Stone G, Teirstein P, Rubenstein R, et al: A prospective, multicenter, randomized trial Risk Factors
of percutaneous transmyocardial laser revascularization in patients with nonreca- Men are approximately 4 times more likely than women to develop
nalizable chronic total occlusions, J Am Coll Cardiol 39:1581–1587, 2002.
Stone NJ, Robinson J, Lichtenstein AH, et al: 2013 ACC/AHA guideline on the treat-
ment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A
report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines, Circulation 2013.
Weber MA, Schiffrin EL, White WB, et al: Clinical practice guidelines for the manage-
ment of hypertension in the community, J Clin Hypertens 16:14–26, 2014.
Wenger NK: Cardiac Rehabilitation: A Guide to Practice in the 21st Century,
New York, 1999, Marcel Dekker.
Whooley MA, Jonge P, Vittinghoff E, et al: Depressive symptoms, health behaviors,
and risk of cardiovascular events in patients with coronary heart disease, JAMA
300:2379–2388, 2008.
AORTIC DISEASE: ANEURYSM AND DISSECTION
Method of
David G. Neschis, MD
CURRENT DIAGNOSIS
• Because the majority of patients with abdominal aortic
aneurysms are asymptomatic, the majority of abdominal aortic
aneurysms are detected on imaging studies performed for other
indications.
• Patients older than 50 years who present with abdominal or
back pain of unclear etiology should be considered for evalua-
III The Cardiovascular System
tion of possible abdominal aortic aneurysm.
• Asymptomatic men older than 65 years who have ever smoked
are eligible for abdominal aortic aneurysm screening.
• All patients older than 60 years who have a strong family history
of abdominal aortic aneurysms should be considered for
screening.
• Patients presenting with sudden onset of chest or back pain
without clear etiology should be evaluated for dissection.
• Dissection can mimic numerous other conditions.
CURRENT THERAPY
94
Indications for Repair of Aneurysm
• Fusiform abdominal aortic aneurysms greater than 5.5 cm in
maximum diameter
• Most saccular aneurysms and pseudoaneurysms
• Thoracic and thoracoabdominal aortic aneurysms of greater
than 6 cm in maximal diameter
• Aneurysms that are symptomatic or are rapidly enlarging
Indications for Repair of Aortic Dissection
• Dissections involving the ascending aorta
• Dissections involving only the descending aorta are usually
managed medically unless complicated by the following:
unrelenting pain, end organ ischemia, or significant aneurysmal
degeneration to greater than 6 cm in maximal diameter
Abdominal Aortic Aneurysms
Epidemiology
A ruptured abdominal aortic aneurysm is a devastating event lead-
ing to approximately 15,000 deaths per year, and it is the 13th
leading cause of death in the United States. It is the 10th leading
cause of death in men. Once rupture occurs, there is an 85% chance
of death overall and approximately 50% mortality in the patients
who make it to the hospital alive. Clearly, the goal is to identify this
life-threatening lesion and repair prior to rupture. Abdominal aor-
tic aneurysms are approximately four times more prevalent in men
than in women. The overall incidence in persons older than 60 years
is approximately 3% to 4%, with incidence as high as 10% to 12%
in an elderly hypertensive population.
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an abdominal aortic aneurysm. Clearly, older persons, particularly
those older than 60 years, are at higher risk. Tobacco use is prob-
ably the strongest preventable risk factor, with tobacco users being
approximately eight times more likely to be affected than non-
smokers. Hypertension is present in approximately 40% of
patients with abdominal aortic aneurysms. Family history also
plays a significant role. In fact, men who have first-degree female
relatives who had aneurysms are approximately 18 times more
likely than the general population to develop an abdominal aortic
aneurysm. There is also a strong correlation between abdominal
aortic aneurysms and other peripheral artery aneurysms. Patients
with bilateral popliteal artery aneurysms have an approximately
50% to 60% risk of having an abdominal aortic aneurysm.
Pathophysiology
An aneurysm is a dilatation of a blood vessel that could occur in
any blood vessel in the body, even in the veins. Most commonly
it is defined as a dilatation of approximately 1.5 to 2 times at that
diameter of the adjacent normal vessel.
