Objective: Low free triiodothyronine (fT3) is common in elderly patients with cardiovascular disease. The purpose of this study was to evaluate the relationship between low fT3 and contrast-induced acute kidney injury (CI-AKI), including the long-term outcomes, in elderly patients after a percutaneous coronary intervention (PCI).
Methods: A total of 350 patients aged ≥75 years who underwent PCI between January 2012 and December 2015 were consecutively enrolled. The perioperative thyroid function, including fT3, was measured before PCI. A low fT3 was defined as fT3 <3.1 pmol/L with normal thyrotropin and free thyroxine. CI-AKI was defined as an absolute serum creatinine (SCr) increase ≥0.30 mg/dL or a relative increase in SCr ≥50% from the baseline value within 48 hours after contrast media exposure. A multivariate logistic regression analysis was applied to analyze whether low fT3 was an independent risk factor for CI-AKI. The Cox regression analysis was used to evaluate the relationship between low fT3 and long-term prognosis.
Results: A total of 46 (13.1%) patients developed CI-AKI. The incidence of CI-AKI was significantly higher in the low fT3 group than in the normal group (26.5% vs. 9.9%, p<0.01). A multivariable logistic analysis demonstrated that a low fT3 level was significantly related to CI-AKI [odds ratio (OR) =2.41; 95% confidence interval (CI), 1.11–5.27; p=0.027]. The Cox regression analysis showed that a low fT3 was associated with long-term mortality [adjusted hazard ratio (HR)= 2.00; 95% CI, 1.04–3.83; p=0.037] during the follow-up of mean 1.67 years.
Conclusion: A low fT3 concentration was independently associated with CI-AKI and poor prognosis in elderly patients who had undergone PCI.

Objective: The relationship between prognosis and heart rate remains unclear among patients diagnosed with heart failure with mid-range ejection fraction (HFmrEF). The aim of the present study was to assess the effect of heart rate in this group of patients.
Methods: Of the 197 patients diagnosed with HFmrEF, 92 had a heart rate <70 beats/min (bpm), and 105 had a heart rate ≥70 bpm. We analyzed the outcomes including all-cause death and HF-related hospitalization and evaluated the quality of life.
Results: The outcome demonstrated a lower incidence in patients with heart rate <70 bpm. The outcome-free survival illustrated significant difference in survival rate (p=0.045). The Minnesota Living with Heart Failure Questionnaire total scores and physical subscale in the lower heart rate group decreased compared with the heart rate ≥70 bpm group (p=0.048 and p=0.03, respectively). In the following analysis of patients with sinus rhythm, beta blockers showed great positive effects on patients with heart rate <70 bpm (p=0.046), as for the quality of life in patients with beta blocker, heart rate <70 bpm showed lower total and physical scores (p=0.025 and p=0.017, respectively).
Conclusion: Our results showed that heart rate is an important prognostic factor in patients with HFmrEF. Patients with heart rate <70 bpm was related with a lower risk of outcomes and better quality of life. Beta blockers reduced the outcome rate in patients with sinus rhythm.

Objective: Identification of the asymptomatic target organ damage (AOD) helps to stratify the overall risk of cardiovascular (CV) diseases and guides a treatment decision in hypertensive patients without a symptomatic CV or renal disease. The endothelial-cell-specific molecule 1 (endocan) is regarded as a novel marker of endothelial dysfunction. Its release is increased in hypertensive patients, especially those with symptomatic CV and renal disease. In the present study, we aimed to evaluate the endocan levels in asymptomatic hypertensive patients with or without AOD.
Methods: The study included 132 asymptomatic hypertensive patients, and 101 of who had at least one AOD.
Results: Serum endocan levels did not differ between patients with and without AOD (3.81±0.78 vs. 3.83±0.63 ng/mL, p=0.88). An analysis according to the presence of any specific AOD did not show any difference between groups. No significant correlation was found between serum endocan levels and any of the continuous variables related to AOD, such as the pulse pressure, carotid intimae-media thickness, cardio-ankle vascular index, ankle-brachial index, left ventricular mass index, Sokolow–Lyon index, Cornell voltage-duration product, and estimated glomerular filtration rate.
Conclusion: Endocan may not serve as a useful biomarker at asymptomatic vascular stages of hypertension, despite its role in indicating disease severity and inflammatory activation in advanced symptomatic CV and renal disease.

