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CHAPTER 11 Other Cardiac Topics
A B
Fig. 11.1 Postpartum anterior wall myocardial infarction from spontaneous coronary dissection of the left
anterior descending and diagonal arteries demonstrated by (A) left coronary angiography showing diffusely
narrowed coronary lumen (proximal left anterior descending artery indicated by the arrow), and (B) intravascular ultrasound confirming hematoma in the medial-adventitial layer of the vessel. The imaging catheter is
central in the lumen. Black arrows indicate the vessel media and the white arrow the hematoma. The intima
of the vessel is thin and normal.
Spontaneous Coronary Artery Dissection
Spontaneous coronary artery dissection (SCAD) is defined as a separation of the arterial wall and subsequent coronary artery obstruction
caused by the formation of an intramural hematoma that is not associated with atherosclerosis, trauma or iatrogenic injury (Fig. 11.1). While
SCAD is the most common cause of pregnancy-associated myocardial
infarction, pregnancy-associated SCAD represents a relatively small
proportion of SCAD cases. The prevalence is 1.81 SCAD events per
100,000 pregnancies during pregnancy or in the postpartum period.
SCAD has been reported as early as 5 weeks’ gestation and up to a year
or more postpartum, particularly in lactating women.
The cause of pregnancy-associated SCAD is not fully understood; however, hormonal changes of pregnancy are thought to alter the architecture
of the arterial wall, weakening the wall and making it prone to rupture,
intramural hematoma, and the subsequent development of clinical symptoms. Risk factors for pregnancy-associated SCAD include black race,
chronic hypertension, lipid abnormalities, chronic depression, migraines,
advanced maternal age, multiparty, and treatment for infertility.
Women with pregnancy-associated SCAD have poorer prognosis
than women with SCAD not related to pregnancy. They have larger
infarcts, more proximal artery dissections, and lower mean left ventricular ejection fraction immediately and at follow-up. Maternal
complications of pregnancy-associated SCAD include cardiogenic
shock, ventricular fibrillation, and mechanical circulatory support.
In-hospital mortality has been reported to be as high as 4%.
Fig. 11.2 Atrial myxoma vascularization identified on cardiac cathe-
CARDIAC TUMORS
Cardiac tumors are broadly divided into primary and secondary
tumors. Primary cardiac tumors, defined as benign or malignant neoplasms that arise from any tissue of the heart, are extremely rare, with
an autopsy incidence of 0.001% to 0.03%. Secondary, or metastatic,
cardiac tumors are 30 times more common than primary tumors, with
an autopsy incidence of 1.7% to 14%.
It is not uncommon for patients with cardiac tumors to initially
have no symptoms or physical findings, but rather present with abnormalities on imaging. Alternatively, patients may present with a constellation of nonspecific symptoms or findings on physical examination.
The initial evaluation is typically imaging such as a two-dimensional
transthoracic echocardiogram or magnetic resonance imaging (MRI). Once
a mass is identified and described, additional imaging may be undertaken
terization. Selective right coronary angiography demonstrates that the
vascular supply to the tumor originates from atrial branches. The vascularized tumor is indicated by the arrow.
such as three-dimensional echocardiography with contrast, transesophageal echocardiography for anatomic information, MRI with gadolinium,
coronary angiography to define coronary anatomy, position emission
tomography (PET) for staging, and/or computed tomography (CT) to
delineate other intrathoracic structures. When assessing a cardiac mass, the
clinical context is critical to the diagnosis. The differential diagnosis of a
cardiac mass is broad and includes tumors, thrombi, infection, and artifact.
Benign Primary Cardiac Tumors
Most primary cardiac tumors are benign, and myxoma is the most
common primary tumor of the heart (Fig. 11.2). Most myxomas are
133
134 SECTION II Cardiovascular Disease
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TABLE 11.2 Cardiac Trauma Categorized
by Mechanism of Injury
Penetrating Nonpenetrating (Blunt)
Stab wounds (e.g., knives, swords, ice picks) Motor vehicle accident
Gunshot wounds (e.g., handguns, nail guns) Vehicular-pedestrian accident
Shotgun wounds Falls from height
Blast fragments Crush (e.g., industrial accidents)
Blast (e.g., explosives)
found in the left atrium. Less commonly, they may be found in the
right atrium, right ventricle, and left ventricle in decreasing frequencies. While most myxomas occur sporadically, a familial pattern of
myxomas can occur in an autosomal dominant manner. In a particular syndrome called the Carney complex, patients may present
with cardiac myxomas, cutaneous myxomas, breast fibroadenomas,
hyperpigmented nevi, hyperactive adrenal or testicular glands, and
pituitary tumors. The Carney complex occurs in young individuals
and should be considered in myxomas in atypical locations in the
heart. Surgical removal is the only definitive treatment of cardiac
myxomas. Myxomas tend to recur with rates varying from 5% to
14%; therefore, it is imperative that lifelong follow-up continue after
surgical removal.
Less common benign tumors include rhabdomyomas, fibromas,
lipomas, and papillary fibroelastomas. Rhabdomyomas are the most
common cardiac tumors found in children and are usually located in
the ventricle. They are often associated with a family history of tuberous sclerosis. Surgery can often be avoided unless the patient develops
clinical evidence of arrhythmias and heart failure. Fibromas are composed of fibroblasts or collagen and typically occur in childhood. They
are most often located on the interventricular septum and patients may
present with chest pain, pericardial effusion, heart failure, arrhythmias,
and sudden death. While both occur in the ventricle, the distinguishing
feature of fibromas, in contrast to rhabdomyomas, is the presence of
calcification. Lipomas are rare and occur most frequently in the left
ventricle and the right atrium, although they can be found anywhere
in the heart and the pericardium. They are frequently asymptomatic
but can grow large enough to cause obstructive symptoms. Papillary
fibroelastomas are pedunculate tumors with filiform attachments that
typically arise from the aortic or mitral valve. They carry an elevated
risk of embolic phenomena and, when situated on the aortic valve, can
cause coronary ostial occlusion. Complete surgical resection is recommended because of the risk of systemic embolism. Recurrence rates
are low and long-term anticoagulation is not recommended unless the
patient has other indications.
Malignant Primary Cardiac Tumors
Malignant primary cardiac tumors commonly cause symptoms
via three mechanisms: obstruction, embolization, and arrhythmia.
