1854 PART 6 Disorders of the Cardiovascular System

very large effusions. In patients with suspected pericardial effusion or

tamponade, echocardiography can usually be performed rapidly, at the

bedside, and even by operators with limited skill. The distance from

the parietal to the visceral pericardial layer can be measured, and when

this exceeds ~1 cm, an effusion is considered significant. Echocardiographic features suggestive of tamponade include diastolic collapse of

the right ventricular free wall, suggestive of pericardial pressures that

exceed right ventricular filling pressures, and Doppler evidence of

respiratory flow variation, which is the Doppler equivalent of pulsus

paradoxus. Despite the benefits of echocardiography in suspected

pericardial tamponade, the diagnosis of tamponade remains a clinical

diagnosis, and other important features, such as patient’s blood pressure in the presence of pulsus paradoxus, need to be taken into account

when considering therapeutic options.

Chronic inflammation of the pericardium leads to thickening and

calcification of the parietal pericardium, resulting in pericardial constriction in which diastolic filling can be severely impaired. In these

cases, filling of the ventricles comes to an abrupt halt when the volume

of ventricular filling is impaired by the constricting pericardium.

Assessment of pericardial thickness in these patients is important, but

it is just as important to note that approximately one in five patients

with severe pericardial constriction have no significant pericardial

thickening by imaging or at surgery. Thus, a lack of thickened pericardium does not rule out pericardial constriction, and patients’ signs and

symptomatology and physiologic evidence of constriction should be

assessed independently. Pericardial constriction typically demonstrates

marked respiratory changes in diastolic flow on Doppler echocardiography, in contrast to restrictive cardiomyopathy, but substantial overlap

exists. CT and CMR offer tomographic, whole-heart assessment of

pericardial thickening and other anatomy abnormalities in pericardial

constriction, such as enlarged atria, vena cavas, and pleural and pericardial effusions (Figs. 241-33 and 241-34 and Videos 241-8 and 241-9).

CMR offers the additional information of pericardial fibrosis and

inflammation by LGE imaging and evidence of constrictive physiology

(e.g., regional relaxation concordance due to myocardial adhesions,

abnormal septal bounce with Valsalva maneuver) (Fig. 241-34).

■ CARDIAC THROMBUS AND MASS

Echocardiography is usually the modality that first detects a cardiac

mass with differential diagnoses including thrombus, tumor, or vegetation. Given their unrestricted tomographic views and multiplanar

three-dimensional imaging, CMR and CT can complement echocardiography by further characterizing the physical features of the cardiac

mass. Compared to CT, CMR has the advantage of higher tissue contrast differentiation, more robust cine imaging, and the use of multifaceted techniques within the same imaging session to determine the

physiologic characteristics of the mass. Gadolinium contrast enhancement patterns of increased capillary perfusion can detect vascularity

within a mass, which differentiates a tumor from a thrombus. Structures that are known to mimic a cardiac mass include (1) anatomic

variants, such as the Eustachian valve, Chiari network, crista sagittalis

or terminalis, and the right ventricular moderator band, and (2) “pseudotumors,” such as interatrial septal aneurysm, coronary or aortic

aneurysm, lipomatous hypertrophy of interatrial septum, hiatal hernia,

or a catheter/pacemaker lead. Coexisting abnormalities that raise the

likelihood of a cardiac thrombus (Fig. 241-35) include regional wall

motion abnormality from an infarction or ventricular aneurysm, atrial

fibrillation leading to slow flow in the left atrial appendage, or presence of venous catheters or recent endovascular injury. CMR has the

advantage of being able to assess regional wall motion and infarction or

ventricular aneurysm in matching scan planes, adjacent to the cardiac

thrombus, using cine and LGE imaging, respectively. For ventricular

thrombus, gadolinium-enhanced LGE imaging can detect thrombus at

a higher sensitivity than echocardiography by depicting high-contrast

difference between the dark thrombus and its adjacent structures and

by imaging in three dimensions. In addition, mural thrombus does not

enhance on first-pass perfusion and often has a characteristic “etched”

appearance (black border surrounding a bright center) on LGE

imaging, thus providing higher diagnostic specificity than anatomic

information alone (Fig. 241-36). Comparing the signal intensities of

a mass before and after contrast injection may confirm the lack of

tissue vascularity (i.e., thrombus) by the lack of signal enhancement

after contrast administration. Like intracardiac thrombus, regions

of microvascular obstruction also appear dark, but microvascular

obstruction is confined within the myocardium and surrounded by

infarction and thus can be differentiated from intracardiac thrombus.

Cardiac CT imaging is ideally suited for small thrombus in the left

atrial appendage, especially in cases where transesophageal echocardiography is suboptimal or not feasible.

The majority of cardiac malignancy is metastatic, which is about

twentyfold more common than primary cardiac malignancies. Metastasis to the heart can be the result of direct invasion (e.g., lung and breast),

lymphatic spread (e.g., lymphomas and melanomas), or hematogenous

spread (e.g., renal cell carcinoma). Primary benign cardiac tumors are

seen mostly in children and young adults and include atrial myxoma,

rhabdomyoma, fibroma, and endocardial fibroelastoma (Fig. 241-37).

Atrial myxomas are often seen as a round or multilobar mass in the

left atrium (75%), right atrium (20%), or ventricles or mixed chambers

(5%). They typically have inhomogeneous brightness in the center

on cine steady-state free precession imaging due to their gelatinous

FIGURE 241-32 Pericardial effusion with tamponade physiology. The right ventricle

(arrow) is small and collapsing in end diastole due to increased pericardial pressure.

