Cardiovascular Medicine

PATHOPHYSIOLOGY

  

↑LVOT(outflow obstruction) ↑LV D pressure ↑LV hyperthropy and LV mass LV disfunction

Aortic stenoisis  

↑LV D diastolic pressure back Pulmonary edema

SYMPTOMS

DIAGNOSIS

• Echocardiography

Aortic valve

 Valve morphology

 Severuty of stenosis:

Orifice planimetric area

o Transvalvular gradient (imagine)

o Orifice «functional» area

o

Left ventricle

Volume, Geometry, Systolic function , Diastolic function and pulmonary pressure

• Cardiac computed tomography

Precise measures of aortic root and ascending aorta (good spatial resolution)

• Cardiac magnetic resonance imaging

Gold standard for chamber measurement

• Cardiac catheterization

Measure the hemodynamic alterations.

TREATMENT

• Aortic valve replacement (SURGERY)

• Cardiac surgery (biological or mechanical prosthesis);

• Transcatheter aortic valve replacement (biological) TAVI.

AORTIC REGURGITATION

the aortic leaflets (primary AR) and/or

the aortic root (secondary AR)

ETIOLOGY

 Congenital leaflets abnormalities (bicuspid aortic valve) OR aortic root abnormalities

 Acquired leaflets abnormalities (senile calcifications, infective endocarditis, rheumatic disease, radiation- or toxic-

induced valvulopathy) OR aortic root abnormalities (systemic hypertension, idiopathic aortic root dilatation…) 21

PATHOPHYSIOLOGY

SYMPTOMS

DIAGNOSIS

Same as Aortic Stenosis

• Echocardiography

 Quantification of the severity of regurgitation:

regurgitant volume

o indirect signs (left ventricular dilatation with pressure overload)

o

TREATMENT

• Aortic valve replacement or repair

• Cardiac surgery (repair vs biological or mechanical prosthesis)

• Transcatheter aortic valve replacement (biological). Less evidence than for aortic stenosis.

2 leaflets

MITRAL REGURGITATION

Divided into two categories, based on whether the mitral leaflets exhibit significant pathological abnormality or not.

 In primary MR, an intrinsic abnormality of the leaflets causes the MR:

Myxomatous degeneration (mitral valve prolapse)

o Fibroelastic deficiency (>60 years). It is characterized by single chordal rupture with thin leaflet and prolapse

o of an isolated scallop. The associated mitral regurgitation jet is usually eccentric and directed opposite to the

prolapsing.

Barlow’s disease (40–60 years old). It is characterized by excess leaflet tissue, diffuse thickening and

o redundancy, typically affecting multiple segments of both leaflets and chordae

These 2 forms of mitral valve prolapse represent the two ends of a spectrum, most of is between these two extremes.

 In secondary MR leaflets are intrinsically normal but disease of cardiac chambers

ventricular functional regurgitation: LV enlargement or focal myocardial scarring, causing posteriorly directed

o or central MR. Ventricular function is loss.

atrial functional regurgitation. LA is severely enlarged. As opposed to ventricular functional regurgitation the

o leaflets are usually flattened or only slightly tethered into the LV cavity. In most of the cases of atrial functional

regurgitation, the regurgitation jet is central.

DIAGNOSIS

Echocardiography - Cardiac magnetic resonance imaging - Cardiac catheterization

TREATMENT

• Mitral valve replacement or repair - Alfieri’s stitch

• Cardiac surgery (repair vs biological or mechanical prosthesis)

• Transcatheter aortic valve replacement (biological) 22

TRICUSPID REGURGITATION

The tricuspid apparatus comprises a nonplanar elliptical annulus (TA), the leaflets, the chordae tendineae, and a variable

number of papillary muscles.

Tricuspid regurgitation (TR) is a major public health problem.

The TV usually (but not invariably) consists of three leaflets

 # leaflets vary from 2-7

 Extra leaflets are called “accessory leaflets”

 Accessory leaflets are common

Functional (or secondary) TR is the most frequent etiology, and its prevalence increases with aging.

It contributes to maintain a vicious circle (TR tends to beget more TR), with progressive volume overload of the right heart

and further right chamber remodeling, pressure overload of the right atrium (RA), visceral congestion, enhanced ventricular

interdependence with impaired left heart preload, low cardiac output or low cardiac output reserve.

Leaflets are named according to their anatomical location: anterior, septal and posterior.

The anterior leaflet is the largest one, extending curtain-like around approximately half the free wall of the right ventricle

(RV) from the infundibular outflow region to the inferior part of the RV, while the posterior leaflet is generally the smallest

with a triangular shape and evident scalloped indentations. The septal leaflet is short radially, but long circumferentially

and has a semicircular shape.

The tricuspid annulus (TA) is a saddle-shaped dynamic structure, in-between the leaflets on one side, and the atrial and

ventricular myocardium on the other side.

The TA is a virtual structure, largely composed of adipose tissue, with a smaller amount of fibrotic tissue. This allows the

geometry and dimensions of the annulus to change significantly during the cardiac cycle, BUT at the same time

predisposes it to dilate.

