Clinical Heart Failure
Left ventricular cardiac mechanics associated with symptomatic heart failure are complex and often counterintuitive. Several investigators have shown that impaired longitudinal strain is a frequent finding in symptomatic HFpEF patients (Figure 2) and predictive of poor outcomes13,14. Although a deterioration in longitudinal mechanics is common, global circumferential strain (GCS), LV twist, and twist/untwist rates may remain normal or even increase to supranormal values6 early in the disease course (Figure 1). This allows for preservation of the ejection fraction via compensatory contributions from the subepicardial layer to circumferential and LV twist deformation. If subepicardial dysfunction is present and compensation is not possible, ejection fraction falls15. Circumferential and twist deformation may remain normal or increased early in the disease course. However, time to peak twist and untwist are often prolonged and signals subtle impairments of systolic and diastolic function16. Advanced HFpEF is characterized by a progressive deterioration of twist/untwist mechanics, as well as circumferential, radial, and longitudinal deformation17,18.
Resting deformation can be used to predict invasive hemodynamics. In HFpEF patients, the ratio of mitral E to global longitudinal strain rate in isovolumic relaxation can predict left ventricular filling pressure19. Furthermore, the ratio of resting global circumferential strain to global longitudinal strain can serve as potential predictor of a pathologic rise in pulmonary capillary wedge pressure during exercise 20.
Exercise imaging for diastolic function and cardiac mechanical assessment can aid tremendously in the initial HFpEF diagnostic work-up. Recent guidelines recommend functional exercise echocardiographic stress testing in patients at intermediate likelihood of HFpEF following an initial morphofunctional assessment21. Despite impaired resting longitudinal deformation, those with preclinical disease can augment longitudinal mechanics during exertion to a greater extent than those who have progressed to symptomatic heart failure. This in part explains the initial onset of exertional symptoms alone in patients transitioning from preclinical disease into frank clinical heart failure 22. Furthermore, impaired GLS during exercise has been independently associated with an increased occurrence of all-cause mortality and HF hospitalizations23.