Pulmonary Vascular Disease |

High Incidence of Silent Parenchymal Lung Disease in Patients With Exercise Induced Pulmonary Hypertension Associated With CTD FREE TO VIEW

Demir Baykal*, MD; Theresa Lawrence, MD; Cynthia Elliott, MD
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Gwinnett Consultants in Cardiology, Lawrenceville, GA

Chest. 2012;142(4_MeetingAbstracts):817A. doi:10.1378/chest.1389207
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SESSION TYPE: DVT/PE/Pulmonary Hypertension Posters I

PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: Pulmonary hypertension (PAH) is a common among CTD patients. Presence or absence of associated comorbidities with exercise induced pulmonary hypertension may incur therapatic implications.

METHODS: We studied 28 symptomatic CTD patients with normal rest PA pressures on transthoracic echocardiogram, 17 of which were NYHA class 2 and 11 were NYHA class 3. The diagnostic testing included pulmonary function tests (DLco % predicted, FVC % predicted, FVC/DLco % predicted), chest HRCT, exercise echocardigram . Cardiac outputs were also calculated in the cath lab using thermodilution method.

RESULTS: 16 patients had exercise induced pulmonary hypertension on exercise echocardiogram defined as more than 20 mmHg increment in systolic PA pressure, 13 of whom were verified to have exercise induced PAH in the cath lab with mean PA pressure exceeding 30mmHg. 3 of the remaining 12 with normal treadmill hemodynamic response was found to have exercise induced PAH in the cath lab (The mean PA pressure was 36mmHg group, whereas it was 25mmhg in the normal hemodynamic response group. The mean FVC % predicted was 69 in the exercise induced PAH group as opposed to 90 in the control group (p=0.02) DLco % predicted and FVC/DLco % predicted were not significantly different between the groups. 11 of the 16 exercise induced PAH patients had abnormalities on chest HRCT including mild honeycombing, ground glass appearance, alveolar interstitial infiltrates and 1 pulmonary fibrosis unexpectedly. Only 1 of the normal hemodynamic response patients had alveolar interstitial infiltrates. The mean cardiac output of control group was 5.1 L/min/sq at rest and increased to 7.1 L/min/sq at peak exercise whereas rest and peak exercise cardiac output values were 4.8 and 6.5 L/min/sq per exercise induced PAH group, the difference not reaching statistical significance with ANOVA analysis.

CONCLUSIONS: Exercise induced pulmonary hypertension is common among symptomatic connective tissue disease population. Parenchymal lung disease and/or PFT abnormalities are prevalent in this group and may explain exercise induced pulmonary hypertension via diminished pulmonary flow reserve secondary to extrinsic compression of lung vasculature

CLINICAL IMPLICATIONS: Exercise induced pulmonary hypertension may be a reason to screen for silent parenchymal lung disease in dyspneic connective tissue disease population .

DISCLOSURE: Demir Baykal: Consultant fee, speaker bureau, advisory committee, etc.: speakers fee

Theresa Lawrence: Consultant fee, speaker bureau, advisory committee, etc.: speaker fee

The following authors have nothing to disclose: Cynthia Elliott

No Product/Research Disclosure Information

Gwinnett Consultants in Cardiology, Lawrenceville, GA




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