Utility of Pulmonary Hypertension for the Prediction of Heart Failure Following Acute Myocardial Infarction

Study Questions:

Is pulmonary hypertension predictive of incident clinical heart failure (HF)?

Methods:

This was a secondary analysis of data collected as part of a longitudinal cohort study designed to determine predictors of HF following hospitalization for acute myocardial infarction (MI). Echocardiography was performed within 2 days of admission and estimated pulmonary artery systolic pressures (PASPs) were determined from the tricuspid regurgitant jet according to Bernoulli’s formula. Patients with prior clinical HF and those without sufficient estimated PASP imaging were excluded. Patients were dichotomized into normal and pulmonary hypertension groups according to PASPs using a threshold of 35 mm Hg. The primary outcome of interest was hospitalization for HF at 1 year.

Results:

Of the 2,023 patients recruited, 1,054 were included in the analysis. The median [interquartile range] PASP was 34 [28-43] mm Hg, and 45% (n = 470) of patients had pulmonary hypertension. Patients with elevated PASPs were older, more likely to be female, and had more comorbidities (i.e., renal dysfunction, diabetes). There were 119 patients (11%) admitted with HF over 1 year of follow-up. Of these, 82% had a PASP >35 mm Hg on admission echo. Pulmonary hypertension on admission echo afforded nearly threefold higher adjusted risk (hazard ratio, 3.1; 95% confidence interval, 1.9-5.1) for HF readmission, and PASP offered a higher area under the receiver operating characteristic curve (AUC) (0.74 ± 0.02) than other echo variables for predicting HF, including left ventricular ejection fraction (LVEF) (AUC 0.67 ± 0.02). Other correlates of risk included reduced EF, mitral regurgitation severity, Killip class, and advanced age.

Conclusions:

The authors concluded that pulmonary hypertension noted at the time of acute MI may be useful for unmasking subclinical HF and predicting development of over HF.

Perspective:

In this analysis, the presence of pulmonary hypertension upon admission was associated with worse outcome after acute MI, even when corrected for other clinical risk factors. In this analysis, 151 (32%) of the 470 patients with pulmonary hypertension had a PASP >50 mm Hg, suggesting pulmonary hypertension was not new on admission. Thus, PASP measurement may ‘expose’ those with subclinical HF likely to be admitted. This analysis is limited by the inherent weakness of using echocardiography to estimate PA pressures. A normal PASP by echo does not ensure an absence of prior pulmonary hypertension in a right ventricle that is failing post-MI. It would be useful to know if follow-up PA pressure estimates upon clinical stability (2-3 months after MI) offer better risk discrimination because LV diastology (and therefore mitral regurgitation and PASP measurements) will change in an acute MI setting. Finally, it is not known if pharmaceutical attempts at improving PA pressures will impact future HF risk.

Clinical Topics: Heart Failure and Cardiomyopathies, Noninvasive Imaging, Pulmonary Hypertension and Venous Thromboembolism, Valvular Heart Disease, Acute Heart Failure, Pulmonary Hypertension, Echocardiography/Ultrasound, Mitral Regurgitation

Keywords: Myocardial Infarction, Follow-Up Studies, Ventricular Function, Left, Tricuspid Valve Insufficiency, Mitral Valve Insufficiency, Comorbidity, Blood Pressure, Risk Factors, Pulmonary Artery, Cyclophosphamide, Heart Failure, Hypertension, Pulmonary, Cardiovascular Diseases, Stroke Volume, Confidence Intervals, ROC Curve, Heart Ventricles, Diabetes Mellitus, Echocardiography


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