cardiovascular disease

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INTRODUCTION

INTERNATIONAL AND LOCAL TRENDS

Cardiovascular disease is caused by disorders of the heart and blood vessels, and includes
coronary heart disease (heart attacks), cerebrovascular disease (stroke), raised blood pressure
(hypertension), peripheral artery disease, rheumatic heart disease, congenital heart disease
and heart failure. Although many cardiovascular diseases (CVDs) can be treated or prevented,
an estimated 17.1 million people die of CVDs each year.
Of an estimated 58 million deaths globally from all causes in 2005, cardiovascular disease (CVD)
accounted for 30%. It is important to recognize that a substantial proportion of these deaths
(46%) were of people under 70 years of age, in the more productive period of life; in addition,
79% of the disease burden attributed to cardiovascular disease is in this age group. Between
2006 and 2015, deaths due to noncommunicable diseases (half of which will be due to
cardiovascular disease) are expected to increase by 17%, while deaths from infectious diseases,
nutritional deficiencies, and maternal and perinatal conditions combined are projected to
decline by 3% (1). Almost half the disease burden in low- and middle-income countries is
already due to noncommunicable diseases (WHO, 2007).
The prevalence of NCD continues to rise in the Philippines and promoting healthy lifestyle is
very much needed and relevant as ever. More than half (58%) of total deaths in the country in
2003 were caused by NCDs. Diseases of the heart and vascular system made up almost one-
third (30.2%) of all deaths (Philippine Health Statistics, 2003).
The four major NCDs in the Philippines are cardiovascular diseases, cancers, chronic obstructive
pulmonary diseases and diabetes mellitus. These diseases are linked by four most common
preventable risk factors related to lifestyle, namely: tobacco use, unhealthy diet, lack of
physical activity and alcohol use.
The Philippines is one of the 23 selected countries that contribute to around 80% of the total
mortality burden attributable to chronic diseases in developing countries, and 50% of the total
disease burden caused by non-communicable diseases worldwide (Lancet, 2007). This is not
surprising since the data shows that 90% of Filipinos have one or more of the six prevalent risk
factors to NCD; i.e., smoking, physical inactivity, hypertension, hypercholesterolemia,
overweight and obesity.

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COMMON ABBREVIATIONS USED
ACS – Acute Coronary Syndrome
AMI – Acute Myocardial Infarction
BMI - body mass index
BMS- bare metal stent
CABG – Coronary Artery Bypass Grafting
CAD – Coronary Artery Disease
CHD - coronary heart disease
CT- Computed Tomography
CVD - cardiovascular disease
DAPT – Dual Anti platelet therapy
DES - Drug-eluting Stent
DASH - Dietary Approaches to Stop Hypertension
ECG – electrocardiogram
INR – International Normalized Ratio
LAD – Left anterior descending
LCA – Left Coronary Artery
LDL - low-density lipoprotein
LVEF – Left Ventricular Ejection Fraction
MRI – Magnetic Resonance Imaging
NCD – Non Communicable Disease
NSTEMI – Non ST segment Myocardial Infarction
OAC – oral anticoagulant
PCI – Percutaneous Coronary Intervention
PT- Prothrombin Time
RCA – Right coronary artery
STEMI – ST segment Myocardial Infarction
WHO - World Health Organization
















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NORMAL ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

Your heart and circulatory system make up your cardiovascular system. Your heart works as a
pump that pushes blood to the organs, tissues, and cells of your body. Blood delivers oxygen
and nutrients to every cell and removes the carbon dioxide and waste products made by those
cells. Blood is carried from your heart to the rest of your body through a complex network of
arteries, arterioles, and capillaries. Blood is returned to your heart through venules and veins. If
all the vessels of this network in your body were laid end to end, they would extend for about
60,000 miles (more than 96,500 kilometers), which is far enough to circle the planet Earth more
than twice!

The one-way circulatory system carries blood to all parts of your body. This process of blood
flow within your body is called circulation. Arteries carry oxygen-rich blood away from your
heart, and veins carry oxygen-poor blood back to your heart.
In pulmonary circulation, though, the roles are switched. It is the pulmonary artery that brings
oxygen-poor blood into your lungs and the pulmonary vein that brings oxygen-rich blood back
to your heart.
In the diagram, the vessels that carry oxygen-rich blood are colored red, and the vessels that
carry oxygen-poor blood are colored blue.
Twenty major arteries make a path through your tissues, where they branch into smaller
vessels called arterioles. Arterioles further branch into capillaries, the true deliverers of oxygen
and nutrients to your cells. Most capillaries are thinner than a hair. In fact, many are so tiny,
only one blood cell can move through them at a time. Once the capillaries deliver oxygen and
nutrients and pick up carbon dioxide and other waste, they move the blood back through wider
vessels called venules. Venules eventually join to form veins, which deliver the blood back to
your heart to pick up oxygen.

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The heart weighs between 7 and 15 ounces (200 to 425 grams) and is a little larger than the size
of your fist. By the end of a long life, a person's heart may have beat (expanded and contracted)
more than 3.5 billion times. In fact, each day, the average heart beats 100,000 times, pumping
about 2,000 gallons (7,571 liters) of blood.
Your heart is located between your lungs in the middle of your chest, behind and slightly to the
left of your breastbone (sternum). A double-layered membrane called the pericardium
surrounds your heart like a sac. The outer layer of the pericardium surrounds the roots of your
heart's major blood vessels and is attached by ligaments to your spinal column, diaphragm, and
other parts of your body. The inner layer of the pericardium is attached to the heart muscle. A
coating of fluid separates the two layers of membrane, letting the heart move as it beats, yet
still be attached to your body.
Your heart has 4 chambers. The upper chambers are called the left and right atria, and the
lower chambers are called the left and right ventricles. A wall of muscle called the septum
separates the left and right atria and the left and right ventricles. The left ventricle is the largest
and strongest chamber in your heart. The left ventricle's chamber walls are only about a half-
inch thick, but they have enough force to push blood through the aortic valve and into your
body.

