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[Hypertrophy and function of the left heart ventricle in hypertension]
1Klinika Kardiologii Akademii Medycznej, Krakowie.
Insights
Left ventricular hypertrophy (LVH) affects over half of hypertension patients and increases mortality. Targeting specific systems can prevent or reverse LVH, improving cardiac function and outcomes.
Area of Science:
- Cardiology
- Hypertension Research
- Medical Science
Background:
- Left ventricular hypertrophy (LVH) is prevalent in over 50% of patients with arterial hypertension.
- Echocardiography has improved the detection of LVH, a condition linked to increased mortality, arrhythmias, and heart failure.
- LVH development involves hemodynamic factors (e.g., elevated blood pressure) and non-hemodynamic factors (e.g., genetic, paracrine, and autocrine cardiac functions).
Purpose of the Study:
- To explore the mechanisms underlying left ventricular hypertrophy in arterial hypertension.
- To investigate the role of hemodynamic and non-hemodynamic factors in LVH development.
- To evaluate the impact of blocking specific systems on LVH and cardiac function.
Main Methods:
- Review of diagnostic studies utilizing electrocardiography and echocardiography.
- Analysis of hemodynamic factors including blood pressure, ejection fraction, cardiac output, and blood viscosity.
- Examination of non-hemodynamic factors such as genetic contributions and local cardiac systems (catecholamines, renin-angiotensin system).
Main Results:
- Blockade of catecholamine and renin-angiotensin systems demonstrated potential for preventing or regressing cardiac hypertrophy in experimental and human studies.
- Regression of LVH correlated with improved systolic and diastolic cardiac function, with diastolic dysfunction often preceding hypertrophy.
- Hypotensive drug efficacy is evaluated based on their ability to improve cardiac function and prevent LVH consequences.
Conclusions:
- Targeting specific neurohormonal systems offers a promising strategy for managing and reversing left ventricular hypertrophy in hypertensive patients.
- Improved cardiac function, particularly diastolic function, is a key outcome of LVH regression.
- Pharmacological treatments for hypertension should consider their impact on LVH and cardiac function, potentially altering treatment guidelines.
Abstract:
Left ventricular hypertrophy in arterial hypertension occurs in over 50% of patients. The detection of such high incidence has been facilitated by the introduction of echocardiography into diagnostic studies. Both earlier electrocardiographic findings and later echocardiographic results show that cardiac hypertrophy leads to an increased mortality and predisposes to cardiac arrhythmias, ischemic heart disease including myocardial infarction and heart failure. The development of hypertrophy is mediated by hemodynamic factors such as elevated blood pressure due to increased peripheral vascular resistance, ejection fraction, increased cardiac output, blood viscosity, as well as by non-hemodynamic factors. Of the latter ones the contribution of a genetic factor is discussed, whereas the role of para- and autocrine cardiac function manifested by local production and action of catecholamines as well as the renin-angiotensin system has been proved. Blockade of these systems makes possible prevention of the development of cardiac hypertrophy or its regression. Such results have been obtained both in experimental studies and in humans with hypertension treated with selected drugs. Regression of hypertrophy is accompanied by an improvement in systolic and especially diastolic cardiac function, the impairment of which is usually diagnosed prior to the detection of hypertrophy. The improvement in cardiac function and possibility of preventing consequences of hypertrophy help us to evaluate the efficacy of hypotensive drugs and their preferential use in this regard. There are also changes in recently recommended models of pharmacological treatment in arterial hypertension.