Abstract
Background: Widened pulse pressure, a marker for increased vascular stiffness, is associated with adverse cardiovascular outcomes. Since diastolic dysfunction may also relate to vascular stiffness and may portend a poor prognosis, our aim was to determine the association between pulse pressure and diastolic dysfunction in patients with preserved LVEF. Methods: 150 consecutive patients with and 300 consecutive controls without diastolic dysfunction and LVEF $50% were studied. We excluded patients with severe valve abnormalities and incomplete documentation. Severity of diastolic dysfunction was graded 1-3 (abnormal relaxation, pseudonormal, restrictive). We compared pulse pressure (at time of echo) in patients with and without diastolic dysfunction and adjusted for baseline covariates before and after propensity score matching. We analyzed the data before and after excluding patients with mild diastolic dysfunction to determine the association in the absence of borderline dysfunction. Results: Data from 269 controls were compared to 130 patients with diastolic dysfunction. Of those, 74 (57%) had abnormal relaxation, 45 (35%) had pseudonormal and 11 (8%) had restrictive patterns. Pulse pressure was wider in patients with diastolic dysfunction compared to controls (74 6 24 vs. 65 6 18, p!.0001). After adjustment for baseline covariates this association was not statistically significant. In 63 propensity-matched patient pairs, diastolic dysfunction was associated with a numerically greater but statistically non-significant difference in pulse pressure (74 6 24 vs. 70 6 18 mmHg, p50.26). After excluding patients with mild (grade 1) diastolic dysfunction, pulse pressure was wider in those with diastolic dysfunction (79 6 23 vs. 65 6 19 mmHg, p!.0001), and remained statistically significant after multivariate adjustment. The odds ratio comparing 25 vs. 75 percentile of pulse pressure for presence of diastolic dysfunction was 1.57 (95% CI 1.01-2.43). Other predictors of diastolic dysfunction that remained significant after multivariable adjustment were older age, LVH, hypertension, and low GFR. Conclusion: Patients with more severe diastolic dysfunction have a wider pulse pressure compared to controls. These results are consistent with the hypothesis that increased vascular stiffness contributes to both a widened pulse pressure and diastolic dysfunction, and may help to explain the increased risk in these patients. We speculate that pulse pressure may be a modifiable risk factor to improve diastolic dysfunction and long term outcomes.
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