Obstructive tumors can present with syncope, chest pain, dyspnea or
heart failure. Pericardial invasion and tamponade are rarely the first
manifestation of the disease. Primary cardiac sarcoma is the most common malignant primary cardiac tumor. Once diagnosed, treatment for
cardiac sarcomas is primarily surgical with complete resection as the
goal followed by adjacent chemotherapy. Cardiac sarcomas carry a
very poor overall prognosis.
Secondary Cardiac Tumors
Cardiac metastases are common and can be found in up to 14% of
patients dying with a known malignancy. Cardiac metastases can occur
either by direct extension, by way of the bloodstream or lymphatics, or by
intracavitary diffusion through the inferior vena cava (IVC). Metastases
to the pericardium are most common, followed by epicardium, myocardium, and endocardium. Primary thoracic cancers, including breast and
lung cancer, tend to invade the pericardium directly whereas abdominal
and pelvic tumors reach the right atrium usually through the IVC. Renal
cell carcinoma is the most common tumor to exhibit this tendency.
In men and women, lung cancer is the most frequent cause of cardiac
metastasis. In men, this is followed by esophageal cancer and lymphoma
whereas in women it is followed by lymphoma and breast cancer.
The prognosis of metastatic cardiac tumors is poor, with 1-year
mortality being 50%. Treatment therefore is primarily palliative and
may include radiation therapy, chemotherapy, and surgical resection,
if possible. Malignant pericardial effusion is typically managed with
pericardiocentesis and may need a pericardiotomy to reduce subsequent reaccumulation of pericardial fluid.
TRAUMATIC HEART DISEASE
Traumatic heart disease can be categorized based on the mechanism of
injury (Table 11.2).
Nonpenetrating Cardiac Trauma
Nonpenetrating or blunt cardiac trauma accounts for about 10% of all
traumatic heart disease. Nonpenetrating cardiac trauma can manifest as
a spectrum of pathology including septal rupture, free wall rupture, coronary artery thrombosis or dissection, rupture of the cordae tendinae or
papillary muscle, pericarditis or cardiac tamponade, and arrhythmias.
Commotio cordis is a type of nonpenetrating cardiac trauma that occurs
more often in child athletes as a result of a projectile such as a ball striking
the chest, resulting in ventricular fibrillation and sudden cardiac death.
Nonpenetrating cardiac trauma can present with clinically significant or clinically insignificant injury. Conduction disturbances are
common and a screening 12-lead electrocardiogram (ECG) can be
useful for initial evaluation. Sinus tachycardia is the most common
ECG abnormality. Other possible findings on ECG include T-wave
and ST-segment changes, bradycardia, first- and second-degree atrioventricular block, right bundle branch block, third-degree heart block,
atrial fibrillation, premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation. Elevated cardiac enzymes are not
specific for blunt cardiac trauma and may be related to severity of noncardiac injury or underlying coronary disease. In one study, only 485 of
patients with elevated troponin were clinically found to have significant
blunt cardiac trauma. A negative troponin, however, had a negative predictive value of 93%. The major use of transthoracic echocardiography
in the evaluation of nonpenetrating cardiac trauma is for the assessment
of pericardial effusion, the presence of which is concerning for chamber
rupture. Transesophageal echocardiography is a more sensitive test for
the evaluation of more subtle features of blunt cardiac injury.
Most patients who present with suspected blunt cardiac injury can
be managed with observation and monitoring. Patients in cardiogenic
shock in whom structural injury is confirmed should be promptly
referred to cardiothoracic surgery for surgical repair.
Penetrating Cardiac Trauma
Penetrating cardiac injury is the most common cause of significant cardiac injury, most often by firearms and knives. Due to their anterior location on the chest wall, the right and left ventricles are at the greatest risk
for injury. Most penetrating cardiac injuries involve the myocardium,
sparing additional structures, and are managed effectively with surgical
intervention and rarely requiring reoperation for a residual defect.
Penetrating injury to the epigastrium and precordium should raise
suspicion for penetrating cardiac injury. The clinical presentation
CHAPTER 11 Other Cardiac Topics
135
TABLE 11.3 Key Features of Available Left Ventricular Percutaneous Assist Devices
IABP Impella 2.5 Impella CP Impella 5.0 TandemHeart V-A ECMO
Mechanism Aorta LV → Aorta LV → Aorta LV → Aorta LA → Aorta RA → Aorta
Flow (L/min) 0.3-0.5 1.0-2.5 3.7-4.0 Max 5.0 2.5-5.0 3.0-7.0
Max implant time — 7-10 days 7-10 days 2-3 weeks 2-3 weeks 3-4 weeks
Ability to oxygenate No No No No No Yes
Cardiac Power ↑ ↑↑ ↑↑ ↑↑ ↑↑ ↑↑↑
Afterload ↓ ↓ ↓ ↓ ↑ ↑↑↑
MAP ↑ ↑↑ ↑↑ ↑↑ ↑↑ ↑↑
LVEDP ↓ ↓ ↓↓ ↓↓ ↓↓ ↔
PCWP ↓ ↓↓ ↓↓ ↓↓ ↓↓ ↔
LV preload — ↓↓ ↓↓ ↓↓ ↓↓ ↓
Coronary perfusion ↑ ↑ ↑ ↑ — —
IABP, Intraaortic balloon pump; LA, left atrium; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; MAP, mean arterial pressure; PCWP,
pulmonary capillary wedge pressure; RA, right atrium; V-A ECMO, veno-arterial extracorporeal membrane oxygenation.
could be varied from normal vital signs to circulatory collapse. This is
because after a weapon injuring the myocardium and pericardium is
withdrawn, blood filling the pericardium may not be able to escape. As
pericardial fluid accumulates, ventricular filling is impaired and stroke
volume decreases. In response to a decrease in stroke volume, there is a
catecholamine surge resulting in tachycardia and increased right-sided
filling pressures. As little as 60 mL to 100 mL of blood in the pericardial
sac can result in clinical pericardial tamponade where the limits of distensibility are reached and there is bowing of the interventricular septum, further compromising left ventricular function, reducing cardiac
output, and resulting in irreversible shock. The classic findings of Beck
triad (muffled heart sounds, hypotension and distended neck veins) is
rarely seen. Pulsus paradoxus (a fall in systolic blood pressure of 20 mm
Hg or more during inspiration) and Kussmaul sign (increase in jugular venous distention on inspiration) may be present but not reliably
predictive of pericardial tamponade. Narrowing of the pulse pressure,
however, is a reproducible sign of tamponade. In the case of penetrating cardiac injury, definitive treatment involves surgical intervention.