ETIOLOGY

 Primary (depending on organic alterations of either the leaflets or the subvalvular apparatus)

 Functional (secondary), where the leaflets and the subvalvular apparatus are intact, and malcoaptation is produced by

a disturbance of the efficient coordination of the elements of the valve complex.

 Ventricular functional TR: ↑ RV enlargement is deemed to be an important mechanism This can lead to leaflet

tethering and malcoaptation.

 

functional TR: ↑

Atrial RA dilation that predisposes to leaflet malcoaptation by promoting TA enlargement

Atrial fibrillation (AF) is one of the major determinants of RA and TA remodeling and dilation

DIAGNOSIS

 Echocardiography: TR evaluation - Echocardiography represents the most available and immediate imaging tool to

assess the TV, and gain insights in the mechanisms accounting for TR. The characterization of TV leaflet by 2D

echocardiography is not reliable. 3D echocardiography allows the en-face view of the whole TV from both the

ventricular and atrial perspective, showing the morphology of the leaflets and providing better insights on the

mechanisms of TR. It allows a more precise measurement of the actual TA dimensions, avoiding the geometrical

assumptions and lack of anatomical landmarks that limit two-dimensional echocardiography.

 Cardiac C: Multi-detector row CT has higher spatial resolution than echocardiography. It provides more precise

information on TA dimensions as well as on the identification of landmarks for tricuspid intervention. It can explore

the relationship of the TA with the right coronary artery, important in the planning of transcatheter interventions on

the TV.

 Cardiac CMR allows optimal visualization and measure of the right chambers and extracardiac/vessels anatomy, but

it is not well suited for the assessment of the thin TV leaflets. It is gold-standard method to measure right heart

chamber dimensions. The ability to visualize the dynamic TV apparatus without body habitus limitations and need

for ionizing radiation.  

Multimodality imaging of TV Assessment of mechanisms and severity of TR Assessment spatial relationship with



neighbouring structures Candidacy, planning and monitoring transcatheter intervention

TREATMENT

 TV repair or replacement) remains the treatment of choice for patients who are deemed to be not at increased risk for

such intervention. Triclip device - Forma repair system - Cardioband device

 Transcatheter interventions 23

PHYSIOLOGY OF THE PULMONARY CIRCULATION

6 -

The pulmonary circulation is a low-pressure, high flow system.

The right ventricle is a low-pressure flow generator.

Physiology of the pulmonary circulation

Fick’s law of diffusion state that the extent of gas moving through a tissue membrane is proportional to the surface of the

membrane and inversely proportional to its thickness. 2.

Alveolo-capillary blood-gas barrier is extraordinarily thin (≈0,3 μm) and covers a surface of 50-100 m

Anatomy of the right ventricle

Anterior position, behind the sternum.

Three components:

 Inlet (tricuspid valve, chordae tendinae and papillary muscles);

 Trabeculated apical myocardium;

 Outlet (infundibolum).

Complex shape

 Influenced by the interventricular septum

RV systolic function 24

Contractility

Ventricular interdependence

Continuity between the muscle fibers of the RV and LV:

 functionally binds the ventricles together;

 represents the anatomic basis of free ventricular wall traction caused by LV contraction;

 contributes, along with the interventricular septum and pericardium, to ventricular interdependence.

The RV is connected in series with the LV and is, therefore, obligated to pump on average the same effective stroke volume.

Right ventricular physiology

RV contraction is sequential, starting with the contraction of the inlet and trabeculated myocardium and ending with the

contraction of the infundibulum (approximately 25 to 50 ms apart).

The RV contracts by 3 separate mechanisms:

1. Inward movement of the free wall (bellows effect)

2. Contraction of the longitudinal fibers, (shortens the long axis, draws the tricuspid annulus toward the apex)

3. LV contraction acting with a traction on RV free wall at the points of attachment (contribution for 20-40% at RV

ejection → in the presence of RV scarring, the septum is able to maintain circulatory stability as long as the RV is

not dilated)



RV preload Related to BLOOD RETURN in RV

 RV preload = fluid in the ventricles before contraction;

 An increase in RV preload improves myocardial contraction (Physiological limit)

Beyond the physiological range, excessive RV volume loading can compress the LV and impair global ventricular

function through the mechanism of ventricular interdependence.

The pericardium imposes greater constraint on the thinner, more compliant, low-pressure RV.

Pathophysiology of RV failure



RV afterload Related to ARTERY BACKPRESSURE

RV afterload = load to overcome during ejection; How much energy does it take to push the blood forward.

 pulmonary vascular resistance (PVR) → steady flow component

 pulmonary arterial compliance (PAC) → pulsatile component

 pulmonary vascular impedance → frequency domain 25

7 - VENOUS THROMBOEMBOLISM

Venous thromboembolism (VTE) encompasses

- deep vein thrombosis (DVT), a blood clot that forms in a deep vein, usually the leg, groin or arm.

- pulmonary embolism (PE).

It is the third most frequent cardiovascular disease.



Pulmonary embolism Small PE may pass unperceived, tha