A complete assessment of hemodynamic load, including pulsatile components, is necessary to understand the transition from compensated hypertrophy to heart failure in hypertensive models.
Answers are grounded in this paper and cite their sources.
Incomplete hemodynamic assessment may mislead HF transition studies in hypertension; hypothesis-generating for comprehensive measures in translational research.
During the first three-quarters of their life, increased left ventricular mass in the SHR is accompanied by enhanced ventricular function, manifest by he heart adapts to the increased stress of hypertension through the process of concentric left ventricular remodeling. 1 Thickening of the left ventricular wall, which is achieved by normal stroke volume and cardiac indexes in the sethypertrophy of existing myocytes, serves to normalize ting of a markedly increased mean arterial pressure.wall stress, or the force per unit cross-sectional area.Contractility, assessed by the ejection fraction index -This adaptation develops in parallel with increasing afterload relation, is normal. 7Furthermore, pressureblood pressure in young spontaneously hypertensive generating capacity, assessed by the peak developed rats and results in a long period of stable ventricular pressure ( Left ventricular systolic 0 End-diastolic function despite the increased blood pressure.This pressures ) during a brief aortic occlusion, is enhanced stable phase is followed by a transitional period in proportion to the increased left ventricular mass. 5wherein progressive increases in left and ultimately, Left ventricular mass is increased in the setting of a right ventricular mass occur in the setting of diminishnormal left ventricular volume in a pattern that is ing ventricular function and arterial pressure ( Figure consistent with classic pressure overload or concentric 1 ) , making the stimulus to ongoing hypertrophy unleft ventricular hypertrophy.The result in an adaptive clear. 2 Furthermore, antihypertensive treatment that increase in the left ventricular mass-to-volume ratio, effectively normalizes mean arterial pressure during which explains the ability of the ventricular to dethis phase has a variable effect on left ventricular velop a higher isovolumic pressure.mass, depending on the class of pharmacologic agent Because cardiac index is maintained during the staused, raising the possibility of a dissociation between ble phase of hypertension in the SHR, the increased hemodynamic load and left ventricular mass during mean arterial pressure is accompanied by elevation the transition to failure in the spontaneously hyperof the total peripheral resistance index, a measure of tensive rat ( SHR ) .Recent studies presented in this steady flow load on the left ventricle.This increased review demonstrate that failure to fully measure hesteady flow load is accompanied by considerable abmodynamic load may account for some of the discrepnormalities of pulsatile load at 12 months of age in ancies between hemodynamics and left ventricular SHR. 8 Pulse wave velocity and characteristic impedmass in this phase and underscore the importance ance are both higher in SHR than in age-matched norof a sustained workload on the transition to severe motensive Wistar rats ( NWR ) during this compenhypertrophy and left ventricular dysfunction.sated phase, indicating an increase in conduit vessel THE STABLE PHASE: COMPENSATORY stiffness in the SHR ( Table 1 ) .Because the heart is an CONCENTRIC LEFT VENTRICULAR intermittent or pulsatile pump, a complete assessment HYPERTROPHY of hemodynamic load must consider both the pulsatile and steady flow components of load.The pulsatile Previously, we evaluated ventricular function and component can contribute considerably to total load mass throughout the 20-to 24-month lifespan of in pathologic conditions such as hypertension.
No takes yet. Share an insight, caveat, or question.
G. H. Mitchell (1997) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: