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Risk stratification and dental management of the


patient with cardiovascular diseases. Part I:
Etiology, epidemiology, and principles of medical
management
Tad Steinhauer, DDS1/Samer A. Bsoul, BDS, MS2/
Geza T. Terezhalmy, DDS, MA3
The heart pumps blood through a system of blood vessels under the control of an electric
conduction system to deliver oxygen to all cells of the body. When the blood volume
becomes greater than the limited volume capacity of the vascular system, the patient
develops hypertension. When the myocardium does not get enough oxygen because of
coronary artery disease, the patient will experience angina pectoris. If oxygen deprivation
to the myocardium persists, the patient may develop myocardial infarction. When the conduction system malfunctions, arrhythmias occur and the heart is unable to pump blood
through the vascular system at a regular rate and rhythm. When the heart is no longer
able to pump enough blood to meet the metabolic demands of the body for oxygen, the
patient is said to have developed heart failure. In addition, many of the above conditions
can lead to thromboembolic complications. These cardiovascular diseases are the leading
cause of death in the United States and most other Western countries. In the United
States alone, more than 1 million annual deaths and as many as three times that number
of serious consequences can be attributed to these conditions. To provide care to patients
with cardiovascular disease, oral health care providers must understand the disease, its
treatment, and its impact on the patients ability to undergo and respond to dental care.
(Quintessence Int 2005;36:119137)

Key words: cardiac arrhythmia, cardiovascular disease, coronary artery disease, dental
treatment, heart failure, hypertension, medical management, thromboembolic
disorders

Assistant Professor, Department of Restorative Dentistry,

HYPERTENSION

Section of Removable Prosthodontics, Southern Illinois


University School of Dental Medicine, Alton, Illinois.
2

Resident, Oral Medicine Program, Department of Dental


Diagnostic Science, The University of Texas Health Science
Center at San Antonio Dental School, San Antonio, Texas.

Professor and Head, Division of Oral Medicine, Department


of Dental Diagnostic Science, The University of Texas Health
Science Center at San Antonio Dental School, San Antonio,
Texas.

Reprint requests: Dr Geza Terezhalmy, Division of Oral


Medicine, Department of Dental Diagnostic Science,
University of Texas Health Science Center at San Antonio,
Dental School, Mail code 7919, 7703 Floyd Curl Drive, San
Antonio, TX 78229-3900. E-mail: terezhalmy@uthscsa.edu

Fluid homeostasis is chiefly controlled by the


renin-angiotensin-aldosterone system. The
juxtaglomerular apparatus (JGA) senses low
salt load and low blood pressure. In
response, renin is released into the vascular
compartment, where it reacts with angiotensinogen, converting it to angiotensin I. Angiotensin I, a weak vasoconstrictor, is then converted to angiotensin II via the angiotensinconverting enzyme (ACE). Angiotensin II, a
powerful vasoconstrictor, also acts on the

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adrenal cortex to stimulate the production of


aldosterone, which in turn promotes
increased uptake of sodium and water and
thus the volume expansion necessary to
restore blood pressure. When homeostatic
mechanisms fail and the blood volume
becomes greater than the limited volume
capacity of the vascular system, the patient
develops high blood pressure.

Etiology and epidemiology


Hypertension is characterized by the elevation of systolic and/or diastolic arterial blood
pressures and may be either primary or secondary. Secondary hypertension, by definition, has an identifiable cause1,2:
Renal disease (renal parenchymal disease, renal artery stenosis)
Adrenal abnormalities (primary aldosteronism, Cushing syndrome, pheochromocytoma)
Coarctation of the aorta
Hyperthyroidism
Pregnancy (eclampsia)
Central nervous system disorders (head
injury, infection, hemorrhage, and brain
tumors)
Autonomic hyperactivity
Sleep apnea
Drug related: (1) noncompliance (known
hypertensive patients); or (2) drugdrug
interactions
Drug induced: (1) cyclooxygenase (COX-1
and COX-2) inhibitors; (2) sympathomimetics (decongestants, anorectics,
cocaine, and amphetamines); (3) steroid
hormones (adrenal steroids and hormones of reproduction); (4) cyclosporine
and tacrolimus; or (5) licorice
Primary or essential hypertension is of
unknown etiology, but it appears to be related to hereditary and environmental factors.
Although the exact mechanism is unclear,
the heritable component of hypertension has
been documented in familial and twin studies.3 In genetically susceptible persons, environmental factors (dietary sodium, obesity,
and stress) appear to increase the likelihood
of hypertension. Several populations are
known to be prone to salt sensitivity, includ-

ing African Americans, those with a family


history of hypertension, the obese, and the
elderly.47 Specialized cells located in the
JGA sense tubular sodium ion concentrations and signal changes in glomerular filtration rate and renin production.8 The JGA also
has a dense sympathetic nerve supply, and
sympathetic stimulation has also been
shown to increase renin synthesis.9
Defects in sodium transport have also
been described in patients with high blood
pressure.10,11 Abnormal sodium transport
across the cell membrane increases intracellular sodium concentrations, which leads to
increased intracellular calcium ion concentration and further increased vascular
smooth muscle sensitivity to sympathetic
stimulation. There is also evidence that persons with hypertension may have decreased
nitric oxide activity. Nitric oxide is a vasodilating substance produced by endothelial
cells.12 The mosaic theory holds that multiple
factors sustain elevated blood pressure even
though initially only one aberrant factor may
have been responsible.13 Whereas the causes and mechanisms responsible for the
development of hypertension are still controversial, the long-term effects of hypertension
on various organ systems have been extensively elucidated. Common to the pathogenesis of all tissue and organ damage are
resistance vascular changes described histologically as either arteriolosclerosis or arteriosclerosis. Additionally, hypertension leads
to increased atherosclerosis.14
In most populations of the world, modified
by genetic and environmental factors, the
blood pressure consistently increases with
age.1522 Recent data suggest that individuals
with healthy blood pressure at 55 years of
age have a 90% lifetime risk of developing
hypertension.23 Hypertension affects approximately 58 million people in the United States
and as many as 1 billion individuals worldwide. Of these, probably fewer than 5% have
a curable cause.24 Hypertension and hypertensive renal disease is the 13th leading
cause of death in the United States.25 The
World Health Organization estimates that
high blood pressure is responsible for one in
every eight deaths worldwide, which makes
it the third leading cause of mortality.26

