A RARE CAUSE OF REVERSIBLE

CARDIOMYOPATHY

DR.P.PRAVEEN KUMAR
SR IN CARDIOLOGY
COIMBATORE MEDICAL COLLEGE HOSPITAL
 CASE SCENARIO
Miss.X , 22 years old, unmarried with no previous comorbidities was
referred to our hospital on 23-8-19 as a case of Anaemia With CCF.

CHIEF COMPLAINTS

•Breathlessness for past 1 week.

•Bilateral pedal edema for 1 week.

•Abdominal distension for 1 week.

•Fever for past 2 days.
HISTORY OF PRESENT ILLNESS

H/o breathlessness for past 1 week. Initially NYHA grade II dyspnea, progressed to
NYHA grade IV dyspnea for past 2 days. h/o orthopnea +. h/o PND +.

H/o bilateral pedal edema for past 1 week.

No H/o chest pain, palpitation or syncope.

H/o giddiness, easy fatiguability for 1 week.

H/o fever for past 2 days, high grade , continous fever, ass with chills and rigor.

No h/o cough/ expectoration/ hemoptysis.

No H/o lower abdominal pain , vomitting, loose stools, bleeding p/v, draining p/v or
reduced urine output.
PAST HISTORY
Not a known Case of Diabetes ,hypertension, Cad, bronchial asthma,
epilepsy, thyroid, Congenital heart disease. No history of previous any
surgery.

PERSONAL HISTORY
Non-smoker, Non-alcoholic, unmarried,
LMP not known.
ON EXAMINATION
conscious,
oriented,
febrile,
dyspnoeic,
tachynoeic,
pallor+,
Icteric,
b/l pedal edema grade 4,
No cyanosis/clubbing
CVS - S1S2+,tachycardia,
RS - NVBS+, b/l basal crepitations,
P/A - uterus 26 weeks size, not acting, not tense and tender.

VITALS
Temperature – 100 F,
PR-158/min,
BP-70/?,
RR-38/min,
Spo2 -89 % in room air.
INVESTIGATIONS

• Hemogram • D-dimer - > 50000,

WBC-36,300 (P74,L20) • FDP - Positive .
Hb-7.6gms,
•FIBRINOGEN – 238 ng/ml ( N 200-400)
Platelet-3,40,000.
• Renal parameters •PT - >60 sec, aPTT- 110 sec
urea-78, • PS - Normocytic normochromic anaemia,
creatinine-1.8 mg/dl.
• Liver parameters Neutrophilia and thrombocytopenia.
bilirubin-total-2. 8, (platelet count was decreasing in trend).
direct-1.0,
SGOT-1253,
SGPT-1256, USG Abdomen and pelvis shows
SAP-189. -Intrauterine fetal demise of 27 weeks
• Serum electrolytes
Na+-137, gestation, GB wall edema, B/L Mild HUN,
k+-4.5,S no free fluid in abdomen and pelvis, and
• Serum LDH -1645IU.
Right mild pleural effusion noted.
• Preliminary Urine culture ,blood culture, high
vaginal swab – no growth.
• Repeat Blood culture – E.coli
CHEST XRAY

ECG
HR-130/min,
NSR,
Axis
Low voltage complexes
Tachycardia induced ST-T
changes.

TROPONIN T - POSITIVE
• Bed side ECHO done shows-
Severe global hypokinesia of left ventricle,
LA, LV dilated,
RA, RV dilated,
severe biventricular dysfunction ,LVEF-24 %.
All valves – structurally normal.
Mild MR,
large RV clot 19*12mm,
Mild TR, RVSP 31 mmHg,
moderate PAH,
TAPSE 12mm.
Grade II diastolic dysfunction.
No pericardial effusion. Bilateral pleural effusion.

