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Assessment of the systolic function and contractility of the hypertensive left ventricle
Insights
Hypertension causes cardiac hypertrophy, which can be concentric or eccentric. Different types of left ventricular hypertrophy show distinct contractile properties, impacting heart function under stress.
Area of Science:
- Cardiovascular Physiology
- Cardiac Remodeling
- Hypertension Research
Background:
- Sustained hypertension induces cardiac hypertrophy, a complex adaptation.
- Cardiac hypertrophy can manifest as concentric or eccentric remodeling.
- Left ventricular (LV) systolic function may vary with hypertrophy type and afterload.
Purpose of the Study:
- To investigate differences in contractile properties between concentric and eccentric LV hypertrophy.
- To assess cardiac function during baseline and acute hemodynamic overload.
- To clarify the role of contractile properties in altered systolic function in hypertensive heart disease.
Main Methods:
- Evaluated LV fiber shortening velocity and fractional shortening.
- Compared normotensive subjects with concentric and eccentric LV hypertrophy groups.
- Utilized a cold pressor test (CPT) for acute hemodynamic overload.
- Analyzed the end-systolic stress-end-systolic volume relation (force-length line slope).
Main Results:
- Group 1 (normal LV) showed normal function.
- Group 2 (concentric hypertrophy) exhibited enhanced function at baseline and during CPT.
- Group 3 (eccentric hypertrophy) displayed depressed function, worsening with CPT.
- The force-length relationship slope was steeper in concentric and less steep in eccentric hypertrophy.
Conclusions:
- Concentric and eccentric LV hypertrophy possess distinct contractile properties.
- These differences influence cardiac function under normal and stressed conditions.
- Further research is needed to determine if these represent distinct disorders or stages of disease.
Abstract:
Sustained hypertension is a stimulus for development of cardiac hypertrophy, which may be either concentric or eccentric. For a given rise of aortic pressure, left ventricle (LV) wall stress (afterload) may remain normal or reduced in the former and become enhanced in the latter condition, and the LV systolic function may vary in a direction opposite to that of wall stress. It is unknown whether there are also differences in contractile properties that may have a role in the shift from normal systolic function. To clarify this we evaluated the velocity of LV fiber shortening and the fractional fiber shortening in normotensive and hypertensive subjects with normal heart size (group 1), or concentric LV (group 2) or eccentric LV (group 3) hypertrophy during baseline and after an acute hemodynamic overload induced by a cold pressor test (CPT). We found that the functional pattern in the two conditions was similar to normal in group 1, significantly enhanced during baseline and CPT in group 2, and was depressed during baseline and more so during CPT in group 3. These findings suggest that the contractile properties of the two types of hypertrophy are different, supported by the slope of the force-length line defined by the end systolic stress-end systolic volume relation in the baseline and during the hemodynamic overload imposed by the CPT. This line was steeper than normal in group 2 and less steep than normal in group 3. It remains to be defined whether the two types of hypertrophy are a separate disorder or represent a different stage of the same disease.