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Noteworthy sequelae after COVID-19 pneumonia in a patient with heart failure due to cardiomyopathy

Published:December 22, 2022DOI:https://doi.org/10.1016/j.jccase.2022.12.006

      Abstract

      Coronavirus disease 2019 (COVID-19) is endemic worldwide. Cardiovascular disease, particularly myocarditis, is one of the most common comorbidities in patients with COVID-19. However, heart failure due to COVID-19-triggered cardiomyopathy is not well understood. Additionally, “pseudo” heart failure symptoms have been reported in patients with a compensated condition, in which the heart works well enough that symptoms are unnoticeable or very easy to manage. Here, we report a case of heart failure due to cardiomyopathy in a patient with COVID-19 and postural orthostatic tachycardia syndrome after heart failure treatment.

      Learning objective

      Postural orthostatic tachycardia syndrome (POTS) symptoms after coronavirus disease 2019 may be mistaken for heart failure symptoms; thus, it is essential to suspect POTS when symptoms such as shortness of breath and palpitations are noted upon standing, along with the relevant physical findings.

      Keywords

      Introduction

      Coronavirus disease 2019 (COVID-19) is endemic worldwide. Cardiovascular disease is one of the most common comorbidities in patients with COVID-19. In some cases, heart failure is exacerbated by COVID-19 pneumonia. The typical symptoms of heart failure are shortness of breath on exertion and edema. However, the signs of heart failure are sometimes difficult to distinguish among the sequelae of COVID-19, which some patients may experience following COVID-19. Nevertheless, some COVID-19 “long haulers” may actually have a condition known as postural orthostatic tachycardia syndrome (POTS). Here, we report the case of a patient with new-onset POTS following COVID-19 pneumonia after treatment for heart failure.

      Case report

      A 34-year-old male patient with a history of hypertension and sleep apnea syndrome developed a cough. The patient was diagnosed with COVID-19 pneumonia, which worsened, and was admitted to the emergency department. Echocardiography initially revealed a low left ventricular ejection fraction (LVEF) of 24 % (Video 1). Subsequently, 2–3 weeks after being diagnosed with COVID-19 pneumonia, the patient was further examined and treated for heart failure.
      Cardiac catheterization revealed no significant coronary artery stenosis. Cardiac magnetic resonance imaging (MRI) and endomyocardial biopsy were performed to assess possible myocarditis (Fig. 1). These tests and others did not show any findings indicative of myocarditis, hypertrophic cardiomyopathy, sarcoidosis, or amyloidosis as possible heart failure causes.
      Fig. 1
      Fig. 1Diagnosis of cardiomyopathy. Histological images show no inflammation on hematoxylin and eosin staining (A) and slightly fibrous collagen on Masson's trichrome staining (B).
      The patient had been previously diagnosed with cardiomegaly based on a physical examination. Thus, we diagnosed decompensation of the original cardiomyopathy due to COVID-19.
      After receiving medical therapy for a month, including oral administration of 25 mg spironolactone, 5 mg bisoprolol, 5 mg enalapril, and 20 mg furosemide and cardiac rehabilitation, the patient's walking distance increased, and shortness of breath on exertion disappeared.
      Fig. 2
      Fig. 2Results of an orthostatic test for diagnosing postural orthostatic tachycardia syndrome. In the orthostatic test, there was an increase in heart rate (HR) of 33 bpm without orthostatic hypotension. At the same time, the patient complained of intermittent palpitations and dyspnea in the standing position.
      Fig. 3
      Fig. 3Result of the orthostatic test after ivabradine administration. After ivabradine administration, there was no significant increase in heart rate (HR) or subjective symptoms such as palpitations or dyspnea in the orthostatic test.
      After discharge, the patient's heart failure appeared to improve, LVEF recovered (Video 2), and N-terminal-pro-brain natriuretic peptide level decreased from 3685 pg/mL to 332 pg/mL. However, fatigue, feeling unwell, intermittent palpitation, and dyspnea persisted upon getting up from the sitting position. The result of an orthostatic dysregulation test showed an increase in heart rate (HR) from 77 bpm in the supine position to 110 bpm in the absence of hypotension during 10-min standing (Fig. 2). These results met the POTS criteria. Because the patient was already on a maximum dose of beta-blockers for heart failure treatment, concomitant oral ivabradine of 5 mg was administered daily to manage this positional change in HR. In an orthostatic dysregulation test performed after ivabradine administration, no significant increase in HR and subjective symptoms, such as palpitations or dyspnea, were noted (Fig. 3). No such symptoms were subsequently observed, and the patient's progress was good.

