Ischemic Heart Disease

Dr Asfaw Tadesse
 Ischemic heart disease (IHD)
• 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.
• The most common cause of myocardial ischemia
is atherosclerotic disease of an epicardial
coronary artery (or arteries)
• IHD is likely to become the most common cause
of death worldwide by 2020.
 Epidemiology
• IHD causes more deaths and disability and incurs
greater economic costs than any other illness in the
developed world.
• IHD is the most common, serious, chronic, life-
threatening illness in the USA ,where:
 13 million persons have IHD,
 >6 million have angina pectoris, and
 >7 million have sustained a MI
• In the developed world, it is growing among low-
income groups rather than high-income groups
• primary prevention has delayed the disease to
later in life in all socioeconomic groups
 …………IHD
• Obesity, insulin resistance, and type 2 DM are
increasing and are powerful risk factors for IHD.
• A high-fat and energy-rich diet, smoking, and a
sedentary lifestyle are associated with the
emergence of IHD.
• With urbanization in the developing world, the
prevalence of risk factors for IHD is increasing
rapidly in these regions such that a majority of
the global burden of IHD is now occurring in low-
income and middle-income countries
 ………………..IHD
• Patients with ischemic heart disease fall into two
large groups:
– patients with chronic coronary artery disease (CAD)
who most commonly present with stable angina and
– patients with Acute Coronary Syndromes (ACSs)
• acute coronary syndromes (ACSs) is composed of
patients with
– acute myocardial infarction (MI) with ST-segment
elevation on their presenting ECG(STEMI) and
– those with unstable angina and non-ST-segment
elevation MI (UA/NSTEMI)
 Stable angina pectoris
• Stable angina pectoris is characterized by
chest or arm discomfort that may not be
described as pain but is reproducibly
associated with physical exertion or stress
and is relieved within 5–10 min by
 rest and/or
sublingual nitroglycerin
 Pathophysiology of AP
• Imbalance of myocardial supply and demand is
central for myocardial ischemia
• The major determinants of myocardial oxygen demand
(MVO2) are
 heart rate,
 myocardial contractility, and
 myocardial wall tension (stress).
• An adequate supply of oxygen to the myocardium
requires:
– a satisfactory level of oxygen-carrying capacity of the
blood and
– an adequate level of coronary blood flow.
• Majority of blood flows through the coronary
arteries occurs during diastole
 …………AP
• reducing the lumen of the coronary arteries,
atherosclerosis limits appropriate increases in
perfusion when the demand for flow is
augmented, as occurs during exertion or
excitement
• When a stenosis reduces the diameter of an
epicardial artery:
 By 50% there is a limitation on the ability to increase
flow to meet increased myocardial demand.
 by ~80%blood flow at rest may be reduced cause
myocardial ischemia
 Risk factors for CAD / IHD
• Age: the risk of CAD increases progressively with age.
• Gender : IHD is more prevalent in men than in women
– The difference is more marked in premenopausal women compared to
men of similar age
• Lipid abnormalities :
– increased serum LDL level and reduced HDL level with hypertriglyceridemia
favors the deposition of lipids and cholesterol in atherosclerotic plaques
• Smoking :
– cigarette smokers are 60% more likely to develop CAD than non smokers
• Hypertension: increases the risk of CAD both in men and women.
• DM : is associated with significant increase in the risk of CAD
• Family history: a familial predisposition to CAD exists
• Oral contraceptive pills: use of OCP is associated with increased
risk of CAD.
• Other risk factors: Gout, Obesity.
 Clinical features
• It is an episodic clinical syndrome due to
transient myocardial ischemia.
• Males constitute ~70% of all patients with angina
pectoris
• The typical patient with angina is a man older
than 50 years or a woman older than 60 years of
age who complains of chest discomfort,
• In general Angina is can be:
– Chronic stable angina
– Unstable angina
– Varian ( Prinzmetal’s ) angina
 Characterstics of Angina(chest pain)
• Quality: squeezing, Pressure like, heaviness, smothering,
or choking , suffocating, heavy
– almost never sharp or stabbing
– is not pleuritic
• Location :substernal radiating to the neck, jaw, epigastrium or arms
– Pain above the mandible & below the umblicus, and that
localized by tip of finger is rarely Anina
• Duration: lasts 2-5 minutes
– Constant pain lasting many hrs, very brief episodes of pain
not angina
• Provoking Factors: exertion & emotional sterss
• Relieving factors: rest, sub lingual nitroglycerine
– delay > 5-10 mins……..ACS or not ischemia
• The pain in angina is often reproducible with the same
degree of physical exertion.
