A National Perspective on the Impact of the COVID-19 Pandemic on Heart Failure Hospitalizations in the United States.

Nationwide data of the COVID-19 pandemic's impact on heart failure (HF) hospitalizations is lacking. We conducted this study to elucidate the impact of the COVID-19 pandemic on HF hospitalizations. Additionally, we assessed the differences in hospitalization characteristics during the pandemic and the impact that a concurrent diagnosis of COVID-19 has on various outcomes and predictors of inpatient mortality among patients admitted for HF. The National Inpatient Sample (NIS) database was queried for all hospitalizations with a primary diagnosis of HF between 2017 and 2020. Monthly HF hospitalizations were trended longitudinally over this period. Beginning April 1, 2020, concurrent COVID-19 infections were identified. Subsequently, we stratified HF hospitalizations between April 2020 and December 2020 (HF-2020) based on if concomitant COVID-19 was diagnosed, forming the HF-COVID+ve and HF-COVID-ve groups respectively. HF-2020 was also compared with prepandemic HF hospitalizations between April 2019 and December 2019 (HF-2019). Baseline characteristics were compared, and adjusted outcomes were obtained. During the initial COVID-19 surge in April 2020, HF admissions were reduced by 47% compared to January 2020. Following this decline, HF hospitalizations increased but did not reach prepandemic levels. HF-2020 admissions had an increased complication burden compared to HF-2019, including acute myocardial infarction (8.9% vs 6.6%, P < 0.005) and pulmonary embolism (4.1% vs 3.4%, P < 0.005) indicating a sicker cohort of patients. HF-COVID+ve hospitalizations had 2.9 times higher odds of inpatient mortality compared to HF-COVID-ve and an increased adjusted length of stay by 2.16 days (P < 0.005). A pandemic of the same magnitude as COVID-19 can overwhelm even the most advanced health systems. Early resource mobilization and preparedness is essential to provide care to a sick cohort of patients like acute HF, who are directly and indirectly effected by the consequences of the pandemic which has worsened hospitalization outcomes.

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.

Symptomatology, prognosis and clinical findings of myocarditis as an adverse event of COVID-19 mRNA vaccine: a systematic review

Funding Acknowledgements Type of funding sources: None. Background Myocarditis, an inflammation of the myocardium in the absence of ischemic injury, may be caused by viruses, drugs, and vaccines. The Myocarditis following COVID-19 vaccinations is most commonly seen in young adult males and commonly after the second dose of the mRNA vaccine. It usually presents with chest pain, dyspnoea, palpitations but has a diverse clinical presentation and varied therapeutic response. We aim to systematically collate the symptomatology, prognosis, and clinical findings of COVID-19 vaccine adverse events causing Myocarditis. Method Following the PRISMA statement 2020, a systematic search was conducted to isolate confirmed cases of COVID-19 vaccine-induced Myocarditis. By applying the BOOLEAN logic, the following keywords were used: COVID-19, SARS-CoV-2, Myocarditis, Mortality. Four databases were searched from January 2021 through August 2021: PubMed, Science Direct, Google Scholar, and Cochrane Library;the reference lists of screened studies were searched as well (umbrella methodology). Results In total, 12 case reports, 10 case series and 1 cohort study with a total of 107 patients were included in the final analysis. A total of 101 male patients were recorded, and 6 were female showing male dominance. The mean age of all participants was 24.73 years(SD = 13.18), ranging from 14 to 70. The most common presenting symptoms were chest pain (47.66%), fever (35.51%), and myalgia (25.23%). Lab findings showed elevated Troponin I, CRP, and ESR levels in the majority of patients. ECG was abnormal in most of the patients, which include sinus rhythm (24%), ST-elevation (42.05%) and T wave inversion (13.08%). Echo findings include decreased Ejection fraction in 19.62% of patients while 13.08% of patients having a hypokinetic left ventricular wall. Further, CMR finding suggestive of confirmed myocarditis cases in 36% patients while rest are suspected one. Overall mortality(1.86%) was low among patients. Conclusion There is increasing evidence for Myocarditis as a rare adverse event of COVID-19 mRNA vaccination in young adults. This evidence is strongest amongst young male patients. The majority of the patients complain of chest pain and fever. In lab findings Troponin I, CRP and ESR are usually increased and ST elevation is common in the ECG. This entity is mainly treated with nonsteroidal anti-inflammatory drugs, Colchicine, Beta-blockers, ACE inhibitors, Steroids. However, prognosis and outcomes are favourable with a very low mortality rate.

