CARDIAC ADVERSE EVENTS AFTER VACCINATION-A SYSTEMATIC REVIEW

Background: Myocarditis and pericarditis can present as mild to life-threatening inflammatory symptoms involving the heart. This has been associated with several drugs and vaccines. We present adverse cardiac events reported after vaccination. Methods: A systematic review of the literature using Medline, Embase, Cochrane, and Scopus was performed to identify cases of adults who developed adverse cardiac events after vaccination from inception through July 2021. Data is reported using descriptive statistics. Results: There were 33 studies describing adverse cardiac events after vaccination with a total of 270 patients. The majority described adverse cardiac events following smallpox vaccine administration, followed by COVID-19 vaccination (12.96%), influenza vaccination (2.59%), tetanus vaccination (0.74%), and pneumococcal vaccination (0.74%). Approximately 85% of cases were male, and 96% of the patients were younger than 65 years old. From the cardiac events, 63.3% described were myocarditis, 13.33% were myopericarditis, 6.66% were acute coronary syndrome, 2.96% were pericarditis and 0.70% developed a pericardial effusion. Troponin levels were elevated in 68.2% of patients. Most developed cardiac events seven days post vaccination and 23.49% developed symptoms within seven days. Management was not described in the majority of the reports. In the cases where treatment was described anti-inflammatory medications were used in 56.09%, colchicine was used in 41.46% and steroids were used in 19.51% of patients. One patient required extra-corporeal membrane oxygenation. All patients recovered except one mortality with smallpox vaccine where biopsy showed eosinophilic epicardial inflammation on autopsy. Conclusion: Adverse cardiac events after vaccination have been reported with different vaccines. Management varies for these patients. These events are rare, and unlikely to be fatal.

Respiratory symptoms of the 2019 novel coronavirus when the source of the symptoms is intra-cardiac thrombus not the pneumonia

Case Report The 2019 Novel Coronavirus (COVID-19) is currently causing a global pandemic. Common symptoms are fever, cough, myalgia, fatigue, headache, dyspnea, sore throat, vomiting, and diarrhea. Patients may present with end-organ failure, ARDS, shock, acute kidney injury, or even death. We present a case of COVID-19 with shortness of breath caused by an intra-cardiac thrombus. Case presentation An 84-year-old woman with COPD and diastolic heart failure presented with shortness of breath. She had hypoxemia on room air upon presentation. Lungs were clear on physical examination. COVID-19 PCR was positive. Her chest radiograph demonstrated no pulmonary infiltrates. Transthoracic echocardiography (TTE) demonstrated a large, irregularly shaped echogenic mass in both the right atrium and right ventricle consistent with a large thrombus. The mass in the right atrium was 3.9∗3.6 cm;the portion in the ventricle was 3.2∗2.2 cm. A previous TTE study in this patient did not reveal an intra-cardiac thrombus. No deep venous thrombosis was found. She was begun on anticoagulation and refused catheter-directed therapy. She improved and was discharged to her home. Discussion Thromboembolic complications of COVID-19 have been described in the literature. The most common are deep venous thrombosis and pulmonary embolism in critically ill patients despite the use of prophylactic anticoagulation. Several studies have reported post-mortem biopsies with widespread microthrombi. Arterial thrombosis with stroke and limb ischemia has also been described. Our case had an unusual presentation since the cause of her shortness of breath was the intra-cardiac thrombus. The pathogenesis beyond the hypercoagulability in COVID is not well understood. Some studies propose direct endothelial injury by the COVID-19 virus, causing microvascular inflammation, endothelial exocytosis, and endothelitis. Some experts propose a hypercoagulable state in COVID-19 patients based on elevated factor VIII, elevated fibrinogen, circulating prothrombotic microparticles, and neutrophil extracellular traps (NETs). Yet, no definitive mechanism has been identified. (Figure Presented).

