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Impairment of pulmonary vascular reserve and right ventricular systolic reserve in pulmonary arterial hypertension.

Domingo E, Grignola JC, Aguilar R, Arredondo C, Bouteldja N, Messeguer ML, Roman A - BMC Pulm Med (2014)

Bottom Line: Cardiovascular reserve was estimated as the change (delta, Δ) during DST compared with rest, including ΔmPAP with respect to ΔCO (ΔmPAP/ΔCO).PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher ΔmPAP/ΔCO (p < 0.05).The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.

View Article: PubMed Central - HTML - PubMed

Affiliation: Pathophysiology Department, School of Medicine, Hospital de Clínicas, Universidad de la República, Avda Italia 2870, PC 11600 Montevideo, Uruguay. jgrig@fmed.edu.uy.

ABSTRACT

Background: Exercise capacity is impaired in pulmonary arterial hypertension (PAH). We hypothesized that cardiovascular reserve abnormalities would be associated with impaired hemodynamic response to pharmacological stress and worse outcome in PAH.

Methods: Eighteen PAH patients (p) group 1 NYHA class II/III and ten controls underwent simultaneous right cardiac catheterization and intravascular ultrasound at rest and during low dose-dobutamine (10 mcg/kg/min) with trendelenburg (DST). We estimated cardiac output (CO), pulmonary vascular resistance (PVR) and capacitance (PC), and PA elastic modulus (EM). We concomitantly measured tricuspid annular plane systolic excursion (TAPSE), RV myocardial peak systolic velocity (Sm) and isovolumic myocardial acceleration (IVA) in PAH patients. Based on the rounded mean + 2 SD of the increase in mPAP in our healthy control group during DST (2.8 + 1.8 mm Hg), PAH p were divided into two groups according to mean PA pressure (mPAP) response during DST, 1: ΔmPAP > 5 mm Hg and 2: ΔmPAP ≤ 5 mm Hg. Cardiovascular reserve was estimated as the change (delta, Δ) during DST compared with rest, including ΔmPAP with respect to ΔCO (ΔmPAP/ΔCO). All patients were prospectively followed up for 2 years.

Results: PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher ΔmPAP/ΔCO (p < 0.05). Neither hemodynamic, IVUS and echocardiographic data were different between both PAH groups at rest. In group 1, DST caused a higher ΔEM, ΔmPAP/ΔCO, ΔPVR, and ΔTAPSE than group 2, with a lower IVA increase and a negative ΔSV (p < 0.05). TAPSE correlated with mPAP and RVP (p < 0.05) and, IVA and Sm correlated with CO (p < 0.05). ΔEM correlated with ΔmPAP and ΔIVA with ΔCO (p < 0.05). There were two deaths/pulmonary transplantations in group 1 and one death in group 2 during the follow-up (p > 0.05).

Conclusions: Pulmonary vascular reserve and RV systolic reserve are significantly impaired in patients with PAH. The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.

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Related in: MedlinePlus

Relationship between mean pulmonary artery pressure (mPAP) and cardiac output at rest and during pharmacological and positional stress. (Filled circle: PAH patients; filled square: control patients).
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Figure 1: Relationship between mean pulmonary artery pressure (mPAP) and cardiac output at rest and during pharmacological and positional stress. (Filled circle: PAH patients; filled square: control patients).

Mentions: All PAH patients tolerated the stress protocol. No dobutamine infusion had to be interrupted at the doses employed for this study and no complications were observed. No patients included in this study presented greater than mild tricuspid regurgitation (≤ grade 2/4), and there were no relevant changes in its severity during the complete protocol. Only six of 18 PAH patients increased SV, and the heart rate increase was significantly lower than control subjects (29 ± 3.8 vs. 41 ± 2 bpm, P = 0.034), therefore the CO increment was mainly dependent on heart rate increase. mPAP, pPAP and EM increased significantly and PC significantly decreased during stress (Table 2). However, they showed an increase in all the RV systolic function indexes during stress (TAPSE 16.8 ± 1.3 vs. 20.2 ± 1.1 mm, P = 0.02; Sm 12.0 ± 0.5 vs. 14.7 ± 0.8 cm ⋅ s-1, P = 0.003; IVA 3.8 ± 0.3 vs. 7.8 ± 0.9 m ⋅ s-2, P = 0.0003). The CO increase was less marked than in healthy controls (P < 0.05), and consequently, ΔmPAP/ΔCO was higher (9.6 ± 3.1 vs. 0.7 ± 0.1 mm Hg/L/min, P = 0.046) in PAH patients than in controls (Figure 1). High quality RV velocity curves were obtained both at rest and stress in 16 out of 18 patients.