PERCUTANEOUS MECHANICAL CIRCULATORY
SUPPORT
Mechanical circulatory support (MCS) is a term that refers to mechanical
pumps designed to assist or replace the function of the left ventricle, right
ventricle or both ventricles of the heart. There are several MCS systems
available including the intra-aortic balloon pump (IABP), extracorporeal
membrane oxygenation (ECMO) or extracorporeal life support (ECLS),
ventricular assist devices (VADs), and total artificial hearts (TAHs).
Further details on the disease process and management of chronic heart
failure are covered in Chapter 5. The following discussion will focus on
temporary or percutaneous MCS as indicated in patients with cardiogenic
shock refractory to medical therapy when the objective is rapid augmentation of cardiac output, reduction of ventricular filling pressures, and
life support. Longer-term support, with VADs, TAHs, and cardiac transplantation are covered elsewhere. A comparison of the key features of the
available percutaneous assist devices is summarized in Table 11.3.
Percutaneous Left Ventricular Assist Devices
Intra-Aortic Balloon Pump
The IABP remains the most commonly used form of circulatory support. A polyethylene helium-filled balloon is placed percutaneously
through the femoral artery into the thoracic aorta, just distal to the left
subclavian artery. Timing of balloon inflation and deflation is based on
the ECG or the arterial waveform of the patient. The balloon inflates
with the onset of diastole and deflates at the onset of left ventricular
systole. Balloon inflation during diastole increases diastolic blood
pressure, referred to as diastolic augmentation, allowing for maximal
delivery of oxygenated blood to the coronary arteries. Deflation during
systole decreases the afterload and myocardial oxygen consumption
while modestly enhancing cardiac output. The IABP reduces myocardial oxygen demand but provides only modest ventricular unloading.
Patients must have some left ventricular function and electrical stability for an IABP to be most effective because the device only results in an
increase in cardiac output of 0.5 to 1.0 liter per minute.
The major contraindication for IABP is greater than mild aortic valve regurgitation because the diastolic inflation of the balloon
may worsen the degree of regurgitation. Severe peripheral arterial
disease or aortic disease increases the risk of vascular complication
such as thromboembolism and lower extremity and visceral ischemia.
Potential major complications include balloon leak, severe bleeding
(e.g., retroperitoneal), thromboembolic events, major limb or visceral
ischemia, vascular trauma, thrombocytopenia from platelet deposition
in the IABP membrane, and infection.
Impella
The Impella (Abiomed, Danvers, Mass.) is a nonpulsatile axial flow
Archimedes-screw pump that propels blood from the left ventricle
into the proximal ascending aorta. Depending on the version used,
these devices can deliver up to 5.0 L/min of maximal flow. Designed
to be placed via the femoral artery, delivery can either be percutaneous (Impella 2.5 and CP) or via a surgical cutdown (Impella 5.0).
At the tip of the catheter there is a flexible pigtail loop that stabilizes
the device in the left ventricle. The main body of the device contains
the pump inlet and outlet areas, motor housing, and pump pressure
monitor. Unlike the IABP, the Impella does not require ECG or arterial pressure timing and therefore provides stability despite transient
arrhythmias.
The hemodynamic effects of the Impella are to unload the left
ventricle and increase forward flow, reducing myocardial oxygen consumption, improving mean arterial pressure, and reducing pulmonary
capillary wedge pressure. Compared to the IABP, the Impella delivers a significant increase in cardiac output. Adequate right ventricular
function is necessary to maintain left ventricular preload and hemodynamic support. In cases where there is significant biventricular failure
or unstable ventricular arrhythmias, a concomitant right ventricular
assist device may be necessary.
136 SECTION II Cardiovascular Disease
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Contraindications to the use of the Impella are the presence of a
mechanical aortic valve, left ventricular thrombus, severe aortic stenosis, moderate to severe aortic insufficiency, severe peripheral arterial
disease, and the inability to tolerate systemic anticoagulation. Possible
complications of Impella use include limb ischemia, vascular complications, hemolysis due to mechanical erythrocyte shearing, and bleeding requiring blood transfusion.
TandemHeart
The TandemHeart (TandemLife, Pittsburgh, Penn.) is a percutaneous
centrifugal pump that provides up to 4 L/min of mechanical circulator
support via a continuous-flow centrifugal pump. The TandemHeart is
inserted through the femoral vein and advanced across the interatrial
septum into the left atrium. Oxygenated blood is then withdrawn from
the left atrium via a 21-Fr inflow cannula and reinjected into the lower
abdominal aorta or iliac arteries via a 15-Fr to 17-Fr outflow cannula.
The need for transseptal puncture is a limitation to the widespread
use of this device. The potential complications of the TandemHeart
include the need for blood transfusion, sepsis/systemic inflammatory
response syndrome, bleeding around the cannula, gastrointestinal
bleeding, coagulopathy, stroke, left atrial perforation, and devicerelated limb ischemia.
Right Ventricular Support
Acute right ventricular (RV) failure may occur in a number of clinical
settings such as acute myocardial infarction, fulminant myocarditis,
acute pulmonary embolism, pulmonary hypertension, postcardiotomy
shock, postcardiac transplantation, and following LVAD implantation.
The mainstay of therapy for RV failure is inotropic and pulmonary
vasodilator support and volume status optimization. Vasopressors
are often used to maintain coronary perfusion pressure and inhaled
nitric oxide can be used to reduce RV afterload. When these measures
are insufficient to augment RV systolic function, mechanical circulatory support may be required to unload the RV, ensure adequate LV
preload, and optimize tissue perfusion.
There are both surgical and percutaneous options for RV mechanical circulatory support. The surgical right ventricular assist device
(RVAD) was associated with worse outcomes when compared to
patients with RV failure who did not need an RVAD. Unfavorable outcome data and the need for repeat sternotomy for both insertion and
removal of the device has limited clinical utilization. There are two
percutaneous devices currently available for RV support: (1) Impella
RP (Abiomed, Danvers, Mass.), an axial catheter-based pump and
(2) the Protek Duo (Cardiac Assist Inc., Pittsburgh, Penn.), a catheter
with an extracorporeal centrifugal pump. The Impella RP provides RV
unloading with up to 4 L/min of continuous flow from the inlet in the
inferior vena cava through a cannula to the outlet in the pulmonary
artery. The pump is inserted via a 23-Fr sheath in the femoral vein into
the atrium and across the tricuspid and pulmonic valves into the main
pulmonary artery. The Protek Duo is a dual-lumen cannula that is
inserted percutaneously via the internal jugular vein. The inflow lumen
is positioned in the right atrium and the outflow lumen is positioned in
the main pulmonary artery. The extracorporeal pump allows flows up
to 5 L/min and an oxygenator can also be introduced into the circuit to
allow for oxygenation support.