LAYERS OF THE HEART

The heart is composed of three layers of tissue: the pericardium, myocardium and
endocardium. Pericardium The pericardium or pericardial sac is a double-layered, closed sac
that surrounds the heart. It is composed of a tough, fibrous outer layer termed the fibrous
pericardium, which consists of fibrous connective tissue, and a thin, transparent inner layer
termed the serous pericardium, which consists of simple squamous epithelium (Seeley et al
2008). The fibrous pericardium prevents overdistension of the heart and anchors it in the
mediastinal space. It is attached inferiorly to the diaphragm (Seeley et al 2008). The serous
pericardium is divided into two layers. The parietal pericardium lines the fibrous pericardium
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and the visceral pericardium covers the surface of the heart. The space between the two layers
is termed the pericardial space and is lubricated by a thin layer of serous fluid (pericardial fluid),
which helps to reduce friction as the heart beats in the pericardial sac (Berne and Levy 2001).
Inflammation of the pericardium is called pericarditis and can be caused by trauma, infection or
myocardial infarction. Myocardium The myocardium is the middle layer of the heart – a strong
muscular layer composed of cardiac muscle, which is responsible for pumping blood around the
body. Cardiac muscle is unique. It is striated like skeletal muscle, but is not under voluntary or
conscious nervous control. Cardiac muscle cells contain one or sometimes two nuclei located
centrally (Seeley et al 2008), and because the cells are particularly active they contain
numerous mitochondria. Cardiac muscle cells, in addition to being bound end-to-end, are
bound to adjacent cells at contact points known as intercalated discs, increasing the area of
contact between cells. Each intercalated disc contains many gap junctions – these are areas of
low electrical resistance that allow action potentials to pass easily between cells (Seeley et al
2008). This arrangement of cardiac muscle cells is known as a syncytium (joined cells) and
enables cardiac muscle cells to act as a single unit, resulting in co-ordinated contraction of the
atria and ventricles (Thibodeau and Patton 2010). A further advantage of the syncytium
structure is that cardiac muscle fibres form a continuous sheet of muscle that wrap around the
cavities of the heart. When the fibres contract around the cavities, they generate pressure
ejecting blood out of the heart into and around the pulmonary and systemic circulatory
systems. Endocardium The endocardium is the innermost layer of the heart. It consists of
flattened epithelial cells that line the heart and blood vessels. This smooth inner lining assists
blood flow through the cardiovascular system. Folds of endothelium make up the valves that
control the flow of blood through the heart (Thibodeau and Patton 2010).

The Coronary Artery

Coronary Circulation
The heart muscle, like every other organ or tissue in your body, needs oxygen-rich blood to
survive. Blood is supplied to the heart by its own vascular system, called coronary circulation.
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The aorta (the main blood supplier to the body) branches off into two main coronary blood
vessels (also called arteries). These coronary arteries branch off into smaller arteries, which
supply oxygen-rich blood to the entire heart muscle.
The right coronary artery supplies blood mainly to the right side of the heart. The right side of
the heart is smaller because it pumps blood only to the lungs.
The left coronary artery, which branches into the left anterior descending artery and the
circumflex artery, supplies blood to the left side of the heart. The left side of the heart is larger
and more muscular because it pumps blood to the rest of the body.

CORONARY ARTERY DISEASE (CAD)


Coronary artery disease (CAD) is a type of blood vessel disorder that is included in the general
category of atherosclerosis. The term atherosclerosis comes from two Greek words: athere,
meaning “ fatty mush, ” and skleros, meaning “ hard. ” This combination implies that
atherosclerosis begins as soft deposits of fat that harden with age. Consequently,
atherosclerosis is commonly referred to as “hardening of the arteries.” Although this condition
can occur in any artery in the body, the atheromas (fatty deposits) prefer the coronary arteries.
The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease,
coronary heart disease, and CAD all describe this disease process.
Coronary heart disease (CHD) occurs when fatty deposits known as atherosclerosis line the
coronary arteries—the major vessels of the heart (Figure 1). This causes a reduction in
blood supply and oxygen to heart muscle (National Institute for Health and Care Excellence
(NICE), 2010a). The pain experienced as a result of the build-up of atherosclerosis or ‘plaque’
is known as angina. The symptoms displayed as a result of plaque that is fixed is known
as stable angina. If this plaque becomes less stable, then the formation of a thrombus
or clot may occur. This will manifest as an acute coronary syndrome (ACS). Myocardial
infarction (MI) or heart attack is damage to cardiac muscle due to complete blockage of
a coronary artery that prevents oxygen from reaching it (Thygesen et al, 2007).
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Atherosclerosis is the major cause of CAD. It is characterized by deposits of lipids within the
intima of the artery. Endothelial injury and inflammation play a central role in the development
of atherosclerosis. The endothelium (the inner lining of the vessel wall) is normally nonreactive
to platelets and leukocytes, as well as coagulation, fibrinolytic, and complement factors.
However, the endothelial lining can be injured as a result of tobacco use, hyperlipidemia,
hypertension, toxins, diabetes, hyperhomocysteinemia, and infection causing a local
inflammatory response 2( Fig. 34-1, A) . C-reactive protein (CRP), a protein produced by the
liver, is a nonspecific marker of inflammation. It is increased in many patients with CAD 3 (see
Table 32-6). The level of CRP rises when there is systemic inflammation. Chronic elevations of
CRP are associated with unstable plaques and the oxidation of low-density lipoprotein (LDL)
cholesterol.
CAD is a progressive disease that develops over many years. When it becomes symptomatic,
the disease process is usually well advanced. The stages of development in atherosclerosis are
(1) fatty streak, (2) fibrous plaque, and (3) complicated lesion.
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Atherosclerosis begins with damage to endothelial cells that line the artery wall. Healthy
endothelial cells are generally impermeable to cholesterol and other damaging substances in
the blood and protect the artery against the development of atherosclerosis. Healthy
endothelial cells release nitric oxide (NO) that allow the artery to relax and increase blood flow
in response to a demand such as physical activity. Damage to the endothelium results in
reduced ability of the endothelial cells to release NO and increased permeability to circulating
proteins and cholesterol. Increased permeability results in the formation of atherosclerotic
plaque. Plaques are prone to tear or “rupture,” releasing plaque contents into the blood
stream, prompting a blood clot to form. Plaque rupture and clot formation can lead to unstable
angina, acute myocardial infarction, and cardiac death. Risk factors for atherosclerosis also lead
to stroke and peripheral arterial disease. Additional consequences of atherosclerosis are
congestive heart failure, arrhythmias, unstable angina, and chronic stable angina. As described
above, uncontrolled risk factors result in endothelial dysfunction, and an accumulation of lipids
and other cells in the sub-intimal space of the artery wall. This can lead to myocardial ischemia,
unstable angina, myocardial infarction or sudden cardiac death. Ischemia is the term that
describes both physical symptoms of angina as well as changes in the electrocardiogram that
indicates lack of blood flow to heart muscle tissue. Ischemic symptoms are primarily related to
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an increase in myocardial oxygen demand coupled with a decrease in blood flow and, thus,
decreased oxygen supply. Increased demand occurs regularly throughout the day such as with
physical activity, emotional upset, eating large meals, and exposure to cold. Additionally, poorly
controlled risk factors, such as hypertension that increases myocardial oxygen demand, can
lead to ischemia and anginal symptoms. Prevention of atherosclerosis relies heavily on
intensive management of the cardiac risk factors including medical therapies and lifestyle
change. For persons with chronic stable angina, these interventions are particularly important
in reducing potential lifethreatening vascular events.


