Abstract P603: Age and Angiotensin-(1-12) Expression in Human Atrial Tissue of Patients with Left Heart Disease

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jessica VonCannon ◽  
Jasmina Varagic ◽  
Sayaka Nagata ◽  
Sarfaraz Ahmad ◽  
Adair Locke ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ventricular Remodeling ◽  
Underlying Mechanism ◽  
Right Atrial ◽  
Mrna Levels ◽  
Ang Ii ◽  
Left Heart ◽  
Atrial Tissue ◽  
Left Heart Disease ◽  
Age Related

In the human heart formation of angiotensin (Ang) II results from the hydrolysis of an alternate angiotensin substrate, -Ang-(1-12)-, by chymase rather than angiotensin converting enzyme. In our recent study a higher Ang-(1-12) expression and upregulation of chymase mRNA and enzymatic activity was found in left (LAA) versus right atrial appendages (RAA) of subjects with left heart disease. Since aging is associated with prominent changes in cardiac structure and function, we assessed the relationships among age, Ang-(1-12), and chymase gene expression and activity in both LAA and RAA in 44 patients undergoing cardiac surgery for the correction of valvular heart disease, resistant atrial fibrillation or ischemic heart disease. Immunohistochemistry for Ang-(1-12) detection was performed using an affinity purified polyclonal antibody directed to the COOH terminus of the full length of the sequence of human Ang-(1-12). Quantitative real-time polymerase chain reaction was used to detect chymase mRNA levels whereas chymase activity was assessed by HPLC. We report that Ang-(1-12) immunostaining in atrial appendages (r=0.30; p<0.05), but not chymase mRNA expression or activity, correlated directly with patients age. While a tendency for higher Ang-(1-12) expression in LAA (Intensity: 5.88 ± 0.91 units; n=11) when compared to RAA (Intensity: 3.948 ± 0.55 units; n=15) was noted in patients younger than 65 yrs, this difference was more prominent and statistically significant in patients older than 65 yrs of age (LAA Intensity: (n=12): 7.39 ± 1.06 units versus RAA Intensity (n=13): 4.74 ±0.54 units; p < 0.05). The results of the present study suggest an age-related increase in Ang-(1-12) expression in human atrial tissue that may be more prominent in the LAA of patients with left heart disease. We suggest that higher availability of Ang-(1-12) for direct Ang II formation may be an underlying mechanism responsible, at least in part, for age- and disease-related atrial and ventricular remodeling and dysfunction.

scholarly journals Different effects on right ventricular function in different etiology of secondary tricuspid regurgitation

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
WC Tsai ◽  
WY Lee ◽  
MS Huang ◽  
WH Lee
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Right Ventricular ◽  
Tricuspid Regurgitation ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Right Atrial ◽  
Left Heart ◽  
Left Heart Disease ◽  
Rv Function

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Ministry of Science and Technology, Excutive Yuan, Taiwan Background Tricuspid regurgitation (TR) is traditionally classified as primary or secondary TR. The effects of TR on right ventricular (RV) function were not consistent. We hypothesized that secondary TR is not a unique group, sophisticated sub-grouping can be useful for studying effects of TR on RV function. Methods 207 consecutive patients identified as significant TR (moderate and severe) by echocardiography were recruited. Standard measurements for right heart were done according to guideline. Lateral tricuspid annulus systolic tissue velocity (S’) and RV fractional area change (FAC) were used for RV function. We classified these patients into primary TR and 6 subgroups of secondary TR according to a new systemic approach. Results Mean age of subjects was 71.2 ± 14.7 years, and there were 84 (40.6%) male. There were 29 (14%) primary TR. Secondary TR was further classified into 6 groups included 18 (8.7%) pacemaker related, 81 (39.1 %) left heart diseases, 6 (2.9%) congenital heart diseases, 3 (1.4%) RV myopathy, 27 (13.0%) pulmonary hypertension, and 43 (20.8%) idiopathic TR. Among 4 major groups (congenital heart disease and RV myopathy were not included in analysis due to low numbers) of secondary TR, S’ was significant higher in idiopathic TR and RV FAC were higher in pacemaker related and idiopathic TR. RV dysfunction was defined as FAC &lt; 35%. RV dysfunction presented mostly in pulmonary hypertension related TR and leastly in idiopathic TR (59.3% vs. 14%, p &lt;0.001). Multivariate analysis using idiopathic TR as reference and controlled TR maximal velocity, RV end-diastolic area, right atrial area, and severity of TR, left heart disease related TR had higher risk of RV dysfunction (OR 4.178, 95% CI 1.490-11.703, p = 0.007). Conclusions Effects of TR on RV function were different among different subgroups of secondary TR. Left heart disease related TR had highest risk for RV dysfunction. Secondary TR should not be regarded as a single disease.

