II.8.

INFECTIVE ENDOCARDITIS

Infective endocarditis represents a microbial infection of the

endocardial surface of the heart caused by bacteremia (bacteria enter the
bloodstream) typically originating from oral sources. Valvular involvement
is common and is characterized by the presence of vegetation on the flow
surface of a valve. It is a severe pathology with high mortality rates despite
optimal diagnosis and treatment.

Transthoracic echocardiography (TTE) and transesophageal

echocardiography (TEE) remain the main imaging resources for identifying
vegetation, valvular dysfunction, impact on ventricular function and
cardiovascular hemodynamics (pulmonary artery pressure- PAP), although
newer methods such as positron emission tomography (PET) with
radiolabeled leukocytes have emerged.

Echocardiography is indicated in any case of unexplained fever

lasting more than 48 hours, bacteremia, new regurgitant murmur, new
conduction disorders or embolic events. A level IIb indication is also given
to cases of Staphyloccocus aureus bacteraemia caused by nosocomial
infections as 30% of these are associated with endocarditis.

Transthoracic echocardiography remains the preferred initial

diagnostic test for patients with intermediate risk of infective endocarditis.
However, it has the following limitations: it does not visualize vegetations
smaller than 2 mm or those attached to a severely remodelled valve. If the
window is suboptimal, the patient has an intracardiac device or a mechanical
prosthesis, the next diagnostic step is represented by transesophageal
echocardiography- TEE which is significantly more sensitive (90%
compared to 50-80%). A negative result does not exclude the diagnosis of
infective endocarditis but justifies repeating the examination in 7-10 days.

In case of clinical suspicion of endocarditis, the evaluation starts

with a transthoracic echocardiography (ETT) and can then be continued with
a transesophageal echocardiography (ETE). Transesophageal
echocardiography is preferred as an initial examination in high-risk patients
according to Duke criteria or in patients who are not good candidates for a
transthoracic examination. High-risk patients include those with prosthetic
heart valves, congenital heart disease, history of endocarditis, new onset of
heart murmur, heart failure, and patients with stigmata of infective
endocarditis. Transesophageal echocardiography allows for a very good
visualization of the heart base and aorta. The mitral and aortic valves are
particularly well visualized in transesophageal examination. (figure 1)

Figure 1. Transesophageal echocardiography apical 4-chamber incidence (Ap4C) showing

a large vegetation involving the anterior mitral valve; it is located on the left atrial slope (left
image) and is associated with hemodynamically significant mitral regurgitation on color
Doppler (right image). From the personal collection of Prof. Dr. Floria M.
 Vegetation is a mixture of microorganisms, inflammatory cells,
platelets and fibrin. It appears as a mobile mass with irregular shape,
attached to the free edge of the valve leaflets. It tends to form upstream, i.e.
on the ventricular side in the case of the aortic valve and on the atrial side in
the case of the mitral valve (on the flow surface of the valve) . It can be
sessile or pedunculated, with independent movement. The presence of wide
mobility and oscillations due to the jet with increased velocities is
characteristic. The lack of mobility is a counter argument for endocarditis
and requires differential diagnosis.

Although typically attached to valves (Figure 2), vegetations can

also be attached to the tendinous cords/chordae tendinae, the walls of cardiac
cavities (ventricular or aortic endocardium, affected by jet- lesions), or
foreign bodies such as pacing wires, prosthetic heart valves. The intracardiac
mass itself is homogeneous, with similar echogenicity to that of the
myocardium, tending to become more echodense during treatment.
Occasionally, vegetations can be cystic or more dense and calcified. Since
the infectious process alters the structure and function of the valve, it often
associates a degree of regurgitation.
 Figure 2. Vegetations sites. RA: right atrium; RV: right ventricle; LA: left
atrium; LV: left ventricle; IVC: inferior vena cava; Ao: aorta; valva mitrala: mitral valve,
valva pulmonara: pulmonary valve; valva aortica: aortic valve; comunicare interventriculara:
interventricular communication; Adapted from Brauwald (page 409).

Although the diagnosis of vegetation can be suspected on

echocardiographic examination, the images must be interpreted in context.
The differential diagnosis includes thrombus, fibroelastoma, Lambl's
excrescences, non-infectious Libman-Sacks endocarditis, variations of the
Eustachian valve, Chiari’s network and prosthetic valve sutures. Vegetations,
masses with calcified structure or those similar to the pericardium are less
likely.