Clinical Classification of angina pain
Typical angina (definite)
1) Substernal chest discomfort with a characteristic
quality and duration
2) provoked by exertion or emotional stress
3) relieved by rest or NTG.

Atypical angina (probable)

- Meets 2 of the above characteristics
Non-cardiac chest pain
-Meets one or none of the typical anginal
characteristics
 …………………cont’d
History
• In a patient presenting with a history of recurrent
chest pain, obtain a detailed symptom history,
including onset, quality, location, duration, radiation,
and precipitating and relieving factors.
• Determine the presence or absence of typical angina
pain
• If the patient's symptoms are consistent with typical
angina, sub-classify the angina as
– Stable angina (unchanged for 2 or more months) or
– unstable angina(rest, new-onset, or increasing) angina
 ………………..cont’d
• Ask about any episodes of dyspnea, palpitations, or
dizziness with or without chest pain.
• If the patient has experienced any such episodes, ask
about the same symptom variables that are applicable
to typical angina
• Assess potential risk factors for CAD, including
– those related to lifestyle,
– habits,
– past medical history,
– family history, and hormone therapy
• Ask about a history of symptoms of CHF
 Physical Examination
• Assess the vital signs, especially for
– hypertension,
– tachycardia,
– bradycardia,
– arrhythmia, and
– tachypnea
• signs of anemia, thyroid disease, hypercholesterolemia
& atherosclerosis (carotid bruit)
• Sn PAD, CVS examinations,
 Diagnostic workup
1-Electrocardiography
A)Resting ECG
– ECG taken when the patient is not in pain may be
normal
Normal in ½ of patients…normal resting LV
function……..favorable Px
– New horizontal or down sloping of ST segment
depression and new T-wave inversion are suggestive
of myocardial ischemia………adverse Px
– ST segment elevation associated with pain which
returns to normal as the pain wanes suggest variant
angina
 ………Work UP
B) Non Invasive Stress Testing:
Testing
– establish the diagnosis of IHD
– estimate prognosis
– guide appropriate treatment
* Exercise ECG
* Stress myocardial perfusion imaging
* Stress Echo
Stress ECG(Exercise ECG)
– Exercise ECG is the initial Dxic test of choice
– Recording ECG during exercise ↑es the Sn & Sp of ECG.
– helps to quantify the patient’s exercise tolerance.
– The presence of new horizontal or down sloping of ST segment
depression has Sn of 70 % and Sp of 90 %.
• Stress Testing to determine the prognosis & management of patients
with suspected or known CAD
• should be performed in those at intermediate or high pretest
probability…
Indications
– At the time of initial evaluation for possible angina
– After a significant change in cardiac symptoms
Absolute CI for Exercise ECG
 ……………..Cont’d
• Other lab
– CXR- in pts with symptoms and signs of CHF
– Hemoglobin or CBC, fasting blood glucose,
– Serum lipid profile
Differential Diagnosis
• Consider other cause of chest pain like
– Pleurisy
– Pneumonia
– Pericarditis
– Ischemia associated with AS or HCMP
 Treatment for Angina
• Therapy for angina should be directed either
– reducing myocardial oxygen demand, or
– to compensate for impaired flow through diseased
coronary arteries or
– at increasing myocardial oxygen supply (i.e. blood flow)
General measures
• Lifestyle Measures
– Counsel patients about cessation of smoking
– Diet
– Regular exercise
– Weight reduction
 Medical therapy
a) Nitrates
– produce venodilation and to lesser extent arteriolar dilation
– short-acting nitrates (e.g., 0.4 mg sublingual nitroglycerin) for
acute attacks
– Consider long-acting nitrates in patients who have refractory
chest pain despite maximal tolerated beta-blocker therapy
– To avoid nitrate tolerance in patients requiring long-acting
nitrates, prescribe a 10-12-hour nitrate-free period daily.
• Nitroglycerine-
– 0.3-0.6 mg sublingual as soon as the pain starts or 5 minutes
before a stressful activity.
• Isosorbide dinitrate slow release:
– 10-60 mg PO TID or 2.5 -10 mg sublingual every 4-6 hrs
 …………….cont’d
b) β-blockers:
• reduce heart rate and myocardial contractility.
reduce cardiac oxygen demand.
