Concomitant amyloidosis is the primary cause of endothelial and coronary microvascular dysfunction in carpal tunnel syndrome.

Study objectives: Patients with carpal tunnel syndrome (CTS) show manifestations of arterial abnormalities, including carotid intimal thickening and increased vascular stiffness. As carpal tunnel syndrome is associated with amyloidosis, we hypothesized that previously observed abnormalities can largely be related with concomitant amyloidosis rather than CTS itself. Design: Prospective observational study. Setting: Medeniyet University Goztepe Hospital. Participants: 61 patients with CTS (of whom 32 had biopsy-proven amyloidosis) and 36 healthy controls. Interventions: Subjects underwent ultrasound examinations for the measurement of coronary flow velocity reserve (CFVR), flow-mediated vasodilatation (FMD) and carotid intimal-media thickness (CIMT). Main outcome measures: Comparison of CFVR, FMD and CIMT in CTS patients with or without amyloidosis. Results: Patients with either CTS or CTS with concomitant amyloidosis (CTS-A) had significantly lower FMD (9.7 % ± 4.0 % in CTS and 10.3 % ± 4.6 % in CTS-A groups, p < 0.05 for both) and CFVR (2.4 (2.1-2.8) in CTS and 1.8 (1.6-2.1) in CTS-A groups, p < 0.001 for both) as compared to controls, while CIMT was only increased in CTS-A group (0.70 (0.60-0.80), p < 0.001). The reduction in CFVR was solely related to an increased basal flow velocity in CTS patients while there was also a reduced hyperemic flow velocity in patients with CTS-A. Conclusion: Most arterial phenomena in CTS patients could be attributable to concomitant amyloidosis, although endothelial dysfunction was present even in patients with CTS without amyloidosis.

Plasminogen activator inhibitor-1 levels as an indicator of severity and mortality for COVID-19.

OBJECTIVE: Coronavirus disease-19 (COVID-19) is a multisystemic disease that can cause severe illness and mortality by exacerbating symptoms such as thrombosis, fibrinolysis, and inflammation. Plasminogen activator inhibitor-1 (PAI-1) plays an important role in regulating fibrinolysis and may cause thrombotic events to develop. The goal of this study is to examine the relationship between PAI-1 levels and disease severity and mortality in relation to COVID-19. METHODS: A total of 71 hospitalized patients were diagnosed with COVID-19 using real time-polymerase chain reaction tests. Each patient underwent chest computerized tomography (CT). Data from an additional 20 volunteers without COVID-19 were included in this single-center study. Each patient's PAI-1 data were collected at admission, and the CT severity score (CT-SS) was then calculated for each patient. RESULTS: The patients were categorized into the control group (n=20), the survivor group (n=47), and the non-survivor group (n=24). In the non-survivor group, the mean age was 75.3±13.8, which is higher than in the survivor group (61.7±16.9) and in the control group (59.5±11.2), (p=0.001). When the PAI-1 levels were compared between each group, the non-survivor group showed the highest levels, followed by the survivor group and then the control group (p<0.001). Logistic regression analysis revealed that age, PAI-1, and disease severity independently predicted COVID-19 mortality rates. In this study, it was observed that PAI-1 levels with >10.2 ng/mL had 83% sensitivity and an 83% specificity rate when used to predict mortality after COVID-19. Then, patients were divided into severe (n=33) and non-severe (n=38) groups according to disease severity levels. The PAI-1 levels found were higher in the severe group (p<0.001) than in the non-severe group. In the regression analysis that followed, high sensitive troponin I and PAI-1 were found to indicate disease severity levels. The CT-SS was estimated as significantly higher in the non-survivor group compared to the survivor group (p<0.001). When comparing CT-SS between the severe group and the non-severe group, this was significantly higher in the severe group (p<0.001). In addition, a strong statistically significant positive correlation was found between CT-SS and PAI-1 levels (r: 0.838, p<0.001). CONCLUSION: Anticipating poor clinical outcomes in relation to COVID-19 is crucial. This study showed that PAI-1 levels could independently predict disease severity and mortality rates for patients with COVID-19.

Comparison of Medical Treatments According to the Characteristics of Idiopathic Premature Ventricular Contractions: Beta-blockers or Calcium Channel Blockers?