AORTIC VALVE ENDOCARDITIS

It is usually identified in parasternal long and short axis. Careful

angulation from medial to lateral in the long axis and from inferior to
superior in the short axis is necessary since the vegetations are often located
eccentrically. A mass attached to the ventricular aspect of the valve with
independent motion and prolapsing into the outflow tract in diastole is
diagnostic for vegetation (Figure 3 and 4). The rapid oscillatory motion is
best appreciated on M-mode.
Figure 3. Schematic representation of an aortic valve vegetation. It shows an irregular,
mobile mass attached to the ventricular aspect of the valve with prolapse into the left
ventricular outflow tract during diastole. The figure also indicates the presence of aortic
regurgitation. (AR). This image is adapted from Catherine Otto's (page 402).

Figure 4. Transesophageal echocardiography in apical 3-chamber view: aortic echodense

vegetation attached to the noncoronary valve leaflet with crossing into the left ventricular
ejection tract in diastole (left image) and leading to significant aortic regurgitation (right
image). From the personal collection of Prof. Dr. Floria M.

The definitive diagnosis is more difficult when the valve anatomy is

abnormal. A vegetation on a calcified valve is covered by the acoustic
shadowing cone and its reverberations. In this situation, independent
movement and diastolic prolapse in the ventricular septum are particular
signs that are very helpful. Changes in dynamics compared to previous
examinations increase the probability of a valve infection. Stationary
examinations decrease the chance of an acute process.
 Findings that can be confused with vegetations on the aortic valve
include artifacts from calcified nodules, prostethic valves, the normal
apposition zone of the cusps and the normal thickening of the cusps in the
central coaptation surface area (nodules of Arantius). In a high percentage of
patients, Lambl's excrescences are present (Figure 5), which are linear echo
structures representing small fibroelastic protrusions from the ventricular
aspect of the cusp coaptation surface area. Their frequency increases with

age.

Figure 5. Transesophageal echocardiography in long-axis view: Lambl's excrescence - a

thin linear echogenic structure at the closure of the aorta that can be mistaken for a
vegetation. From the personal collection of Prof. Dr. Floria M.
 The presence of anomalies in both apical and parasternal views
decreases the possibility of an artifact because the relationship between the

ultrasound beam and the aortic valve is completely different between these
two windows. Regarding TEE, the aortic valve can be evaluated from a
apical transgastric view, but often the image quality is not better compared to
the transthoracic examination due to the distance between the transducer and
the aortic valve (Figure 6).

Figure 6. Transthoracic ecocardiography in parasternal long-axis incidence: bulky

vegetation on the ventricular side of the aortic valve, which is degeneratively remodelled.
From the personal collection of [Link]. Floria M.

MITRAL VALVE ENDOCARDITIS

Mitral valve vegetations are typically located on the atrial side

(Figure 7). The diagnostic criteria include: independent rapid movement,
prolapse into the left atrium during systole, and valve dysfunction. One
possible artifact is the presence of an apparent mass on the atrial side of the
anterior mitral valve in the apical 4-chamber view, caused by calcification or
aortic prostethic valve. Differential diagnosis is necessary with myxomatous
degeneration of the cardiac valves, partial flail of the cusps or papillary
muscle rupture. Comparison with previous examinations helps differentiate

between an acute process and an underlying chronic valvular disease.

Endocarditis can also occur on a normal anatomical valve. Mitral
regurgitation often accompanies mitral valve endocarditis (a sign of valve
dysfunction)

Figure 7. Transesophageal echocardiography in the apical 3-chamber view - typical mitral

valve vegetation on the atrial side; the vegetation is attached to the anterior mitral leaflet; in
the left image, it measures (10.6 / 18.9 mm). From the personal collection of Prof. Dr. Floria
M.

Transesophageal echocardiography. The mitral valve is well

visualized from the high esophageal incidence. Since the plane of the mitral
annulus is perpendicular to the ultrasound beam, excellent 2D images can be
obtained by slowly rotating the transducer from 0 to 180 degrees. Special
attention is required for the standard 4-chamber incidence (at 0 degrees), 2-
chamber incidence (at 60 degrees) and long-axis incidence (at 120 degrees).
The degree of mitral regurgitation is evaluated by color Doppler in the same
incidences. Given the large distance between the mitral valve and the
thoracic wall in both apical and parasternal transthoracic examinations, TEE
provides images of superior quality. It identifies the site of attachment of the
vegetation and allows for the identification of a possible perforation.

