Learning Objectives

Week 4: Ischemic Heart Diseases

11 October 2019

1. Relationship Between High Blood Glucose and Hyperlipidemia

 People with diabetes are more prone to having unhealthy high cholesterol levels, which
contributes to cardiovascular disease (CVD)
 Diabetes tends to lower "good" cholesterol levels and raise triglyceride and "bad" cholesterol
levels, which increases the risk for heart disease and stroke. This common condition is called
diabetic dyslipidemia
 Studies show a link between insulin resistance, which is a precursor to type 2 diabetes, and
diabetic dyslipidemia, atherosclerosis and blood vessel disease. These conditions can develop
even before diabetes is diagnosed

2. Nitrate vs. Nitroglycerin

 Nitroglycerin is a type of nitrate
 Nitrates can be used to prevent chest pain (angina), limit the number of attacks, relieve the pain
of current attack, or treat the symptoms of heart failure
 Nitrate
o Do not alter the underlying cause of angina
 Angina is usually caused by narrowing
of the heart arteries due to a build-up of
a fatty substance called atheroma
o However, nitrate medicines are good at
easing and preventing angina pains
o Work by relaxing the walls of blood vessels,
which makes them slightly wider  heart can
get more blood flow and oxygen  helps to
treat symptoms of angina
o It also relaxes other blood vessels in the body,
which takes the strain off the heart a little
o Types
 Short-Acting Nitrate Preparations
 Glyceryl Trinitrate (GTN) (tablets or sprays)  commonly used to ease angina
 Isosorbide Dinitrate (tablets or sprays)  sometimes used as an alternative to
GTN for the immediate relief of angina pains when they develop
 Long-Acting Nitrate Preparations
 If you have frequent angina pains, long acting nitrate preparations help to prevent
the pains from developing
 Isosorbide Mononitrate
o Works in the same way as the other nitrates  relaxes the walls of the blood
vessels  boosts the blood flow
 Takes longer to start working, so is not much use for immediate pain relief
 However, it works for much longer after each dose than a short-acting preparation
(which loses its effect after 20 minutes or so)
o Side Effects
 Throbbing headache
 Flushed face
 Dizziness
 Lightheadedness (from the nitrate causing low BP)
 Slightly nauseous
 Sublingual (applied under the tongue)  slight burning sensation under the tongue
o They help with the symptoms of chest pain, but don't change the cause for the chest pains
o So, although they can make you feel better, they don't prevent heart attacks

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 Nitroglycerin
o Belongs to nitrates
o Used to prevent chest pain (angina) in
people with a certain heart condition
(coronary artery disease [CAD])
 Angina occurs when the heart
muscle is not getting enough blood
o Works by relaxing and widening blood
vessels so blood can flow more easily to
the heart
o This medication will not relieve chest
pain once it occurs
o Not intended to be taken just before
physical activities (e.g. exercise) to
prevent chest pain
 Other medications may be needed in
these situation
o Taken by mouth, usually 3-4 times daily
 It is important to take the drug at the
same times each day
o Dosage is based on the medical condition
and response to treatment
o Do not suddenly stop taking this
medication without consulting the doctor
o Side Effects  headache, dizziness, lightheadedness, nausea, and flushing
 Headache is often a sign that the medication is working. Doctor may recommend to
treat this with over-the-counter pain reliever (e.g. acetaminophen, aspirin)
o Relaxing smooth muscle and blood vessels in the body  increases the amount of blood
and oxygen that reaches the heart  heart doesn't work as hard  reduces chest pain
o Principal pharmacological action of nitroglycerin  relaxation of vascular smooth muscle
o Although venous effects predominate, nitroglycerin produces (in a dose-related manner)
dilation of both arterial and venous beds
 Dilation of postcapillary vessels, including large veins, promotes peripheral pooling
of blood, decreases venous return to the heart, and reduces left ventricular end-
diastolic pressure (preload)
 Nitroglycerin also produces arteriolar relaxation, thereby reducing peripheral vascular
resistance and arterial pressure (afterload), and dilates large epicardial coronary
arteries; however, the extent to which this latter effect contributes to the relief of
exertional angina is unclear