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Blood pressure (mm Hg)

220
200
180

Systolic
Diastolic
Range

> 160
140159

160
140

120139
> 100
< 120

120

9099
8089

100
80

< 80

60
Normal

Prehypertension

Stage 1
hypertension

Stage 2
hypertension

Fig 1 Classification system for blood pressure adopted by JNC 7.36

Clinical manifestations
Primary hypertension is asymptomatic until
complications develop in target organs, particularly in the kidneys, cardiovascular system, cerebrovascular system, peripheral vascular system, and eyes. The kidneys are
major targets for the ill effects of hypertension, although this damage may be occult
until late in the progression of the disease.27
Clinically, the ultimate pathophysiologic condition is hypertensive nephrosclerosis characterized by decreased glomerular filtration
and tubular dysfunction, which can progress
to end-stage renal disease. Hypertensive
nephrosclerosis may predispose patients to
refractory hypertension, especially in African
Americans.27 Large-scale studies have also
demonstrated a linear relationship between
increasing blood pressure and cardiovascular disease.28 The risk of cardiovascular disease doubles for individuals aged 40 to 70
years with each increment of 20 mm Hg in
systolic or 10 mm Hg in diastolic blood pressure across the entire blood pressure range
from 115/75 to 185/115 mm Hg.29 Chief cardiovascular complications include arteriosclerotic and atherosclerotic changes in
coronary arteries.3033 Coronary artery disease (CAD) leads to angina pectoris and
myocardial infarction. Other cardiovascular
complications include left ventricular (LV)
hypertrophy, which progresses to cardiac
myopathy, dilation, and ultimately failure.3033

Hypertensive events (arteriosclerotic and atherosclerotic vessel disease and increased


vascular resistance) also increase the incidence of ischemic and hemorrhagic
stroke.34,35 Hypertension-induced peripheral
vascular disease is characterized by the
absence of one or more major pulses in the
extremities, while hypertensive retinopathy is
characterized by hemorrhages or exudates,
with or without papilledema.

Diagnosis
The diagnosis of primary hypertension is
based on evidence of elevated systolic
and/or diastolic blood pressure in the
absence of secondary causes. The Seventh
Joint National Committee on Detection,
Evaluation, and Treatment of High Blood
Pressure (JNC 7) provides a new classification of blood pressure for adults aged 18
years or older (Fig 1).36 When systolic and
diastolic pressures fall into different categories, the higher category is used to determine treatment strategies. Patients with prehypertension are at increased risk for progression to hypertension. Those in the
130/80 to 139/89 mm Hg blood pressure
range have twice the risk of developing hypertension as those with lower values.36
The basic evaluation recommended for
patients with elevated blood pressure
includes a review of the medical history, physical examination, and laboratory studies.35,3739

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Ta b l e 1

Therapeutic goals and pharmacologic strategies for hypertension

Therapeutic goal

Pharmacologic strategies

Reduce volume overload


Block 1-adrenergic receptors
Dilate blood vessels

Diuretics
1-adrenergic receptor antagonists
ACE inhibitors
Angiotensin II-receptor antagonists
Calcium-channel blocking agents
1-adrenergic receptor antagonists
2-adrenergic receptor agonists

Reduce sympathetic outflow from the


central nervous system
ACE = angiotensin-converting enzyme.

The medical evaluation of patients with documented elevated blood pressure has three
objectives: (1) rule out identifiable causes of
high blood pressure (see above); (2) identify
cardiovascular risk factors or concomitant disorders that may affect prognosis or treatment
strategies (see below); and (3) assess the
presence or absence of target-organ damage.35 Major cardiovascular risk factors
are35,3739:
Obesity
Dyslipidemia
Diabetes mellitus
Age (> 55 years for men, > 65 years for
women)
Family history of cardiovascular disease (<
55 years for men, < 65 years for women)
Social history (cigarette smoking, alcohol
use/abuse, sedentary lifestyle)
Fewer than 5% of the patients with high
blood pressure have secondary hypertension.21 Indications for specialized diagnostic
procedures to rule out secondary hypertension are: onset of hypertension before age
30 or after age 60, diastolic blood pressure
greater than 120 mm Hg, abrupt onset of
hypertension, hypertensive retinopathy, or
refractory hypertension.3739 Renovascular
disease is the most likely etiologic factor in
younger and older patients suffering from
severe hypertension.

Principles of medical management


The goals of prevention and management of
hypertension are to reduce morbidity and
mortality associated with resistance vascular

disease. This may be achieved by maintaining systolic blood pressure below 140 mm
Hg and diastolic pressure below 90 mm Hg.
Treatment to lower levels may be useful, particularly to prevent stroke, preserve renal
function, and prevent or slow the progression
to heart failure. While the mainstay of treatment for hypertension is pharmacologic,
adoption of a healthy lifestyle is critical for the
prevention of high blood pressure, and it is
an indispensable part of the management of
those with hypertension. Major lifestyle modifications shown to lower blood pressure
include aerobic exercising for 30 to 45 minutes, three to five times a week; weight reduction (in overweight and obese individuals);
adopting a diet rich in fruits, vegetables, and
low-fat dairy products that are rich in potassium and calcium; reduction of dietary sodium;
and moderation of alcohol consumption.35
Pharmacologic strategies include reducing volume overload, blocking adrenergic
receptors in the heart, dilating peripheral
blood vessels, and reducing sympathetic
outflow from the central nervous system
(Table 1). Clinical trial outcome data prove
that thiazide-type diuretics, 1-adrenergic
blocking agents, ACE inhibitors, angiotensin
II-receptor blocking agents, and calciumchannel blocking agents all reduce the complications of hypertension.35 Thiazide diuretics are the initial drugs of choice for most
patients with hypertension. If the initial drug
at full dose has no effect on the blood pressure or causes troublesome side-effects,
substituting a drug from a different class is
recommended. If the initial drug produces
only a partial response but is well-tolerated,

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adding another drug from a different class is


indicated. Most patients with hypertension
will require two or more antihypertensive
agents to achieve their target blood pressure,
especially if the blood pressure is 20/10 mm
Hg above goal. Once antihypertensive drug
therapy is initiated, patients require follow-up
and adjustment of medications at monthly
intervals until the blood pressure is at target.
After the blood pressure is at goal and stable,
follow-up visits are usually at 3- to 6-month
intervals.

