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Physiologic and pathologic myocardial hypertrophy--physiologic and pathologic regression of hypertrophy?
1Department of Pathophysiology, Faculty of Medicine, Bratislava, Slovak Republic. simko@fmed.uniba.sk
Insights
Left ventricular hypertrophy (LVH) can improve heart function but also lead to negative outcomes. Achieving LVH regression is a therapeutic goal, though its complete normalization remains complex.
Area of Science:
- Cardiology
- Physiology
- Pathology
Background:
- Left ventricular hypertrophy (LVH) presents a dual biological value, enhancing cardiac performance while potentially leading to adverse effects.
- Pathologic LVH is associated with fibrosis, reduced coronary flow reserve, and protein remodeling, increasing cardiovascular morbidity and mortality.
Purpose of the Study:
- To explore the complexities of left ventricular hypertrophy (LVH) regression.
- To investigate the implications of different therapeutic approaches for managing hemodynamic overload and LVH.
Main Methods:
- Review of existing literature on the mechanisms and outcomes of LVH regression.
- Analysis of the differences between physiologic and pathologic LVH and their responses to treatment.
Main Results:
- LVH regression is a complex process influenced by both hemodynamic and non-hemodominant factors.
- Complete normalization of myocardial structure and function post-regression is not guaranteed.
- Physiologic growth may induce LVH without adverse prognostic alterations, unlike pathologic forms.
Conclusions:
- LVH regression is a key therapeutic target, but its success is multifaceted.
- The optimal treatment strategy for hemodynamic overload and LVH requires careful consideration of variable regression patterns and biological implications.
Abstract:
Hypertrophy of the left ventricle is an adaptive phenomenon of ambiguous biological value. It enables improvement of the heart performance without substantial enhancement of energetic demands. On the other hand, pathologic left ventricular hypertrophy (LVH) is characterized by increased fibrosis, diminished coronary flow reserve and protein remodeling, resulting in increased cardiovascular morbidity and mortality. Achievement of LVH regression is thus considered a principal therapeutic aim. However, the reversal of LVH is a very complex process in which both hemodynamic and non-hemodynamic alterations participate. Reversal of LVH does not mean the re-expression of the original genotype and normalization of myocardial structure and function. It does not guarantee that the heart will be normal in all aspects. Regression of hypertrophy induced by different therapeutic means may exhibit different properties and patterns, with variable biological implications. Physiologic growth stimulators seem to induce LVH without prognostically undesirable alterations. It is a challenge to determine which approach to treatment of hemodynamic overload and concomitant LVH is optimal.