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3. Why Did They Give Atenolol (Tenormin)?
 A 1-selective blocker that affects heart and circulation (blood flow through arteries and veins)
 Used to treat angina (chest pain) and hypertension
 Lower the risk of death after a heart attack
 Do not use this if you have a serious heart condition (e.g. "AV block," bradycardia, or CHF)
 Do not stop taking atenolol suddenly. Stopping suddenly may make your condition worse
 May take up to 2 weeks before you get the full effect of atenolol
 Side Effects  dizziness, feeling tired, depressed mood.
 Indication
o Management of hypertension alone and in combination with other antihypertensives
o Management of angina pectoris associated with coronary atherosclerosis
o Management of acute myocardial infarction in hemodynamically stable patients with a
heart rate greater than 50 beats per minutes and a systolic blood pressure above 100 mmHg
 Atenolol acts as an antagonist to sympathetic innervation and prevents increases in heart rate,
electrical conductivity, and contractility in the heart due to increased release of norepinephrine
from the peripheral nervous system
 Together the decreases in contractility and rate produce a reduction in cardiac output resulting
in a compensatory increase in peripheral vascular resistance in the short-term. This response
later declines to baseline with long-term use of atenolol
 More importantly, this reduction in the work demanded of the myocardium also reduces oxygen
demand which provides therapeutic benefit by reducing the mismatch of oxygen supply and
demand in settings where coronary blood flow is limited, such as in coronary atherosclerosis
 Reducing oxygen demand, particularly due to exercise, can reduce the frequency of angina
pectoris symptoms and potentially improve survival of the remaining myocardium after
myocardial infarction
 Atenolol exerts some effects on the respiratory system although to a much lesser extent than
non-selective beta-blockers
o Interaction with β2 receptors in the airways can produce bronchoconstriction by blocking
the relaxation of bronchial smooth muscle mediated by the sympathetic nervous system
o The same action can interfere with β-agonist therapies used in asthma and chronic
obstructive pulmonary disease
 By reducing the heart rate, the force of muscle contraction, and the BP against which the heart
must pump, atenolol reduces the work of heart muscle and the need of oxygen for the muscle
o Since angina occurs when oxygen demand of the heart muscle exceeds the supply, atenolol
is helpful in treating angina

4. Mechanism of Action of All the Medications in Tutorial 2 Page B and C

 Atenolol 50 mg 2x/day
o Most of the explanations of its mechanism of action are in #3
o Adult Dosage for MI
 50 mg orally twice a day or 100 mg orally once a day
 If IV -blockers are contraindicated or inappropriate, oral therapy should continue for
at least 7 days post-myocardial infarction (MI)
 Treatment with -blockers post MI should generally continue for 1 to 3 years if there
are no contraindications
 Use  management of hemodynamically stable patients with definite or suspected
acute myocardial infarction to reduce cardiovascular mortality
 Nitroglycerine sublingual when required
o Forms free radical nitric oxide (NO)  activates guanylate cyclase  increase of
guanosine 3'5' monophosphate (cyclic GMP) in smooth muscle and other tissues 
dephosphorylation of myosin light chains, which regulate the contractile state in smooth
muscle  vasodilatation
 This also decrease platelet aggregation
o Most of it is discussed in #2

