Lower levels of triiodothyronine are associated with poor hemodynamic profile and all-cause mortality in heart failure

2021 ◽  
Vol 15 (4) ◽  
pp. 273-283
Author(s):  
Elif HO Cetin ◽  
Mehmet S Cetin ◽  
Hasan C Könte ◽  
Kadir Ocak ◽  
Nezaket M Yaman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Uric Acid ◽  
Pulmonary Capillary Wedge Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Survival Function ◽  
Poor Prognostic Factor ◽  
Pulmonary Capillary ◽  
All Cause Mortality ◽  
Wedge Pressure

Background: We aimed to assess the association of triiodothyronine (T3) hormone with invasive hemodynamic parameters and all-cause mortality in heart failure with reduced ejection fraction (HFrEF). Results: About 483 HFrEF patients were enrolled. Patients with the lowest T3 tertile had advanced New York Heart Association (NYHA) classes, had higher uric acid, brain natriuretic peptide. T3 level had a positive correlation with cardiac index (CI) and a negative correlation with pulmonary vascular resistance and pulmonary capillary wedge pressure. Adjusted with NYHA III–IV classes, uric acid, aspartate aminotransferase and CI, T3 level was found to be an independent predictor of all-cause mortality. In Kaplan–Meier analysis, the lowest T3 tertile had the lowest survival function. Conclusion: Free T3 is positively correlated with CI and negatively correlated with pulmonary vascular resistance and pulmonary capillary wedge pressure in patients with HFrEF. Lower levels of T3 seems to be a poor prognostic factor in this particular patient population.

Lung and myocardial thallium-201 kinetics in resting patients with congestive heart failure: Correlation with pulmonary capillary wedge pressure

1992 ◽  
Vol 123 (2) ◽  
pp. 427-432 ◽  
Author(s):  
Eulogio E. Martinez ◽  
Steven F. Horowitz ◽  
Helio J. Castello ◽  
Mario L.V. Castiglioni ◽  
Antonio C.C. Carvalho ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Capillary Wedge Pressure ◽  
Thallium 201 ◽  
Pulmonary Capillary ◽  
Failure Correlation ◽  
Wedge Pressure

Effects of pneumatic antishock garment inflation in normovolemic subjects

1989 ◽  
Vol 67 (1) ◽  
pp. 339-345 ◽  
Author(s):  
B. J. Rubal ◽  
M. R. Geer ◽  
W. H. Bickell
Keyword(s):  
Cardiac Output ◽  
Pulmonary Capillary Wedge Pressure ◽  
Vascular Resistance ◽  
Heart Function ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Ventricular Afterload ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure

This study examines the effects of inflation of pneumatic antishock garments (PASG) in 10 normovolemic men (mean age 44 +/- 6 yr) undergoing diagnostic catheterization. Seven subjects had normal heart function and no evidence of coronary artery disease (CAD); three patients had CAD. High-fidelity multisensor catheters were employed to simultaneously record right and left heart pressures before PASG inflation and after inflation to 40, 70, and 100 mmHg. A thermal dilution catheter was used to obtain pulmonary capillary wedge pressure and cardiac output. Counterpressure increases greater than or equal to 40 mmHg were associated with significant changes in left and right heart pressures. Right and left ventricular end-diastolic pressures increased 100% (P less than 0.01); mean pulmonary arterial and aortic pressures increased 77 and 25%, respectively (P less than 0.01); systemic vascular resistance increased 22% (P less than 0.05) and pulmonary vascular resistance did not change in normal subjects at maximum PASG inflation. Heart rate, cardiac output, and aortic and pulmonary arterial pulse pressures did not change during inflation in either group. Right and left ventricular end-diastolic pressures and pulmonary capillary wedge pressure were greater (P less than 0.05) in the CAD group compared with the normal subjects during PASG inflation. The data suggest that the primary mechanism whereby PASG inflation induces changes in central hemodynamics in normovolemic subjects is through an acute increase in left ventricular afterload. PASG changes in afterload and pulmonary capillary wedge pressure imply that these devices should be used with caution in patients with compromised cardiac function.

Abstract 4869: Pulmonary Vasoconstriction Occurs out of Proportion to Increases in Pulmonary Capillary Wedge Pressure During Exercise in Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Gregory D Lewis ◽  
Ravi V Shah ◽  
Maryann Martinovic ◽  
Kenneth D Bloch ◽  
Marc J Semigran
Keyword(s):  
Heart Failure ◽  
Pulmonary Capillary Wedge Pressure ◽  
Exercise Capacity ◽  
Exercise Testing ◽  
Left Ventricular ◽  
Work Rate ◽  
Left Ventricular Ejection ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Capillary ◽  
Wedge Pressure

Secondary pulmonary hypertension (PH) is an important prognostic indicator in patients with systolic heart failure (HF), but the pattern of increase in pulmonary arterial pressure (PAP) during exercise and its relationship to exercise capacity and pulmonary capillary wedge pressure (PCWP) have not been comprehensively investigated. We hypothesized that HF patients would develop an increase in PAP out of proportion to the increase in PCWP during exercise and that the rate of PAP increase during exercise would predict exercise capacity in HF. Thirty-three patients with systolic HF (mean±SD, age 58 ± 7 years, left ventricular ejection fraction 0.27 ± 0.05, peak oxygen uptake 11.2 ± 3.2 ml/kg/min) and 10 normal subjects (age 53±9, sex, VO2) underwent cardiopulmonary exercise testing with simultaneous hemodynamic monitoring. There was a linear relationship between PAP and work rate in watts (R>0.85 for all subjects) whereas no consistent relationship between PCWP and work rate was present (R=0.02– 0.93). HF patients had a 3-fold greater rate of increase in PAP per watt than normals (slope=0.23±0.02 vs. 0.07±0.002 mmHg/W respectively, p<0.0001). In HF patients, PAP increased out of proportion to PCWP, as indicated by the slope of the gradient between PAP and PCWP (0.11±0.005 mmHg/W in HF vs. 0.01±0.005 mmHg/W in normals, p<0.0001). In HF patients, PAP slope, but not PCWP slope, inversely correlated with exercise capacity as measured by peak VO 2 (R=−0.41, p=0.04 and R=−0.12, p=0.56, respectively). Fifteen of the HF subjects underwent repeated exercise testing after 12-weeks of treatment with the pulmonary vasodilator sildenafil, with a resultant decrease in slope of the PAP-PCWP gradient from 0.11±0.02 to 0.07±0.01 mmHg, P<0.05. In patients with systolic HF there is a linear increase in PAP/watt that is out of proportion to the increase in PCWP/watt and inversely correlated with exercise capacity. Abnormal pulmonary vasoconstriction in response to physical activity in HF may represent a target for therapeutic intervention in HF. This research has received full or partial funding support from the American Heart Association, AHA National Center.

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