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Objectives: Cases of fulminant myocarditis after mRNA COVID-19 vaccination have been reported. The most severe may need venoarterial extracorporeal membrane oxygenation (V-A ECMO) support. Here we report two cases successfully rescued with V-A ECMO. Method(s): We included all the cases supported with V-A ECMO for refractory cardiogenic shock due to myocarditis secondary to a mRNA SARS-COV2 vaccine in the high-volume adult ECMO Program in Vall Hebron University Hospital since January 2020. Result(s): We identified two cases (table). One of them was admitted for out-of-hospital cardiac arrest. In both, a peripheral V-A ECMO was implanted in the cath lab. An intra-aortic balloon pump was needed in one case for left ventricle unloading. Support could be successfully withdrawn in a mean of five days. No major bleeding or thrombosis complications occurred. Definite microscopic diagnosis could be reached in one case (Image, 3). Treatment was the same, using 1000mg of methylprednisolone/day for 3 days. A cardiac magnetic resonance 10 days after admission showed a significant improvement in systolic function and diffuse oedema and subepicardial contrast intake in different segments (Image, 1-2). Both patients were discharged fully recovered. Conclusion(s): V-A ECMO should be established in cases of COVID-19 vaccine-associated myocarditis with refractory cardiogenic shock during the acute phase. (Table Presented).
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Background: Eosinophilic myocarditis is a rare inflammatory cardiomyopathy with a poor prognosis. SARS-CoV-2 (COVID-19) illness has been associated with myocarditis, particularly of lymphocytic etiology. Although there have been cases of eosinophilic myocarditis associated with COVID-19 vaccination, there have been few reported cases secondary to COVID-19 illness, with the majority being diagnosed via post-mortem autopsy. Case: A 44-year-old woman with no significant medical history other than recent COVID-19 illness 6 weeks prior presented with progressive dyspnea. Patient developed acute dyspnea and diffuse pruritic rash after taking hydroxyzine. Labs were significant for mild eosinophilia. Echocardiography showed biventricular systolic dysfunction with left ventricular ejection fraction of 40%, and a moderate pericardial effusion that was drained percutaneously. She underwent left heart and right heart catheterization showing elevated biventricular filling pressures, Fick cardiac index of 1.6 L/min/m2, and no coronary disease. She was started on intravenous diuretics and transferred to our facility for further management. Her course was complicated by cardiogenic shock requiring intra-aortic balloon pump (IABP) support. Mixed venous saturations continued to decline and the patient was placed on veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support. The patient underwent endomyocardial biopsy (EMB) showing marked interstitial infiltration of eosinophils and macrophages with myocyte injury (see image). She was intubated with mechanical ventilation as well due to worsening pulmonary edema and hypoxemia. She was started on intravenous steroids with improvement of hemodynamics and myocardial function and eventually VA- ECMO was decannulated to low-dose inotropic support which in turn was ultimately weaned after 3 days of mechanical support. Conclusion(s): Eosinophilic myocarditis is a rare and under-recognized sequela of acute COVID-19 infection associated with high mortality rates. It requires prompt diagnosis and aggressive supportive care, including temporary mechanical circulatory support. There are few literature-reported cases of COVID-19 myocarditis requiring use of both IABP and VA-ECMO, none of which were used in biopsy-proven eosinophilic myocarditis, with most of these cases resulting in either fatal or unreported outcomes. Most cases of covid myocarditis required IV glucocorticoids therapy in conjunction with IVIG or interferon therapy. Here, we present a rare case of cardiogenic shock secondary to biopsy-proven eosinophilic myocarditis associated with recent COVID-19 illness with a survival outcome after temporary use of IABP and VA-ECMO support, as well as aggressive immunosuppressive therapy.Copyright © 2022