IMPRESSION :
DILATED CARDIOMYOPATHY.
SEVERE BIVENTRICULAR DYSFUNCTION.
RV CLOT.
MILD PULMONARY HYPERTENSION.
RV CLOT
PULMONARY CT ANGIOGRAM
Bilateral lung parenchyma appears normal.
11*13mm thrombus in right ventricle.
Mild bilateral pleural effusion.
Mild ascites.
No evidence of pulmonary embolism.
 DIFFERENTIAL DIAGNOSIS
• SEVERE ANAEMIA WITH CCF

• ACUTE CORONARY SYNDROME

• DILATED CARDIOMYOPATHY - ? ISCHAEMIC ? IDIOPATHIC

• PULMONARY/ AMNIOTIC FLUID EMBOLISM

• PERIPARTUM CARDIOMYOPATHY

• TAKOTSUBO CARDIOMYOPATHY

• SEPSIS INDUCED CARDIOMYOPATHY

• MYOCARDITIS
• Mean while patient spontaneously expelled
dead male fetus of weight 850 grams.
• Followup ECHO done on Day 9 shows

Normal LV systolic function,

grade 1 LV diastolic dysfunction,
no RV dysfunction,
thormbus not visualised,
LVEF-51 %.
 DIFFERENTIAL DIAGNOSIS
SEVERE ANAEMIA WITH CCF
ACUTE CORONARY SYNDROME
DILATED CARDIOMYOPATHY
- ? ISCHAEMIC ? IDIOPATHIC
PULMONARY/ AMNIOTIC FLUID EMBOLISM
PERIPARTUM CARDIOMYOPATHY
TAKOTSUBO CARDIOMYOPATHY
SEPSIS INDUCED CARDIOMYOPATHY
 MYOCARDITIS
Admission Hb was 9 gm/dl and developed severe anaemia over
the stay in hospital due to DIC/SEPSIS.
No ecg changes in serial ecg, No RWMA,
Echo supports diagnosis.. Cause not clear.
It also seemed unlikely that our patient had pre existing cardiac
disease which was exacerbated by severe sepsis because she
reported previous good health before. LV function recovered.
CTPA negative.
Did not meet definition of last month of pregnancy with no
associated cause other than pregnancy
Contractile function of the mid-to-apical segments of the left
ventricle is depressed and there is hyperkinesis of basal walls,
producing a balloon-like appearance of the distal ventricle.
Catecholamine levels was not elevated.
there is global ventricular dysfunction and dilated left ventricle
without regional dysfunction with recovery in 7-10 days
We did not believe myocarditis was likely because of the
normal troponin level and electrocardiogram.
• Takotsubo cardiomyopathy typically occurs when the
contractile function of the mid-to-apical segments of the
left ventricle is depressed and there is hyperkinesis of
basal walls, producing a balloon-like appearance of the
distal ventricle.

• Several studies have reported that this syndrome is

induced by increased catecholamine levels.

• In sepsis-induced cardiomyopathy, there is global

ventricular dysfunction and dilated left ventricle without
regional dysfunction with Rapid recovery in 7-10 days.
 DIAGNOSIS

• IUD/SEPTIC ABORTION/ SEPTIC SHOCK.

• DIC/MODS.

• CARDIOMYOPATHY WITH RV CLOT –

SECONDARY TO SEPSIS /DIC.
 TREATMENT
• Patient was treated with fluid resuscitation.
• inotropic support – Inj.Noradrenaline and I.j.Dobutamine.
• i.v Antibiotics – Inj.Meropenem , Inj.Metronidazole and T.Azithromycin.
• Periodic monitoring of coagulation profile and PRBC and FFP substitution.
• Serum Albumin was persistently low and Inj.Albumin 25% was given for 10
days.
• T.Carvidilol 3.125 BD.
• Inj.Frusemide iv 20-20-20
• T.Spironolactone. 25mg 1-0-0.

