Skip to main content
Dryad logo

Right ventricular contractility and load in HIV associated pulmonary hypertension

Citation

Rajaratnam, Arun et al. (2020), Right ventricular contractility and load in HIV associated pulmonary hypertension, Dryad, Dataset, https://doi.org/10.5061/dryad.v6wwpzgt8

Abstract

Background: People living with human immunodeficiency virus (PLWH) are at risk of developing pulmonary hypertension (PH) and right ventricular (RV) dysfunction, but understanding of the relationship of RV function to afterload (RV-PA coupling) is limited. We evaluated the clinical and hemodynamic characteristics of human immunodeficiency virus (HIV)-associated PH.

Methods: We performed a retrospective review of patients with a diagnosis of HIV undergoing right heart catheterization (RHC) from 2000-2016 in a tertiary care center. Inclusion criteria were diagnosis of HIV, age ≥ 18 years and availability of RHC data. PH was classified as either pulmonary arterial hypertension (PAH; mean pulmonary arterial pressure [mPAP] ≥ 25mmHg with pulmonary artery wedge pressure [PAWP] ≤ 15mmHg) or pulmonary venous hypertension (PVH; mPAP ≥ 25mmHg with PAWP > 15). We collected demographics, CD4 cell count, HIV viral load, RHC and echocardiographic data. The single beat method was used to calculate RV-PA coupling from RHC.

Results: Sixty-two PLWH with a clinical likelihood for PH underwent RHC. Thirty-two (52%) met PH criteria (15 with PAH, 17 with PVH). Average time from diagnosis of HIV to diagnosis of PH was 11 years. Eleven of 15 individuals with PAH were on antiretroviral therapy (ART) while all 17 patients with PVH were on ART. Compared to PLWH without PH, those with PH had an increased likelihood of having a detectable HIV viral load and lower CD4 cell counts. PLWH with PAH or PVH had increased RV afterload with normal RV contractility, and preserved RV-PA coupling. 

Conclusion: PLWH with PH (PAH or PVH) were more likely to have a detectable HIV viral load and lower CD4 count at the time of RHC. PLWH with PAH or PVH had increased RV afterload, normal RV contractility, with preserved RV-PA coupling suggestive of an early onset, mild, and compensated form of PH. These results should be confirmed in larger studies.

Methods

Subjects were selected from a de-identified database of all patients who underwent a right heart catheterization (RHC) at the University of Pittsburgh Medical Center between 2000 and 2016. We selected individuals with a diagnosis of HIV (ICD-9 code: 042) in the Electronic Health Record. Patients were categorized into 2 groups:  Pulmonary Hypertension (PH, defined as mean pulmonary arterial pressure [mPAP] ≥ 25mmHg) and No Pulmonary Hypertension (No PH, defined as mPAP≤ 25mmHg). PH was further sub-categorized as either pulmonary arterial hypertension (PAH; defined as mPAP ≥ 25mmHg with pulmonary artery wedge pressure [PAWP] ≤ 15mmHg) or pulmonary venous hypertension (PVH; defined as mPAP ≥ 25mmHg with PAWP > 15). Data collected included demographics, medical history, medications, CD4 cell count, and HIV viral load. We analyzed echocardiographic and cardiac catheterization data that were collected within 6 months of each other for complete LV systolic and diastolic measurements and RV systolic measurements. The IRB of the University of Pittsburgh approved the study.

Usage Notes

Table S1. Missing data for subject characteristics

 

 

 

 

No Pulmonary Hypertension

N=30

 

Pulmonary Hypertension

N=32

 

 

 

Age (years)

0

0

Female

0

0

African-American

1

1

CAD

0

0

IVDU

0

0

History of Smoking 

0

0

Hypertension

0

0

Vasodilator use

0

6 (40%)

0

3 (18%)

Anti-retroviral use

0

0

CD4 <400 

4

6

CD4 count (cells/mm3)

4

6

 

Table S2. Missing data for hemodynamic and echocardiographic data.

 

 

No Pulmonary Hypertension 

N=30

Pulmonary Hypertension 

N=32

Heart rate (bpm) 

13

15

ePASP (mmHg)  

7

9

EF (%)  

3

5

RVOT VTI (m)

15

16

mPAAT (cm)

16

16

TAPSE (cm)

14

16

FAC (%)

17

                16

MPAP (mmHg)

3

5

PAWP (mmHg)

3

7

CO (L/min/m2)

7

6

PVR (Woods Units)

9

8

Ees (mmHg/mL)*

12

8

Ea (mmHg/mL)*

12

8

Ees/Ea*

12

8

Diastolic StiffnessBeta,*

12

8

* Single beat analysis was available for 1patients in the No Pulmonary Hypertension group and 24 patients in the Pulmonary Hypertension group.

 

 

Table S3. Missing data for subject characteristics

 

PAH

N= 15

PVH

N=17

 

 

 

Age (years)

0

0

Female

0

0

African-American

1

1

CAD

0

0

IVDU

0

0

History of Smoking 

0

0

Hypertension

0

0

Vasodilator use

0

6 (40%)

0

3 (18%)

Anti-retroviral use

0

0

CD4 <400 

2

4

CD4 count (cells/mm3)

2

4

 

Table S4. Missing data for hemodynamic and echocardiographic data.

 

PAH

N=13

PVH

N=14

Heart rate (bpm) 

3

7

ePASP (mmHg)  

2

2

EF2 (%)  

0

0

RVOT VTI (m)

4

7

mPAAT (cm)

4

7

TAPSE (cm)

4

7

FAC1 (%)

4

                 7

MPAP (mmHg)

0

0

PAWP (mmHg)

2

0

CO (L/min/m2)

2

1

PVR  (Woods Units)

2

1

Ees (mmHg/mL)*

3

7

Ea (mmHg/mL)*

3

7

Ees/Ea2*

3

7

Diastolic StiffnessBeta,*

3

7

* Single beat analysis was available for 10 patients in the Pulmonary Arterial Hypertension group and 7 patients in the Pulmonary Venous Hypertension group.

 

Please note on the uploaded dataset the tab marked 'demographics', 'viral dais not patient linked to 'hemodynamics', given the differences in available data ( i.e sample number) and for concerns of sensitive data, and for ease of analysis.

Funding

National Institutes of Health, Award: NIH 2P01HL103455

National Institutes of Health, Award: R01HL098032

National Institutes of Health, Award: RO1HL096973

National Institutes of Health, Award: R01AG058659

National Institutes of Health, Award: K24123342