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Erschienen in: Cardiovascular Ultrasound 1/2015

Open Access 01.12.2015 | Case report

A case report of ventricular dysfunction post pericardiocentesis: stress cardiomyopathy or pericardial decompression syndrome?

verfasst von: Chadi Ayoub, Michael Chang, Leonard Kritharides

Erschienen in: Cardiovascular Ultrasound | Ausgabe 1/2015

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Abstract

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.
Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s12947-015-0026-3) contains supplementary material, which is available to authorized users.
Chadi Ayoub and Michael Chang contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

All authors have approved the final article, contributed to conception, literature review, analysis and interpretation of the material, to the drafting of the manuscript and its critical revision; All authors agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Abkürzungen
SCM
Stress Cardiomyopathy
LV
Left ventricle
RV
Right ventricle
PDS
Pericardial decompression syndrome
APO
Acute pulmonary oedema
ECG
Electrocardiogram
TTE
Transthoracic echocardiography
bpm
Beats per minute
HR
Heart rate
RR
Respiratory rate

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 beta-blocker 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 re-accumulation 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 relaxed and well adjusted in regards to his diagnosis. No LV dysfunction was detected on serial follow-up echocardiograms after the second pericardiocentesis (Fig. 10).

Discussion

Our patient developed biventricular apical dysfunction following successful and judicious pericardiocentesis, with features typical of stress or “Takotsubo cardiomyopathy”. The case is instructive for its comparison with PDS and the clinical pattern of initial improvement followed by deterioration respectively due to pericardial aspiration and myocardial pathology.
In light of the timing of onset of biventricular impairment immediately post procedure PDS is an important differential diagnosis. Other differentials such as laceration to the ventricle or left anterior descending (LAD) coronary artery were clinically unlikely. The former was excluded by the absence of new pericardial bleed post procedure. Laceration of the LAD was also clinically unlikely given relatively small rise in cardiac enzymes and absence of large infarct, the presence of concurrent RV dysfunction, spontaneous recovery of ventricular function in a short period of time; additionally CT scan showed no evidence of haematoma or injury to the LAD.
Accordingly, we reviewed the literature describing SCM and PDS. Whereas SCM has been rarely reported after pericardiocentesis, much has been published on PDS. The incidence of PDS or new left or right systolic dysfunction has been reported to range from 5 % to 36 % of patients post pericardiocentesis [3, 4], especially after malignant pericardial effusions. Although the first case report of PDS in 1983 noted APO with preserved LV function [5], most subsequent reports describe severe impairment of left, right or bi- ventricular function, which may be segmental or global (Tables 1 and 2).
Table 1
Summary of reported cases of LVF post pericardiocentesis: Clinical characteristics
Report
Age/Gender
Clinical Scenario
Chronicity of effusion
Type of pericardi-ocentesis
Nature of pericardial fluid
Fluid drained
Time to onset of symptoms
Symptom
Signs
VanDyke (1983) [5]
42 M
Unwell for 10 days
Days
P
Exudate (malignant)
680 mls
Minutes
Dyspnoea
LVF
Shenoy (1984) [22]
57 M
Recent myocardial infarction
Days
P
Transudate
1000 mls
Minutes
Dyspnoea
LVF
Glasser (1988) [23]
33 M
Respiratory tract infection 3 months prior, history of Down’s and Ventricular Septal Defect
Weeks
S
Transudate
2000 mls
Minutes
Dyspnoea
LVF
Downey (1991) [24]
50 M
Traumatic (3 weeks post motor vehicle accident)
Weeks
P
Not specified
450 mls then 1500 mls
Minutes
Dyspnoea
LVF
Wolfe (1993) [19]
46 F
2 weeks, history of breast cancer prior
Weeks
P
Exudate
650 mls
Weeks
Dyspnoea
LVF
Wolfe (1993) [19]
50 F
2 weeks, history of breast cancer prior
Weeks
P
Exudate
650 mls
Weeks
Dyspnoea
LVF
Hamaya (1993) [25]
16 F
Unwell, lymphoma with pericardial effusion for 3 years
Months
P
Not specified
700 mls
Weeks
Dyspnoea
CS, and no APO
Braverman (1994) [26]
27 F
Unwell for 3 weeks (Atrial Septal Defect closure 13 years prior)
Weeks
P then S
Transudate
500 mls then 100 mls
Days
Dyspnoea, pleuritic chest pain
LVF, RVF, CS
Anguera (1996) [27]
68 F
History of bowel cancer, anorexia and dyspnoea for 1 month
Weeks
P
Malignant
800 mls
Minutes
-
CS
Sunday (1999) [8]
60 F
3 days of dyspnoea, lung cancer with pericardial involvement
Days
S
Exudate
700 mls
Minutes
Dyspnoea
CS, LVF
Chamoun (2003) [6]
36 F
2 months post Mitral valve replacement and Tricuspid repair
Days
P
Exudate
1070 mls
Hours
Dyspnoea
CS, LVF
Chamoun (2003) [6]