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Clinical Information Patient Initials or Identifier Number: SHS Relevant Clinical History and Physical Exam: Mr. SHS was admitted in August 2022 for acute decompensated heart failure secondary to NSTEMI, complicated with ventricular tachycardia (VT). CPR was performed for6 minutes on the day of admission and was subsequently transferred to the Cardiac Care Unit. His hospital stay was complicated with Covid-19 infection(category 2b) which he recovered well from. During admission, he developed recurrent episodes of angina. Physical examination was otherwise unremarkable. His ejection fraction was 45%. Relevant Catheterization Findings: Cardiac catheterization was performed, which revealed significant calcification of left and right coronary arteries. There was a left main stem bifurcation lesion (Medina 0,1,1) with subtotal occlusion over ostial the LAD, receiving collaterals from RCA and 90% stenosis over ostial LCx. RCA was dominant, heavily calcified with no significant stenosis. He was counselled for CABG (Syntex score26) but refused. As he was symptomatic, he was planned for PCI to the left coronary system. [Formula presented] [Formula presented] [Formula presented] Interventional Management Procedural Step: The left main was engaged with a 7F EBU 3.5guiding catheter via transradial approach. Sion Blue wired into LAD and LCx. IVUS catheter couldn't cross the LAD and LCx lesions, hence we decided for up front rotational atherectomy. Sion blue was exchanged to Rotawire with the assistance of Finecross microcatheter. A 1.5mm burr was used at 180000 rpm. After the first run of rotablation, patient developed chest pain and severe hypotension (BP ranging 50/30). 4 inotropes/vasopressors were commenced. The shock was refractory hence an intraarterial balloon pump was inserted. Symptoms and blood pressure improved. Another 2 runs of atherectomy done (patient developed hypotension after each run). IVUS examination then showed calcification of proximal to mid LAD with an IVUS Calcium score of 3. LAD was further predilated with Scoreflex balloon 3.0/20mm at 8-22ATM. LCx was predilated with Scoreflex balloon 2.0/15mm at 12-14ATM. DCB Sequent Please NEO2.0/30mm was deployed at 7ATM at ostial to proximal LCx. Proximal to mid LAD was stented with Promus ELITE 2.5/32mm at 11ATM, which was then post dilated with stent balloon at 11ATM. Ostial LM to proximal LAD (overlap) was stented with Promus ELITE 4.0/28mm at 11ATM. LMS POT was then done with NC Balloon 4.0/15mm at 24ATM. LCx was rewired and kissing balloon technique with NC balloon 4.0/15mm at 14ATM (LAD) and NC balloon 2.0/10mm at 12ATM (LCx) was done, followed by a final POT with NC balloon 4.0/15mm at 14ATM. Final IVUS showed good MSA. [Formula presented] [Formula presented] [Formula presented] Conclusion(s): This patient developed hemodynamic instability with each rotational atherectomy run, hence we decided not to perform rotablation to the circumflex artery. His hemodynamic condition improved with the use of intra aortic balloon pump. IABP use can reduce procedural event rate and potentially reduce long term mortality in appropriately selected patients who are at high risk of adverse events. He was followed up a month following the procedure and remained asymptomatic. For complex, calcified coronary lesions involving the left main stem, coronary artery bypass graft surgery is an alternative option.Copyright © 2023
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Background Graft versus host disease (GVHD) most often occurs 100-365 days after hematopoietic stem cell transplant (HSCT). Manifestations most often are dermatologic, hepatic or pulmonic, and are rarely cardiac. We present a unique case of GVHD inducing cardiogenic shock necessitating advanced heart failure therapies. Case This is a 34 year-old male with a history of acute lymphoblastic leukemia who completed chemoradiation and HSCT from an HLA perfect sibling in 1992. In May 2020, he presented with dyspnea for 6 weeks. An echocardiogram at that time showed an EF of 10% and severe biventricular dilatation. He was originally hospitalized