FIGURE 241-33 A female patient developed pericardial constriction and right

heart failure, secondary to radiation therapy for breast cancer. Note the multiple

pericardial adhesions (red arrows).

Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1855CHAPTER 241

contents and may have a pedunculated attachment to the fossa ovalis.

Primary malignant cardiac tumors are rare and may include angiosarcoma, fibrosarcoma, rhabdomyosarcoma, and liposarcoma.

■ ROLE OF IMAGING IN INFECTIOUS AND

INFLAMMATORY DISEASE

Patients with suspected endocarditis often undergo echocardiography

for the purpose of identifying vegetations or intramyocardial abscesses.

Vegetations are generally highly mobile structures that most typically

are attached to valves or present in areas of the heart with turbulent

flow. The absence of a vegetation on echocardiography does not rule

out endocarditis, because small vegetations below the resolution of the

imaging techniques can be present. Echocardiography remains the best

technique for assessment of vegetations because its high temporal resolution allows visualization of the typical oscillating motion, although

large vegetations can be visualized with other techniques (Fig. 241-38).

The size and location of a vegetation do not necessarily provide any

specific information about the type of infection. Abscesses, particularly around the aortic and mitral annuli, are particularly concerning

in patients with endocarditis and should be suspected in patients

C D

A B

E F

G H I

FIGURE 241-34 Representative cardiac magnetic resonance (CMR) and CT features of pericardial disease. A. Four-chamber late gadolinium enhanced image showing

severe, diffuse enhancement of both the visceral (arrowheads) and parietal (arrows) layers of the pericardium. The black signal between the two layers represents effusion.

B. Axial T2-weighted image showing severe thickening and increased signal of both the visceral (arrowheads) and parietal (arrows) layers of the pericardium. C. Fourchamber steady-state free precession (bright-blood) image in early diastole showing the apical interventricular septum bowed to the left (white arrowhead) due to the

increased right-sided ventricular volume at the expense of the left ventricular volume. Dilated atria (white arrows) are also a feature of constriction. D. Axial T1-weighted

double inversion recovery (black-blood) image showing increased thickness of the pericardium >4 mm (black arrowhead). E. Four-chamber late gadolinium enhanced image

showing diffuse enhancement of the thickened pericardium (white arrows). F. Axial steady-state free precession (bright-blood) image showing dilated inferior vena cava

(IVC) (white arrowheads), which is greater than twice the size of the normal aorta (white arrow). Under normal conditions, the IVC should be similar in size to the aorta.

G. Lateral chest radiograph showing calcification of the pericardium anteriorly (arrows). H. Corresponding sagittal view from computed tomography angiography (CTA)

showing the calcified pericardium (arrowheads). I. Three-dimensional rendered segmented image from the CTA showing the extent of the pericardial calcification. (Images

courtesy of Dr. Michael Steigner, Brigham and Women’s Hospital.)

1856 PART 6 Disorders of the Cardiovascular System

FIGURE 241-35 Cardiac thrombus (arrow) in an apical aneurysmal region following

acute myocardial infarction.

*

FIGURE 241-36 Late gadolinium enhancement image of a massive anterior

infarction complicated by a dyskinetic left ventricular aneurysm and intracavitary

thrombus (red asterisk).

*

FIGURE 241-37 A case of a cardiac fibroma. A patient presented with shortness of breath and was found to have a large myocardial mass on echocardiography. Cine

cardiac magnetic resonance imaging confirmed the large myocardial mass involving the anterolateral wall. Shortly after gadolinium contrast was injected, the myocardial

mass demonstrated intense accumulation of contrast on late gadolinium enhancement imaging (right panel, asterisk). This is a case of cardiac fibroma. The patient also has

gingival hyperplasia and bifid thoracic ribs, a part of the rare Gorlin’s syndrome.

with prolongation of cardiac intervals in the setting of endocarditis.

Visualization of both vegetations and possible abscesses is best done

with transesophageal echocardiography, particularly in patients with

prosthetic valves. Indeed, transesophageal echocardiography is the first

test of choice in a patient with a mechanical mitral or aortic valve and

suspected endocarditis (Fig. 241-38). Vegetations should be measured

because their size has prognostic importance and can be used to decide

whether a patient should be taken to surgery.

PET metabolic imaging is emerging as a potentially useful imaging

technique to identify the source of infection in patients with prosthetic

valves, vascular grafts, and implantable pacemakers/defibrillators,

especially in patients in whom echocardiography and/or blood cultures

are negative. There is an emerging literature documenting the potential

value of macrophage-targeted metabolic imaging with 18F-FDG and

PET (Fig. 241-39). Likewise, FDG PET is also useful to identify vascular inflammation and monitor the response to immunosuppressive

therapy (Fig. 241-40).

■ EVALUATION OF COMMON CONGENITAL

ABNORMALITIES IN THE ADULT

While a discussion of complex congenital heart disease is beyond the

scope of this chapter, several common congenital abnormalities are

present in adults, and cardiac imaging is essential to diagnosing and

managing these conditions. Abnormalities of the interatrial septum

probably represent the most common adult congenital cardiac abnormalities. Patent foramen ovale (PFO) can be identified in almost 25%

of patients. In patients with PFO, a one-way flap in the region of the

fossa ovalis is normally kept closed by the left atrial pressure, which

is generally higher than right atrial pressure for much of the cardiac

cycle. However, right-to-left flow through a PFO can occur any time

the right atrial pressure exceeds the left atrial pressure, including with

maneuvers or conditions in which intrathoracic pressure is increased.