– Propranolol: 20 -80 mg PO BID to QID
– Metoprolol: 25-200 mg Po BID
– Atenolol: 50 -150 mg PO daily
• Contraindicated in patients with asthma and severe form of CHF
C) Calcium channel blockers:
– decrease the tone of the smooth muscle of coronary arteries.
– These drugs are especially effective in preventing coronary spasm that
cause variant angina.
angina
• Nifedipine XL: 30 mg PO O daily
• Verapamil: 180-240 mg daily
• Amlodipine: 5-10 mg daily
– Consider calcium channel blockers when beta-blockers are
contraindicated or are not tolerated.
– Consider using combination therapy cautiously (e.g., a β-blocker and
calcium antagonist or nitrate) for patients who fail to respond adequately
to monotherapy
 ……….treatment of AP
Anti-platelet agents :
• Aspirin: to prevent the occurrence of MI.
– Dose: 75 – 150 mg PO daily.
Lipid lowering drugs :
– prescribe a lipid-lowering medication (statins) and a low-fat,
low-cholesterol diet for patients with CAD and elevated LDL
– Goal= LDL level of < 100 mg/dl
ACE inhibitor : may be beneficial in all patients
– with significant CAD or
– in those with previous MI who also have DM and/or LV systolic
dysfunction
Treat comorbidities that can provoke or exacerbate angina
(e.g., HPN, DM, hyperthyroidism, pulmonary disorders, anemia)
 …………………………..cont’d
• Acute Care/Hospitalization:
– Always refer patients presenting with new-onset, rest, or
increasing angina to an emergency department, and hospitalize
a patient with clinical evidence of unstable angina or
myocardial infarction
• Complications
– In patients with chronic stable angina, be sensitive particularly
to accelerating symptoms, indicating development of unstable
angina
Prognosis
• The main prognostic indicators in patients with ischemic heart
disease (IHD) are:
– The status of left ventricular (LV) function
– The location and severity of coronary artery narrowing
– The severity or activity of myocardial ischemia
– The presence of complex arrhythmias
 Acute coronary syndrome(ACS)
• Refer to any constellation of clinical symptoms that
are compatible with acute myocardial ischemia
• Three primary presentations that suggest an ACS :-
– Rest angina, which is usually more than 20 minutes
in duration .
– New onset angina that markedly limits physical
activity.
– Increasing angina that is more frequent, longer in
duration, or occurs with less exertion than previous
angina.
 Unstable Angina
• It is an Angina pectoris or equivalent ischemic
discomfort with at least one of three features:-
– (1) Occurs at rest (or with minimal exertion), usu. >10 min
– (2) Severe and of new onset (< 4–6 weeks); and/or
– (3) Crescendo pattern (i.e., more severe, prolonged, or
frequent than previously).
• No elevation in troponins or CK-MB, with or without ECG
changes indicative of ischemia (eg, ST segment depression
or transient elevation or new T wave inversion).
 Acute myocardial infarction(AMI)
(NSTEMI/ STEMI)
• AMI- is ischemic myocardial cell necrosis.
Epidemiology
• Every year in the United States,
– ~1.3 million patients are admitted to hospitals with
UA/NSTEMI
– ~300,000 patients are admitted with acute STEMI
• Cardiovascular disease is responsible for almost 50% of
all deaths in the U.S.A and other developed countries
and
– for 25% deaths in the developing world
• Nearly half of these deaths occur before the patients
receive medical care either from emergency medical
technicians or in a hospital
 Risk factors
Major
• Family (hx) (MI before age 55 in a Minor
male or 65 in a female)  Male sex
• Diabetes  Postmenopausal
female
• Smoking
 Elevated plasma
• Hyperlipidemia homocysteine
• Hypertension
• ?Obesity
• Age: male >45, female >55
 PATHOPHYSIOLOGY
STEMI:
-occurs when coronary blood flow decreases
abruptly
-plaque rupture, fissures and/or ulceration
-formation of platelet monolayer

↓
- Platelet aggregates and cross link occur
 …………………CONTD
Occlusion of the culprit artery by thrombous
Depending on the degree of obstruction of the
lumen
The severity and duration of the imbalance
between myocardial oxygen supply and demand
determine whether the damage is reversible ( ≤20
min for total occlusion in the absence of
collaterals) or whether it is permanent, with
subsequent myocardial necrosis (>20 min).