Extracorporeal Membrane Oxygenation
ECMO provides cardiopulmonary support in patients whose heart
and/or lungs no longer provide adequate physiologic support. ECMO
can be either veno-venous (V-V ECMO) for isolated pulmonary failure
only or veno-arterial (V-A ECMO) for pulmonary and cardiac failure.
Cannulas are placed in the right side of the heart, from the vena cava,
to drain blood into the ECMO circuit for oxygenation. Blood can then
either be returned to the right side of the heart in V-V ECMO or to the
arterial system (proximal or distal aorta) in V-A ECMO. The bypass
circuit in ECMO is composed of a centrifugal, nonpulsatile pump
for blood propulsion, and a membrane oxygenator for gas exchange.
V-A ECMO requires anticoagulation while V-V ECMO does not.
Complications relate to bleeding, thromboembolism, and mechanical
complications such as hemolysis and arterial insufficiency.
V-V ECMO offers gas exchange and is useful for conditions resulting
in severe impairment of gas exchange such as ARDS or pulmonary embolism. V-V ECMO does not provide hemodynamic support. Alternatively,
V-A ECMO provides additional hemodynamic support with flows sometimes exceeding 6 L/min depending on the cannula French size and length
and properties of the pump. V-A ECMO alone, however, does not reduce
ventricular wall stress and the use of a concomitant MCS such as IABP or
percutaneous VAD is usually needed to vent or unload the left ventricle.
NONCARDAIC SURGERY IN THE PATIENT WITH
CARDIOVASCULAR DISEASE
Noncardiac surgery in patients with known cardiovascular disease may be
associated with an increased risk for death or cardiac complications such as
MI, congestive heart failure, and arrhythmias. To determine an individual
patient’s risk for a procedure, the consulting physician must have knowledge of the type and severity of the patient’s cardiac disease, the comorbid
risk factors, and the type and urgency of surgery. In general, the preoperative evaluation and management are the same as in the nonoperative
setting; for patients who are at risk, additional noninvasive and invasive
testing may be performed if the results would affect treatment or outcome.
Estimation of a patient’s perioperative risk can be determined by a
careful clinical evaluation, including a history, physical examination,
ECG, and type of surgery. Risk models can then be applied to guide the
clinician with regards to additional testing and treatment. The most
widely used risk model was developed in a study of 4315 patients 50
years or older undergoing major noncardiac procedures in a tertiary
care teaching hospital and has been validated over the past 15 years.
The index includes six independent predictors of complications in a
revised cardiac risk index (RCRI): high-risk type of surgery, history of
cerebrovascular disease, preoperative treatment with insulin, history
of ischemic heart disease, history of congestive heart failure, and preoperative serum creatinine concentration greater than 2.0 mg/dL. The
evaluating clinician can risk stratify the patients into low, intermediate,
or high cardiovascular risk on the basis of having zero, one to two, or
three or more risk factors, respectively. Another risk model was developed from the American College of Surgeons 2007 National Surgical
Quality Improvement Program database (NSQIP), which identified
five predictors of perioperative myocardial infarction or cardiac arrest:
type of surgery, dependent functional status, abnormal creatinine
level, American Society of Anesthesiologists class, and increasing age.
Once the clinical evaluation is complete and the type of surgery
is known, the need for additional testing and treatment can be determined. Very high-risk patients are defined as those with recent myocardial infarction (within 60 days), unstable angina, decompensated
heart failure, and hemodynamically important valvular disease. These
patients are at very high risk of preoperative myocardial infarction,
heart failure, fatal arrhythmia, and cardiac death. All such patients
should be optimally treated and referred to a cardiologist for evaluation.
If emergency surgery is contemplated, little in the way of cardiac
assessment can be performed, and recommendations may be directed
at perioperative medical management and surveillance. If surgery is
not urgent, additional evaluation is based on the clinical assessments
of the risk and type of surgery.
CHAPTER 11 Other Cardiac Topics
137
Disease-Specific Approaches
Ischemic Heart Disease
About 70% of MIs occur within the first 6 days after an operation,
with the peak incidence between 24 and 72 hours. Multiple stresses
associated with surgery such as volume shifts, anemia, and infection
can increase the heart rate and blood pressure perioperatively and can
provoke myocardial ischemia. Identification of known or symptomatic
stable coronary artery disease or risk factors for coronary artery disease
can guide further evaluation or changes in perioperative management.
Patients with stable angina represent a continuum from mild to
severe. In mild cases, patients manifest angina only after strenuous
exercise and do not have signs of left ventricular dysfunction. These
patients can be stabilized with optimal medical therapy with aspirin,
β-adrenergic blocking agents and statins. On the severe end of the
continuum, patients with angina on mild exertion are at high risk for
development of perioperative major cardiovascular events and warrant
consideration of additional cardiovascular testing.
Coronary angiography and revascularization should be reserved for
individuals in whom this treatment would otherwise result in significant improvement in symptoms or long-term survival. Current data do
not support a clear benefit of preoperative coronary revascularization.
The preoperative management of patients with a history of
recent coronary artery revascularization on antiplatelet therapy is
challenging as clinicians balance the cardiac risks of discontinuing
therapy with the bleeding risks of continuing antiplatelet agents.
Several large observational studies have shown an increased risk of
adverse cardiovascular events in patients undergoing noncardiac
surgery, particularly within 6 weeks of receiving a coronary stent.
While the risk extends to 12 months, it stabilizes without significant decrease in risk from 6 to 12 months. The American College
of Cardiology (ACC) and American Heart Association (AHA)
guidelines recommend the following algorithm for patients with
a coronary stent. If surgery is elective and can be safely delayed,
the optimal timing is 12 months after PCI. For those in whom surgery cannot be delayed and are within 30 days of bare metal or 6
months of a drug-eluting stent, dual-antiplatelet therapy with aspirin and P2Y12 inhibitor should be continued. If the risk of bleeding
is prohibitive, the P2Y12 inhibitor is temporarily interrupted (for
5 to 7 days) and aspirin is continued throughout the perioperative
period because typically aspirin provides benefits that outweigh the
bleeding risk. Possible exceptions to this include intracranial procedures, transurethral prostatectomy, intraocular procedures, and
operations with extremely high bleeding risk. In clinical practice,
the decision is made with a multidisciplinary team approach considering a number of factors such as the risk of stent thrombosis if
DAPT needs to be interrupted, the consequences of delaying the
surgical procedure, the increased intra- and periprocedural bleeding risks, and possible consequences of such bleeding if DAPT is
continued.