Objective: Premature ventricular contractions (PVCs) are a common arrhythmic condition. The first approach in patients with symptomatic and frequent PVC is medical treatment, primarily beta-blockers (BB) or calcium channel blockers (CCB), but it is still unclear which of the two should be chosen. This study investigated which drug treatment would be beneficial according to patient and electrocardiography (ECG) characteristics in patients with idiopathic PVC. Methods: We retrospectively analyzed 156 patients with PVC who came to the cardiology outpatient clinic. Seventy-one patients were responsive to BB, and 85 were responsive to CCB. Their demographic and ECG characteristics were compared. Results: The male ratio was higher (p<0.001), and the left ventricular ejection fraction was lower in BB responders than in CCB responders (p<0.001). Although the mean heart rate was higher in BB responders (p<0.001), the initial PVC burden was lower in BB responders than in CCB responders (p<0.001). The PVC QRS duration was longer in BB responders than in CCB responders (p<0.001). Similarly, the coupling interval variability was higher in BB responders (p=0.006). Conclusions: The evaluation of clinical and ECG parameters in patients with frequent idiopathic PVCs may determine whether BBs or CCBs should be chosen as initial treatment. Further prospective studies are needed to verify our findings and establish their clinical applicability.

The successful management of type III coronary perforation.

The coronary artery perforation during percutaneous coronary intervention is a nightmare for interventional cardiologists and is always hard to manage timely and properly. We present a 60-year-old male with periprocedural coronary perforation during ST-segment elevation myocardial infarction. A coronary balloon was inflated in the proximal left anterior descending (LAD) artery just after perforation and the 600 cc of hemorrhagic fluid was drained with the pericardial drainage set. The covered stent was deployed in the LAD and he was discharged on the 7th day. At an 18-month follow-up, he is on dual-antiplatelet therapy and the exercise stress test shows no ischemic changes.

A Associação de TWEAK com Calcificação da Artéria Coronária em Pacientes com Doença Renal Crônica / The Association of TWEAK with Coronary Artery Calcification in Patients with Chronic Kidney Disease

Resumo Fundamento O receptor fraco indutor de apoptose semelhante a fator de necrose tumoral solúvel (sTWEAK) é um membro da superfamília de TNF que tem um papel crítico na proliferação e inflamação na circulação arterial. Objetivos Este estudo prospectivo tem o objetivo de mostrar a relação entre os níveis de sTWEAK e calcificação da artéria coronária (CAC) em pacientes com doença renal crônica (DRC). Métodos Este estudo prospectivo incluiu 139 pacientes consecutivos que passaram por angiografia coronariana por tomografia computadorizada, por qualquer motivo, para síndromes coronarianas agudas, de agosto de 2020 a fevereiro de 2021. Um total de 12 pacientes foi excluído do estudo devido aos critérios de exclusão. Os pacientes foram divididos em dois grupos com base em terem um escore CAC menor que 400 (n=84) ou um escore de 400 ou mais (n=43). A significância foi presumida em p-valor bilateral <0,05. Resultados À medida que o escore CAC aumentou, os níveis de sTWEAK diminuíram de forma estatisticamente significativa e detectou-se uma relação forte entre níveis de sTWEAK e escore CAC (r: -0,779, p<0,001). A análise ROC revelou que o nível de corte ideal de sTWEAK para prever o escore CAC de 400 era 761 pg/mL com uma sensibilidade de 71% e especificidade de 73% (AUC: 0,78; IC 95%: 0,70-0,85; p <0,001). Conclusões Embora os estudos em larga escala tenham demonstrado uma correlação positiva entre os níveis de TFGe e sTWEAK, alguns estudos detectaram que o aumento nos níveis de sTWEAK estão associados a mortalidade e gravidade do sistema da artéria coronária em pacientes com DRC. Nossos resultados comprovam nossa hipótese de que os níveis de sTWEAK mostram calcificação coronária em vez de outros tipos de placas ateroscleróticas.

