Atherosclerosis and Ischemic Heart Disease: Utline

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Medicine II 4.03a 2 Sem/A.Y. 2016-2017


Atherosclerosis and Ischemic Heart Disease
Rodney M. Jimenez, M.D. January 12, 2017

OUTLINE • Hypertension (BP 140/90 mmHg or on antihypertensive


I. Atherosclerosis medication)
II. Ischemic Heart Disease • Low high-density lipoprotein (HDL) cholesterol [<1.0
mmol/L (<40mg/dL)]
III. Stable Angina Pectoris
• Diabetes mellitus
IV. Coronary Revascularization Procedures
• Family history of premature coronary heart disease (CHD)
o CHD in male first-degree relative <55 years
Lecturer Previous Trans Book Internet o CHD female first-degree relative <65 years
! 4 & " • Age (men: 45 y/o; women: 55 y/o)
! Why 55 years old in females? Because there is
I. ATHEROSCLEROSIS already no hormonal protection from estrogen and
progesterone
A. PATHOPHYSIOLOGY • Lifestyle risk factors
2
o Obesity (BMI 30 kg/m )
o Physical inactivity (! sedentary lifestyle)
o Atherogenic diet (! eating fatty food)
• Emerging risk factors
o Lipoprotein (a)
o Homocysteine
o Prothrombotic factors
o Proinflammatory factors:
! C-reactive protein (CRP) is a proven risk factor
even if LDL levels are low.
o Impaired fasting glucose
o Subclinical atherosclerosis (! asymptomatic
atherosclerosis)
Figure 1. Formation of Atherosclerosis. (See Appendix) ! 1)
Low-density lipoprotein (LDL) is present in the arterial C. LDL CHOLESTEROL GOALS AND CULPRITS FOR THERAPEUTIC
bloodstream 2) along with monocytes and cell adhesion LIFESTYLE CHANGES (TLC) DRUG THERAPY IN DIFFERENT RISK
molecules. 3) The monocytes will phagocytize LDL, adhere to CATEGORIES
the endothelium then 4) enter the tunica media and intima layer
of the arteries. 5) There, the macrophages will be engulfed by Table 1. ! These goals categorize LDL levels and how you
the scavenger receptors, which 6) will trigger an inflammation will treat them. If you have 190 mg/dL of LDL, even if you’re
cascade, 7) forming foam cells, fibrosis and apoptosis. asymptomatic and don’t have any risk factors, just the LDL
alone, you need to consider drug therapy, a high-intensity drug
& Atherosclerosis affects various regions of the circulation therapy should still be considered. If you are under a VERY
preferentially and has distinct clinical manifestations that HIGH RISK category for cardiovascular events, the goal is
depend on the particular circulatory bed affected <70.) (REMEMBER AND UNDERSTAND THIS TABLE.)
o Atherosclerosis of the coronary arteries – myocardial
infarction
o Atherosclerosis of the arteries supplying the central
nervous system – strokes and transient cerebral
ischemia
o Atherosclerosis in the peripheral circulation –
intermittent claudication and gangrene and can
jeopardize limb viability
o Atherosclerosis involving the splanchnic circulation –
mesenteric ischemia
o Atherosclerosis in renal arteries – renal artery stenosis
& Atherogenesis typically occurs over a period of many years,
usually many decades
& Clinical manifestations of atherosclerosis may be chronic or
acute
o Chronic – development of stable, effort-induced angina
pectoris or predictable and reproducible intermittent
claudication ! If the risk category is VERY HIGH, meaning the patient has
o Acute – such as myocardial infarction, stroke, or acute coronary syndrome (ACS) or coronary heart disease
sudden cardiac death may first herald the presence of documented with diabetes mellitus, or has multiple
atherosclerosis cardiovascular risk factors (hypertension, cigarette
& Other individuals may never experience clinical smoking, or obesity), the goal should be less than 70.
manifestations of arterial disease despite the presence of ! In HIGH-risk category, if LDL is less than 100 mg/dl, the
widespread atherosclerosis demonstrated postmortem goal should be less than 100, not less than 70.
! If you are MODERATELY HIGH with 2 risk factors only,
B. MAJOR RISK FACTORS* THAT MODIFY LDL GOALS the goal is less than 130.
*Exclusive of LDL Cholesterol ! In LOWER with 0-1 risk factors, the goal should be less
• Cigarette smoking than 160.