Heart Failure
Studies have shown that heart failure is associated with increased
perioperative cardiac morbidity after noncardiac surgery. During the
postoperative period, congestive heart failure most commonly occurs
in the first 24 to 48 hours, when fluid administered during surgery is
mobilized from the extravascular space. However, heart failure may
also result from myocardial ischemia and new arrhythmias. Initial
management includes identification and treatment of the underlying
cause. In addition, intravenous diuretics usually provide rapid relief of
pulmonary congestion. If heart failure is complicated by hypotension
or poor urine output, insertion of a pulmonary artery catheter may be
helpful to guide additional therapy.
Valvular Heart Disease
In regard to valvular heart disease the greatest risk for complications
after noncardiac surgery is in those with aortic or mitral stenosis.
Patients with symptomatic, severe aortic or mitral stenosis should
be evaluated for valve replacement before high-risk noncardiac surgery. In patients with mild to moderate aortic or mitral stenosis, careful attention to volume status and heart rate control are necessary to
optimize left ventricular filling and avoid pulmonary congestion. In
patients with valve disease or prosthetic heart valves, prophylactic antibiotics are recommended if appropriate. Lifelong anticoagulation with
an oral vitamin K antagonist (VKA) is recommended for all patients
with mechanical prosthetic heart valves. In addition to the thrombogenic nature of the intravascular prosthetic material, mechanical valves
create abnormal flow conditions and areas of high-shear stress, both
of which can result in platelet activation leading to valve thrombosis
and embolic events. The preoperative management of patients with
mechanical heart valves in whom interruption of anticoagulation therapy is needed for diagnostic or surgical procedures should account for
the type of procedure, risk factors, and type, location, and number of
heart valve prostheses. The ACC/AHA guidelines recommend continuation of VKA anticoagulation with a therapeutic INR in patients
undergoing minor procedures (such as dental extractions or cataract
removal) where uncontrolled bleeding risk is low. The guidelines recommend bridging anticoagulation with either intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin during
the time interval when INR is subtherapeutic in patients who are
undergoing invasive or surgical procedures with (1) mechanical aortic valves and any thromboembolic risk factor, (2) older-generation
mechanical aortic valves, or (3) mechanical mitral valves.
Arrhythmias and Conduction Defects
Patients with symptomatic, high-grade conduction disturbances,
such as third-degree atrioventricular (AV) block, have an increased
perioperative risk for cardiac complications and should have a temporary pacemaker inserted before surgery. Patients with first-degree
AV block, Mobitz type I AV block, or bifascicular block (right bundle
branch block and left anterior fascicular block) do not require prophylactic pacemaker insertion.
Atrial arrhythmias such as atrial fibrillation are common after
surgery and usually are not associated with significant complications
if the ventricular rate is well controlled. Mounting evidence suggests
that new-onset postoperative atrial fibrillation following noncardiac
surgery carries a similar risk of thromboembolism as in patients with
nonvalvular atrial fibrillation. Therefore, the long-term management
of these patients should be similar with regards to anticoagulation.
Ventricular premature beats and nonsustained ventricular tachycardia are also common after noncardiac surgery and do not require
specific therapy unless they are associated with myocardial ischemia
or heart failure. In most instances, treatment of the underlying cause
(e.g., hypoxia, metabolic abnormalities, ischemia, volume overload)
results in significant improvement or resolution of the rhythm disturbance without specific antiarrhythmic therapy.
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12
Vascular Diseases and Hypertension
Thomas Sperry, Wanpen Vongpatanasin
INTRODUCTION
Diseases of the systemic and pulmonary vasculature are among the
most common clinical problems encountered in internal medicine. Yet
these important diseases are not often given the emphasis they deserve;
they fall between the cracks of traditional medical subspecialties. Early
clinical recognition is important because effective therapy often can
prevent or at least delay needless suffering and death. This chapter
reviews the causes, clinical manifestations, diagnostic evaluations, and
therapeutic approaches to the major forms of systemic and pulmonary
vascular diseases, as well as arterial hypertension.
SYSTEMIC VASCULAR DISEASE
Peripheral Arterial Disease
Peripheral arterial disease (PAD) refers to atherosclerotic vascular disease of mainly the lower extremities. The prevalence increases with age,
ranging from 2% to 6% for adults under the age of 60 years to 20% to
30% for those over age 70. As with coronary atherosclerosis, the major
reversible risk factors are cigarette smoking, diabetes mellitus, hyperlipidemia, and hypertension. The diagnosis of PAD may at times be
elusive, as only 30% to 50% of patients with PAD become symptomatic. PAD may present with symptoms of intermittent claudication,
critical limb ischemia, or acute limb ischemia. Roughly 10% to 15%
of patients present with the classic syndrome of intermittent claudication, which refers to ischemic muscle pain or weakness brought on
by exertion and promptly relieved by rest. A larger proportion of PAD
patients (50%) have more atypical leg symptoms different from classic claudication, which either may not limit an individual from walking or may not resolve within 10 minutes of rest. Claudication is also
associated with a significant 10-year risk of morbidity and mortality.
Approximately 10% to 20% of patients will develop worsening claudication or critical limb ischemia, 5% will require amputation, 10%
to 20% will require revascularization, and up to 30% will die of a cardiovascular event (e.g., heart attack, stroke) as a result of concomitant
coronary and/or cerebrovascular atherosclerosis. To minimize progression of PAD and avoid complications, risk factor modification is
absolutely essential. This includes tight control of blood pressure (BP),
plasma lipids, and blood glucose. Complete cessation of tobacco use
is a must.
The diagnosis of PAD begins with a careful history and physical
examination and is confirmed with noninvasive laboratory testing.