Objective: Intravascular ultrasound (IVUS) has developed as a preferable choice for optimizing the stenting procedures mainly because it will have good access to vessel size, lesion length, or severity accurately. However, it still remains unclear about the benefits of IVUS guidance in drug-eluting stent (DES) implantation for patients with unprotected left main coronary artery (ULMCA) stenosis. The aim of the present study was to evaluate the clinical outcomes with respect to IVUS-guided DES implantation for these patients.
Methods: A total of 336 consecutive patients from December 2010 to December 2015 were enrolled in the study. The patients were then randomly assigned into two groups: IVUS-guided group (n=167) and control group (n=169). The primary endpoint was the incidence of composite major adverse cardiac events (MACEs), including cardiac death, myocardial infarction (MI), and target vessel revascularization (TVR). The risk of stent thrombosis (ST) was chosen as the safety endpoint.
Results: After a 1-year follow-up, the occurrence of composite MACE in the IVUS-guided group was significantly lower than that in the control group (13.2% vs. 21.9%, p=0.031), which might mainly result from the significant reduction in the risk of cardiac death (1.8% vs. 5.9%, p=0.048). Dramatically, the risk of MI did not differ significantly between the two groups (11.4% vs. 13.6%, p=0.478), though a tended reduction in TVR was observed under IVUS guidance (4.2% vs. 8.9%, p=0.068). There was no statistical significance between the two groups with respect to the risk of target lesion revascularization (IVUS-guided vs. control: 1.2% vs. 3.0%, p=0.239) and ST (IVUS-guided vs. control: 1.2% vs. 3.0%, p=0.246).
Conclusion: The possible feasibility of IVUS-guided DES implantation for patients with ULMCA stenosis was supported by the present study. Larger and more powerful randomized trials were still warranted to research the whole benefits of IVUS guidance for these patients.

Objective: Omentin is a recently identified novel adipocytokine mainly expressed in the epicardial adipose tissue. Although it has favorable effects on cardiovascular disease, the impact of omentin on the hearts is still an understudied issue. The aim of the present study was to investigate the possible effects of omentin on isolated rat heart.
Methods: Using the Langendorff method, 28 adult male Sprague–Dawley rat hearts were isolated and perfused with modified Krebs–Henseleit solution (mK–Hs). Concentrations of 100, 200, and 400 ng/mL omentin were given to the hearts for 30 min. The control group (n=7) was perfused with mK–Hs alone. Gene expressions in the left ventricle tissue were determined by real-time polymerase chain reaction. Left ventricular cyclic adenosine monophosphate and cyclic guanosine monophosphate (cGMP) concentrations were determined by using enzyme-linked immunosorbent assay.
Results: All concentrations of omentin significantly decreased left ventricular developed pressure and maximal rate of pressure development that are the indexes of cardiac contractility. At the same time, omentin decreased both phosphoinositide 3-kinase γ (PI3Kγ) and sarcolemmal L-type Ca2+ channel (CaV1.2) mRNA levels. Moreover, this peptide at concentrations of 200 and 400 ng/mL increased endothelial nitric oxide synthase (eNOS) mRNA. Furthermore, concentrations of 200 and 400 ng/mL omentin increased the amount of cGMP.
Conclusion: We conclude that acute omentin treatment decreases cardiac contractility. Elevated eNOS mRNA and cGMP levels with reduced CaV1.2 mRNA are likely to lead to negative inotropy.