CORONARY ARTERY
DISEASE
Aerobic metabolism (conversion of pyruvic
acid to CO2 and H2O) accounts for the majority of the energy produced in cardiac muscles. Anaerobic metabolism is used only in
extreme hypoxia. The factors that increase
the oxygen demand of the heart are: heart
rate, wall tension, and contractile state. The
faster the heart rate, the more oxygen it uses.
The larger the heart, the more oxygen is
required for its contraction. The greater the
force of myocardial contraction, the greater
the amount of oxygen consumed. If there is a
temporary deficiency of oxygen to a portion
of the myocardium, painful coronary insufficiency takes place and the patient is said to
have suffered from an attack of angina pectoris. If the deficient supply of oxygen to a
portion of the myocardium is permanent,
necrosis will develop and myocardial infarction occurs.

Etiology and epidemiology


The hypoxia or anoxia associated with CAD
is due primarily to atherosclerosis. CAD is an
inflammatory disease affecting the large- and
medium-sized arteries of the heart.40,41 Early
lesions reflect functional alterations of arterial
endothelial cells in response to chronic lowgrade irritation caused by disturbances in the
pattern of blood flow. Such injury leads to the
accumulation of amorphous and membranous lipids and monocytes (macrophages
and T-lymphocytes). Further endothelial
injury leads to increased vascular permeabil-

ity and increased interaction among the


endothelium, platelets, and monocytes.
Monocytes, platelets, and endothelial cells
release various vasoactive molecules, such
as cytokines, chemokines, and growth factors, which lead the migration and proliferation of smooth muscle cells and the formation of fibrous tissue. These fibrous lesions
undergo reorganization, exhibiting a core of
necrotic tissue and lipid. When the fibrous
lesions are large enough, they become
occlusive. In later stages, these lesions may
become disrupted and contribute to thrombus formation.
Atherosclerotic plaques and thrombus formation contribute to acute coronary syndromes such as angina pectoris, myocardial
infarction, sudden death caused by arrhythmias, and stroke. In the United States, heart
diseases are the leading cause of death
among both men and women, and cerebrovascular disease is the fourth and third
leading cause of death among men and
women, respectively.25 The progression of
early atherosclerotic lesions to clinical manifestation appears to be more rapid in persons with well-known coronary risk factors,
which include low-density lipoprotein (LDL),
homocysteine, hypertension, and infection.
In addition, CAD increases with tobacco use;
diets high in fat and calories; diets low in
fruits, vegetables, and vitamins E and C; poor
stress management; a sedentary lifestyle;
diabetes mellitus; and hypothyroidism.
Low-density lipoprotein. Most of the cholesterol in plasma is normally carried in the
form of LDL. LDL, modified by oxidation, glycation, aggregation, association with proteoglycans, or incorporation into immune complexes, is a major cause of injury to endothelial and smooth muscle cells.41 After oxidation, LDL may be internalized by macrophages. This internalization tends to minimize the effect of LDL on endothelial and
smooth muscle cells. However, LDL is
chemotactic and can upregulate the expression of genes for macrophage-stimulating
factor and monocyte chemotactic protein
derived from endothelial cells. Consequently,
it can amplify the inflammatory response;
increase the binding of LDL to the endothelium and smooth muscle cells; and perpetuate

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a cycle of inflammation, lipoprotein modification, and more inflammation.


Homocysteine. Homocysteine is toxic to
the endothelium, promotes oxidative damage, stimulates smooth muscle cells, is prothrombotic (activates platelets, plasma-clothing factors, and leukocytes), increases collagen synthesis, and decreases nitric oxide
availability.41,42 Patients with elevated homocysteine are at increased risk of atherosclerosis of coronary, cerebral, and peripheral
arteries and death.41,4345
Hypertension. Angiotensin II is the principal product of the renin-angiotensin cascade.
It is a potent vasoconstrictor, often elevated
in hypertensive patients. Angiotensin II binds
to receptors of vascular smooth muscles,
which leads to increased intracellular calcium ion concentrations, increased smooth
muscle contractions, and smooth muscle
hypertrophy.41 It also increases lipoxygenase
activity and has a proinflammatory effect,
which reduces the formation of nitric oxide
and increases leukocyte adhesion, peripheral resistance, and free-radical formation, contributing to hypercholesterolemia.41
Infection. Both herpes viruses and
Chlamydia pneumoniae have been identified
in atheromatous lesions.41 Although there is
no direct evidence that these organisms
cause the lesion of atherosclerosis, the possibility exists that infection in combination
with other factors may contribute to the
pathogenesis of atherosclerosis in some
patients.

Clinical manifestations
Myocardial ischemia develops either when
myocardial oxygen demand increases to a
level exceeding the capacity of the diseased
coronary arteries to deliver blood or when
coronary vasoconstriction increases coronary resistance so that flow decreases to critical levels.46 Vasoconstriction can be mediated through neural pathways; caused by
endothelial injury secondary to substances
released by aggregating platelets and cigarette smoking; or associated with exposure to
cold or exercising. The myocardial ischemia
caused by either an excessive increase in
myocardial oxygen demand or by vasoconstriction may be silent, may be accompanied

by exertional dyspnea, or may be accompanied by chest pain or angina pectoris.