CHRONIC STABLE ANGINA

CAD is a progressive disease, and patients may be asymptomatic for many years or may develop
chronic stable chest pain. When the demand for myocardial oxygen exceeds the ability of the
coronary arteries to supply the heart with oxygen, myocardial ischemiaoccurs. Angina, or chest
pain, is the clinical manifestation of reversible myocardial ischemia. Either an increased demand
for oxygen or a decreased supply of oxygen can lead to myocardial ischemia. The primary
reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis. For
ischemia secondary to atherosclerosis to occur, the artery is usually blocked (stenosed) 75% or
more. On the cellular level, the myocardium becomes hypoxic within the first 10 seconds of
coronary occlusion. Myocardial cells are deprived of oxygen and glucose needed for aerobic
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metabolism and contractility. Anaerobic metabolism begins, and lactic acid accumulates. Lactic
acid irritates myocardial nerve fibers and transmits a pain message to the cardiac nerves and
upper thoracic posterior nerve roots. This accounts for referred cardiac pain to the shoulders,
neck, lower jaw, and arms. In ischemic conditions, cardiac cells are viable for approximately 20
minutes. With restoration of blood flow, aerobic metabolism resumes, contractility is restored,
and cellular repair begins. Chronic stable angina refers to chest pain that occurs intermittently
over a long period with the same pattern of onset, duration, and intensity of symptoms.



ACUTE CORONARY SYNDROME

When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS)
develops and encompasses the spectrum of unstable angina (UA), non – ST-segmentelevation
myocardial infarction(NSTEMI), and ST-segmentelevation myocardial infarction (STEMI) ( Fig.
34-8 ). Although each remains a distinct diagnosis, this nomenclature (ACS) reflects the
relationships among the pathophysiology, presentation, diagnosis, prognosis, and interventions
for these disorders. ACS is associated with deterioration of a once stable atherosclerotic plaque.
The once stable plaque ruptures, exposing the intima to blood and stimulating platelet
aggregation and local vasoconstriction with thrombus formation. This unstable lesion may be
partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a
thrombus (manifesting as STEMI). What causes a coronary plaque to suddenly become unstable
is not well understood, but systemic inflammation (described earlier) is thought to play a role.
Patients with suspected ACS require immediate hospitalization.
UNSTABLE ANGINA
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Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a worsening
pattern. The patient with chronic stable angina may develop UA, or UA may be the first clinical
sign of CAD. Unlike chronic stable angina, UA is unpredictable and is an emergency. The patient
with previously diagnosed chronic stable angina describes a significant change in the pattern of
angina. It occurs with increasing frequency and is easily provoked by minimal or no exertion,
during sleep, or even at rest. The patient without previously diagnosed angina describes anginal
pain that has progressed rapidly in the past few hours, days, or weeks, oft en ending in pain at
rest.

ACUTE MYOCARDIAL INFARCTION

A myocardial infarction (MI) occurs because of sustained ischemia, causing irreversible
myocardial cell death (necrosis). Thrombus formation causes 80% to 90% of all acute MIs.
When a thrombus develops, there is no blood flow to the myocardium distal to the blockage,
resulting in necrosis. Contractile function of the heart stops in the necrotic area(s). The degree
of altered function depends on the area of the heart involved and the size of the infarction. The
acute MI process takes time. Cardiac cells can withstand ischemic conditions for approximately
20 minutes before cell death begins. The earliest tissue to become ischemic is the
subendocardium (the innermost layer of tissue in the cardiac muscle). If ischemia persists, it
takes approximately 4 to 6 hours for the entire thickness of the heart muscle to become
necrosed. If the thrombus is not completely blocking the artery, the time to complete necrosis
may be as long as 12 hours. MIs are usually described based on the location of damage (e.g.,
anterior, inferior, lateral, septal, or posterior wall infarc tion). Most involve some portion of the
leftventricle. Th e location of the infarction correlates with the involved coronary circulation.
For example, the right coronary artery provides blood supply to the inferior wall. Blockage of
the right coronary artery results in an inferior wall MI. Anterior wall infarctions result from
blockages in the leftanterior descending artery. Blockages in the leftcircumflex artery usually
cause lateral and/or posterior wall MIs. Damage can occur in more than one location, especially
if more than one coronary artery is involved (e.g., anterolateral MI, anteroseptal MI).