Epidemiology, clinical ramifications, and cellular pathogenesis of COVID-19 mRNA-vaccination-induced adverse cardiovascular outcomes: A state-of-the-heart review.

The coronavirus disease 2019 (COVID-19) has overwhelming healthcare systems globally. To date, a myriad of therapeutic regimens has been employed in an attempt to curb the ramifications of a severe COVID-19 infection. Amidst the ongoing pandemic, the advent and efficacious uptake of COVID-19 vaccination has significantly reduced disease-related hospitalizations and mortality. Nevertheless, many side-effects are being reported after COVID-19 vaccinations and myocarditis is the most commonly reported sequelae post vaccination. Majority of these diseases are associated with COVID-19 mRNA vaccines. Various studies have established a temporal relationship between these complications, yet the causality and the underlying pathogenesis remain hypothetical. In this review, we aim to critically appraise the available literature regarding the cardiovascular side effects of the various mRNA vaccines and the associated pathophysiology.

Chilaiditi syndrome: A structural displacement in a heart failure patient.

BACKGROUND: Chilaiditi's sign is often found incidentally on chest or abdominal radiograph and can be accompanied by clinical symptoms such as abdominal pain, gastrointestinal complications, and less commonly associated with dyspnea. CASE PRESENTATION: In this interesting case, we discover lingering dyspnea in our 79 year old male with a past medical history of asthma and heart failure with preserved ejection fraction admitted for acute heart failure exacerbation with reduced ejection fraction along with a new incidental finding of Chilaiditi's sign on chest radiograph. Patient received optimal diuretics and guideline-directed medical treatment for heart failure exacerbation, but mild dyspnea with pleuritic chest pain persisted. Dyspnea with pleurisy was likely attributed to a structural anatomical defect (Chilaiditi's sign) that can be picked up on imaging. CONCLUSION: Chilaiditi syndrome can be an incidental cause of ongoing persistent dyspnea, and if symptoms are severe, intervention can be warranted for symptomatic resolution. LEARNING OBJECTIVE: Chilaiditi syndrome should be considered as a possible diagnosis among patients with a history of heart failure and incidental Chilaiditi's sign on chest radiographic imaging who suffer from persistent dyspnea and pleurisy despite optimal diuretics and guideline-directed medical treatment.

Coronavirus disease 2019 (COVID-19): Multisystem review of pathophysiology.

Coronavirus disease-19 (COVID-19) pandemic is associated with high morbidity and mortality. COVID-19, which is caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS CoV-2), affects multiple organ systems through a myriad of mechanisms. Afflicted patients present with a vast constellation of symptoms, from asymptomatic disease to life-threatening complications. The most common manifestations pertain to mild pulmonary symptoms, which can progress to respiratory distress syndrome and venous thromboembolism. However, in patients with renal failure, life-threatening cardiac abnormalities can ensue. Various mechanisms such as viral entry through Angiotensin receptor (ACE) affecting multiple organs and thus releasing pro-inflammatory markers have been postulated. Nevertheless, the predictors of various presentations in the affected population remain elusive. An ameliorated understanding of the pathology and pathogenesis of the viral infection has led to the development of variable treatment options, with many more that are presently under trial. This review article discusses the pathogenesis of multiple organ involvement secondary to COVID-19 infection in infected patients.

Safety and Efficacy of Renin-Angiotensin-Aldosterone System Inhibitors in COVID-19 Population.