The presence of a PFO can increase the likelihood of the paradoxical embolus, and thus the presence of a PFO should be determined

in patients with stroke or systemic embolus of unknown etiology.

Because the one-way flap of the PFO will be closed during much of

the cardiac cycle, color flow Doppler will usually not reveal a PFO.

Instead, agitated saline (bubble study) is the best way to assess for PFO

or atrial septal defect. Saline is agitated and injected peripherally and

then enters the right atrium. If no shunt is present, only the right side

of the heart will be pacified because the air bubbles will be too small to

traverse the lungs. Because PFO is a one-way flap, maneuvers should

be used to temporarily increase right atrial pressure. Either a Valsalva

maneuver or sniff maneuver can be effective.

Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1857CHAPTER 241

LA

LV

LA

LV

FIGURE 241-38 Vegetation on native mitral valve (left panel, arrow). Left atrium (LA) and left ventricle (LV) are indicated. Middle panel shows a vegetation on a mechanical

prosthesis (St. Jude) indicated by an arrow; right panel shows vegetation on prosthesis after excision.

FIGURE 241-41 Large secundum-type atrial septal defect (arrow) noted in the subcostal view with color flow Doppler showing flow through the defect (right).

CT

Before

treatment

After

treatment

FDG PET PET/CT fusion

L

A

P

R

FIGURE 241-39 Representative cross-sectional computed tomography (CT; left), fluorodeoxyglucose (FDG) positron emission tomography (PET; middle), and fused CT

and PET (right) images before and after antibiotic treatment in a patient with fever and suspected infection of the stent placed in the descending portion of the aortic arch

(arrow) for treatment of aortic coarctation. The FDG images before treatment demonstrate intense glucose uptake within the stent, consistent with inflammation/infection.

The lower panel demonstrates significant attenuation of the FDG signal after treatment. (Images used with permission from Dr. Sharmila Dorbala, Brigham and Women’s

Hospital.)

CTA PET PET/CT fusion

Ao Ao

Ao LV LV

LV

FIGURE 241-40 Representative coronal computed tomography (CT) angiographic (CTA; left panel), fluorodeoxyglucose (FDG) positron emission tomography (PET; middle

panel), and fused CT and PET (right panel) images in a patient with suspected aortitis. The CTA images demonstrate thickening of the ascending aorta (Ao), which

correlates with intense, focal FDG uptake consistent with active inflammation. LV, left ventricle.

1858 PART 6 Disorders of the Cardiovascular System

0

–50

0

50

100

150

200

250

300

350

400

450

500

550

600

650

700

750

800

ms 0 10 20 30 40 50

Flow volume

A B

C

60 70 80

Main pulmonary artery

Ascending aorta

90 100

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Time |ms|

FIGURE 241-42 A and B are phase contrast images that display blood flow (phase images on A) and anatomy (structural images on B) of the aorta (red) and pulmonary

artery (green). C demonstrates the flow curves of the aorta (red) and the pulmonary artery (green). Note that the total flow (area under the curve) was substantially higher

in the pulmonary artery than the aorta, indicative of a marked elevated pulmonary-to-systemic shunt ratio, as a result of the partial anomalous pulmonary venous return that

drained into the superior vena cava.

Atrial septal defects occur most commonly in the region of the fossa

ovalis, referred to as secundum-type defects (Fig. 241-41). Additional

atrial septal defects include defects of the sinus venosus and atrium

primum. Color flow Doppler echocardiography is usually sufficient for

diagnosis of a secundum-type atrial septal defect, but agitated saline is

generally needed for the diagnosis of other types of atrial septal defects.

Ventricular septal defects can generally be visualized by color flow

Doppler as turbulent high-velocity jets from the left to the right ventricle. In cases where the jet origin is unclear, continuous wave Doppler

can estimate the velocities. These would be expected to be extremely

high to reflect the pressure gradient between the left and right ventricles. Defects can occur in both the muscular and membranous portions

of the ventricular septum.

In patients with either atrial or ventricular septal defects, estimation of the severity of the left-to-right shunt is essential and can be an

important determinant in management decisions. Shunts are generally

assessed by echocardiography by assessing the relationship between

pulmonary flow and aortic flow, the Qp/Qs ratio. Shunts and cardiac

anatomy of most congenital heart diseases can also be accurately evaluated by CMR (Fig. 241-42).

■ FURTHER READING

Di Carli MF et al: The future of cardiovascular imaging. Circulation

133:2640, 2016.

VIDEO 241-1 Cine steady-state free precession (SSFP) imaging (left) in short axis

in a patient who had a large anterior myocardial infarction. Only one cut of a stack

of short axis is shown. This method allows quantification of left ventricular (LV)

and right ventricular (RV) volumes in diastole and systole and calculation of the LV

ejection fraction, stroke volumes, and cardiac output (a product of LV stroke volume

and heart rate). Note that in this case there is anterior and anteroseptal akinesia

(lack of systolic wall thickening, as shown by the left cine movie, red arrows)

matching by a near-transmural myocardial infarction as seen by the matching late

gadolinium enhancement (LGE) image (right picture, white arrows).

Johnson NP et al: Invasive FFR and noninvasive CFR in the evaluation of ischemia: What is the future? J Am Coll Cardiol 67:2772,

2016.

