2019 Research Forum

A Case Of Acute Onset Heart Failure In A Previously Healthy 26-Year-Old Female David Aguirre MD, Fowrooz Joolhar MD, Nosheen Hasan MD R2, Sarah El-Halees MS IV Department of Internal Medicine, Kern Medical

PHYSICAL EXAM & IMAGES

INTRODUCTION

DISCUSSION

Heart failure is a relatively uncommon diagnosis in healthy young adults, particularly that of new and rapid onset. We present a unique case of a young female with multiple possible etiologies of worsening heart failure, with one likely exacerbating another. 27-year-old female with history of IV drug use presented to an outside hospital at 35 weeks gestation with pelvic pain. She delivered emergently via C-section, but was found to be bacteremic with MSSA. Chest X-ray obtained revealed many cavitary lesions suspicious for septic emboli, which was later confirmed via CT. TTE showed mobile vegetation on TV suggestive of endocarditis, tricuspid regurgitation, and hypokinesis of LV with EF of 35%. Patient was treated with IV Nafcillin. Two weeks later, patient experienced worsening dyspnea, thoracentesis removed 1350ml of transudative fluid. A repeat TTE revealed an echo-density suggestive of ruptured chordae tendineae, and EF of 20%. Lisinopril, Carvedilol, and Digoxin were started for HF management. Left heart catheterization ruled out ischemic causes leading to primary diagnosis of postpartum cardiomyopathy. She left against medical advice, but presented to our institution 2 days later dyspneic at rest with diffuse anasarca. Physical exam revealed a holosystolic murmur at the lower left sternal border, bibasilar lung crackles, and 3+ pitting edema of lower extremities. Labs indicated BNP of 1793, and positive toxicology for amphetamines and opiates. Patient was restarted on IV Nafcillin, Lisinopril, Carvedilol, with aggressive diuresis (net loss of 44lbs). New findings of TEE revealed dilated cardiomyopathy, severely reduced right ventricular function, and a LV EF of 10-15%. Patient was not a candidate for valve replacement, thus managed medically. Upon clinical improvement and completed endocarditis treatment, patient was discharged, however, lost to follow up. CASE PRESENTATION

The patient likely had an underlying non- ischemic methamphetamine-induced dilated cardiomyopathy with a component of peripartum cardiomyopathy which is supported by her initial decreased LV EF of 35%. She concomitantly also had an acute tricuspid infective endocarditis with subsequent chordae tendinae rupture that then lead to a severely reduced right ventricular function. The combination of both, the decreased LV EF and reduced right ventricular function, in the setting of fluid overload due to physiological hemodynamic changes in pregnancy and her severe hypoalbuminemia that lead to the rapid biventricular heart failure with a LV EF of <15%. proapoptotic effects. While methamphetamine induced cardiac injury mechanisms are better understood and include coronary vasospasm, ischemia, mitochondrial injury and/or direct toxic effects of the drug. Chronic use of the drug leads to myocardial fibrosis and dilated cardiomyopathy. References: 1. Rodriguez ZiccardiM, SiddiqueMS. Peripartum Cardiomyopathy. [Updated 2019 Jan 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2018 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482185 2. Sliwa K, SkudickyD, Bergemann A, Candy G, Puren A, Sareli P. Peripartum cardiomyopathy:Analysisof clinicaloutcome, left ventricular function,plasma levelsof cytokinesand Fas/APO-1.J Am Coll Cardiol.2000;35:701–5.[ PubMed ]) 3. Won, S., et al., Methamphetamine-associatedcardiomyopathy.ClinCardiol,2013. 36: p. 737-42.) 4. Hussain, S. T., Witten, J., Shrestha, N. K., Blackstone,E. H., & Pettersson, G. B. (2017). Tricuspidvalve endocarditis. Annalsof cardiothoracic surgery , 6 (3), 255-261. 5. Soma-Pillay,P., Catherine, N.-P., Tolppanen,H., Mebazaa, A., Tolppanen,H., & Mebazaa, A. (2016). Physiologicalchanges inpregnancy. Cardiovascular Journal of Africa , 27 (2), 89–94. http://doi.org/10.5830/CVJA-2016-021 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4928162/ 6. Kaye, S. and McKetin,R. (2005) Cardiotoxicityassociatedwith methamphetamineuse and signsof cardiovascularpathology amongmethamphetamineusers , Sydney: NationalDrug and Alcohol ResearchCentre. CONCLUSION Peripartum cardiomyopathy often develops rapidly in last trimester of pregnancy or within 6 months of delivery. Although no specific causative factors have been identified for peri-partum cardiomyopathy, it has been hypothesized that it may be secondary to oxidative stress that causes the myocytes to release a protein that cleaves prolactin, a pregnancy hormone, into smaller fragments that possess angiostatic and

Neck: Jugular Venous Distension: Paradoxical increase in JVP upon inspiration (Kassmaul’s Sign), Severe “V”wave Cardiac: 4/6 Holosystolic murmur at lower left sternum, however, murmur

Lung: Decreased breath sounds bilaterally, crackles heard throughout all lung lobes. Extremities: >3+ Pitting edema extending to the hips bilaterally.

Figure 1

HR 119 Vitals

Trop < 0.05

Cardiac

BNP 1793

Albumin 1.7

Figure 1: Yellow arrow pinpoints pulmonary opacity, likely the septic emboli. Purple arrow labels the pleural effusion.

auscultated throughout. Palpable thrill.

Tender to palpation

Figure 3

Figure 2

Figure 2: Yellow arrow identifies TV vegetation. Figure 3: Illustrates moderate tricuspid regurgitation.

Figure 4

Figure 5

Figure 4 and 5 have yellow arrows labeling the ruptured chordae tendineae.

Figure 6

Figure 7

Figure 6 and 7 depict the severe tricuspid regurgitation in the setting of the ruptured chordae tendineae. LV EF 10-15%.

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