Abstract Background The soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) is a member of the TNF superfamily that plays a critical role in proliferation and inflammation in the arterial circulation. Objectives This prospective study aimed to show the relationship between the sTWEAK levels and coronary artery calcification (CAC) in patients with chronic kidney disease (CKD). Methods This prospective study included 139 consecutive patients undergoing computed coronary angiography for any reason except for acute coronary syndromes from August 2020 to February 2021. A total of 12 patients were excluded from the study due to exclusion criteria. Patients were divided into two groups with regard to having a CAC score of less than 400 (n=84) and 400 or more (n=43). Significance was assumed at a 2-sided p<0.05. Results As the CAC score increased, sTWEAK levels presented a statistically significant decrease, and a strong relationship between sTWEAK levels and the CAC score (r: -0.779, p<0.001) was observed. The ROC analysis revealed that the optimal cut-off level of sTWEAK for predicting the CAC score of 400 was 761 pg/mL with a sensitivity of 71% and a specificity of 73% (AUC: 0.78; 95% CI:0.70-0.85; p < 0.001) Conclusions Even though the large-scale studies showed a positive correlation between eGFR and the sTWEAK levels, some studies found the increased sTWEAK levels to be associated with mortality and the severity of the coronary artery system in patients with CKD. Our results support our hypothesis that the sTWEAK level shows coronary calcification rather than other types of atherosclerotic plaques.

Coronary flow velocity reserve is reduced in patients with an exaggerated blood pressure response to exercise.

Coronary artery disease and cardiovascular mortality are increased in patients with an exaggerated blood pressure response to exercise. The exact cause of this increase remains unknown, but previous studies have indicated the presence of endothelial dysfunction in peripheral arteries and subclinical atherosclerosis in these patients. The present study aimed to clarify whether coronary microvascular dysfunction is also present in patients with exaggerated blood pressure response to exercise. A total of 95 patients undergoing exercise testing were consecutively enrolled. Flow-mediated vasodilatation and carotid intima-media thickness were measured using standardized methods. A transthoracic echocardiography examination was performed to measure coronary flow velocity reserve. Patients with an exaggerated blood pressure response to exercise had significantly lower coronary flow velocity reserve than the controls (2.06 (1.91-2.36) vs. 2.27 (2.08-2.72), p = 0.004), and this difference was caused by a reduction in hyperemic flow velocity (57.5 (51.3-61.5) vs. 62.0 (56.0-73.0), p = 0.004) rather than a difference in basal flow (26.5 (22.3-29.8) vs. 26.0 (24.0-28.8), p = 0.95). Patients with an exaggerated blood pressure response to exercise also had a significantly greater carotid intima-media thickness and significantly lower flow-mediated vasodilatation than controls. However, an exaggerated blood pressure response to exercise remained a significant predictor of coronary microvascular dysfunction after adjusting for confounders (OR: 3.60, 95% CI: 1.23-10.54, p = 0.02). Patients with an exaggerated blood pressure response to exercise show signs of coronary microvascular dysfunction, in addition to endothelial dysfunction and subclinical atherosclerosis. This finding might explain the increased risk of coronary artery disease and cardiovascular mortality in these patients.

Prognostic significance of HDL-C on long-term mortality in patients with COVID-19 pneumonia in the Turkish population: A potential mechanism for population differences.

Coronavirus disease 2019 (COVID-19) is diagnosed by the evidence of the presence of multiple phenotypes, including thrombosis, inflammation, and alveolar and myocardial damage, which can cause severe illness and mortality. High-density lipoprotein cholesterol (HDL-C) has pleiotropic properties, including anti-inflammatory, anti-infectious, antithrombotic, and endothelial cell protective effects. The aim of this study was to investigate the HDL-C levels and one-year mortality after the first wave of patients with COVID-19 were hospitalized. Data from 101 patients with COVID-19 were collected for this single-center retrospective study. Lipid parameters were collected on the admission. The relationship between lipid parameters and long-term mortality was investigated. The mean age of the non-survivor group (n = 38) was 68.8 ± 14.1 years, and 55% were male. The HDL-C levels were significantly lower in the non-survivors group compared with the survivors (26.9 ± 9.5 vs 36.8 ± 12.8 mg/dl, respectively p < 0.001). Multivariate regression analysis determined that age, C-reactive protein, D-dimer, hypertension, and HDL-C as independent predictors for the development of COVID-19 mortality. HDL-C levels <30.5 mg/dl had 71% sensitivity and 68% specificity to predict one-year mortality after COVID-19. The findings of this study showed that HDL-C is a predictor of one-year mortality in Turkish patients with COVID-19. COVID-19 is associated with decreased lipid levels, and it is an indicator of the inflammatory burden and increased mortality rate. The consequences of long-term metabolic dysregulations in patients that have recovered from COVID-19 still need to be understood.