ETIOLOGY AND RISK FACTORS

Non-modifiable risk factors
Age
CHD is more prevalent in people aged over 60 years (NICE, 2010a). The effects of decreasing
cardiac function owing to the ageing process can affect cardiac output leading to
hypertension and a reduced ability to exercise, which itself can lead to a reduction in
cardiac output (Chummum, 2009).
Heredity (Including Race)
There is a higher risk if a patient’s father or brother is under the age of 55 years when
diagnosed with CHD, or a sister or mother under the age of 65 years; however, the relevance of
this should be considered in the case of the older person. Family history is also taken in the
context of other risk factors such as hypertension, dyslipidaemia and smoking (Wrigley and
Lathlean, 2010).
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For people 35 to 47 years of age, the age-adjusted death rate from CHD for African-American
women is 72% higher than that for white women and native Americans. The prevalence of CHD
is lower in Mexican-Americans (Braunwald et al., 2002).
Gender
Men
• Initial cardiac event for men is more often Ml than angina.
• Men report more typical signs and symptoms of angina and MI.
• Men receive more evidence-based therapies (e.g., aspirin, statins, diagnostic catheterization,
PCI) when acutely ill from CAD (e.g., MI) than women.
• Mortality rates from CAD have fallen more rapidly for men than women.
Women
• Women experience the onset of heart disease approximately 10 yrs later than men.
• CAD is the leading cause of death for women, regardless of race or ethnicity.
• Initial cardiac event for women is more often angina than MI.
• More women than men with MI die of sudden cardiac death before reaching the hospital.
• Before menopause, women have higher HDL cholesterol levels and lower LDL cholesterol
levels than men. After menopause LDL levels increase.

Modifiable Risk Factors
Smoking
Those that smoke inhale toxins and chemicals which accelerate atherosclerosis and
increase the risk of MI (Hart et al, 2006). Adults over the age of 60 years actually have
the lowest prevalence of smoking; however, it should be considered that they may be ex-
smokers (Health and Social Care Information Centre, 2013).
Smoking prevalence was shown to be as high as 31% in the population in 2008; with 53%
among males and 12.5% among females. Trend in smoking or tobacco use among adolescents is
seen to be rising (Table 1.5).


Diet and weight
Several dietary factors will lead to an increased risk of CHD in all age groups (Stanner,
2009). While fats are an essential part of the diet to promote cell growth, saturated fats can
raise the levels of LDL, which is then deposited in arteries. Excess salt in the diet can lead to
hypertension. Being obese or underweight have a detrimental effect on the heart. Obesity
increases cardiac workload, whereas malnourishment may lead to muscle wastage, including
cardiac muscle.
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Obesity or overweight can best be assessed using the Body Mass Index (BMI). The BMI is a
measure of body fat based on height and weight. It is calculated by dividing the person’s weight
in kilograms (kg) by the height in meters squared (m2). Overweight is a BMI between 23.0 to
24.9 and obesity is a BMI of 25 and above. The body mass index distribution of Filipino adults >
20 years old is shown to be increasing from 1998 to 2008 (see Table 1.6).

Inactivity
A lack of exercise will lead to increased body weight, insulin resistance, raised cholesterol and
hypertension—all precursors to heart disease (Stanner, 2009).
In the list of risk factors for NCD, physical inactivity tops the list for Filipinos in 2003. As much as
60.5 percent of Filipinos lack physical activity.


High cholesterol
High cholesterol can be hereditary. Total cholesterol is comprised of low-density lipoprotein
(LDL), high-density lipoprotein (HDL) and triglycerides. The ideal goal is for total cholesterol
to be less than 5 mmol/l (European Society of Cardiology (ESC), 2013). However, the ratio of
total cholesterol to HDL is also important, and this should be less than 4 mmol/l.
Hypertension
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High blood pressure is defined as blood pressure that is persistently higher than 140/90
mmHg regardless of age (British Hypertension Society, 2011). Hypertension can contribute to
atherosclerosis.
The prevalence of hypertension by age group is shown to be increasing over the years: 21%
(1998), 22.5% (2003) and 25.3% (2008) (Figure 1.1).

Diabetes
Both type 1 and type 2 diabetes increase risk. Insulin resistance causes vascular
inflammation and eventually atherosclerosis. The incidence of diabetes is predicted to rise
especially in the older person with a subsequent rise in CHD (Rydén et al, 2013).
Diabetes is an independent risk factor for coronary artery disease; this means that having
diabetes even without other risk factors may lead to heart disease. That is because diabetes
accelerates development of atherosclerosis.
The prevalence of high fasting blood sugar was shown to have increased overall from 1998 to
2008. Table 1.8 shows the trend from 1998-2008. Hyperglycemia is based on fasting blood
sugar greater than or equal to 126 mg/dl.


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LABORATORY AND DIAGNOSTIC EXAMINATIONS

COMPUTED TOMOGRAPHY ANGIOGRAPHY
CT angiography (CTA) is an excellent technique in which ECG gating and administration of
intravenous contrast material are used to visualize and measure calcified areas of coronary
areas of coronary plaque and luminal stenosis. Although considered inferior to cardiac
catheterization, CTA can provide visualization of small, tortuous arteries (as small as 1 mm in
diameter). Coronary CTA can provide valuable information on distribution, severity,
morphology, and composition of coronary arterial plaque, along with prognostic information on
the severity of both obstructive (>50% blockage) and nonobstructive (<50% blockage) disease.

TRANSTHORACIC ECHOCARDIOGRAPHY
Echocardiography is useful in assessing the ability of the heart walls to contract and relax. The
transducer is placed on the chest, and images are relayed to a monitor screen. Wall motion is
abnormal in ischemic or infarcted areas.

ELECTROCARDIOGRAPHY (ECG)
ECG is the recording of the electrical activity of the heart. Traditionally this is in the form of a
transthoracic (across the thorax or chest) interpretation of the electrical activity of
the heart over a period of time, as detected by electrodes attached to the surface of the skin
and recorded or displayed by a device external to the body. An ECG recorded in the presence of
pain may document transient ischemic attacks with ST-segment elevation or depression.