Impairment of pulmonary vascular reserve and right ventricular systolic reserve in pulmonary arterial hypertension.

Domingo E, Grignola JC, Aguilar R, Arredondo C, Bouteldja N, Messeguer ML, Roman A - BMC Pulm Med (2014)

Relationship between mean pulmonary artery pressure (mPAP) and cardiac output at rest and during pharmacological and positional stress. (Filled circle: PAH patients; filled square: control patients).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4007147&req=5

Figure 1: Relationship between mean pulmonary artery pressure (mPAP) and cardiac output at rest and during pharmacological and positional stress. (Filled circle: PAH patients; filled square: control patients).
Mentions: All PAH patients tolerated the stress protocol. No dobutamine infusion had to be interrupted at the doses employed for this study and no complications were observed. No patients included in this study presented greater than mild tricuspid regurgitation (≤ grade 2/4), and there were no relevant changes in its severity during the complete protocol. Only six of 18 PAH patients increased SV, and the heart rate increase was significantly lower than control subjects (29 ± 3.8 vs. 41 ± 2 bpm, P = 0.034), therefore the CO increment was mainly dependent on heart rate increase. mPAP, pPAP and EM increased significantly and PC significantly decreased during stress (Table 2). However, they showed an increase in all the RV systolic function indexes during stress (TAPSE 16.8 ± 1.3 vs. 20.2 ± 1.1 mm, P = 0.02; Sm 12.0 ± 0.5 vs. 14.7 ± 0.8 cm ⋅ s-1, P = 0.003; IVA 3.8 ± 0.3 vs. 7.8 ± 0.9 m ⋅ s-2, P = 0.0003). The CO increase was less marked than in healthy controls (P < 0.05), and consequently, ΔmPAP/ΔCO was higher (9.6 ± 3.1 vs. 0.7 ± 0.1 mm Hg/L/min, P = 0.046) in PAH patients than in controls (Figure 1). High quality RV velocity curves were obtained both at rest and stress in 16 out of 18 patients.

Bottom Line: Cardiovascular reserve was estimated as the change (delta, Δ) during DST compared with rest, including ΔmPAP with respect to ΔCO (ΔmPAP/ΔCO).PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher ΔmPAP/ΔCO (p < 0.05).The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.

View Article: PubMed Central - HTML - PubMed

Affiliation: Pathophysiology Department, School of Medicine, Hospital de Clínicas, Universidad de la República, Avda Italia 2870, PC 11600 Montevideo, Uruguay. jgrig@fmed.edu.uy.

ABSTRACT

Background: Exercise capacity is impaired in pulmonary arterial hypertension (PAH). We hypothesized that cardiovascular reserve abnormalities would be associated with impaired hemodynamic response to pharmacological stress and worse outcome in PAH.

Methods: Eighteen PAH patients (p) group 1 NYHA class II/III and ten controls underwent simultaneous right cardiac catheterization and intravascular ultrasound at rest and during low dose-dobutamine (10 mcg/kg/min) with trendelenburg (DST). We estimated cardiac output (CO), pulmonary vascular resistance (PVR) and capacitance (PC), and PA elastic modulus (EM). We concomitantly measured tricuspid annular plane systolic excursion (TAPSE), RV myocardial peak systolic velocity (Sm) and isovolumic myocardial acceleration (IVA) in PAH patients. Based on the rounded mean + 2 SD of the increase in mPAP in our healthy control group during DST (2.8 + 1.8 mm Hg), PAH p were divided into two groups according to mean PA pressure (mPAP) response during DST, 1: ΔmPAP > 5 mm Hg and 2: ΔmPAP ≤ 5 mm Hg. Cardiovascular reserve was estimated as the change (delta, Δ) during DST compared with rest, including ΔmPAP with respect to ΔCO (ΔmPAP/ΔCO). All patients were prospectively followed up for 2 years.

Results: PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher ΔmPAP/ΔCO (p < 0.05). Neither hemodynamic, IVUS and echocardiographic data were different between both PAH groups at rest. In group 1, DST caused a higher ΔEM, ΔmPAP/ΔCO, ΔPVR, and ΔTAPSE than group 2, with a lower IVA increase and a negative ΔSV (p < 0.05). TAPSE correlated with mPAP and RVP (p < 0.05) and, IVA and Sm correlated with CO (p < 0.05). ΔEM correlated with ΔmPAP and ΔIVA with ΔCO (p < 0.05). There were two deaths/pulmonary transplantations in group 1 and one death in group 2 during the follow-up (p > 0.05).

Conclusions: Pulmonary vascular reserve and RV systolic reserve are significantly impaired in patients with PAH. The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.

Show MeSH
Related in: MedlinePlus