Which ventricle is broken?

Download Which ventricle is broken?

Post on 28-Dec-2016




0 download

Embed Size (px)


  • wl C

    Article history:

    Received 27 April 2013

    Accepted 3 October 2013

    physical exam, she was alert and oriented albeit in severe

    remarkable for JVP of 8 cm, S3, bilateral basal crackles and

    lower extremity edema.

    In the emergency room her respiratory rate worsened and

    she was started on bi-level non-invasive positive pressure

    ventilation with FiO2 of 50%. Her ECG showed biatrial

    e changes. D-dimer,

    395 respectively. CT

    bolism. Echocardio-

    %, LV apical ballon-

    lonning (Figs. 1 and 2

    of 50e60 mmHg. The

    following day, patient had a left and right cardiac catheteri-

    obstructive coronary

    tension and elevated

    son lost his job recently and this created significant emotional

    distress. She improved clinically on treatment and repeat

    echocardiogram in 3 days (Video 5) showed improved LVEF to

    45% and cardiac MRI (Video 6) on day 7 showed normal EF and

    normal LV and RV wall motion.

    * Corresponding author. 856 West Nelson Street, Apt 908, Chicago, IL 60657, USA. Tel.: 1 312 547 0499; fax: 1 773 296 7486.

    Available online at www.sciencedirect.com


    j o u r n a l o f i n d i a n c o l l e g e o f c a r d i o l o g y 3 ( 2 0 1 3 ) 1 9 2e1 9 3E-mail address: bhavith.aruni@advocatehealth.com (B. Aruni).of 111/83 mmHg, heart rate of 121, respiratory rate of 22, and

    saturating 100% on 15 L O2. General physical exam was

    wedge pressure. Patient was followed in intensive care unit on

    NIPPV and IV diuresis. Further questioning revealed that herrespiratory distress. She was immediately placed on O2 by the

    paramedics and her initial vital signs showed blood pressure

    zation (Video 3, 4) that showedmild non-

    artery disease andmild pulmonary hyper1. Case report

    A 65-year-old woman with past medical history of hyperten-

    sion, and COPD presented with acute onset shortness of

    breath, diaphoresis and nausea. She denied chest pain and the

    remainder of her review of systems was unremarkable. On

    enlargement with non-specific ST-T wav

    troponin I and BNP were 35, 0.45 and

    angiogram did not show pulmonary em

    gram revealed ejection fraction (EF) < 25

    ning, RV showed dyskinetic apexwith bal

    and Video 1, 2) and elevated RV pressureAvailable online 23 October 2013


    Stress-induced cardiomyopathy


    Right ventricle1561-8811/$ e see front matter Copyright http://dx.doi.org/10.1016/j.jicc.2013.10.001A 65-year-old lady with hypertension and COPD presented with acute onset shortness of

    breath, diaphoresis and nausea without chest pain. She was tachycardic and volume

    overloaded on examination. ECG showed biatrial enlargement with non-specific ST-T

    changes. D-Dimer, troponin and BNP were elevated. Echocardiogram revealed ejection

    fraction (EF)

  • 2. Discussion

    Stress-induced cardiomyopathy presents similar to myocar-

    dial infarction with mild elevation of cardiac enzymes. The

    most common presenting symptom is acute substernal chest

    pain but some patients present with dyspnea, syncope, shock

    j o u rn a l o f i n d i a n c o l l e g e o f c a r d i o l o g y 3 ( 2 0 1 3 ) 1 9 2e1 9 3 193Supplementary video related to this article can be found at


    function. The small number of studies have shown that RVFig. 1 e Subcostal View showing left and right ventricles in

    End-Diastole on the day of presentation. LA e Left Atrium;

    RA e Right Atrium; LV e Left Ventricle; RV e Right


    Fig. 2 e Subcostal view showing left and right ventricular

    apical ballooning in End-Systole on the day of

    presentation. LA e Left Atrium; RA e Right Atrium; LV e

    Left Ventricle; RV e Right Ventricle.Conflicts of interest

    All authors have none to declare.

    r e f e r e n c e s

    1. Haghi D, Papavassiliu T, Fluchter S, et al. Variant form of theacute apical ballooning syndrome (takotsubo cardiomyopathy):observations on a novel entity. Heart. 2006 Mar;92(3):392e394.

    2. Elesber AA, Prasad A, Bybee KA, et al. Transient cardiac apicalballooning syndrome: prevalence and clinical implications ofright ventricular involvement. J Am Coll Cardiol. 2006;47:1082e1083.

    3. Fitzgibbons TP, Madias C, Seth A, et al. Prevalence and clinicalcharacteristics of right ventricular dysfunction in transientstress cardiomyopathy. Am J Cardiol. 2009;104:133e136.3. Conclusion

    Right ventricular involvement in stress cardiomyopathy is

    being reportedmore frequent, and the incidence will continue

    to rise as imaging modalities continue to improve. It is

    important to recognize RV involvement as it is associatedwith

    increased complications.involvement in SIC follows similar wall motion abnormality

    pattern as the LV.2 RV involvement usually indicates lower LV

    function, higher artery pressure, higher incidence of tricuspid

    regurgitation, higher BNP level and longer hospital stay.3or electrocardiographic abnormalities.

    Until the initial reports in 2006, RV involvement had not

    been systematically evaluated in SIC. This could partly be

    attributed to the well-known difficulties in echocardiographic

    assessment of RV morphology, function and to the often

    impressive LV dysfunction which might have diverted atten-

    tion away from the RV.

    However, there is emerging evidence that the RV is also

    affected in up to 25% in different small series.1 Cardiovascular

    magnetic resonance (CMR) imaging does not have the tech-

    nical limitations like echocardiographic assessment and is

    regarded as the gold standard for the assessment of RV

    Which ventricle is broken?1 Case report2 Discussion3 ConclusionConflicts of interestReferences