46 F
Metastatic cancer
Weeks
P
Exudate
1000 mls
Hours
Dyspnoea
CS, LVF
Geffroy (2004)
[7]
53 M
1 month post chemotherapy for cancer
Weeks
S
Exudate
1500 mls
Not specified
Dyspnoea, hypoxia
CS, LVF, RVF
Ligero (2006) [20]
41 F
Lung cancer with hepatic metastases
Days
P
Exudate
1000 mls
Hours
Dyspnoea
LVF, RHF
Bernal (2007) [28]
45 F
Acute myeloid leukemia
Days
P
Exudate
500 mls
Hours
Dyspnoea
CS, LVF
Dosios (2007) [9]
66 F
Hematoma, 10 day history of dyspnoea
Days
S
Exudate
500 mls initially
Hours
-
CS
Sevimli (2008) [17]
42 F
Infective - tuberculous pericarditis
Days
S
Exudate
500 mls
Hours
Dyspnoea
CS and LVF
Khalili (2008) [29]
32 F
2 months post aortic and mitral valve replacement surgery
Weeks
P
Transudate
1000 mls
Hours
Dyspnoea
CS
Flores (2009) [30]
80 M
Unwell for weeks, multiple myeloma, stent 2 weeks prior
Weeks
P
Transudate
1200mls
Days
Dyspnoea
CS and LVF
Karamichalis (2009) [31]
19 F
2 months post motor vehicle accident
Weeks
P
Exudate
1600 mls
Hours
Dyspnoea
LVF
Lee (2010) [18]
14 M
Infective – tuberculous pericarditis
Days
P
Exudate
Not specified
Hours
Dyspnoea
CS, LVF
Lim (2011) [32]
44 F
Hypothyroidism related heart failure. Dyspnoea and fatigue for 4 months
Weeks
S
Exudate
1.3L
9 h
-
CS
Abdelsalam (2012) [10]
65 F
Stage IV Non small cell lung cancer for 6 months, 1 week of dyspnoea
Weeks
S
Malignant
Complete drainage of pericardial effusion intraoperatively
Seconds
Asystole during surgery
CS
Weijers (2013) [11]
69 F
Weight loss and dyspnoea
-
P
-
800 mls
6 h
-
LVF
Liang (2014) [1]
56 F
Polymyositis. Progressive dyspnoea on exertion
-
P
-
275 mls initially, with ongoing drain
Several hours
Pleuritic chest pain
Nil
Versaci (2015) [16]
78 F
3 months post mitral valve repair
Days
P
Possibly transudate
500 mls
Hours
Dyspnoea
LVF
Abbreviations: P percutaneous, S surgical, CS cardiogenic shock (hypotension, tachycardia), LVF Left heart failure, RVF right heart failure
Table 2
Summary of reported cases of LVF post pericardiocentesis: Electrocardiographic, biochemical, echocardiographic and outcome parameters
Report
LV function pre tap
LV function post tap
RV function post tap
Regional wall motion abnormality
Bio marker
ECG
Coronary artery imaging
Inotrope, IABP or Intubation
Death
LV recovery
VanDyke (1983) [5]
Normal
Normal (EF 67%)
-
Nil
Normal
Normal
-
Intubation
No
Normal LV
Shenoy (1984) [22]
-
Mild LV impairment
Normal
Septal hypokinesis
Normal
T wave abnormality and ST elevation V5-6
-
-
No
Normalised few days later
Glasser (1987) [23]
-
Pulmonary capillary wedge pressure normal
Normal (RVP increased)
-
-
-
-
Intubation
No
Clinical improvement
Downey (1991) [24]
-
Inferred to be normal
Normal
-
-
Normal
-
No
No
Normal LV
Wolfe (1993) [19]
Normal, EF > 50%
EF 30%
-
Severe global hypokinesis of LV
-
-
-
-
No
Normalised after 7 days
Wolfe (1993) [19]
Normal, EF > 50%
EF 25%
-
Antero-apical akinesis and apical dyskinesis
-
-
-
-
-
Normalised after 2 weeks
Hamaya (1993) [25]
Normal
-
-
Not provided
Normal
ST elevation
-
Inotropes and intubation
No
-
Braverman (1994) [26]
EF 20%
EF 20%
EF <15%
Not provided
-
-
-
-
-
EF 45% in 9 days then normalised after a few weeks
Anguera (1996) [27]
-
Mildly impaired. Normal capillary wedge pressure
Severely dilated and severely impaired contractility, EF <15%
Paradoxical septal motion
-
-
Normal coronary arteries
Inotropes
No
Complete recovery of biventricular fn after 10 days
Sunday (1999) [8]
EF 65%
EF 30%
Severely impaired contractility
Global hypokinesis
-
-
-
Intubation
Yes
No
Chamoun (2003) [6]
Normal, EF > 50%
EF 20%
-
Regional wall motion abnormality
-
SR
Normal coronary arteries
Inotropes and IABP
No
Normalised 2 weeks later
Chamoun (2003) [6]
Normal, EF > 50%
EF 20%
-
Akinesis of mid anterior wall and septum /dilatation of LV
-
SR
-
No
No
Normalised 2 weeks later
Geffroy (2004) [7]
Normal, EF > 50%
EF >50%
EF <15%
Akinetic and dilated RV
Elevated
Old RBBB
Normal coronary arteries
Inotropes and intubation
Yes
-
Ligero (2006) [20]
Normal, EF 75%
EF 25%
Severe impairment
Akinesis of anterior, septum and apex
Normal CK
Normal
Normal coronary arteries
Inotropes
No
Normalised 10 days later
Bernal (2007) [28]
Normal, EF 60-65%
EF 30%
-
Akinesis of mid anterior wall, anteroseptal akinesis with apical sparing
Elevated
Sinus tachycardia
CMR: no myocardial infarction
Inotropes and intubation
No
Normalised 1 weeks later
Dosios (2007) [9]
Normal LV fn
EF 25%
Moderately dilated, impaired
Global hypokinesis
Elevated
-
-
Inotropes and intubation
Yes
-
Sevimli (2008) [17]
Normal, EF > 50%
EF 20%
-
Akinesis in the left ventricular apex, and severe hypokinesis in the septum
-
Precordial TWI, normalised later
Normal coronary arteries
No
No
Normalised 10 days later
Khalili (2008) [27]
EF 35%
<10%
EF <15%
Global hypokinesis
-
Widening of QRS
-
Inotropes and IABP-
Yes
-
Flores (2009) [28]
EF 60%
13%
-
Global hypokinesis
Normal
Normal
Old RCA Branch lesion
Inotropes
No
Normalised 10 days later
Karamichalis (2009) [31]
-
-
-
 