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! Then check the level when to initiate (drug) TLC or ! There are 4 spectra (from low risk to highest risk of dying):
CONSIDER DRUG THERAPY. 1. Chronic stable angina pectoris (CSAP)
• Sample question: 2. Unstable angina pectoris
o When do you consider drug therapy, at what level if 3. Non-ST elevation acute coronary syndrome
you have 2 risk factors? You will just provide drug 4. ST-elevation myocardium infarction (STEMI)
therapy if you have 2 risk factors, if the level is 160.
A. PATHOPHYSIOLOGY
D. CLINICAL IDENTIFICATION OF THE METABOLIC SYNDROME • Ischemic Heart Disease is a condition in which there is an
inadequate supply of blood and oxygen to portion of the
Table 2. Clinical Identification of the Metabolic Syndrome – Any myocardium
Three Risk Factors. • Imbalance between myocardial oxygen supply and
demand
! Even if there a decrease of blood flow (e.g. blood vessel
constriction) but there is still enough oxygen for the
muscle, it is not ischemia.
& The most common cause of myocardial ischemia is
atherosclerotic disease of an epicardial coronary artery (or
arteries) sufficient to cause a regional reduction in
myocardial blood flow and inadequate perfusion of the
myocardium supplied by the involved coronary artery

! You are considered to have a metabolic syndrome when


you have at least three of these factors.
! Abdominal obesity, regardless of the weight and BMI, is
considered to be an independent risk factor
o In females, hips should be bigger than abdominal
circumference
o In males, they could be equal
Figure 3. Pathophysiology of IHD. 4 A picture of the balance
& Metabolic Syndrome of oxygen supply and demand for the myocardium. When there
is ischemia, one of which is imbalanced.
• Also known as syndrome X, insulin resistance syndrome
• Consists of a constellation of metabolic abnormalities that
DETERMINANTS OF MYOCARDIAL OXYGEN DEMAND
confer increased risk of cardiovascular disease (CVD) and
diabetes mellitus • Heart rate
• Major features of the metabolic syndrome include: ! Increase in oxygen demand results to tachycardia
o Central obesity • Myocardial contractility
o Hypertriglyceridemia • Myocardial wall tension (stress)
o Low levels of HDL cholesterol ! If there is thicker myocardium there is bigger demand
o Hyperglycemia
o Hypertension REQUIREMENTS FOR AN ADEQUATE SUPPLY OF O2 TO
• Individuals with metabolic syndrome are twice as likely to THE MYOCARDIUM
die of cardiovascular disease as those who do not, and • Oxygen-carrying capacity of the blood
their risk of an acute myocardial infarction or stroke is ! If there is enough hemoglobin (Hg), then there is also
three-fold higher enough O2 capacity; if a patient is anemic, then there
• With appropriate cardiac rehabilitation and changes in is decreased in capacity
lifestyle (e.g. nutrition, physical activity, weight reduction, & Determined by the inspired level of oxygen,
and in some cases, pharmacologic therapy), the pulmonary function, and hemoglobin concentration
prevalence of the syndrome can be reduced and function
• Adequate coronary blood flow
II. ISCHEMIC HEART DISEASE (IHD) ! If there is constriction, then there is decreased in
coronary blood flow
o Flow occurs in PHASIC fashion
o Majority occurring during DIASTOLE
& About 75% of the total coronary resistance to flow occurs
across three sets of arteries: (1) large epicardial arteries
(Resistance 1 = R1), (2) prearteriolar vessels (R2), and (3)
arteriolar and intramyocardial capillary vessels (R3). In the
absence of significant flow-limiting atherosclerotic
obstructions, R1 is trivial; the major determinant of
coronary resistance is found in R2 and R3.

