Page 18 - Journal of Structural Heart Disease Volume 3, Issue 4

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Original Research Article
scatheter device closure of ASDs at di erent eleva- tions, we sought to determine whether elevation is an independent risk factor for the development of PAH in these patients.
We evaluated individual RHC hemodynamic data as well as data contributing to the clinical classi ca- tions of PH and PAH (with PAH referring to pulmonary vascular disease with elevated pulmonary artery pres- sures and normal left heart pressures). We found that patients living at moderate altitude showed a trend toward higher pulmonary artery pressures and that more patients living at moderate altitude met the clinical de nition of PH than those living at low alti- tude. We suspect this is secondary to lower oxygen tension and more hypoxic vasoconstriction, as defect size, shunt fraction, and the presence of other causes of PH or use of PH medications were similar between groups.
In looking at PVR and PAH, the presence of which is the main contributor to morbidity in these pa- tients and thus was our choice for primary outcome, we found that although PVR was signi cantly high- er in the moderate altitude group, it was not elevat- ed to the clinically important threshold that de nes PAH. We believe that the higher pulmonary arterial pressures seen in the moderate altitude group con- tribute to higher calculated PVR (as mPAp makes up one half of the numerator in the PVR calculation, (mPAp-PCWp)/Qp), but there is likely no signi cant di erence between groups in actual pulmonary vas- cular disease.
Patients with unrepaired ASDs or ASD physiology and defect size ≥ 4 mm were chosen because these patients are most likely to have a hemodynamically signi cant shunt that may predispose to the develop- ment of pulmonary vascular changes and PAH. By ex- cluding patients with a patent foramen ovale or small defects, we intended to avoid a false underestimation of PAH prevalence in patients with interatrial com- munications. By excluding other types of congenital heart disease, such as ventricular septal defects, aor- topulmonary connections, or other causes of left-to- right shunt and excessive pulmonary blood ow, we intended to prevent a false overestimation of the bur- den of PAH. We did not exclude patients with multiple PH risk factors or multifactorial PH/PAH because it is quite common for a patient to have more than one
cause of PH/PAH, such as having an ASD and obstruc- tive sleep apnea. By looking primarily at PAH (and not PH), we focused on patients with true pulmonary vascular disease rather than those with excessive pul- monary blood ow and/or increased pulmonary pres- sures from lung or left heart disease.
There are several limitations of this study. First, in- accurate hemodynamic analysis using false data can often be a challenge when studying cardiac catheter- izations. Speci cally, a catheterization lab’s computer software generates results of complex calculations of multiple variables, of which the software attempts to select variables from the data it ‘sees’ and/or a human operator chooses. This can result in reported calcu- lations or results that are not physiologically correct. To avoid the problem of comparing software-gener- ated results, we reviewed the catheterization reports closely for the values that should be used in the calcu- lations and performed the calculations independent- ly. In some cases, assumptions were still necessary. For instance, we used pulse oximeter saturation as a sur- rogate for pulmonary vein and systemic arterial satu- rations when these data were not available or used a value of 95% as the pulmonary vein and systemic sat- uration when no pulse oximeter saturation was avail- able. Furthermore, the assumed value of 95% may vary at moderate elevation compared to sea level.
Second, we made several assumptions about our patients. We assumed that the zip code of a patient’s residence at the time of chart review was the same zip code and elevation at which he or she was living at the time of the catheterization. For catheterizations 7–10 years ago, however, this may not be the case. We also assumed that a patient was living at a particular elevation long enough for it to impact his or her risk of developing PAH. Unfortunately, data regarding du- ration of residence at that elevation prior to catheter- ization was not available.
Third, residence in Denver or at elevations similar to Denver’s may not be high enough to reveal a dif- ference in the development of PAH compared with residence at sea level. Previously, 8200 ft (2500 m) or higher has been described as a threshold at which signi cant pulmonary vascular disease can develop [12], and Denver’s population is well below that mark at 5280 ft (1600 m). Although elevation-related in- creases in pulmonary pressures are certainly present
Nicolarsen, J. et al.
Altitude and Pulmonary Arterial Hypertension