Elevated FAI Index of Pericoronary Inflammation on Coronary CT Identifies Increased Risk of Coronary Plaque Vulnerability after COVID-19 Infection.

Inflammation is a key factor in the development of atherosclerosis, a disease characterized by the buildup of plaque in the arteries. COVID-19 infection is known to cause systemic inflammation, but its impact on local plaque vulnerability is unclear. Our study aimed to investigate the impact of COVID-19 infection on coronary artery disease (CAD) in patients who underwent computed tomography angiography (CCTA) for chest pain in the early stages after infection, using an AI-powered solution called CaRi-Heart®. The study included 158 patients (mean age was 61.63 ± 10.14 years) with angina and low to intermediate clinical likelihood of CAD, with 75 having a previous COVID-19 infection and 83 without infection. The results showed that patients who had a previous COVID-19 infection had higher levels of pericoronary inflammation than those who did not have a COVID-19 infection, suggesting that COVID-19 may increase the risk of coronary plaque destabilization. This study highlights the potential long-term impact of COVID-19 on cardiovascular health, and the importance of monitoring and managing cardiovascular risk factors in patients recovering from COVID-19 infection. The AI-powered CaRi-Heart® technology may offer a non-invasive way to detect coronary artery inflammation and plaque instability in patients with COVID-19.

Lung Transplantation for COVID-19 Pulmonary Sequelae.

BACKGROUND: The role of lung transplantation for coronavirus disease 2019 (COVID-19)-related lung failure is evolving as the pandemic persists. METHODS: From January 2021 to April 2022, 20 patients (median age 62 y; range 31-77) underwent lung transplantation for COVID-related lung failure at our institution. We reviewed their clinical and intraoperative characteristics and early outcomes including postoperative complications. RESULTS: Eleven patients (55%) had chronic lung disease when they contracted COVID-19. All 20 patients required hospitalization for antivirus treatment. Median lung allocation score was 74.7 (33.1-94.0). Thirteen patients (65%) underwent single-lung transplants, and 7 patients (35%) underwent double-lung transplants. Concomitant coronary artery bypass graft surgery was performed in 2 (10%) patients because of severe coronary artery disease. Postoperatively, venovenous extracorporeal membrane oxygenation was needed in 3 patients (15%) because of severe primary graft dysfunction; all were eventually weaned. Ten patients (50%) experienced deep venous thrombosis, and 1 eventually developed a major pulmonary embolus. The median intensive care unit stay and hospital stays were 6.5 d (3-44) and 18 d (7-77), respectively. During a median follow-up of 201 d (47-418), we experienced 1 late mortality due to COVID-19-related myocarditis. Among the 13 patients with single-lung transplant, 5 demonstrated improvement in their native lungs. CONCLUSIONS: Lung transplantation yielded favorable early outcomes in a heterogeneous patient cohort that included older patients, obese patients, and patients with coronary artery disease or preexisting chronic lung disease. Our data also shed light on the transforming role of lung transplantation for the pulmonary sequelae of a complex multisystem COVID-19 disorder.

Effects of Medical Face Masks on Physical Performance in Patients With Coronary Artery Disease or Hypertension.

In this randomized, prospective monocentric study, 40 subjects with coronary artery disease or hypertension (cardiovascular disease [CVD] group) were assigned to either surgical mask (SM) or class 2 filtering facepiece mask (FFP2). They performed cycle ergometry exercise tests with progressive intensity until exhaustion with the assigned mask and another test with no mask (NM) in random order. A control group of 10 healthy subjects randomly performed 3 exercise tests with NM, SM, and FFP2, respectively. Blood pressure, heart rate, 12-lead electrocardiogram, exertion, shortness of breath, and capillary blood gases from the earlobe were documented. Across all groups, exercise testing with face masks resulted in a significantly reduced peak power output in watts compared with testing with NM (CVD group: SM vs NM: -5.0 ± 7.0%, p = 0.005; FFP2 vs NM: -4.7 ± 14%, p = 0.03; control group: SM vs NM: -6.8 ± 4.4%, p = 0.008; FFP2 vs NM: -8.9 ± 6.3%; p = 0.01) without differences in hemodynamic parameters, such as maximum heart rate and systolic blood pressure. Wearing an FFP2 compared with NM resulted in significant higher carbon dioxide partial pressure (CVD group: FFP2: 36.0 ± 3.2 mm Hg vs NM: 33.3 ± 4.4 mm Hg, p = 0.019; control group: FFP2: 32.6 ± 2.8 mm Hg vs NM: 28.1 ± 1.7 mm Hg, p <0.001) with corresponding differences in hydrogen carbonate and base excess, but not to a clinically critical extent. In conclusion, exercise testing with SM and FFP2 resulted in a significant reduction of peak power output without differences in hemodynamic parameters in subjects with preexisting CVD and in healthy subjects.

Diagnosis of coronary artery rethrombosis after effective systemic thrombolytic therapy in patients with ST-segment elevation myocardial infarction.

