Cardiovascular outcomes of type 2 myocardial infarction among COVID-19 patients: a propensity matched national study.

BACKGROUND: Myocardial infarction Type II (T2MI) is a prevalent cause of troponin elevation secondary to a variety of conditions causing stress/demand mismatch. The impact of T2MI on outcomes in patients hospitalized with COVID-19 is not well studied. METHODS: The Nationwide Inpatient Sample database from the year 2020 was queried to identify COVID-19 patients with T2MI during the index hospitalization. Clinical Modification (ICD-10-CM) codes 'U07.1' and 'I21.A1' were used as disease identifiers for COVID-19 and T2MI respectively. Multivariate adjusted Odds ratio (aOR) and propensity score matching (PSM) was done to compare outcomes among COVID patients with and without T2MI. The primary outcome was in-hospital mortality. RESULTS: A total of 1,678,995 COVID-19-weighted hospitalizations were identified in the year 2020, of which 41,755 (2.48%) patients had T2MI compared to 1,637,165 (97.5%) without T2MI. Patients with T2MI had higher adjusted odds of in-hospital mortality (aOR 1.44, PSM 32.27%, 95% CI 1.34-1.54) sudden cardiac arrest (aOR 1.29, PSM 6.6%, 95% CI 1.17-1.43) and CS (aOR 2.16, PSM 2.73%, 95% CI 1.85-2.53) compared to patients without T2MI. The rate of coronary angiography (CA) in T2MI with COVID was 1.19%, with significant use of CA among patients with T2MI complicated by CS compared to those without CS (4% vs 1.1%, p < 0.001). Additionally, COVID-19 patients with T2MI had an increased prevalence of sepsis compared to COVID-19 without T2MI (48% vs 24.1%, p < 0.001). CONCLUSION: COVID-19 patients with T2MI had worse cardiovascular outcomes with significantly higher in-hospital mortality, SCA, and CS compared to those without T2MI. Long-term mortality and morbidity among COVID-19 patients who had T2MI will need to be clarified in future studies. [Figure: see text].

In-Hospital Outcomes of COVID-19 Associated Myocarditis (from a Nationwide Inpatient Sample Database Study).

The prevalence of COVID-19 infection-related myocarditis, its in-hospital cardiovascular outcomes, and its impact on hospital cost and stay at national level are not well studied in the literature. The Nationwide Inpatient Sample Database from 2020 was queried to identify patients with COVID-19 and myocarditis versus those without myocarditis. Cardiovascular outcomes and resource utilization were studied among cohorts with COVID-19, with and without myocarditis, using descriptive statistics, multivariate regression matching, and propensity score matching using STATA version 17. Of 1,678,995 patients, 3,565 (0.21%) had COVID-19 with myocarditis, and 1,675,355 (99.78%) had COVID-19 without myocarditis. On multivariate regression analysis, we found higher odds of in-hospital mortality (adjusted odds ratio [aOR] 1.59, 95% confidence interval [CI] 1.27 to 1.9) in patients with myocarditis than in those without myocarditis, in addition to higher odds of major adverse cardiovascular and cerebrovascular events (aOR 3.54, 95% CI 2.8 to 4.4), acute kidney injury (aOR 1.29, 95% CI 1.27 to 1.9), heart failure (aOR 2.77, 95% CI 2.3 to 3.4), cardiogenic shock (aOR 10.2, 95% CI 7.9 to 13), myocardial infarction (aOR 5.74, 95% CI 4.5 to 7.3), and use of mechanical circulatory support (aOR 2.81, 95% CI 1.6 to 4.9). The propensity-matched cohort also favored similar outcomes. In conclusion, patients with COVID-19 and myocarditis had worse clinical outcomes, having a higher rate of in-hospital mortality, major adverse cardiovascular and cerebrovascular events with longer length of hospital stay, and higher hospitalization costs. Large prospective trials are necessary to validate these findings with diagnostic measures, including biopsy and cardiac magnetic resonance imaging for the extent of myocardial involvement.

In-Hospital Outcomes of Takotsubo Cardiomyopathy During the COVID-19 Pandemic: Propensity Matched National Cohort.

Takotsubo Cardiomyopathy (TTS) is an acute reversible left ventricular dysfunction with regional ballooning secondary to various physical or psychological triggers, including COVID-19. The impact of TTS on outcomes in COVID-19 patients is not well studied. The Nationwide in-patient sample database from 2019 to 2020 was utilized to identify TTS patients with and without COVID-19. Clinical Modification (ICD-10-CM) codes U07.1 and I51.81 were used as disease identifiers for COVID-19 and TTS, respectively. Multivariate logistic regression was performed to report adjusted odds ratios (aOR) and propensity score match (PSM) was done to compare outcomes among TTS patients with and without COVID. The primary outcome was in-hospital mortality. A total of 83,215 TTS patients for the period 2019-2020 were included in our study, of which 1665 (2%) had COVID-19. COVID-19 with TTS group had higher adjusted odds of in-hospital mortality (aOR 7.23, PSM 32.7% vs 10.16%, p = <0.001), cardiogenic shock; (aOR 2.32, PSM 16.7% vs 9.5%, P < 0.001) and acute kidney injury; (aOR 2.30, PSM 47.5% vs 33.1%, P< 0.001) compared to TTS without COVID-19. TTS hospitalizations with COVID-19 were associated with longer lengths of stay (12 ± 12 vs 7 ± 9 days) and higher total cost ($47,702 ± $67,940 vs $26,957 ± $44,286) compared to TTS without COVID. TTS with COVID-19 group had a higher proportion of males compared to TTS without COVID-19 group (37.8% vs 18.5%). TTS with COVID-19 group had a greater proportion of non-white race. The proportion of Blacks, Hispanics, and Asian/Pacific Islander was higher in the COVID-19 TTS group compared to TTS without COVID-19 group (12.9% vs 8.4%, 20.4% vs 6.5%, 5 vs 2.2%, respectively). TTS in the setting of COVID-19 illness has worse outcomes in terms of in-hospital mortality, cardiogenic shock, and acute kidney injury. Male sex and non-white race were more likely to be affected by TTS in the setting of COVID-19. The out-of-hospital morbidity and mortality in patients who suffered TTS during COVID-19 illness need further study. Studies are needed to provide mechanistic insights into the interaction between COVID-19 and TTS.

Endotheliitis, endothelin, and endothelin receptor blockers in COVID-19.

We summarize the role of endothelin as a potent vasoconstrictor, pro-inflammatory, pro-oxidative agent in the pathophysiologic effects and end-organ dysfunction of coronavirus disease 2019 (COVID-19). Endotheliitis is an under-recognized pathophysiologic process that causes various types of dysfunction in end organs, including heart, lung, kidney, and brain. Endothelin receptor blockers, such as bosentan and sitaxentan, can pave a path ahead in the realm of COVID-19 therapies. These agents have a potential role against COVID-19 and should be studied in research trials to determine their efficacy in treatment of this severe disease.