Post-cardiac injury syndrome after a concealed accessory pathway ablation.

The incidence of pericardial effusion for supraventricular tachycardias is less than 1%, and its combination with pleural effusion is rare. We present a case of severe pericardial and pleural effusion after a left-sided concealed accessory pathway ablation. The 480 cc of pericardial fluid was drained with the pericardial drainage system due to cardiac tamponade with hemodynamic compromise. The chest X-ray and thorax computed tomography showed moderate left-sided pleural effusion after pericardiocentesis. We considered the inflammatory response as the pathophysiology of the situation; we started ibuprofen 800 mg t.i.d. and colchicine 0.5 mg o.d. At a 3-week follow-up, her X-ray revealed the resolution of pleural effusion, and the echocardiography showed no pericardial effusion. .

The Association of TWEAK with Coronary Artery Calcification in Patients with Chronic Kidney Disease. / A Associação de TWEAK com Calcificação da Artéria Coronária em Pacientes com Doença Renal Crônica.

BACKGROUND: The soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) is a member of the TNF superfamily that plays a critical role in proliferation and inflammation in the arterial circulation. OBJECTIVES: This prospective study aimed to show the relationship between the sTWEAK levels and coronary artery calcification (CAC) in patients with chronic kidney disease (CKD). METHODS: This prospective study included 139 consecutive patients undergoing computed coronary angiography for any reason except for acute coronary syndromes from August 2020 to February 2021. A total of 12 patients were excluded from the study due to exclusion criteria. Patients were divided into two groups with regard to having a CAC score of less than 400 (n=84) and 400 or more (n=43). Significance was assumed at a 2-sided p<0.05. RESULTS: As the CAC score increased, sTWEAK levels presented a statistically significant decrease, and a strong relationship between sTWEAK levels and the CAC score (r: -0.779, p<0.001) was observed. The ROC analysis revealed that the optimal cut-off level of sTWEAK for predicting the CAC score of 400 was 761 pg/mL with a sensitivity of 71% and a specificity of 73% (AUC: 0.78; 95% CI:0.70-0.85; p < 0.001). CONCLUSIONS: Even though the large-scale studies showed a positive correlation between eGFR and the sTWEAK levels, some studies found the increased sTWEAK levels to be associated with mortality and the severity of the coronary artery system in patients with CKD. Our results support our hypothesis that the sTWEAK level shows coronary calcification rather than other types of atherosclerotic plaques.

FUNDAMENTO: O receptor fraco indutor de apoptose semelhante a fator de necrose tumoral solúvel (sTWEAK) é um membro da superfamília de TNF que tem um papel crítico na proliferação e inflamação na circulação arterial. OBJETIVOS: Este estudo prospectivo tem o objetivo de mostrar a relação entre os níveis de sTWEAK e calcificação da artéria coronária (CAC) em pacientes com doença renal crônica (DRC). MÉTODOS: Este estudo prospectivo incluiu 139 pacientes consecutivos que passaram por angiografia coronariana por tomografia computadorizada, por qualquer motivo, para síndromes coronarianas agudas, de agosto de 2020 a fevereiro de 2021. Um total de 12 pacientes foi excluído do estudo devido aos critérios de exclusão. Os pacientes foram divididos em dois grupos com base em terem um escore CAC menor que 400 (n=84) ou um escore de 400 ou mais (n=43). A significância foi presumida em p-valor bilateral <0,05. RESULTADOS: À medida que o escore CAC aumentou, os níveis de sTWEAK diminuíram de forma estatisticamente significativa e detectou-se uma relação forte entre níveis de sTWEAK e escore CAC (r: -0,779, p<0,001). A análise ROC revelou que o nível de corte ideal de sTWEAK para prever o escore CAC de 400 era 761 pg/mL com uma sensibilidade de 71% e especificidade de 73% (AUC: 0,78; IC 95%: 0,70-0,85; p <0,001). CONCLUSÕES: Embora os estudos em larga escala tenham demonstrado uma correlação positiva entre os níveis de TFGe e sTWEAK, alguns estudos detectaram que o aumento nos níveis de sTWEAK estão associados a mortalidade e gravidade do sistema da artéria coronária em pacientes com DRC. Nossos resultados comprovam nossa hipótese de que os níveis de sTWEAK mostram calcificação coronária em vez de outros tipos de placas ateroscleróticas.

