pericarditis constrictiva

Dr. Abel, Calloapaza Pari [email protected]

MR. Cirugía de Tórax y Cardiovascular

HNHU El presente trabajo expresa la opinión personal del autor sobre el tema.

Definición.

Etiología y Epidemiologia.

Cuadro Clínico.

Métodos Diagnósticos.

Opciones terapéuticas.

Pronostico.

Imágenes.

PERICARDITIS CONSTRICTIVA

Constrictive pericarditis is the end stage of an inflammatory

process involving the pericardium.

Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.

In the developed world the cause is most commonly: (1 –

3).

idiopathic,

postsurgical, or

radiation injury.

Tuberculosis was the most common cause of constrictive

pericarditis in the developed world before development of

effective drug therapy. It remains important in developing

countries.

1. Troughton RW, Asher CR, Klein AL: Pericarditis. Lancet 2004; 363:717.

2. Hoit BD: Management of effusive and constrictive pericardial heart disease. Circulation 2002; 105:2939.

3. Little WC, Freeman GL: Pericardial disease. Circulation 2006; 113:1622.

Although constriction can follow an initial insult by as little

as several months, it usually takes years to develop.

The end result is dense fibrosis, often calcification, and

adhesions of the parietal and visceral pericardium.

Usually scarring is more or less symmetrical and impedes

filling of all heart chambers.

In a subset of patients the process develops relatively

rapidly and is reversible. This variant is seen most

commonly following cardiac surgery. 1

1. Haley JH, Tajik AJ, Danielson GK, et al: Transient constrictive pericarditis: Causes and

natural history. J Am Coll Cardiol 2004; 43:271.

The clinical presentation is usually dominated by signs and

symptoms of right-heart failure.

The pathophysiological consequence of pericardial

scarring is markedly restricted filling of the heart. This

results in elevation and equilibration of filling pressures in

all chambers and the systemic and pulmonary veins. In

early diastole the ventricles fill abnormally rapidly because

of markedly elevated atrial pressures and accentuated

early diastolic ventricular suction, the latter related to small

end-systolic volumes. 1. Troughton RW, Asher CR, Klein AL: Pericarditis. Lancet 2004; 363:717.

2. Hoit BD: Management of effusive and constrictive pericardial heart disease. Circulation 2002; 105:2939.

3. Little WC, Freeman GL: Pericardial disease. Circulation 2006; 113:1622.

Systemic venous congestion results in hepatic congestion,

peripheral edema, ascites, and sometimes anasarca and cardiac

cirrhosis. Reduced cardiac output is a consequence of impaired

ventricular filling and causes fatigue, muscle wasting, and weight

loss.

In “pure” constriction, contractile function is preserved, although

ejection fraction can be reduced as a consequence of reduced

preload.

The myocardium is occasionally involved in the chronic inflammation

and fibrosis, leading to true contractile dysfunction that can at times

be quite severe. The latter predicts a poor response to

pericardiectomy.


Schematic representation of transvalvular and central venous flow velocities in constrictive

pericarditis. During inspiration the decrease in left ventricular filling results in a leftward

septal shift, allowing augmented flow into the right ventricle. The opposite occurs during

expiration. EA = mitral inflow; HV = hepatic vein; LA = left atrium; LV = left ventricle; PV =

pulmonary venous flow; RA = right atrium; RV = right ventricle.

At a relatively early stage these signs and symptoms include lower

extremity edema, vague abdominal complaints, and some degree of

passive hepatic congestion.

Signs and symptoms ascribable to elevated pulmonary venous

pressures such as exertional dyspnea, cough, and orthopnea may

also appear with progressive disease. Atrial fibrillation and tricuspid

regurgitation, which further exacerbate venous pressure elevation,

may also appear at this stage. In the end stage of constrictive

pericarditis, the effects of a chronically low cardiac output are

prominent including severe fatigue, muscle wasting, and cachexia.


El hallazgo semiológico más propio de la pericarditis constrictiva es

el signo de Kussmaul o aumento de la presión venosa yugular

(ingurgitación yugular) durante la inspiración, como

consecuencia de un aumento del retorno venoso, secundario a la

presión negativa intratorácica, pero con restricción al llene

ventricular derecho y sin que haya un aumento simultáneo del gasto

cardíaco. Dado que el corazón está recubierto por una coraza

rígida, la distensibilidad de este se ve muy disminuida y cualquier

aumento de volumen se transmite en forma retrógrada, es por eso

que las yugulares se ingurgitan al inspirar (no como normalmente se

esperaría: al inspirar, las yugulares colapsan)

1. Haley JH, Tajik AJ, Danielson GK, et al: Transient constrictive pericarditis: Causes and

natural history. J Am Coll Cardiol 2004; 43:271.

O… en valsalva.

Jugular Neck Distention.flv

Medicine.2009; 10(43) :2870-5

Constrictive pericarditis Doppler schema of respirophasic changes in mitral and tricuspid inflow. Reciprocal

patterns of ventricular filling are assessed on pulsed Doppler examination of mitral (MV) and tricuspid (TV)

inflow. (Courtesy of Bernard E. Bulwer, MD; with permission.)

No specific ECG findings exist.

Nonspecific T wave abnormalities are often

observed, as well as reduced voltage.

Left atrial abnormality may also be present.

Atrial fibrillation is present in significant numbers of

patients.