INTRODUCTION: The safety of renin-angiotensin-aldosterone system inhibitors (RAASi) among COVID-19 patients has been controversial since the onset of the pandemic. METHODS: Digital databases were queried to study the safety of RAASi in COVID-19. The primary outcome of interest was mortality. The secondary outcome was seropositivity improvement/viral clearance, clinical manifestation progression, and progression to intensive care units. A random-effect model was used to compute an unadjusted odds ratio (OR). RESULTS: A total of 49 observational studies were included in the analysis consisting of 83,269 COVID-19 patients (RAASi n = 34,691; non-RAASi n = 48,578). The mean age of the sample was 64, and 56% were males. We found that RAASi was associated with similar mortality outcomes as compared to non-RAASi groups (OR 1.07; 95% CI 0.99-1.15; p > 0.05). RAASi was associated with seropositivity improvement including negative RT-PCR or antibodies, (OR 0.96; 95% CI 0.93-0.99; p < 0.05). There was no association between RAASi versus control with progression to ICU admission (OR 0.99; 95% CI 0.79-1.23; p > 0.05) or higher odds of worsening of clinical manifestations (OR 1.04; 95% CI 0.97-1.11; p > 0.05). Metaregression analysis did not change our outcomes for effect modifiers including age, sex, comorbidities, RAASi type, or study type on outcomes. CONCLUSIONS: COVID-19 is not a contraindication to hold or discontinue RAASi as they are not associated with higher mortality or worsening symptoms. Continuation of RAASi might be associated with favorable outcomes in COVID-19, including seropositivity/viral clearance.

Delayed hemodialysis in COVID-19: Case series with literature review.

BACKGROUND: Increased incidence of kidney injury has been seen in patients with COVID-19. However, less is known about COVID-19 susceptibility and outcomes in end-stage renal disease (ESRD) patients on hemodialysis (HD). Reduced angiotensin-converting enzyme 2 (ACE-2) from SARS-CoV-2 binding and increased angiotensin II (Ang-II) activity have been suggested as mechanisms for COVID-19 renal pathophysiology. MATERIALS AND METHODS: In this case series, we analyzed the data of 3 patients with ESRD who had a delay in receiving their regular HD. Reduced oxygen requirement, resolved hyperkalemia, and normalized fluid status were used for the basis of discharge. RESULTS: Presenting symptoms included fever, dyspnea, and dry cough. Laboratory markers were characteristic for COVID-19, such as lymphopenia, elevated D-dimer, C-reactive protein (CRP), and interleukin 6 (IL-6). All 3 of our reported patients required urgent HD upon admission. However, we report no fatalities in our case series, and our patients did not have a severe course of illness requiring endotracheal intubation. We reviewed COVID-19 pathophysiology and how patients with ESRD on HD may be particularly at risk for infection. CONCLUSION: New renal failure or ESRD sequelae, such as hyperkalemia, uremic encephalopathy, and fluid overload, can be exacerbated by a delay in receiving HD due to COVID-19 infection. Both direct COVID-19 infection and the challenges this pandemic creates to health care logistics present unique threats to ESRD patients on HD.

Outcomes of in-hospital cardiac arrest in COVID-19 patients: A proportional prevalence meta-analysis.

BACKGROUND: Limited epidemiological data are available on the outcomes of in-hospital cardiac arrest (CA) in COVID-19 patients. METHODS: We performed literature search of PubMed, EMBASE, Cochrane, and Ovid to identify research articles that studied outcomes of in-hospital cardiac arrest in COVID-19 patients. The primary outcome was survival at discharge. Secondary outcomes included return of spontaneous circulation (ROSC) and types of cardiac arrest. Pooled percentages with a 95% confidence interval (CI) were calculated for the prevalence of outcomes. RESULTS: A total of 7,891 COVID patients were included in the study. There were 621 (pooled prevalence 8%, 95% CI 4-13%) cardiac arrest patients. There were 52 (pooled prevalence 3.0%; 95% CI 0.0-10.0%) patients that survived at the time of discharge. ROSC was achieved in 202 (pooled prevalence 39%;95% CI 21.0-59.0%) patients. Mean time to ROSC was 7.74 (95% CI 7.51-7.98) min. The commonest rhythm at the time of cardiac arrest was pulseless electrical activity (pooled prevalence 46%; 95% 13-80%), followed by asystole (pooled prevalence 40%; 95% CI 6-80%). Unstable ventricular arrhythmia occurred in a minority of patients (pooled prevalence 8%; 95% CI 4-13%). CONCLUSION: This pooled analysis of studies showed that the survival post in-hospital cardiac arrest in COVID patients is dismal despite adequate ROSC obtained at the time of resuscitation. Nonshockable rhythm cardiac arrest is commoner suggesting a non-cardiac cause while cardiac related etiology is uncommon. Future studies are needed to improve the survival in these patients.

Does Pulmonary Embolism in Critically Ill COVID-19 Patients Worsen the In-Hospital Mortality: A Meta-Analysis.

