scholarly journals Studies on left ventricular function during acute right heart failure and during extracorporeal circulatory ejection support for the right heart.

1989 ◽  
Vol 18 (4) ◽  
pp. 547-549
Author(s):  
M. Miyamoto
Keyword(s):  
Heart Failure ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Right Heart ◽  
The Right

Left Ventricular Function in Chronic Obstructive Pulmonary Disease with and without Cardiac Failure

1973 ◽  
Vol 45 (3) ◽  
pp. 267-279 ◽  
Author(s):  
V. Ježek ◽  
F. Schrijen
Keyword(s):  
Heart Failure ◽  
Chronic Obstructive Pulmonary Disease ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Chronic Obstructive ◽  
Right Heart ◽  
Obstructive Pulmonary Disease ◽  
Abnormal Response

1. The circulatory response to supine exercise and to angiotensin infusion was measured in patients with chronic obstructive pulmonary disease (COPD). 2. Left ventricular function assessed from left ventricular end-diastolic pressure (LVEDP)-stroke volume or stroke work relationships was almost always normal in the patients without cardiac failure. The patients with right heart failure showed an abnormal response with a pronounced rise of LVEDP during both exercise and infusion of angiotensin. The values of LVEDP showed a significant correlation with RVEDP and with arterial oxygen saturation and carbon dioxide tension under both experimental conditions. No abnormality in the response of cardiac output, mean systolic ejection ratio or systolic ejection time was observed. In thirteen out of fifteen patients subjected to both exercise and infusion of angiotensin, the results of the two tests agreed in showing left ventricular function to be normal or abnormal; two patients showed an abnormal response to exercise, but a normal response to angiotensin. 3. The possible causes of the abnormality of left ventricular function in COPD with right heart failure are discussed. Changes in left ventricular compliance and the effect of chronic hypoxaemia and hypercapnic acidosis on myocardial contractility seem to be the most probable explanation.

Right Heart Function during Left Ventricular Assistance in an Open-Chest Porcine Model of Acute Right Heart Failure

1994 ◽  
Vol 17 (4) ◽  
pp. 224-229 ◽  
Author(s):  
Y. Abe ◽  
K. Kotoh ◽  
P.H. Deleuze ◽  
M. Miyama ◽  
G.J. Cooper ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Volume Loading ◽  
Right Heart ◽  
Open Chest ◽  
The Right ◽  
Ventricular Assistance ◽  
Left Ventricular Assistance

Changes in the right ventricular function measured with a thermodilution ejection fraction catheter have been recorded in open-chest normal pigs and pigs with acute right heart failure (RVF) undergoing left ventricular assistance with a pneumatic-sactype device (LVAD). To produce acute right heart failure, 5 pigs underwent ligation of the right ventricular free wall coronary arteries. Compared with normal pigs, cardiac output in ligated pigs fell by 21% (7.5 ± 0.5 vs 9.5 ± 1.2 L/min; p < 0.05) and the right ventricular end diastolic pressure rose (11.4 ± 2.6 vs 5.7 ± 3.6 vs mmHg: p <0.05). With the left ventricular assist device connected, the right atrial pressure was increased to 3, 5, 7, 10 and 12 mmHg by volume loading while maintaining the haematocrit at 35 ± 6%. The right ventricular stroke work index (RVSWI) increased with volume loading in normal pigs. In RVF pigs, RVSWI increased significantly with the LVAD (59.2 ± 5.8 vs 23.5 ± 7.8 mmHg ml/min/kg, p<0.01), approaching that of normal pigs (62.3 ± 4.8 mmHg ml/min/kg). Similar changes were observed in the cardiac output and right ventricular stroke volume. These results show that, in this model of open-chest, mild, acute right heart failure, left ventricular assistance allows right ventricular function to return to normal, despite volume overloading, by decreasing right ventricular after load and increasing right ventricular compliance

P5370Pulmonary pressure overload stimulates cardiac stem or progenitor cell-derived cardiac regeneration in the right ventricular area

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kanda ◽  
T Nagai ◽  
N Kondou ◽  
K Tateno ◽  
M Hirose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Progenitor Cell ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Free Wall ◽  
Right Heart ◽  
The Right

