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.