Frequently, the first clinical manifestations of
CAD are acute myocardial infarction and sudden death caused by arrhythmias.46

Diagnosis
Dyslipidemia. The National Cholesterol
Education Programs Adult Treatment Panel
II, sponsored by the National Institutes of
Health and endorsed by the American Heart
Association (AHA), recommends the routine
measurement of nonfasting total cholesterol
and high-density lipoprotein (HDL) every 5
years.47,48 The American College of Physicians and American Academy of Family Physicians suggest periodic cholesterol measurement in men aged 35 to 65 years and
women aged 45 to 65 years.49 The primary
goal of screening younger people is to promote lifestyle changes, which may provide
long-term benefits later in life. Total cholesterol levels below 200 mg/dL are classified as
desirable blood cholesterol; those 200 to
239 mg/dL are classified as borderline-high
blood cholesterol; and those 240 mg/dL and
above are classified as high blood cholesterol. Patients with desirable blood cholesterol levels (< 200 mg/dL) are given general
dietary and risk reduction education and
advised to have another serum cholesterol
test within 5 years. Patients with borderlinehigh blood cholesterol (200 to 239 mg/dL)
and two other CAD risk factors (hypertension,
diabetes mellitus, severe obesity, family history of CAD, and cigarette smoking) and those
with high blood cholesterol (> 240 mg/dL)
should undergo lipoprotein analysis.
LDL is considered the main risk factor for
CAD. Consequently, LDL levels serve as the
key index for clinical decision making about
cholesterol-lowering therapy. Levels of LDL of
160 mg/dL or higher are classified as highrisk LDL, and those 130 to 159 mg/dL are
classified as borderline-high-risk LDL.
Patients with high-risk LDL levels and those
with borderline-high-risk LDL who have two
other risk factors should have a complete clinical evaluation and begin cholesterol-lowering
treatment. However, LDL represents only a
proportion of the atherogenic lipoproteins
accumulated in plasma and has significant

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limitations in assessing the risk of coronary


heart disease in some patient populations,
such as in individuals with hypertriglyceridemia or mixed hyperlipidemia or even in normolipidemic individuals with diabetes mellitus.50 These limitations are explained by the
abnormal composition of the triglyceride-rich
lipoproteins found in these conditions. NonHDL, which reflects total cholesterol minus
HDL cholesterol (ie, all apolipoprotein Bcontaining atherogenic lipoproteins), may be a
better predictor of cardiovascular risk, and it
may also be a better marker for assessing the
beneficial effects of treatment in patients with
mixed hyperlipidemia or hypertriglyceridemia.
Angina pectoris. Angina pectoris may be
defined as a temporary inability of the coronary arteries to supply the myocardium with
a sufficient amount of oxygenated blood.
The result is hypoxia and chest pain.
Hypoxia, and at times anoxia, results from
certain underlying diseases that tend to limit
or impair coronary blood flow. The most
common of these diseases, as discussed
earlier, is obstruction by fatty deposits, or atherosclerosis. The diagnosis of angina pectoris is based on history and clinical signs
and symptoms. Typical angina presents as
chest tightness or heaviness brought on by
exertion and relieved by rest. The pain frequently radiates to the neck, left shoulder,
down the left arm, and left side of the jaw.
Signs and symptoms may be exacerbated by
cold weather, heavy meals, or states of high
emotion. The clinical examination is important in evaluating patients with chest pain,
allowing the clinician to estimate with a high
degree of accuracy the likelihood of clinically
significant CAD; however, coronary angiography remains the most accurate method for
diagnosing clinically important obstructive
CAD.51 The AHA also recommends the use
of resting 12-lead electrocardiograms (ECG)
in all patients with symptoms suggestive of
angina pectoris.52 Special studies may
include stress testing using nuclear and
echocardiographic imaging, and blood oxygen leveldependent (BOLD) magnetic resonance imaging (MRI).5356
Myocardial infarction. The diagnosis of
acute myocardial infarction is based on the
presence of two of the following three criteria:

(1) signs and symptoms compatible with


myocardial ischemia, (2) typical ECG changes,
and (3) the measurement of creatine kinase
(CK) and myocardial-bound CK (CK-MB)
enzymes.5762 Acute myocardial infarction
resulting from an occlusive thrombus is recognized on an ECG by an ST-segment elevation
in relation to the end of the PR segment.
However, 51% to 85% of patients with chest
pain and ST-segment elevation may have LV
hypertrophy, left bundle-branch block, early
repolarization, or ventricular aneurysm. Elevations in the serum troponin T and troponin I
levels, which are sensitive markers for myocardial injury, have also been used both to test for
acute myocardial infarction and predict
adverse cardiac events.63 MRI is a promising
new approach to diagnosing acute myocardial
infarction.64

Principles of medical management


Whereas the mainstay of treatment for
ischemic heart disease is pharmacologic,
lifestyle modifications such as smoking cessation, dietary control, and increased exercise are also important. The goals of pharmacologic intervention in the management of
CAD (Table 2) are to control symptoms and
reduce mortality by preventing formation,
slowing progression, and causing regression
of atherosclerotic lesions; improve coronary
circulation; reduce the workload of the heart;
and prevent thromboembolic episodes.6568

Surgical intervention
There are two routinely available procedures
for the surgical management of patients with
CAD: (1) percutaneous coronary intervention, such as balloon angioplasty and stent
implantation; and (2) coronary artery bypass
graft (CABG) surgery.68 The advantages of
percutaneous coronary intervention for the
treatment of ischemic heart disease include
a low level of procedure-related mortality,
short hospital stay, and early return to activity. Disadvantages include a risk of acute
coronary occlusion during angioplasty and a
significant risk of restenosis. CABG procedures carry increased risk of mortality in the
first 12 months after surgery but thereafter
appear to reduce the risk of death from CAD
for up to 5 to 10 years.

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Ta b l e 2

Therapeutic goals and pharmacologic strategies for coronary heart


disease

Therapeutic goal

Pharmacologic strategies

Inhibit progression of atherosclerosis

Lipid-lowering agents
HMG-Co-A reductase inhibitors
Nitrates
Calcium-channel blocking agents
1-adrenergic receptor antagonists
Antithrombotic agents
Anticoagulants

Improve circulation in coronary arteries


Reduce workload
Prevent thrombus formation
Prevent coagulation

CARDIAC ARRHYTHMIA
The primary pacemaker of the heart is the
sinoatrial (SA) node. Under the influence of
the autonomic nervous system, the SA node
generates electric impulses at regular intervals and with a frequency of 60 to 100 beats
per minute. The impulses spread rapidly
through the atria and enter the atrioventricular (AV) node. After a brief delay at the AV
node, the impulses propagate over the HisPurkinje system as depolarization progresses
over the ventricles in an anatomically synchronous and hemodynamically effective
fashion. Interruption of this system compromises tissue oxygenation and may lead to
death.