Can plasma TWEAK levels predict coronary slow flow in patients with chronic kidney disease?

BACKGROUND: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in patients with chronic kidney disease (CKD), and it has demonstrated that its level declines as estimated glomerular filtration rate (eGFR) decreases. Most studies have found that the decreased TWEAK levels were seen in atherosclerosis and associated with plaque calcification. The objective of this prospective study was to clarify any relationship between coronary slow-flow (CSF) and TWEAK levels in patients with CKD under conservative treatment. METHODS: This prospective study included 93 consecutive patients with CKD (mean creatinine level was 1.8±0.4 mg/dL) undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020. A total of 93 patients were divided into two groups concerning having CSF (n=35) or no-CSF (n=58). RESULTS: Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs. 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, TWEAK levels increased statistically significantly (r:0.635/ p<0.001). Receiver operating characteristic (ROC) analysis showed that TWEAK levels of 516 pg/mL could predict CSF in patients with CKD. CONCLUSIONS: Our study has shown that plasma TWEAK levels were an independent predictor for CSF in patients with CKD. In addition, our study has found that elevated TWEAK levels may not reflect the healthy arteries as it was hypothesized in the past.

Coronary microvascular dysfunction is common in patients hospitalized with COVID-19 infection.

BACKGROUND AND AIMS: Microvascular disease is considered as one of the main drivers of morbidity and mortality in severe COVID-19, and microvascular dysfunction has been demonstrated in the subcutaneous and sublingual tissues in COVID-19 patients. The presence of coronary microvascular dysfunction (CMD) has also been hypothesized, but direct evidence demonstrating CMD in COVID-19 patients is missing. In the present study, we aimed to investigate CMD in patients hospitalized with COVID-19, and to understand whether there is a relationship between biomarkers of myocardial injury, myocardial strain and inflammation and CMD. METHODS: 39 patients that were hospitalized with COVID-19 and 40 control subjects were included to the present study. Biomarkers for myocardial injury, myocardial strain, inflammation, and fibrin turnover were obtained at admission. A comprehensive echocardiographic examination, including measurement of coronary flow velocity reserve (CFVR), was done after the patient was stabilized. RESULTS: Patients with COVID-19 infection had a significantly lower hyperemic coronary flow velocity, resulting in a significantly lower CFVR (2.0 ± 0.3 vs. 2.4 ± 0.5, p < .001). Patients with severe COVID-19 had a lower CFVR compared to those with moderate COVID-19 (1.8 ± 0.2 vs. 2.2 ± 0.2, p < .001) driven by a trend toward higher basal flow velocity. CFVR correlated with troponin (p = .003, r: -.470), B-type natriuretic peptide (p < .001, r: -.580), C-reactive protein (p < .001, r: -.369), interleukin-6 (p < .001, r: -.597), and d-dimer (p < .001, r: -.561), with the three latter biomarkers having the highest areas-under-curve for predicting CMD. CONCLUSIONS: Coronary microvascular dysfunction is common in patients with COVID-19 and is related to the severity of the infection. CMD may also explain the "cryptic" myocardial injury seen in patients with severe COVID-19 infection.

A rare cause of idiopathic right outflow tract premature ventricular contraction: Type-4 renal tubular acidosis.

The premature ventricular contractions (PVCs) have usually good prognosis in patients without structural heart disease. In case of left ventricular ejection fraction depression or symptoms, antiarrhythmic drugs or cardiac ablations could be an option for management. We present a case of a patient with high burden of PVC admitted for cardiac ablation. Preoperative assessment revealed hyperkalemia and metabolic acidosis which ended up with type-4 renal tubular acidosis (RTA). Its rare cause and management may draw attention to the possibility of type -4 RTA as the cause of the PVC, and hyperkalemia.

Endothelial dysfunction in patients with acromegaly and It's association with Endocan.