B. MYOCARDIAL ISCHEMIA
• A reduction of coronary blood flow caused by fixed and/or
Figure 2. Ischemic Heart Disease. Atherosclerosis limits dynamic epicardial coronary artery (i.e. conductive vessel)
appropriate increase in the perfusion when the demand for flow stenosis, an abnormal constriction or deficient relaxation of
is augmented, e.g. exertion or excitement.

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coronary microcirculation (i.e. resistance vessels), or o Example: not expected in young females and those
reduced oxygen-carrying capacity of the blood without a family history - unless the patient is an illicit
! Resistance vessels - enmeshed within the drug user
myocardium
! Conductive vessels - epicardial or outside the
myocardium
& Inadequate perfusion causes myocardial tissue oxygen
tension to fall. This may cause transient disturbances of
the mechanical, biochemical, and electrical functions of the
myocardium.
o Mechanical: Abrupt development of severe ischemia
(as occurs with total or subtotal coronary occlusion), is
associated with almost instantaneous failure of
normal muscle relaxation and then contraction.
o Biochemical: There is decreased fatty acid oxidation
and increased glucose conversion to lactate,
decreasing intracellular pH and myocardial stores Figure 4. This diagram presents how atherosclerotic
of ATP and creatine phosphate. Impaired cell plaque build-up impedes blood flow.
membrane function leads to the leakage of potassium
and the uptake of sodium by myocytes as well as
increase in cytosolic calcium.
o The severity and duration of the imbalance between
myocardial oxygen supply and demand determine
whether the damage is reversible (<20min for total
occlusion in the absence of collaterals) or permanent,
with subsequent myocardial necrosis (>20min).
Figure 5. Atherosclerosis.
Coronary Flow Reserve (CFR)
• The ability of the coronary arteries to increase blood flow in
• Fixed coronary atherosclerotic lesion of at least 50% show
response to increased cardiac metabolic demand.
myocardial ischemia during increased myocardial
metabolic demand as the result of a significant reduction in
III. STABLE ANGINA PECTORIS Coronary Flow Reserve (CFR).
• First spectrum of IHD ! 50% of the area is already coronary artery disease
• The episodic clinical syndrome is due to transient ! If 50% stenosed or blocked, when you exert effort,
myocardial ischemia there is chest pain as supply is decreased
! Chest pain during exertion, relieved by rest • These patients are not able to increase their coronary
! When there is exertion, there is increase in myocardial blood flow during stress to match the increased myocardial
demand, leading to ischemia. But at rest, there is not metabolic demand, thus they experience angina.
enough constriction to cause ischemia. • Fixed atherosclerotic lesions of at least 90% almost
! Example: Your HR is 60 at rest so your demand is not
completely abolish the flow reserve; patients with these
increased. But if one gets angry or climbs the stairs,
lesions may experience angina at REST.
there is increased HR
! Even when lying down, you already feel chest pain.
! The demand of the body increases, the heart pumps
more blood toward the muscles, but the heart itself PRINZMETAL’S VARIANT ANGINA (PVA)
would have decreased coronary blood flow (CFR).
Myocardial demand increases but the supply is
decreased because of the constriction (due to
coronary artery disease)
• Males constitute ~70% of all patients with angina pectoris
and an even greater proportion of those less than 50 years
of age
• However, it is important to note that angina pectoris in
women and diabetics is often atypical in presentation
o Diabetics would present with shortness of breath
• Atherosclerosis
o Most common cause of epicardial coronary artery Figure 6. Focal vasospasm as presented in Prinzmetal Angina.
stenosis and, hence, angina pectoris
& Chronic severe coronary narrowing and myocardial ! One of the kinds of Stable Angina
ischemia frequently are accompanied by the • Resting angina associated with ST-segment elevation
development of collateral vessels, especially when the caused by focal (epicardial) coronary artery spasm.
narrowing develops gradually. When well developed, & The cause of the spasm is not well defined, but it may be
such vessels can by themselves provide sufficient related to hypercontractility of vascular smooth muscle due
blood flow to sustain the viability of the myocardium at to adrenergic vasoconstrictors, leukotrienes, or serotonin
rest, but not during conditions of increased demand. & Coronary spasm can also reduce CFR significantly, leading
! Always remember if the patient would have a setting for to severe transient myocardial ischemia and occasionally
coronary artery disease. Knowing the risk factors are infarction.
important (REMEBER THE TABLE!) ! Does NOT ALWAYS lead to infarction unless spasm is
sustained

