Rapid development of artificial intelligence (AI) is gaining grounds in medicine. Its huge impact and inevitable necessity are also reflected in cardiovascular imaging. Although AI would probably never replace doctors, it can significantly support and improve their productivity and diagnostic performance. Many algorithms have already proven useful at all stages of the cardiac imaging chain. Their crucial practical applications include classification, automatic quantification, notification, diagnosis, and risk prediction. Consequently, more reproducible and repeatable studies are obtained, and personalized reports may be available to any patient. Utilization of AI also increases patient safety and decreases healthcare costs. Furthermore, AI is particularly useful for beginners in the field of cardiac imaging as it provides anatomic guidance and interpretation of complex imaging results. In contrast, lack of interpretability and explainability in AI carries a risk of harmful recommendations. This review was aimed at summarizing AI principles, essential execution requirements, and challenges as well as its recent applications in cardiovascular imaging.

Coronavirus disease 2019 (COVID-19) caused by “Severe Acute Respiratory Syndrome Coronavirus-2” (SARS-CoV-2) infection emerged in Wuhan, a city of China, and spread to the entire planet in early 2020. The virus enters the respiratory tract cells and other tissues via ACE2 receptors. Approximately 20% of infected subjects develop severe or critical disease. A cytokine storm leads to over inflammation and thrombotic events. The most common clinical presentation in COVID-19 is pneumonia, typically characterized by bilateral, peripheral, and patchy infiltrations in the lungs. However multi-systemic involvement including peripheral thromboembolic skin lesions, central nervous, gastrointestinal, circulatory, and urinary systems are reported. The disease has a higher mortality compared to other viral agents causing pneumonia and unfortunately, no approved specific therapy, nor vaccine has yet been discovered. Several clinical trials are ongoing with hydroxychloroquine, remdesivir, favipiravir, and low molecular weight heparins. This comprehensive review aimed to summarize coagulation abnormalities reported in COVID-19, discuss the thrombosis, and inflammation-driven background of the disease, emphasize the impact of thrombotic and inflammatory processes on the progression and prognosis of COVID-19, and to provide evidence-based therapeutic guidance, especially from antithrombotic and anti-inflammatory perspectives.

Objective: Computed tomography pulmonary angiography (CTPA) is used for the main diagnosis in acute pulmonary embolism (APE). Determining the thrombus location in the pulmonary vascular tree is also important for predicting disease severity. This study aimed to analyze the correlation of the thrombus location and the clot burden with the disease severity and the risk stratification in patients with APE.
Methods: The study included patients with APE diagnosed by CTPA who were admitted to the hospital between January 28, 2016, and July 1, 2019. Data collected were markers of severity in APE, including patient demographics, comorbidities, length of hospital stay, pulmonary embolism severity index (PESI) score, modified PESI score, Wells score, risk stratification according to the American Heart Association, systolic blood pressure (SBP), right ventricle diameter to left ventricle diameter ratio, pulmonary arterial pressure, brain natriuretic peptide, troponin, D-dimer, and plasma lactate levels, and vessel location of the thrombus, clot burden score, ratio of the pulmonary artery trunk diameter/aortic diameter, superior vena cava diameter (SVC) by CTPA, and survival. All parameters were analyzed in correlation with clot load and vessel location.
Results: Thrombus vascular location was found to be correlated with risk stratification and negatively correlated with SBP. Simplified Mastora score was correlated with risk stratification, SVC diameter, and D-dimer and negatively correlated with SBP. Occlusion of both the pulmonary artery trunk and any pulmonary artery with thrombus was associated with massive APE.
Conclusion: The level of the occluded vessel on CTPA may provide the ability to risk-stratify, and the clot burden score may be used for assessing both risk stratification and cardiac strain.

Objective: This prospective study aimed to investigate the myocardial energy metabolism in severe mitral regurgitation (MR) and explore its effect on postoperative differentiation of ejection fraction (EF).
Methods: A total of 85 patients with severe MR were prospectively enrolled from October 2018 to June 2019. During the study period, a total of 50 patients underwent mitral valve surgery and 49 patients were finally enrolled due to 1 missing data. Left ventricular function, circumferential end-systolic stress (cESS), and myocardial energy expenditure (MEE) were measured by transthoracic echocardiography preoperatively and 3 months after surgery. Patients were divided into 2 groups according to absolute difference of postoperative differentiation of EF.
Results: Nine patients underwent mitral valve repair and 40 underwent prosthetic valve replacement. Patients with reduced EF had higher MEE demonstrated with cESS and MEE. Negative correlation between preoperative EF and N-terminal pro-brain natriuretic peptide (NT-proBNP), cESS, MEEs, and MEEm and positive correlation between preoperative EF and effective regurgitant orifice area were found. Complications occurred in 12 patients during hospitalization. Basal NT-proBNP, left atrium (LA), and cESS were significantly higher in postoperatively decreased EF group. Taking into consideration the covariates of multiple logistic regression analysis, LA and cESS were found to be independent predictors of EF reduction postoperatively.
Conclusion: Higher LA and cESS are independent predictors of postoperative EF reduction. Preoperative high end-systolic stress could predict postoperative EF reduction and hence could be helpful for determining the timing of mitral valve surgery. Although MEE was higher in postoperatively decreased EF group, it did not reach statistical significance.