Etiology and epidemiology


Arrhythmia or dysrrhythmia is usually the
result of either abnormal impulse generation
or abnormal impulse conduction. Epidemiologic data indicate that structural coronary
arterial abnormalities and their consequences are the cause of 80% of fatal
arrhythmias69; dilated and hypertrophic cardiomyopathies account for the second
largest number (10% to 15%).69 Other cardiac disorders, such as valvular or congenital
heart disease, primary electrophysiologic
disorders, and genetically determined ionchannel abnormalities, account for only a
small proportion of the cases (< 5%).69

Clinical manifestations
A disturbance in the rhythm of the heart, or
arrhythmia, may manifest as bradyarrhythmia
or bradycardia (slow rhythm) or tachyarrhythmia or tachycardia (rapid rhythm).70
Common disorders of impulse generation
are as follows:

Sinus bradycardia. The heart rate is less


than 60 beats per minute, and the rhythm
is regular. Impulses originate from the
sinoatrial node at a slow rate under the
influence of increased parasympathetic
(vagal) tone. Sinus bradycardia is common in athletes, in patients with hypothyroidism, in patients with increased intracranial pressure, and during treatment
with drugs with negative chronotropic
action (eg, 1-adrenergic receptor antagonists, calcium-channel blocking agents,
digoxin). Symptoms include light headedness, fainting, chest pain, hypotension,
and dyspnea.
Sinus tachycardia. The heart rate is
between 100 and 180 beats per minute,
and the rhythm is regular. Impulses originate from the sinoatrial node at a rapid
rate under the influence of increased sympathetic tone or vagal blockade. Sinus
tachycardia is found in patients after exercise or smoking; in patients with hyperthyroidism, anxiety, toxic states, fever, anemia, severe hemorrhage, debilitation, or
acute or chronic heart disease; and in
patients taking stimulants (eg, tea, coffee)
or medications with positive chronotropic
effects).
Atrial flutter. The heart rate is 250 to 350
beats per minute, and the rhythm is regular. Impulses originate from a single abnormal focus in the atria. The AV node is
unable to transmit all of the impulses, and
the ventricles tend to respond to every
second or third impulse.
Atrial fibrillation. The heart rate is 350 to
450 beats per minute, and the rhythm is
irregular. Impulses originate from multiple
atrial foci, which travel in a random manner in the atria. The ventricles respond to

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only about 120 to 180 of the impulses.


The patient with atrial fibrillation often
presents with palpitations. Stasis of blood
in the fibrillating atrium can lead to blood
clot formation and systemic embolism,
which may present as stroke-like illness or
sudden confusion; acutely painful, pale,
pulseless limbs; and an acute abdomen.
Premature ventricular contractions (PVC).
PVCs are characterized by a pronounced
pause in an otherwise normal rhythm.
Impulses originate from an ectopic ventricular focus. PVCs are considered
benign if fewer than six such pauses are
noted per minute. PVCs may be an occasional finding in otherwise healthy adults,
and the incidence increases with age,
fatigue, emotional stress, and the use of
coffee and tobacco. PVCs are significant
in a patient with cardiovascular disease
(coronary heart disease, valvular disease,
hypertension, congestive heart failure).
Ventricular tachycardia. Ventricular tachycardia usually evolves from an ectopic
focus in the right or left ventricle, which
depolarizes at a rate of 140 to 220 beats
per minute. It is a serious arrhythmia that
occurs in patients with organic heart disease and may be precipitated by drugs
such as digoxin and tricyclic antidepressants.
Ventricular fibrillation. The heart rate is
350 to 450 beats per minute, and the
rhythm is irregular. The myocardium
depolarizes in a chaotic manner. Coordinated ventricular activity ceases. The
heart ceases to pump, blood pressure
falls, and unconsciousness occurs. If left
untreated, death will follow in about 3 to 5
minutes. CAD is the most common cause
of ventricular fibrillation and it is the main
cause of sudden death, which occurs
most frequently in the first few hours after
a myocardial infarction.
A common disorder of impulse conduction, on the other hand, is an AV block. AV
blocks are characterized by a delay or failure
in impulse conduction from the atria to the
ventricles. This occurs at three levels: first
degree, with a delay in impulse conduction;
second degree, with an intermittent failure in

conduction; and third degree, with permanent failure in conduction.

Diagnosis
In the investigation of arrhythmias, it is customary to take a twelve-lead ECG: three limb
leads (lead I, lead II, and lead III), three augmented limb leads (aVR, aVL, and aVF), and
six precordial leads (V1, V2, V3, V4, V5, and
V6). An ECG is a graph of voltage variants
plotted against time (Fig 2). The paper on
which the ECG is recorded is ruled in lines
spaced 1-mm apart horizontally and vertically. When the tracing is properly standardized,
each vertical space represents a voltage
change of 0.1 mv and each horizontal space
represents a time interval of 0.04 second.
Each fifth line, horizontally and vertically, is
wider than the others. The time interval
between the heavy horizontal lines is 0.2 second. The voltage change between heavy vertical lines is 0.5 mv.
The P wave of an ECG reflects atrial depolarization. The PR segment is a measure of
the time interval from the beginning of atrial
depolarization to the beginning of ventricular
depolarization. This interval is usually 0.2
second for heart rates over 60 beats per
minute. The QRS interval is the depolarization complex of the ventricular musculature.
The duration of the QRS interval is measured
from the beginning of the first wave of the
complex to the end of the last wave and normally does not exceed 0.1 second. The T
wave is the wave of ventricular repolarization.
The vast majority of arrhythmias can be diagnosed by evaluating atrial rhythm (P waves),
ventricular rhythm (QRS complex), AV conduction (the relationship between P waves
and QRS complexes), and the presence of
unusual complexes (early, late, or unusual
contour).7174 Counting the number of R-R
intervals within 16 heavy vertical lines (15
time spaces) and multiplying it by 20 determines the heart rate.