Ischemic pain occurs in the leg muscles supplied by arterial segments
that are distal to the site of stenosis. Calf claudication is the hallmark
of femoral-popliteal disease, whereas discomfort in the thigh, hip, or
buttock associated with impotence indicates aortoiliac disease (Leriche
syndrome). Depending on the severity of the stenosis, the pain is experienced at a predictable walking distance and is promptly relieved by
rest. Claudication must be differentiated from the pseudoclaudication
of lumbar degenerative spinal canal stenosis. In the latter condition,
walking can also aggravate leg pain, but it is not relieved simply by the
cessation of exercise. Rather, assuming positions that minimize lumbar
extension such as stooping forward or sitting alleviates the pain. The
characteristic physical findings of PAD are absent or diminished pulses
distal to the stenosis, bruits over the diseased artery, hair loss, thin
shiny skin, and muscle atrophy. Severe ischemia causes pallor, cyanosis, decreased skin temperature, ulceration, and gangrene.
Noninvasive techniques are quite good in the diagnosis of PAD.
The ankle-brachial index (ABI) is the ratio of the highest systolic BP
measured from either the dorsalis pedis or posterior tibialis artery to
the highest systolic BP obtained from the brachial artery of either arm
using a Doppler stethoscope. The normal ABI range is 1.0 to 1.4. An
ABI of 0.9 or less indicates PAD. This simple noninvasive test has a
sensitivity and specificity of 68% to 84% and 84% to 99%, respectively,
when compared to vascular imaging. In the occasional patient with a
high likelihood of PAD but with borderline (between 0.9-1.0) or normal ABI, ABI obtained during exercise treadmill testing may prove
useful in the diagnosis. In some patients with diabetes mellitus or renal
failure, the media of the affected leg vessels become so heavily calcified
that they resist compression except during very high levels of cuff inflation. The result is a falsely elevated ankle BP and an artificially normal
or supernormal ABI of greater than 1.4 (Table 12.1). Measurement of
toe BP to obtain toe-brachial index in that situation is recommended
to verify presence of PAD. Patients with a toe-brachial index of less
than or equal to 0.70 are considered to have hemodynamically significant PAD.
Duplex ultrasonography is an important adjunct to the ABI, with
a similar sensitivity and specificity. This test is particularly useful to
diagnose PAD in patients with noncompressible vessels from medial
wall calcification. The Doppler velocity waveform remains abnormal, despite a spuriously normal or elevated ABI. Magnetic resonance
(MR) angiography and computed tomographic (CT) angiography also
TABLE 12.1 Interpretation of Ankle-
Brachial Index
Ankle-Brachial Index Interpretation
1.00-1.40 Normal
0.90-0.99 Borderline
0.70-0.89 Mild PAD
0.40-0.69 Moderate PAD
<0.40 Severe PAD
>1.40 Noncompressible vessels
PAD, Peripheral arterial disease.
139
140 SECTION II Cardiovascular Disease
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permit excellent visualization of vascular stenosis and identification
of runoff vessels. With these noninvasive imaging modalities, spatial
resolution is comparable with that of traditional invasive angiography,
which now is reserved for patients undergoing revascularization.
The medical management of PAD includes lifestyle and risk factor
modification, as well as antiplatelet therapy. Smoking cessation reduces
the risk of limb loss, myocardial infarction, and death. Lipid-lowering
therapy with high-intensity statin therapy should be initiated and
intensified to reduce the rate of vascular events regardless of cholesterol levels. In addition, PAD patients with LDL-C greater than 70 mg/
dL despite maximally tolerated statin therapy should be considered for
additional lipid-lowering therapy such as ezetimibe. Those with persistently elevated LDL-C despite statin and ezetimibe may then be considered for PCSK9 inhibition. Antihypertensive medication should be
initiated and intensified until BP is less than 130/80 mm Hg. Choice of
antihypertensive regimen should be based on corresponding comorbidities, but there is some evidence to support the use of ACE inhibitors or angiotensin-receptor blockers. β-Adrenergic blockers do not
reduce walking capacity or worsen intermittent claudication in patients
with PAD. Aspirin reduces the risk of myocardial infarction, death,
and stroke. However, clopidogrel is an effective alternative treatment
and is more effective than aspirin in reducing cardiovascular events.
Newer antiplatelet agents, such as ticagrelor, have not been proven to
be more effective than clopidogrel in reducing cardiovascular events
or limb ischemia in patients with symptomatic PAD. More recently,
the combination of low-dose factor Xa inhibitor rivaroxaban (2.5 mg
twice daily) and low-dose aspirin of (≤100 mg) was shown to reduce
the risk of cardiovascular events and limb amputation in PAD patients
when compared to low-dose aspirin alone. While the overall bleeding
risk is increased with the combination therapy, fatal bleeding is not.
Therefore, this combination should be considered in PAD patients with
high cardiovascular risk but low bleeding risk. Each patient also needs
an exercise prescription as exercise training improves walking capacity and quality of life. This exercise training should be conducted in a
medical facility or clinic at a minimal frequency of three times weekly
for 12 weeks, preferably for 30 to 45 minutes per session. Cilostazol, a
phosphodiesterase-3 inhibitor, is effective in improving claudication
symptoms but is not effective in preventing cardiovascular events. Side
effects of cilostazol include headache, diarrhea, dizziness, and palpitation. However, cilostazol must be avoided in patients with congestive
heart failure because its use in such patients may increase mortality.
Pentoxifylline should not be used in PAD as it is no more effective than
placebo for intermittent claudication.
Revascularization (percutaneous or surgical) is indicated for
patients with severe claudication that is resistant to medical therapy,
limb-threatening ischemia, or ischemia-induced impotence (Fig. 12.1).
A variety of devices are now available for aortoiliac, femoropopliteal,
and infrapopliteal percutaneous interventions, including drug-coated
balloons, cutting balloons, laser atherectomy, self-expanding stents,
and drug-coated stents. However, efficacy of these newer devices has
not been directly compared to each other or to surgical revascularization. In general, surgical revascularization is more suitable for longer areas of stenosis and remains the best option for some patients.
The decision between surgery versus endovascular intervention also
depends on a patient’s life expectancy and other comorbid conditions.
Overall, the selection of surgery versus percutaneous intervention as
the initial mode of revascularization in patients with limb-threatening
ischemia is complex and should be a decision made amongst an interdisciplinary team of physicians.
