Left Ventricular Hypertrophy Is More Prominent in Patients with Primary Aldosteronism than in Patients with Other Types of Secondary Hypertension.

Tanabe, Akiyo; Naruse, Mitsuhide; Naruse, Kiyoko; Hase, Mitsuyasu; Yoshimoto, Takanobu; Tanaka, Masami; Seki, Toshiro; Demura, Reiko; Demura, Hiroshi

doi:10.1291/hypres.20.85

Cited by 143 publications

(84 citation statements)

References 23 publications

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“…We have reported that prevalence and severity of LV hypertrophy is larger in patients with primary aldosteronism than in Cushing's syndrome and pheochromocytoma with similar blood pressure levels. 27 These studies suggest that aldosterone may play an important role in the development of target organ damage in hypertension. To elucidate the pathophysiological significance of aldosterone breakthrough during long-term administration of AT1A, effects of coadministration of low-dose SPRL with AT1A were investigated.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Breakthrough During Angiotensin II Receptor Antagonist Therapy in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2002

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Abstract-Aldosterone breakthrough during ACE inhibitor therapy has been reported. This study investigates changes in plasma aldosterone concentration (PAC) and its mechanism and effects on target organ damage during long-term angiotensin II type 1 (AT1) receptor antagonist (AT1A) therapy in hypertensive rats. An AT1A (candesartan, 1 mg/kg per day PO) was administered in stroke-prone spontaneously hypertensive rats from 4 weeks of age for 34 weeks. PAC was significantly decreased during the first 4 weeks but showed aldosterone breakthrough after 8 weeks of AT1A administration. Plasma angiotensin II concentration was significantly elevated, whereas no change was seen in plasma ACTH or serum potassium. The mechanism(s) of aldosterone breakthrough were investigated by giving high doses of candesartan (3 mg/kg per day PO), dexamethasone (200 g/kg per day IP), or the AT2 antagonist (PD123319, 10 mg/kg per day SC) during the last week of the 24-week AT1A treatment period. Dexamethasone and AT2 antagonist but not high-dose AT1A produced a significant decrease in PAC, with a larger decrease produced by the AT2 antagonist. To clarify the effects of the residual aldosterone, effects of coadministration of low-dose spironolactone (10 mg/kg per day SC), an aldosterone antagonist, on left ventricular hypertrophy and expression of brain natriuretic peptide mRNA were determined. Low-dose spironolactone further improved left ventricular hypertrophy and brain natriuretic peptide mRNA expression despite no additional depressor effect. These results suggest that aldosterone breakthrough occurs during long-term AT1A therapy, mainly by an AT2-dependent mechanism. Residual aldosterone may attenuate the cardioprotective effects of AT1A.

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Section: Discussionmentioning

confidence: 99%

Aldosterone Breakthrough During Angiotensin II Receptor Antagonist Therapy in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2002

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“…Mineralocorticoid excess, such as occurs with primary hyperaldosteronism (PA), is a low renin state in which cardiac hypertrophy is a prominent finding. 32 When matched for several factors (blood pressure, duration of hypertension, age, gender, BMI, race), subjects with PA have Dietary sodium RAAS and LVH JS Williams et al more cardiac hypertrophy developing at an earlier age than subjects with essential hypertension. 33 Although primary hyperaldosteronism was excluded in this cohort, it is possible that subjects with lower renin hypertension, as defined in this study, are part of a continuum of mineralocorticoid excess relative to the level of sodium intake.…”

Section: Discussionmentioning

confidence: 99%

Influence of dietary sodium on the renin–angiotensin–aldosterone system and prevalence of left ventricular hypertrophy by EKG criteria

Williams

Jeunemaı̂tre

et al. 2004

J Hum Hypertens

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We investigated the interplay of dietary sodium and renin-angiotensin-aldosterone system (RAAS) activity with the prevalence of left ventricular hypertrophy (LVH) in essential hypertension. Electrocardiograms (EKG) were reviewed for the presence of LVH in 160 hypertensive patients. We then compared the rate of LVH to levels of plasma renin activity (PRA) and serum aldosterone under high and low sodium diet conditions. On high sodium diet, serum aldosterone was significantly higher (7.770.93 vs 5.770.35 ng/dl, P ¼ 0.02) in participants with LVH. With low sodium diet and upright posture, PRA was significantly lower in subjects with LVH vs those without (5.671.1 vs 7.670.56 ng/ml/h, P ¼ 0.026). Aldosterone levels on low sodium diet were not different between those with and those without LVH. PRA was then dichotomized at the lowest quartile under low sodium/upright posture conditions to define a 'low renin' group. In a multivariate logistic regression containing renin status (low renin vs normal/high renin), aldosterone on a high sodium diet, age, body mass index, gender, race, duration of hypertension, systolic and diastolic blood pressure and salt-sensitivity only low-renin status on a low sodium diet (P ¼ 0.019) and serum aldosterone on a high sodium diet (P ¼ 0.04) were significant predictors of LVH. Thus, reduced modulation of renin activity in response to sodium restriction and an increased aldosterone on a high sodium diet appear to identify characteristics of hypertensive patients predisposed to abnormal cardiac remodelling.

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“…[1][2][3][4][5] Growing lines of evidence have consistently supported the view that secondary hypertension due to primary aldosteronism is much more frequent (8-20%) than previously suspected . [6][7][8][9][10] It is important to diagnose primary aldosteronism during the early stage before the progression to end-organ damage because primary aldosteronism due to unilateral adrenal lesion, mostly aldosterone producing adenoma, can be cured by surgery.…”

Section: Introductionmentioning

confidence: 93%

Primary hyperaldosteronism- a resistant endocrine hypertension- A case report

et al. 2009

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A thirty years old lady presented with uncontrolled hypertension and dizziness during working for last 5 years. She had history of termination of pregnancy due to treatment-resistant hypertension. Even in the post-partum period her blood pressure remains uncontrolled with more than three antihypertensive drugs. Her serum K + level was low and USG of KUB & adrenal glands showed slightly increased right renal cortical echotexture; CT scan of abdomen revealed right Adrenal adenoma. She underwent unilateral adrenalectomy. Now, she has no complaints and her blood pressure is normal without any antihypertensive drugs. There is no target organ damage.

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Left Ventricular Hypertrophy Is More Prominent in Patients with Primary Aldosteronism than in Patients with Other Types of Secondary Hypertension.

Cited by 143 publications

References 23 publications

Aldosterone Breakthrough During Angiotensin II Receptor Antagonist Therapy in Stroke-Prone Spontaneously Hypertensive Rats

Aldosterone Breakthrough During Angiotensin II Receptor Antagonist Therapy in Stroke-Prone Spontaneously Hypertensive Rats

Influence of dietary sodium on the renin–angiotensin–aldosterone system and prevalence of left ventricular hypertrophy by EKG criteria

Primary hyperaldosteronism- a resistant endocrine hypertension- A case report

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