key: cord-289816-rlwoy8ms authors: Tedeschi, Delio; Rizzi, Andrea; Biscaglia, Simone; Tumscitz, Carlo title: Acute myocardial infarction and large coronary thrombosis in a patient with COVID‐19 date: 2020-08-07 journal: Catheter Cardiovasc Interv DOI: 10.1002/ccd.29179 sha: doc_id: 289816 cord_uid: rlwoy8ms This is a case report of a 60‐year‐old male, without any cardiovascular risk factor and no cardiac history admitted to hospital with a diagnosis of interstitial pneumonia caused by coronavirus disease 2019 (COVID‐19). After 7 days, the blood tests showed a significant rise of inflammatory and procoagulant markers, along with a relevant elevation of high‐sensitivity Troponin I. Electrocardiogram and transthoracic echocardiogram (TTE) were consistent with a diagnosis of infero‐posterolateral acute myocardial infarction and the patient was transferred to the isolated Cath Lab for primary percutaneous coronary intervention (PCI). The angiography showed an acute massive thrombosis of a dominant right coronary artery without clear evidence of atherosclerosis. Despite the optimal pharmacological therapies and different PCI techniques, the final TIMI flow was 0/1 and after 3 hr the clinical condition evolved in cardiac arrest for pulseless electric activity. Acute coronary syndrome–ST‐elevation myocardial infarction is a relevant complication of COVID‐19. Due to high levels of proinflammatory mediators, diffuse coronary thrombosis could occur even in patients without cardiac history or comorbidities. This clinical case suggests that coronary thrombosis in COVID‐19 patients may be unresponsive to optimal pharmacological (GP IIb–IIIa infusion) and mechanical treatment (PCI). was transferred from another hospital to our institution. The patient claimed he had been previously in contact with a colleague positive to COVID-19. A nasopharyngeal swab for COVID-19 detection was collected, and after 48 hr the test result confirmed the active infection. The patient's symptoms started with low-grade fever, dry cough, asthenia, and muscle pain on March 10. After a couple of days, the fever became higher and unresponsive to paracetamol. The patient had no history of other preexisting pathological conditions except amoxicillin allergy. The results of physical examination on March 20 revealed blood pressure of 130/85 mmHg, heart rate of 101 bpm, body temperature of 36 C, oxygen saturation (SpO 2 ) of 85% while breathing ambient air, respiratory rate of 18 breath/min; the SpO 2 reached 94% after oxygen supplement by Venturi mask at 8 L/min, and FiO 2 of 40%. Routine blood tests at admission revealed normal white blood cell count (6,500 μl) with 84% neutrophil and 9.9% lymphocyte, normal platelet count (146 × 10 3 μl), normal hemoglobin concentration, high levels of C-reactive protein (PCR 134 mg/L), and slight increase of lactate dehydrogenase (LDH 372 U/L) normal levels of BNP (proBNP 43 pg/ml). The serum creatinine was 1.09 mg/dl and eGFR at 70 ml/ min ( Table 1) . The arterial gas analysis showed a pH of 7.41, oxygen partial pressure of 71 mmHg, carbon dioxide partial pressure of 38 mmHg, and bicarbonate level of 22 mmol/L. The chest X-ray revealed evidence of pneumonia with bilateral multiple interstitial ill-defined patchy opacities ( When admitted, the patient was treated with dexamethasone (12 mg iv), hydroxychloroquine (200 mg twice daily), antiviral drugs (lopinavir/ritonavir-2 tablets 200/50 mg twice daily), oxygen support (Venturi mask FiO2 40%), antibiotic prophylaxis with ceftriaxone (2 g iv), and venous thromboembolic (VTE) prophylaxis with enoxaparin (4,000 U.I. sc). After 48 hr, n-acetylcysteine (600 mg twice daily) and furosemide (20 mg iv twice daily) were administered. During the first 5 days of the hospital stay, the clinical conditions and the vital signs of the patient were stable (afebrile, SpO 2 90-92% at 10 L/min, and FiO 2 40%). On the sixth day, the patient showed a significant worsening of the shortness of breath and oxygen saturation (SpO2 87%), indeed respiratory support by CPAP machine was started (FiO2 100%, PEEP 12 cmH 2 O). On the seventh day (March 27) the patient showed a significant psychomotor agitation along with slight chest