scholarly journals Serum-Free Thyroxine Levels Were Associated with Pulmonary Hypertension and Pulmonary Artery Systolic Pressure in Euthyroid Patients with Coronary Artery Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-8
Author(s):  
Bingjie Wu ◽  
Jingjing Jiang ◽  
Minghui Gui ◽  
Lin Liu ◽  
Qiqige Aleteng ◽  
...  

The aim of this study was to evaluate the association between thyroid hormone levels, pulmonary hypertension (PH), and pulmonary artery systolic pressure (PASP) in euthyroid patients with coronary artery disease (CAD). A cross-sectional study was conducted in individuals who underwent coronary angiography and were diagnosed as CAD from March 2013 to November 2013. 811 subjects (185 women and 626 men) were included in this study. PASP was measured by transthoracic Doppler echocardiography. 86 patients were diagnosed as PH and had significantly higher free thyroxine (FT4) levels than those without PH. Multiple logistic regression analysis demonstrated an independent association of FT4 levels with PH after adjustment of gender, age, body mass index, systolic blood pressure, left ventricular ejection fraction, hypertension, and medication use of calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and nitrates. Serum-free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were not associated with PH. Furthermore, multivariate linear regression analysis showed that FT4 levels emerged as an independent predictor for PASP, while FT3 and TSH levels were not associated with PASP. Our study demonstrated that, in euthyroid patients with CAD, FT4 was an independent risk factor for PH, and FT4 levels were independently associated with PASP.

2008 ◽  
Vol 55 (5) ◽  
pp. 819-826 ◽  
Author(s):  
Chan-Hee JUNG ◽  
Eun-Jung RHEE ◽  
Hun-Sub SHIN ◽  
Sook-Kyoung JO ◽  
Jong-Chul WON ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Nima Ghasemzadeh ◽  
Raghda Alanbari ◽  
Salim Hayek ◽  
Mosab Awad ◽  
Mohamed Khayata ◽  
...  

Background: Elevated pulmonary artery systolic pressure (PASP) is associated with a worse outcome in heart failure (HF), but the prognostic role of PASP in patients with coronary artery disease (CAD) remains unknown. Methods: 863 patients with known or suspected CAD (age: 64±13 years, 62% male) enrolled in the Emory Cardiovascular Biobank were followed for a median 455 days for all-cause death. Transthoracic echocardiographic parameters included measurement of left ventricular ejection fraction (LVEF, range: 5-80%) and diastolic function parameters. Youden’s index from the receiver operating curve analysis was used to determine the best discriminatory cutoff for PASP (cutoff=43 mmHg). Cox regression was performed to determine independent predictors of mortality. Results: 88 (10%) subjects died during follow-up. PASP correlated with left ventricular ejection fraction (LVEF, N=644, r=-0.20, p<0.0001), C-reactive protein (CRP, N=539, r=0.12, p=0.004), and mitral valve inflow E/A ratio (N=359, r=0.32, p<0.0001), mitral valve deceleration time (N=260, r=-0.16, p=0.007),and left atrial size (LAs, N=694, r=0.25, p<0.0001). High PASP predicted incident mortality in a model adjusted for age, gender, diabetes, hypertension, dyslipidemia, smoking, glomerular filtration rate, CRP, heart failure, Gensini angiographic severity score, as well as aspirin, statin, beta-blocker, and angiotensin converting enzyme-inhibitor use (HR: 3.3, p=0.000001). The association of PASP with death was independent of LVEF (HR=3.2, p=0.00002). Thus, high PASP also predicted mortality in subjects with LVEF>50% and no history of HF (HR: 4.7, p=0.004). In separate models, this association was also independent of LAs and E/A. Conclusion: High PASP >43 mmHg is an independent predictor of mortality in patients with CAD even in those with preserved LVEF without HF. Whether high PASP predicts future development of HF and hospitalization for HF exacerbation needs to be investigated.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
B Balcer ◽  
I Dykun ◽  
S Hendricks ◽  
F Al-Rashid ◽  
M Totzeck ◽  
...  

