Advanced Right Ventricular Assessment: Pulmonary Artery Compliance and RV-PA Coupling

Abstract Surgical repair of Tetralogy of Fallot has excellent outcomes, with over 90% of patients alive at 30 years. The ideal time for surgical repair is between 3 and 11 months of age. However, the symptomatic neonate with Tetralogy of Fallot may require earlier intervention: either a palliative intervention (right ventricular outflow tract stent, ductal stent, balloon pulmonary valvuloplasty, or Blalock-Taussig shunt) followed by a surgical repair later on, or a complete surgical repair in the neonatal period. Indications for palliation include prematurity, complex anatomy, small pulmonary artery size, and comorbidities. Given that outcomes after right ventricular outflow tract stent palliation are particularly promising – there is low mortality and morbidity, and consistently increased oxygen saturations and increased pulmonary artery z-scores – it is now considered the first-line palliative option. Disadvantages of right ventricular outflow tract stenting include increased cardiopulmonary bypass time at later repair and the stent preventing pulmonary valve preservation. However, neonatal surgical repair is associated with increased short-term complications and hospital length of stay compared to staged repair. Both staged repair and primary repair appear to have similar long-term mortality and morbidity, but more evidence is needed assessing long-term outcomes for right ventricular outflow tract stent palliation patients.

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Species differences in effect of gram-negative endotoxin on circulation

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.6.1197 ◽

1961 ◽

Vol 200 (6) ◽

pp. 1197-1202 ◽

Cited By ~ 64

Author(s):

Hiroshi Kuida ◽

Robert P. Gilbert ◽

Lerner B. Hinshaw ◽

Joel G. Brunson ◽

Maurice B. Visscher

Keyword(s):

Pulmonary Artery ◽

Right Ventricular ◽

Species Differences ◽

The Other ◽

Short Segment ◽

Gram Negative ◽

Microscopic Studies ◽

Significant Mechanism ◽

Dramatic Fall ◽

Made In

Studies were made in 5 monkeys, 7 rabbits, and 33 cats of the effect of gram-negative endotoxin on aortic, pulmonary artery (PAP), and portal venous (PVP) pressures; and on changes in weight of a short segment of intestine. Studies of blood pooling were also made in 12 cats. The responses in these species were compared with those previously observed in the dog. Although variable degrees of hypotension developed at one time or another in all animals following injection of endotoxin, the early precipitous hypotension that characteristically occurs in the dog was observed only in the cat. However, in this species the dramatic fall in pressure could be ascribed to pulmonary vascular constriction and acute right ventricular hypertension and failure, and not to splanchnic pooling. PAP also became elevated in the monkey and the rabbit, but usually was of lesser magnitude and did not appear to explain the development of the relatively late hypotension that occurred in these species. The absence of significant increases in gut weight and the minor increments in PVP in all animals indicate that in none of these species is hepatic vein constriction and splanchnic pooling a significant mechanism in producing early shock as it is in the dog. Pathologic gross and microscopic studies in the monkey and gross examinations in the other species supported this conclusion.

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Delineating the molecular and histological events that govern right ventricular recovery using a novel mouse model of pulmonary artery de-banding

Cardiovascular Research ◽

10.1093/cvr/cvz310 ◽

2019 ◽

Vol 116 (10) ◽

pp. 1700-1709 ◽

Cited By ~ 2

Author(s):

Mario Boehm ◽

Xuefei Tian ◽

Yuqiang Mao ◽

Kenzo Ichimura ◽

Melanie J Dufva ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Mouse Model ◽

Pulmonary Artery ◽

Right Ventricular ◽

Exercise Capacity ◽

Pressure Overload ◽

Left Ventricular ◽

Sequence Of Events ◽

Reverse Remodelling ◽

Rv Function

Abstract Aims The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement of pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model of gradual RV recovery from pressure overload and use it to delineate RV reverse-remodelling events. Methods and results Surgical pulmonary artery banding (PAB) around a 26-G needle induced RV dysfunction with increased RV pressures, reduced exercise capacity and caused liver congestion, hypertrophic, fibrotic, and vascular myocardial remodelling within 5 weeks of chronic RV pressure overload in mice. Gradual reduction of the afterload burden through PA band absorption (de-PAB)—after RV dysfunction and structural remodelling were established—initiated recovery of RV function (cardiac output and exercise capacity) along with rapid normalization in RV hypertrophy (RV/left ventricular + S and cardiomyocyte area) and RV pressures (right ventricular systolic pressure). RV fibrotic (collagen, elastic fibres, and vimentin+ fibroblasts) and vascular (capillary density) remodelling were equally reversible; however, reversal occurred at a later timepoint after de-PAB, when RV function was already completely restored. Microarray gene expression (ClariomS, Thermo Fisher Scientific, Waltham, MA, USA) along with gene ontology analyses in RV tissues revealed growth factors, immune modulators, and apoptosis mediators as major cellular components underlying functional RV recovery. Conclusion We established a novel gradual de-PAB mouse model and used it to demonstrate that established pulmonary hypertension-associated RV dysfunction is fully reversible. Mechanistically, we link functional RV improvement to hypertrophic normalization that precedes fibrotic and vascular reverse-remodelling events.

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