TRICUSPID VALVE ENDOCARDITIS

Tricuspid valve endocarditis occurs most often in iv drug users and

is associated with large vegetations due to Staphylococcus aureus infection.
In right ventricular inflow tract incidence, a bulky, mobile echostructure
attached to the atrial side of the valve with systolic prolapse into the right
atrium can be visualized. Given the bulky mass a frequent complication is
pulmonary septic embolism. Apical and subcostal 4-chamber incidence is
recommended to assess the severity of regurgitation, atrial and right
ventricular dilatation to assess the severity of regurgitation, atrial and right
ventricular dilatation.

In TEE, the tricuspid valve is visualized from the 4-chamber and

transgastric views. Due to its proximity to the chest wall ETT is often
diagnostic.
Figure 8. Transesophageal mid-esophageal ultrasound in patient with history of iv drug use
and infective endocarditis. A mass attached to the tricuspid valve on the atrial side is
visualized in diastole. AD: right atrium; AS: left atrium; VA: aortic valve; VT: tricuspid
valve. From the personal collection of Prof. Dr. Floria M.

INFECTION ON INTRACARDIAC DEVICES

Infection of intracardiac pacemaker or implantable cardioverter

defibrillators (ICD) present in the right cavities are vulnerable due to
transient bacteremia. In addition, pocket infections can spread to the
catheters thus involving the heart. Their number has increased with the
number of wearers of such devices.

Small fibrin filaments (strands) or small thrombi can be observed

on intracavitary leads. There is no diagnostic clue to differentiate non-
infectious masses attached to leads from infectious ones. Therefore, any
vegetation-like formation attached on the leads should be interpreted in a
clinical setting. Infection should be suspected when you get a positive blood
culture. The ability of TEE to detect infection in the distal portion of the
superior vena cava is limited, but the adjacent portion of the heart and the
leads can be adequately evaluated. TTE has a limited role. Fibrin formations
attached to intracardiac catheters resemble valvular vegetations: mobile
masses with independent movement. In the case of right heart devices, the
presence of a patent foramen ovale is important to highlight, as it represents
a pathway for the spread of infection to the left heart, with a risk of systemic
embolism.

The diagnosis is important because removal of the leads is necessary,

in addition to prolonged antibiotic treatment. This can pose significant
problems for a pacemaker-dependent patient. For vegetations larger than 25
mm, surgery is preferred over percutaneous removal.

Figure 9. Figure [Link] ultrasound short-axis incidence in the great vessels with
focus on the right cavity where vegetation is seen near the tricuspid valve (white arrow) on a
pacemaker lead. From the personal collection of Prof. Dr. Floria M
Figure 10. Transesophageal echocardiography- short-axis incidence in the great vessels with
focus on the right cavity where the vegetation is seen near the tricuspid valve (white arrow)
on a pacemaker lead. AD: right atrium; AS: left atrium; VA: aortic valve; VT: tricuspid
valve. From the personal collection of Prof. Dr. Floria M.

COMPLICATIONS OF INFECTIVE ENDOCARDITIS

Paravalvular abscesses

Paravalvular abscess appears on ultrasound examination as either a

hyper- or hypoechoic area. It may be located on the valve annulus adjacent to
the affected leaflet, more commonly on the aortic valve. Aortic annular
abscess (Figure 11,12) presents as increased increased echogenicity, a eco
lucent area at the base of the septum or thickening of the posterior aortic

root.

Figure 11. Transesophageal ultrasound A. Midesophageal short-axis view : thickening and

echolucency of the aortic root in the region of the left coronary and non-coronary cusp; B.
Long-axis mid-esophageal view: extension of the abscess from the aortic root to the
ascending aorta. RA: right atrium; RV: right ventricle; LA: left atrium. Adapted from
Braunwald (page 410).

Figure 12. Transesophageal ecocardiography A. Long-axis view: thickening of the posterior

aortic wall and irregular echolucency and echodensity in the aortic annulus and sinus B.
Short-axis incidence: bicuspid aortic valve, thickening, dilatation and irregular aortic
sinuses. RA: left atrium; LV: left ventricle; Ao: aorta. Adapted from Otto (page 410).