Naoum C et al: Cardiac computed tomography and magnetic resonance imaging in the evaluation of mitral and tricuspid valve disease:

Implications for transcatheter interventions. Circ Cardiovasc Imaging 10:pii:e005331, 2017.

Solomon SD et al: Essential Echocardiography, a Companion to

Braunwald’s Heart Disease. Philadelphia, Elsevier, 2018.

Steel KE, Kwong RY: Application of cardiac magnetic resonance

imaging in cardiomyopathy. Curr Heart Fail Rep 5:128, 2008.

Vandoorne K, Nahrendorf M: Multiparametric imaging of

organ system interfaces. Circ Cardiovasc Imaging 10:pii:e005613,

2017.

Diagnostic Cardiac Catheterization and Coronary Angiography

1859CHAPTER 242

VIDEO 241-2 This is cine cardiac magnetic resonance (CMR) imaging of a

patient in the long-axis four-chamber view. Note that the basal aspect of the right

ventricular (RV) free wall is thickened, aneurysmal, and akinetic (red arrows). The

global RV systolic function is mildly reduced, and the RV is dilated. CMR can image

the RV using tomographic views and can quantify the RV volumes and ejection

fraction volumetrically. This is a patient who presented with syncopal spells and

inducible ventricular tachycardia on subsequent workup. He was diagnosed to have

arrhythmogenic right ventricular dysplasia.

VIDEO 241-4 The video shows cardiac magnetic resonance (CMR) myocardial

perfusion imaging during vasodilating stress, in three parallel short-axis views.

A bolus of gadolinium contrast was injected intravenously while rapid imaging

acquisition occurred. The contrast enhances the right ventricle first, then travels

through the pulmonary circulation, enters the left ventricle (LV), and then perfuses

the LV myocardium. Myocardial perfusion defects with this technique show as

black subendocardial rims, reflecting lack of contrast accumulation due to ischemia

and/or scar. In this case, the anterior wall has a severe perfusion defect (red arrow).

Figure 241-14 shows the late gadolinium enhancement (LGE) image of a mid shortaxis view. There is no evidence of infarction in the anterior wall, which would be

seen as bright white areas, indicating that the stress perfusion defect primarily

represents myocardial ischemia. This patient had a significant stenosis of the left

anterior descending coronary artery.

VIDEO 241-8 This video shows the heart in long and short axis. Note the large atria,

thickened pericardium, and extensive pericardial adhesions. Given the extensive

pericardial adhesions, there is little shearing motion of the ventricles against the

parietal pericardium.

VIDEO 241-9 This video shows the heart in long axis with a four-chamber view.

The steady-state free precession (bright-blood) cine shows the early diastolic filling

bounce of the apical interventricular septum due to constrictive physiology.

VIDEO 241-6 A patient with severe aortic regurgitation quantified by cardiac

magnetic resonance (CMR). Notice the dark flow jet during diastolic across the

aortic valve. For quantitation of the aortic regurgitation severity, a cross-sectional

cut was made just below the aortic valve, perpendicular to the aortic regurgitation

jet, using phase contrast flow imaging. Apart from aortic regurgitation fraction and

volume, CMR also can volumetrically quantify ventricular sizes and dimensions of

the aorta, which are useful in monitoring patients with aortic valve diseases.

VIDEO 241-5 A 60-year-old female presented with intermittent chest pain of

3 days in duration but was pain-free at the time of assessment in the emergency

department. Admission electrocardiogram (ECG) demonstrated T-wave inversion

in the anterior precordial lead, but cardiac enzymes were normal. A resting

cardiac magnetic resonance (CMR) study reviewed a large area of anteroseptal

hypokinesia (left picture, region of hypokinesia shown by the red arrows), matching

with a large resting perfusion defect (middle picture, perfusion defect shown by the

blue arrows). Late gadolinium enhancement (LGE) imaging (right picture), however,

did not show any enhancement to indicate any infarction in the anteroseptal wall,

suggesting that the hypocontractile and hypoperfused anteroseptal wall was viable.

Urgent coronary angiography demonstrated an acute thrombus in the mid left

anterior descending coronary artery, which required coronary stenting. This case

represents an example of acute coronary syndrome with hibernating but viable

myocardium in the anteroseptal wall. The anteroseptal wall recovered contractile

function when reassessed 6 months later.

VIDEO 241-3 Exercise echocardiogram showing rest images on left and poststress

images on right, with parasternal long-axis, upper panel, and apical four-chamber,

lower panel, end-systolic frames. Following exercise, the distal septal/apical region

becomes akinetic. A = upper left (UL); B = upper right (UR); C = lower left (LL); D =

lower right (LR).

VIDEO 241-7 These are T2*

 images of the heart (left panel) and the liver (right

panel) of a patient who has hemochromatosis. Note that iron and the liver are

markedly darkened in these movies, indicating high load of iron in the heart muscle

and liver. The rate of signal reduction (decay) in the myocardium and liver can

be calculated as T2*

 value expressed in milliseconds. In this case, the T2*

 was at

10 ms. T2*

 <20 ms in patients with cardiomyopathy has been shown to indicate iron

toxicity as the etiology of the cardiomyopathy, and it carries prognostic value for

such patients at risk of cardiac iron toxicity.

Diagnostic cardiac catheterization and coronary angiography are

considered the gold standard in the assessment of the anatomy and

physiology of the heart and its associated vasculature. In 1929, Forssmann demonstrated the feasibility of cardiac catheterization in humans

when he passed a urological catheter from a vein in his arm to his

right atrium and documented the catheter’s position in the heart by

x-ray. In the 1940s, Cournand and Richards applied this technique

to patients with cardiovascular disease to evaluate cardiac function.