scholarly journals P1361 Loading conditions might mimic right ventricular longitudinal dysfunction in patients with chronic left heart disease and forward failure

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
O Bech-Hanssen ◽  
M Fredholm ◽  
S E Bartfay ◽  
K Karason ◽  
G Dellgren ◽  
...  
Keyword(s):  
Heart Disease ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Venous Pressure ◽  
Right Atrial ◽  
Volume Index ◽  
Loading Conditions ◽  
Left Heart ◽  
Peak Vo2 ◽  
Left Heart Disease

Abstract Background and aim Right ventricular failure (RVF) in patients with chronic left heart disease (LHD) has important prognostic implications. RV longitudinal function parameters (tricuspid annular plane systolic excursion, TAPSE; peak systolic longitudinal strain, RV-Str; tricuspid annulus systolic velocity, TAPSm) are today commonly used to define RV dysfunction. In the present study we hypothesized that longitudinal RV dysfunction (LDF) might be due to loading conditions and not necessarily RV dysfunction. Methods We retrospectively included 66 patients with LHD (age 52 ± 13 years, males 79%) that underwent right heart catheterization (RHC), ergospirometry (n = 47) and echocardiography (Echo) within 48 hours. Patients were divided into three groups from Echo data: normal RV function (TAPSE ≥17 mm + normal central venous pressure (CVP) from collapsibility of cava inferior, n = 18); LDF (TAPSE &lt; 17 mm + normal CVP, n = 22) and RVF (CVP≥10 mmHg, n = 26). Results Patients with RVF had compared with normal and LDF lower peak VO2, more advanced LHD, enlarged RV and higher RV afterload (Table). Patients with LDF had compared with normal reduced stroke volume index (SVI). The patients with normal and LDF did not differ regarding right atrial pressure (RAP) response during exercise (P = 0.84). The longitudinal parameters did not differ between patients with LDF and RVF. Conclusions Longitudinal parameters in patients with chronic LHD and normal CVP should be interpreted with caution. Loading conditions with reduced stroke volume might mimic LDF. Normal (n = 18) LDF (n = 22) RVF (n = 26) Overall P-value Normal vs LDF Normal vs RVF LDF vs RVF Peak VO2 (mlO2/min/m2) 14.8 ± 3.3 13.5 ± 3 11 ± 2 0.001 0.29 &lt;0.001 0.005 RAP (mmHg) 4 ± 3 4 ± 4 12 ± 3 &lt;0.001 0.55 &lt;0.001 &lt;0.001 PASP (mmHg) 32 ± 13 37 ± 14 47 ± 11 &lt;0.001 0.28 &lt;0.001 0.002 PCWP (mmHg) 10 ± 6 14 ± 7 22 ± 5 &lt;0.001 0.03 &lt;0.001 &lt;0.001 SVI(ml/m2) 43 ± 10 34 ± 6 30 ± 9 &lt;0.001 &lt;0.001 &lt;0.001 0.15 PVR (Wood unit) 2.0 ± 1.1 2.0 ± 0.8 2.3 ± 1.1 0.29 - - - RVdA (cm2) 19 ± 3 22 ± 7 26 ± 7 0.003 0.16 &lt;0.001 0.04 RVsax (mm) 23 ± 4 25 ± 8 34 ± 8 &lt;0.001 0.42 &lt;0.001 &lt;0.001 TAPSE (mm) 21 ± 4 12 ± 3 12 ± 3 &lt;0.001 &lt;0.001 &lt;0.001 0.98 TAPSm (cm/s) 11 ± 3 8 ± 2 8 ± 2 &lt;0.001 &lt;0.001 &lt;0.001 0.55 RV-Str (%) -24 ± 5 -16 ± 5 -15 ± 5 &lt;0.001 &lt;0.001 &lt;0.001 0.87 PASP, pulmonary systolic pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RVdA, RV diastolic area; RVsax, RV short axis diameter.