The definition of a pseudoaneurysm is often misunderstood. The
attempt to describe a pseudoaneurysm in terms of the number of
layers of the artery wall involved does nothing to help resolve this
confusion. A pseudoaneurysm is a walled-off defect in the artery
wall. A circular shell of adventitial and surrounding connective tis-
sue contains the blood, preventing free hemorrhage. However,
there remains continued flow out and back into the arterial lumen,
resulting in a classic to-and-fro pattern on duplex ultrasound. The
most common cause of a pseudoaneurysm is iatrogenic, from nee-
dle puncture, but it also can be caused by trauma or focal rupture of
the artery at the site of an atherosclerotic ulcer.
The etiology of true aneurysms is not clear, although in the past
these have been attributed to atherosclerosis. However, it is well
known that the majority of patients with abdominal aortic aneu-
rysms do not have associated significant occlusive disease. Bio-
chemical studies have demonstrated decreased quantities of
elastin and collagen in the walls of aneurysmal aortas. It is believed
that a family of enzymes known as matrix metalloproteinase
(MMP), particularly those that have collagenase and elastase activ-
ity, are likely involved in development of arterial aneurysms. The
propensity for growth and rupture is based on Laplace’s law,
T ¼ PR, where T represents wall tension (or in other words the pro-
pensity to rupture), P is the transmitted pressure, and R is the
radius. This explains why patients with hypertension and those
with larger aneurysms are at higher risk for aortic rupture.
Prevention
Currently the most effective means to prevent aneurysm rupture is
early detection and elective repair. Avoidance of smoking and
aggressive control of blood pressure would likely be helpful in pre-
venting aneurysmal development and growth. Patients with known
abdominal aortic aneurysms that are relatively small and at low risk
for rupture are generally serially followed with imaging studies over
time. These patients are advised to avoid straining (e.g., heavy lift-
ing), avoid smoking, and keep their blood pressure well controlled.
Investigation is ongoing in efforts to develop a medication that
may be helpful in slowing the growth of abdominal aortic aneu-
rysms. It has been known since 1985 that tetracycline antibiotics
have activity against MMPs. There had been several animal studies
and at least one small human study suggesting that doxycycline
(Vibramycin)1 may be effective at slowing the growth of abdominal
aortic aneurysms. Currently, larger human studies are ongoing. At
this point, there are no formal recommendations regarding the use
of doxycycline for the purpose of slowing aneurysmal growth.
Clinical Manifestations
Approximately 75% of abdominal aortic aneurysms are asymp-
tomatic and discovered incidentally. Unfortunately, physical
1
Not FDA approved for this indication.
examination is an unreliable method for detecting aneurysms or
determining aneurysm size. In heavier patients it may be simply
impossible to adequately palpate the aorta. The majority of aneu-
rysms are incidental findings identified on imaging studies per-
formed for other reasons. Occasionally, an aneurysm is first
detected upon operation for another condition.
Unfortunately, when an aneurysm becomes symptomatic, this is
usually a sign of impending rupture. Symptoms related to abdom-
inal aortic aneurysms can include abdominal or back pain. The
classic triad of findings in the setting of abdominal aortic aneurysm
rupture includes abdominal pain, hypotension, and a pulsatile
abdominal mass. This triad, however, occurs in only approxi-
mately 20% of the patients. Often a high index of suspicion needs
to be maintained.
The episode of hypotension associated with aneurysm rupture
may be manifested as an episode of syncope or near-syncope before
the patient arrives at the hospital. It is quite possible for the patient
to have a contained rupture of the abdominal aorta and appear
quite stable with a normal blood pressure in the emergency depart-
ment. Although uncommon, a primary fistula between the aneu-
rysm and gastrointestinal tract can occur and manifest as
gastrointestinal bleeding.
Diagnosis
Several imaging modalities are available that can accurately diag-
nose and measure abdominal aortic aneurysms. Real-time B-mode
ultrasound scanning has the advantage of being almost universally
available, relatively inexpensive, and essentially risk free. The
major disadvantage, however, is that it is technician dependent.
Computed tomography (CT) scans can provide a very accurate rep-
resentation of the aorta in a very short study time (Figures 1 and 2).
The use of iodinated contrast is not necessary to obtain a gross size
measurement of the aorta. The contrast, however, helps delineate
the flow lumen more clearly, and it is quite valuable in planning
repair. Disadvantages include the use of ionizing radiation and
the use of iodinated contrast material. MRI is also accurate in
determining the size of the aneurysm; however, study times are lon-
ger, equipment is less widely available, and the expense is consid-
erable. Angiography, while excellent for evaluating the status of
important aortic branches and for evaluating occlusive disease, is
not an accurate study for the purpose of determining maximal
diameter of the aneurysm. Often aneurysms are filled with lami-
nated thrombus, and the flow lumen, which was seen on aortogra-
phy, is not representative of the true aneurysm size.