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 Atorvastatin 20 mg only night
o Why only at night?  #5
o As with other statins, atorvastatin is a competitive inhibitor of HMG-CoA reductase. Unlike
most others, however, it is a completely synthetic compound. HMG-CoA reductase
catalyzes the reduction of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) to
mevalonate, which is the rate-limiting step in hepatic cholesterol biosynthesis. Inhibition
of the enzyme decreases de novo cholesterol synthesis, increasing expression of low-
density lipoprotein receptors (LDL receptors) on hepatocytes. This increases LDL uptake
by the hepatocytes, decreasing the amount of LDL-cholesterol in the blood. Like other
statins, atorvastatin also reduces blood levels of triglycerides and slightly increases levels
of HDL-cholesterol
o Recent studies have shown that in people with acute coronary syndrome, high-dose statin
treatment may play a plaque-stabilizing role. At high doses, statins have anti-inflammatory
effects, incite reduction of the necrotic plaque core, and improve endothelial function,
leading to plaque stabilization and, sometimes, plaque regression. However, there is an
increased risk of statin-associated adverse effects with such high-dose statin treatment
o Adult Dosage for Prevention of Cardiovascular Disease
 Initial dos  10 mg or 20 mg orally once a day
 Initial dose of 40 mg may be used in patients who require a reduction in low
density lipoprotein (LDL-C) of more than 45%
 Maintenance dose  10 mg to 80 mg orally once a day
 Following initiation and/or upon titration, lipid levels should be evaluated within 2 to
4 weeks and dosages adjusted accordingly
 Uses:
 In patients without clinically evident coronary heart disease (CHD), but with
multiple risk factors for CHD such as age, smoking, hypertension, low HDL-C,
or a family history of early CHD, to reduce the risk of myocardial infarction and
stroke, and to reduce the risk for revascularization procedures and angina
 In patients with type 2 diabetes, and without clinically evident CHD, but with
multiple risk factors for CHD such as retinopathy, albuminuria, smoking, or
hypertension, to reduce the risk for myocardial infarction and stroke
 In patients with clinically evident CHD, to reduce the risk of nonfatal myocardial
infarction and fatal and nonfatal stroke; to reduce the risk for revascularization
procedures; to reduce the risk of hospitalization for CHF; and to reduce the risk
of angina
 Aspirin 80 mg in the morning
o Why only in the morning?  #5
o Aspirin and other non-steroid anti-inflammatory drugs (NSAIDs) inhibit the activity of the
enzyme now called cyclooxygenase (COX) which leads to the formation of prostaglandins
(PGs) that cause inflammation, swelling, pain and fever
o In treatment and prevention of cardiovascular disease,
 Involves inhibition of platelet activation and aggregation
 The main mechanism of action was the irreversible inhibition of the platelet-dependent
enzyme cyclooxygenase (COX), thereby preventing the synthesis of prostaglandins
 Two COX isoenzymes, COX-1 and COX-2
 In platelets, the COX-1 enzyme produces thromboxane A2, a powerful promoter of
platelet aggregation. Thus, aspirin irreversibly inactivating COX-1 and blocks the
generation of thromboxane A2, derives a potential antiplatelet effect
 Platelet activation and aggregation with subsequent activation of the clotting cascade
play critical roles in the onset of acute occlusive vascular events, such as MI and
occlusive cerebrovascular accident (CVA). Because platelets do not have nucleus and
thus cannot regenerate COX, they become an excellent target for antithrombotic
therapy, while aspirin shows both immediate and long-term effects on platelets