Abstract Background Anemia is a frequent comorbidity in patients with coronary artery disease (CAD). Besides a complemental effect on myocardial oxygen undersupply of CAD and anemia, available data suggests that it may independently impact the prognosis in CAD patients. We aimed to determine the association of anemia with long-term survival in a longitudinal registry of patients undergoing conventional coronary angiography. Methods The present analysis is based on the ECAD registry of patients undergoing conventional coronary angiography at the Department of Cardiology and Vascular Medicine at the University Clinic Essen between 2004 and 2019. For this analysis, we excluded all patients with missing hemoglobin levels at baseline admission or missing follow-up information. Anemia was defined as a hemoglobin level of &lt;13.0g/dl for male and &lt;12.0g/dl for female patients according to the world health organization's definition. Cox regression analysis was used to determine the association of anemia with morality, stratifying by clinical presentation of patients. Hazard ratio and 95% confidence interval are depicted for presence vs. absence of anemia. Results Overall, data from 28,917 patient admissions (mean age: 65.3±13.2 years, 69% male) were included in our analysis (22,570 patients without and 6,347 patients with anemia). Prevalence of anemia increased by age group (age &lt;50 years: 16.0%, age ≥80 years: 27.7%). During a mean follow-up of 3.2±3.4 years, 4,792 deaths of any cause occurred (16.6%). In patients with anemia, mortality was relevantly higher as compared to patients without anemia (13.4% vs. 28.0% for patients without and with anemia, respectively, p&lt;0.0001, figure 1). In univariate regression analysis, anemia was associated with 2.4-fold increased mortality risk (2.27–2.55, p&lt;0.0001). Effect sizes remained stable upon adjustment for traditional risk factors (2.38 [2.18–2.61], p&lt;0.0001). Mortality risk accountable to anemia was significantly higher for patients receiving coronary interventions (2.62 [2.35–2.92], p&lt;0.0001) as compared to purely diagnostic coronary angiography examinations (2.31 [2.15–2.47], p&lt;0.0001). Likewise, survival probability was slightly worse for patients with anemia in acute coronary syndrome (2.70 [2.29–3.12], p&lt;0.0001) compared to chronic coronary syndrome (2.60 [2.17–3.12], p&lt;0.0001). Interestingly, within the ACS entity, association of anemia with mortality was relevantly lower in STEMI patients (1.64 [1.10–2.44], p=0.014) as compared to NSTEMI and IAP (NSTEMI: 2.68 [2.09–3.44], p&lt;0.0001; IAP: 2.67 [2.06–3.47], p&lt;0.0001). Conclusion In this large registry of patients undergoing conventional coronary angiography, anemia was a frequent comorbidity. Anemia relevantly influences log-term survival, especially in patients receiving percutaneous coronary interventions. Our results confirm the important role of anemia for prognosis in patients with coronary artery disease, demonstrating the need for specific treatment options. Figure 1. Kaplan Meier analysis Funding Acknowledgement Type of funding source: None


2003 ◽  
Vol 285 (4) ◽  
pp. H1576-H1581 ◽  
Author(s):  
Fraser D. Russell ◽  
Deborah Meyers ◽  
Andrew J. Galbraith ◽  
Nick Bett ◽  
Istvan Toth ◽  
...  

Human urotensin-II (hU-II) is the most potent endogenous cardiostimulant identified to date. We therefore determined whether hU-II has a possible pathological role by investigating its levels in patients with congestive heart failure (CHF). Blood samples were obtained from the aortic root, femoral artery, femoral vein, and pulmonary artery from CHF patients undergoing cardiac catheterization and the aortic root from patients undergoing investigative angiography for chest pain who were not in heart failure. Immunoreactive hU-II (hU-II-ir) levels were determined with radioimmunoassay. hU-II-ir was elevated in the aortic root of CHF patients (230.9 ± 68.7 pg/ml, n = 21; P < 0.001) vs. patients with nonfailing hearts (22.7 ± 6.1 pg/ml, n = 18). This increase was attributed to cardiopulmonary production of hU-II-ir because levels were lower in the pulmonary artery (38.2 ± 6.1 pg/ml, n = 21; P < 0.001) than in the aortic root. hU-II-ir was elevated in the aortic root of CHF patients with nonischemic cardiomyopathy (142.1 ± 51.5 pg/ml, n = 10; P < 0.05) vs. patients with nonfailing hearts without coronary artery disease (27.3 ± 12.4 pg/ml, n = 7) and CHF patients with ischemic cardiomyopathy (311.6 ± 120.4 pg/ml, n = 11; P < 0.001) vs. patients with nonfailing hearts and coronary artery disease (19.8 ± 6.6 pg/ml, n = 11). hU-II-ir was significantly higher in the aortic root than in the pulmonary artery and femoral vein, with a nonsignificant trend for higher levels in the aortic root than in the femoral artery. The findings indicated that hU-II-ir is elevated in the aortic root of CHF patients and that hU-II-ir is cleared at least in part from the microcirculation.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.


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