OBJECTIVE: This study aims to assess endocan levels in patients with acromegaly who have active disease or disease in remission and to investigate a relation between endocan levels and endothelial dysfunction in these patients. DESIGN: The study is a case-control study. Study was conducted at Istanbul Medeniyet University Goztepe Training and Research Hospital between 2013 and 2019. Patients who were older than 18 years with acromegaly diagnosis were recruited if they agreed to participate. Patients with uncontrolled diabetes (DM), hypertension (HT), hyperlipidemia, decompensated heart failure, immune or infectious diseases, moderate-severe valve disease and stage 3 or more advanced chronic kidney disease were excluded. There were 30 healthy control subjects who agreed to participate to the study. Patients with acromegaly were divided into two groups as: disease active patients and patients in remission. Serum endocan levels were measured with enzyme linked immunosorbent assay (ELISA) method endothelial function was assessed with flow mediated dilatation (FMD). RESULTS: There were 85 patients included to the study. Twenty-three patients had active disease, 31 were in remission and 31 were healthy controls. FMD was higher in controls compared to patients in active disease and patients in remission (p < 0.001). There was no difference between patients with active disease for FMD and patients in remission (p = 0.088). There was statistically significant correlation between FMD and endocan and insulin like growth hormone-1 (IGF-1) levels of patients with acromegaly. As FMD increased endocan and IGF-1 decreased. A moderate negative relation between FMD and endocan was identified (p < 0.001, r:-0.409) as well as FMD and IGF-1 levels (p:0.011, r:-0.377). Along with endocan and IGF-1, DM, HT, sex, body mass index, age and uric acid were associated with changes in FMD. CONCLUSIONS: Endocan levels and endothelial function measured with FMD have an inverse relationship. Endocan may prove to be a marker for endothelial dysfunction in acromegaly.

Elevated D-dimer levels on admission are associated with severity and increased risk of mortality in COVID-19: A systematic review and meta-analysis.

BACKGROUND: In this systematic review and meta-analysis, we aimed to investigate the correlation of D-dimer levels measured on admission with disease severity and the risk of death in patients with coronavirus disease 2019 (COVID-19) pneumonia. MATERIALS AND METHODS: We performed a comprehensive literature search from several databases. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed in abstracting data and assessing validity. Quality assessment was performed using the Newcastle-Ottawa quality assessment scale (NOS). D-dimer levels were pooled and compared between severe/non-severe and surviving/non-surviving patient groups. Weighted mean difference (WMD), risk ratios (RRs) and 95% confidence intervals (CIs) were analyzed. RESULTS: Thirty-nine studies reported on D-dimer levels in 5750 non-severe and 2063 severe patients and 16 studies reported on D-dimer levels in 2783 surviving and 697 non-surviving cases. D-dimer levels were significantly higher in patients with severe clinical status (WMD: 0.45 mg/L, 95% CI: 0.34-0.56; p < 0.0001). Non-surviving patients had significantly higher D-dimer levels compared to surviving patients (WMD: 5.32 mg/L, 95% CI: 3.90-6.73; p < 0.0001). D-dimer levels above the upper limit of normal (ULN) was associated with higher risk of severity (RR: 1.58, 95% CI: 1.25-2.00; p < 0.0001) and mortality (RR: 1.82, 95% CI: 1.40-2.37; p < 0.0001). CONCLUSION: Increased levels of D-dimer levels measured on admission are significantly correlated with the severity of COVID-19 pneumonia and may predict mortality in hospitalized patients.

Echocardiographic features of patients with COVID-19 infection: a cross-sectional study.