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! Does NOT ALWAYS require a setting of • A number of extravascular forces produced by contraction
atherosclerosis / lipid deposit in the intima but causes of adjacent myocardium and intraventricular pressures can
spasm influence coronary microcirculation resistance and thus
! Sometimes spontaneous, sometimes initiated by reduce CFR.
COLD TEMPERATURE • Extravascular compressive forces are highest in the
o Ex: patient would be taking a cold shower and he subendocardium and decrease toward the subepicardium.
would feel chest pain • Left ventricular (LV) hypertrophy together with a higher
! Can be prevented by Calcium Channel Blockers myocardial oxygen demand (e.g. during tachycardia)
! But the most common pathology found in patients with this cause greater susceptibility to ischemia in subendocardial
variant is atherosclerosis layers.
o Focal disease to cause a spasm, but not significantly
obstructing during rest nor exertion
& Atherosclerotic plaques in at least one proximal
coronary artery occur in about half of patients, and in
these patients, spasm usually occurs within 1cm of the
plaque.
& Focal spasm is most common in the right coronary
artery, and can occur in many arteries simultaneously.
& Coronary angiography demonstrates transient coronary
spasm as the diagnostic hallmark of PVA
• Approximately 30% of patients with chest pain - have
normal or minimal atherosclerosis of coronary arteries.
• Caused by functional and structural alterations of small Figure 8. Left Ventricular Hypertrophy. ! This is one of the
coronary arteries and arterioles (i.e. resistance vessels). causes of angina. One of the factors of oxygen demand is
• Resistance vessels are responsible for as much as 95% of myocardial wall stress. Conditions that could cause thickness in
coronary artery resistance, with the remaining 5% being the myocardium are aortic stenosis, athletic heart, chronic
from epicardial coronary arteries (i.e. conductive vessels). hypertension, sarcoidosis, and hypertrophic cardiomyopathy.
All these conditions would increase susceptibility for myocardial
MICROVASCULAR ANGINA ischemia as these compress the myocardial vessels.

• Myocardial ischemia can also be the result of factors


affecting blood composition such as,
o Reduced oxygen-carrying capacity of blood, as is
observed with severe anemia (hemoglobin, <8g/dL)
o Elevated levels of carboxyhemoglobin
! Carboxyhemoglobin increases the propensity for
ischemia by carbon monoxide because carbon
monoxide has a higher binding-capacity for
hemoglobin than oxygen
• The latter may be the result of inhalation of carbon
monoxide in a closed area or of long-term smoking.

A. CLINICAL PRESENTATION OF STABLE ANGINA


• Retrosternal chest discomfort (pressure, heaviness,
squeezing, burning, or choking sensation) as opposed to
frank pain
• Pain localized primarily in the epigastrium, back, neck, jaw,
or shoulders
Figure 7. Large and small coronary arteries as presented in • Pain precipitated by exertion, eating, exposure to cold, or
a patient with angina. emotional stress, lasting for about 1-5 minutes and relieved
by rest or nitroglycerin
• Coronary arterioles not visualized during regular coronary • Pain intensity that does not change with respiration
catheterization (arterioles meshed into the myocardium). (pleuritis), cough, or change in position
• Angina due to dysfunction of small coronary arteries and & Myocardial ischemic discomfort does not radiate to the
arterioles is called microvascular angina. trapezius muscles, which is more typical of pericarditis
& There is an abnormal constriction or failure of normal • Pain on the RIGHT side is more common (REMEMBER!)
dilation of the coronary resistance vessels
! Ex. If you did an angiogram, but there was no lesion
found in the epicardium. Sometimes, the chest pains
would be from the microvascular angina, which could
only be seen by perfusion imaging.
• Several diseases, such as diabetes mellitus, hypertension,
and systemic collagen vascular diseases (e.g. systemic
lupus erythematosus, polyarteritis nodosa)
• Believed to cause microvascular abnormalities with
subsequent reduction in CFR.
Figure 9. Common points of pain in stable angina.

