Transcript Constrictive Pericarditis

Constrictive
Pericarditis
Nisha I. Parikh, MD MPH
July 21st 2009
Echo Conference
Summary of Talk
Background
 Clinical features
 Echocardiographic diagnosis

M-mode
 Doppler
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Constriction versus restriction
 Treatment and prognosis
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Historical Perspective
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The history of constrictive pericarditis is
replete with famous names in medicine
Richard Lower described a patient with
dyspnea and an intermittent pulse in 1669
Lancisi first reported on the constrictive
syndrome in 1828
Corrigan described the pericardial knock in
1842
Kussmaul described his sign and the
associated paradoxical pulse in 1873.
Pericardium
Parietal and visceral layers
Usually 5-10 mL fluid
Pericardium
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When larger amounts of fluid
accumulate (pericardial effusion) or
when the pericardium becomes
scarred and inelastic, one of three
pericardial compressive syndromes
may occur
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1. Cardiac tamponade — characterized by the
accumulation of pericardial fluid under pressure.
2. Constrictive pericarditis —result of scarring and
consequent loss of elasticity of the pericardial sac.
Typically chronic. The pathological changes are
inflammation, sometimes calcification. Grossly,
pericardium thicker than normal -80% of time.
3. Effusive-constrictive pericarditis —characterized by
constrictive physiology with a coexisting pericardial
effusion, usually with tamponade.
Epidemiology
9% of patients with acute pericarditis
for any reason go on to develop
constrictive physiology.
 Acute pericarditis is only clinically
diagnosed in 1 in 1,000 hospital
admissions
 Frequency of a diagnosis of
constrictive pericarditis is less than
1 in 10,000 hospital admissions.
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Constrictive Pericarditis HPI
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67 % presented with symptoms of
heart failure (HF)
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8 % with chest pain
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6 % with abdominal symptoms
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4 % with atrial arrhythmia
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5 % with symptoms of cardiac
tamponade
Constrictive Pericarditis Etiology
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Idiopathic or viral — 42 to 49 %
Post cardiac surgery — 11 to 37 %
Post radiation therapy — 9 to 31 %
Connective tissue disorder — 3 to 7 %
Postinfectious (tuberculous or purulent
pericarditis) — 3 to 6 %
Miscellaneous causes (malignancy, trauma,
drug-induced, asbestosis, sarcoidosis,
uremic pericarditis) — 1 to 10 %
Constricitve Pericarditis - PE
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Elevated JVP
Peripheral edema
Ascites
Hepatomegaly
Pleural effusion
S3
Pulsus paradoxus
Kussmaul’s sign
Cachexia- late stages
Kussmaul’s sign
The observation of a jugular venous
pressure (JVP) that rises with
inspiration.
 Respiratory variation in intrathoracic
pressure with inspiration is not
transmitted to the heart chambers.
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Physiology of constriction
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In the pericardial compressive
syndromes, the pericardium is
inelastic and total cardiac volume
cannot change
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The result is enhanced ventricular
interaction or…
ventricular interdependence
Physiology of constriction
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Pericardial constriction leads to impairment
of ventricular filling, usually affecting all four
cardiac chambers, preventing ventricular
filling in mid and late diastole.
As a result, the majority of ventricular filling
occurs rapidly in early diastole and the
ventricular volume does not increase after
the end of the early filling period.
Pericardial Effusion
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M-Mode
Pericardial effusion
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M-mode Cannot determine volume of
accumulated fluid accurately
Pericardial thickening
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This can be visualized by
transesophageal echo (often requiring
multiple views), however, this is best
seen using other imaging modalities
such as CT or MRI.
Calcified Pericardium
Pericardial calcifications CT
Pericardial calcification on
echo
Normal pericardium
is highly reflective
 Bright pericardial
echo cannot alone
diagnose
constrictive
pericarditis
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Specific echo exam for
constriction
Neither sensitive nor specific
 Must diagnose via a combination of
physical exam/ history findings and
echo findings
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M-mode findings in
constriction
Abrupt relaxation of the posterior wall
with flattening of endocardial motion
during diastole
 Abnormal septal motion:
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Mimics conduction disturbances
 Mimics RV p/v overload
 Early diastolic notching followed by
paradoxical and then normal motion of
the ventricular septum
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diastolic septal bounce:
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Thought to be due to the rapid filling
during early diastole leading to
asymmetrical filling of the right and left
ventricals which creates a fluctuating
pressure gradient that manifests as an
abrupt shift of the septum.
? Subtle septal bounce
“Bouncy Septum”
Dilation and lack of
respiratory variation in IVC
Doppler echo findings in
constriction
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Mitral inflow
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Exaggerated E/A ratio
Short deceleration time
Exaggerated respiratory variation in E-wave
velocity >25%
Seen more reliably when patients are well
hydrated
Can also be seen in pulmonary disease
Hepatic Veins
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Expiratory increase in diastolic flow reversal
Hepatic flow reversal
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Secondary to elevated right atrial
pressures. Hepatic vein doppler
reveals pressure tracings significant
for a prominant "a" wave and
prominent "y" descent.
Atrial dilation
Mild
 Secondary to elevated atrial
pressures
 More severe atrial dilatation seen in
restrictive cardiomyopathy.
