Plasma aldosterone and left ventricular diastolic function in treatment-naïve patients with hypertension:

Cristiana Catena1, Nicolas Verheyen2, Stefan Pilz2

  • 1From the Divisions of Cardiology (C.C., N.V.) and Endocrinology and Metabolism (S.P., A.T.), Department of Medicine, Medical University of Graz, Graz, Austria; Department of Internal Medicine and Cardiology, Charitè University Medicine, Campus Virchow Klinikum and German Heart Center, Berlin, Germany (E.K.-K., B.P.); and Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Sciences, University of Udine, Udine, Italy (L.A.S.). cristiana.catena@uniud.it.

Insights

In hypertensive patients, higher plasma aldosterone levels correlate with left ventricular hypertrophy. However, aldosterone does not independently affect left ventricular diastolic function, despite its known cardiac effects.

Area of Science:

  • Cardiology
  • Endocrinology
  • Hypertension Research

Background:

  • Aldosterone exerts hypertrophic and profibrotic effects on the heart.
  • The link between plasma aldosterone and left ventricular diastolic function in hypertension remains incompletely understood.
  • Comorbidities can influence left ventricular diastolic filling, necessitating study in uncomplicated hypertensive populations.

Purpose of the Study:

  • To investigate the association between plasma aldosterone levels and left ventricular diastolic function.
  • To examine this relationship in treatment-naïve patients with primary hypertension without confounding comorbidities.
  • To assess diastolic function using both conventional echocardiography and tissue-Doppler imaging.

Main Methods:

  • Study included 115 treatment-naïve hypertensive patients and 100 matched normotensive controls on a standard diet.
  • Measurements included plasma aldosterone and active renin levels.
  • Left ventricular diastolic function was assessed using conventional echocardiography and tissue-Doppler imaging; left ventricular mass index was calculated.

Main Results:

  • Left ventricular hypertrophy was present in 21% of hypertensive patients.
  • Diastolic dysfunction was identified in 20% by conventional echocardiography and 58% by tissue-Doppler imaging.
  • Patients with diastolic dysfunction exhibited higher age, male sex, BMI, blood pressure, alcohol intake, LV mass index, and relative wall thickness, but lower plasma aldosterone levels.

Conclusions:

  • Plasma aldosterone levels are associated with left ventricular hypertrophy in hypertensive individuals.
  • Aldosterone does not demonstrate an independent relationship with left ventricular diastolic properties in this cohort.
  • Tissue-Doppler imaging revealed a higher prevalence of diastolic dysfunction compared to conventional echocardiography.

Related Concept Videos

Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
2.7K
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
1.2K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.5K
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
1.5K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.9K
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
579