The aortic abscess (Figure 13) can extend to the anterior mitral valve,
causing thickening of the valve leaflet and the appearance of vegetation, and
eventually valve rupture. Rupture of an annular abscess can cause various
complications depending on the exact location of the breach:

 The abscess of the right coronary cusp opens into the right ventricle
or right atrium with frequent involvement of the septal leaflet of the
tricuspid valve.
 The abscess of the non-coronary cusp tends to fistulize into the left
atrium, through the fibrous and avascular mitro-aortic continuity,
compared to the surrounding tissue.
 The fistula can connect the aortic root to the left atrium.
 Figure 13. Transesophageal echocardiography (TEE) Mid-esophageal 4-chamber
view: abscess of intervalvular fibrous tissue in the context of mitral mechanical
prosthesis endocarditis (yellow arrow). The two black shadow cones represent artifacts
caused by the mechanical prosthesis. The fistula is located between the abscess and the
left atrium (white arrow). Color Doppler examination confirms the communication
created by the fistula. RA: left atrium; LV: left ventricle; RV: right ventricle. Adapted
from Braunwald (page 412).

The fistula can have a direct communication or a tortuous path. It is

best visualized through TEE. By reducing the Doppler color window, the
frame rate is increased and the flow can be visualized. Continuous Doppler
examination along the fistulous tract measures the pressure difference
between the aorta and the connected cavity.

If the abscess ruptures into a blood-filled cavity, a pseudoaneurysm

is formed. Color Doppler examination detects unidirectional flow and
pulsatile perivalvular space.

The perforation of the valve may be present even when there is no

evident vegetation in the proximity. It starts with the protrusion of the
affected cusp, with progressive formation of an aneurysm until complete
perforation. The anterior mitral valve can perforate through jet lesions with
 bacterial load from aortic valve endocarditis. Due to false positive results,
color Doppler examination is required to establish the diagnosis of
perforation.

Surgery/ Autopsy Echocardiography

Vegetation Infected mass attached to the Mobile/ immobile

endocardial structures or intracardiac mass, localized
intracardiac devices on the valves or other
endocardial structures or on
the intracardiac devices
Abcess Perivalvular cavity with Thickened and homogeneous
necrosis and purulent valve area with an echodense
material, without or echolucent appearance.
communication with the
cardiovascular lumen
Pseudoaneuryism Perivalvular cavity Pulsatile ecofree perivalvular
communicating with the space with detectable doppler
cardiovascular lumen flow
Perforation Interruption of the continuity Disruption of endocardial
of the endocardial tissue tissue continuity, traversed
by ecodoppler flow
Fistulla Communication between two Communication between two
adjacent cavities through a adjacent cavities through a
perforation perforation with color
Doppler signal.
Valvular Saccular dilatation of valve Saccular proeminence tissue
aneueysm tissue of the valve
Prosthetic Prosthetic dehiscence Paravalvular regurgitation
cardiac valve detected by TTE/TEE, with
dehiscence or without prosthetic valve
rocking motion
When the subvalvular apparatus is involved, the infection can cause
chordae tendineae rupture and rarely of papillary muscles, a situation that is
sometimes difficult to distinguish from spontaneous chordal rupture or
posterior papillary muscle that follows a acute myocardial infarction.
Figure 14. Sonographic vs anatomic definition of infective endocarditis complications.
After Floria M and Arsenescu Georgescu MC (page 27).

All these complications (Figure 14) are associated with significant

regurgitation jets, whereas valve stenosis is unusual and is only found in
prosthetic valve endocarditis.

PROSTETIC VALVE ENDOCARDITIS

Patients with mechanical prosthetic valves suspected of infective

endocarditis, due to the artifacts caused by the prosthesis, should be
evaluated by transesophageal echocardiography, which is even more
necessary in patients with multiple valve prostheses. Compared to native
valve prostheses, the ring is the first site of infection and not the valve
leaflets, which produces a mild regurgitation. The reverberations and
posterior acoustic shadowing limit the echocardiographic detection of
anomalies. This problem is especially relevant in the transthoracic
examination of the mitral prosthesis. The left atrium is obscured by the
prosthesis, so neither mitral ring infection nor valvular incompetence can be
detected. The acoustic barrier is a smaller problem for the aortic valve as
aortic regurgitation can be evaluated both apically and parasternally without
being obscured by the prosthesis. However, because the anterior part of the
prosthetic valve shadows the posterior part, the evaluation of the valve cusps
is suboptimal.

