Association of glomerular hyperfiltration with carotid artery plaque in the general population.

BACKGROUND AND AIMS: Glomerular hyperfiltration (GHF) is a hemodynamic change of the kidney as an adaptive response to nephron loss. Although GHF is associated with metabolic risk factors and cardiovascular disease (CVD), the mechanisms that explain these relationships remain largely unknown. This is partially caused by a non-unified definition of GHF based on pathophysiologic vascular changes. Thus, the objective of this study was to evaluate the association between various definitions of GHF and carotid plaque in a health checkup cohort. METHODS: A total of 4493 individuals without history of CVD who had carotid ultrasonography (USG) results available between January 2016 and June 2018 were enrolled. GHF was defined as >90th percentile of eGFR residuals after adjusting for confounding factors. Carotid plaque score was calculated based on carotid USG results. RESULTS: Of 4493 individuals (mean age, 52.3 ± 10.1 years; 3224 [71.8%] males), 449 subjects were included in the GHF group (mean eGFR, 107.0 ± 7.1 ml/min/1.73 m2) and 4044 subjects were included in the non-GHF group (mean eGFR, 92.5 ± 12.3 ml/min/1.73 m2). When the GHF group was compared to the non-GHF group, GHF was associated with the presence of significant carotid plaque (carotid plaque score ≥2) (adjusted OR: 1.46; 95% CI: 1.16 to 1.83; p = 0.001). GHF defined in this study showed higher sensitivity to the presence of carotid plaque than other definitions of GHF. CONCLUSIONS: GHF status was associated with risk of carotid plaque in individuals without history of CVD. Presence of subclinical carotid plaque was associated with risk of future CVD. Therefore, GHF based on creatinine could be a useful surrogate marker for surveillance of CVD in asymptomatic individuals.

Increased EAT volume after anthracycline chemotherapy is associated with a low risk of cardiotoxicity in breast cancer.

PURPOSE: Chemotherapy-induced cardiotoxicity is a critical issue for patients with breast cancer. Change of epicardial adipose tissue (EAT) is associated with cardiac dysfunction. The objective of this study was to investigate the relationship between EAT and chemotherapy-induced cardiotoxicity. METHODS: This retrospective study analyzed EAT on chest computed tomography (CT) of patients with early breast cancer using automatic, quantitative measurement software between November 2015 and January 2020. Changes in EAT before and after initiation of chemotherapy were compared according to the type of anticancer drug. Subclinical cardiotoxicity was defined as worsening ≥ 10% in left ventricular ejection fraction to an absolute value > 50% with a lower limit of normal measured with standard echocardiography. RESULTS: Among 234 patients with breast cancer, 85 were treated with adjuvant anthracycline-based (AC) and 149 were treated with non-anthracycline-based (non-AC) chemotherapy. There was a significant increase in EAT volume index (mL/kg/m2) at the end of chemotherapy compared to that at the baseline in the AC group (3.33 ± 1.53 vs. 2.90 ± 1.52, p < 0.001), but not in the non-AC group. During the follow-up period, subclinical cardiotoxicity developed in 20/234 (8.6%) patients in the total population [13/85 (15.3%) in the AC group and 7/149 (4.8%) in the non-AC group]. In the multivariable analysis, EAT volume index increment after chemotherapy was associated with a lower risk of subclinical cardiotoxicity in the AC group (Odds ratio: 0.364, 95% CI 0.136-0.971, p = 0.044). CONCLUSIONS: Measurement of EAT during anthracycline-based chemotherapy might help identify subgroups who are vulnerable to chemotherapy-induced cardiotoxicity. Early detection of EAT volume change could enable tailored chemotherapy with cardiotoxicity prevention strategies.

Role and Prognosis of Extracorporeal Life Support in Patients Who Develop Cardiac Arrest during or after Office-Based Cosmetic Surgery.