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  Aspirin also blocks the formation of COX-dependent vasoconstrictors, in which
contribute to endothelial dysfunction in atherosclerosis.
 Thus, improvement of endothelial dysfunction with aspirin may improve vasodilation,
reduce thrombosis, and inhibit progression of atherosclerosis
 Furthermore, aspirin reduces the inflammatory response in patients with coronary
artery disease (CAD) and may inhibit the progression of atherosclerosis by protecting
low-density lipoprotein from oxidation
 Morphine (2 mg IV), Oxygen, Aspirin 320 mg, Clopidogrel 300 mg
o Part of the MONACO initial management
o Mandatory ga?  ga selalu
o Morphine  dikasih kalo pain msh ada walaupun udah minum nitrate
 Morphine is used for the management of chronic moderate-to-severe pain
 Opioids, including morphine, can manage pain effectively when used for a short
amount of time
 The use of opioids for longer periods needs to be monitored as they can develop a
physical dependence, addiction disorder and drug abuse
 The binding of morphine in the opioid receptors blocks the transmission of nociceptive
signals, it activates the signaling of pain-modulating neurons in the spinal cord and
inhibits the transmission from primary afferent nociceptors to the dorsal horn sensory
projection cells
o Oxygen  baru kasih ketika saturasi oksigen < 90%
o Nitrates  kalo pasien dateng chest painnya pas dirumah, dan pas ke UGD ga sakit, gausah
 Kalo infarct ventricle kanan, jangan dikasih
 Mechanism of action ada di #2
o Aspirin  160-320 mg, chewable!
 Dia itu antiplatelet
 Wajib dikasih!
 Karena rupture plaque stimulate platelet  dikasih antiplatelet
 Mechanism of action ada diatas, masih #4
o Clopidogrel  300 mg PO, or Ticagrelor 180 mg PO
 Clopidogrel  antiplatelet  banyak macemnya
 Dual antiplatelet therapy  pada pasien ACS
 Selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12
receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa
complex, thereby inhibiting platelet aggregation (this action is irreversible)
 Keep platelets apart and stopping them sticking together and forming clots
 Helps reduce the risk of a future stroke or heart attack in this way
 The drug achieves this effect as it is a platelet inhibitor  reduces platelets in the blood
 Streptokinase (1,500,000 IU)
o Plasminogen is an inactive molecule that becomes activated to plasmin when the Arg/Val
bond is cleaved. Plasmin breaks down fibrin clots created by the blood clotting cascade
o Streptokinase forms a highly specific 1:1 enzymatic complex with plasminogen which
converts inactive plasminogen molecules into active plasmin
o Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins  degradation
of blood clots
o More information in #8
 Heparin (IV)
o Heparin binds to the enzyme inhibitor antithrombin III (AT), causing a conformational
change that results in its activation through an increase in flexibility of its reactive site loop
o The activated AT then inactivates thrombin, factor Xa and other proteases
o More information in #8

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5. Difference Between Drinking Medications in the Morning vs. Night
 The best time to take them is really dependent upon the type of medication
 Certain medications do work more efficiently in the mornings or evenings
 For other types of drugs, taking them consistently at the same time of day is more important
than when you take them
 Other medications, like those for asthma attacks, should be taken on an as-needed basis, which
may be in the morning, the evening or both, depending on the day
 Morning Medications
o Heartburn Medications
 Certain preventive medications should be taken 30 minutes before the first meal of the
day, even if symptoms usually occur at night or at bedtime
 Taken on an empty stomach to prevent future relapses of heartburn
 The proton pumps in your body that reduce the production of stomach acids are most
active in the morning
o Thyroid Replacement Drugs
 Taken first thing in the morning, either with food or on an empty stomach
 Your provider can adjust the dosage based on the levels of hormone in the blood and
how consistently you’re taking the medication
o Phosphonates
 Given to treat and prevent osteoporosis (a condition in which the bones become weak
and brittle) and should be taken in the morning with a full glass of water to ensure the
medication works most efficiently
 These should be taken at a time when you know you won’t be laying down again. Once
you take this, you should be standing or at least sitting upright for about 30 minutes
 Evening Medications
o Sleep Aids
 As expected, if you take medications that help you sleep, it’s best to take them in the
evening, about 15 to 20 minutes before bedtime, or as otherwise prescribed
o Blood Pressure Medications/-Blockers
 Talk to your health care provider about the ideal time of day to take them, though as a
general rule of thumb, evening is best
 Providers may specify to take these in the evening because of side effects that can
occur. Many people will sleep through those side effects
 Common side effects of b-blockers include:
o Dizziness o Dry mouth, skin, or eyes
o Weakness o Headache
o Drowsiness or fatigue o Upset stomach
o Cold hands and feet o Diarrhea or constipation
 Common side effects of high blood pressure medications include:
o Cough o Feeling nervous
o Diarrhea or constipation o Tired, drowsy, or a lack of energy
o Dizziness or lightheadedness o Headache
o Erection problems o Nausea or vomiting
o Statin and Cholesterol Medications
 Take statins at bedtime, advises the British Heart Foundation
 Cholesterol production in the liver is highest after midnight and lowest during the
morning and early afternoon  statins most effectively taken just before bedtime
 Between 2 a.m. and 4 a.m. is when your cholesterol is being produced and most active
 Take cholesterol medications at night so you get the highest concentration of the drug
at the right time
o Allergy Medications
 Many allergy medications can cause drowsiness, and if your allergies are keeping you
awake and congested during sleeping hours, you may need to take these at night

