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Hemodynamic hypertrophied left ventricular patterns in systemic hypertension
G de Simone1, L Di Lorenzo, D Moccia
1Cardiology Unit, Second Medical School, University of Naples, Italy.
Insights
Systemic hypertension leads to left ventricular (LV) hypertrophy, with eccentric hypertrophy being more common. LV contractile capacity may rely on increased muscle mass rather than enhanced inotropic state in hypertensive patients.
Area of Science:
- Cardiology
- Physiology
- Hypertension Research
Background:
- Systemic hypertension frequently causes left ventricular (LV) hypertrophy.
- Understanding the hemodynamic adaptations in hypertrophied LV is crucial for managing hypertensive heart disease.
Purpose of the Study:
- To investigate the hemodynamic patterns of the hypertrophied left ventricle in untreated systemic hypertension.
- To differentiate between concentric and eccentric LV hypertrophy adaptations to pressure overload.
Main Methods:
- M-mode echocardiography was used to assess 42 untreated hypertensive patients and 45 normotensive controls.
- Key hemodynamic parameters including cardiac dimensions, wall thickness, and contractility indices were measured.
Main Results:
- Hypertensive patients exhibited increased cardiac dimensions, wall thickness, and cardiac output compared to controls.
- Eccentric hypertrophy (74%) was associated with increased dimensions and LV contractility, while concentric hypertrophy (26%) showed normal dimensions but higher contractility.
- Normalized stress/volume and systolic pressure/dimension ratios indicated preserved LV contractile function.
Conclusions:
- Left ventricular hypertrophy in hypertension presents with distinct patterns of eccentric and concentric remodeling.
- LV contractile capacity appears to be maintained by increased myocardial mass rather than an elevated inotropic state.
Abstract:
The hemodynamic pattern of hypertrophied left ventricle in systemic hypertension was studied by M-mode echocardiography in 42 untreated hypertensive patients with left ventricular (LV) mass index greater than 2 standard deviations from the sex-specific mean of 114 normal subjects (normal values of our laboratory), and in 45 normotensive volunteers. Hypertensive patients showed cardiac dimensions, relative diastolic wall thickness, ratio of systolic pressure to end-systolic dimension, cardiac index and stroke index greater than normotensive control subjects (0.01 less than p less than 0.0001). Pressure/dimension ratio was correlated to relative wall thickness (p less than 0.005). End-systolic stress/volume ratio was normal as was systolic pressure to dimension ratio normalized for end-diastolic wall thickness. LV hypertrophy was concentric in 26% and eccentric in 74% of patients and suggested 2 different heart adaptations to overload: eccentric hypertrophy was associated with increased cardiac dimensions, high peak stress, normal systolic function and moderately increased LV contractility; concentric hypertrophy was associated with the highest blood pressure values, normal cardiac dimension, normal peak stress, normal systolic function and much increased LV contractility. Because stress/volume ratio and wall thickness-corrected systolic pressure/dimension ratio were normal in hypertensive patients, LV contractile capacity might be supported by the increase in myocardium available for contraction, rather than by increase in inotropic state.