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Is left ventricular systolic dysfunction in hypertensive patients with heart failure normalized by long-term
1Second Department of Internal Medicine, Ehime University School of Medicine.
Insights
Hypertensive heart failure develops when left ventricular (LV) mass exceeds approximately 300g or an LV mass index of 180g/m2. Long-term antihypertensive therapy did not normalize LV dysfunction in these patients.
Area of Science:
- Cardiology
- Hypertension Research
- Heart Failure Studies
Background:
- Essential hypertension often leads to left ventricular (LV) hypertrophy.
- The threshold for developing hypertensive heart failure and the reversibility of LV dysfunction are not fully understood.
Purpose of the Study:
- To determine the critical left ventricular (LV) mass associated with hypertensive heart failure.
- To investigate if long-term antihypertensive therapy can normalize LV dysfunction in patients with heart failure due to hypertension.
Main Methods:
- Measured LV dimensions, mass, mass index, LV ejection time (LVET), and pre-ejection period (PEP) in normal subjects and essential hypertensives.
- Classified hypertensives into groups based on LV hypertrophy and heart failure status.
- Analyzed changes after long-term antihypertensive therapy (mean 16 months).
Main Results:
- Critical LV mass for heart failure onset was identified around 300g (LV mass index of 180g/m2).
- Significant LV ejection time shortening occurred only in the heart failure group.
- Prolonged pre-ejection period correlated with increased LV mass.
- LV dilatation and impaired contractility were not normalized by chronic antihypertensive therapy.
Conclusions:
- A left ventricular (LV) mass of approximately 300g or an LV mass index of 180g/m2 signifies the transition to hypertensive heart failure.
- Chronic antihypertensive therapy does not reverse LV dilatation or improve myocardial contractility in patients with a history of congestive heart failure due to hypertension.
Abstract:
The critical left ventricular (LV) mass when hypertensive heart failure appears, and whether LV dysfunction in hypertensives with heart failure is normalized by long-term antihypertensive therapy were investigated. LV dimension, LV mass, LV mass index, LV ejection time (LVET) and pre-ejection period (PEP) were measured in 27 normal subjects and 56 essential hypertensives, the latter divided into three groups: group I, without LV hypertrophy; group II, with LV hypertrophy; and group III, with hypertensive heart failure. LV mass and LV mass index were 135.0 +/- 23.8 g and 85.8 +/- 11.7 g/m2, respectively, in normal controls, 133.0 +/- 30.8 g and 82.0 +/- 18.4 g/m2 in group I, 222.3 +/- 38.0 g and 136.1 +/- 19.9 g/m2 in group II, and 422.0 +/- 30.3 g and 235.7 +/- 19.6 g/m2 in group III of essential hypertensives. The upper limits of LV mass and LV mass index in group II (mean + 2SD) were about 300 g and 180 g/m2, respectively. Significant shortening of LVET was observed only in group III, but PEP was prolonged with an increase in LV mass. LV diastolic dimension and PEP were not normalized by long-term antihypertensive therapy (mean: 16 months). These results indicate that the critical LV mass marking the transition from non-failing hypertrophied left ventricle to failing ventricle associated with essential hypertension is about 300 g, or LV mass index of 180 g/m2, and that LV dilatation and depressed myocardial contractility in essential hypertensives with a past history of congestive heart failure were not normalized by chronic antihypertensive therapy.