Transthoracic examination can provide some clues even if definitive

diagnostic elements are missing. For example, if color Doppler examination
is non-diagnostic due to posterior acoustic shadowing or artifacts,
continuous-wave Doppler examination provides evidence for prosthetic
regurgitation suggesting cusp infection or annular destruction. ETE is
recommended for severity evaluation. Other indicators of valve prosthesis
dysfunction are: increased anterograde flow velocity through the prosthesis
(resulting from increased blood volume due to regurgitation); increased
velocity of the tricuspid regurgitation jet (resulting from pulmonary
hypertension).

Rarely, endocarditis can cause valve stenosis by protrusion of the

infected mass into the valve opening or by infected pannus upstream of the
valve. Visualization of the infected mass is more likely through TEE.
Prosthetic valve stenosis is recognized by an increased transvalvular pressure
gradient and decreased valve area, calculated by PHT (pressure half-time) or
continuity equation. Individually, for each patient, a change in the
appearance or characteristics of the flow is a stronger argument for the
diagnosis than a single examination at a certain moment.

Several components of the prosthesis must be carefully examined:

- Suture ring: normal regular contour without discontinuities; both pannus

and thrombus can interrupt the suture ring contour.
- Bioprosthetic valves (Figure 15): must be carefully examined for
vegetations. These valves can degenerate due to natural or atherosclerotic
degradation. The appearance is similar, the volume of regurgitation is
more significant, being only slightly present in normofunctional valves.
- Mechanical valves: examination is difficult due to artifacts. Symmetric
opening and closing angle must be monitored. A non-physiologic valve
gradient suggests obstruction.
- Valve apparatus: dehiscence of the valve apparatus from the myocardium
causes a rocking motion if the dehiscence is significant. A turbulent,
asymmetric jet regurgitation is observed with color Doppler examination.
Dehiscence can be caused by infection, friable myocardium, excessive
calcifications. The perivalvular area should be examined for suggestive
echolucent areas for abscesses. Valvular ultrasound artifacts can cause
similar echolucency but will not be accompanied by a regurgitation jet.

Figure 15. Transesophageal echocardiography at Upper esophageal aortic arch long axis in
a patient with endocarditis of bioprosthetic pulmonary valve complicated by stenosis:
extensive vegetation (A - arrow); turbulence on color Doppler imaging suggesting high
velocities (B); severe stenosis on continuous wave Doppler imaging with a maximum
gradient of 111 mmHg (C). RVOT: right ventricular outflow tract; PA: pulmonary artery.
Adapted from Braunwald (page 413).

Clinical manifest embolism occurs in one-third of patients with

infective endocarditis, more commonly in the first few days after initiating
antibiotic treatment and rarely after successful completion of the therapeutic
regimen. For left-sided endocarditis, the most common sites for emboli are
the brain, spleen and in aortic valve involvement, the coronary system. For
right-sided endocarditis, the lung is the most common site and rarely it can
generate systemic emboli in the presence of a patent foramen ovale.

Predictors for embolism:

o Vegetation size (a vegetation over 10 mm has higher embolic risk)

o Increased mobility (especially anterior mitral valve)
o Increase in size during antibiotic treatment
o Decrease in size (insufficient data)
o Low echogenicity (hyperechoic vegetations are better organized so
less likely to embolize)

Guideline recommendations for reporting valve masses:

o Echogenicity/echotexture: differentiation of echogenicity similar to

myocardium from more echogenic and highly echogenic patterns,
with "shadowing" – in case of calcifications;
o Size: width and thickness in millimeters;
o Shape: sessile or pedunculated, amorphous, irregular, lobulated,
elongated, linear, round, etc.;
o Location: atrial or ventricular aspect in the case of atrioventricular
valves, respectively aortic/vascular or ventricular aspect of the aortic
valve, on the free edge of the valve leaflets, the body or base of the
cusps or on the tendinous cords;
o Movement: dependent or independent of valve motion;
o Associations: valvular regurgitation, valve stenosis, mycotic valve
aneurysms, valve destruction, perivalvular abscesses, perforation,
prosthetic valve dehiscence;
o Description of the position of the valve prosthesis annulus (fixed),
presence of rocking movement, mechanism of opening/closing
(normal valve or disc excursion in diastole in the case of the mitral
valve prosthesis).

Differential diagnosis in infective endocarditis:

1. Libman-Sacks or verrucous endocarditis (figure 16) consists of
variable-sized, usually small (1-4 mm), granular warts composed of
immune complexes, platelet thrombi, without bacteria. Libman-Sacks is
a form of nonbacterial thrombotic endocarditis. They are found in 43% of

patients with systemic lupus erythematosus, especially localized on the

free edge of the mitral cusps.