Treatment
The decision on when to intervene in an abdominal aortic aneu-
rysm is based on a careful analysis of the patient’s risk for rupture
Figure 1 Large abdominal aortic aneurysm. Notice how the majority of
this aneurysm is filled with laminated thrombus. The flow lumen is only
mildly dilated, and this aneurysm could be missed on angiography alone.
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Figure 2 Classic image of a ruptured abdominal aortic aneurysm, which in
this case can be seen even without the use of intravascular contrast. Note the
lack of symmetry and obliteration of tissue planes in the retroperitoneum on
the left.
Aortic Disease: Aneurysm and Dissection
versus the risk of operative repair. Historically, open repair can be
performed with less than 5% in-hospital mortality. Based on his-
torical studies it was estimated that the risk of rupture for an
approximately 5-cm aneurysm was about 1% per year, which
increased dramatically to 6.6% for aneurysms between 6 and
7 cm. It has been fairly well established for years that aneurysms
larger than 5.5 cm are generally recommended for repair and those
less than 4 cm are generally observed over time. There remains a
gray area for moderate aneurysms in the 4- to 5.5-cm category.
Two large prospective randomized trials were developed to
answer this question. These include the United Kingdom Small
Aneurysm Trial and the Department of Veterans Affairs Aneurysm
Detection and Management (ADAM) trial. Both these studies ran-
domized patients with moderately sized aneurysms to observation
versus open repair. Results of both trials were fairly similar. The
rupture rate for aneurysms under observation was 0.5% to 1%
per year, and neither trial showed a difference in long-term sur-
vival. Both studies concluded that it was relatively safe to observe 95
patients with aneurysms less than 5.5 cm in diameter, particularly
in men who would be compliant with the follow-up regimen. The
diameter of the aneurysm, however, should not be the only data
point used for a decision on whether to repair.
Women seem to have a higher rupture rate for a particular aneu-
rysm diameter than men, perhaps because they are starting with
smaller aortas to begin with. Patients with COPD may be at higher
risk for rupture as well. Saccular or eccentric-shaped aneurysms
may also have a higher propensity to rupture and should not be
subject to diameter recommendations for fusiform aneurysms
(Figures 3 and 4). Additionally, rapidly growing aneurysms—
growing at a rate faster than approximately 0.5 cm per year—
should be considered for repair.
Once it has been determined that repair is indicated, a number of
options are available. Traditional open repair involves a relatively
large abdominal incision, cross clamping of the aorta, and replace-
ment of the aneurysmal segment with a graft of polyethylene tere-
phthalate (Dacron) or polytetrafluoroethylene (PTFE; Teflon).
Often the iliac arteries are involved, and in these cases a bifurcated
graft is placed. Open repair is quite durable and very effective at
preventing aneurysm-related deaths. Long-term complications
are rare, and patients following open repair generally enjoy 95%
freedom from issues related to the repair over the course of their
lifetime. Disadvantages, however, include the large incision and
an approximate 1-week hospital stay. Recovery to a relatively nor-
mal level of function occasionally takes months. In the past, many
patients were deemed too old or frail to be expected to undergo
open surgery.
III The Cardiovascular System

Figure 3 Axial CT slice and reconstructed images of a saccular abdominal aortic aneurysm. This lesion could also be described as a pseudoaneurysm. For
these, treatment is recommended because it is thought that the risk of rupture is higher than for a similarly sized fusiform abdominal aortic aneurysm.

Figure 4 Angiogram of patient in Figure 3, demonstrating

aneurysm before and after deployment of an endograft,
which successfully excluded the lesion from the circulation.

96

Endograft repair has revolutionized the practice of vascular sur-
gery. Using small incisions placed at the groin and performing the
procedure under fluoroscopic guidance, devices can now be
advanced into the aorta from the femoral artery. Using angiogra-
phy as a guide, the graft typically is deployed below the renal arter-
ies and effectively excludes the aneurysm from the circulation.
Advantages include small incisions and very short hospital stays.
Patients are typically discharged on the first or second day after
aneurysm repair. Recovery to normal activity is also quite
rapid, taking approximately 1 to 2 weeks. Use of this modality
has allowed treatment of older and frailer patients who previously
were denied treatment due to concerns of operative risk.