COVID-19 patients with cardiac involvement have a high mortality rate. The aim of this study was to investigate the echocardiographic features in COVID-19 patients between severe and non-severe groups. For this single-center study, data from patients who were treated for COVID-19 between March 25, 2020 and April 15, 2020 were collected. Two-dimensional echocardiography (2DE) images were obtained for all patients. Patients were divided into two groups based on the severity of their COVID-19 infections. 2DE parameters indicating right ventricular (RV) and left ventricular (LV) functions were compared between the two groups. A total of 90 patients hospitalized for COVID-19 were included in this study. The mean age of the severe group (n = 44) was 63.3 ± 15.7 years, and 54% were male. The mean age of non-severe group (n = 46) was 49.7 ± 21.4 years, and 47% were male. In the severe group, RV and LV diameters were larger (RV, 36.6 ± 5.9 mm vs. 33.1 ± 4.8 mm, p = 0.003; LV 47.3 ± 5.8 mm vs. 44.9 ± 3.8 mm, p = 0.023), the LE ejection fraction (LVEF) and the RV fractional area change (RV-FAC) were lower (LVEF, 54.0 ± 9.8% vs. 61.9 ± 4.8%, p < 0.001; RV-FAC, 41.4 ± 4.1% vs. 45.5 ± 4.5%, p < 0.001), and pericardial effusions were more frequent (23% vs. 0%) compared to patients in the non-severe group. A multiple linear regression analysis determined that LVEF, right atrial diameter, high-sensitivity troponin I, d-dimer, and systolic pulmonary artery pressure, were independent predictors of RV dilatation. The results demonstrate that both right and left ventricular functions decreased due to COVID-19 infection in the severe group. 2DE is a valuable bedside tool and may yield valuable information about the clinical status of patients and their prognoses.

Prognostic significance of cardiac injury in COVID-19 patients with and without coronary artery disease.

OBJECTIVE: COVID-19 is a disease with high mortality, and risk factors for worse clinical outcome have not been well-defined yet. The aim of this study is to delineate the prognostic importance of presence of concomitant cardiac injury on admission in patients with COVID-19. METHODS: For this multi-center retrospective study, data of consecutive patients who were treated for COVID-19 between 20 March and 20 April 2020 were collected. Clinical characteristics, laboratory findings and outcomes data were obtained from electronic medical records. In-hospital clinical outcome was compared between patients with and without cardiac injury. RESULTS: A total of 607 hospitalized patients with COVID-19 were included in the study; the median age was 62.5 ± 14.3 years, and 334 (55%) were male. Cardiac injury was detected in 150 (24.7%) of patients included in the study. Mortality rate was higher in patients with cardiac injury (42% vs. 8%; P < 0.01). The frequency of patients who required ICU (72% vs. 19%), who developed acute kidney injury (14% vs. 1%) and acute respiratory distress syndrome (71%vs. 18%) were also higher in patients with cardiac injury. In multivariate analysis, age, coronary artery disease (CAD), elevated CRP levels, and presence of cardiac injury [odds ratio (OR) 10.58, 95% confidence interval (CI) 2.42-46.27; P < 0.001) were found to be independent predictors of mortality. In subgroup analysis, including patients free of history of CAD, presence of cardiac injury on admission also predicted mortality (OR 2.52, 95% CI 1.17-5.45; P = 0.018). CONCLUSION: Cardiac injury on admission is associated with worse clinical outcome and higher mortality risk in COVID-19 patients including patients free of previous CAD diagnosis.

Combined past preeclampsia and gestational diabetes is associated with a very high frequency of coronary microvascular dysfunction.

BACKGROUND: A history of preeclampsia (pPE) and gestational diabetes (pGDM) are female-specific risk markers for atherosclerosis and future cardiovascular risk. In addition to increasing the risk of established risk factors for atherosclerosis, such as hypertension or diabetes, evidence suggests that pregnancy-related complications can also directly accelerate atherosclerosis by inducing endothelial dysfunction. A combination of both conditions is seen in a subset of patients with pregnancy, though it is not known whether this combination increases the overall risk for cardiovascular events. AIMS: Present study aimed to find the impact of combined pPE/pGDM on the prevalence of coronary microvascular dysfunction (CMD). METHODS: A total of 24 patients with combined pPE/pGDM, 19 patients with isolated pPE and 63 patients with pGDM were included to the present study and a further 36 healthy women with no previous pregnancy-related complications served as controls. Coronary flow reserve was measured using echocardiography and CMD was defined as a coronary flow reserve ≤2.5. RESULTS: Patients with combined pPE/pGDM had a high prevalence of CMD (91%), which was significantly higher than controls (5.6%, p < 0.001) and patients with pGDM (55%, p = 0.01). A history of pPE on top of pGDM was associated with an increased risk of CMD (HR:6.28, 95%CI:1.69-23.37, p = 0.006) after multivariate adjustment, but pGDM did not increase the odds for CMD in those with pPE. CONCLUSIONS: Combined pPE/pDM is associated with a very high prevalence of CMD, which may indicate an increased risk for future cardiovascular events.

