Via Research Recognition Day 2024 VCOM-Carolinas

Clinical Case-Based Reports

A Form Fruste Presentation of Hypertrophic Cardiomyopathy Discovered by COVID-19 Infection: A Case Report Emily Ranta, OMS-III 1 , Chelsea McCoy, DO 2 1 - VCOM-Carolinas, Spartanburg, South Carolina 2- Newberry Country Memorial Hospital, Newbery, South Carolina

Abstract

Discussion

Case Report Continued

COVID-19 and Hypertrophic Cardiomyopathy (HOCM) HOCM is a well-documented condition causing a thickened heart muscle and affecting the interventricular septum with obstruction. It generally presents with chest pain, syncope, arrythmia, and shortness of breath. 2 In regard to COVID-19, literature suggests that 25% of patients with HOCM require hospitalization, with 6% requiring the ICU. 3 The reason for this has not been well-elucidated, but as seen in this case, perhaps it is related to autonomic dysfunction, which is a well-documented side effect of COVID-19. Autonomic Dysfunction and COVID-19 Numerous studies suggest that COVID-19 has a profound effect on the autonomic system, leading to the development of orthostatic intolerance syndromes. 4,5,6 This pathophysiology of this has been described as one high catecholamine levels causing paradoxical vasodilation resulting in vagus nerve stimulation causing hypotension, dizziness, and syncope. 4,5 One systematic review found that 54 articles involving 154 cases demonstrated the most common presentation of post-COVID autonomic dysfunction included orthostatic intolerance and syncope 5 , as was seen in this patient. Autonomic Dysfunction Effect on HOCM As HOCM worsens with decreased pre-load, COVID-19 induced autonomic dysfunction is a serious outcome that must be considered in patients with HOCM or LV outlet obstructions. In general, normal management for HOCM includes long-acting beta-blockers to decrease outlet obstructions, which should be utilized in cases such as this one. 7 This alone may not be enough, though, if the worsening symptoms are due to autonomic dysfunction, especially in COVID-19 cases. It is important to use the appropriate anti-viral medications, Remdesivir, as well as avoiding exacerbating factors such as diuretics. Additionally, other medications, including midodrine should be considered to increase venous return to the heart. 8 The case becomes more difficult though with more co-morbidities such as heart failure and thus, further research is needed to determine how to safely treat these patients.

Second Encounter Continued Given the severity of his symptoms, his renal function, and his chest x-ray findings, he was admitted for an acute COVID-19 induced pneumonia and an acute kidney injury. He was started on gentle IV fluids, dexamethasone, ceftriaxone, azithromycin, and remdesivir. During his stay, his renal function was fluid-responsive with his BUN and Cr down trending to 82 and 2.7 respectively but in several instances, he became volume overloaded so there was a delicate balance between fluids and diuretics. In contrast to his improving renal function, he continued to have severe shortness of breath, requiring up to 15 L of oxygen. Despite finishing his antivirals, a round of dual antibiotic coverage, and steroids his condition did not improve, and his chest x-ray remained unchanged if not worse from the original. Finding the Diagnosis Physical therapy was consulted, but he continued to have orthostatic syncopal and O 2 desaturation episodes. Thus, cardiology was brought in for further evaluation. An ECHO revealed hyperdynamic left ventricular systolic function with near cavity obliteration and moderate to severe concentric left ventricular hypertrophy ( Figures 3 and 4 ). With his symptoms and the ECHO findings, the cardiologist determined the patient had severe autonomic dysfunction induced by COVID causing a form fruste presentation of HOCM.

This case follows a patient who presented with shortness of breath and weakness who was found to have COVID-19 pneumonia that ultimately disrupted his autonomic system, rendering him incapable to standing without syncopal episodes. Failed consults with physical therapy led to further work-up including a cardiology consult and imaging. An echocardiogram (ECHO) revealed a left ventricular (LV) outlet obstruction, similar to that of hypertrophic cardiomyopathy (HOCM). He was subsequently started on additional medications including midodrine and metoprolol Succinate which aided in his recovery and discharge. Given the global prevalence of HOCM is .2% and the majority of patients are diagnosed in their teens or twenties, this case uniquely demonstrates how autonomic dysfunction can reveal undetected HOCM 1 . A literature review revealed several studies demonstrating COVID- 19’s association with autonomic changes in heart rate and orthostatic blood pressure, which were seen in this case. Recommendations for treatment include one used in case, midodrine. This is consistent with the symptoms seen in this study. The uniqueness of this case is the undetected LV outlet obstruction that was worsened by COVID-19 induced autonomic dysfunction. First Encounter This was a 78-year-old African American male with a past medical history of diabetes, hypertension, chronic kidney disease, and sarcoidosis who initially presented to the ED with SOB, cough, and weakness and was found to have COVID-19 and an AKI, with physical exam findings of rales in the lungs and a CMP revealing a Cr of 5.1 and a BUN of 103, significantly elevated from his baseline. He was treated with fluids, IV remdesivir and dexamethasone. His symptoms improved and he was switched to oral prednisone and discharged. Second Encounter After two days, he returned to the ED with worsening SOB, cough, and weakness, and an oxygen saturation of 80%. Laboratory values revealed poor renal function, with a Cr of 4.1 and BUN of 139. A chest x-ray revealed bilateral bibasilar opacities consistent with pneumonia ( Figure 1 ). At this point, an electrocardiogram was conducted which revealed sinus rhythm with non-specific T wave changes as seen in Figure 2 . Case Presentation

Figure 3 (right): Moderate to severe hypertrophy in apical 4 chamber view (yellow dashed lines)

References

Figure 4 (left): Moderate to severe hypertrophy in parasternal long axis view (red dashed lines)

Treatment and Outcome After these findings, offending pre-load reducing agents such as diuretics were discontinued and he was started on metoprolol succinate 50 mg, midodrine 5 mg BID, and oral prednisone 40 mg. His oxygen requirements slowly decreased from 15 L to 8 L, but he continued to have some syncopal episodes, so his midodrine was increased to TID. With this change, he began working with physical therapy, ambulating 100 ft while stable on 4 L of oxygen, and having no syncopal episodes. His labs, including his renal function, continued to improve with his last BUN and Cr before discharge at 31 and 1.6, respectively. He was ultimately discharged to a rehabilitation facility with the above new medications.

Please scan the QR code to the right for references used in the poster.

The authors of this case report would like to thank the patient and Newberry County Memorial Hospital for their contribution to this case.

Figure 2: Sinus rhythm with 1 st degree heart block. Nonspecific T wave changes

Figure 1: Bilateral bibasilar opacities

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2024 Research Recognition Day