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Constrictive Pericarditis – other
tests?
CT – not very sens/spec
 Cardiac MRI – growing in favor
 BNP – usually only a mild elevation
due to limited wall stretch
 Cath – GOLD STANDARD
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Effusive constrictive
pericarditis
Combination of tamponade and
constriction
 Common etiologies: malignancy and
radiation therapy
 Pericardial thickening may prevent RA
collapse
 Hemodynamic compromise and JVD
persist even after tap
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Effusive Constrictive
Pericarditis- Prospective Study
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Methods From 1986 through 2001, all patients with effusive–constrictive pericarditis were prospectively
evaluated. Combined pericardiocentesis and cardiac catheterization were performed in all patients, and
pericardiectomy was performed in those with persistent constriction. Follow-up ranged from 1 month to
15 years (median, 7 years).
Results
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1184 patients with pericarditis were evaluated,
218 with tamponade.
190 underwent combined pericardiocentesis and catheterization.
Fifteen of these patients had effusive–constrictive pericarditis and were included in the study. All patients
presented with clinical tamponade;
however, concomitant constriction was recognized in only seven patients.
At catheterization, all patients had elevated intrapericardial pressure (median, 12 mm Hg; interquartile range,
7 to 18) and elevated right atrial and end-diastolic right and left ventricular pressures. After
pericardiocentesis, the intrapericardial pressure decreased (median value, –5 mm Hg; interquartile range, –5
to 0), whereas right atrial and end-diastolic right and left ventricular pressures, although slightly reduced,
remained elevated, with a dip–plateau morphology. The causes were diverse, and death was mainly related
to the underlying disease.
Pericardiectomy was required in seven patients, all of whom had involvement of the visceral pericardium.
Three patients had spontaneous resolution.
Conclusions Effusive–constrictive pericarditis is an uncommon pericardial syndrome that may be missed
in some patients who present with tamponade. Although evolution to persistent constriction is frequent,
idiopathic cases may resolve spontaneously. In our opinion, extensive epicardiectomy is the procedure
of choice in patients requiring surgery.
Constriction versus
Restriction
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Restrictive Cardiomyopathy
Pure diastolic dysfunction
 Systolic function preserved
 Usually due to infiltrative process
 Several echo signs overlap with
constrictive pericarditis
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Restrictive versus Constrictive
Restrictive Cardiomyopathy
History
Constrictive Pericarditis
Infiltrative disease
Pericarditis, trauma, surgery
Mantle radiation, cardiac
surgery
Mantle radiation, cardiac
surgery
Respiratory
effects
No bulging
Increased ventricular
interaction- bulging of the
septum towards LV
CMR
C/w infiltrative disease
Increased pericardial
thickness (> 5 mm
Comparison of Pericardial Constriction and
Restrictive Cardiomyopathy
Constrictive Pericarditis
Restrictive
Cardiomyopathy
Right Atrial Pressure
RV/LV filling pressures
RV=LV
LV > RV
PASP
Mild elevation 35-40
mmHg
Moderate-to-severe (≥ 60
mmHg)
2D Echo
Pericardial thickening, no
effusion
LVH, normal systolic
function
Doppler Echo
* E > a on LV inflow
* Prominent y descent in
hepatic vein
* Pulm venous flow =
prominent a wave,
reduced systolic phase
* Resp variation in IVRT
and E velocity
* Atria: mildly enlarged
* Early in disease E < a
* Late in disease E > a
* Constant IVRT
* Absence of significant
respiratory variation
* Marked enlarged atria
Tissue Doppler to
distinguish entities
Dimunitive E’
<8 cm/s
E’ similar to E
>12cm/s
Treatment
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Definitive treatment is surgical
Earlier the better
Extensive decortication favored, especially at the
diaphragmatic-ventricular contact regions.
Complications
 excessive bleeding
 atrial and ventricular arrhythmias
 ventricular wall ruptures.
Published surgical mortality 5-15%.
Perioperative mortality rate (within 30 days) was found to
be 6.1%.
 progressive heart failure
 Sepsis
 renal failure
 respiratory failure
 arrhythmia
Post-op course
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80-90% achieve NYHA class I or II
postoperatively.
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Abnormal diastolic filling (which can be
correlated with clinical status) often remains
Only 60% of patients have complete
normalization of cardiac hemodynamics.
In 58 patients who underwent total
pericardectomy for constriction, 30% still had
some significant symptoms after 4 years.
These patients were more likely to have a
persistent restrictive or constrictive pattern to
their transmitral and transtricuspid Doppler
signals as determined by respiratory recording.
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Survival post
pericardiectomy
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Long-term survival after pericardiectomy depends on
the underlying cause.
Idiopathic with best prognosis (88% survival at 7 yrs),
Constriction due to cardiac surgery (66% at 7 years).
Worst prognosis occurs in postradiation constrictive
pericarditis (27% survival at 7 years). (likely represents
confounding comorbidities).
Predictors of poor outcomes in patients who undergo
pericardiectomy
 history of prior radiation
 worsening renal function
 pulmonary hypertension
 systolic heart failure
 Hyponatremia
 advanced age.
Thanks
For
Listening!!