These three physicians were awarded the Nobel Prize in 1956. In 1958,

Sones inadvertently performed the first selective coronary angiography when a catheter in the left ventricle slipped back across the aortic

valve, engaged the right coronary artery, and power-injected 40 mL of

contrast down the vessel. The resulting angiogram provided superb

anatomic detail of the artery, and the patient suffered no adverse

effects. Sones went on to develop selective coronary catheters, which

were modified further by Judkins, who developed preformed catheters

and allowed coronary artery angiography to gain widespread use as

a diagnostic tool. In the United States, cardiac catheterization is the

second most common operative procedure, with more than 1.0 million

procedures performed annually.

CARDIAC CATHETERIZATION

■ INDICATIONS, RISKS, AND PREPROCEDURE

MANAGEMENT

Cardiac catheterization and coronary angiography are indicated to

evaluate the extent and severity of cardiac disease in symptomatic

patients and to determine if medical, surgical, or catheter-based interventions are warranted (Table 242-1). They are also used to exclude

severe disease in symptomatic patients with equivocal findings on noninvasive studies and in patients with chest-pain syndromes of unclear

etiology for whom a definitive diagnosis is necessary for management.

Cardiac catheterization is not mandatory prior to cardiac surgery in

some younger patients who have uncomplicated congenital or valvular

heart disease that is well defined by noninvasive imaging and who do

not have symptoms or risk factors that suggest concomitant coronary

artery disease.

The risks associated with elective cardiac catheterization are relatively low, with a reported risk of <0.1% for myocardial infarction,

0.01% for stroke, and 0.05% for death. For elective and emergent

procedures, the in-hospital mortality is 1.4%. These risks increase

substantially if the catheterization is performed emergently, during

acute myocardial infarction, or in hemodynamically unstable patients.

Additional risks of the procedure include tachy- or bradyarrhythmias

that require countershock or pharmacologic therapy, acute renal failure

leading to transient or permanent dialysis, vascular complications that

necessitate surgical repair or percutaneous intervention, and significant access-site bleeding. Of these risks, vascular access-site bleeding

is the most common complication, occurring in 1.5–2.0% of patients,

with major bleeding events associated with a worse short- and longterm outcome.

In patients who understand and accept the risks associated with

cardiac catheterization, there are no absolute contraindications when

the procedure is performed in anticipation of a life-saving intervention.

Relative contraindications do, however, exist; these include decompensated congestive heart failure; acute renal failure; severe chronic

renal insufficiency, unless dialysis is planned; bacteremia; acute stroke;

active gastrointestinal bleeding; excessive anticoagulation or recent

lytic administration; severe, uncorrected electrolyte abnormalities; a

242 Diagnostic Cardiac

Catheterization and

Coronary Angiography

Jane A. Leopold, David P. Faxon

1860 PART 6 Disorders of the Cardiovascular System

shock, pulmonary edema, and cardiorespiratory arrest. Patients with

a history of significant contrast allergy should be premedicated for at

least 24 hours prior to planned coronary angiography with corticosteroids and antihistamines (H1

-blockers) and studies performed with

nonionic, low-osmolar contrast agents that have a lower reported rate

of allergic reactions.

Contrast-induced acute kidney injury, defined as an increase in creatinine >0.5 mg/dL or 25% above baseline that occurs 48–72 h after contrast administration, occurs in ~2–7% of patients with rates of 20–30%

reported in high-risk patients, including those with diabetes mellitus,

congestive heart failure, chronic kidney disease, anemia, older age, or

who present with an ST-segment elevation myocardial infarction. Dialysis is required in 0.3–0.7% of patients and is associated with a fivefold

increase in in-hospital mortality. For all patients, adequate intravascular

volume expansion with intravenous 0.9% saline (1.0–1.5 mL/kg per

hour) for 3–12 h before and continued 6–24 h after the procedure

limits the risk of contrast-induced acute kidney injury by >50%. Pretreatment with N-acetylcysteine (Mucomyst) has not reduced the risk

of contrast-induced acute kidney injury consistently and, therefore, is

no longer recommended routinely. Diabetic patients treated with metformin should stop the drug 24 h prior to the procedure and not restart

until 48 h after contrast administration to limit the associated risk of

lactic acidosis. Other strategies to decrease risk include the administration of sodium bicarbonate (3 mL/kg per hour) 1 h before and 6 h

after the procedure (similar outcome to saline infusion); use of low- or

iso-osmolar contrast agents; and limiting the volume of contrast to

<50 mL per procedure.

Cardiac catheterization is performed after the patient has fasted

for 6 h and has received intravenous conscious sedation to remain

awake but sedated during the procedure. All patients with suspected

coronary artery disease are pretreated with 325 mg aspirin. In patients

in whom the procedure is likely to progress to a percutaneous coronary intervention, an additional antiplatelet agent should be started:

clopidogrel (600-mg loading dose and 75 mg daily), prasugrel (60-mg

loading dose and 10 mg daily), or ticagrelor (180-mg loading dose and

90 mg twice daily). Prasugrel should not be selected for individuals

with prior stroke or transient ischemic attack and is not recommended

for patients 75 years of age or older. Warfarin is held starting 2–3 days

prior to the catheterization to allow the international normalized ratio

(INR) to fall to <1.7 and limit access-site bleeding complications. The

direct oral anticoagulants (DOACs) should be stopped 24–48 h prior

to the test. Cardiac catheterization is a sterile procedure, so antibiotic

prophylaxis is not required.