Takotsubo cardiomyopathy due to hemophagocytic lymphohistocytosis secondary to COVID-19 pneumonia

Case Report Hemophagocytic lymphohistiocytosis (HLH) is a potentially fatal disease characterized by excessive immune response and cytopenia. Severe COVID-19 infection induces a life-threatening inflammatory syndrome associated with intense cytokine release that similar to HLH. We present a patient who developed takotsubo cardiomyopathy due to HLH. Case 24-year olrd man with a past medical history of obesity was admitted at the medical intensive care unit (MICU) due to acute respiratory distress syndrome secondary to COVID- 19 pneumonia. During the MICU stay, the patient required a high dose of vasopressors and ventilatory support. For Covid management, the patient received tocilizumab, high dose steroids (20 mg daily of dexamethasone), and empiric antibiotic coverage with vancomycin and cefepime. On day six of MICU admission, the patient developed hypertriglyceridemia (TGL) that was initially thought to be secondary to propofol, but after discontinuing propofol the patient continued to have increasing TGL levels. On day 8 of MICU admission, the suspicion of HLH increased, HSscore was calculated, and the patient had a 70-80% probability of having HLH (181 points: Temperature of 103 °F, ferritin 2580 ng/ml, TGL:771 mg/dl, Fibrinogen 220 mg/dl, AST:116 u/L). On day 10 of MICU admission, troponins increased from 7.5 to 2,966 ng/L, telemetry showed diffuse ST elevations, but ECG did not show any ischemic changes. At that time, his clinical parameters included HR: 96 bpm, BP: 92/42 mmHg, O2 Sat:93% on mechanical ventilation with pressure support FIO2: 100%, Hb: 11.6 g/dl, WBC:10.36 k/dl, Plt: 210 k/dl. Acute stress cardiomyopathy secondary to HLH was suspected. Transthoracic echocardiogram demonstrated preserved ejection fraction and inferoapical akinesia consistan as takotsubo cardiomyopathy. On day 11 of MICU admission, the patient had a cardiac arrest and after 30 minutes of cardiopulmonary resuscitation no return of spontaneous circulation was achieved. Discussion HLH induces a cytokine cascade that causes an excessive inflammatory response and multi-organ dysfunction that can be secondary to infections such as Covid-19. Takotsubo cardiomyopathy also known as stress cardiomyopathy, is a reversible dysfunction characterized by acute hypokinesia/ akinesia of the apical and middle segments of the left ventricle that extends beyond a unique coronary territory. We conclude that the trigger for takotsubo cardiomyopathy in this case was related to excess catecholamine release secondary to HLH.

Thrombus or vegetation? The importance of following the duke criteria for infective endocarditis before proceeding with advanced cardiac imaging

Case Report We present a case of a middle-age male who based on the Duke criteria (DC), we were able to rule out infective endocarditis (IE) before proceeding with advanced imaging. Case We present a case of a 51-year-old man with past medical history of heroin and cocaine use disorder, that was admitted to the intensive care unit (ICU) becouse COVID-19 pneumonia. On day 1 of admission, transthoracic echocardiogram (TTE) showed moderate tricuspid regurgitation. In the ICU, blood cultures (BC) were positive for Staphylococcus coagulase-negative species, patient received a course of vancomycin for 7 days. On day 17, the patient had repeat TTE, which showed new nodular thickening of the tricuspid valve associated with tricuspid regurgitation. BC were sent that same day, and they grew out Staphylococcus coagulase-negative species. At that time, it was not clear if new tricuspid valve findings were secondary to vegetation or a thrombus. The DC for infective endocarditis was applied to determine whether the findings on the TTE were due to IE. Major criteria include positive blood cultures and findings of vascular vegetation on echocardiography. After analyzing the BC and meeting with the microbiology personnel, it was found that the Staphylococcus coagulase-negative species found were different from each other. However, there was a possible vegetation present, shown on echocardiography. The patient had predisposing heart condition of tricuspid regurgitation and a history of IV drug abuse. Fever was absent. As for vascular phenomena, the patient did not have skin changes and no pulmonary embolism was found following chest CT protocol. As for immunologic phenomena, the patient did not have Roth spots or glomerulonephritis. Lastly, for microbiological evidence, the patient's blood cultures were possibly positive due to contamination. Based on the DC the patient had a possible diagnosis of IC but it was rejected because a patient had a firm alternative diagnosis, mainly a ventricular thrombus. The patient received anticoagulation treatment for thrombus, and he was discharged on his 24th day of hospitalization without complications. Discussion The diagnosis of IE remains difficult due to low specificity of the laboratory and imaging tests. Our patient had all the risk factors to believe it was endocarditis instead of a thrombus. Based on the DC, endocarditis was ruled out and the patient responded well to anticoagulation. More studies are needed to clarify the utility of the DC as a method to differentiate IE from thrombus before proceeding with advanced imaging.