D-DIMER TEST
D-dimer tests are ordered, along with other laboratory tests and imaging scans, to help rule out
the presence of a thrombus.

LEFT VENTRICULAR EJECTION FRACTION (LVEF)
An EF is a percentage of blood that is pumped out of the heart during each beat. Ejection
fraction is a key indicator of heart health.

Hyperdynamic = LVEF greater than 70%
Normal = LVEF 50% to 70% (midpoint 60%)
Mild dysfunction = LVEF 40% to 49% (midpoint 45%)
Moderate dysfunction = LVEF 30% to 39% (midpoint 35%)
Severe dysfunction = LVEF less than 30%

CARDIAC MRI
In cardiac MRI, a static magnet, pulsed radiofrequency energy, and gradient magnetic fields are
used to image the body. These studies can be performed with patients at rest or during the
intravenous administration of a pharmacological stress agent such as dobutamine. Cardiac MRI
may be useful for assessment or detection of dynamic cardiac anatomy and ventricular
function, cardiomyopathies and fibrosis, myocardial ischemia and viability through the use of
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pharmacologically induced stress, cardiac masses or pericardial disease disease, valvular
disease, and complex congenital and coronary anomalies.

PT/INR
International normalized ratio (INR) is a calculation made to standardize prothrombin time. INR
is based on the ratio of the patient's prothrombin time and the normal mean prothrombin time.
Prothrombin time is a test to learn how fast the blood clots in patients receiving oral
anticoagulant medication. This test may be used in patients with prosthetic heart valves,
venous thromboembolism, or antiphospholipid syndrome. A blood sample is collected for this
test. The prothrombin time (PT) test is ordered to help diagnose unexplained bleeding, often
along with a partial thromboplastin time (PTT) test. The PT test evaluates the extrinsic and
common pathways of the coagulation cascade, while the PTT test evaluates the intrinsic and
common pathways. Using both examines the integrated function of all of the coagulation
factors. Occasionally, the tests may be used to screen people for any previously undetected
bleeding problems prior to surgical procedures.
The PT and INR are used to monitor the effectiveness of the anticoagulant. The doctor will use
the INR to adjust a person's drug dosage to get the PT into the desired range that is right for the
person and their condition.

OTHER LABORATORY AND DIAGNOSTIC EXAMINATIONS

SERUM CARDIAC MARKERS
Serum cardiac markers are proteins released into the blood from necrotic heart muscle after an
MI. These markers are important in the diagnosis of MI. The onset, peak, and duration of levels
of these markers are shown in. Cardiac-specific troponin has two subtypes: cardiac-specific
troponin T (cTnT) and cardiac-specific troponin I (cTnI). These markers are highly specific
indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine
kinase (CK) MB (CK-MB). Serum levels of cTnI and cTnT increase 4 to 6 hours aft er the onset of
MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days. CK levels begin to rise
about 6 hours after an MI, peak at about 18 hours, and return to normal within 24 to 36 hours.
The CK enzymes are fractionated into bands. The CK-MB band is specific to myocardial cells and
also helps quantify myocardial damage. Myoglobin is released into the circulation within 2
hours after an MI and peaks in 3 to 15 hours. Although it is one of the first serum cardiac
markers to appear after an MI, it lacks cardiac specificity. Its role in diagnosing MI is limited.

LOW DENSITY LIPOPROTEIN
The LDH is plentiful in heart muscle and is released into the serum when myocardial damage
occurs.

STRESS TESTING
Stress testing is one of the most commonly used method of noninvasive assessment of
coronary artery disease. Stress testing involves the use of exercise (for patients who are
physically able) or drugs such as vasodilators and dobutamine (for patients who are physically
unable to exercise) to increase myocardial demand and is used to determine the presence of
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ischemia. Assessment data are collected by using continuous ECG monitoring,
echocardiography, nuclear imaging, or various combinations of these 3 methods.

MULTIDETECTOR COMPUTED TOMOGRAPHY (MTCT)
Another method of noninvasive diagnostic testing is computed tomography (CT). With the
advent of multidetector CT, improvements in spatial and temporal resolution have improved
visualization of the coronary arteries, making this imaging method more reliable for detecting
coronary artery disease. With MDCT, an arm with an x-ray tube located within a moveable
platform (a gantry) rotates around a patient with 165-ms or faster imaging at 3.0-mm intervals.
MDCT testing is conducted during a single breath hold. ECG gating is used, and images are
acquired solely during specific part of the cardiac cycle. Images are obtained during end systole
and mid diastole when the heart motion is the least.

CAC SCORING
The atherosclerotic process involves deposition of calcium in the coronary arteries. Any calcium
deposition in the coronary arteries is considered abnormal.

ELECTRON BEAM CT
In EBCT, an electron beam rotates around the patient who is supine on the table with the arms
extended over the head or at the side. The beam is directed at a stationary tungsten target that
lies beneath the patient. EBCT allows the acquisition of 1.5-3-mm sections with an exposure
time of 50 to 100 ms during a single breath hold. No intravenous contrast material is used, and
the patient does not need to avoid ingesting anything by mouth beforehand. The procedure
requires approximately 10 to 15 minutes. Patients usually experience little to no discomfort,
and the CT tube is typically much larger than that of a traditional magnetic resonance imaging
(MRI) device, so claustrophobia is not much of a concern.

MANAGEMENT
MEDICAL MANAGEMENT

Major goals of care for clients with AMI include the following:
 Initiating prompt care
 Reducing pain
 Delivering successful treatment for the acute pain and reperfusion of the myocardium
 Preventing complications
 Rehabilitating and educating the client and significant others.