■ TECHNIQUE

Cardiac catheterization and coronary angiography provide a detailed

hemodynamic and anatomic assessment of the heart and coronary

arteries. The selection of procedures is dependent on the patient’s

symptoms and clinical condition, with some direction provided by

noninvasive studies.

Vascular Access Cardiac catheterization procedures are performed

using a percutaneous technique to enter the femoral or radial artery

and femoral, brachial, or internal jugular vein as the access sites for

left and right heart catheterization, respectively. A flexible sheath is

inserted into the vessel over a guidewire, allowing diagnostic catheters

to be introduced into the vessel and advanced toward the heart using

fluoroscopic guidance. The radial artery (or rarely the brachial artery)

access site is advantageous in patients with peripheral arterial disease

that involves the abdominal aorta, iliac, or femoral vessels; severe iliac

artery tortuosity; morbid obesity; or preference for early postprocedure

ambulation. Use of radial artery access is the preferred access route

due to a lower rate of access-site bleeding complications and improved

patient comfort. A normal modified Allen’s test or Barbeau test confirming dual blood supply to the hand from the radial and ulnar arteries is recommended prior to access at this site. The internal jugular or

antecubital veins serve as the preferred access sites to the right heart

when the patient has an inferior vena cava filter in place or requires

prolonged hemodynamic monitoring.

TABLE 242-1 Indications for Cardiac Catheterization and

Coronary Angiography

CORONARY ARTERY DISEASE

Asymptomatic or Symptomatic

High risk for adverse outcome based on noninvasive testing

Sudden cardiac death

Sustained (>30 s) monomorphic ventricular tachycardia

Nonsustained (<30 s) polymorphic ventricular tachycardia

Symptomatic

Canadian Cardiology Society Class II, III, or IV stable angina on medical therapy

Acute coronary syndrome (unstable angina and non-ST-segment elevation

myocardial infarction)

Chest-pain syndrome of unclear etiology and equivocal findings on

noninvasive tests

ST-Segment Elevation Acute Myocardial Infarction

Reperfusion with primary percutaneous coronary intervention

Persistent or recurrent ischemia

Pulmonary edema and/or reduced ejection fraction

Cardiogenic shock or hemodynamic instability

Risk stratification or positive stress test after acute myocardial infarction

Mechanical complications—mitral regurgitation, ventricular septal defect

Valvular Heart Disease

Suspected severe valve disease in symptomatic patients—dyspnea, angina,

heart failure, syncope

Infective endocarditis with need for cardiac surgery

Asymptomatic patients with aortic regurgitation and cardiac enlargement or ↓

ejection fraction

Prior to cardiac surgery or transcatheter aortic valve replacement or other

percutaneous valvular interventions in patients with suspected coronary artery

disease

Congestive Heart Failure

New-onset angina or suspected undiagnosed coronary artery disease

New-onset cardiomyopathy of uncertain cause or suspected to be due to

coronary artery disease

Congenital Heart Disease

Prior to surgical correction or percutaneous interventions, when symptoms or

noninvasive testing suggests coronary disease

Suspicion for congenital coronary anomalies

Pericardial Disease

Symptomatic patients with suspected cardiac tamponade or constrictive

pericarditis

Cardiac Transplantation

Preoperative and postsurgical evaluation

Other Conditions

Hypertrophic cardiomyopathy with angina

Diseases of the aorta when knowledge of coronary artery involvement is

necessary for management

history of an anaphylactic/anaphylactoid reaction to iodinated contrast

agents without premedication; and a history of allergy/anaphylaxis/

bronchospasm to aspirin in patients for whom progression to a percutaneous coronary intervention is likely and aspirin desensitization has

not been performed.

Contrast allergy and contrast-induced acute kidney injury merit

further consideration, because these adverse events may occur in

otherwise healthy individuals and prophylactic measures exist to

reduce risk. Allergic reactions to contrast agents occur in <5% of cases,

with severe anaphylactoid (clinically indistinguishable from anaphylaxis, but not mediated by an IgE mechanism) reactions occurring

in 0.1–0.2% of patients. Mild reactions manifest as nausea, vomiting,

and urticaria, while severe anaphylactoid reactions lead to hypotensive

Diagnostic Cardiac Catheterization and Coronary Angiography

1861CHAPTER 242

Right Heart Catheterization This procedure measures pressures

in the right heart and pulmonary artery. Right heart catheterization

is no longer a routine part of diagnostic cardiac catheterization, but

it is reasonable in patients with unexplained dyspnea, pulmonary

hypertension, valvular heart disease, pericardial disease, right and/or

left ventricular dysfunction, congenital heart disease, and suspected

intracardiac shunts. Right heart catheterization most commonly uses

a balloon-tipped flotation catheter that is advanced sequentially to the

right atrium, right ventricle, pulmonary artery, and pulmonary wedge

position (as a surrogate for left atrial pressure) using fluoroscopic guidance; in each cardiac chamber, pressure is measured and blood samples

are obtained for oxygen saturation analysis to screen for intracardiac

shunts and calculate a cardiac output.