BACKGROUND: Mortality in critically ill COVID (coronavirus disease) patients secondary to pulmonary embolism (PE) has conflicting data. We aim to evaluate the mortality outcomes of critically ill patients with and without PE (WPE). METHODS: Three studies were identified after a digital database search on PE in ICU (intensive care unit) patients until September 2020. The primary outcome was mortality. Outcomes were compared using a random method odds ratio and confidence interval of 95%. RESULTS: A total of 439 patients were included in the study. Diabetes, hypertension, and renal replacement requirement had no statistically significant association between PE and WPE, p = 0.39, p = 0.23, and p = 0.29 respectively. The study revealed that males have higher odds of PE, OR-1.98, 95%CI-1.01-3.89; p = 0.05. In-hospital mortality results were comparable between PE and WPE after subgroup analysis and correction of heterogeneity, p = 0.25. CONCLUSION: PE in critically ill COVID patients had similar in-hospital mortality outcomes as WPE patients. The findings are only hypotheses generated from observational studies and need future randomized, prospective clinical trials for a definitive conclusion.

COVID-19 Infection Complicated by a Complete Occlusion of the Left Circumflex Artery With Acute Restenosis After Drug-Eluting Stent Placement.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause a hypercoagulable state that can complicate the management of patients presenting with acute myocardial infarction (MI). We present the case of a patient with coronavirus disease 2019 (COVID-19) with ST elevation MI who was treated with percutaneous coronary intervention and stenting to the left circumflex artery. He was treated appropriately with anticoagulation with appropriate activated clotting time. However, the coronary angiogram course was complicated with heavy thrombosis that involved the left circumflex artery and the left anterior descending artery. Physicians are urged to suspect heparin resistance in COVID-19 patients, particularly if those patients have venous thromboembolism or acute coronary syndrome while taking heparin.

Safety and Efficacy of Hydroxychloroquine in COVID-19: A Systematic Review and Meta-Analysis.

BACKGROUND: During the initial phases of the coronavirus disease 2019 (COVID-19) epidemic, there was an unfounded fervor surrounding the use of hydroxychloroquine (HCQ); however, recently, the Centers for Disease Control and Prevention (CDC) has recommended against routine use of HCQ outside of study protocols citing possible adverse outcomes. METHODS: Multiple databases were searched to identify articles on COVID-19. An unadjusted odds ratio (OR) was used to calculate the safety and efficacy of HCQ on a random effect model. RESULTS: Twelve studies comprising 3,912 patients (HCQ 2,512 and control 1400) were included. The odds of all-cause mortality (OR: 2.23, 95% confidence interval (CI): 1.58 - 3.13, P value < 0.00001) were significantly higher in patients on HCQ compared to patients on control agent. The response to therapy assessed by negative repeat polymerase chain reaction (PCR) (OR: 1.83, 95% CI: 0.50 - 6.75, P = 0.36), radiological resolution (OR: 1.98, 95% CI: 0.47 - 8.36, P value = 0.36) and the need for invasive mechanical ventilation (IMV) (OR: 1.21, 95% CI: 0.34 - 4.33, P value = 0.76) were identical between the two groups. Overall, four times higher odds of net adverse events (NAEs) were observed in the HCQ group (OR: 4.59, 95% CI 1.73 - 12.20, P value = 0.02). The measures for individual safety endpoints were also numerically lower in the control arm; however, none of these values reached the level of statistical significance. CONCLUSIONS: HCQ might offer no benefits in terms of decreasing the viral load and radiological improvement in patients with COVID-19. HCQ appears to be associated with higher odds of all-cause mortality and NAEs.

COVID-19 cardiovascular epidemiology, cellular pathogenesis, clinical manifestations and management.

Coronavirus Disease 2019 (COVID-19) is a rapidly progressing global pandemic that may present with a variety of cardiac manifestations including, but not limited to, myocardial injury, myocardial infarction, arrhythmias, heart failure, cardiomyopathy, shock, thromboembolism, and cardiac arrest. These cardiovascular effects are worse in patients who have pre-existing cardiac conditions such as coronary artery disease, hypertension, diabetes mellitus, and coagulation abnormalities. Other predisposing risk factors include advanced age, immunocompromised state, and underlying systemic inflammatory conditions. Here we review the cellular pathophysiology, clinical manifestations and treatment modalities of the cardiac manifestations seen in patients with COVID-19.