Therapeutic challenges in treating a newly diagnosed aplastic anemia in a patient with coexistent COVID-19 infection

Introduction Aplastic anemia is a syndrome of bone marrow failure characterized bone marrow hypoplasia. Immunosuppressive therapy is one modality of its management. We report a case in which use of this modality was hindered by lack of data showing the effects of its use during the novel COVID- 19 infection. Case presentation A 20-year-old man with a newly diagnosed pancytopenia presented with fever, cough, headaches, and exertional dyspnea. When his vital signs were obtained, he was afebrile but his blood pressure, heart rate and oxygen saturation were within normal range. Physical exam was unremarkable. Laboratory tests showed that the white blood cell count was 1.42 K/mL, hemoglobin level was 9.7 g/dl, and platelet count was 13 K/mL. He was tested for COVID-19 infection and was found to be positive. A peripheral blood smear showed pancytopenia. A bone marrow biopsy showed hypocellular marrow with trilineage hypoplasia. Flow cytometry showed no significant trilineage abnormalities. Vitamin 12 and folate levels were within normal range. Testing for antinuclear antibodies, rheumatoid factor, HIV, hepatitis C, and hepatitis B were negative. Ultrasound of the abdomen showed no enlargement of the spleen. The PNH FLAER test was done twice and was inconclusive possibly due to hemolysis or severe pancytopenia. The patient was diagnosed with aplastic anemia, but the cause was unclear. Anti-thymocyte globulin, cyclosporine, and steroids were considered for treating the aplastic anemia, but there was concern about their unknown effect on his active COVID-19 infection. Immunosuppressive therapy was decided to be held until he was cured from his COVID-19 infection, and he was discharged after his blood cell indices improved. Discussion Being an infection caused by a novel virus, COVID 19 can cause a therapeutic dilemma when no data are available about the effects of certain therapies on the infection. In our patient, immunosuppressive therapy was needed to treat the aplastic anemia but there was no published literature on the effect of this treatment on the course of the infection. This should become less of an issue with time as data surrounding COVID-19 infection and its effects on other diseases and treatment modalities grow.

COVID-19 causing myoglobinuria requiring hemodialysis in young adult

Introduction Cases of rhabdomyolysis causing myoglobinuria in post-COVID-19 patients have been seen occasionally, and exact mechanisms behind this seem multi-factorial. Some patients have severe myoglobinuria with highly elevated creatinine phosphokinase levels requiring urgent hemodialysis to keep creatinine and blood urea nitrogen levels under control and protect the kidneys from long-term damage. Case presentation We present a case of a 24-year-old man with autism who was admitted to the hospital for COVID-19 viral pneumonia and discharged without major complications. After 3 weeks, he came to the ER with a decreased mental status and asterixis, and labs indicated creatinine had increased from baseline 0.7 mg/dl to 2.9 mg/dl and eventually increased to 6.4 mg/dl despite IV hydration. Creatinine phosphokinase was ordered, and it was 289,500 mcg/L. The patient likely suffered acute tubular necrosis secondary to rhabdomyolysis. Urgent hemodialysis was initiated, and the patient showed clinical improvement after one week and was taken off dialysis in 2 weeks. During an outpatient Nephrology clinic visit, the creatinine level was close to baseline level at 0.9 mg/dl, and the patient was asymptomatic. Discussion Different viruses have been described to cause myositis and rhabdomyolysis. The list is long but not limited to influenza A and B, coxsackie, Epstein-Barr, herpes simplex, parainfluenza, adenovirus, cytomegalovirus, measles, varicellazoster, human immunodeficiency, and dengue. In addition, reports about myoglobinuria post-COVID-19 infection have been emerging. The mechanism is unclear, but one theory suggests muscular necrosis from the direct viral invasion of myocytes, and another one suggests a toxic effect on myocytes by the host response, i.e., cytokine release and other immunological factors. Hence, early clinical recognition of this entity can be lifesaving in some cases.

