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Myocardial Virus and Gene Expression in SARS CoV-2 Positive Patients 
with Clinically Important Myocardial Dysfunction


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Myocardial dysfunction has emerged as an important pathophysiologic component of some critically ill patients with SARS CoV-2 (CoV-2) infections,1-5 either from myocarditis4, 5 or myocardial dysfunction without overt evidence of inflammatory disease. 1-3 There are multiple unanswered questions regarding cardiac involvement in CoV-2 disease including: does the virus invade cardiac myocytes; if so, does it utilize the same host cellular machinery as in other cells; what are the relative roles of direct viral tissue injury vs. inflammatory myocardial disease; what cytokines are active in the myocardium; and what are the effects on functionally important cardiac myocyte genes and gene networks.




Ten patients with PCR confirmed CoV-2 infection and evidence of cardiac involvement contributing to clinical compromise will be recruited from the UCH ICU and inpatient hospital units. Patients will have no other known etiology for cardiomyopathy other than COVID-19 infection. Patients may be supported with mechanical ventilation but will need to be in a stable respiratory condition with improving oxygen requirements prior to enrollment. In addition, investigators will have direct conversations with the treating ICU or Hospitalist team caring for the patient on the day prior to and day of the procedure to review the status of the patient and ensure no acute changes have occurred that may increase the risk of transportation out of the unit. Additional Inclusion criteria include: 1) age >18 years; 2) clear evidence of myocardial involvement including a Troponin I value of (≥0.05 ng/ml (the 99% upper bound)) AND a) an LVEF < 50% OR b) a global longitudinal strain of > -16.0, OR c) ST-T change suggesting STEMI, NSTEMI or myopericarditis in the presence of patent coronary arteries, OR d) new onset sustained VT or VF 3) Laboratory-confirmed SARS-CoV-2 infection as determined by polymerase chain reaction (PCR) testing or other commercial or public health assay 4) Patient and/or legally authorized representative must be competent to understand and agree with informed consent form. Exclusion Criteria: 1) Hemodynamic instability as evidenced by escalating doses of inotropic agents or vasopressors within the prior 24 hours 2) Respiratory instability as evidenced by increasing oxygen requirements over the 24 hours prior to consent or FiO2 requirement >; 60 %. 3) evidence that respiratory failure is the primary reason for myocardial dysfunction; 4) Moderate to severe pulmonary hypertension (mean PAP >35 mmHg); 5) INR >1.8 on no anticoagulation or contraindication to withdrawing anticoagulation; 6) platelets <100k/mm3.

Type of Study



University of Colorado Hospital

Principal Investigator
Natasha Altman,  MD

Natasha Altman, MD

Study ID

Protocol Number: 20-0852

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