BACKGROUND: Cardiac arrest during or after office-based cosmetic surgery is rare, and little is known about its prognosis. We assessed the clinical outcomes of patients who developed cardiac arrest during or after cosmetic surgery at office-based clinics. METHODS: Between May 2009 and May 2016, 32 patients who developed cardiac arrest during or after treatment at cosmetic surgery clinics were consecutively enrolled. We compared clinical outcomes, including complications, between survivors (n=19) and non-survivors (n=13) and attempted to determine the prognostic factors of mortality. RESULTS: All 32 of the patients were female, with a mean age of 30.40±11.87 years. Of the 32 patients, 13 (41%) died. Extracorporeal life support (ECLS) was applied in a greater percentage of non-survivors than survivors (92.3% vs. 47.4%, respectively; p=0.009). The mean duration of in-hospital cardiopulmonary resuscitation (CPR) was longer for the non-survivors than the survivors (31.55±33 minutes vs. 7.59±9.07 minutes, respectively; p=0.01). The mean Acute Physiology and Chronic Health Evaluation score was also higher among non-survivors than survivors (23.85±6.68 vs. 16.79±7.44, respectively; p=0.01). No predictor of death was identified in the patients for whom ECLS was applied. Of the 19 survivors, 10 (52.6%) had hypoxic brain damage, and 1 (5.3%) had permanent lower leg ischemia. Logistic regression analyses revealed that the estimated glomerular filtration rate was a predictor of mortality. CONCLUSION: Patients who developed cardiac arrest during or after cosmetic surgery at office-based clinics experienced poor prognoses, even though ECLS was applied in most cases. The survivors suffered serious complications. Careful monitoring of subjects and active CPR (when necessary) in cosmetic surgery clinics may be essential.

Beta 2-adrenergic receptor agonists are novel regulators of macrophage activation in diabetic renal and cardiovascular complications.

Macrophage activation is increased in diabetes and correlated with the onset and progression of vascular complications. To identify drugs that could inhibit macrophage activation, we developed a cell-based assay and screened a 1,040 compound library for anti-inflammatory effects. Beta2-adrenergic receptor (ß2AR) agonists were identified as the most potent inhibitors of phorbol myristate acetate-induced tumor necrosis factor-α production in rat bone marrow macrophages. In peripheral blood mononuclear cells isolated from streptozotocin-induced diabetic rats, ß2AR agonists inhibited diabetes-induced tumor necrosis factor-α production, which was prevented by co-treatment with a selective ß2AR blocker. To clarify the underlying mechanisms, THP-1 cells and bone marrow macrophages were exposed to high glucose. High glucose reduced ß-arrestin2, a negative regulator of NF-κB activation, and its interaction with IκBα. This subsequently enhanced phosphorylation of IκBα and activation of NF-κB. The ß2AR agonists enhanced ß-arrestin2 and its interaction with IκBα, leading to downregulation of NF-κB. A siRNA specific for ß-arrestin2 reversed ß2AR agonist-mediated inhibition of NF-κB activation and inflammatory cytokine production. Treatment of Zucker diabetic fatty rats with a ß2AR agonist for 12 weeks attenuated monocyte activation as well as pro-inflammatory and pro-fibrotic responses in the kidneys and heart. Thus, ß2AR agonists might have protective effects against diabetic renal and cardiovascular complications.

Delayed Surgery for Aortic Dissection after Intravenous Thrombolysis in Acute Ischemic Stroke.

We report a case of aortic dissection masquerading as acute ischemic stroke followed by intravenous thrombolysis. A 59-year-old man presented with dizziness. After examination, the patient had a seizure with bilateral Babinski signs. Soon after identifying multiple acute infarctions in both hemispheres on diffusion-weighted brain magnetic resonance (MR) imaging, tissue plasminogen activator (t-PA) was administered. Both common carotid arteries were invisible on MR angiography, and subsequent chest computed tomography revealed an aortic dissection. The emergency operation was delayed for 13 hours due to t-PA administration. The patient died of massive bleeding.

Successful extracorporeal life support in sudden cardiac arrest due to coronary anomaly.

Extracorporeal life support (ECLS) has recently been reported to have a survival benefit in patients with cardiac arrest. It is now used widely as a lifesaving modality. Here, we describe a case of sudden cardiac arrest (SCA) in a young athlete with an anomalous origin of the right coronary artery from the left coronary sinus. Resuscitation was successful using ECLS before curative bypass surgery. We highlight the efficacy of ECLS for a patient with SCA caused by a rare, unexpected aetiology. In conclusion, ECLS was a lifesaving modality for SCA due to an anomalous coronary artery in this young patient.

Fatal massive and recurring pulmonary embolism followed by thrombocytopenia developed after heparin and warfarin treatment in a patient with metastatic breast cancer with an incidental large right atrial thrombus.

A thromboembolic complication such as pulmonary embolism in patients who had cancer and mobile thrombi in the heart is a rare but fatal complication. Surgical thromboembolectomy is considered as the classical treatment of choice. In case of inoperable patient, catheter-directed therapy may be an alternative treatment. We report an interesting case of metastatic breast cancer with a large and mobile right atrial thrombus complicated by a massive and subsequently recurring pulmonary embolism, followed by thrombocytopenia developed after heparin and warfarin treatment.