The cardiac silhouette can be enlarged secondary to a coexisting pericardial

effusion.

Pericardial calcification is seen in a minority of patients and should raise the

suspicion of tuberculous pericarditis, but calcification per se is not diagnostic of

constrictive physiology.

The lateral chest film is useful to detect pericardial calcification along the right

heart border and in the atrioventricular groove.

Isolated calcification of the LV apex or posterior wall suggests ventricular

aneurysm rather than pericardial calcification.

Pleural effusions are occasionally noted and can be a presenting sign of

constrictive pericarditis.

When left heart filling pressures are markedly elevated, pulmonary vascular

congestion and redistribution can be present.


Chest radiograph showing marked pericardial calcifications

in a patient with constrictive pericarditis.

CT provides detailed images of the pericardium and is especially

helpful in detecting even minute amounts of pericardial calcification.

Its major disadvantage is the frequent need for iodinated contrast

medium administration to best display findings of pericardial

pathology. The thickness of the normal pericardium measured by CT

is less than 2 mm.

MRI provides a detailed and comprehensive examination of the

pericardium without the need for iodinated contrast or ionizing

radiation. It is somewhat less sensitive for detecting calcification

than CT.

1. Wang ZJ, Reddy GP, Gotway MB, et al: CT and MR imaging of pericardial disease. Radiographics

2003; 23:S167-S180.

2. Oyama N, Oyama N, Komuro K, et al: Computed tomography and magnetic resonance imaging of the

pericardium: Anatomy and pathology. Magn Res Med Sci 2004; 3:145.

CT scan performed during an infusion of contrast material shows enhancement of the soft-tissue-

density pericardium (arrowheads), which is up to 6 mm thick.

Computed Body Tomography by JKT Lee, SS Sagel, and RJ Stanley (Eds) with permission of Raven

Press, New York, ©1989.

Panel A. Echocardiographic transmitral flow pattern with exaggerated respiratory variation in inflow velocities (>25%).

Panel B. Transaxial CT image (slice thickness 3.0 mm) of the heart at mid-ventricular level, demonstrating severe calcification of the pericardium (arrows). In addition, bilateral pleural effusion is seen. AO, descending aorta; PE, pleural effusion.

Panel C. Three-dimensional volume rendering technique reconstruction of the whole chest. Nearly circumferential pericardial calcification is seen (structures of high CT density, such as bone and calcification, are rendered in white colour).

Panel D. Three-dimensional volume rendering technique reconstruction of the heart. To exclude the non-calcified part of the heart, a threshold of 130 Hounsfield units (common threshold for coronary calcification in CT imaging) was chosen.

In mid-diastole, the thickened pericardium

begins to restrict right ventricular filling,

causing a rapid increase in ventricular

pressure. Early changes of septal

flattening and bowing of the

interventricular septum toward the left

ventricle (normally concave in shape

toward the left ventricle during diastolic

filling) are seen. This pressure change

results in diastolic septal dysfunction, the

septal bounce described in

echocardiography.

Frontiers in Bioscience 14, 2688-2703, January 1, 2009

Constrictive pericarditis four-chamber, ECG-gated cine SSFP MR.flv

M-mode and two-dimensional echocardiography findings include: Pericardial thickening,

Abrupt displacement of the interventricular septum during early diastole (septal “bounce”), and

Signs of systemic venous congestion such as dilation of hepatic veins and distention of the inferior vena cava with blunted respiratory fluctuation.

Premature pulmonic valve opening as a result of elevated RV early diastolic pressure may also be observed.

Exaggerated septal shifting during respiration is often present. 1

1. Maisch B, Seferovic PM, Ristic AD, et al: Guidelines on the diagnosis and

management of pericardial diseases executive summary; the Task Force on the

Diagnosis and Management of Pericardial Diseases of the European Society of

Cardiology. Eur Heart J 2004; 25:587.

Cardiac catheterization in patients with suspected constrictive

pericarditis provides documentation of the hemodynamics of

constrictive physiology and assists in discriminating between

constrictive pericarditis and restrictive cardiomyopathy.

Although there is limited need for contrast ventriculography,

coronary angiography is used to detect occult coronary artery

disease in those being considered for pericardiectomy. In

addition, on rare occasions external pinching or compression of

the coronary arteries or outflow tract regions by the constricting

pericardium is detected.

Cardiac Catheterization and Angiography

Constrictive Pericarditis

Constriction Restriction

Prominent y descent in venous pressure Present Variable

Paradoxical pulse ≈⅓ cases Absent

Pericardial knock Present Absent

Equal right-left side filling pressures Present Left at least 3-5 mm Hg > right

Filling pressures >25 mm Hg Rare Common

Pulmonary artery systolic pressure >60

mm Hg

No Common

“Square root” sign Present Variable

Respiratory variation in left-right

pressures/flows

Exaggerated Normal

Ventricular wall thickness Normal Usually increased

Atrial size Possible LA enlargement Biatrial enlargement

Septal “bounce” Present Absent

Tissue Doppler E′ velocity Increased Reduced

Pericardial thickness Increased Normal


Constrictive Pericarditis

Constrictive pericarditis is a progressive disease.

With the exception of patients with transient constrictive

pericarditis, surgical pericardiectomy is the only

definitive treatment.


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pericarditis constrictiva

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