Principles of medical management


Electric impulses carried to ventricular
myocardial cells cause powerful contractions
that propel blood throughout the body. An
understanding of the mechanisms by which
action potentials are propagated through

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Atrial contraction

sic cardiac electric activity. Today, most pacemakers in the United States use adaptive-rate
pacing to modify pacing rate for changing
metabolic needs.76 A single-chamber pace-

Ventricular contraction

Myocardial
repolarization

ST
segment
T

Q
PR
interval

S
QRS
interval

Fig 2 Elements of an ECG.

conducting cells facilitates understanding of


a drugs mechanism of antiarrhythmic action.
The charge inside resting cardiac cells is
electronegative. As an action potential is initiated, five distinct electrophysiologic phases
can be identified. In phase 0, voltagedependent sodium channels open, and the
rapid influx of sodium ions depolarizes the
cell. In phase 1, the inactivation of sodium ion
influx and the transient efflux of potassium
cause rapid repolarization. Phase 2, or the
plateau phase, is characterized by low membrane conductance and the activation of a
slow inward calcium ion current. During
phase 3, in response to the continued efflux
of potassium ions, the process of repolarization to resting potential continues. In phase 4,
the outward potassium current is inactivated,
and an inward sodium ion current reduces
transmembrane potential. Interruption of this
system jeopardizes tissue oxygenation and
may lead to death. The goals of treatment of
cardiac arrhythmias are to restore synchronous myocardial contraction and prevent
thromboembolic episodes (Table 3).75

Nonpharmacologic management
of arrhythmias
The basic function of a pacemaker is to stimulate (or pace) the heart and to sense intrin-

maker stimulates either the atria or ventricles


according to programmed timing intervals.
By sensing intrinsic atrial and/or ventricular
depolarization, the pacemaker can inhibit
unnecessary or inappropriate stimuli. Dualchamber devices time delivery of ventricular
stimuli relative to sensed atrial depolarization
to maintain proper AV synchrony. Most pacemakers use bipolar transvenous leads, which
may be placed in the subpectoral region or
at the belt line in the anterior abdominal wall.
In the former, the leads traverse through the
subclavian vein and superior vena cava and
are implanted subendocardially in the right
ventricle. Generators placed in the abdominal wall have subcutaneous leads piercing
the apical pericardium and the epicardium to
enter the myocardium. Indications for permanent pacemakers include symptomatic sinus
bradycardia, SA node dysfunction, symptomatic AV node disease, long Q-T syndrome,
hypertrophic obstructive cardiomyopathy,
and dilated cardiomyopathy.77,78 Pacemakers
powered by lithium-iodide batteries have an
expected service life of 5 to 12 years.
Implantable cardioverter defibrillators
(ICD) incorporate all the capabilities of contemporary pacemakers but are longer lived
and multiprogrammable. They have transvenous leads and multiple tachycardia detection zones with programmable detection criteria, and they provide tiered therapy such as
antitachycardia pacing, followed by shocks if
needed.76,79,80 ICDs can also store dysrhythmia event records and treatment results. An
ICD can be used for the prevention of sudden death in a patient with life-threatening
ventricular tachydysrhythmias.76 An implanted atrial ICD or combined atrial and ventricular ICD may be prescribed for patients with
paroxysmal atrial tachydysrhythmias or susceptibility to both atrial and ventricular tachydysrhythmias.81,82 ICDs are also used for primary prevention in patients with asymptomatic CAD and nonsustained ventricular
tachydysrhythmias.83,84 Other circumstances
in which ICDs have been used for primary
prevention include following coronary artery

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Ta b l e 3

Therapeutic goals and pharmacologic strategies for cardiac


arrhythmia75

Therapeutic goal

Pharmacologic strategies

Restore synchronous myocardial


contraction

Class I antiarrhythmic agents


Make cardiac cell membrane less permeable to the influx of sodium
ions and slow depolarization and repolarization
Class II antiarrhythmic agents
Block 2-adrenergic receptors and slow depolarization, lengthen
AV conduction, reduce cardiac contractility, and slow the heart rate
Class III antiarrhythmic agents
Inhibit potassium and sodium channels and prolong both
repolarization and the refractory period
Class IV antiarrhythmic agents
Slow influx of calcium ions and slow depolarization, repolarization,
and AV conduction
Unclassified
Decrease conduction velocity, primarily at the AV node
Antithrombotic agents
Anticoagulants

Prevent thrombus formation


Prevent coagulation
AV = atrioventricular.

bypass surgery in patients with severe LV


dysfunction (ejection fraction < 35%) and
after abnormal findings of signal-averaged
electrocardiography, as well as in some
patients awaiting heart transplantation.85,86

HEART FAILURE
Cardiac muscle contraction is under the regulatory control of the autonomic nervous system. On a cellular level, the combination of a
catecholamine with its membrane-bound 1adrenergic receptor activates the enzyme
adenylate cyclase. The resultant increase in
intracellular cyclic adenosinemonophosphate (AMP) then promotes myocardial contraction by facilitating transmembrane calcium flux. In cardiac muscle, the 1-adrenergic
pathway can therefore be characterized as a
series of events that begins with the combination of a 1-agonist with a receptor and
concludes with an increase in muscle contraction. Consequently, in patients with normal heart function, the pumping actions of
the left and right sides of the heart complement each other and produce a continuous
flow of blood to the tissues. When the heart
is no longer able to pump an adequate supply of blood to meet the metabolic needs of
tissues, heart failure, a state of circulatory stasis, follows.

