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The heart in hypertension
1Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
Insights
Hypertension causes unique heart changes, influenced by both hemodynamic and non-hemodynamic factors. Reversing left ventricular hypertrophy (LVH) may not eliminate associated cardiovascular risks.
Area of Science:
- Cardiology
- Hypertension Research
- Cardiovascular Physiology
Background:
- Cardiac changes in hypertension differ from other afterload-associated diseases due to distinct etiologies and mechanisms.
- Hemodynamic alterations play a key role in adaptive cardiac changes, but non-hemodynamic factors are increasingly recognized.
- Non-hemodynamic factors include demographics (age, race, gender), comorbidities, growth factors, and therapeutic history.
Purpose of the Study:
- To explore the complex functional and structural cardiac alterations in hypertension.
- To investigate the roles of both hemodynamic and non-hemodynamic factors in hypertensive heart disease.
- To examine the implications of left ventricular hypertrophy (LVH) reversal on cardiovascular risk.
Main Methods:
- Review of recent scientific knowledge on cardiac changes in hypertension.
- Analysis of hemodynamic and non-hemodynamic influences on cardiac adaptation.
- Evaluation of the relationship between LVH, its reversal, and cardiovascular outcomes.
Main Results:
- Hypertension-induced cardiac remodeling is multifactorial, involving hemodynamic and non-hemodynamic elements.
- Adaptive cardiac changes, while preventing failure, independently increase cardiovascular morbidity and mortality risk.
- The impact of reversing LVH on this independent risk remains uncertain and requires further investigation.
Conclusions:
- Cardiac remodeling in hypertension is complex and influenced by diverse factors beyond hemodynamics.
- The independent cardiovascular risk conferred by the hypertensive heart warrants further study, especially concerning LVH reversal.
- Reversal of LVH does not guarantee elimination of associated risks; underlying mechanisms require elucidation.
Abstract:
Knowledge concerning the functional and structural changes of the heart in hypertension has increased remarkably over the past three decades. These changes may not at all be the same as with other diseases associated with increased afterload since the etiology, pathophysiological mechanisms, and other associated diseases are very different. Hemodynamic alterations associated with hypertension have a major role in the adaptive cardiac changes; but recent knowledge indicates that they are not exclusive. Nonhemodynamic factors are also very important; they not only include the now-accepted demographic considerations of age, race, gender and associated diseases but also consider newly discovered growth factors as well as prior and present therapy. The heart that provides a physiological adaptation to the increasing overload produced by disease in order to stem the tide from eventual cardiac failure also confers an independent risk of premature cardiovascular morbidity and mortality. It is too early to infer that reversal of the LVH reverses this risk. But, even if this does occur, mechanisms other than only LVH reversal must be considered. Therefore, at this time, the implications and consequences of reversed LVH has yet to be demonstrated.