Objective: The aim compares the blood gases, vital signs, mechanical ventilation requirement, and length of hospitalization in patients with hypertensive pulmonary edema treated with standard oxygen therapy (SOT) and high-flow oxygen therapy (HFOT).
Methods: This prospective observational study was conducted in patients with tachypneic, hypoxemic, hypertensive pulmonary edema. The patients’ 0th, 1st, and 2nd hour blood gas results; 0th, 1st, and 2nd hour vital signs; requirement of endotracheal intubation, length of hospitalization, and the prognosis were recorded on the study form.
Results: A total of 112 patients were included in this study, of whom 50 underwent SOT and 62 received HFOT. The initial blood gas analysis revealed significantly lower levels of pH, PaO2, and SpO2 and significantly higher levels of PaCO2 in the HFOT group. Patients in the HFOT group had significantly higher respiratory rate and pulse rate and significantly lower SpO2 values. The recovery of vital signs was significantly better in the HFOT group (p<0.05). Similarly, follow-up results of arterial blood gas analysis were better in the HFOT group (p<0.05). Both length of stay in the emergency department (p<0.05) and length of intensive care unit hospitalization s significantly shorter in the HFOT group (p<0.05).
Conclusion: HFOT can be much more effective in patients with hypertensive pulmonary edema than SOT as it shortens the length of stay both in the emergency service and in the intensive care unit. HFOT also provides better results in terms of blood gas analysis, heart rate, and respiratory rate in the follow-up period.

Objective: Elevated systolic blood pressure (SBP) can significantly increase the bleeding risk in patients with atrial fibrillation (AF). However, it is unclear whether elevated diastolic blood pressure (DBP), in the presence of well-controlled SBP is also associated with bleeding. Therefore, we aimed to examine the specific relationship between DBP and bleeding in patients with AF treated with anticoagulants and had well-controlled SBP.
Methods: We analyzed data from 542 of 929 patients with nonvalvular AF (NVAF) treated with dabigatran from the Monitor System for the Safety of Dabigatran Treatment study (MISSION-AF) who had a SBP of 120–140 mm Hg at the time of enrollment. The association between DBP and bleeding was analyzed using multivariate logistic regression and smooth curve fitting (penalized spline method). Threshold saturation effect analysis was used to show the nonlinear relationship between DBP and bleeding.
Results: After 3 months of follow-up, 49 bleeding events occurred. Compared with participants with DBP <80 mm Hg, those with DBP ≥80 mm Hg had a 118% higher bleeding risk [hazard ratio (HR): 2.18; 95% confidence interval (CI): 1.19, 3.98; p<0.05]. The smooth curve showed a nonlinear relationship between DBP and bleeding risk, and the inflection point of DBP was 80 mm Hg. When DBP was ≥80 mm Hg, the bleeding risk increased by 59% (HR: 1.59; 95% CI: 1.16, 2.19; p<0.05) for every 5 mm Hg increase in DBP.
Conclusion: Upon achieving an optimal SBP (120–140 mm Hg), a higher DBP might be associated with a higher bleeding risk in patients with NVAF treated with dabigatran.

Objective: Stent thrombosis (ST) is a common phenomenon in acute coronary syndromes (ACS) when compared to stable coronary artery disease. This study analyzed the patient- and operator-related risk factors of ST in ACS.
Methods: Coronary angiograms of 1738 consecutive ACS patients admitted in a large tertiary center between year 2014 and 2016 were analyzed retrospectively for the presence of ST. The paired angiograms [ST in ACS during and after percutaneous coronary intervention (PCI)] of the patients were analyzed by two independent observers, with focus on lesion characteristics and procedure techniques. Clinical and laboratory data were collected.
Results: Stent thrombosis was found in 29 (1.6%) ACS patients, with a combination of at least one clinical/laboratory risk factor and one lesion/operator risk factor identified in 28 (96%) out of the 29 ACS patients with ST. The following risk factors for ST were found: Renal insufficiency (OR=4.14, p<0.001, 95% CI=1.73-9.88), type 2 diabetes (OR=2.21, p=0.034, 95% CI=1.06-4.61), excessive alcohol consumption (OR=3.12, p=0.023, 95% CI=1.17-8.33), stent implantation for ST-elevation myocardial infarction (STEMI) (OR=2.28, p=0.029, 95% CI=1.08-4.81), left main (LM) or left anterior descending artery (LAD) as culprit lesion (OR=2.80, p=0.010, CI 95%=1.27-5.95), and absence of antiplatelet therapy prior to ST (OR=3.58, p=0.002, 95% CI=1.60-7.96). The following lesion/operator possible risk factors were identified: Bifurcation lesion (n=7; 24%), heavy coronary calcifications (n=13; 44%), in-stent restenosis with secondary plate rupture (n=6, 20%), inappropriate stent size selection (n=6, 20%), and errors in periprocedural drug administration (n=4, 14%).
Conclusion: ST occurred in 1/62 ACS patients after PCI. A combination of clinical/laboratory and lesion/operator risk factors were present in almost all ACS patients with ST. This finding may support the search for strictly individualized strategies for the treatment of ACS patients with ST after PCI.