at an outside institution for hypoxia where a left heart catheterization showed normal coronaries and goal directed therapy was initiated. After 2 negative COVID tests, he was discharged with a LifeVest. One month later, despite medication compliance, he returned in cardiogenic shock after his LifeVest was activated for ventricular tachycardia (VT). Decision-making He was started on inotropic therapy and an intra-aortic balloon pump (IABP) was placed 1:1 prior to transfer to our tertiary center. After support was started, a right heart catheterization showed a right atrial pressure of 13 mmHg, a wedge of 17, and a cardiac index of 2.6. His course was complicated by VT storm. Differentials for his non-ischemic cardiomyopathy (NICMO) included myocarditis (viral vs. giant cell) with a possible component of chemotherapy/radiation induced NICMO. Immediate AHFT work-up was started. He was unable to be weaned off his IABP or inotropic support. The decision was made to pursue emergent left ventricular assist device placement (LVAD) and achieve a definitive diagnosis with a core biopsy. Pathology resulted with myocyte hypertrophy, chronic inflammation with eosinophils concerning for chronic GVHD. Conclusion There have only been a handful of case reports describing cardiac manifestations of GVHD, and none with NICMO and cardiogenic shock requiring an LVAD. Despite this, suspicion should remain present for GVHD in HSCT patients regardless of time frame from oncologic therapies or specificity of HLA match when presenting in cardiogenic shock.Copyright © 2023 American College of Cardiology Foundation
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SESSION TITLE: COVID-19 Case Report Posters 3 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: The SARS-CoV-2 pandemic quickly spread throughout the world after it was first identified in Wuhan, China in 2019. Severe cases of hypoxic respiratory failure have since filled hospitals over the past few years. We present a case of an immunosuppressed patient with persistent respiratory failure from SARS-CoV-2, with a failure to mount antibody response, treated with convalescent plasma. CASE PRESENTATION: We present a 54-year-old female with a past medical history significant for rheumatoid arthritis on immunosuppression with methotrexate, prednisone, sulfasalazine, and rituximab who presented with diarrhea, cough, and shortness of breath. She was unvaccinated and tested positive for COVID-19 pneumonia, which was treated with corticosteroids and Remdesevir. CT thorax revealed diffuse infiltrates (Figure-1). She had progressive hypoxia requiring ICU stay and her course was complicated by inferior wall STEMI, requiring Intra-aortic balloon pump and intubation given worsening hypoxia. She had progressive improvement and was discharged from the hospital on 4 L of supplemental oxygen after a 30-day hospital stay. She presented two days after discharge with cough, fevers and increasing oxygen requirements up to 100% high flow nasal cannula. She was septic and was treated with steroids and antibiotics. She was febrile despite broad spectrum antibiotics. CT thorax demonstrated diffuse infiltrates worsened from the previous and steroid dosing was increased (Figure-2). No obvious source of infection was found, and further evaluation revealed positive Covid-19 RT-PCR. Despite her initial infection occurring two months prior, COVID-19 anti-spike and anti-nucleocapsid antibodies were negative. She was treated with two doses of convalescent plasma and had improvement in her oxygenation, going from 80% high-flow nasal cannula to 6L of supplemental oxygen within two days of administration. DISCUSSION: It's unclear whether immunosuppressed patients with rheumatologic disease are at an increased risk of severe SARS-CoV-2 infection. However, the use of immunosuppressants places patients at risk of an improper immune response to infection. In immunocompetent patients, the typical time to negative SARS-CoV-2 RT-PCR is 3 weeks after positivity (1), and most patients develop antibodies within 2-3 weeks after viral exposure (2). Anti-CD20 monoclonal antibodies like rituximab, commonly used for rheumatologic diseases, can hinder humoral immunity, and