Endograft repair, however, is clearly not without its disadvan-
tages. Currently, the durability of endograft repair is unknown,
and these patients are subject to frequent serial imaging. Also, there
is a higher incidence of graft-related complications, which can
occur in up to 35% of patients. These include the development
of leaks of blood into the aneurysm sac outside the graft device,
issues related to graft failure and migration, and graft limb throm-
bosis. These grafts are also quite expensive.

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 Two major prospective randomized trials studying traditional
open versus endograft repair are often cited. These include the
United Kingdom–based EVAR-1 trial (first Endovascular Aneu-
rysm Repair trail) and the Dutch-based DREAM trial (Diabetes
REduction Assessment with ramipril and rosiglitazone Medication
trial). Both studies randomized patients who were believed to be
good risks for open repair to endograft versus traditional open
repair. The results of both of these studies were relatively similar
in that both studies demonstrated a clear early survival benefit for
patients in the endograft group. However, this came at a cost of
an increased incidence of graft-related complications in the endo-
graft group and a higher cost for the endograft group. Additionally,
at 2 to 4 years, there was no clear difference in long-term survival in
either group.
Ultimately, the decision about whether to proceed with open or
endograft repair is a decision between surgeon and patient based
on the patient’s aortic anatomy, overall health, and the patient’s
and physician’s preference. It would appear, however, that older
and frail patients with good anatomy should be strongly consid-
ered for endograft repair.
Monitoring
Patients with abdominal aortic aneurysms should be evaluated
for the presence of femoral and popliteal aneurysms (particularly
in men) and for thoracic aortic aneurysms. After open repair, a
follow-up CT scan with contrast should be considered approxi-
mately 5 years out to evaluate for the integrity of the graft (i.e., pseu-
doaneurysms), as well as development of new aneurysms. Patients
who have undergone endograft repair require more-intensive
monitoring. Typical regimens include a contrast-enhanced CT scan
approximately 2 weeks after repair, then 6 months after repair, and
then based on the perceived stability of the graft, approximately
yearly thereafter. Some centers have used duplex ultrasonography
for evaluating patients after endograft repair in efforts to reduce
the amount of ionizing radiation the patients receive. However, it
should be remembered that duplex ultrasound is highly technician
dependent, and follow-up of patients with endograft repairs using
only duplex ultrasound should be performed in experienced centers.
Thoracic Aortic Aneurysms
Thoracic aortic aneurysms (TAAs) are limited to the chest cavity.
Although they are less common than infrarenal abdominal aortic
aneurysms, they share similar risk factors. The male-to-female ratio
incidence of the TAA is approximately 1:1.
In the past, the threshold for repair was at a diameter greater
than 6 cm. This threshold was chosen due to the higher operative
risks associated with repair of the thoracic aorta. Now with the
availability of endograft, patients with good anatomy are generally
recommended for repair at a diameter similar to those for the
infrarenal aorta.
Open repair involves performing a thoracotomy and cross-
clamping the aorta. Repair in this location is often performed with
the addition of extracorporeal bypass to maintain perfusion to the
viscera and spinal cord drain performance of the repair. Although
the risk of paraplegia in the treatment of infrarenal aortic is exceed-
ingly low, the risk of paraplegia from a repair of an isolated TAA is
approximately 6%. Endograft devices for repair of TAA are now
widely available and have reduced the incidence of paraplegia to
approximately 3%.
Thoracoabdominal Aortic Aneurysms
By definition, thoracoabdominal aortic aneurysms require
entrance to both the thoracic and abdominal cavity to perform
repair. These lesions are usually true aneurysms of the aorta and
should not be confused with dissection. Repair of thoracoabdom-
inal aortic aneurysms is quite complex and carries risks of death
and paraplegia as high as 20% in some settings. These procedures
are generally performed at larger institutions with considerable
experience with this condition. Unfortunately, endograft devices
for the repair of thoracoabdominal aortic aneurysms are limited
to a handful of centers in the United States.
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Thoracic Aortic Dissection
Thoracic aortic dissection is the most common aortic emergency,
even more common than ruptured abdominal aortic aneurysm.
This potentially fatal condition is rare in patients younger than
50 years and is approximately two times more common in men
than women. Patients at risk include patients with a history of con-
nective tissue disorders and patients with severe, poorly controlled
hypertension.
An aortic dissection occurs when there is loss of integrity of the
intima and blood dissects into the media. Once in the media, there
is a natural plane through which dissection is quite easy.
