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Left ventricular wall stress and systolic function in untreated primary hypertension
Insights
Hypertension increases left ventricular (LV) wall stress despite thicker heart walls. However, LV systolic function remains normal or enhanced in hypertensive men, suggesting increased myocardial contractility.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Hypertension Research
Background:
- Elevated blood pressure (BP) is a major risk factor for cardiovascular disease.
- Left ventricular (LV) remodeling is a key adaptation to chronic hypertension.
- Understanding the impact of hypertension on LV mechanics and function is crucial for risk stratification.
Purpose of the Study:
- To investigate left ventricular (LV) wall stress, wall thickness, and systolic function in normotensive and hypertensive men.
- To determine if increased LV wall thickness adequately compensates for elevated blood pressure to maintain normal LV wall stress.
- To assess the relationship between LV wall stress and LV systolic function across different blood pressure categories.
Main Methods:
- Noninvasive investigation of untreated men aged 49 years.
- Categorization into four blood pressure groups: normotensive, borderline, mild, and moderate hypertension.
- Assessment of left ventricular (LV) wall stress, wall thickness, and systolic function.
Main Results:
- LV wall thickness increased with hypertension but did not sufficiently normalize LV wall stress.
- End-systolic wall stress remained elevated in hypertensive groups, even with pronounced wall thickening.
- LV systolic function was normal or supranormal in hypertensive men, correlating inversely with end-systolic wall stress.
- Hypertensive groups exhibited higher than expected LV ejection phase indices compared to normotensive controls.
Conclusions:
- Hypertension leads to increased LV wall stress that is not fully compensated by LV hypertrophy.
- Despite elevated wall stress, hypertensive men maintain normal or enhanced LV systolic function.
- Increased myocardial contractility, possibly due to adrenergic stimulation or cellular adaptations, underlies preserved LV function in hypertension.
Abstract:
A noninvasive investigation was undertaken in four blood pressure (BP) groups of untreated 49-year-old men derived by screening a random population sample: normotensive men (n = 20) and subjects with borderline (n = 30), mild (n = 45), or moderate BP elevation (n = 24). We here report the findings regarding left ventricular (LV) wall stress, LV wall thickness, and LV systolic function. Although there was an increase in LV wall thickness with hypertension, the raised BP was not compensated for by a sufficient degree of LV wall thickening to keep wall stress within normal limits in the hypertensive groups. Among a subset of individuals with pronounced increase in wall thickness peak systolic wall stress approached the normal range, but end-systolic wall stress was still high. In spite of high wall stress LV systolic function was normal or supranormal in the hypertensive men. The LV ejection phase indices showed a close inverse correlation with end-systolic wall stress (r = -0.67 to -0.84) in all four BP groups, but no correlation or only a weak correlation with peak systolic wall stress (r = 0.18 to -0.40). As judged from the relationship between end-systolic wall stress and ejection phase indices of LV function in the normotensive controls, all hypertensive groups had higher than expected values for LV ejection phase indices, which indicates an increased myocardial contractility secondary to adrenergic stimulation or to a more efficient contractile machinery in the myocardial cells.