1349403 - Myocardial structure and elastance components of blood pressure predict adverse outcomes

In patients with pulmonary arterial hypertension (PAH) it is widely believed that increasing pulmonic blood pressure progresses to right heart failure. However, others have recently identified that approximately half of the deaths in PAH patients are related to non-pulmonary/right heart conditions. Here we show that cardiovascular adverse events (CVAE) are more strongly associated with the systemic as opposed to pulmonic blood pressure derived from a cardiovascular magnetic resonance (CMR) imaging model.

Methods:

Data from PAH patients (n=40) with right heart catheterization measures of pulmonary arterial systolic pressure (PAPs) and CMR functional scans of the heart were analyzed to isolate the myocardial elastance and ventricular structural components of blood pressure. Sinusoidal transforms of key cardiac measures obtained using CMR were separately fit to systemic systolic blood pressure (SBP) and PAPs to model the maximum myocardial elastance component of left and right ventricular contributions to pulmonic and systemic systolic BP. Additionally, the structural component of systolic blood pressure was obtained from a linear combination of left and right ventricular mass and patient age. The summation of the maximal myocardial elastance and structural components of pressure was used to model left and right systolic BP. During follow-up up to one year, CVAEs noted were myocardial infarction, angina, hypotension, atrial fibrillation and orthostatic syncope. The structural and elastance components of BP were entered into models to find the association with CVAEs.

Results: The model fit to SBP had an r² of 0.59, while the model fit to PAPs had an r² of 0.75, and 6 (15%) patients experienced at least one CVAE. The measured PAPs did not significantly associate with CVAEs, Figure 1A.  Similarly, the measured SBP did not significantly associate with CVAEs, Figure 1B. However, the difference between the left ventricular structural and left ventricular maximal myocardial elastance contributions to pressure were significantly associated with CVAEs (p < 0.05), Figure 1C. Most CVAEs occurred when the systemic elastance component exceeded the ventricular structural component. This condition likely indicates conditions when the structural integrity of the ventricle is compromised by the high force of contraction. The ROC curve had an area under the curve of 0.78, and CVAEs could be detected with 83% sensitivity and 82% sensitivity, Figure 1D.

Conclusion:

By separating components of pressure into the ventricular structural and maximal myocardial elastance we were able to show that MACE predominated when the elastance exceeded the structural component. Importantly, this observation was made for the systemic blood pressure, despite the patients having PAH. Moreover, reliance on ubiquitous PAP measurement leads to an under-representation of MACE whereas detecting the fundamental perturbation of the RV/LV interaction results in a tripling of MACE detection.