impair vaccine response (3). Given our patient's immunosuppressive regimen, we suspect she failed to mount an immune response to COVID-19, resulting in 56 days of infection without an adequate antibody response, successfully treated with convalescent plasma. CONCLUSIONS: Patients with significant immunosuppression regimens may fail to produce antibody responses to SARS-CoV-2, resulting in prolonged infection. Reference #1: Rodríguez-Grande, C., Adán-Jiménez, J., Catalán, P., Alcalá, L., Estévez, A., Muñoz, P., Pérez-Lago, L., de Viedma, D. G., Adán-Jiménez, J., Alcalá, L., Aldámiz, T., Alonso, R., Álvarez, B., Álvarez-Uría, A., Arias, A., Arroyo, L. A., Berenguer, J., Bermúdez, E., Bouza, E., … de la Villa, S. (2021). Inference of active viral replication in cases with sustained positive reverse transcription-PCR results for SARS-CoV-2. Journal of Clinical Microbiology, 59(2). https://doi.org/10.1128/JCM.02277-20 Reference #2: Boechat, J. L., Chora, I., Morais, A., & Delgado, L. (2021). The immune response to SARS-CoV-2 and COVID-19 immunopathology – Current perspectives. In Pulmonology (Vol. 27, Issue 5). https://doi.org/10.1016/j.pulmoe.2021.03.008 Reference #3: Eisenberg, R. A., Jawad, A. F., Boyer, J., Maurer, K., McDonald, K., Prak, E. T. L., & Sullivan, K. E. (2013). Rituximab-treated patients have a poor response to influenza vaccination. Journal of Clinical Immunology, 33(2). https://doi.org/10.1007/s10875-012-9813-x DISCLOSURES No relevant relationships by Issa Makki No relevant relationships by John Parent No relevant relationships by Jay Patel No relevant relationships by Ruchira Sengupta
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SESSION TITLE: The Cardiac Intensivist 2 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Hydroxychloroquine and chloroquine are medications derived from aminoquinoline. They are disease-modifying antirheumatic drugs used in the treatment of systemic lupus erythematosus (SLE). Although well tolerated, they do have side effects such as retinopathy, vacuolar myopathy, neuropathy, and as seen in our patient, cardiotoxicity. CASE PRESENTATION: Patient is a 48 year old female with a past medical history significant for chronic kidney disease secondary to autosomal dominant polycystic kidney disease, SLE on hydroxychloroquine who presented to the emergency department complaining of weakness. On arrival the patient was found to be in cardiogenic shock. Her transthoracic echocardiogram revealed a reduced ejection fraction of 37% and a large pericardial effusion concerning for tamponade physiology. Her COVID-19 PCR test was positive. She was taken for emergent pericardiocentesis which revealed 300cc of exudative fluid. Patient’s right heart catheterization revealed mean pulmonary capillary wedge pressure of 23 mmHg, pulmonary artery pressures of 44 mmHg/24 mmHg, mean 31mmHg, cardiac index 1.1L/min/m² by thermodilution, 1.7 L/min/m² by Fick. Following right heart catheterization and intra aortic balloon pump placement, the patient was admitted to the medical intensive care unit (MICU) and placed on intravenous inotropic and vasopressor support. Shortly after arrival to the MICU, patient had an increase in vasopressor requirements. Bedside ultrasound revealed cardiac tamponade. Patient had approximately 400cc of bloody pericardial fluid removed from her pericardial drain. The decision was made for emergent venoarterial extracorporeal membrane oxygenation (ECMO) to be initiated. Endomyocardial biopsy was performed which revealed vacuolization in the cytoplasm of several myocytes as well as lymphocytes in the interstitium of the endocardium. The vacuoles found in the cardiac myocytes were PAS positive. These biopsy results are consistent with hydroxychloroquine cardiotoxicity. The patient’s hydroxychloroquine was discontinued. In addition to hemodynamic support, she also received intravenous immunoglobuluin and systemic steroids. After a prolonged hospitalization she was successfully discharged. DISCUSSION: Cardiotoxicity is a rare adverse reaction seen with hydroxychloroquine. A 2018 systematic review revealed 127 cases of cardiac toxicity associated with the use of hydroxychloroquine or chloroquine. Most patients had been treated