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  Other medications (e.g. Benadryl, Claritin) can be taken throughout the day, as they
are low- or non-sedating types of antihistamines
o Aspirin
 Also known as acetylsalicylic acid (ASA)
 Used for pain reliever, anti-inflammatory drug and as a blood thinner
 People with a high risk of blood clots, stroke, and heart attack can use aspirin long-
term in low doses (75-150 mg, but ideally 81 mg)
 Based on a new study from American Heart Association (AHA), aspirin is best taken
at night  aspirin at night may be more protective than an aspirin in morning
 Cardiovascular events are about three times more likely to occur in the morning, when
blood pressure and platelet activity are at peak levels
 Most heart attacks happen between 6 a.m. and 10 a.m. The rate is 40 percent higher
than any other time of the day or night
 These early morning hours are when the blood is the “thickest” and most likely
to clog the arteries supplying blood to the heart
 That means you want your aspirin to the on board and thinning things out in that
critical time of the morning. But aspirin doesn’t work within minutes
 Unlike its ability to ease a pounding headache within 15 to 30 minutes, blood thinning
is another story  needs a few hours to make the blood flow more smoothly
 Researchers from Leiden University Medical Center conducted a study in Netherlands
to examine nearly 300 patients with heart disease who were taking aspirin
 During two separate three-month periods, half of the patients were instructed to
take 100 mg of aspirin first thing in the morning, while the other half were told
to take the drug right before bed
 It was found that morning platelet activity was lower when aspirin was taken at
night, and patients did not suffer any additional side effects from the dosage
 However, the study did not detect a difference in morning blood pressure levels
between the two patient groups

6. Exercise for Patients with a History of Myocardial Infarction

 Patients after MI who choose to exercise regularly have improved survival rates and a reduced
incidence of non-fatal reinfarction
 The recommendation for patients who have had a myocardial infarction/undergoing
percutaneous coronary intervention (PCI) and who have a low-probability of further cardiac
events is for them to have a minimum of three months’ rehabilitation before they resume
participation in competitive sports. If they are receiving dual antiplatelet therapy (DAPT),
because of the risk of bleeding, they should be advised to avoid contact sports
 Advice on eligibility to participate in sport must be combined with recommendations to perform
proper warm-up and cool-down procedures and ensure adequate hydration. Patients should also
be made aware of the need to be mindful of any symptoms occurring during resumed exercise.
Continuous long-term cardiac evaluation, at least annually, is then advised. The risk factor
profile should be managed pharmacologically and with lifestyle modifications
 A study by GIH and Centre for Health and Performance at Gothenburg University, Sweden,
was conducted
o Levels of physical activity were reported 6–10 weeks and 12 months after the heart attack.
The difference between answers was considered a change in physical activity over the year
following the heart attack
o On both occasions, patients were asked how many times they had exercised for 30 minutes
or longer during the previous seven days. Patients were categorized as constantly inactive,
reduced activity, increased activity, or constantly active
o A total of 1,087 patients died during an average follow-up of 4.2 years. The researchers
analyzed the association between the four categories of physical activity and death, after
adjusting for age, sex, smoking, and clinical factors. Compared to patients who were

