The trusted source for
healthcare information and
Elevated Pulmonary Artery Pressures in CAD
Abstract & Commentary
By Michael H. Crawford, MD, Professor of Medicine, and Chief of Clinical Cardiology, at the University of California, San Francisco. Dr. Crawford is on the speaker's bureau for Pfizer.
Synopsis: Elevated echo-Doppler estimates of pulmonary artery pressure predict heart failure and death in CAD patients.
Source: Ristow B, et al. Elevated Pulmonary Artery Pressure by Doppler Echocardiography Predicts Hospitalization for Heart Failure and Mortality in Ambulatory Stable Coronary Artery Disease. J Am Coll Cardiol. 2007;49:43-49.
Elevated estimates of pulmonary artery pressures by echo-Doppler are valuable information in many clinical situations. However, its value in coronary artery disease patients is not known. Thus, Ristow and associates evaluated the Heart and Soul Study database for echo estimates of pulmonary pressures and related them to cardiovascular (CV) outcomes. The Heart and Soul Study is a prospective cohort study on the influence of psychosocial factors on CV events in patients with known coronary artery disease (CAD). Echocardiograms were done at intake in all patients and the peak tricuspid regurgitation (TR) and pulmonic regurgitation (PR) velocity was recorded when present. The echocardiograms were read independently in a blinded fashion. The upper limit of normal for peak TR gradient was taken as 30 mmHg and 5 mmHg for the end-diastolic (ED) PR gradient. Outcomes were determined independently by patient phone calls and inspection of hospital records, death certificates and coroner's reports.
Results: Outcome adjudication was complete for 717 of 741 participants enrolled from July 2001 to December 2002. Of these 717 patients, 466 (65%) had ED PR, 573 (80%) had TR and 392 (55%) had both gradients measured. At least one TR or ED PR measurement was present in 90%. An ED PR gradient > 5 mmHg was found in 21% and 22% had a TR gradient > 30 mmHg. Several baseline characteristics differed significantly in the elevated pulmonary pressure patients; in general, they were older, sicker and had more comorbidities. Thus, multivariate adjustments were made for these differences in calculating the odds of the primary outcomes of heart failure (HF) hospitalization, CV death and all-cause mortality. During the mean follow-up of 3 years, there were 63 HF hospitalizations, 19 CV deaths, and 86 total deaths. Elevated ED PR or TR gradients were associated with higher rates of HF hospitalization and all-cause death, but not CV death. On multivariate analysis, every 5 mmHg increase in ED PR was associated with a 2.5 fold increase in HF hospitalization and a 70% increase in total mortality. Every 10 mmHg increase in TR gradient resulted in a 50% increase in HF hospitalization. Statistically both measures had similar predictive power. The authors concluded that increases in echo-Doppler measurements of ED PR or TR gradients predict HF hospitalization and death in ambulatory patients with CAD.
That elevated estimates of pulmonary pressures are a bad prognostic sign in CAD patients is not surprising. What is unique about this study is the use of ED PR. This is a simple measurement available in most adults that is derived from one short axis parasternal view. TR gradients must be obtained in multiple views and the highest taken because of variations in jet direction. ED PR gradient was as useful as TR, but it was obtainable in fewer patients (65% vs 80%). However, one or both measures were available in 90% of their patients. ED PR is also attractive because it is an estimate of end diastolic pulmonary pressure, which is a surrogate for left ventricular filling pressure. Thus, it is not surprising that it was good at predicting HF hospitalizations (OR 2.7), but so was TR gradient (OR 3.4).
There are some potential limitations to this study. The population was largely male. There were few CV deaths, so the power to predict this outcome was reduced. Neither the ED PR nor the TR gradients were corrected for estimated right atrial pressure, which would have more accurately reflected pulmonary artery pressures. This is surprising since this group popularized using inferior vena cava measurements to estimate right atrial pressure. They argue that in this ambulatory population most would have normal right atrial pressures and it would add little to the predictive value of the gradients. This may be true, but it would have been nice to see it proven. Also, they did not try to estimate pulmonary vascular resistance by measuring cardiac output by echo-Doppler. This would have been interesting, but would have added complexity to the study.
The authors recommend that echocardiographic laboratories routinely measure ED PR and TR gradients to estimate pulmonary pressures and I agree with them. This is a simple addition that provides powerful information to the clinician.