Dataset Information

ST-segment elevation in patients presenting with COVID-19: case series.

ABSTRACT:

Background

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the now pandemic disease, coronavirus disease (COVID-19). A number of reports have emerged suggesting these patients may present with signs and symptoms consistent with ST-segment elevation myocardial infarction without coronary artery occlusion.

Case summary

We report an international case series of patients with confirmed COVID-19 infection who presented with suspected ST-segment elevation myocardial infarction. Three patients with confirmed COVID-19 presented with electrocardiogram criteria for ST-segment elevation myocardial infarction. No patient had obstructive coronary disease at coronary angiography. Post-mortem histology in one case demonstrated myocardial ischaemia in the absence of coronary atherothrombosis or myocarditis.

Discussion

Patients with COVID-19 may present with features consistent with ST-segment elevation myocardial infarction and patent coronary arteries. The prevalence and clinical outcomes of this condition require systematic investigation in consecutive unselected patients.

SUBMITTER: Saririan M

PROVIDER: S-EPMC7898565 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background Adenosine is used to treat no-reflow in the infarct-related artery (IRA) during ST-segment-elevation myocardial infarction intervention. However, the physiological effect of adenosine in the IRA is variable. Coronary steal-a reduction of blood flow to the distal coronary bed-can occur in response to adenosine and this is facilitated by collaterals. We investigated the effects of adenosine on coronary flow reserve (CFR) in patients presenting with ST-segment-elevation myocardial infarction to better understand the physiological mechanism underpinning the variable response to adenosine. Methods and Results Pressure-wire assessment of the IRA after percutaneous coronary intervention was performed in 93 patients presenting with ST-segment-elevation myocardial infarction to calculate index of microvascular resistance, CFR, and collateral flow index by pressure. Modified collateral Rentrop grade to the IRA was recorded, as was microvascular obstruction by cardiac magnetic resonance imaging. Coronary steal (CFR <0.9), no change in flow (CFR=0.9-1.1), and hyperemic flow (CFR >1.1) after adenosine occurred in 19 (20%), 15 (16%), and 59 (63%) patients, respectively. Patients with coronary steal had higher modified Rentrop score to the IRA (1 [0, 1.75] versus 0 [0, 1], P<0.001) and a higher collateral flow index by pressure (0.25±0.10 versus 0.15±0.10, P=0.004) than the hyperemic group. The coronary steal group also had significantly higher index of microvascular resistance (61.68 [28.13, 87.04] versus 23.93 [14.67, 37.00], P=0.006) and had more disease (stenosis >50%) in the donor arteries (52.63% versus 22.03%, P=0.02) than the hyperemic group. Conclusions Adenosine-induced coronary steal may be responsible for a reduction in coronary flow reserve in a proportion of patients presenting with ST-segment-elevation myocardial infarction. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT03145194. URL: https://www.isrctn.com; Unique identifier: ISRCTN3176727.