Post-immunization multisystemic inflammatory response in non-COVID patient

Case Report Moderna vaccine postvaccination symptoms include local and systemic reactions. Local side effects include pain after injection, erythema, induration, tenderness, and lymphadenopathy. Systemic reactions include fever, headache, fatigue, myalgia, arthralgia, nausea/vomiting, or chills. We describe a case of severe postvaccination symptoms that occurred after administration of Moderna vaccine in an individual with no prior history of COVID infection. Case 73-year-old male with a past medical history of diabetes, atrial fibrillation, hypertension, and hyperlipidemia presented to the Emergency Department secondary to an elevated white blood cell count (WBC). Patient started with weakness, low appetite, fever, chills, and headaches 2 days after receiving the Moderna vaccine. COVID-19 antigen and PCR test were negative. He was hemodynamically stable and afebrile. Laboratories showed WBC of 35.16 K/μL, sodium of 120 mmol/L, alanine transaminase of 84 IU/L, and aspartate transaminase of 116 IU/L. The patient denied having unintentional weight loss, fever, adenopathy, rash, pruritus, new medications, or recent infection. Chest x-ray did not show pleural effusion, consolidation or pneumothorax. Patient was started on broad spectrum antibiotics, and on hypertonic saline, fluid restriction and desmopressin for severe hyponatremia. Liver ultrasound ruled out cirrhosis;his hepatitis panel was negative. Peripheral blood smear showed normocytic anemia, neutrophilia, monocytosis, lymphopenia, and thrombocytosis. Workup for myeloproliferative process including Jak2, CALR, MPL, BCR -ABL, was negative. No bone marrow biopsy was performed as the smear results were considered a reactive process. Blood and urine cultures were negative. The patient was briefly transferred to ICU secondary to worsening hyponatremia, decreased mental status, and acute kidney injury (AKI). He developed erythematous non-pruritic rash on his arms and upper chest on day 13 which resolved after oral antihistamines. Transaminitis, hyponatremia, and AKI resolved, and patient was discharged 18 days later with WBC of 14.42 K/μL. Discussion Post-immunization side effects have been widely described after COVID vaccination. A new entity called adult multisystem inflammatory syndrome (MIS-A) which includes some of those symptoms has been described. Diagnostic criteria include severe illness requiring hospitalization in a person ≥ 21 years, positive COVID test during admission or in the previous 12 weeks, extrapulmonary organ system dysfunction, severe inflammation on laboratory test, and absence of severe respiratory illness. Our patient had characteristics consistent with MIS-A, except for negative COVID test. To our knowledge, there is only one reported case of multisystemic inflammatory syndrome associated with vaccine. Although MIS-A criteria establish that a patient must have a positive COVID test, it is worthwhile examining if there is any role of the vaccination per se on its presentation.

A case of dvt and pe and cardiac arrest in a patient with factor v leiden mutation and covid