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B. DIAGNOSTIC TESTS OF STABLE ANGINA BETA-ADRENERGIC BLOCKING AGENTS


• Chest radiography • Work by competing with endogenous catecholamine for
o Usually normal in angina pectoris but may show beta-adrenergic receptors
cardiomegaly in patients with previous MI, ischemic • Reduce myocardial oxygen consumption via several
cardiomyopathy, pericardial effusion, or acute effects, including decrease in resting and exercise heart
pulmonary edema rates and reductions in myocardial contractility and
! To rule out other causes of chest pain afterload
• Graded exercise stress testing ! Decrease in heart rate, decrease in demand
o This is the most widely used test for the evaluation of (REMEMBER!)
patients presenting with chest pain and can be • Classified as nonselective, beta-1 selective, and having
performed alone and in conjunction with intrinsic sympathomimetic effects
echocardiography or myocardial perfusion scintigraphy • Ex. Metoprolol, Bisoprolol, Carvedilol, Atenolol
! The speed of the treadmill increases with every stage
• Pharmacologic stress testing CALCIUM CHANNEL BLOCKERS
o Almost the same as graded exercise stress test, but ! Dihydropyridines; decrease the heart, decrease in
with the use of pharmacologic agents that would vasoconstrictions
increase the heart rate of the patients like, Dobutamine • Reduce transmembrane flux of calcium via calcium
(with increase in doses) channels.
• Coronary artery calcium (CAC) scoring by fast CT • Cause smooth muscle relaxation, resulting in peripheral
o The primary fast CT methods for this application are arterial vasodilation and afterload reduction.
electron-beam CT (EBCT) and multi-detector CD • Indicated when symptoms persist despite treatment with
(MDCT) beta-blockers or when beta-blockers are contraindicated.
• Other tests that may be useful include the following:
• Also indicated in patients with Prinzmetal angina with or
o ECG
without nitrates.
§ Including exercise with ECG monitoring and
• Ex. Amlodipine, Verapamil, Diltiazem
ambulatory ECG monitoring
o Selective coronary angiography
LONG – ACTING NITRATES
§ Definitive diagnostic test for evaluating the
anatomic extent and severity of CAD • Reduce LV preload and afterload by venous and arterial
dilation, which subsequently reduces myocardial oxygen
C. MANAGEMENT OF STABLE ANGINA consumption and relieves angina.
• Also cause dilation of epicardial coronary arteries,
• General treatment measures include the following:
which is beneficial in patients with coronary spasm.
o Encouragement of smoking cessation
• In addition, nitroglycerin has antithrombotic and antiplatelet
! Smoking causes vasoconstriction and increase in
effects in patients with angina pectoris.
heart rate
• No evidence suggests that nitrates improve survival or slow
o Treatment of risk factors (e.g. hypertension, diabetes
progression of coronary artery disease.
mellitus, obesity, hyperlipidemia)
! Only addresses symptoms of acute chest pains
• In patients with CAD, efforts should be made to lower the
• Ex. Isosorbide mononitrate/dinitrate
low-density lipoprotein (LDL) level (e.g. with a statin).
Current Adult Treatment Panel III (ATP III) guidelines
ANGIOTENSIN – CONVERTING ENZYME (ACE) INHIBITORS
are as follows: REMEMBER!!!
o In high-risk patients, a serum LDL cholesterol level of • Angiotensin-converting enzyme (ACE) Inhibitors have been
<100 mg/dL is the goal shown to reduce rates of death, MI, stroke, and need for
o In very high-risk patients, an LDL cholesterol level revascularization procedures in patients with coronary
goal of <70 mg/dL is a therapeutic option artery disease or diabetes mellitus and at least one other
o In moderately high-risk persons, the recommended cardiovascular risk factor, irrespective of the presence of
LDL cholesterol level is <130 mg/dL, but an LDL hypertension or heart failure.
cholesterol level of 100 mg/dL is a therapeutic option • The 2009 Canadian Hypertension Education Program
o Non-high-density lipoprotein (HDL) cholesterol level is recommends beta-blockers and ACE inhibitors as first- line
a secondary target of therapy in persons with high therapy that patients with angina, recent myocardial
triglyceride levels (>200 mg/dL); the goal in such infarction or heart failure
persons is a non-HDL cholesterol level 30 mg/dL • Ex. Captopril, Ramipril, Enalapril
higher than the LDL cholesterol level goal ! Majority of the guidelines recommend the giving of Beta
Blockers and ACE Inhibitors as first line therapy for patients
ANTIPLATELETS with angina. ACE inhibitors also slow the progression of
! Not really recommended; known as blood thinners atherosclerosis. The actions of angiotensin are
• Aspirin vasoconstriction, apoptosis or myocardial cell death. If
o Prevents platelet aggregation by irreversible angiotensin is increased, it’s a toxin to muscle.
cyclooxygenase inhibition with subsequent
suppression of thromboxane A2 IV. CORONARY REVASCULARIZATION PROCEDURES
o Antiplatelet effect can last as long as 7 days ! If they are not relieved by medication treatment, there are
• Clopidogrel 2 main coronary revascularization procedures,
o Selectively inhibits ADP binding to platelet receptor percutaneous coronary intervention (PCI) with or
and subsequent ADP-mediated activation of GPIIb/ without coronary stenting and coronary artery bypass
IIIa complex, thereby inhibiting platelet aggregation grafting (CABG), which can be done. First, we introduce
o Consider in patients with contraindication to aspirin oral medical therapy. However, if the condition does not
improve and they continue their old lifestyle and they still
have chest pain, you do revascularization procedures.

