Key result
Developmental pressure-overload induced left ventricular thickening in giraffes emerges as an evolved adaptation that may offer a roadmap for identifying therapeutic strategies for HFpEF.
Why the study?
The proximate mechanisms underlying the unique cardiovascular physiology of giraffes, which exhibit left ventricular thickening without impaired diastolic relaxation or exercise capacity, are not yet characterized.
The unique cardiovascular adaptations of the giraffe may serve as a natural model to study resistance to HFpEF and identify novel therapeutic strategies.
Giraffe myocardial adaptations may model HFpEF resistance; leaves open translation to human pressure-overload therapies.
Heart failure with preserved ejection fraction (HFpEF) is a leading form of human cardiovascular disease and commonly associated with systemic hypertension. Unique evolved adaptations in giraffe myocardia may be a natural animal model of resistance to HFpEF. In humans, pressure-overload induced left ventricular thickening (PLVT) impairs diastolic relaxation, elevates left atrial pressures and may progress to heart failure with symptoms including exercise intolerance. In healthy giraffe, the left ventricle thickens as developmental neck lengthening widens the vertical distance between the heart and head increasing pressures needed to maintain constant brain perfusion. Yet, diastolic relaxation and exercise capacity are unimpaired, a critical adaptation for prey species such as giraffe. The proximate mechanisms underlying this unique cardiovascular physiology are not yet characterized. Developmental PLVT in giraffe emerges as a species-specific evolved adaptation which offers a roadmap for identifying innovations in therapeutic and prevention strategies for HFpEF.
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Natterson-Horowitz et al. (2020) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Giraffe as a natural animal model vs. Humans was evaluated. Developmental pressure-overload induced left ventricular thickening in giraffes emerges as an evolved adaptation that may offer a roadmap for identifying therapeutic strategies for HFpEF.
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