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 constantly inactive, the risk of death was 37%, 51%, and 59% lower in patients in the
categories of reduced activity, increased activity, or constantly active, respectively
o Shows that patients can reduce their risk of death by becoming physically active after a
heart attack. Patients who reported being physically active 6 to 10 weeks after the heart
attack but became inactive afterwards seem to have a carry-over benefit. But of course, the
benefits for active people are even greater if they remain physically active
o Exercise reduced the risk of death in patients with large and small myocardial infarctions,
and for smokers and non-smokers, for example
o However, the study did not investigate what type of exercise patients undertook. More
research is needed to find out if there is any type of activity that is especially beneficial
after a heart attack
 Patients who join cardiac rehabilitation programs have a faster and safer recovery and better
outcomes after a heart attack
 Everyone recovers at a different pace. This may be related to your activity level before your
heart attack or the amount of damage to your heart muscle. It may take many months to develop
the optimal exercise program
o Start slowly and gradually increase your walking pace over 3 minutes until the activity feels
moderate (slightly increased breathing, but should still be able to talk with someone). If
you feel too short of breath, slow down your walking pace
o Walk at a moderate pace for about 10 minutes the first time and each day try to add one or
two minutes. By the end of a month, aim for walking 30 minutes most days of the week
o Remember to cool down at the end of your exercise by gradually walking slower for the
last 3 minutes of your exercise
o Choose an activity that you enjoy such as walking (outside or on a treadmill), stationary
cycling, rowing or water aerobics. Ask your doctor before lifting weights
o Exercise should be done regularly to gain the benefits; national guidelines suggest most
days of the week if not every day
o Try to exercise at the same time every day, to establish a habit and minimize any variables
that may impact your exercise (timing of meals, medications, work schedule, etc.)
o If you notice any symptoms (e.g. shortness of breath, chest discomfort, palpitations that do
not go away or increasing fatigue), stop your exercise and notify your doctor
o After a heart attack many things may have changed including energy level and medications.
These may affect your exercise tolerance; keep your exercise expectations day to day as
you go through the healing process
o Enroll in an outpatient cardiac rehab program to assist with developing the best exercise
program and assisting with lifestyle changes such as heart healthy diet, quitting smoking,
weight loss and stress management
 Returning to exercise after a heart attack or beginning a new exercise program can be
challenging or anxiety provoking. Start small and steadily build your program over time will
help to set you up for success

7. Treatment ACS
 Treatment should be given for a minimum of 48 hours and up to eight days
 Additional acute treatment options include supplemental oxygen, nitroglycerin, intravenous
morphine, beta blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor
blockers, and statins
 Door-to-balloon inflation (pPCI) goal of 90 minutes
 Door-to-needle (fibrinolysis) goal of 30 minutes

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8. Indications and Contraindications of Streptokinase and Heparin
 Streptokinase
o Indications
 For the treatment of acute evolving transmural myocardial infarction, pulmonary
embolism, deep vein thrombosis, arterial thrombosis or embolism and occlusion of
arteriovenous cannula
 An early thrombolysis with streptokinase can significantly reduce mortality after acute
cardiac infarctions
 According to several studies, approximately 13 of 100 subjects without thrombolysis
die in the first month following an infarction; about three of these deaths can be
avoided with streptokinase
 Whether a combination with heparin represents an additional benefit is not safely
established. Combined with a small dose of aspirin (acetylsalicylic acid), the absolute
mortality is even reduced by 5%
 In most comparative studies streptokinase proved to be equally effective as other
thrombolytic agents. Only one study demonstrated an advantage of alteplase (t-PA,
tissue plasminogen activator) if the thrombolysis was performed within the first six
hours following the infarction
 Acute MI  within 12 hours of onset with persistent ST-segment elevation or recent
left bundle branch block (LBBB)
o Contraindications
 Active internal bleeding
 Severe hypertension
 Cerebrovascular episode in the last year
 Unconscious patient
 Hemorrhagic diathesis (a tendency to suffer from a particular medical condition)
 Known active peptic ulcer
 Recent surgery
 Abdominal aneurysm or another potential source of clot such as large fibrillating LA
 Possible pregnancy
 Heparin IV
o Indications
 Heparin acts as an anticoagulant, preventing the formation of clots and extension of
existing clots within the blood. While heparin does not break down clots that have
already formed (unlike tissue plasminogen activator), it allows the body's natural clot
lysis mechanisms to work normally to break down clots that have formed
 Heparin is generally used for anticoagulation for the following conditions:
 Acute coronary syndrome
 Atrial fibrillation

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  Deep-vein thrombosis and pulmonary embolism
 Cardiopulmonary bypass for heart surgery
 Hemofiltration
 Indwelling central or peripheral venous catheters
 Heparin is used to treat and prevent blood clots caused by certain medical conditions
or medical procedures
 It is also used before surgery to reduce the risk of blood clots
o Contraindications
 Known hypersensitivity
 Past or present heparin-induced thrombocytopenia
 Active bleeding
 Severe hypertension
 Etc.