Etiology and epidemiology


Heart failure is a clinical syndrome defined
as chronic inadequate contraction of the
heart muscle, resulting in insufficient cardiac
output. It is a manifestation of one or more
underlying conditions, including systemic or
pulmonary hypertension, CAD, myocardial
infarction, cardiomyopathy, congenital heart
disease, or rheumatic fever.87,88 In association
with these heart diseases, the clinical manifestation of heart failure reflects impairment
of either the left or right ventricle. LV failure
characteristically develops in patients with
CAD, hypertension, and most forms of congenital heart defects. Right ventricular (RV)
failure is most commonly caused by LV failure, which increases pulmonary venous
pressure and leads to pulmonary arterial
hypertension. Other causes of RV failure
include tricuspid valve regurgitation, mitral
valve stenosis, primary pulmonary hypertension, pulmonary emboli, pulmonary artery or
valve stenosis, and RV infarction. Either systolic or diastolic dysfunction or characterizes
heart failure. In diastolic dysfunction, resistance to ventricular filling (ventricular stiffness) probably reflects myocyte loss and
increased interstitional collagen deposition.
In systolic dysfunction, which is primarily a
ventricular contractile dysfunction, the heart
fails to provide adequate circulatory output,
giving rise to hypoperfused tissues and congested organs. Consequently, although heart

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failure begins with impaired ventricular function, much of what follows is caused by the
retention of salt and water.89,90
The kidneys are responsible for regulating
the balance of salt and water by conserving
both during periods of deprivation and
excreting diluted urine when water consumption is high. This activity requires an
abundant blood supply. Consequently, renal
function is dependent on an adequate cardiac output, 25% of which is apportioned to
the kidneys. Normal salt and water homeostasis is maintained by negative-feedback
mechanisms. Key among them is the reninangiotensin-aldosterone system.91,92 Renin,
released from the juxtaglomerular and macula densa cells of the kidneys, cleaves four
amino acids from circulating angiotensinogen, produced by the liver, to form angiotensin I. The ACE, which is bound to the plasma membrane of endothelial cells, cleaves
two amino acids from angiotensin I to form
angiotensin II. Angiotensin II promotes the
constriction of renal and systemic arterioles
and sodium reabsorption in the proximal
segments of the nephrons. It also stimulates
the adrenal cortex to secrete aldosterone,
which promotes the reabsorption of sodium,
in exchange for potassium, in the distal segments of the nephrons.
The contribution of aldosterone to the
retention of sodium in patients with congestive heart failure is now well established.9396
Aldosterone secretion in patients with heart
failure is regulated by several major stimuli.
These include angiotensin II and elevations in
serum potassium concentrations. Plasma corticotropin concentrations are also critically
increased, contributing to the increase in
aldosterone secretion.97 Finally, because of
reduced hepatic perfusion, decreased metabolic clearance of aldosterone by the liver can
account for significant increase in plasma
aldosterone concentrations.98 In addition to its
classic mineralocorticoid properties, aldosterone has other adverse effects that can contribute to the pathophysiology of heart failure.
These effects include coronary and renovascular remodeling (fibrosis), endothelial cell
and baroreceptor dysfunction, and inhibition
of myocardial norepinephrine uptake.99101
The persistent activation of the renin-

angiotensin-aldosterone system induces inappropriate intravascular and extravascular volume expansion; induces fibrosis of the heart,
kidneys, and other organs; and contributes to
the progressive nature of heart failure, which
leads to episodes of symptomatic heart failure
and sudden death.

Clinical manifestations
The American College of Cardiology and
AHA guidelines for the evaluation and management of heart failure state that there are
four stages of heart failure.102 Patients with
stage A heart failure are at risk of developing
heart failure because of the presence of conditions strongly associated with the development of heart failure, such as hypertension,
CAD, diabetes mellitus, history of cardiotoxic
drug therapy, alcohol abuse, history of rheumatic fever, or family history of cardiomyopathy. Patients with stage B heart failure have
structural heart disease associated with the
development of heart failure but have not
shown symptoms or signs of heart failure.
These patients have a prior myocardial infarction, LV hypertrophy or fibrosis, LV dilatation
or hypocontractility, or asymptomatic valvular
disease. Patients with stage C heart failure
have current or prior symptoms of heart failure associated with structural heart disease.
Patients with stage D heart failure have
advanced structural disease and marked
symptoms of heart failure at rest despite maximal medical therapy and required specialized interventions. Heart failure is usually a
relatively slow, progressive condition. By the
time it is recognized clinically, congestive
heart failure has become the end stage of a
sustained disproportion between the load on
the heart and the ability of the heart muscle
to handle the load. The traditional clinical
manifestations of heart failure represent
stages C and D, which manifest impairment
of either the left or right ventricle.103105
Left ventricular failure. LV failure characteristically develops in hypertension, CAD,
cardiomyopathy, and most forms of congenital heart defects. It may manifest as tachycardia, fatigue on exertion, dyspnea on mild
exercise, and intolerance to cold. Paroxysmal
nocturnal dyspnea and nocturnal cough
reflect the redistribution of excess fluid into

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the lungs with the recumbent position.


Occasionally, bronchospasm, wheezing, and
hemoptysis are present.
Right ventricular failure. RV failure usually develops from LV failure, tricuspid regurgitation, mitral or pulmonary valve stenosis,
and pulmonary hypertension or emboli. The
principle symptoms include fatigue; an
awareness of fullness in the neck (jugular
vein distension); fullness in the abdomen,
with an enlarged liver with tenderness in the
upper right quadrant; and, in advanced
cases, abdominal swelling secondary to
ascites and pitting edema of the lower
extremities.

Diagnosis
Clinical signs and symptoms such as exertional dyspnea, orthopnea, edema, tachycardia, pulmonary rales, and jugular vein distension have a high diagnostic specificity for
heart failure. Diagnostic sensitivity and predictive accuracy can be increased with blood
chemistry, ECG, chest radiograph, and
echocardiography.106112
Compensated heart failure. Patients who
experience dyspnea and fatigue only with
heavy muscular work and manifest no signs
of intravascular or extravascular volume
expansion have compensated heart failure.113
These patients have mild to moderate impairment of renal perfusion, and the ratio of sodium to potassium in the urine is greater than
1 because the release of natriuretic peptides
from the distended atria and ventricles stimulates sodium excretion.
Decompensated heart failure. Patients
who experience dyspnea and fatigue at rest
or during mild exertion and manifest signs of
intravascular or extravascular volume expansion have decompensated heart failure.113
Decompensation occurs because these
patients have moderate to marked reductions in renal perfusion. Plasma renin activity
increases, and the resulting increases in
angiotensin II and aldosterone production
override the action of natriuretic peptides.
Urinary sodium retention becomes nearly
complete, and the sodium-to-potassium ratio
is less than 1.