Acute limb ischemia (ALI) is a vascular emergency. Sudden occlusion of a peripheral artery is caused by either arterial embolism or
thrombosis in situ. Arterial emboli usually originate in the cardiac
chambers in the setting of preexisting cardiac disease such as myocardial infarction (e.g., left ventricular mural thrombus), congestive heart
failure, or atrial arrhythmias (e.g., left atrial thrombus in a patient with
atrial fibrillation). Thrombosis in situ usually occurs in arteries with
a preexisting severe stenosis in the setting of long-standing PAD with
or without previous vascular surgery. Patients with arterial embolism
usually experience sudden onset of symptoms without a history of
claudication, whereas those with thrombosis in situ typically have a
history of claudication that has previously been stable and then suddenly assumes a crescendo pattern over a period of days. In either case,
the physical examination reveals a cold, cyanotic (bluish) extremity
with absent pulses distal to the site of arterial occlusion and diminished
Fig. 12.1 Angiogram of the distal abdominal aorta and iliac arteries demonstrates an occluded left common
iliac artery with extensive collateral circulation from the contralateral internal iliac artery (left), which resolved
after successful stent implantation (right). (Courtesy of Bart Domatch, MD, Radiology Department, University
of Texas Southwestern Medical Center, Dallas, Texas.)
CHAPTER 12 Vascular Diseases and Hypertension
141
motor and/or sensory function. A handheld Doppler device is used to
assess signals at different arterial segments and confirms the diagnosis
of acute vascular occlusion. Anticoagulation should be initiated immediately with intravenous heparin titrated to maintain the activated
partial thromboplastin time equal to 2.0 to 2.5 times control. Catheterdirected infusion of thrombolytic therapy offers a similar success rate
in salvaging the limbs as surgical revascularization (thromboembolectomy or bypass surgery). However, survival rate is higher with
catheter-based therapy, likely related to the multiple comorbidities of
patients with ALI. Patients with irreversible tissue necrosis, regardless
of the cause, should be treated with emergent amputation rather than
revascularization to reduce the risk of kidney failure (myoglobinuria),
sepsis, and multiorgan failure.
Aortic Aneurysm
An aortic aneurysm is commonly defined as a dilation of all three layers of the vessel to more than 50% of the expected normal diameter.
The two main types are thoracic aortic aneurysms (TAA), which occur
above the diaphragm, and abdominal aortic aneurysms (AAA), which
occur below the diaphragm. Abdominal aortic aneurysm is a common
vascular disease in older adults, affecting 4% to 8% of men and 0.5% to
1.5% of women over the age of 65 years. Thoracic aortic aneurysm is
much less prevalent (0.4% to 0.5%). Besides age, the major risk factors
for abdominal aortic aneurysms are cigarette smoking, hypertension,
and a family history of aortic aneurysms. Atherosclerosis is responsible
for most cases of abdominal aortic aneurysm, while other causes such
as genetic (Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz,
Turner syndrome, or bicuspid aortic valve), vasculitis with connective
tissue disease (Takayasu’s arteritis, giant-cell arteritis), chronic infection (syphilitic aortitis), and trauma may cause thoracic or abdominal
aortic aneurysms. Abdominal aortic aneurysms gradually grow in size
over time at an average rate of 1 to 4 mm per year. The risk of rupture is
low until the diameter reaches 5 cm, and then it increases exponentially.
The risk of aortic rupture is 1% per year for aneurysms between 3.5 and
4.9 cm in diameter and 5% per year for aneurysms larger than 5 cm.
Most cases of aortic aneurysms are asymptomatic and detected
incidentally during routine screening or imaging for other indications.
However, some patients with AAA may develop vascular complications
such as aneurysm expansion with compression of adjacent structures.
Occasionally, mural thrombi form within the aneurysm and embolize,
causing acute occlusion of distal arterial segments. Patients with iliac
aneurysm may develop hydronephrosis or recurrent urinary tract infection from ureteral compression. Others develop neurologic symptoms
from compression of sciatic or femoral nerves. The classic physical
finding is a pulsatile nontender mass below the umbilicus (distal to the
origin of the renal arteries). In thin patients, normal aortic pulsations
are often palpable but above the umbilicus. Hypotension and acute
abdominal pain should prompt consideration of aneurysm rupture,
which requires emergent operative repair. Duplex ultrasonography is
an accurate and reliable diagnostic tool for abdominal aortic and iliac
aneurysms. Routine screening for AAA with ultrasonography is recommended for all men between the ages of 65 and 75 years who have ever
smoked or men above the age of 60 with family history of AAA among
first-degree relatives. Such screening has a proven mortality benefit. CT
and MR angiography allow visualization of the thoracic and abdominal
aorta, as well as the iliac arteries and its branches (Fig. 12.2).
Medical treatment for aortic aneurysm includes smoking cessation,
tight BP control to less than 130/80 mm Hg, and intensive statin therapy. Although transforming growth factor-β has been implicated in the
pathogenesis of aortic aneurysm in Marfan syndrome, which is mediated by angiotensin-II receptor activation, losartan was not shown to
more effective than beta adrenergic receptor blockade in reducing the
rate of aortic root enlargement. β-Adrenergic blockade has not proven
beneficial in patients with abdominal aortic aneurysm from other
causes. Similarly, a randomized clinical trial failed to demonstrate
superiority of angiotensin-converting enzyme inhibitors (ACEI) over
calcium-channel blockers in preventing AAA expansion. However,
small sample size and inclusion of patients with well-controlled hypertension may have limited the investigators’ ability to detect a difference. Patients who develop symptoms from thoracic aneurysms of any
size should undergo repair. For asymptomatic patients, presence of
large aneurysms (diameter 5.5 cm or above) or rapid aneurysm expansion regardless of the size are also indications for aneurysm repair
(Table 12.2). Open surgical repair remains the treatment of choice for
thoracic aneurysms involving the aortic root, ascending aorta, or aortic
arch. However, thoracic endovascular aortic repair (TEVAR) has now
emerged as the procedure of choice for descending thoracic aneurysm
given lower early morbidity and mortality compared to open surgical repair in several observational studies. Elective abdominal aortic
aneurysm repair carries a perioperative mortality rate of 2% to 6%.
Fig. 12.2 CT angiogram of the distal abdominal aorta shows abdominal
aortic aneurysm with the largest diameter of 6.2 cm and severe stenosis at the origin of the right common iliac artery. (Courtesy of Bart
Domatch, MD, Radiology Department, University of Texas Southwestern Medical Center, Dallas, Texas.)