-
Bradycardia
-
Inotropes and tracheostomy
Yes
-
Lee (2010) [18]
-
EF 20 -30%
-
Typical features of Takotsubo’s (diagnosed as such)
-
Precordial TWI, normalised later
Normal coronary arteries
No
Yes
No
Lim (2011) [32]
EF normal, 73%
EF 46%
-
Segmental wall motion abnormality
-
-
-
Inotropes and IABP
Yes
-
Abdelsalam (2012) [10]
Vigorous
EF 10-15%
Dilated and impaired fn
Takotsubo pattern of akinesia
-
ST elevation
-
Inotropes and IABP
Yes
-
Weijers (2013) [11]
Normal
Poor LV fn
-
General hypokinesia and anterior and septal akinesia
Normal
TWI and Q waves in anterolateral lead
-
-
No
Complete recovery of LV fn several months later
Liang (2014) [1]
Normal, EF 69%
EF 39% (on MRI)
Impaired
Severe mid and apical hypokinesis of both Ventricles (diagnosis : Takotsubo’s cardiomyopathy)
-
-
Normal coronary arteries
-
No
LV normalised 1 week later
Versaci (2015) [16]
Normal, EF >50%
EF 28%
-
LV ballooning, typical feature of Takotsubo’s cardiomyopathy
Elevated
QS wave in V1–V4 with negative T wave and ST elevation in V5–V6
Normal coronary arteries
No
No
Normalised after 10 days
LV Left ventricle, RV Right ventricle, fn function, EF Ejection fraction, IABP Intra-aortic balloon pump, RVP right ventricular pressure
A number of mechanisms have been proposed to explain the pathogenesis of LV systolic dysfunction in PDS. Acute withdrawal of exaggerated sympathetic drive during relief of tamponade may trigger paradoxical haemodynamic instability [5]. Mechanical, inter-ventricular volume mismatch may also contribute, with sudden relief of pericardial constraint leading to abrupt, disproportionate increase in RV volume and a paradoxical rise in pulmonary artery pressure, resulting in raised LV end diastolic pressure and transient left heart failure [59]. Others have proposed myocardial stunning from coronary perfusion mismatch with acute distension of cardiac chambers after decompression [6, 10, 11]. Taken together, it is likely that a combination of hormonal and mechanical pathophysiologic mechanisms contribute to LV dysfunction and the final clinical sequelae in PDS.
The classic echocardiographic feature in SCM is transient LV apical ballooning, although other segmental patterns have been described [12, 13]. A stressor leading to sympathetic overdrive and excessive catecholamine release is the currently accepted trigger in the development of SCM [12]. The catecholamine surge precipitates 1) ‘peripheral arterial vasospasm leading to increased afterload and transient increase in LV end-systolic pressure’, 2) ‘acute multiple coronary artery vasospasm leading to myocardial ischaemia’, and 3) direct catecholamine- β-adrenoceptor - mediated myocardial stunning in the apex [14]. These three pathophysiologic pathways are thought to contribute to the ischaemia, morphologic features and potential haemodynamic sequelae that can be seen in SCM.
More recent case reports have made reference to LV apical ballooning related to PDS as similar to SCM [10, 11, 1517], and have postulated the physiological stressor being cardiac tamponade along with emotional stress [16]. It is therefore possible that the transient ventricular systolic dysfunction in PDS is actually a variant form of stress cardiomyopathy. We carefully reviewed 25 cases of heart failure post pericardiocentesis in the literature (Tables 1 and 2), and we believe that seven cases (two considered to be SCM [1, 18] by the authors and five classified as PDS [10, 16, 17, 19, 20]) could be considered to have echocardiographic features of SCM.
SCM has relatively characteristic clinical presentation, with rise of cardiac enzymes [21], and often associated with ischaemic ECG changes (up to 44 % of those with SCM have T-wave inversion and 41 % ST elevation [13, 21]). The clinical manifestations in PDS are more variable, ranging from asymptomatic in some to severe low cardiac output states in others. The primary clinical symptom in PDS has been reported as dyspnoea (Table 1). This is in contrast to chest pain being predominant in SCM (69-83 % of presentations) [13, 21]. In the majority of cases of PDS in the literature (Table 2) there was no cardiac enzyme rise, and ischaemic type changes on ECG were seen in a minority (seven of twenty five cases). In all the cases where ischaemic ECG changes where present except for one, there was concomitant apical and peri-apical regional wall motion abnormality, which could be classified as SCM also.
Generally SCM has a benign course, with recovery of LV function and good prognosis [12], whilst PDS has poorer outcomes and increased mortality [4]. Reports of PDS suggested normalization of LV dysfunction in 12 of 25 cases classified as PDS. Of the 12 cases that did recover LV function, four had LV impairment with classic SCM pattern of LV impairment on echocardiogram [16, 17, 19, 20]. The normalisation of LV function in our patient 2 weeks subsequently is more in keeping with SCM.
Current literature has not specifically addressed risk factors for the development of ventricular dysfunction after pericardiocentesis. In our patient, the malignant nature of the effusion, the presence of tamponade and larger size of pericardial effusion [4], may have increased his predisposition to develop ventricular dysfunction. Amount and rate of fluid removed on initial decompression are also associated with development PDS [4, 5], however there are no guidelines regarding the maximum amount of pericardial fluid that can be drained immediately. There is consensus to stop initial drainage with improvement of symptoms or hemodynamic parameters, followed by gradual decompression through indwelling catheter [5].
Our patient’s apical systolic dysfunction post pericardiocentesis was associated with chest discomfort, transient loss of R waves and rise in cardiac enzymes are typical of classic SCM. The clinical sequence of HR and RR improving immediately post decompression and then increasing again hours after the procedure, was a useful clinical marker of myocardial dysfunction, prompting investigation which identified new ventricular impairment. It is likely that the frequency of transient LV dysfunction is underestimated in these patients.

