MEAN PULMONARY ARTERIAL PRESSURE AT FINAL BALLOON PULMONARY ANGIOPLASTY PREDICTS THE IMPROVEMENT OF EXERCISE CAPACITY AFTER ONE-YEAR IN CTEPH PATIENTS

The present method enables the noninvasive assessment of mean pulmonary arterial pressure from magnetic resonance phase mapping by computing both physical and biophysical parameters. The physical parameters include the mean blood flow velocity over the cross-sectional area of the main pulmonary artery (MPA) at the systolic peak and the maximal systolic MPA cross-sectional area value, whereas the biophysical parameters are related to each patient, such as height, weight, and heart rate. These parameters have been measured in a series of 31 patients undergoing right-side heart catheterization, and the computed mean pulmonary arterial pressure value (PpaComp) has been compared with the mean pressure value obtained from catheterization (PpaCat) in each patient. A significant correlation was found that did not differ from the identity line PpaComp = PpaCat ( r = 0.92). The mean and maximal absolute differences between PpaComp and PpaCat were 5.4 and 11.9 mmHg, respectively. The method was also applied to compute the MPA systolic and diastolic pressures in the same patient series. We conclude that this computed method, which combines physical (whoever the patient) and biophysical parameters (related to each patient), improves the accuracy of MRI to noninvasively estimate pulmonary arterial pressures.

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Mean pulmonary arterial pressure after percutaneous mitral valvuloplasty predicts long-term adverse outcomes

Revista Portuguesa de Cardiologia ◽

10.1016/j.repc.2011.09.018 ◽

2012 ◽

Vol 31 (1) ◽

pp. 19-25 ◽

Cited By ~ 4

Author(s):

Elisabete Jorge ◽

Rui Baptista ◽

Henrique Faria ◽

João Calisto ◽

Vítor Matos ◽

...

Keyword(s):

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Adverse Outcomes ◽

Mitral Valvuloplasty ◽

Mean Pulmonary Arterial Pressure ◽

Pulmonary Arterial

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Increased Pulmonary Arterial Compliance after Balloon Pulmonary Angioplasty Predicts Exercise Tolerance Improvement in Inoperable CTEPH Patients with Lower Pulmonary Arterial Pressure

Heart & Lung ◽

10.1016/j.hrtlng.2021.11.003 ◽

2022 ◽

Vol 52 ◽

pp. 8-15

Author(s):

Shintaro Umemoto ◽

Kohtaro Abe ◽

Kazuya Hosokawa ◽

Koshin Horimoto ◽

Keita Saku ◽

...

Keyword(s):

Arterial Pressure ◽

Exercise Tolerance ◽

Pulmonary Arterial Pressure ◽

Arterial Compliance ◽

Balloon Pulmonary Angioplasty ◽

Pulmonary Arterial ◽

Tolerance Improvement

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Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs

Journal of Applied Physiology ◽

10.1152/jappl.1982.52.3.705 ◽

1982 ◽

Vol 52 (3) ◽

pp. 705-709 ◽

Cited By ~ 24

Author(s):

B. R. Walker ◽

N. F. Voelkel ◽

J. T. Reeves

Keyword(s):

Cardiac Output ◽

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Pressor Response ◽

Conscious Dogs ◽

Pulmonary Pressure ◽

Time Control ◽

Mean Pulmonary Arterial Pressure ◽

Before And After ◽

Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

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Pulmonary Vasodilator Therapy in Children with Single Ventricle Physiology: Effects on Saturation and Pulmonary Arterial Pressure

Pediatric Cardiology ◽

10.1007/s00246-020-02424-w ◽

2020 ◽

Vol 41 (8) ◽

pp. 1651-1659

Author(s):

Ida Jeremiasen ◽

Karin Tran-Lundmark ◽

Nikmah Idris ◽

Phan-Kiet Tran ◽

Shahin Moledina

Keyword(s):