Principles of medical management


While the mainstay of treatment for heart failure is pharmacologic, lifestyle modification is
an essential part of management. Patients
with heart failure should avoid excessive fluid
intake. They should use spices and herbs
instead of sodium chloride to flavor food.
They should also avoid exposure to heavy air
pollution. Air conditioning is essential for
patients with heart failure who live in a hot
and humid environment. Ethyl alcohol intake
should be avoided. Regular physical activity
such as walking should be encouraged in
patients with mild to moderate heart failure to
improve functional capacity and decrease
symptoms. The pharmacologic management of heart failure is aimed at the identification and correction of both the underlying
disorder and precipitating factors. Specific
goals include a reduction of cardiac workload and myocardial oxygen consumption,
improvement in myocardial contractility, control of sodium and fluid retention, increased
peripheral tissue perfusion and oxygenation,
and prevention of thromboembolic episodes
(Table 4).102,114

Surgical intervention
Heart transplantation is the primary surgical
treatment for patients with end-stage heart
failure, with 1-year survival of 86% and 5-year
survival of 69%.115117 Because heart transplantation is an option to only a small number of patients, classic interventions such as
revascularization procedures, valve repair, or
valve replacement have been improved and
modified to meet the special need of patients
with heart failure.118

THROMBOEMBOLIC
COMPLICATIONS OF
CARDIOVASCULAR
DISEASES
The clotting of blood involves the sequential
initiation, interaction, and completion of several stages of hemostasis. The vascular
stage is initiated by tissue injury, and the
response or outcome is vasoconstriction.
The platelet phase is initiated by adhesion

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Ta b l e 4

Therapeutic goals and pharmacologic strategies for heart failure

Therapeutic goal

Pharmacologic strategies

Reduce workload

Diuretics
ACE inhibitors
1-adrenergic receptor antagonists
Vasodilators
Cardiac glycosides
Antithrombotic agents
Anticoagulants

Improve myocardial contractility


Prevent thrombus formation
Prevent coagulation
ACE = angiotensin-converting enzyme.

and aggregation of platelets mediated


through the release of adenosine diphosphate (ADP), resulting in platelet plug formation. In the plasma phase of hemostasis, fibrin generation takes place via a cascading
group of interactions involving numerous
blood-clotting factors.

Etiology and epidemiology


A blood clot, or thrombus, that forms in a
blood vessel or heart chamber may be either
arterial or venous in origin. The formation of
an arterial thrombus begins when platelets
aggregate and become surrounded by fibrin
and erythrocytes. Eventually, arterial thrombi,
like atherosclerotic plaques, occlude blood
vessels and cause tissue ischemia. Venous
thrombi develop in areas of slow blood flow.
The clot forms rapidly and lacks the organization of the arterial thrombus. Although
venous occlusion does occur, a far greater
concern is the tendency of small emboli to
detach from venous thrombi. The emboli
travel to and wedge into pulmonary arteries,
preventing deoxygenated blood from entering the portion of the lung.

Clinical manifestations
Arterial thrombi contribute to transient
ischemic attacks and stroke, occlusion of coronary artery grafts, coronary artery rethrombosis after thrombolysis, myocardial infarction
and death in unstable angina, increased incidence of periprocedural myocardial infarction
in patients undergoing coronary angioplasty,
mural thrombosis after myocardial infarction,
and recurrent myocardial infarction.119121
Arterial thrombi can also contribute to systemic
embolism in patients with prosthetic heart
valves or atrial fibrillation and death in patients

with valvular heart disease. Venous thrombi are


responsible for venous thrombosis and pulmonary embolism.122

Principles of medical management


The goals of treatment are to reduce morbidity and mortality from thromboembolic events
(Table 5). Antithrombotic agents are effective
in preventing transient ischemic attacks, in
preventing occlusion of coronary grafts, in
preventing myocardial infarction and death in
unstable angina, in reducing the incidence of
periprocedural myocardial infarction in
patients who have undergone coronary
angioplasty, in reducing nonfatal vascular
events and vascular mortality in the secondary prevention of myocardial infarction, and in
reducing the incidence of myocardial infarction.119121 Oral anticoagulants, such as warfarin, are effective in the primary and secondary prevention of venous thromboembolism,
in the prevention of systemic embolism in
patients with prosthetic heart valves or atrial
fibrillation, and in the prevention of stroke,
recurrent infection, and death in patients with
valvular heart disease. Heparin is effective in
the prevention and treatment of venous
thrombosis and pulmonary embolism, in the
prevention of mural thrombosis after myocardial infarction, in the treatment of patients
with unstable angina and acute myocardial
infarction, and in the prevention of coronary
artery rethrombosis after thrombolysis.122

CONCLUSION
Hypertension is the most common primary
diagnosis in the United States. While a blood

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pressure of 180/110 mm Hg is not an independent risk factor for cardiovascular complications during noncardiac procedures, elevated blood pressure is a reliable indicator of
CAD. Cardiac ischemia during noncardiac
procedures correlates with intra- and postoperative morbidity. Structural coronary arterial
abnormalities and their consequences are
the cause of the majority of arrhythmias leading to sudden death. Finally, hypertension
and CAD are major causes of congestive
heart failure, which has also been identified
as a further risk factor for coronary events.
The physiologic response to the trauma of
an oral/dental procedure and the administration of anesthetic agents can affect cardiac
function. Consequently, oral health care
providers must have an understanding of cardiovascular diseases. Such an obligation is
tempered only by the extent to which such
diseases relate to the dental professions
anatomic field of responsibility and the extent
to which such illnesses require modification
of dental therapy or alter prognosis. This
overview provides the framework for considering cardiac risk in association with
oral/dental procedures and for determining a
patients clinical risk profile to be used in
making treatment decisions that may influence both short- and long-term outcomes.

Ta b l e 5

Therapeutic goals and


pharmacologic strategies
for thromboembolic
complications of
cardiovascular diseases
Pharmacologic
strategies

Therapeutic goal

Prevent thrombus formation


Prevent coagulation

Antithrombotic agents
Anticoagulants

7. Beilin LJ. Non-pharmacological management of


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8. Grienling KK, Alexander RW. Cellular mechanisms in
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9. Lindop GB.The effects of hypertension on the structure of human resistance vessels. In: Swales JD (ed).
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