discomfort. The daily blood tests showed a significant rise of pro-coagulant and inflammatory markers D-Dimer (1,392 ng/ml), white blood count Abbreviations: eGFR, estimated glomerular filtration rate; LDH, lactate dehydrogenase; N/A, not applicable; Pro BNP, pro-brain natriuretic peptide. F I G U R E 1 Chest radiography at presentation: bilateral multiple interstitial ill-defined patchy opacity (12,300 μl), PCR (359 mg/L), LDH (761 U/L), ferritin (1,629 ng/ml) along with a significant elevation of high sensitivity troponin I levels (12,990 ng/ml) ( Table 1) . Angiography showed a high grade thrombus burden diffused in all RCA extensions (Figure 3c) . We decide to proceed with manual thrombus aspiration, as first strategy, using a 6 Fr Eliminate aspiration catheter (Terumo Medical) without achieving any effective recanalization. Images of diffuse intracoronary thrombosis with persistent TIMI 0-1 flow was documented. Eptifibatide 180 μg/kg IV bolus was given, followed by continuous infusion of 2 μg/kg/min; the ACT value was 304 s; after some minutes we administered a second eptifibatide 180 μg/kg intracoronary bolus through the tip of Eliminate aspiration catheter, placed in distal RCA. In order to maximize the thrombectomy effect, we proceeded with a manual thrombus aspiration using a 6 F guide extension catheter Guideliner (Teleflex Medical) as described in previously published case series. 2 The Guideliner was carefully advanced to the distal part of RCA, and aspiration with a 50 cc syringe via a Y connector through the side port was performed during slow retrieval of the catheter (Figure 3d ). Previous studies 3-6 have linked acute infections with an increased risk for acute myocardial infarction (AMI). In fact, the host inflammatory response to the infection often results in the release of proinflammatory cytokines and activation of platelets, leukocytes, and endothelial cells that can activate procoagulant pathways with prothrombotic status and consequently higher risk of acute cardiovascular events such as AMI. 3, 4 Many possible biological factors related to the COVID-19 infection could be involved in the physiopathological cascade that could precipitate cardiovascular complications, especially ACS 7 : • High levels of systemic proinflammatory cytokine and mediators of atherosclerosis may determine the plaque rupture through local inflammation. • Procoagulant effects of systemic inflammation may cause coronary thrombosis: plaque thrombosis, stent thrombosis, and spontaneous thrombosis. reports showed that patients with COVID 19 and severe respiratory distress often develop complications such as liver dysfunction or renal failure which can be related to procoagulant status. [12] [13] [14] In our report, the 60 years old male developed an AMI-STEMI just when blood tests showed an important elevation of proinflammatory and thrombotic activity mediators while these results were normal in the preceding days. The main angiographic finding was an acute massive thrombosis of a dominant RCA without evidence of clear coronary stenosis or atherosclerotic plaques. Considering the diffuse thrombosis was resistant to pharmacologic and mechanical therapy, this case supports the hypothesis that the proinflammatory and prothrombotic status related to COVID-19 infection was the main factor that triggered the coronary thrombosis. As the intracoronary imaging test was not performed (OCT-IVUS), the limitations of this report is the lack of clear information about the pathogenetic mechanisms underlying the RCA thrombosis. Furthermore, as the autopsy was not performed, we assume that fatal outcome was due to a combination of severe oxygen desaturation, acute ischemic heart failure, and consequent severe acidosis. However, we cannot exclude concomitant pulmonary thromboembolism or thrombosis of other organs as precipitating factors of cardiac arrest. This case report highlights the clinical impact of ACS-STEMI in COVID-19 patients. High levels of proinflammatory and hyperthrombotic activity could significantly affect the final outcome, even in young patients without cardiac past history or significant comorbidities. 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