Characterization of a Pulmonary Hypertension Model Caused by Left Heart Disease in Mouse

2020 ◽  
Author(s):  
L. K. Pallos ◽  
J. M. Dietrich ◽  
A. Simon ◽  
E. Carls ◽  
M. Matthey ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Left Heart ◽  
Left Heart Disease

Roundtable: Pulmonary Hypertension Due to Left Heart Disease

2015 ◽  
Vol 14 (2) ◽  
pp. 105-110
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Guest Editor ◽  
Mayo Clinic ◽  
Diagnosis And Treatment ◽  
Left Heart ◽  
Health Network ◽  
University Of Utah ◽  
School Of Medicine ◽  
Left Heart Disease

Guest editor Teresa De Marco, MD, along with Brian Shapiro, MD, Mayo Clinic, Jacksonville, FL, convened a panel of experts to discuss the challenges in diagnosis and treatment and the emerging science regarding pulmonary hypertension due to left heart disease. Contributing to the engaging discussion were James Fang, MD, University of Utah School of Medicine; Barry Borlaug, MD, Mayo Clinic, Rochester, MN; and Srinivas Murali, MD, Allegheny Health Network, Pittsburgh, PA.

Pulmonary Hypertension secondary to Left Heart Disease

2018 ◽  
Vol 16 (6) ◽  
pp. 555-560 ◽  
Author(s):  
Ghazal Kabbach ◽  
Debabrata Mukherjee
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Left Heart ◽  
Left Heart Disease

scholarly journals Under pressure: pulmonary hypertension associated with left heart disease

2015 ◽  
Vol 24 (138) ◽  
pp. 665-673 ◽  
Author(s):  
Harrison W. Farber ◽  
Simon Gibbs
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Survival Rates ◽  
Left Ventricular ◽  
Left Heart ◽  
Mean Pulmonary Arterial Pressure ◽  
Left Heart Disease ◽  
Right Heart Catheterisation ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial

Pulmonary hypertension (PH) associated with left heart disease (PH-LHD) is the most common type of PH, but its natural history is not well understood. PH-LHD is diagnosed by right heart catheterisation with a mean pulmonary arterial pressure ≥25 mmHg and a pulmonary capillary wedge pressure >15 mmHg. The primary causes of PH-LHD are left ventricular dysfunction of systolic and diastolic origin, and valvular disease. Prognosis is poor and survival rates are low. Limited progress has been made towards specific therapies for PH-LHD, and management focuses on addressing the underlying cause of the disease with supportive therapies, surgery and pharmacological treatments. Clinical trials of therapies for pulmonary arterial hypertension in patients with PH-LHD have thus far been limited and have provided disappointing or conflicting results. Robust, long-term clinical studies in appropriate target populations have the potential to improve the outlook for patients with PH-LHD. Herein, we discuss the knowledge gaps in our understanding of PH-LHD, and describe the current unmet needs and challenges that are faced by clinicians when identifying and managing patients with this disease.

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