with the medication for a prolonged period of time and the toxicity is dose dependent. The mechanism behind hydroxychloroquine and chloroquine induced cardiomyopathy is believed to be secondary to lysosomal dysfunction as a result of toxic phospholipid accumulation in cardiomyocytes. CONCLUSIONS: In patients with new onset cardiomyopathy, a detailed medication reconciliation should be conducted to evaluate for toxins such as hydroxychloroquine and chloroquine. Reference #1: Della Porta, A., Bornstein, K., Coye, A., Montrief, T., Long, B., & Parris, M. A. (2020). Acute chloroquine and hydroxychloroquine toxicity: A review for emergency clinicians. The American Journal of Emergency Medicine. Reference #2: Abbi, B., Patel, S., Kumthekar, A., Schwartz, D., & Blanco, I. (2020). A Case of Cardiomyopathy With Long-term Hydroxychloroquine Use. JCR: Journal of Clinical Rheumatology, 26(8), e300. Reference #3: Chatre, C., Roubille, F., Vernhet, H., Jorgensen, C., & Pers, Y. M. (2018). Cardiac complications attributed to chloroquine and hydroxychloroquine: a systematic review of the literature. Drug safety, 41(10), 919-931. DISCLOSURES: no disclosure on file for Joseph Adams;no disclosure on file for Suliman Alradawi;No relevant relationships by George Kalapurakal No relevant relationships by Mohammed Siddiqui
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CASE: A 52-yo male with hypertension and former smoker was transferred from outside hospital with dyspnea and hemoptysis. He had presented with chest pain and abnormal ECG to an urgent care 2 days earlier but declined to visit the emergency room in fear of the pandemic. This time, he had respiratory distress requiring intubation and transfer to a higher level of care. He developed cardiogenic shock and profound refractory hypoxia. ECG showed sinus tachycardia, Q waves V1-V3. Chest X-ray had right-side pulmonary edema. An urgent transthoracic echocardiogram (TTE) revealed evidence of papillary muscle rupture (PMR) and LVEF of 65%. An emergent coronary angiogram showed multivessel disease, and a simultaneous transesophageal echocardiogram confirmed torrential mitral regurgitation and PMR. An intra-aortic balloon pump was placed. Patient then underwent urgent CABG/valve replacement and was discharged 10 days later. At 4-month follow-up patient was asymptomatic in clinic. IMPACT/DISCUSSION: Here we present a case of Non-ST-segment elevation myocardial infarction (NSTEMI) whose presentation was delayed due to fear on contracting COVID-19, resulting in papillary muscle rupture (PMR). Acute mitral regurgitation (MR) due to PMR is a life-threatening mechanical complication occurring in 3/1000 patients with myocardial infarction (MI) per year. Prepandemic studies showed that mechanical complications had decreased their incidence over time given the numerous advances in reperfusion therapies. The mortality of such complications remained elevated in numerous studies (4-fold higher than patients without mechanical complications), especially for patients presenting with late-STEMI. Mechanical complications are significantly less common in patients with NSTEMI, such as our patient. The COVID-19 pandemic marked a surge in delayed presentations of MI, resulting in rising incidence of complications worldwide. Certain studies have demonstrated that the pandemic itself is an independent risk factor for delayed presentations of acute coronary syndrome. Echocardiogram remains the diagnostic modality of choice with sensitivity of 65-85% to detect complications from MI, however high clinical suspicion is key to prompt early use of this imaging modality. Our case illustrates that awareness of delayed presentations amongst clinicians may grant early diagnosis and good outcomes. CONCLUSION: Mechanical complications with catastrophic presentations had decreased after the reperfusion treatment era, however the advent of the COVID-19 pandemic has raised concerns for an increasing incidence of delayed presentations of acute coronary events resulting in lethal complications. High clinical suspicion is paramount in diagnosis and outcomes associated to patients suffering from papillary muscle rupture as well as other mechanical complications of MI.