ISCHEMIA(NSEMI) OR/& NECROSIS(STEMI)
 Clinical presentation
Symptoms:
severe prolonged chest pain (TYPICAL Sx)
description, location, duration ,radiation, ppting or relieving factors,
associated symptoms
Signs:
tachycardia/ bradycardia ,↑ JVP ,Dyskinitic LV
impulse ,dysrthmia, S3/S4 gallop ,systolic
murmur ,pericardial friction rub
May be clinical silent like in
DM, OLD AGE ,female, Postoperative….
 Diagnosis of AMI
History-characteristic chest pain
P/E-findings are not characheteristic.
Laboratory: divided into 4 groups
– ECG(ST- elevation or depression),Q- wave
– serum cardiac markers(CK-MB, troponin……)
– cardiac imaging
– non specific indexes of tissue necrosis and inflammation
Approach to IHD
 Management of AMI
• immediate referral to hospitals with intensive
care unit (ICU) facility is mandatory
• Early(cotrol the pain,treat hypoxemia,…..)
• Long term improvement
– Prevention of:
recurrent thrombosis →by ASA
LV remodelling →by ACEI
Recurrent ischemia & threatening arrythmia→by BB
Slow/prevent disease progression →by statin
Prevent embolization →by anticoagulant
• Emergency management :
– Management of patients should start before they
reach the hospital emergency room
1. General measures
– Reassure and make the patient comfortable
– Supply O2 by mask
– Secure IV line
– Give Aspirin 160-325 mg tablets –helps to prevent
further platelet aggregation
 Management in the ED
Goals:
1. control of cardiac discomfort (pain)
2. emergency referal
3. triage of lower-risk patients to the
appropriate location in the hospital, and
4. avoidance of inappropriate discharge of
patients with STEMI.
Treatment of pain(discomfort)
Nitroglycerin: sublingual up to three doses of 0.4 mg at
about 5 minutes interval
Morphine:
 very effective analgesic for the pain associated with
STEMI.
 may reduce cardiac output and arterial pressure.
 Brady cardia /heart block in pt with posteroinferior
infarction.
Dose:- 2-4mg Q 5 MIN
 ….pain control
β-Blockers:-
 pain control
 IV β blockers improves mortality outcome
metopprolol 5 mg Q 5min for a total of 3
doses ,15min after the last IV dose, 50mg po Q 10hrs
for 48hrs and then 100mg po Q 12hrs
Oxygen
if normal saturation arterial O2 supplemental O2 is
of limited clinical benefit and not cost-effective
if hypoxia is present Nasal prongs/face mask (2-4L/min)
for the 1st 6-12hrs.
 Limitation of infarct size
• through reperfusion or revascularization
– Thrombolysis/Fibrinolysis
– Direct percutanous transluminal coronary
angioplasty
 Hospital phase management
 Coronary artery care unit
 for 8-12hrs if NSTEMI and
 24hrs STEMI, CHF, hypotension, arrhythmias
 Continuously monitoring of V/S , …
 ECG:
o debrillation
o non invasive transthoracic pacemakers
o other intervasions
 ………………..cont’d
Activity
 bed rest for at least 12hrs-STEMI
 Encourage activities if no complication with 1st
24hrs
2nd or 3rd day-ambulate in the room, shower
At least 3x walk of 185m /600feet/
Diet -NPO or clear fluid by mouth for the 1st 4-12 hrs
-typical coronary diet <30% calories as fat
<300mg cholesterol
50-55% complex CHO
Bowels
bed side commond
dioctyl sodium sulfosuccinate,20mg po/d

Sedation
diazepam 5 mg 3x or 4x po/d
oxazepam
lorazepam
 …………..hospital
2. Pharmacological therapy
a) Antithombotic agents and anti platelet agents :
– Unfractionated heparin :
– Anti platelet agents : ASA 75-150 mg Po daily to prevent
recurrence of AMI
b) β-Blockers:
– have short term and long term benefits for patients with AMI.
– The short term benefit is they relive pain and decrees the risk of
malignant arrhythmias
• Metoprolol: 25-200 mg BID
• Atenolol: 50-150 mg Po daily
c) ACE inhibitors ;
– reduce the mortality rate and improve long term
survival in post AMI patients by preventing cardiac
remodeling which may have lead to progressive heart
failure
 Complications of AMI
• Malignant arrhythmias
• conduction disturbances
• Heart failure
• Cardiogenic shock