Introduction Heterozygous Factor V Leiden (FVL) mutation is the most common inherited thrombophilia, most common in people of Northern European descent and in some Middle Eastern population. It increases risk of developing a deep venous thrombosis (DVT) by 5-to 7-fold, and is considered a weak risk factor, and most people never develop blood clots. Case report 19-year-old woman presented with left lower quadrant abdominal pain, left groin pain, chest tightness and shortness of breath that had started 1 week prior to presentation. Patient had tested positive for COVID-19 six months but had only minor symptoms and recovered without needing treatment. She had completed 2nd dose of Moderna Covid vaccine two weeks ago and had been using oral contraceptive pills (OCP) for two years. Family history was significant for a paternal uncle with history of blood clots. Physical exam revealed swelling and erythema in left lower extremity up to groin area. Doppler ultrasound showed an acute DVT in the left external iliac vein, common femoral vein, deep femoral vein, superficial femoral vein, and proximal popliteal vein. Spiral computed tomography imaging of chest showed pulmonary emboli (PE) in the segmental branches of the pulmonary arteries with mild dilation of the right ventricle. Cardiac echogram (TTE) showed intact right ventricular function. Patient underwent mechanical aspiration thrombectomy with extirpation of DVT, but the procedure was complicated by PEA arrest requiring CPR for about 50-60 mins. During episode, bedside TTE showed evidence of right ventricular dilation and RV strain concerning for a massive PE. She was cannulated for V-A ECMO then underwent therapeutic hypothermia, and was successfully decannulated after six days. Patient eventually recovered and was neurologically intact. She was discharged home on warfarin and aspirin. Hypercoagulable work-up was remarkable for heterozygous FVL mutation R506Q. Both her father and mother were found to have heterozygous FVL mutation and her sister was found to have homozygous FVL mutation. Discussion People with FVL have additional risk factors that contribute to the development of DVT, and FVL alone does not increase the risk of developing arterial thrombosis, heart attacks and strokes. DVTs in heterozygous FVL population are considered provoked DVTs requiring anti-coagulation for a definite period, like that in general population. Curiously, patients with severe COVID-19 infection requiring ventilator support were found to have factor V levels high above the normal reference range and were found to have elevated risk for blood clots. Use of OCPs, and perhaps a recent COVID infection, although mostly asymptomatic, might have contributed to hypercoagulability in our patient. FVL mutation is not considered a contraindication to having COVID vaccination and patients with hereditary clotting disorders are recommended to have the vaccine.

Pulmonary cryptococcosis in the 2019 novel coronavirus, when the coinfection affects the mortality

Introduction: The 2019 Novel Coronavirus (COVID-19) is currently causing a pandemic all over the world. Many patients suffer from respiratory syndromes, including acute respiratory distress syndrome (ARDS). Coinfection with fungi is rare in these fragile patients but does increase the mortality risk in them. We present a case of COVID-19 who presented with shortness of breath and was found to have associated pulmonary cryptococcosis.Case presentation: A 78-year-old woman with hypertension and diabetes mellitus was transferred to our hospital with an upper GI bleed. Initially, she presented to another hospital after she was tested positive for COVID-19 and subsequently admitted due to shortness of breath. She was transferred to our critical care unit for a higher level of care after reporting melena and having a hemoglobin drop. She was in respiratory distress when admitted and was intubated. A culture from a deep tracheal aspirate grew Cryptococcus neoformans on admission. Cryptococcal antigen in her blood was negative. The patient was started on fluconazole. More history from her family indicated that she was immunocompetent with no chronic corticosteroid therapy or HIV. Lumbar puncture was done and showed an opening pressure of 34 cm H2O with 25 RBCs/mm3 and 5 WBCs/mm3, but it was performed after she received fluconazole for several days. The patient died with ARDS. Discussion: Cryptococcosis is a potentially life-threatening fungal infection usually caused by inhalation of C. neoformans or C. gatti spores. Severe cryptococcal disease occurs in immunocompromised patients but can also occur in immunocompetent adults. The association between fungal infection and COVID-19 has been reported with Aspergillus species. Yet, few reports are available about coinfection with Cryptococcus species and COVID-19. Considering that COVID-19 causes ARDS, coinfection with Cryptococcus species almost certainly increases inflammation in the lung and the risk for poor outcomes. Since corticosteroids are a necessary treatment in COVID-19 with respiratory symptoms and hypoxemia, initiating them in patients with cryptococcal infection should be closely monitored for the possibility of dissemination. Clinicians should obtain cultures for Cryptococcus species from blood and the central nervous system in COVID-19 patients with pulmonary cryptococcosis and balance the need for corticosteroids with the risk of cryptococcal dissemination.