1349192 - Increased left ventricular kinetic energy and contractility due to underfilling in patients with precapillary pulmonary hypertension

Precapillary pulmonary hypertension (PH_precap) is a vascular condition with elevated pressure and resistance in the pulmonary circulation (1), leading to right ventricular heart failure. However, altered pulmonary hemodynamics also impact the left ventricle (LV), although the mechanisms are not fully understood. Cardiac magnetic resonance imaging (CMR) can provide detailed measurements of cardiac functions, and has the potential to improve the understanding of the pathophysiological mechanisms in PH_precap.  Intracardiac hemodynamics can be measured by kinetic energy (KE) computed from CMR with 4D flow, and LV contractility can be estimated from CMR by non-invasive pressure-volume loops. Therefore, the aim of this study was to investigate if LV KE and contractility in patients with PH_precap differ from healthy controls.

Methods:

Patients with PH_precap (n=19; pulmonary arterial hypertension, n=12, 63%, and chronic thromboembolic pulmonary hypertension, n=7, 37%) and age- and sex matched controls (n=14) underwent CMR at 1.5T (MAGNETOM Aera, Siemens Healthcare, Erlangen, Germany) (Table 1). Cine images, 2D flow phase contrast images, and 4D flow using a prototype sequence were acquired. Left ventricular peak KE and contractility were computed using the software Segment v.3.3 R10057 (Medviso, Lund, Sweden), as previously published (2,3). The Mann-Whitney U test was used for group comparisons, regression analysis for associations, and Spearman analysis for correlations.

Results:

Systolic and diastolic LV KE did not differ between patients and controls (Table 1, Figure 1). However, when indexed to stroke volume, systolic and diastolic LV KE were increased in patients (Table 1, Figure 1). Likewise, contractility was increased in patients (Table 1). In both patients with PH_precap and controls, there is a positive association between stroke volume and kinetic energy (r²=0.75 and r²=0.53), and a negative association between stroke volume and contractility (r²=0.44 for both) (Figure 2). There was no correlation between contractility and systolic KE (p=0.07 and p=1.0) (Figure 2).

Conclusion:

Patients with PH_precap have increased peak left ventricular KE when indexed to SV as well as an increased contractility compared to controls. This suggests that increased KE could be caused by a sympathetic upregulation, which may be due to underfilling of the LV in patients with PH_precap. Furthermore, the associations between stroke volume and contractility in both groups, indicate that the intrinsic LV function in patients with PH_precap is similar to that of the healthy heart.