The aim of the study was to evaluate the diagnostic significance of ST-segment re-elevation episodes registered with telemetric ECG monitoring in patients with ST-segment elevation myocardial infarction (STEMI) treated with thrombolytic therapy (TLT). The study included 117 patients with STEMI following effective TLT. The elective coronary angiography followed by percutaneous coronary interventions was performed in the interval from 3 to 24 hours after a successful systemic TLT. Before and after cardiac catheterization, the telemetric ECG monitoring was performed using AstroCard Telemetry system (Meditec, Russia). During the study, two groups of patients were formed. Group 1 included 85 patients (72.6%) without new ST-segment deviations on telemetry. 77 patients (90.6%) had no recurrent coronary artery thrombosis at angiography. Eight patients (9.4%) from group 1 were diagnosed with thrombosis of the infarct-related coronary artery. Group 2 included 32 patients (27.4%) who underwent TLT and then had ST-segment re-elevation episodes of 1 mV or more in the infarct-related leads, lasting for at least 1 minute. In group 2, in 27 of 32 patients (84.4%), thrombosis of the infarct-related coronary artery was confirmed (p<0.01 compared with group 1). In 71.9% cases, the recurrent ischemic episodes were asymptomatic ('painless myocardial ischemia') (p<0.01). Thus, in patients with STEMI and successful TLT, re-elevation of ST-segment during remote ECG monitoring is strongly related to angiographically documented coronary artery thrombotic reocclusion. The absence of chest pain during recurrent myocardial ischemia requires continuous ECG telemetry to select patients for the rescue percutaneous coronary interventions at an earlier stage.

Understanding the association between endothelial dysfunction and left ventricle diastolic dysfunction in development of coronary artery disease and heart failure.

Cardiovascular diseases (CVDs)  have been the most common cause of death worldwide for decades. Until recently the most affected patients were middle-aged and elderly, predominantly men, with more frequent ST elevation myocardial infarction  (STEMI) caused by obstructive coronary artery disease (CAD). However, in the last two decades we have noticed an increased incidence of ischemia with non-obstructive coronary arteries (INOCA), which includes myocardial infarction with non-obstructive coronary arteries (MINOCA) and non-myocardial infarction syndromes, such as microvascular and vasospastic angina, conditions that have been particularly pronounced in women and young adults - the population we considered low-risky till than. Therefore, it has become apparent that for this group of patients conventional methods of assessing the risk of future cardiovascular (CV) events are no longer specific and sensitive enough. Heart failure with preserved ejection fraction (HFpEF) is another disease, the incidence of which has been rising rapidly during last two decades, and predominantly affects elderly population. Although the etiology and pathophysiology of INOCA and HFpEF are complex and not fully understood, there is no doubt that the underlying cause of both conditions is endothelial dysfunction (ED) which further promotes the development of left ventricular diastolic dysfunction (LVDD). Plasma biomarkers of ED, as well as natriuretic peptides (NPs), have been intensively investigated recently, and some of them have great potential for early detection and better assessment of CV risk in the future.

Arterial and venous thrombosis in coronavirus 2019 disease (Covid-19): relationship with mortality.

BACKGROUND: Patients with coronavirus disease 2019 (Covid-19) may experience venous thrombosis while data regarding arterial thrombosis are sparse. METHODS: Prospective multicenter study in 5 hospitals including 373 patients with Covid-19-related pneumonia. Demographic data, laboratory findings including coagulation tests and comorbidities were reported. During the follow-up any arterial or venous thrombotic events and death were registered. RESULTS: Among 373 patients, 75 (20%) had a thrombotic event and 75 (20%) died. Thrombotic events included 41 venous thromboembolism and 34 arterial thrombosis. Age, cardiovascular disease, intensive care unit treatment, white blood cells, D-dimer, albumin and troponin blood levels were associated with thrombotic events. In a multivariable regression logistic model, intensive care unit treatment (Odds Ratio [OR]: 6.0; 95% Confidence Interval [CI] 2.8-12.6; p < 0.001); coronary artery disease (OR: 2.4; 95% CI 1.4-5.0; p = 0.022); and albumin levels (OR: 0.49; 95% CI 0.28-0.87; p = 0.014) were associated with ischemic events. Age, sex, chronic obstructive pulmonary disease, diabetes, heart failure, coronary heart disease, intensive care unit treatment, in-hospital thrombotic events, D-dimer, C-reactive protein, troponin, and albumin levels were associated with mortality. A multivariable Cox regression analysis showed that in-hospital thrombotic events (hazard ratio [HR]: 2.72; 95% CI 1.59-4.65; p < 0.001), age (HR: 1.035; 95% CI 1.014-1.057; p = 0.001), and albumin (HR: 0.447; 95% CI 0.277-0.723; p = 0.001) predicted morality. CONCLUSIONS: Covid-19 patients experience an equipollent rate of venous and arterial thrombotic events, that are associated with poor survival. Early identification and appropriate treatment of Covid-19 patients at risk of thrombosis may improve prognosis.

Cardiovascular and Cerebrovascular Complications With COVID-19.

The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 has affected the health of people across the globe. Cardiovascular diseases (CVDs) have a significant relationship with COVID-19, both as a risk factor and prognostic indicator, and as a complication of the disease itself. In addition to predisposing to CVD complications, the ongoing pandemic has severely affected the delivery of timely and appropriate care for cardiovascular conditions resulting in increased mortality. The etiology behind the cardiac injury associated with severe acute respiratory syndrome coronavirus-2 is likely varied, including coronary artery disease, microvascular thrombosis, myocarditis, and stress cardiomyopathy. Further large-scale investigations are needed to better determine the underlying mechanism of myocardial infarction and other cardiac injury in COVID-19 patients and to determine the incidence of each type of cardiac injury in this patient population. Telemedicine and remote monitoring technologies can play an important role in optimizing outcomes in patients with established CVD. In this article, we summarize the various impacts that COVID-19 has on the cardiovascular system, including myocardial infarction, myocarditis, stress cardiomyopathy, thrombosis, and stroke.

Coronary Artery Dilation in an Asymptomatic Pediatric Patient with COVID19 Antibodies.

We describe a 16-year-old asymptomatic male who presented with coronary artery dilation (z score + 2.3) identified on echo performed solely for presence of COVID-19 antibodies. This case raises the question of whether cardiac screening should be considered for all patients with a history of COVID-19.

Possible mechanisms responsible for acute coronary events in COVID-19.

The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.