Takotsubo cardiomyopathy presentation.pptx

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1. Takotsubo cardiomyopathy “broken heart syndrome” Pathophysiology presentation Lukas Scholz, Theresa Schreck, Maja Schulte, Gabriel Shamsul, David Spägele

2. Agenda What is Takotsubo cardiomyopathy ? Risk Factors + Prognosis Pathology + Anatomy Symptoms Diagnosis + DD Treatment Case Sources

3. Agenda What is Takotsubo cardiomyopathy ? Risk Factors + Prognosis Pathology + Anatomy Symptoms Diagnosis + DD Treatment Case Sources

4. What is Takotsubo cardiomyopathy? Defined as an acute, stress-induced, reversible dysfunction of the left ventrice that mimics acute coronary syndrome. 90% of reported cases are women aged 58 to 75. Also known as broken-heart syndrome due to intense (negative) emotional stress being one of the major triggers. Emotional stress activates the sympathetic nervous system, leading to a massive catecholamine discharge and subsequent cardiotoxicity, causing multivessel spasm and dysfuntion  myocardial stunning (abnormal revional LV wall motion persisting for hours to weeks following transient ischemia). Left ventricle shape becomes similar to a Japanese Octopus trap (Tako-Tsubo).

5. Pathology / Anatomy

6. Symptoms Retrosternal chest pain with angina features Dyspnea Syncope Arrythmia Signs of: Heart failure Cardiogenic shock

7. Diagnosis ECG: ECG is abnormal in > 95% of patients ST elevations  Prolonged QT interval Laboratory: Ischemic indicators Imaging: Most important is echocardiography Coronary angiography MRI for additional evaluation of the status of the heart

8. Differential Diagnosis Pathological laboratory values and ECG could be missleading Usually ishemic heart diseases need to be excluded Any disease that shows chest pain or heartmalformations Acute and chronic diseases need to be considered Imagine is most likely to rule them out

9. Treatment of hemodynamically stable patients Treatment is according to symptoms and complications Reduce stressors (e.g anxiolytics ) should treat with ACE inhibitors (e.g Lisinopril) If good with ACE‘s we can use low dose beta-blockers (e.g metoprolol) Deep Vein Thrombosis prophylaxis is advised

10. Treatment of hemodynamically unstable patients LVOT obstruction low dose beta-blockers might be used under monitoring IV fluids for better systolic function might be used Advanced: LV assist device Avoid : Inotropes (e.g catecholamines =risk for cardiogenic shock ) Vasodilators No LVOT obstruction Ionotropic support can be given , but should be monitored closely (e.g levosimendan ) Vasopressors , if ionotrops are insufficient If recurrent Takotsubo‘s : consider „ Intra-aortic balloon pump“

11. Treatment

12. Case study An 83-year-old woman presented to the emergency department (ED) with extreme thirst. She described an unquenchable thirst along with an ominous feeling that began the previous night. She denied shortness of breath, palpitations, chest pain, lower extremity edema, and recent stressors or illnesses. She had a history of chronic lower extremity deep vein thrombosis, diastolic congestive heart failure, hypothyroidism, and asthma. Echocardiogram 2 years prior showed a normal ejection fraction (EF).

13. An 83-year-old woman presented to the emergency department (ED) with extreme thirst . She described an unquenchable thirst along with an ominous feeling that began the previous night. She denied shortness of breath, palpitations, chest pain, lower extremity edema, and recent stressors or illnesses . She had a history of chronic lower extremity deep vein thrombosis , diastolic congestive heart failure , hypothyroidism , and asthma . Echocardiogram 2 years prior showed a normal ejection fraction (EF). Heart failure Angina ?, HF No other signs of HF DVT + hypothyroidism risk factors for CV disease Susceptibiliity for cardiac diseases , myocardial hypokinesia or akinesias , No hint for vavlular insufficiencies / stenosis Shunts, hypertrophic cardiomyopathy NOT CHRONIC Age risk factor for everything Female : ASD, mitral valve disease, cardiac involvement in collagenases, TC

14. On presentation, serum studies were significant for a: troponin level of 4.241 ng/mL (0-0.04ng/ml) a brain natriuretic peptide level of 201 pg / mL . (<100 pg /ml)

15. On presentation, serum studies were significant for a: troponin level of 4.241 ng/mL (0-0.04ng/ml) a brain natriuretic peptide level of 201 pg / mL . (<100 pg /ml) (N)STEMI, Myocarditis , PE, unstable angina , Takotsubo Systolic dilation of Ventricle

16. Electrocardiogram showed T-wave inversions in the inferior leads ST segment elevation, T-wave inversion, Pathological Q waves, T prolongation, Conduction abnormalities – L/RBBB Echocardiogram demonstrated an EF of 30%

17. During evaluation in the ED, the patient developed chest pain . After nitroglycerin administration, she became hemodynamically unstable and required pressors to maintain blood pressure. Repeat electrocardiogram was significant for diffuse T-wave inversions. Due to concern for NSTEMI, she was immediately rushed to cardiac catheterization

18. Coronaorgraphy + Echocardiogram

19. Catheterization demonstrated no significant coronary artery disease but did show significant left ventricular to aortic pullback gradient, suggesting Takotsubo cardiomyopathy-related left ventricular outflow tract obstruction (LVOT ). Dynamic gradient was seen as well as an LVOT resting gradient of 20 mm Hg at baseline . Because of her severely elevated left-sided filling pressures in the setting of stress-induced cardiomyopathy, an EF of 30%, and hypotension, we elected to manage her with cautious diuresis and intra-aortic balloon pump (IABP) placement, with planned IABP removal the next morning. Echocardiogram confirmed the diagnosis of Takotsubo cardiomyopathy with an LVOT dynamic obstruction of 85 mm Hg and systolic anterior motion of the mitral valve Systolic anterior motion MV – 25% Parasternal long axis

20. Dynamic obstruction (of LV outflow tract)

21. Her condition improved after initiation of beta blocker and diuretic therapy, and repeat echocardiogram 5 days after admission showed recovered EF with no resting LVOT obstruction. Six days after discharge, the patient presented to the ED after a syncopal episode when standing up from the toilet. Her blood pressure at the scene was 60/40. Her pressures gradually improved to a systolic pressure of 100, but the patient reported heavy chest pressure and was readmitted. CTA showed large pericardial effusio n that was increased in size from her previous visit. Echocardiogram confirmed large pericardial effusion and demonstrated increased intrapericardial pressure and no inferior vena cava collapse. At this time, the patient was not in tamponade clinically. Diagnostic pericardiocentesis was significant for exudative pericardial effusion per Light’s criteria with negative cultures. She also had an elevated erythrocyte sedimentation rate POST-TAKOTSUBO CARDIOMYOPATHY Pericardial effusion + pericarditis in up to 43% of patients ( most asymptomatic )

22. Sources https://www.svhhearthealth.com.au/conditions/takotsubo-cardiomyopathy https://bjcardio.co.uk/2021/03/takotsubo-syndrome-the-broken-heart-syndrome/ https://www.amboss.com/int https://twitter.com/ dhirenshah_in /status/1353002118706290689 https://www.osmosis.org/answers/broken-heart-syndrome https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231567/figure/F1/ https://bjcardio.co.uk/2021/03/takotsubo-syndrome-the-broken-heart-syndrome/

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