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& Revascularization should be considered in the presence of when you do the balloon dilatation it injures the endothelium
unstable phases of the disease, intractable symptoms, again precipitating another thrombotic event.
severe ischemia or high-risk coronary anatomy, diabetes,
and impaired left ventricular (LV) function. B. CORONARY ARTERY BYPASS GRAFTING (CABG)
& Revascularization should be employed in conjunction with & Anastomosis of one or both of the internal mammary
but not replace the continuing need to modify risk factors arteries or a radial artery to the coronary artery distal to the
and assess medical therapy. obstructive lesion is the preferred procedure.
! If you cannot introduce stenting, then you open the chest.
A. PERCUTANEOUS CORONARY INTERVENTION OR PCI (WITH OR Then you bypass. You usually bypass the lungs and the
WITHOUT CORONARY SETTING) heart with a bypass machine. The machine oxygenates the
" Percutaneous coronary intervention (PCI), also known blood because you temporarily stop the heart. Most of the
as coronary angioplasty, is a nonsurgical technique for thoracocardiovascular surgeons stop the heart so they can
treating obstructive coronary artery disease, including easily put the bypass using the internal mammary artery or
unstable angina, acute myocardial infarction (MI), and saphenous vein graft. They put it in the aorta, then distal to
multi-vessel coronary artery disease (CAD). the disease. So that the blood perfusion will improve.
& PCI involving balloon dilatation usually accompanied by 4 If angioplasty does not work and we have multiple lesions,
coronary stenting is widely used to achieve CABG is used.
revascularization of the myocardium in patients with
symptomatic IHD and suitable stenoses of epicardial
coronary arteries.
! In PCI, if constricted with atherosclerosis, you introduce a
balloon and then you inflate the balloon to dilate the
coronary artery. Then you introduce a stent to prevent
recoiling or re-stenosis. Because if you just use a balloon,
it will recoil. We introduce a stent, which acts as a scaffold
to prevent re-stenosis or recoiling.

