We for the first time investigated the role of cardiac power estimated by non-invasive echocardiography in patients with stable HFpEF. In this study, we found that (i) cardiac power normalized to LV mass at rest were both independently associated with all-cause death and HF hospitalization in patients with HFpEF and (ii) the incorporation of rest cardiac power/mass (reflective of comprehensive cardiac function) and NT-proBNP (indicative of myocardial stretch) into a model with established risk factors enhanced the prognostic value for the endpoints.
As is well known, LV diastolic dysfunction plays a fundamental and predominant role in the pathophysiology of HFpEF [10] and elevates filling pressure, which further promotes dyspnea, impairs exercise capacity and increases mortality and incidence for HF hospitalization[11]. Non-invasive echocardiography is an indirect approach to measuring LV diastolic function. Due to its safety and rapidity, echocardiography is usually superior to the invasive right heart catheterization for clinical physicians. However, individual parameters of echocardiography, such as left atrial volume index and the mitral annular diastolic velocity, has their own limitations and fail to accurately determine LV dysfunction as well as the severity. Moreover, a combination of these parameters undoubtedly increases the work burden and is not conducive to clinical application.
Despite having a “preserved” EF, HFpEF also presents abnormity in LV systolic performance [12, 13]. Multiple studies have demonstrated that patients with HFpEF present subtle impairments in systolic function at rest, and this alternation tends to expand during exertion, which impairs LV suction, decreases cardiac output, and elevates LV filling pressures [14, 15]. LV systolic dysfunction in HFpEF also predict increased risk of adverse outcomes [16, 17]. Some scholars question the ability of EF to truly reflect the LV systolic function of HFpEF[18]. HFpEF patients are often complicated with myocardial concentric hypertrophy, which inevitably generates a normal or supernormal EF, even when stroke volume is declined. Therefore, a non-invasive method which can quantify LV pump function better than EF and would be a major step forward.
Cardiac power is a comprehensive quantitative indicator and can evaluate cardiac function via noninvasive echocardiography[4, 5, 19]. It is better than variables such as cardiac output because it covers both pressure load and volume load[20]. Since the power depends on the volume of the muscle that produces the power, standardizing cardiac power with LV mass can better evaluate the applicability of this indicator in different populations[4, 6, 19], and also facilitate the comparison between individuals. In addition, cardiac power may be more promising than EF. It has been reported to be the strongest predictor of in-hospital mortality in patients with cardiac shock because of acute myocardial infarction [20], and presently have been used to evaluate the response of patients with advanced HF to mechanical circulatory support system [21].
In the present study, we found that the HFpEF patients with lower rest cardiac power/mass were more likely to be older and had higher NYHA class and NT-proBNP level, as well as more comorbidities, indicating that the patients in this subgroup might have a worse baseline condition and more risk factors of adverse outcomes. After adjustment of multiple covariates, such as age and comorbidity, our study brought new evidence that rest cardiac power/mass were independently associated with all-cause death and HF hospitalization in patients with HFpEF. Meanwhile, rest cardiac power/mass significantly promoted the prediction efficiency of both traditional risk factors and NT-proBNP, supporting a pathophysiological link between the reduced cardiac performance and the mortality and HF progression later on in life as aging and comorbidities advance. Furthermore, we performed sensitivity analysis, and the results showed that although not all subgroups showed a statistically significant association, the risk of adverse outcome within these subgroups was higher in patients with lower rest cardiac power/mass than in those with higher rest cardiac power/mass, indicating the stable and independent prediction efficacy of rest cardiac power/mass among HFpEF patients. Clinically, rest cardiac power/mass is easily obtained by measuring blood pressure and stroke volume. And the latter can be measured by Doppler echocardiography. What is more excitingly is that the technical setup of cardiac power is very similar to what is used in a standard diastolic stress test, so whether the integrated application of the two tests provides incremental diagnostic or prognostic significance in HFpEF patients deserves further exploration.
Our study has some limitations: (1) this study is a retrospective study design; (2) compared to invasive measurements, the non-invasive measurements of stroke volume may be inclined to errors; and (3) the prognostic value of peak or reserved cardiac power indexed to LV mass is not evaluated in patients with HFpEF.