A case report of ventricular dysfunction post pericardiocentesis: stress cardiomyopathy or pericardial decompression syndrome?
Ayoub et al. Cardiovascular Ultrasound
A case report of ventricular dysfunction post pericardiocentesis: stress cardiomyopathy or pericardial decompression syndrome?
Chadi Ayoub 0 1 2
Michael Chang 0 1 2
Leonard Kritharides 1 2
0 Equal contributors
1 The University of Sydney , Sydney, NSW , Australia
2 Department of Cardiology, Concord Repatriation General Hospital , Concord 2139, NSW , Australia
We report a case of transient biventricular dysfunction post therapeutic pericardiocentesis, with classic features of stress cardiomyopathy (SCM). In our patient, the clinical and echocardiographic features were more in keeping with Takotsubo-type SCM than pericardial decompression syndrome (PDS). Our case is instructive in challenging our understanding of the aetiology of LV dysfunction complicating pericardiocentesis, and in highlighting the importance of careful clinical evaluation (altered heart rate and dyspnoea) in suspecting acute LV dysfunction after initial clinical improvement with pericardial aspiration.
Pericardiocentesis; Stress cardiomyopathy; Pericardial decompression syndrome; Ventricular dysfunction; Echocardiography
-
Background
We report a case of reversible biventricular dysfunction
following successful pericardiocentesis with classic
features of stress or “Takotsubo” cardiomyopathy (SCM).
Reports of SCM after pericardiocentesis are rare [1],
as distinct from so-called pericardial decompression
syndrome (PDS) which encompasses a spectrum of
features of cardiac decompensation after large volume
pericardiocentesis, including pulmonary oedema, adult
respiratory distress syndrome, severe bi-ventricular
failure and cardiogenic shock [2]. Our case is
instructive in challenging our understanding of the aetiology of
LV dysfunction complicating pericardiocentesis, and
in highlighting the importance of careful clinical
observations (heart rate and dyspnoea) in suspecting
acute LV dysfunction after initial clinical improvement
with pericardiocentesis.
Case report
A 62-year-old male presented with progressive dyspnoea
for 10 days. He had a background of stage IV metastatic
non-small lung carcinoma treated for 6 months with
non-cardiotoxic chemotherapy (carboplatin and
gemcitabine), and recently commenced on target therapy
(Erlotinib). Clinical examination revealed signs
consistent with cardiac tamponade, including significant
pulsus paradoxus, tachycardia (heart rate 101),
tachypnea (respiratory rate 25), elevated jugular venous
pressure and muffled heart sounds. He was normotensive at
130/90mmHg. The patient was extremely anxious and
spontaneously expressed concern about his imminent
death.
His electrocardiogram (ECG) (Fig. 1) demonstrated
electrical alternans and bedside transthoracic
echocardiography (TTE) revealed a large pericardial effusion
with features of cardiac tamponade, including diastolic
compression of both right atrium and ventricle (Fig. 2,
Additional file 1: Video 1 and Additional file 2: Video 2)
and large mitral inflow variation (Fig. 3). Urgent
pericardiocentesis was performed with a restricted
aspiration of only 600 ml drained initially over the first hour,
and a total drainage of 1.8 l of heavily blood-stained
pericardial fluid over 36 h. During initial aspiration of
pericardial fluid there was immediate symptomatic
relief and haemodynamic improvement (heart rate [HR]
decreased to 80/min, respiratory rate [RR] decreased to
15 breaths/min and BP increased to 150/70 mmHg).
Overnight (9 h post procedure) the patient developed
chest discomfort, dyspnea, tachycardia (HR 110) and
tachypnoea (RR 24). TTE the next morning showed no
re-accumulation of pericardial fluid, but detected new
severe impairment in function of both ventricles, with
akinesis of the apex and peri-apical region (Figs. 4 and 5,
Additional file 3: Video 3 and Additional file 4: Video 4).
Biomarkers demonstrated a rise in highly sensitive
troponin from 8 to 224ng/L, but creatinine kinase did not rise
significantly (107 to 116U/L). ECG after chest pain
demonstrated resolution of the electrical alternans, with
new loss of R waves in the anterior leads (Fig. 6).
Based on a presumptive diagnosis of SCM, angiotensin
converting enzyme inhibitor and long acting
betablocker were commenced, chemotherapy withheld and
the patient discharged for early clinical and
echocardiographic review. Serial follow up TTEs showed
normalization of bi-ventricular function after two weeks
(Figs. 7 and 8, Additional file 5: Video 5 and Additional
file 6: Video 6), and restoration of R waves on subsequent
ECGs (Fig. 9). Subsequent computed tomography
examination showed normal coronary arteries with a calcium
score of zero and no evidence of LAD laceration or
dissection.
The patient presented three months later with
reaccumulation of pericardial effusion and tamponade.
Therapeutic pericardiocentesis was performed with
500 ml of blood stained pericardial fluid drained
immediately, with 1.9 L in total over 36 h. On this
presentation he was relaxe (...truncated)