Left Heart Catheterization This procedure measures pressures

in the left heart as a determinant of left ventricular performance. With

the aid of fluoroscopy, a catheter is guided to the ascending aorta and

across the aortic valve into the left ventricle to provide a direct measure

of left ventricular pressure. In patients with a tilting-disc prosthetic

aortic valve, crossing the valve with a catheter is contraindicated, and

the left heart may be accessed via a transseptal technique from the right

atrium using a needle-tipped catheter to puncture the atrial septum

at the fossa ovalis. Once the catheter crosses from the right to the left

atrium, it can be advanced across the mitral valve to the left ventricle.

This technique is also used for mitral valvuloplasty. Heparin is given

for prolonged procedures to limit the risk of stroke from embolism

of clots that may form on the catheter. For patients with heparininduced thrombocytopenia, the direct thrombin inhibitors bivalirudin

(0.75 mg/kg bolus, 1.75 mg/kg per hour for the duration of the procedure) or argatroban (350 μg/kg bolus, 15 μg/kg per min for the duration of the procedure) may be used.

■ HEMODYNAMICS

A comprehensive hemodynamic assessment involves obtaining pressure measurements in the right and left heart and peripheral arterial

system and determining the cardiac output (Table 242-2). The shape

and magnitude of the pressure waveforms provide important diagnostic information; an example of normal pressure tracings is shown

in Fig. 242-1. In the absence of valvular heart disease, the atria and

ventricles are “one chamber” during diastole when the tricuspid

and mitral valves are open, whereas in systole, when the pulmonary

and aortic valves are open, the ventricles and their respective outflow

tracts are considered “one chamber.” These concepts form the basis

by which hemodynamic measurements are used to assess valvular

stenosis. When aortic stenosis is present, there is a systolic pressure

gradient between the left ventricle and the aorta; when mitral stenosis

is present, there is a diastolic pressure gradient between the pulmonary

capillary wedge (left atrial) pressure and the left ventricle (Fig. 242-2).

Hemodynamic measurements also discriminate between aortic stenosis and hypertrophic obstructive cardiomyopathy where the asymmetrically hypertrophied septum creates a dynamic intraventricular

pressure gradient during ventricular systole. The magnitude of this

obstruction is measured using an end-hole catheter positioned at the

left ventricular apex that is pulled back while recording pressure; once

the catheter has passed the septal obstruction and is positioned in the

apex of the left ventricle, a gradient can be measured between the left

ventricular apex and the aorta. Hypertrophic obstructive cardiomyopathy is confirmed by the Brockenbrough-Braunwald sign: following

a premature ventricular contraction, there is an increase in the left

ventricular–aorta pressure gradient with a simultaneous decrease in

the aortic pulse pressure. The finding of a decrease in pulse pressure is

absent in aortic stenosis.

Regurgitant valvular lesions increase volume (and pressure) in the

“receiving” cardiac chamber. In severe mitral and tricuspid regurgitation, the increase in blood flow to the atria takes place during

ventricular systole, leading to an increase in the v wave (often two

times greater than the mean pressure). The size of the v wave is a

measure of the compliance of the left atrium but is not a reliable

measure of the severity of the mitral regurgitation. Severe aortic

regurgitation leads to a decrease in aortic diastolic pressure with a

concomitant rise in left ventricular end-diastolic pressure, resulting in equalization of pressures between the two chambers at end

diastole.

Hemodynamic measurements are also used to differentiate between

cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy (Table 242-3). In cardiac tamponade, right atrial pressure is

increased with a decreased or absent “y” descent, indicative of impaired

right atrial emptying in diastole, and there is diastolic equalization of

pressures in all cardiac chambers. In constrictive pericarditis, right

atrial pressure is elevated with a prominent “y” descent, indicating

rapid filling of the right ventricle during early diastole. A diastolic dip

and plateau, or “square root sign,” in the ventricular waveforms due

to an abrupt halt in ventricular filling during diastole, elevated right

ventricular and pulmonary artery pressures, and discordant pressure

changes in the right and left ventricles with inspiration (right ventricular systolic pressure increases while left ventricular systolic pressure

decreases) are observed. In the absence of constriction, the two ventricular pressures are concordant. The latter hemodynamic phenomenon

is the most specific for constriction. Restrictive cardiomyopathy may

be distinguished from constrictive pericarditis by a marked increase

in right ventricular and pulmonary artery systolic pressures (usually

>60 mmHg), a separation of the left and right ventricular diastolic

pressures by >5 mmHg (at baseline or with acute volume loading),

and concordant changes in left and right ventricular diastolic filling

pressures with inspiration (both increase).

Cardiac Output Cardiac output is measured by the Fick method or

the thermodilution technique. Typically, the Fick method and thermodilution technique are both performed during cardiac catheterization,

although the Fick method is considered more reliable in the presence of

tricuspid regurgitation and in low-output states. The Fick method uses

oxygen as the indicator substance and is based on the principle that

the amount of a substance taken up or released by an organ (oxygen

consumption) is equal to the product of its blood flow (cardiac output)

and the difference in the concentration of the substance in the arterial

TABLE 242-2 Normal Values for Hemodynamic Measurements

Pressures (mmHg)

Right atrium

Mean 0–5

a wave 1–7

v wave 1–7

Right ventricle

Peak systolic/end diastolic 17–32/1–7

Pulmonary artery

Peak systolic/end diastolic 17–32/1–7

Mean 9–19

Pulmonary capillary wedge (mean) 4–12

Left atrium

Mean 4–12

a wave 4–15

v wave 4–15

Left ventricle

Peak systolic/end diastolic 90–130/5–12

Aorta

Peak systolic/end diastolic 90–130/60–85

Mean 70–100

Resistances ([dyn-s]/cm5

)