Although there are various classification systems for aortic dis-
section, the Stanford classification is perhaps the most widely used
and the most useful. In this classification, any dissection that
involves the ascending aorta, whether it involves the ascending
aorta alone or both the ascending and descending thoracoabdom-
inal aorta, are classified as type A. Dissections that do not involve
the ascending aorta are classified as type B. This classification is
useful because type A dissections require urgent surgery. Type B
dissections are typically managed medically unless they are associ-
ated with complications such as unremitting pain, aneurysmal
expansion, and end-organ ischemia. By convention, aortic dissec-
tions that are evaluated within 14 days after the onset of symptoms
Aortic Disease: Aneurysm and Dissection
are considered acute, and those evaluated beyond 14 days are con-
sidered chronic.
Helical CAT scanners with the use of contrast are excellent at
defining the location and extent of aortic dissection. However,
being alert to the potential for this diagnosis requires a high index
of suspicion. Aortic dissection can mimic a variety of common con-
ditions based on the extent of the dissection and the aortic branches
involved (Table 1). Uncomplicated type B dissections are typically
managed medically. This is usually performed in an intensive care
setting with the use of intravenous medications to control contrac-
tility and, if necessary, hypertension.
In the past, due to the friability of dissected aortic tissue, the
results of operative repair for type B dissections have been partic-
ularly poor. Currently, endograft repair with the purpose of
excluding the entry point of dissection and reestablishing flow to
the true lumen is gaining popularity in the treatment of complex
dissection. This at times may be supplemented by stenting of
affected aortic side branches and fenestration to establish a connec-
tion between the true and false lumen to restore perfusion to certain
organs. Once the acute phase has passed and medically treated 97
patients are under good hypertensive control, these patients are
then converted to an oral medication regimen and transferred
out of the intensive care setting. Patients need to be followed up
with serial CT imaging after discharge to evaluate for aneurysmal
TABLE 1 Dissection: The Great Mimic
TERRITORY INVOLVED OR AFFECTED
BY DISSECTION MIMICS
Rupture into pericardial sac Cardiac tamponade
Dissection through aortic valve Acute aortic insufficiency
Dissection occluding coronary arteries Myocardial infarction
Involvement of cerebral vessels Stroke
Involvement of subclavian arteries Upper extremity ischemia
(cold arm)
Dissection running down descending Severe back pain and
thoracic aorta paralysis
Mesenteric artery obstruction Mesenteric ischemia
Renal artery obstruction Oliguria and acute renal
failure
Iliac artery occlusion Lower extremity ischemia
(cold leg)
 degeneration of the false lumen. This evaluation should occur every
6 months until the patient is stable and then yearly thereafter.
In cases where the total aortic diameter grows to greater than
6 cm, repair for the purpose of preventing rupture is indicated,
although this is often technically more complicated than treating
a fusiform aneurysm in the absence of a previous dissection.
Patients should strictly adhere to their blood pressure medication
regimen for life.
References
Blankensteijn JD, de Jong SE, Prinssen M, et al: Two-year outcomes after conventional
or endovascular repair of abdominal aortic aneurysms, N Engl J Med 352
(23):2398–2405, 2005.
Crawford ES, Crawford JL, Safi HJ, et al: Thoracoabdominal aortic aneurysms: Pre-
operative and intraoperative factors determining immediate and long-term results
of operations in 605 patients, J Vasc Surg 3(3):389–404, 1986.
Daily PO, Trueblood HW, Stinson EB, et al: Management of acute aortic dissections,
Ann Thorac Surg 10(3):237–247, 1970.
EVAR Trial Participants: Endovascular aneurysm repair versus open repair in patients
with abdominal aortic aneurysm (EVAR trial 1): Randomised controlled trial,
Lancet 365(9478):2179–2186, 2005.
EVAR Trial Participants: Endovascular aneurysm repair and outcome in patients unfit
for open repair of abdominal aortic aneurysm (EVAR trial 2): Randomised con-
trolled trial, Lancet 365(9478):2187–2192, 2005.
Lederle FA, Wilson SE, Johnson GR, et al: Immediate repair compared with surveil-
lance of small abdominal aortic aneurysms, N Engl J Med 346(19):1437–1444,
2002.
Lee ES, Pickett E, Hedayati N, et al: Implementation of an aortic screening program in
clinical practice: Implications for the Screen For Abdominal Aortic Aneurysms
Very Efficiently (SAAAVE) Act, J Vasc Surg 49(5):1107–1111, 2009.
Nevitt MP, Ballard DJ, Hallett JW Jr: Prognosis of abdominal aortic aneurysms.
