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Echocardiographic comparison of left ventricular structure and function in hypertensive patients with primary
Ronen Goldkorn1, Alexei Yurenev, Jon Blumenfeld
1Division of Cardiology, New York Presbyterian Hospital-Weill Cornell Medical Center, New York 10021, USA.
Insights
Excess aldosterone in primary aldosteronism does not significantly alter left ventricular (LV) structure or systolic function in hypertensive patients compared to essential hypertension. This suggests aldosterone may not independently impact LV remodeling in human hypertension.
Area of Science:
- Cardiology
- Hypertension Research
- Endocrinology
Background:
- Aldosterone's role in myocardial remodeling and fibrosis is known in experimental renovascular hypertension.
- Its specific effects on left ventricular (LV) structure and function in hypertensive patients remain unclear.
Purpose of the Study:
- To investigate whether excess aldosterone in primary aldosteronism affects LV geometry and systolic function in hypertensive patients.
- To compare LV structure and function between patients with primary aldosteronism and essential hypertension matched for key clinical parameters.
Main Methods:
- A comparative study of 35 patients with primary aldosteronism and 35 controls with essential hypertension.
- Assessment of LV mass, endocardial and midwall fractional shortening, and afterload-corrected midwall shortening (observed/predicted midwall shortening ratio).
- Statistical analysis included logistic regression adjusting for covariates like blood pressure, BMI, and gender.
Main Results:
- Patients with primary aldosteronism and essential hypertension exhibited similar LV dimensions, wall thickness, and mass.
- No significant differences were found in endocardial or midwall fractional shortening, or afterload-corrected midwall shortening between the groups.
- Logistic regression analysis did not reveal statistical differences in LV geometry or systolic function based on aldosterone status.
Conclusions:
- Patients with primary aldosteronism show comparable LV geometry and systolic function to essential hypertension patients when matched for age, gender, and blood pressure.
- These findings challenge the notion of a significant independent association between aldosterone and LV remodeling or function in human hypertension.
Background:
In experimental renovascular hypertension, aldosterone has been implicated in myocardial remodeling and fibrosis, but it is uncertain whether excess aldosterone effects left ventricular structure and function in hypertensive patients.
Methods:
Hypertensive patients from the Cardiovascular Center of the New York Presbyterian Hospital-Weill Cornell Medical Center in New York and the Russian Cardiovascular Research Institute, Moscow, Russia, were studied. The sample included 35 patients with primary aldosteronism and 35 controls with essential hypertension matched for age, gender, and blood pressure (BP). Left ventricular (LV) mass, endocardial and midwall fractional shortening, and circumferential end-systolic stress were calculated. The observed/predicted midwall shortening ratio was used as an index of LV performance corrected for afterload.
Results:
Primary aldosteronism and essential hypertension patients had comparable LV dimensions, wall thickness, mass, mass/body surface area, and mass/height. Endocardial and midwall fractional shortening, and afterload-corrected midwall shortening were similar in primary aldosteronism and essential hypertension groups from both clinics. Moreover, logistic regression analysis using BP, body mass index, height, gender, and center as covariates failed to identify statistical differences in LV geometry or systolic function between primary aldosteronism and essential hypertension patients.
Conclusions:
Patients with primary aldosteronism, a state characterized by chronic aldosterone excess, had similar LV geometry and systolic function compared to essential hypertension patients matched for age, gender, and BP. This argues against important independent associations between aldosterone and these aspects of LV response to human hypertension.