Conclusion

We report a case of transient biventricular dysfunction post pericardiocentesis, with classic features of SCM. LV dysfunction post pericardiocentesis and in PDS is more prevalent than previously thought, and some previous reports of PDS may also be potentially considered as SCM complicating pericardiocentesis. In addition to judicious and gradual decompression to avoid ventricular dysfunction or PDS, patients undergoing therapeutic pericardiocentesis should have careful haemodynamic monitoring, as changes in parameters such as heart rate and respiratory rate can raise suspicion of acute LV impairment.
Written informed consent was unable to be obtained from the patient for publication of this Case report and any accompanying images, as he has passed away. His next of kin are not contactable after their subsequent return to their home country of China. Professor L. Kritharides, Head of Department, approves the publication of this report, with all patient identifiers kept confidential and material presented solely for educational purposes arising from the clinical encounter.
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Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

All authors have approved the final article, contributed to conception, literature review, analysis and interpretation of the material, to the drafting of the manuscript and its critical revision; All authors agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
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Metadaten
Titel
A case report of ventricular dysfunction post pericardiocentesis: stress cardiomyopathy or pericardial decompression syndrome?
verfasst von
Chadi Ayoub
Michael Chang
Leonard Kritharides
Publikationsdatum
01.12.2015
Verlag
BioMed Central
Erschienen in
Cardiovascular Ultrasound / Ausgabe 1/2015
Elektronische ISSN: 1476-7120
DOI
https://doi.org/10.1186/s12947-015-0026-3

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