ABSTRACT
CASE: We report a 50-year-old Caucasian female with a history of systemic lupus erythematosus (SLE) in remission and chronic kidney disease (CKD) stage 5. The patient presented with dyspnea on exertion and orthopnea for two weeks. Six weeks ago, she was diagnosed with COVID-19 after presenting to the ED for substernal chest pain, myalgias, and fatigue. During this admission, she denied any current joint pain, chest pain, or rashes. She denies a history of alcohol or illicit drug use. EKG in the ED showed T-wave inversions in lead I and aVL, stable from prior EKG. The brain natriuretic peptide level was elevated at 3,500 pg/ml. There was no transaminitis, and kidney function was at baseline. Chest x-ray showed pulmonary vascular congestion and cardiomegaly. A transthoracic echocardiogram showed a left ventricular ejection fraction of 15-20% with severe global hypokinesis. The patient had a full cardiomyopathy workup. We ruled out ischemic cardiomyopathy with a negative coronary angiogram. Non-ischemic cardiomyopathy (NICMO) workup was initiated, with a focus on viral or autoimmune myocarditis. While a cardiac MRI would have been the gold standard to assess for myocardial scarring, the patient's CKD status prohibited this possibility. Similarly, an endomyocardial biopsy was not performed due to its low sensitivity for diagnosing viral or autoimmune myocarditis. Without evidence of infiltrative disease, or other exposures, it was deemed that the patient's recent history of COVID-19 infection, in conjunction with underlying SLE, were the causes of her new-onset NICMO. The patient's dyspnea responded to intravenous bumetanide. We initiated guideline-directed medical therapy with carvedilol and isosorbide-dinitrate. She continues regular follow-up in the outpatient heart failure clinic. IMPACT/DISCUSSION: Classification and evaluation of NICMO can be broad, and thus the clinical picture plays an essential role in the workup. Acquired cardiomyopathy from prior myocarditis was the most likely etiology of our patient's new-onset NICMO. Our patient had no clinical symptoms of myocarditis prior to her exposure to COVID-19, making it unlikely that SLE was the sole driving factor. There is a known association between COVID-19 and myocarditis. A few proposed mechanisms for COVID-19 induced myocarditis include upregulation of cytokines, particularly interleukin-6, and downregulation of ACE2, leading to microvascular and cardiac pericyte dysfunction. Cytokine release from COVID-19 coupled with subclinical SLE could have acted synergistically to cause this patient's condition. Given the increasing incidence of COVID-19 infections, internists must consider COVID-19 exposures during the workup of new-onset heart failure. CONCLUSION: The workup for NICMO in the COVID-19 era must include detailed history taking for sick contacts and prior history of COVID-19 diagnosis. More research is needed to determine if COVID-19 infection can increase the risk of NICMO in patients with a known history of SLE.
ABSTRACT
Case Report A Rare Presentation of Multivessel Vasospastic Angina in the Setting of Septic Shock Background Prinzmetal or vasospastic angina is an unusual but important consideration when evaluating a patient with chest pain. Unlikely acute coronary syndromes (ACS) which primarily occur as a result of coronary artery occlusion, prinzmetal angina occurs angina occurs mainly as a result of coronary artery vasospasm. We present the unusual case of a patient who suffered cardiac arrest and was found to have >90% occlusion in multiple coronary arteries on a left heart catheterization (LHC) performed within 60 minutes. Case presentation Patient is a 70-year-old female who was initially being treated in the hospital for COVID-19. She spent a few days in the ICU due to requiring high flow nasal cannula but was transferred to the floor after she was weaned down to 3L/min via regular nasal cannula. On day of arrest, patient had increasing oxygen requirements and was on ventimask immediately prior to the code blue. Patient received 2 rounds of CPR and her initial rhythm was found to be ventricular fibrillation. Pt was defibrillated and ROSC was immediately achieved. EKG showed ST elevations in inferior leads. Patient was, however, alert and oriented x3 on initial evaluation by critical care team. She was not intubated after the arrest. She was transferred to the intensive care unit, given 300 mg intravenous amiodarone and therapeutic dose lovenox. On LHC, her left anterior descending artery (mid/ distal portion), distal diagonal vessel, left circumflex artery (mid portion), distal portion of the obtuse marginal and right coronary artery were found to be severely spasmodic. Patient had recurrence of angina after the catheterization which was transiently relieved with nitro. Patient had sustained relief of angina after starting nitro drip. Patient was also started on amiodarone drip upon transfer back to the ICU. Discussion The obvious side-effect of our therapeutic treatment was hypotension that was initially responsive to intravenous fluids. Patient, however, became hypoxic a few hours later and needed to be diuresed to return to baseline oxygen requirement. Patient was then started on norepinephrine drip with goal to maintain mean arterial pressure above 65. After patient was loaded with amiodarone, nitro drip was discontinued. She was then transitioned to oral amiodarone. She was started on isosorbide dinitrate prior discontinuing nitro drip. Patient's blood pressure stabilized as her per oral intake improved and norepinephrine drip soon thereafter. Novel presentations require novel treatment and creative thinking lead to the decision to continue nitro drip to keep her stable, even if it meant the simultaneous use of an anti-hypertensive and a pressor. It is possible that COVID-19 served as a trigger for such a global vasospasm event. Patient was restarted on her home medication of long-acting nitrates which were held on admission due to hypotension.
ABSTRACT
Introduction: As defined by MB-CPK, hsTn-I, MB, or EKG and/or cardiac echo abnormalities, cardiac injury (CI) determines a median survival time (MST) of 10 days for hospitalized COVID patients (HCPs). HCPs without defined CI have an MST beyond 39 days (Huang, et al., see Figure). Hypertension (HTN) presents in 17-41% of HCPs in various studies, with COVID mortality independent of HTN. Therefore, a randomized clinical trial (RCT) is proposed for HCPs with CI and incidental BP elevation to compare IV isosorbide dinitrate (ISDN) with usual anti-HTN care (UC). Vasodilatory ISDN lowers BP, and has been proposed an an anti-SARS-CoV-2 drug. Others report improved survival of ISDN treated Coxsackie B3 virus-infected mice as evidence for anti-viral activity. The endpoint for this CI RCT pilot of 100 ISDN-treat HCPs and 100 UC controls is mortality. Secondary endpoints are interval biomarkers to dissect ISDN anti-viral action. Methods: Log-rank analysis was performed with 1:1 allocation. Accrual time was 180 days with a 60-day follow-up. Power was 0.8 with a type I error of 0.05. Results: For 200 total subjects, an MST greater than 14.9 days in the ISDN arm was significant if UC stays at 10 days (see Figure). Conclusions: Testing repurposed ISDN as a COVID drug is feasible. A successful pilot with improved MST suggests ISDN has anti-SARS-CoV-2 action, since COVID mortality is independent of HTN. Biomarkers could include viral clearance, oxygenation, D-dimer, IL-6, LDH, as well as platelet and lymphocyte counts. The need to treat HCPs with elevated BP per guidelines permits study entry. Cross-over treatment occurs if a regimen fails. Immunomodulators and remdesivir are administered per COVID treatment guidelines for all HCPs. IV ISDN, bolused and/or infused, avoids 1 pass hepatic effects. IV IDSN is approved in most countries, but not in the USA or Canada. A successful pilot would permit larger IV ISDN RCTs as IND RCTs, and can serve as a template for other treatments for HCPs with defined CI.