Abstract 2239: Is Heightened Vascular Stiffness A Predictor Of Future Acute Pulmonary Edema
Hypothesis: We assessed the hypothesis that an inability of the left ventricle to augment stroke volume (SV) during stress due to impaired arterial stiffness may predispose patients to developing pulmonary congestion or edema (PE).
Methods: We performed a case-control study to determine if left ventricular (LV) or vascular function measured using dobutamine cardiovascular magnetic resonance (DCMR) was associated with the future risk of PE in the absence of an acute coronary syndrome, angina, pneumonia, or renal failure. From a population of patients who underwent a DCMR for assessment of ischemia during 1997–2001 followed for an average of 5 years, there were 23 patients who sustained a PE event during the follow-up period (PE+). A gender (40% women) and age (range 44 – 87 years) matched sample of 73 subjects was selected from those who did not sustain a PE event (PE-) during the same time interval. In PE+ and PE- individuals, we measured LVSV reserve (stress SV/rest SV), and ventriculo-vascular stiffness (brachial pulse pressure [PP] / LVSV indexed for body surface area [SVi]) at rest and during DCMR stress.
Results: The mean ± standard deviation of the age in years (66 ± 11, PE+; 64 ± 10, PE−: p=0.55), gender (42% women, PE+; 41% women PE−: p= 1.0), peak stress heart rate (121bpm, PE+; 124bpm PE−: p = 0.35), and peak stress systolic blood pressure (151 mm Hg, PE+; 142 mm Hg, PE−: p = 0.22) were similar among the groups. Resting LV ejection fraction was 45 ± 14% in PE+, and 49 ± 11% in PE-participants (p = 0.15). PE+ participants exhibited reduced LVSV reserve relative to PE-participants (0.9 ± 0.2 versus 1.1 ± 0.1, respectively, p = 0.009); they also exhibited increased ventriculo-vascular stiffness at peak dobutamine stress (4.5 ± 2.9 mmHg/ml/m2 versus 2.7 ± 1.0 mmHg/ml/m2, respectively, p <0.0001). After adjusting for age, gender, and resting LVEF, differences in LVSV reserve and PP/SVi at peak stress remained different between PE+ and PE- participants (p=<0.001).
Conclusions: In conclusion, these results suggest that the failure to increase left ventricular stroke volume and diminish arterial stiffness during dobutamine stress may indicate patients at risk for subsequent development of pulmonary edema.