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Pulmonary artery systolic pressure is not only a strong predictor of death in heart failure patients, but also provides prognostic information independent of known predictors of outcomes, according the results of a community-based study.

Compared with the lowest tertile, patients with pulmonary artery systolic pressure in the highest tertile were more than twice as likely to die from all-cause death and cardiovascular disease at one year, noted Veronique L. Roger, MD, MPH, from the Mayo Clinic in Rochester, Minn., and colleagues.

When pulmonary artery systolic pressure was added to traditional risk factors such as age, sex, comorbidity index results, anemia, ejection fraction, diastolic function, and chronic obstructive pulmonary disorder, it resulted in a net reclassification improvement of 14.1%, according to the study published in the Jan. 17 issue of the Journal of the American College of Cardiology.

Roger and colleagues noted that much more is known about idiopathic pulmonary hypertension than the type associated with heart failure. In addition, studies that did find a link between pulmonary hypertension and a poor outcome in heart failure patients were limited in ways that hinder broad conclusions. For example, studies often excluded those with chronic obstructive pulmonary disorder or did not assess diastolic function.

They also noted that the only other population-based study on this topic was limited to patients with preserved ejection fractions (J Am Coll Cardiol 2009; 53: 1119-26).

"Therefore, the prevalence, clinical characteristics, and prognosis of pulmonary hypertension among all community patients with heart failure remains uncertain," they wrote.

To help fill in those gaps, the investigators prospectively examined all inpatients and outpatients presenting with heart failure in Olmsted County, Minn., using Doppler echo estimations of pulmonary artery systolic pressure to gauge pulmonary hypertension.

The final study population was 1,049 patients who had consented and had undergone an echo exam at a median of one day within the heart failure diagnosis.

The mean age of patients was 76, with 51% being women and slightly more than half of the patients having a modified Charlson comorbidity index of 3 or greater. The rate of incident and prevalent cases of heart failure was essentially equal (51% versus 49%).

Researchers divided patients into tertiles: those with <41 mm Hg, those with 41 to 54 mm Hg, and those with >54 mm Hg. Even with an upper limit of normal pulmonary pressure defined as 35 mm Hg, only 21% of patients had normal pulmonary pressures.

The median pulmonary artery systolic pressure was 48 mm Hg. A few patient characteristics associated with a higher systolic pressure included older age, anemia, atrial fibrillation, higher NYHA functional class, lower creatinine clearance, and higher B-type natriuretic peptide (P<0.001 for all except atrial fibrillation, P=0.015).

Researchers followed patients for a mean of 2.7 years and found that one-year all-cause mortality rates rose from 8% in the first tertile to 28% in the third tertile. Compared with the first tertile, those in the second and third tertiles had unadjusted hazard ratios of 1.72 and 2.64, respectively.

After adjusting for traditional risk factors, the risk remained, albeit somewhat attenuated: HR 1.45 and HR 2.07, respectively.

Researchers also found a significant association between pulmonary artery systolic pressure and cardiovascular (CV) death, as mortality rates went from 4% in the lowest tertile to 17% in the highest tertile.

The adjusted risk of CV death was significant, although lower than the unadjusted risk (HRs 1.75 and 2.50, second and third tertiles, respectively). Ejection fraction did not have a significant relationship with pulmonary systolic pressure, the researchers noted.

Adding systolic pressure measurement to traditional risk factors increased discriminatory power for identifying patients at a higher risk of all-cause and CV death. For both metrics, the c-statistic significantly increased.

Roger and colleagues suggested that Doppler echo can readily assess pulmonary hypertension in the community and that it would be beneficial to do so given the results of their study.

In an accompanying comment, Myung Park, MD, from the University of Maryland School of Medicine in Baltimore, and Mandeep R. Mehra, MBBS, from Brigham and Women's Hospital in Boston, noted that there were variances in the degrees of usefulness of pulmonary hypertension as a marker.

While the indicated discrimination improvement showed a gain of 4.2% in one-year mortality, the net reclassification improvement suggested a predictive gain of 14.1% over the established risk markers. The challenge is to translate this to clinical application, "particularly since the underlying pathology is rather variable" and therapeutic directives still "poorly defined."

Why pulmonary hypertension has incremental prognostic value and what therapeutic targets might be viable are questions to be answered, they said. Possibilities include that these patients are more ill or have genetic factors that predispose to a worse prognosis. Does inflammation play a role? Is it simply related to the "hemodynamic response to chronically elevated left-sided filling pressures coupled with dynamic interaction between the two ventricles?" Perhaps all these factors play a role, Park and Mehra said.

They would have liked it if Roger and colleagues examined the relationship between right ventricular function and pulmonary hypertension. But Roger et al. acknowledged the study was limited by the inability to account for right ventricular size and function as the information was not always available.

Another limitation, they said, was that echo estimates of pulmonary artery systolic pressure have lower reproducibility and reliability than a Swan-Ganz catheter, but the invasive method could not be used in this study.

From the American Heart Association:

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