Arterial Pressure ◽

Single Ventricle ◽

Pulmonary Arterial Pressure ◽

Vasodilator Therapy ◽

Single Ventricle Physiology ◽

Pulmonary Vasodilators ◽

Mean Pulmonary Arterial Pressure ◽

Pulmonary Vasodilator ◽

Pulmonary Arterial ◽

Stage 1

AbstractIn children with single ventricle physiology, increased pulmonary vascular resistance may impede surgical progression or result in failing single ventricle physiology. The use of pulmonary vasodilators has been suggested as a potential therapy. However, knowledge on indication, dosage, and effect is limited. A retrospective case notes review of all (n = 36) children with single ventricle physiology, treated with pulmonary vasodilators by the UK Pulmonary Hypertension Service for Children 2004–2017. Therapy was initiated in Stage 1 (n = 12), Glenn (n = 8), or TCPC (n = 16). Treatment indications were high mean pulmonary arterial pressure, cyanosis, reduced exercise tolerance, protein-losing enteropathy, ascites, or plastic bronchitis. Average dose of sildenafil was 2.0 mg/kg/day and bosentan was 3.3 mg/kg/day. 56% had combination therapy. Therapy was associated with a reduction of the mean pulmonary arterial pressure from 19 to 14 mmHg (n = 17, p < 0.01). Initial therapy with one or two vasodilators was associated with an increase in the mean saturation from 80 to 85%, (n = 16, p < 0.01). Adding a second vasodilator did not give significant additional effect. 5 of 12 patients progressed from Stage 1 to Glenn, Kawashima, or TCPC, and 2 of 8 from Glenn to TCPC during a mean follow-up time of 4.7 years (0–12.8). Bosentan was discontinued in 57% and sildenafil in 14% of treated patients and saturations remained stable. Pulmonary vasodilator therapy was well tolerated and associated with improvements in saturation and mean pulmonary arterial pressure in children with single ventricle physiology. It appears safe to discontinue when no clear benefit is observed.

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Gestational resistance to the pulmonary vasoconstrictor effect of the TxA2 mimetic U-46619: possible mechanism

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.272.6.r1734 ◽

1997 ◽

Vol 272 (6) ◽

pp. R1734-R1739 ◽

Cited By ~ 2

Author(s):

G. Losonczy ◽

G. Brown ◽

I. Mucha ◽

R. Klocke ◽

V. Muller ◽

...

Keyword(s):

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Vascular System ◽

Late Gestation ◽

Mechanically Ventilated ◽

Mean Pulmonary Arterial Pressure ◽

Vascular Sensitivity ◽

Specific Receptors ◽

Pulmonary Arterial ◽

Dose Dependent

Pregnancy is associated with the reduction of vascular sensitivity to vasoconstrictor compounds. We have examined whether pregnancy in rabbits induces hyposensitivity of the pulmonary vascular system to U-46619. Anesthetized, mechanically ventilated nonpregnant (NP; n = 7) and late-pregnant (P; n = 7) rabbits were studied. The intravenous injection of 0.03, 0.1, and 0.3 microgram/kg U-46619 led to a dose-dependent elevation of mean pulmonary arterial pressure (MPAP) in NP rabbits from a baseline value of 15 +/- 1 to 22 +/- 1 mgHg. There was no significant MPAP response to intravenous administration of U-46619 in P rabbits. The pulmonary arterial pressure response of isolated, ventilated, and buffer-perfused lungs of P rabbits was also blunted (P < 0.001 vs. NP). Pulmonary arterial membrane binding of [125I]BOP, another thromboxane (Tx)A2 analog, indicated 48 +/- 16 fmol receptors/mg protein in P rabbits and 193 +/- 48 fmol receptors/mg protein in NP samples (P < 0.025). Receptor affinity [1/dissociation constant (KD)] was also lower in the tissue of P rabbits (P < 0.01 vs. NP). The urinary excretion of the stable TxA2 metabolite 11-dehydro-TxB2 was lower in P than in NP rabbits (P < 0.02), which made homologous desensitization an unlikely explanation for the changes of vascular TxA2 receptors. These results show that, in late gestation, rabbit pulmonary vascular sensitivity to U-46619 is reduced simultaneously with, and as a possible consequence of, downregulation of specific receptors.

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