Systemic vascular resistance 900–1400

Pulmonary vascular resistance 40–120

Oxygen Consumption Index ([L-min]/m2

) 115–140

Arteriovenous oxygen difference (vol %) 3.5–4.8

Cardiac index ([L-min]/m2

) 2.8–4.2

1862 PART 6 Disorders of the Cardiovascular System

mmHg

0

25

50

ECG

RA RV PA PCWP

FIGURE 242-1 Normal hemodynamic waveforms recorded during right heart catheterization. Atrial pressure

tracings have a characteristic “a” wave that reflects atrial contraction and a “v” wave that reflects pressure

changes in the atrium during ventricular systole. Ventricular pressure tracings have a low-pressure diastolic filling

period and a sharp rise in pressure that occurs during ventricular systole. d, diastole; PA, pulmonary artery; PCWP,

pulmonary capillary wedge pressure; RA, right atrium; RV, right ventricle; s, systole.

mmHg

0

100

mmHg

0

200 50

 25

ECG ECG

LV

Ao

Aortic

gradient

LV

PCW

Mitral

gradient

FIGURE 242-2 Severe aortic and mitral stenosis. Simultaneous recording of left ventricular (LV) and

aortic (Ao) pressure tracings demonstrates a 62-mmHg mean systolic gradient (shaded area) that

corresponds to an aortic valve area of 0.6 cm2

 (left). Simultaneous recording of LV and pulmonary

capillary wedge (PCW) pressure tracings reveals a 14-mmHg mean diastolic gradient (shaded area)

that is consistent with critical mitral stenosis (mitral valve area = 0.5 cm2

). d, diastole; e, end diastole;

s, systole.

and venous circulation (arterial-venous oxygen difference). Thus, the

formula for calculating the Fick cardiac output is:

Cardiac output (L/min) = (oxygen consumption [mL/min])/

(arterial-venous oxygen difference [mL/L])

Oxygen consumption is estimated as 125 mL oxygen/minute × body

surface area, and the arterial-venous oxygen difference is determined

by first calculating the oxygen-carrying capacity of blood (hemoglobin

[g/100 mL] × 1.36 [mL oxygen/g hemoglobin] × 10) and multiplying

this product by the fractional oxygen saturation. The indicator dilution

method measures the concentration of a substance that is injected

proximally, adequately mixes with blood, and is then

sampled distally. In contemporary practice, thermodilution cardiac outputs are measured using temperature

as the indicator. Measurements are made with a thermistor-tipped catheter that detects temperature deviations

in the pulmonary artery after the injection of 10 mL of

room-temperature normal saline into the right atrium.

Vascular Resistance Resistance across the systemic

and pulmonary circulations is calculated by extrapolating from Ohm’s law of electrical resistance and is equal

to the mean pressure gradient divided by the mean flow

(cardiac output). Therefore, systemic vascular resistance

is ([mean aortic pressure − mean right atrial pressure]/

cardiac output) multiplied by 80 to convert the resistance from Wood units to dyn-s-cm−5. Similarly, the

pulmonary vascular resistance is ([mean pulmonary

artery − mean pulmonary capillary wedge pressure]/

cardiac output) × 80. Pulmonary vascular resistance

is lowered by oxygen, nitroprusside, calcium channel

blockers, prostacyclin infusions, and inhaled nitric

oxide; these therapies may be administered during

catheterization to determine if increased pulmonary

vascular resistance is fixed or reversible.

Valve Area Hemodynamic data may also be used to

calculate the valve area using the Gorlin formula that

equates the area to the flow across the valve divided by

the pressure gradient between the cardiac chambers surrounding the valve. The formula for the assessment of

valve area is: Area = (cardiac output [cm3

/

min]/[systolic ejection period or diastolic

filling period][heart rate])/44.3 C × square

root of the pressure gradient, where C =

1 for aortic valve and 0.85 for the mitral

valve. A valve area of <1.0 cm2

 and a mean

gradient of >40 mmHg indicate severe

aortic stenosis, while a valve area of <1.5

cm2

 and a mean gradient >5–10 mmHg are

consistent with moderate-to-severe mitral

stenosis; in symptomatic patients with a

mitral valve area >1.5 cm2

, a mean gradient

>15 mmHg, pulmonary artery pressure

>60 mmHg, or a pulmonary artery wedge

pressure >25 mmHg after exercise is also

considered significant and may warrant

intervention. The modified Hakki formula

has also been used to estimate aortic valve

area. This formula calculates the valve area

as the cardiac output (L/min) divided by

the square root of the pressure gradient.

Aortic valve area calculations based on the

Gorlin formula are flow-dependent, and

therefore, for patients with low cardiac

outputs, it is imperative to determine if

a decreased valve area actually reflects a

fixed stenosis or is overestimated by a low

cardiac output and stroke volume that is

insufficient to open the valve leaflets fully. In these instances, cautious

hemodynamic manipulation using dobutamine to increase the cardiac

output and recalculation of the aortic valve area may be necessary.

Intracardiac Shunts In patients with congenital heart disease or

unexplained hypoxemia, detection, localization, and quantification

of the intracardiac shunt should be evaluated. A shunt should be suspected when there is unexplained arterial desaturation or increased

oxygen saturation of venous blood. A “step up” or increase in oxygen

content indicates the presence of a left-to-right shunt while a “step

down” indicates a right-to-left shunt. The shunt is localized by detecting a difference in oxygen saturation levels of 5–7% between adjacent