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Background: Prosthetic valve dehiscence is a manifestation of endocarditis which may be difficult to diagnose based on imaging. Case: A 68-year-old female with mechanical mitral valve replacement (MVR) complicated by recurrent endocarditis requiring two redo MVR presented with subacute chills, nausea, fatigue and dyspnea. Evaluation revealed leukocytosis, elevated NT-proBNP, acute kidney injury, negative blood cultures, and negative SARS-CoV2. Transthoracic echocardiography (TTE) showed normal prosthetic valve function. She was managed for acute decompensated heart failure and placed on empiric antibiotics. She continued to have chills, night sweats and developed hypotension. Blood cultures remained negative, and no source of infection was identified on imaging. Decision-making: To aid in differentiation shock, patient underwent right heart catheterization. This revealed severe cardiogenic shock, with cardiac index of 1.3 L/min/m2. Repeat TTE demonstrated dehiscence of the prosthetic mitral valve, which was confirmed on transesophageal echocardiogram (Figure 1). An intra-aortic balloon pump was placed, and inotropic support provided. Patient underwent successful redo MVR using a bioprosthetic valve. Tissue microbiology was positive for coagulase negative staph. Conclusion: Unmasking the etiology of vague clinical presentations may pose a challenge. Our case highlights the importance of a high index of suspicion and serial imaging when patients present with B-type symptoms. [Formula presented]
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Background: We report an unusual case of Takotsubo cardiomyopathy (TTC) caused by radial spasm during percutaneous coronary intervention (PCI), resulting in a fatal outcome. Case: A 70-year-old Caucasian female presented with an acute anterior myocardial infarction (MI) with anterior ST segment elevation. Coronary angiography showed critical proximal left anterior descending artery stenosis, and she underwent successful PCI via the right radial artery. Post-MI echocardiogram showed anterior wall hypokinesis with a left ventricular ejection fraction (LVEF) of 45%. The right coronary artery (RCA) had 70% stenosis in the mid-vessel and a staged outpatient intervention was planned. Decision-making: The staged procedure was delayed by seven months due to the COVID-19 pandemic. The same right radial access was selected but she developed significant radial spasm. Despite vasodilators, radial spasm persisted, so balloon-assisted tracking technique was used to advance guiding catheter. Fractional flow reserve of the RCA stenosis was positive at 0.76. PCI was then successfully performed using a 3x48 mm Xience stent. Thirty minutes later, she developed severe chest pain with widespread ST segment elevation. Repeat angiography via the right femoral artery showed patent coronary arteries. Echocardiography showed new apical ballooning pattern, typical of TTC with LVEF was 35%. She was discharged after 48 hours, but she re-presented a week later with cardiogenic shock. She had florid pulmonary oedema and an echo showed new torrential mitral regurgitation due anterior mitral leaflet chordal rupture. The apical ballooning that was observed a week earlier had resolved. An intra-aortic balloon pump was inserted, and the patient underwent emergency repair of the mitral valve. The procedure was technically successful, but the patient died on postoperative day one, due to multi-organ failure. Conclusion: We believe that TTC in our patient was caused by radial artery spasm. To our knowledge, this is the first case of TTC caused by radial spasm. Furthermore, chordal rupture secondary to TTC has been reported only once before.