PHARMACOLOGIC MANAGEMENT

IV Nitroglycerin.
IV NTG (Tridil) is used in the initial treatment of the patient with ACS. Th e goal of therapy is to
reduce anginal pain and improve coronary blood flow. IV NTG decreases preload and afterload
while increasing the myocardial oxygen supply. The onset of action is immediate. Titrate NTG to
control and stop chest pain. Because hypotension is a common side effect, closely monitor BP
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during this time. Patients who do become hypotensive are often volume depleted and can
benefit from an IV fluid bolus. Tolerance is another side effect of IV nitrate therapy. An effective
strategy for this phenomenon is to titrate the dose down at night during sleep and titrate the
dose up during the day.

Morphine Sulfate.
Morphine sulfate is the drug of choice for chest pain that is unrelieved by NTG. As a vasodilator,
it decreases cardiac workload by lowering myocardial oxygen consumption, reducing
contractility, and decreasing BP and HR. In addition, morphine can help reduce anxiety and fear.
In rare situations, morphine can depress respirations. Monitor patients for signs of bradypnea
or hypotension, conditions to avoid in myocardial ischemia and infarction.

β-Adrenergic Blockers.
β-Adrenergic blockers decrease myocardial oxygen demand by reducing HR, BP, and
contractility. Th e use of these drugs in patients who are not at risk for complications of MI
(e.g., cardiogenic shock) reduces the risk of reinfarction and the occurrence of HF. The
continuation of β-adrenergic blockers indefinitely is recommended.

Angiotensin-Converting Enzyme Inhibitors.
ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI
with an EF of 40% or less. The use of ACE inhibitors can help prevent ventricular remodeling and
prevent or slow the progression of HF. For patients who cannot tolerate
ACE inhibitors, angiotensin II receptor blockers should be considered.

Antidysrhythmic Drugs.
Dysrhythmias are the most common complications after an MI. In general, they are self-limiting
and are not treated aggressively unless they are life threatening (e.g., sustained ventricular
tachycardia). ( Chapter 36 discusses the drugs used in the treatment of dysrhythmias.)

Lipid-Lowering Drugs.
A fasting lipid panel is obtained on all patients admitted with ACS. All patients with elevated
triglycerides and LDL cholesterol should receive lipid-lowering drugs (see Table 34-5 ).
Stool Softeners. After an MI, the patient may be predisposed to constipation because of bed
rest and opioid administration. Stool softeners (e.g., docusate sodium [Colace]) are given to
facilitate bowel movements. This prevents straining and the resultant vagal stimulation from
the Valsalva maneuver. Vagal stimulation produces bradycardia and can provoke dysrhythmias.

Thrombolytic Therapy
Thrombolytic therapy offers the advantages of availability and rapid administration in facilities
that do not have an interventional cardiac catheterization laboratory or when one is too far
away to transfer the patient safely. Treatment of MI with thrombolytic therapy aims to stop the
infarction process by dissolving the thrombus in the coronary artery and reperfusing the
myocardium. Thrombolytic therapy is given as soon as possible, ideally within the first hour and
19

preferably within the first 6 hours after the onset of symptoms. Mortality is reduced by 25% if
reperfusion occurs within 6 hours.

e.g. Dual antiplatelet therapy (DAPT) and Concomitant oral anticoagulation therapy (OAC).
DAPT (clopidogrel and aspirin) and OAC (acenocoumarol).

SURGICAL

Percutaneous Coronary Intervention
Percutaneous Coronary Intervention (PCI) includes percutaneous luminal coronary angioplasty,
rotational atherectomy, directional antrectomy, laser angioplasty, and implantation of
intracoronary stents.
In the US, approximately 1 in 3 patients with CAD undergo less invasive percutaneous coronary
intervention which is directed at treating culprit lesions. For patients with extensive and diffuse
coronary disease, or complex lesions that are not amenable to treatment with balloon
angioplasty or stenting, PCI is a suboptimal strategy. But for suitable candidates, PCI offers the
advantages of lower periprocedural risk, shorter recovery, and lower initial cost. However, since
the focalized approach results in a less complete revascularization than bypass surgery, a major
limitation of percutaneous intervention is the need for additional procedures to address
restenosis (re-narrowing of lumen to >50% occlusion which occurs in 30% to 57% of patients
after PCI)53-55 and atherosclerotic progression in native vessels.
Percutaneous coronary intervention procedure
After providing informed consent, the patient underwent PCI of the RCA and LAD. A 6-Fr
sheath was inserted into the right femoral artery and a 6-Fr guiding catheter (AL 0.75;
Medtronic, Minneapolis, MN, USA) engaged in the RCA. A 0.010-inch guide wire (Wizard 3 g;
Japan Lifeline, Tokyo, Japan), supported by a microcatheter (Finecross, Terumo, Japan) was
successfully advanced to the distal end of the occluded RCA. Balloon catheters (1.5 and 2.0 mm)
were used to expand the occluded artery and a drug-eluting stent (DES) (Promus 2.5928 mm;
Boston Scientific, Natick, MA,USA) was implanted. Intravascular ultrasound revealed the
satisfactory result that the stent was fully expanded (Fig.1c).
Following the RCA, we performed PCI of the LAD, which showed severe stenosis. A 6-Fr guiding
catheter (JL 4.0;Medtronic) was engaged in the LAD and a DES (Promus 2.5 923 mm; Boston
Scientific) was implanted after balloon predilation. Intravascular ultrasound was then
performed to confirm the stent apposition (Fig.1d)