      Discussion

      Here, the patient had worsened heart failure after COVID-19 pneumonia, and myocarditis was one cause of heart failure worsening after COVID-19. Since the COVID-19 pandemic outbreak, many cases of myocarditis in patients with COVID-19 have been reported [
      • Ashok V.
      • Loke W.I.
      Case report: high-grade atrioventricular block in suspected COVID-19 myocarditis.
      ].
      In this case, to determine the cause of heart failure, we first thoroughly investigated myocarditis and performed cardiac catheterization, cardiac MRI, and endomyocardial biopsy. None of them showed any significant findings that indicated myocarditis. Since the patient had been previously diagnosed with cardiomegaly based on a physical examination, we concluded that the original cardiomyopathy was complicated and exacerbated by COVID-19.
      Despite the successful treatment of heart failure exacerbated by COVID-19 pneumonia, the patient continued to have unpleasant symptoms in the standing position. Based on the patient's symptoms, POTS was suspected to be the cause. POTS is a type of autonomic neuropathy whose characteristic symptom is excessive HR elevation when switching to the standing position. The exact etiology of POTS is unknown, although it can be caused by viral infections, vaccine ingestion, trauma, pregnancy, surgery, some medications, or psychosocial stress [
      • Arnold A.C.
      • Ng J.
      • Raj S.R.
      Postural tachycardia syndrome – diagnosis, physiology, and prognosis.
      ]. It presents with palpitations, dyspnea, and other signs and symptoms, which resemble those of heart failure. Head-up tilt and orthostatic tests are effective for diagnosing POTS. In these tests, after 10 min in the supine position, an HR increase ≥30/min develops within 10 min of the patient's standing in the upright position, with no blood pressure drop. The symptoms worsened and were reduced in the standing and supine positions, respectively, and no other cause of tachycardia was observed. In our case, the patient had HR elevated by >30/min without a decreased blood pressure and a complaint of mood discomfort during the orthostatic test. Following POTS diagnosis, treatment with ivabradine effectively improved the patient's symptoms by significantly reducing the orthostatic HR increase response. Medications used to lower heart rates, such as beta-blockers and calcium-channel blockers, concurrently lower blood pressure and can limit their use. Ivabradine is a specific cardio-selective agent that inhibits the I-funny channel of the sinoatrial node and lowers the HR without concurrently lowering blood pressure. This is the reason ivabradine results in fewer side effects. Previous reports on the benefits of ivabradine showed that it significantly reduced standing pulse rates and its changes in the ivabradine group compared with that in the placebo group. Furthermore, patients who took ivabradine reported significant improvements in physical and social functioning [
      • Taub P.R.
      • Zadourian A.
      • Lo H.C.
      • Ormiston C.K.
      • Golshan S.
      • Hsu J.C.
      Randomized trial of ivabradine in patients with hyperadrenergic postural orthostatic tachycardia syndrome.
      ]. Similarly, in this case, treatment with ivabradine-improved POTS and the patient's overall quality of life. Furthermore, it is speculated that this case was adrenergic POTS, based on the marked increase in both systolic blood pressure and HR upon standing in the orthostatic test. Originally, ivabradine alleviates the symptoms of POTS by lowering only the heart rate without lowering blood pressure. However, in this case, it is believed to have reduced the base blood pressure due to the decreasing systemic circulation associated with heart failure treatment. Long COVID-19 syndrome is prone to neurological manifestations such as POTS [
      • Buoite Stella A.
      • Furlanis G.
      • Frezza N.A.
      • Valentinotti R.
      • Ajcevic M.
      • Manganotti P.
      Autonomic dysfunction in post-COVID patients with and without neurological symptoms: a prospective multidomain observational study.
      ]. Five cases have been reported where alpha-synuclein deposition in nerve fibers, as noted in Parkinson's disease, was observed in skin biopsies of young people with POTS after COVID-19 infection, which would cause autonomic neuropathy [
      • Miglis M.G.
      • Seliger J.
      • Shaik R.
      • Gibbons C.H.
      A case series of cutaneous phosphorylated α-synuclein in long-COVID POTS.
      ].
      In conclusion, we report our experience with COVID-19-related decompensation in a case of pre-existing cardiomyopathy. The patient was diagnosed with POTS after compensation for heart failure exacerbated by COVID-19 and whose POTS symptoms improved with ivabradine administration. However, the symptoms of POTS after COVID-19 may be mistaken for heart failure symptoms; therefore, it is essential to suspect POTS based on symptoms such as shortness of breath upon standing, along with the accompanying related physical findings. In addition, ivabradine may be an effective treatment for chronic heart failure complicated by POTS.
      The following are the supplementary data related to this article.

      Declaration of competing interest

      S. Kuwata and M. Izumo are consultants for Abbott Medical, Japan. The other authors have no conflicts of interest to declare.

      Acknowledgments

      The authors are grateful to the associate editor for the comments provided, which significantly improved the manuscript's clarity.

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