Evaluation of biventricular function in patients with COVID-19 using speckle tracking echocardiography.

A new infectious outbreak sustained by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is now spreading all around the world. The aim of this study was to evaluate the prognostic value of left ventricular global longitudinal strain (LV-GLS) and right ventricular longitudinal strain (RV-LS) in patients with coronavirus disease 2019 (COVID-19). In this prospective, single-center study, data were gathered from patients treated for COVID-19 between April 15 and April 30, 2020. Two-dimensional echocardiography (2-DE) and speckle tracking echocardiography (STE) images were obtained for all patients. Patients were divided into three groups: those with severe COVID-19 infection, those with non-severe COVID-19 infection, and those without COVID-19 infection (the control group). Data regarding clinical characteristics and laboratory findings were obtained from electronic medical records. The primary endpoint was in-hospital mortality. A total of 100 patients hospitalized for COVID-19 were included in this study. The mean age of the severe group (n = 44) was 59.1 ± 12.9, 40% of whom were male. The mean age of the non-severe group (n = 56) was 53.7 ± 15.1, 58% of whom were male. Of these patients, 22 died in the hospital. In patients in the severe group, LV-GLS and RV-LS were decreased compared to patients in the non-severe and control groups (LV-GLS: - 14.5 ± 1.8 vs. - 16.7 ± 1.3 vs. - 19.4 ± 1.6, respectively [p < 0.001]; RV-LS: - 17.2 ± 2.3 vs. - 20.5 ± 3.2 vs. - 27.3 ± 3.1, respectively [p < 0.001]). The presence of cardiac injury, D-dimer, arterial oxygen saturation (SaO2), LV-GLS (OR 1.63, 95% confidence interval [CI] 1.08-2.47; p = 0.010) and RV-LS (OR 1.55, 95% CI 1.07-2.25; p = 0.019) were identified as independent predictors of mortality via multivariate analysis. LV-GLS and RV-LS are independent predictors of in-hospital mortality in patients with COVID-19.

Serum prolidase activity in patients with cardiac syndrome X.

OBJECTIVE: Although the underlying mechanism is not yet fully understood, Cardiac Syndrome X (CSX) is defined as microvascular dysfunction. Prolidase plays a role in collagen synthesis. Increased serum prolidase activity (SPA) has been shown to correlate with collagen turnover. Augmented collagen turn-over may be associated with vascular fibrosis and microvascular dysfunction. In this study, we assessed whether there was a correlation between CXS and prolidase activity. METHODS: This case-control study included 45 consecutive CSX patients (mean age 50.7±6.5 years, 27 women) and 40 healthy controls (mean age 51.2±6.5 years, 25 women). Prolidase activity was determined with the Human Xaa-Pro Dipeptidase/Prolidase enzyme-linked immunosorbent assay kit (Cusabio Biotech Co. Ltd, China). RESULTS: Mean prolidase activity was 898.8±639.1 mU/mL in the CSX group and 434.1±289.8 mU/mL in the control group (p<0.001). In ROC analysis, it was found that the SPA value above 350 mU/mL sympathizes with the diagnosis of CSX. CONCLUSION: Increased SPA in CXS patients may play an essential role in the pathophysiology of CSX, leading to augmented oxidative stress and vascular fibrosis, endothelial dysfunction, and increased microvascular resistance.

Catheter-based management of a catheterization related stroke.

Ischemic stroke is a rare and serious complication of coronary angiography and percutaneous coronary intervention, which has high morbidity and mortality. To our knowledge, there is no large-scale randomized controlled trial for the management of catheter-related ischemic stroke. In this case study, we presented a 46-year-old male with peri-procedural ischemic stroke during the coronary angiography (CAG). The CAG was terminated after the stroke and the left carotid artery was selectively cannulated, and digital subtraction angiography (DSA) revealed total occlusion (Modified Thrombolysis in Cerebral Infarction, mTICI, 0) of the M1 part of the left middle cerebral artery (MCA). A stent-assisted thrombectomy was performed and the DSA revealed restoration of flow to the left MCA with mTICI 3 flow in the distal branches. The next day, the neurological exam showed no sensory, motor deficits. The patient was discharged four days later. In the setting of catheter-related stroke, mechanical thrombectomy seems to be the least time-consuming and effective approach.