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BACKGROUND: Patients with severe COVID-19 pneumonia are hypercoagulable and are at risk for acute pulmonary embolism. Timely diagnosis is imperative for their prognosis and recovery. This case describes an otherwise healthy 55-year-old man with respiratory failure requiring mechanical ventilatory support secondary to COVID-19 pneumonia. Massive acute pulmonary embolism with right heart failure complicated his course. CASE: A healthy 55-year-old man presented to our emergency department (ED) with a sore throat, cough, and myalgia. A nasopharyngeal swab was obtained, and he was discharged for home quarantine. His swab turned positive for SARS-CoV-2 infection on real-time reverse transcriptase-polymerase chain reaction assay (RT-PCR) on day 2 of his ED visit. A week later, he represented with worsening shortness of breath, requiring intubation for hypoxic respiratory failure due to COVID-19 pneumonia. Initially, he was easy to oxygenate, had no hemodynamic compromise, and was afebrile. On day 3, he became febrile and developed significant hemodynamic instability requiring maximum vasopressor support and oxygenation difficulty. His ECG revealed sinus tachycardia with S1Q3T3 pattern. On bedside TTE, there was evidence of right heart strain and elevated pulmonary artery systolic pressure of 45 mmHg. All data was indicative of a massive APE as the etiology for his hemodynamic collapse. A decision was made to forgo computed tomography pulmonary angiography (CTPA), given his clinical instability, and systemic thrombolytic therapy was administered. Within the next 12-24 hours, his hemodynamic status significantly improved. CONCLUSIONS: This case highlights the importance of considering massive APE in COVID-19 patients as a cause of the sudden and rapid hemodynamic decline. Furthermore, timely diagnosis can be made to aid in appropriate management with the help of bedside TTE and ECG in cases where CTPA is not feasible secondary to the patient's hemodynamic instability.
RESUMO
Background Unloading the left ventricle and delaying reperfusion reduces infarct size in preclinical models of acute myocardial infarction. We hypothesized that a potential explanation for this effect is that left ventricular (LV) unloading before reperfusion increases collateral blood flow to ischemic myocardium. Methods and Results Acute myocardial infarction was induced by balloon occlusion of the left anterior descending artery for 120 minutes in adult swine, followed by reperfusion for 180 minutes. After 90 minutes of occlusion, animals were assigned to 30 minutes of continued occlusion (n=6) or to 30 minutes of support with either an Impella CP (n=4) or venoarterial extracorporeal membrane oxygenation (n=5) with persistent occlusion. The primary end point was measures of microcirculatory blood flow including the collateral flow index (CFI) during left anterior descending artery occlusion as (Pw-RA)/(Pa-RA), where Pa, Pw, and RA are aortic, coronary wedge, and right atrial pressure, respectively. Infarct size was quantified using triphenyltetrazolium chloride. Compared with continued occlusion, Impella, not venoarterial extracorporeal membrane oxygenation, reduced infarct size relative to the area at risk. Before reperfusion, Impella reduced LV stroke work by 25% and increased the CFI by 75%, but venoarterial extracorporeal membrane oxygenation did not. Among all groups, the change in CFI between 90 and 120 minutes correlated inversely with the change in LV stroke work (r2=0.44, P=0.01) and infarct size (r2=0.41, P=0.02). Conclusions We report for the first time that 30 minutes of LV unloading during coronary occlusion increases the CFI, which correlates inversely with LV stroke work and infarct size. Venoarterial extracorporeal membrane oxygenation failed to increase the CFI and did not reduce infarct size.
