Exercise during cardiac catheterization distinguishes between pulmonary and left ventricular causes of dyspnea in systemic sclerosis patients


  • Authorship and contributorship

    WDH: designed the study, collected and analyzed data, wrote the paper. IC: collected and analyzed data. JPT: statistical analysis, wrote paper. MA: collected and analyzed data. RF: designed the study, collected and analyze data, wrote the paper. SL: collected data. NFR: designed the study, collected and analyzed data, wrote the paper.

  • Ethics

    The study was approved by the University of Connecticut Institutional Review Board. The data analyzed are from clinical studies performed previously. Data do not identify subjects.

  • Conflict of interest

    Dr Foley has research funding from Actelion Pharmaceuticals and Gilead Sciences.

    Dr Rothfield has research funding from Actelion Pharmaceuticals, Medimmune, United Therapeutics, UCB, Pfizer, Bristol-Myers Squibb and Mediquest Therapeutics.

    The authors have stated explicitly that there are no conflicts of interest in connection with this article.


W. David Hager, MD, Calhoun Cardiovascular Center, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030


Tel: +1 860 679 2771

Fax: +1 860 679 3346

email: Hager@NSO1.UCHC.edu



The cause for shortness of breath among systemic sclerosis (SSc) patients is often lacking. We sought to characterize the hemodynamics of these patients by using simple isotonic arm exercise during cardiac catheterization.


Catheterization was performed in 173 SSc patients when resting echocardiographic pulmonary systolic pressures were <40 but >40 mmHg post stress. Patients with resting mean pulmonary arterial pressures (mPAP) ≤ 25 and pulmonary arterial wedge pressures (PAWP) ≤ 15 mmHg exercised with 1-pound hand weights. Normal exercise was defined as a change in mPAP divided by the change in cardiac output (CO) (ΔmPAP/ΔCO) ratio ≤ 2 for patients <50 years (≤3 for >50). An abnormal ΔmPAP/ΔCO ratio, an exercise transpulmonary gradient (TPG) ≥ 15, a PAWP < 20, a ΔTPG > ΔPAWP and a pulmonary vascular resistance (PVR) which increased defined exercise-induced pulmonary arterial hypertension (EIPAH). An abnormal ΔmPAP/ΔCO ratio, an exercise TPG < 15, a PAWP ≥ 20, a ΔTPG < ΔPAWP and a drop in PVR defined left ventricular diastolic dysfunction (DD). Twelve patients without SSc served as controls.


Pulmonary pressures increased with exercise in 53 patients. Six had EIPAH and 47 had DD. With exercise, mPAP and PAWP were 20 ± 4 and 13 ± 2 in controls, 36 ± 3 and 12 ± 4 in EIPAH and 34 ± 6 and 26 ± 4 in DD. Control ΔmPAP/ΔCO was 0.8 ± 0.7, 7.5 ± 3.9 in EIPAH and 9.1 ± 7.2 in DD. Rest and exercise TPG was normal for control and DD patients but increased (12 ± 4 to 23 ± 4) in EIPAH (P < 0.0001). PVR decreased in DD but increased in EIPAH with exercise.


Exercise during catheterization elucidates the pathophysiology of dyspnea and distinguishes EIPAH from the more common DD in SSc patients.