Figure 16. Transesophageal echocardiography mid-esophageal 3-chamber view in a patient

with antiphospholipid syndrome and embolic stroke: small, round, soft hyperechoic mass
(arrow) attached to the right cusp corresponding to Libman-Sacks endocarditis. AS: left
atrium; SIV: interventricular septum; VA: aortic valve; VD: right ventricle. From the
personal collection of Prof. Dr. Floria M.

2. Marantic endocarditis refers to non-infectious thrombotic endocarditis

associated with malignancies, especially metastatic solid carcinomas,
lung neoplasms, pancreatic and gastric adenocarcinomas with an
uncertain point of origin. Marantic vegetations are composed of platelets
and fibrin and do not differ in structure and location from vegetations in
infective endocarditis.
3. Fibroelastomas are benign cardiac tumors, primarily located on the
valves but downstream on the aortic side of the aortic valve and
ventricular side of the mitral valve. They are homogeneous, round,
irregular, well-defined, and often mobile. They have a dense center with
frontal extension, resembling anemones. They can cause complications
such as stroke, transient ischemic attack, and acute myocardial infarction.
 Figure 17. Transthoracic echocardiography, apical 4-chamber view with zoom on
the mitral valve: mobile echodense mass on the ventricular side of the mitral valve
in a patient with embolic events. AS: left atrium; SIV: interventricular septum; VD:
right ventricle; VS: left ventricle. From the personal collection of Prof. Dr. Floria
M.

4. Lambl's excrescences or strands are filiform structures, with undulating

movements and a thickness of up to 2 mm and a length between 3 and 10
mm, located on the coaptation line of the valves. They are usually
multiple and affect the left heart more frequently.

Figure 18. Transesophageal echocardiography in apical 3-chamber view with zoom on the
aortic valve: Lambl's excrescences - linear (filamentous) echodense formations originating
from the valve coaptation line. They are well visualized in diastole. From the personal
collection of Prof. Dr. Floria M.

5. Mitral annular calcification (figure 19) is represented by calcified

deposits, a fibrous structure in the shape of the letter C (in the short axis
 at the level of the mitral valve), which spares the anterior portion. In the
parasternal short axis view, there is an intensely hyperechoic, coarse
border that surrounds the outer edge of the posterior mitral annulus, with

a posterior acoustic shadowing.

Figure 19. A. Parasternal long axis transthoracic echocardiography: dense hyperechoic

formation of posterior mitral annulus (white arrow); B. Parasternal short axis transthoracic
echocardiography: a C-shaped echodensity compatible with posterior mitral annular
calcification.

6. Prosthetic valve thrombosis more commonly affects the mitral and

tricuspid valves compared to the aortic valve. It can cause pulmonary or
systemic embolism. In the case of mechanical prostheses, it often occurs
at subtherapeutic levels of anticoagulation. Recent thrombi as well as
vegetations, have a similar structure to myocardium and are mobile; their
shape is better defined and their mobility is lower. When high gradients
are present, it is difficult to distinguish between prosthesis mismatch,
pannus formation and degenerative stenosis in the case of bioprostheses.
 Figure 20. Transesophageal echocardiography in the apical 4-chamber view with zoom
on the mitral valve: thrombus on the atrial ventricular aspect of the mitral valve (white
arrow). AS: left atrium; VS: left ventricle. From the personal collection of Prof. Dr.
Floria M.

Figure 21. Transesophageal 3D echocardiography of subvalvular aortic region: pannus

formation on the aortic prosthesis, lining the left ventricular outflow tract, which causes
prosthetic dysfunction stenotic type. From the personal collection of Prof. Dr. Floria M.
 Selective bibliography:

1. Zipes D, Libby P, Bonow R. Braunwald’s Heart Disease. Elsevier 2019

2. Otto Catherine. Clinical Echocardiography. Elsevier 2018
3. Rasalingam R, Macan M, Perez J. The Washington Manual of Echocardiography.
Lippincott 2013
4. Arsenescu Catalina, Floria Mariana. Ghid de ecocardiografie transtoracică, Vol II.
Editura Gr. T. Popa 2015
5. Armstrong W, Ryan T. Feigenbaums Echocardiography Seventh Edition, Lippincott
2010
6. Saric M, Armour Alicia, Arnaout S. Guidelines for the Use of Echocardiography in the
evaluation of a Cardiac Source of Embolism. 2016