A population-based study, N Engl J Med 321(15):1009–1014, 1989.
III The Cardiovascular System
Nienaber CA, Rousseau H, Eggebrecht H, et al: Randomized comparison of strategies
for type B aortic dissection: The INvestigation of STEnt Grafts in Aortic Dissection
(INSTEAD) trial, Circulation 120(25):2519–2528, 2009.
Rentschler M, Baxter BT: Pharmacological approaches to prevent abdominal aortic
aneurysm enlargement and rupture, Ann N Y Acad Sci 1085:39–46, 2006.
ATRIAL FIBRILLATION
Method of
Lin Yee Chen, MD, MS; and Samuel C. Dudley, Jr., MD, PhD
CURRENT DIAGNOSIS
98
• History taking and physical examination for atrial fibrillation
(AF) should be focused on determining symptom severity (to
decide on treatment strategy), risk of thromboembolic stroke,
and associated cardiovascular risk factors.
• Symptoms include palpitations, chest discomfort, shortness of
breath, and reduced exercise capacity. Some patients are
symptom free.
• Investigations include 12-lead electrocardiogram (ECG) for
confirmation, transthoracic echocardiogram to evaluate left
atrial size, left ventricular ejection fraction, and rule out valvular
abnormalities, and blood tests for thyroid, renal, and hepatic
function.
CURRENT THERAPY
• Rate control: Achieve average ventricular rate of less than 110
beats/min by using atrioventricular node (AVN) blockers or
catheter ablation of AVN
• Rhythm control: Prevent AF recurrence by using antiarrhythmic
drugs or catheter ablation (pulmonary vein isolation)
• Stroke prophylaxis: Risk stratification and stroke prevention by
oral anticoagulation or left atrial appendage closure
• Risk factor management or lifestyle modification: Prevent AF by
weight management, intensive blood pressure lowering, and
exercise training
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Epidemiology
AF is the most common sustained arrhythmia in the adult general
population. Globally, the estimated number of individuals with AF
in 2010 was 33.5 million. Between 1990 and 2010, the global esti-
mated age-adjusted prevalence rate of AF increased from 569.5 to
596.2 per 100,000 men and from 359.9 to 373.1 per 100,000
women. This increase in prevalence was accompanied by a sub-
stantial increase in health burden: disability-adjusted life-years
increased by 18.8% in men and 18.9% in women from 1990 to
2010. Finally, the lifetime risk for development of AF in adults
at age 40 is 1 in 4.
Risk Factors and Pathophysiology
Table 1 shows the known risk factors of AF; many of these are also
risk factors for atherosclerotic disease. Traditional cardiovascular
risk factors such as diabetes, hypertension, and obesity can lead to
AF via the following pathway: Cardiovascular risk factors ! left
ventricular diastolic dysfunction ! structural and functional alter-
ations in the atria (enlargement, impaired function, fibrosis, etc.)
! AF. The aforementioned pathway creates the substrate for AF;
premature atrial contractions and supraventricular ectopic beats
are the trigger for AF. Other pathophysiological pathways include
inflammation and increased oxidative stress leading to electrical
remodeling, and, consequently, AF.
Clinical Manifestations
Common symptoms of AF include palpitations, irregular heart
beat sensation, lightheadedness, dyspnea, chest discomfort, and
fatigue. Some patients may have no symptoms at rest but report
poor stamina or easy fatigability with physical activity. Other
patients, particularly in the elderly, may be asymptomatic.
Diagnosis
The absence of distinct P waves with irregularly irregular RR
interval on the ECG are the sine qua non for diagnosing AF.
Rhythm documentation can be obtained via the standard
12-lead ECG, Holter monitors that can record up to 48 hours,
leadless patch monitors that can record up to 2 weeks, or
implantable loop recorders. Newer wearable technologies that
can diagnose AF include smart watches and smart phones with
specialized apps.
TABLE 1 Risk Factors of Atrial Fibrillation
Cardiovascular risk factors
Older age
Male sex
Diabetes mellitus
Overweight and obesity
Hypertension
Chronic kidney disease
Structural heart disease
Valvular heart disease
Cardiomyopathy (dilated, restrictive, and hypertrophic)
Congenital heart disease
Coronary heart disease
Left ventricular diastolic dysfunction
Left atrial enlargement
Family history
Genetics (polygenic and monogenic inheritance)
Inflammation
Low serum magnesium
Heavy alcohol consumption
Poor cardiorespiratory fitness
Low physical activity
Premature atrial contractions or supraventricular ectopy