Coronary Artery Bypass Grafting Surgery
Coronary Artery Bypass Grafting Surgery involves the bypass of a blockage in one or more of
the coronary arteries using the saphenous veins, mammary artery, or radial artery as conduits
or replacement vessels. Before surgery, coronary angiography precisely located lesions and
points of narrowing within the coronary arteries.
During traditional CABG surgery, a median sternotomy incision is made through the sternum so
that the heart and aorta can be seen. The client is then placed on cardiopulmonary bypass
(CPB) or the “heart-lung machine” while the bypasses are performed. After being connected to
the bypass, the heart is stopped (cardioplegia) using a solution of iced saline containing
20

potassium. After the bypasses have been performed, the client is taken off the machine, and
the heart takes over again. All the bypasses originally performed using saphenous veins from
the leg as the new conduit. The distal end of the vein is sutured to the aorta, and the proximal
end is sewn to the coronary vessel distal to the blockage. The veins are reversed so that their
valves do not interfere with blood flow.
Approximately 10% of patients with coronary disease undergo CABG in the US, which is
considered the standard approach for treatment of significant left main disease and multivessel
disease, especially when the proximal left anterior descending (LAD) artery is involved. During
surgical revascularization, most of the epicardial vessel is bypassed, including symptom-causing
culprit lesions and, more importantly, “future” culprit lesions which are thought to be
responsible for most mid- and long-term coronary events. In this way, patients who are treated
with CABG generally receive a more complete and durable revascularization, particularly when
internal mammary artery (IMA) grafts are used, and therefore, less frequently need additional
subsequent procedures. These benefits, however, come at the cost of CABG being a major
surgical procedure with attendant risks, including perioperative myocardial infarction (MI),
stroke, and death, as well as potential complications of general anesthesia and
cardiopulmonary bypass such as cognitive impairment. These factors translate into a longer
hospitalization and overall recovery and higher initial cost, compared to percutaneous
intervention.


Balloon aortic valvuloplasty procedure
A 14-Fr sheath was inserted into the right femoral artery. Balloon aortic valvuloplasty was
performed using the retrograde femoral approach. To stabilize the balloon position across the
valve, the heart was paced at a high rate (200 beats/min) until the blood pressure fell to 50
mmHg before inflation. Pacing was continued until the balloon was fully deflated. Tyshak
(NuMED, Hopkinton, NY, USA) balloons of 15 960 mm, 18960 mm, and 20960 mm, respectively,
were placed across the aortic valve. After inflation of each balloon, the left ventricle to aortic
pressure gradient was markedly reduced and there was no increase in aortic regurgitation.
Finally the aortic valve area was 1.2 cm2 and the mean pressure gradient was 23 mmHg. She
was discharged to her home 4 days after the procedure. One month later, her dyspnea had
greatly improved (New York Heart Association functional class II).

Surgical methods only ease the manifestations. Surgery cannot halt the process of
atherosclerosis, although it may prolong life in some cases.



21

NURSING MANAGEMENT
REDUCE RISK FACTORS


PHYSICAL ACTIVITY
A physical activity program should be designed to improve physical fitness by following the FITT
formula: Frequency (how often), Intensity (how hard), Type (isotonic), and Time (how long).
Everyone should aim for at least 30 minutes of moderate physical activity on most days of the
week. In addition, adding weight training to an exercise program two days a week can help
treat metabolic syndrome and improve muscle strength. Examples of moderate physical activity
include brisk walking, hiking, biking, and swimming. Regular physical activity contributes to
weight reduction, reduction in systolic BP, and, in some men more than women, increase in
HDL cholesterol. The AHA has two programs to encourage people (Start Walking Now at
http://startwalkingnow.org), and especially women (My Heart, My Life at
http://www.startwalkingnow.org), to increase their daily physical activity.


NUTRITIONAL THERAPY
The National Heart, Lung, and Blood Institute recommends therapeutic lifestyle changes for all
people to reduce the risk of CAD by lowering LDL cholesterol. These recommendations
emphasize a decrease in saturated fat and cholesterol and an increase in complex
carbohydrates (e.g., whole grains, fruit, vegetables) and fiber ( Tables 34-3 and 34-4 ). Fat
22

intake should be about 30% of calories, with most coming from mono- and polyunsaturated
fats ( Fig. 34-3 ). Red meat, egg yolks, and whole milk products are major sources of saturated
fat and cholesterol and should be reduced or eliminated from diets. If the serum triglyceride
level is elevated, the guidelines recommend reducing or eliminating alcohol intake and simple
sugars. Omega-3 fatty acids reduce the risks associated with CAD when eaten regularly. For
individuals without CAD, the AHA recommends eating fatty fish twice a week because fatty fish
such as salmon and tuna contains two types of omega-3 fatty acids: eicosapentaenoic acid
(EPA) and docosahexaenoic acid (DHA). Patients with CAD are encouraged to take EPA and DHA
supplements with their diet. The AHA also recommends eating tofu and other forms of
soybean, canola, walnut, and flaxseed because these products contain alpha-linolenic acid,
which becomes omega-3 fatty acid in the body. For more information on the AHA ’ s nutritional
recommendations, see their website listed in the Resources section at the end of this chapter .
Lifestyle changes, including a low-saturated-fat, high-fiber diet; avoidance of tobacco; and
increase in physical activity, can promote the reversal of CAD and reduce coronary events.

PRIORITY NURSING CARE PLAN
1. Acute Pain

ASSESSMENT:
SUBJECTIVE:
Patient verbalized squeezing and pressing sensation at chest that radiates to the left shoulder
and upper arm
OBJECTIVE:
Pain scale: 8 of 10
Pallor and diaphoresis
Elevated PR, RR, BP
Facial grimace
Hands pressing on chest

DIAGNOSIS: Acute Pain related to myocardial ischemia resulting from coronary artery occlusion

PLANNING: The client will experience improved comfort of the chest, as evidenced by a
decrease in the rating of the chest pain, the ability to rest and sleep comfortably, less need for
analgesia or nitroglycerine, and reduced anxiety.

INTERVENTIONS:
1. Assess the characteristic of chest pain, including location, duration, quality, intensity,
presence of radiation, precipitating and alleviating factors, and associated
manifestations. Have the client rate pain on a scale of 0 to 10 and document findings in
nurses’ notes.
2. Assess the respirations, blood pressure, and heart with each episode of pain.
3. Monitor the response to drug therapy. Notify the physician if pain does not abate within
15 to 20 minutes.
23

4. Provide calm, efficient manner that reassures the patient and minimizes anxiety. Stay
with the client until discomfort is relieved.
5. Limit visitors as the client requests.
6. Administer morphine as ordered.
7. Administer nitrates as ordered.

EVALUATION: The client should be pain-free within 15 to 20 minutes after administration of
drug therapy. The client will verbalize feeling of relief of pain and will not exhibit associated
manifestations of pain.