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Background: Acute respiratory distress syndrome (ARDS) is characterized by hypoxemia and non-hydrostatic pulmonary edema. While ARDS is associated with a high mortality rate, its conjunction with cardiogenic shock (CS) can lead to devastating outcomes. ARDS is managed via lung protective ventilation with low tidal volumes and positive end expiratory pressures. Prone positioning has emerged as a supplementary strategy with beneficial effects on gas exchange, respiratory mechanics, and hemodynamics. Our case underlines the feasibility of intra-aortic balloon pump counterpulsation (IABP) with concurrent prone positioning in a patient with ARDS and CS. Case: 71-year-old male with history of coronary artery disease, hypertension, hyperlipidemia, and chronic kidney disease, presented to the emergency department with new onset chest pain. EKG showed ST-segment elevations in leads V1-V2 consistent with acute anterior wall myocardial infarction. Patient underwent percutaneous coronary intervention to the left anterior descending artery.Due to worsening hemodynamics and CS, it was decided to place a left axillary IABP. Hospital course was further complicated by acute pulmonary edema and ARDS requiring emergent intubation and mechanical ventilation. Patient was also started on renal replacement therapy given progression of renal failure. Decision-making: Given the onset of ARDS, the patient was placed in prone position for 12-16 hours/day for 5 days. There was no special technique required during proning, other than additional staff to ensure IABP stability. Gradual improvement in hemodynamics was attained, including an increase in cardiac index from 2.1 to 3.4, and a decrease in pulmonary vascular congestion. Conclusion: With the emergence of COVID-19 pandemic, the incidence of ARDS has increased significantly, with simultaneous occurrence of CS in some of these patients. Prone positioning has become one of the main therapeutic modalities in the management of ARDS. Our case highlights the feasibility of axillary IABP while implementing prone positioning in patients with concomitant ARDS and CS.
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There is ample evidence that the coronavirus can cause fatal blood clots. Angiotensin-converting enzyme 2 (ACE2) receptors act as a gateway for the coronavirus to enter the body and facilitate infection. ACE2 receptors are scientifically linked to disease severity in smokers because nicotine is thought to affect ACE2 expression in different ways. Patients admitted with severe COVID-19 infection with high levels of factor V Leiden are prone to serious damage from blood clots such as deep vein thrombosis or pulmonary embolism. Damage to the vascular endothelium is a complication that can be caused by the coronavirus. It can cause vascular clots, in the formation of which factors such as age, sex, blood type, and underlying diseases are effective. Thrombotic events, especially venous thrombosis, following COVID-19 infection have already been described;nonetheless, data are scarce on arterial thrombosis. Herein we report 4 cases of COVID-19 infection complicated by arterial thrombosis. (Iranian Heart Journal 2022;23(1): 223-227).
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Background: ST-Segment elevation MI (STEMI) is one of the leading cause of mortality in the western world. The coronavirus disease-2019 (COVID-19) pandemic might have implications of the treatment of STEMI patients. Our aim was to evaluate the treatment of STEMI patients during 2 months of the COVID-19 pandemic as compared with the year before. Methods: Data of 90 STEMI patients treated at the Shaare Zedek Medical Center intensive coronary care unit (ICCU) Between March-April 2019 and March-April 2020 were collected. Patients were divided into 2 groups: The pre COVID-19 group and the COVID-19 era group. Data regarding complications upon arrival and during hospitalization, door to balloon time and echocardiographic exams. Results: Fifty one (56%) patients were admitted with STEMI in the pre COVID-19 group and only 39 (44%) in the COVID-19 era group. Of them 13.7% vs. 20.5% were female, p=0.392 with a mean age of 62.1 (±13.5) vs. 63.4 (±11) years old, p=0.635 in the pre vs. post COVID-19 era group, respectively. Interestingly, more Jewish vs. non-Jewish were admitted with STEMI in the COVID-19 era group. There were no differences regarding baseline characteristics, catheterization access, culprit vessel and percutaneous coronary intervention rate. Door to balloon time was also similar in both pre and post COVID-19 era groups 35.4 (±32) vs. 30.5 (±29.1) minutes (p=0.896). Moreover, there was no difference regarding infarct size. Complications including acute renal failure, cardiogenic shock, and the use of intra-aortic balloon pump were similar in both groups. 30-day mortality rate was low and similar in both pre and post COVID-19 era groups (5.9% vs. 2.6%, respectively, p=0.426). Conclusions: During the beginning of COVID-19 era there was a reduction in STEMI admission rate, while no significant difference was found regarding baseline characteristics, door to balloon time, infarct size and mortality rate.