TABLE 12.2 Indications for Surgical
Treatment of Arterial Aneurysms
Symptoms from expansion of aneurysm or compression of adjacent structure
Rupture of aneurysm
Rapid aortic aneurysm expansion of ≥1 cm per year
Asymptomatic with large size
Thoracic aneurysm (ascending or descending aneurysm) with diameter >5.5
cm in adults
For genetic cause of thoracic aneurysm (such as Marfan, Loeys-Dietz,
Ehlers-Danlos, Turner syndrome, or bicuspid aortic valve), a lower
diameter or aortic size may be considered (generally of at least 5 cm or
>4.5 cm in the presence of family history of aortic dissection)
Abdominal aorta >5.5 cm
Iliac aneurysm >3 cm
142 SECTION II Cardiovascular Disease
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Furthermore, a large randomized study failed to demonstrate any benefit of surgery in patients with aneurysms 4.0 to 5.4 cm in diameter.
For these reasons, patients with small aortic aneurysms (4.0 to 5.4 cm
in diameter) should be treated medically with close monitoring of
aneurysm size with periodic imaging studies every 6 to 12 months (see
Table 12.2).
Percutaneous endovascular aneurysm repair (EVAR) is an alternative method to open surgical repair for treatment of abdominal
aortic aneurysm. EVAR offers lower perioperative death than surgical
repair with equivalent long-term survival. However, EVAR should be
reserved for patients with favorable anatomy who are able to return
for follow-up visits and repeated imaging studies of the aneurysm
sites to ensure that the stent graft is free from endovascular leaks or
displacement.
Aortic Dissection
In aortic dissection, the intimal layer is torn from the aortic wall leading to the formation of a false lumen in parallel with the true lumen.
Risk factors include hypertension, cocaine use, trauma, hereditary
connective tissue disease (e.g., Marfan syndrome, Ehlers-Danlos
syndrome), vasculitis (e.g., Takayasu’s arteritis, giant-cell arteritis),
Behçet’s disease, bicuspid aortic valve, and aortic coarctation. Aortic
dissection can be classified as types A and B (Stanford system). Type
A dissection involves the ascending aorta, whereas type B dissection
involves the distal aorta. The DeBakey system subdivides aortic dissection into three subtypes—types I, II, and III. Type 1 dissection
involves the entire aorta, whereas type II involves only the ascending
aorta and type III involves only the descending aorta. Aortic dissection involving the ascending aorta carries a high mortality rate
of 1% to 2% per hour during the first 24 to 48 hours. Patients usually develop acute onset of severe chest or back pain. Abdominal
pain, syncope, and stroke are common. Retrograde propagation of
the dissection can cause pericardial tamponade or coronary artery
dissection with acute myocardial infarction. Dissection involving
the aortic valve causes acute severe aortic insufficiency with acute
pulmonary edema. The dissection plane may propagate in an antegrade direction to compromise flow in the carotid and subclavian
arteries, producing a stroke or acute upper limb ischemia. Patients
with distal (type B) aortic dissection exhibit acute onset of back pain
or chest pain often accompanied by lower extremity ischemia and
ischemic neuropathy.
The physical findings include pulse deficits, neurologic deficits,
or a diastolic murmur of aortic regurgitation. However, acute aortic regurgitation into an unprepared ventricle produces only a short,
soft diastolic murmur that is often missed. The widened pulse pressure and associated physical findings of chronic aortic regurgitation
are absent, and the clinical picture is that of an acutely ill patient with
tachypnea, tachycardia, and a narrow pulse pressure. Hypotension,
jugular venous distention, and pulsus paradoxus should prompt the
diagnosis of pericardial tamponade. Transesophageal echocardiography, MR angiography, or CT angiography confirm the diagnosis
by demonstrating an intimal flap that separates the true lumen from
the false lumen (Fig. 12.3). Type A aortic dissection is uniformly fatal
without emergent surgical repair. With surgery, mortality is reduced
to 10% at 24 hours and 20% at 30 days. Patients with type B aortic dissection should be treated medically because 1-year survival
is higher with medical therapy than it is with surgery (75% versus
50%). However, surgery is indicated if type B dissection compromises blood flow to the legs, kidneys, or other viscera. Tight control
of BP is essential because aortic aneurysm was found to develop in
30% to 50% of patients with type B aortic dissection when studied
over 4 years.
Fig. 12.3 CT angiogram of the aorta shows type B aortic dissection.
The intimal flap (arrow) separates the true lumen (T) from the false
lumen (F) and compromises blood flow to the right kidney causing renal
atrophy and cortical thinning. (Courtesy of Bart Domatch, MD, Radiology Department, University of Texas Southwestern Medical Center,
Dallas, Texas.)
Penetrating Aortic Ulcers and Intramural Hematoma
Penetrating aortic ulcers and intramural hematomas exhibit chest pain
that is indistinguishable from that of aortic dissection. In contrast to
aortic dissection, however, the pathologic condition is localized. No
identifiable intimal flap and thus no branch vessel occlusion are produced. Disruption of the internal elastic lamina produces aortic ulcers
that erode into the medial wall and protrude into the surrounding
structures. Rupture of the vasa vasorum causes formation of localized hematoma underneath the adventitia with resultant asymmetric
thickening of the aortic wall. Patients with either condition typically
are older than those with aortic dissection, have a larger aortic size, and
have a higher prevalence of abdominal aortic aneurysm. Aortic rupture
is the major complication of both penetrating ulcers and intramural
hematomas, particularly with those aneurysms located in the ascending aorta. The diagnosis is made with invasive angiography, CT angiography, or MR angiography (Fig. 12.4). Surgical intervention should
be considered for ulcers and hematomas of the ascending aorta, deeply
penetrating ulcers, or severely bulging hematomas, irrespective of their
location. Ulcers and hematomas of the descending aortic may be managed successfully with β-adrenergic blockade and tight control of BP.
Other Arterial Diseases
Buerger’s disease, or thromboangiitis obliterans is a nonatherosclerotic disease of the arteries, veins, and nerves of the arms and legs
affecting mostly young men before the age of 45 years. The mechanism
is unknown, but all patients have a history of heavy tobacco addiction.
The presenting symptom is claudication of the feet, legs, hands, or
arms. Multiple-limb involvement and superficial thrombophlebitis are
common. The C-reactive protein and Westergren sedimentation rate
typically are normal, and a search for serologic markers for connective
tissue disease (e.g., antinuclear antibody or rheumatoid factor, antiphospholipid antibody) is negative. The diagnosis is based on the typical clinical presentation. If the presentation is atypical, then biopsy is
needed to make the diagnosis. The histologic hallmark is inflammatory
intramural thrombi within the arteries and veins with sparing of internal elastic lamina and other arterial wall structures. The most effective
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