ANGIOPLASTY AND STENT DEPLOYMENT


4 If medical treatment doesn’t work and your patient is high
risk then you start thinking about invasive management
which can be in the form of angioplasty (with coronary
angiogram), implantation of stent, CABG, angioplasty
PTCA without employment of the stent
Figure 11. Coronary bypass surgery

Figure 12. Difference in the approach to the lesion with


percutaneous coronary intervention (PCI) and
coronaryartery bypass grafting (CABG). PCI is targeted at
the “culprit” lesion or lesions, whereas CABG is directed at the
epicardial vessel, including the culprit lesion or lesions and
future culprits, proximal to the insertion of the vein graft, a
difference that may account for the superiority of CABG, at least
in the intermediate term, in patients with multivessel disease.

GUIDE QUESTIONS
1. A 65 year old male with coronary artery disease, post
coronary artery bypass grafting, was rushed to the ER
due to shortness of breath, easy fatigability, and pedal
edema for two days. BP was 100/60 mmHg and HR was
Figure 10. Angioplasty. Insert a catheter with a balloon in it 60 bpm. Auscultation of lungs revealed bilateral mid to
and if it is able to pass the atheroma then it is a way of bringing basal rales and wheezes. The following medications
in the balloon which will be used to dilate the artery. After may be given:
inserting the balloon you remove the endoplasmic catheter a. Captopril, Spironolactone, Furosemide
leaving behind an open artery. However, today we just do not b. B. Enalapril, Metoprolol succinate, Digoxin
leave an open artery after balloon dilatation since soon it will be c. Losartan, Carvedilol, Furosemide
thrombosed again since 1) the artery is already diseased and 2)

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d. Valsartan, Bisoprolol, Digoxin

2. Therapeutic effects of ACE inhibitors include:


a. Decreased water reabsorption by blocking angiotensin
II receptors
b. Increased EF by increasing inotropy and chronotropy
c. Improved cardiac function by reversing LV remodeling
d. All of the above
3. J.K. is a 60 year-old male who sees his cardiologist for
his recurrent chest pain which he claims as chest
heaviness felt behind the sternum. There are times
when he feels the pain even at rest and would last for
3-5 minutes. Sometimes it would occur upon climbing
stairs hurriedly. His treadmill test was negative at 10
METS. It goes away with nitroglycerin. J.K. is probably
suffering from which of the following?
a. Typical angina
B. Unstable angina
C. Prinzmetal angina
D. Pericarditis

Answer Key:
1) A – Beta blockers are not needed for a patient
presenting with pulmonary edema secondary to
impending heart failure , you need following diuretics
to lessen the load of the heart.
2) C
3) C – Typical angina is typically described by exertional
pain that is relieved by nitroglycerin (NTG). Unstable
angina is pain at rest that is unrelieved by NTG.
Prinzmetal angina (also called variant angina) is pain
at rest that is relieved by NTG.

REFERENCES
1. Lecture Notes
2. Recording
3. 2016 Transcription
4. 2017 Transcription
5. Harrison’s Principle of Internal Medicine

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APPENDIX

Figure 1. Formation of Atherosclerosis. ! 1) LDL is present in the arterial bloodstream 2) along with monocytes and cell adhesion
molecules. 3) The monocytes will phagocytize LDL, adhere to the endothelium then 4) enter the tunica media and intima layer of the
arteries. 5) There, the macrophages will be engulfed by the scavenger receptors, which 6) will trigger an inflammation cascade, 7)
forming foam cells, fibrosis and apoptosis.

Table 1. LDL cholesterol goals and culprits for therapeutic lifestyle changes (TLC) drug therapy in different risk categories.

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