Abstract Introduction and purpose The number of patients with right heart failure due to pulmonary hypertension has been increasing. Although several drugs have reportedly improved pulmonary hypertension, no treatments have been established for decompensated right heart failure. The heart has an innate ability to regenerate, and cardiac stem or progenitor cells (e.g., side population [SP] cells) have been reported to contribute to the regeneration process. However, their contribution to right ventricular pressure overload has not been clarified. Here, this regeneration process was evaluated using a genetic fate-mapping model. Methods and results We used Cre-LacZ mice, in which more than 99.9% of the cardiomyocytes in the left ventricular field were positive for 5-bromo-4-chloro-3-indolyl-β-D-galactoside (X-gal) staining immediately after tamoxifen injection. Then, we performed either a pulmonary binding (PAB) or sham operation on the main pulmonary tract. In the PAB-treated mice, the right ventricular cavity was significantly enlarged (right-to-left ventricular [RV/LV] ratio, 0.24±0.04 in the sham group and 0.68±0.04 in the PAB group). Increased peak flow velocity in the PAB group (1021±80 vs 1351±62 mm/sec) was confirmed by echocardiography. One month after the PAB, the PAB-treated mice had more X-gal-negative (newly generated) cells than the sham mice (94.8±34.2 cells/mm2 vs 23.1±10.5 cells/mm2; p<0.01). The regeneration was biased in the RV free wall (RV free wall, 225.5±198.7 cells/mm2; septal area, 88.9±56.5/mm2; LV lateral area, 46.8±22.0/mm2; p<0.05). To examine the direct effects of PAB on the cardiac progenitor cells, bromodeoxyuridine was administered to the mice daily until 1 week after the PAB operation. Then, the hearts were isolated and SP cells were harvested. The SP cell population increased from 0.65±0.23% in the sham mice to 1.87% ± 1.18% in the PAB-treated mice. Immunostaining analysis revealed a significant increase in the number of BrdU-positive SP cells, from 11.6±2.0% to 44.0±18%, therefore showing SP cell proliferation. Conclusions Pulmonary pressure overload stimulated cardiac stem or progenitor cell-derived regeneration with a RV bias, and SP cell proliferation may partially contribute to this process. Acknowledgement/Funding JSPS KAKENHI Grant Number JP 17K17636, GSK Japan Research Grant 2016

scholarly journals ACE Inhibition Modulates Myeloid Hematopoiesis after Acute Myocardial Infarction and Reduces Cardiac and Vascular Inflammation in Ischemic Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 396
Author(s):  
Wolf-Stephan Rudi ◽  
Michael Molitor ◽  
Venkata Garlapati ◽  
Stefanie Finger ◽  
Johannes Wild ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Bone Marrow ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Vascular Inflammation ◽  
Ace Inhibition ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Ischemic Heart Failure

Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function and survival. We aimed to elucidate the impact of early treatment with the ACE inhibitor ramipril on the hematopoietic response after MI, as well as on the chronic systemic and vascular inflammation. Methods and Results: In a mouse model of MI, induced by permanent ligation of the left anterior descending artery, immediate initiation of treatment with ramipril (10 mg/k/d via drinking water) reduced cardiac inflammation and the number of circulating inflammatory monocytes, whereas left ventricular function was not altered significantly, respectively. This effect was accompanied by enhanced retention of hematopoietic stem cells, Lin−Sca1−c-Kit+CD34+CD16/32+ granulocyte–macrophage progenitors (GMP) and Lin−Sca1−c-Kit+CD150−CD48− multipotent progenitors (MPP) in the bone marrow, with an upregulation of the niche factors Angiopoetin 1 and Kitl at 7 d post MI. Long-term ACE inhibition for 28 d limited vascular inflammation, particularly the infiltration of Ly6Chigh monocytes/macrophages, and reduced superoxide formation, resulting in improved endothelial function in mice with ischemic heart failure. Conclusion: ACE inhibition modulates the myeloid inflammatory response after MI due to the retention of myeloid precursor cells in their bone marrow reservoir. This results in a reduction in cardiac and vascular inflammation with improvement in survival after MI.

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