9. ECG Left Bundle Branch Block (LBBB)  How Does It Occur? Can Ischemic Patients Get
LBBB?
 Interruption of conduction through the right or left bundle branches may develop from ischemic
or degenerative damage  affected ventricle does not depolarize in the normal sequence
 Rather than rapid uniform stimulation by the Purkinje fibers, the cells of that ventricle must
rely on relatively slow myocyte-to-myocyte spread of electrical activity traveling from the
unaffected ventricle
o This delayed process prolongs depolarization and widens the QRS complex
o Normal QRS duration  ≤ 0.10 seconds (≤ 2,5 small boxes)
o Incomplete bundle branch block  QRS duration 0.10-0.12 seconds (2.5-3.0 small boxes)
o Complete bundle branch block  QRS duration > 0.12 seconds (> 3.0 small boxes)
 In this situation, normal initial depolarization of the left septum does not occur; rather, the right
side of the ventricular septum is first to depolarize, through branches of the right bundle
 Thus, the initial forces of depolarization are directed toward the left ventricle instead of the
right  initial downward deflection is recorded in V1, and small Q wave in V6 is absent
 Those with LBBB have increased risk for cardiovascular mortality, coronary artery disease,
heart failure, and sudden cardiac death
 The LBBB itself can be the result of an
aging or fibrotic conduction system,
chronic ischemic heart disease, left
ventricular hypertrophy, adverse
ventricular remodeling from congestive
heart failure, or valvular heart disease
 The most widely accepted tools to aid
in the diagnosis of MI in the presence
of LBBB are the Sgarbossa criteria

10. Reciprocal ECG

 Reciprocal change  ST-segment depression occurring on an ECG which also has ST-segment
elevation in at least 2 leads in a single anatomic segment
 In other words, reciprocal change cannot be used if ST-segment elevation is absent
 A very important ECG finding, not only supporting the diagnosis of STEMI but also indicating
a high-risk patient
 Reciprocal change is an important ECG concept to consider for two reasons
o First, it identifies patients with a high-risk ACS presentation
 Reciprocal change in the setting of STEMI identifies a patient with an increased
likelihood of cardiovascular complication (heart block, malignant ventricular
dysrhythmia, cardiogenic shock) and poor outcome (significant left ventricular
dysfunction, death)

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 o Second, the presence of reciprocal change is strong confirmatory evidence that STEMI is
present and has both very high specificity and a positive predictive value greater than 90%
 The concept of reciprocal change cannot be used in patients who have the following patterns
on ECG: left bundle-branch block, right bundle-branch block, right ventricular paced rhythm
from an implanted pacemaker, and left ventricular hypertrophy via voltage criteria with strain.

11. What Determines the Prognosis of ACS?

 Acute myocardial infarction (MI) is associated with a 30% mortality rate
 About 50% of the deaths occur prior to arrival at the hospital
 An additional 5-10% of survivors die within the first year after their myocardial infarction
 Approximately half of all patients with MI are rehospitalized within 1 year of their index event
 Six-month mortality rates in the Global Registry of Acute Coronary Events (GRACE) were
13% for patients with NSTEMI ACS and 8% for those with unstable angina
 Patients who survive a first MI are at an increased risk of future cardiovascular events. Studies
have shown that up to one-half of patients do not receive one or more recommended treatments
during an ACS event
 In general, the short-term mortality rate at 30 days after an ACS event is between 2% and 3%;
the mortality rate is lower after an NSTE-ACS event than after STEMI
 Rehospitalization within 30 days ranges between 17% and 25% for all types of ACS
 The risk of sudden cardiac death increases after an ACS, and is correlated with low ejection
fraction (35% or less)
 Mortality rates at one year begin to equalize between patients with STEMI and NSTE-ACS at
approximately 8% to 10%, with long-term mortality rates higher in patients with NSTE-ACS
o This is believed to be secondary to the older age and increased comorbidities in patients
with NSTE-ACS

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12. Do Cardiac Markers Decrease After Therapy?

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