening ventricular
arrhythmias with beta blockers
Cholesterol lowering with a statin to prevent or slow disease
progression; the benefit of statins may be mediated by pleiotropic
effects in addition to its effect on serum lipids
51
52. CON . . .
Once ACS is diagnosed, the acute management of the patient
involves:-
1. Bed rest in patients with chest pain with continuous
ECG monitoring.
2. Provide oxygen 2-4l/min for the first 6-12hr if patients
has:-
SaO2 <90%
respiratory distress
other high risk features for hypoxemia .
52
53. CON . . .
3.Antithrombotic therapy
Double Antiplatelet
Aspirin and clopidogrel
Clopidogrel can be given in combination with aspirin for 1
yr and it has significant long term benefits in patients with
NSTMI/UA .
Anticoagulants:
Heparin for 5-7 days
53
54. CONT’D . . .
4. Anti ischemic therapy
Nitroglycerin: Three doses of sublingual nitroglycerine
0.4 mg Q 5 minute if pain persists
Beta blockers: IV to relieve pain, prevent reinfarction
and AF. Preferably Metoprolol 5 mg every 2-5 min.
Morphine—if pain persists, morphine sulfate 2-4 mg
IV repeated every 5 minutes.
should be given for relief of persistent chest pain or anxiety despite
nitroglycerine and beta blockers
Contraindicated if hypotensive
54
55. CONT’D….
5.GI prophylaxis and bowl care
omeprazole 20 mg PO BID routine and laxatives for constipation
6.Glucose and electrolyte
Keep RBS level b/n 140-180 mg/dl
Keep serum K+ level >4 meq/l
Magnesium >2 mmol/l
55
56. CON . . .
7. Long term medications
Beta blockers, statins, ACE-I, aspirin and clopidogrel
Clopidogrel and aspirin should be continued for 9-12 month with
aspirin continued thereafter.
56
58. CON . . .
9.Return to activities
Most patients with uncomplicated course can return to
activities after 2-4weeks
Should be advised to slowly increase the level of
exertion watching for symptoms e.g. walking distance.
58
Notas del editor
manifests due to an imbalance in myocardial oxygen supply and Demand, Ventricular fibrillation. Other causes of death include cardiac rupture, pump failure due to massive infarction, acute mechanical complication such as ventricular septal rupture or acute mitral regurgitation, and cardiogenic shock .cause of death in z 1st 48 hrs
change in the life style associated with urbanization including sedentary life style,
smoking, obesity high fat and energy diet and the associated increased prevalence
in Diabetes mellitus it is likely to become the most common cause of death worldwide by 2020