2. Ineffective Tissue Perfusion (Cardiopulmonary)

ASSESSMENT:
SUBJECTIVE:
Patient verbalized squeezing and pressing sensation at chest that radiates to the left shoulder
and upper arm
OBJECTIVE:
Pain scale: 8 of 10
Dyspnea
Pallor and diaphoresis
Elevated PR, RR, BP
Facial grimace
Hands pressing on chest

DIAGNOSIS: Ineffective Tissue Perfusion (Cardiopulmonary) related to thrombus in coronary
artery resulting to altered blood flow to myocardial tissues.

PLANNING: The client will demonstrate improved cardiac tissue perfusion, as evidenced by a
decrease in the rating of pain and resolving ST segments.

INTERVENTIONS:
1. Keep the client on bed rest with a quiet environment
2. Administer oxygen as ordered.
3. Administer thrombolytics or send the client for angioplasty as ordered.
4. Monitor ST segments.

EVALUATION: The return of ST segments to baseline is dependent on the degree of ischemia
and rapidness of treatment. Pain scale rating markedly decreased or alleviated.






24

3. Decreased Cardiac Output

ASSESSMENT
SUBJECTIVE: Patient verbalized having strong and fast heartbeats and the feeling of restlessness
and weakness.
OBJECTIVE:
Tachycardia
Dysrhythmias
Dyspnea
Pallor, cold clammy skin
Weak peripheral pulses
ECG changes
Decreased ejection fraction

DIAGNOSIS: Decreased Cardiac Output related to negative inotropic changes in the heart
secondary to myocardial ischemia, injury and/or infarction.

PLANNING: The client will demonstrate improved cardiac output, as evidenced by normal
cardiac rate, rhythm, and hemodynamic parameters, dysrhythmias, and absence of angina.

INTERVENTIONS:
1. Assess for and document the following: mental status, lung sounds, blood pressure,
heart sounds, urine output, peripheral perfusion, ABG levels and hemodynamic
parameters every 2 to 4 hours and as needed.
2. Maintain hemodynamic parameters by monitoring the effects of beta-blockers and
inotropic agents.
3. Monitor and assess angina for type, severity and duration.


EVALUATION: After 2 to 3 days of admission, the client will have normal hemodynamic
pressures, nomal vital signs, clear breath sounds, no SOBs, normal ABG values, and normal
sinus rhythm with rate between 60 and 100 beats/min.












25

REFERENCES
BOOKS

Black, Joyce M., Hawks, Jane Hokanson. (2005). Medical-Surgical Nursing: Clinical Management
for Positive Outcomes. (7
th
ed.). Philadelphia, PA: Elsevier.

Doenges, Marilynn E., Moorhouse, Mary Frances, Murr, Alice C. (2008). Nurse’s Pocket Guide
Diagnosis, Prioritized Interventions, and Rationales. (11
th
ed.). Philadelphia, PA: F.A Davis.

JOURNALS FROM ONLINE DATABASE

Senior, B., & Swailes, S. (2007). Inside management teams: Developing a
teamwork survey instrument. British Journal of Management, 18, 138-153. doi:10.1111/j.1467-
8551.2006.00507.x

Lacalzada et al. (2013). Recurrent Intraventricular Thrombus Six Months after ST-elevation
Myocardial Infarction in a Diabetic Man: a Case Report. BMC Research Notes, 6:348.
http://www.biomedcentral.com/1756-0500/6/348

Anadolu Kardiyol Derg Ertaş et al. (2012). Drug eluting stents., 12: 676-83 677

Barrett, Julie EM, Davenport, J. (2014). Managing coronary heart diseasein older people: age is
no barrier.

Frostegård, J. (2013). Immunity, atherosclerosis and cardiovascular disease. BMC Medicine,
11:117 http://www.biomedcentral.com/1741-7015/11/117

Hoffman, D., Tranbaugh, R. (2014). Coronary artery bypass graft (CABG) and the diabetic
patient: current perspectives. Dovepress http://dx.doi.org/10.2147/RRCC.S39994

Grech, Ever D. Pathophysiology and investigation of coronary artery disease. British Medical
Journal; May 10, 2003; 326, 7397; ProQuest pg. 1027

Maekawa, Y., Kawamura, A., Furuta, A., Yuasa, S., & Fukuda, K. (2012). A case of severe aortic
stenosis with severe coronary artery disease that was successfully treated by balloon aortic
valvuloplasty and percutaneous coronary intervention. Heart Vessels.27:528–531 DOI
10.1007/s00380-011-0208-3

Berra, K., Fletcher, B., & Miller, N. H. (2008). Chronic stable angina: Addressing the needs of
patients through risk reduction, education and support. Clin Invest Med 2008; 31 (6): E391-
E399.

Libby, P. and Theroux, P. (2005). Pathophysiology of Coronary Artery Disease. AHA Journals doi:
10.1161/CIRCULATIONAHA.105.537878
26

Ramos, L. (2014). Cardiac Diagnostic Testing: What Bedside Nurses Need to Know. American
Association of Critical Nurses doi: http://dx.doi.org/10.4037/ccn2014361

Thygesen, K., Alpert, J. & Harvey D. (2007). Universal definition of myocardial infarction.
European Heart Journal 28, 2525–2538 doi:10.1093/eurheartj/ehm355

INTERNET SOURCES

World Health Organization Prevention of cardiovascular disease : guidelines for assessment and
management of total cardiovascular risk. Retrieved from http://www.who.com

Anatomy of the Heart. Retrieved from http://www.texasheart.org/HIC/Anatomy/anatomy2.cfm

Anatomy of the Heart. www.nlm.nih.gov/medlineplus/ency/imagepages/8672.htm

DISSERTATIONS AND THESIS

Kim, Lauren Ji-Yon (2006). Evaluation of treatments for coronary artery disease utilizing
contemporary statistical methods. University of Pittsburgh, ProQuest, UMI Dissertations
Publishing.