Effect of Respiratory Impairment on the Outcomes of Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction and Coronavirus Disease-2019 (COVID-19).

BACKGROUND: Coronavirus Disease-2019 (COVID-19) may impair outcomes of patients with ST-segment elevation myocardial infarction (STEMI). The extent of this phenomenon and its mechanisms are unclear.Methods and Results:This study prospectively included 50 consecutive STEMI patients admitted to our center for primary percutaneous coronary intervention (PCI) at the peak of the Italian COVID-19 outbreak. At admission, a COVID-19 test was positive in 24 patients (48%), negative in 26 (52%). The primary endpoint was in-hospital all-cause mortality. Upon admission, COVID-19 subjects had lower PO2/FiO2 (169 [100-425] vs. 390 [302-477], P<0.01), more need for oxygen support (62.5% vs. 26.9%, P=0.02) and a higher rate of myocardial dysfunction (ejection fraction <30% in 45.8% vs. 19.2%, P=0.04). All patients underwent emergency angiography. In 12.5% of COVID-19 patients, no culprit lesions were detected, thus PCI was performed in 87.5% and 100% of COVID-19 positive and negative patients, respectively (P=0.10). Despite a higher rate of obstinate thrombosis in the COVID-19 group (47.6% vs. 11.5%, P<0.01), the PCI result was similar (TIMI 2-3 in 90.5% vs. 100%, P=0.19). In-hospital mortality was 41.7% and 3.8% in COVID-19 positive and negative patients, respectively (P<0.01). Respiratory failure was the leading cause of death (80%) in the COVID-19 group, frequently associated with severe myocardial dysfunction. CONCLUSIONS: In-hospital mortality of COVID-19 patients with STEMI remains high despite successful PCI, mainly due to coexisting severe respiratory failure. This may be a critical factor in patient management and treatment selection.

Microthrombi as a Major Cause of Cardiac Injury in COVID-19: A Pathologic Study.

BACKGROUND: Cardiac injury is common in patients who are hospitalized with coronavirus disease 2019 (COVID-19) and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain uncertain. METHODS: We conducted a systematic pathological analysis of 40 hearts from hospitalized patients dying of COVID-19 in Bergamo, Italy, to determine the pathological mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underlying mechanisms of cardiac injury. RESULTS: Of the 40 hearts examined, 14 (35%) had evidence of myocyte necrosis, predominantly of the left ventricle. Compared with subjects without necrosis, subjects with necrosis tended to be female, have chronic kidney disease, and have shorter symptom onset to admission. The incidence of severe coronary artery disease (ie, >75% cross-sectional narrowing) was not significantly different between those with and without necrosis. Three of 14 (21.4%) subjects with myocyte necrosis showed evidence of acute myocardial infarction, defined as ≥1 cm2 area of necrosis, whereas 11 of 14 (78.6%) showed evidence of focal (>20 necrotic myocytes with an area of ≥0.05 mm2 but <1 cm2) myocyte necrosis. Cardiac thrombi were present in 11 of 14 (78.6%) cases with necrosis, with 2 of 14 (14.2%) having epicardial coronary artery thrombi, whereas 9 of 14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and small muscular arteries. We compared cardiac microthrombi from COVID-19-positive autopsy cases to intramyocardial thromboemboli from COVID-19 cases as well as to aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19-infected patients presenting with ST-segment-elevation myocardial infarction. Microthrombi had significantly greater fibrin and terminal complement C5b-9 immunostaining compared with intramyocardial thromboemboli from COVID-19-negative subjects and with aspirated thrombi. There were no significant differences between the constituents of thrombi aspirated from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction. CONCLUSIONS: The most common pathological cause of myocyte necrosis was microthrombi. Microthrombi were different in composition from intramyocardial thromboemboli from COVID-19-negative subjects and from coronary thrombi retrieved from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction. Tailored antithrombotic strategies may be useful to counteract the cardiac effects of COVID-19 infection.

Pathological Evidence for SARS-CoV-2 as a Cause of Myocarditis: JACC Review Topic of the Week.

To investigate whether severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2)-induced myocarditis constitutes an important mechanism of cardiac injury, a review was conducted of the published data and the authors' experience was added from autopsy examination of 16 patients dying of SARS-CoV-2 infection. Myocarditis is an uncommon pathologic diagnosis occurring in 4.5% of highly selected cases undergoing autopsy or endomyocardial biopsy. Although polymerase chain reaction-detectable virus could be found in the lungs of most coronavirus disease-2019 (COVID-19)-infected subjects in our own autopsy registry, in only 2 cases was the virus detected in the heart. It should be appreciated that myocardial inflammation alone by macrophages and T cells can be seen in noninfectious deaths and COVID-19 cases, but the extent of each is different, and in neither case do such findings represent clinically relevant myocarditis. Given its extremely low frequency and unclear therapeutic implications, the authors do not advocate use of endomyocardial biopsy to diagnose myocarditis in the setting of COVID-19.