• The inotropic support was stopped after 7 days and Beta blockers, cardiac
failure drugs continued along with Inj.Albumin transfusion.
SEPSIS-INDUCED CARDIOMYOPATHY
• Sepsis-induced cardiomyopathy is a complication of severe
sepsis and septic shock first described by Parker et al. in 1984
• Reversible myocardial dysfunction of rapid onset, changes in
LV function typically resolves in 7-10 days. Incidence 18-65
percent.
• Its triad of
. Left ventricular dilatation .
Depressed ejection fraction.
Recovery in 7-10 days.
In this myocardium is functionally and structurally injured by
inflammatory cytokines and endotoxins.
Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but reversible myocardial depression in
patients with septic shock. Ann Intern Med.1984;

Zanotti-Cavazzoni SL: Cardiac dysfunction in severe sepsis and septic shock. Curr Opin Crit Care 2009,
15:392-398.
The Mechanisms Of Sepsis-induced
Cardiomyopathy
• First, myocardial ischemia resulting from
inadequate coronary blood flow has been proposed
on the basis of a study in animals.
(Cunnion RE, Schaer GL, Parker MM, et al. The coronary circulation in human septic shock.
Circulation. 1986)

• Second, there are strong arguments that chemical

mediators, such as endotoxins, cytokines, and nitric
oxide, are causative.
(Kumar A, Brar R, Wang P, Dee L, Skorupa G, Khadour F, Schulz R, Parillo JE:Role of nitric oxide and
cGMP in human septic serum-induced depression of cardiac myocyte contractility. Am J Physiol Heart
Circ Physiol 2008, 276)
• Ognibene FP, Rosenberg SA, Lotze M, et al. Interleukin-2 administration causes reversible hemodynamic changes and
left ventricular dysfunction similar to those seen in septic shock. Chest. 1988;94;750–754.

•Zangrillo A, Putzu A, Monaco F, Oriani A, Frau G, De Luca M, et al.Levosimendan reduces mortality in patients with
severe sepsis and septicshock: a meta-analysis of randomized trials. J Crit Care 2015; doi: 10.1016/
 REVIEW OF LITERATURE
• Flesch et al. also demonstrated that exposure of the myocardium to endotoxins caused
depressed cardiac contractility, which was mediated by enhanced inducible nitric
oxide synthase activity and nitric oxide release.
(Flesch M, Kilter H, Cremers B, Laufs U, Sudkamp M, Ortmann M, et al. Effects of endotoxin on human myocardial
contractility involvement of nitric oxide and peroxynitrite. J Am Coll Cardiol. 1999;)
• Vincent et al. demonstrated that anti-TNF antibody administration improved
ventricular function without changing the cardiac filling pressure .
(Vincent JL, et all Administration of anti-TNF antibody improves left ventricular function in septic shock patients.
Results of a pilot study. Chest. 1992;101(3):810–5.)

• In a more recent study, interleukin-1β has also been implicated , further supporting
cytokine’s role in sepsis-induced cardiomyopathy.
(Kumar A, Thota V, Dee L, Olson J, Uretz E, Parillo JE. Tumor necrosis factor alpha and interleukin 1beta are responsible for
in vitro myocardial cell depression induced by human septic shock serum. J Exp Med. 1996;183(3):949–58.)

• In 2001, Kirov et al. evaluated the effects of continuous infusion of methylene blue, an
inhibitor of the nitric oxide pathway, on the hemodynamics and organ function of
patients with septic shock. It counteracted the myocardial depression, maintained
oxygen transport, and reduced the need for concurrent adrenergic support .
(Kwok ES, Howes D. Use of methylene blue in sepsis: a systematic review. J Intensive Care. 2006;21(6):359–63.)
• Standard treatment for sepsis should focus on
infection control and optimization of
hemodynamic parameters by fluid
resuscitation and vasopressor therapy.
(Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, et al. Early goal-directed
therapy in the treatment of severe sepsis and septic shock. N En J Med. 2001;345(19):1368–77.)

• Sepsis survival campaign bundles did not

address sepsis induced cardiomyopathy.
(Dellinger RP, Levy MM, Rhodes A, Annane D, Geriach H, Opal SM, et al.Surviving sepsis campaign:
international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med.
2016;41(2):580–637)
LIMITATIONS
• An endomyocardial biopsy could have been
performed, but the rate of a positive biopsy is
low even in those with high suspicion for
myocarditis and the procedure is invasive.
• A limitation of this report is that we did not
measure levels of myocardial depressant
substances such as tumor necrosis factor and
interleukin 1B as measurement is not standard
in clinical practice.
THANK YOU