Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism

Suzuki, Toshihide; Abe, Hitoshi; Nagata, Seiki; Saitoh, Fumio; Iwata, Satoru; Ashizawa, Atsushi; Kuramochi, Morio; Omae, Teruo

doi:10.1016/0002-9149(88)90264-0

Cited by 46 publications

(20 citation statements)

References 25 publications

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“…17,18 Compared with BP-matched primary (essential) hypertensive patients, those with PA have an excess LVH and a LV mass inappropriately high for the degree of LV workload and BP elevation. [2][3][4]9,[19][20][21][22][23][24][25][26][27][28] Cardiac fibrosis with ensuing altered LV diastolic dysfunction can lead to left atrium dilatation and increased risk of atrial fibrillation (AF) 7,8,29 ; whether these changes regress with specific treatment for PA remains uncertain. 3,4,19,20,26 We, therefore, set out to prospectively investigate the long-term effects of correction of hyperaldosteronism on BP, LV mass, and cardiovascular events in a large cohort of patients with PA.…”

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confidence: 99%

Long-Term Control of Arterial Hypertension and Regression of Left Ventricular Hypertrophy With Treatment of Primary Aldosteronism

et al. 2013

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P rimary aldosteronism (PA) is a common curable cause of high blood pressure (BP).1 PA is of peculiar interest because the excess aldosterone secretion is held to be autonomous from angiotensin II, which allows elucidating the cardiovascular effects of excess aldosterone without the confounding effects of excess angiotensin II. Moreover, as the excess of aldosterone is cured with adrenalectomy in practically all patients, 2 causation between aldosterone excess and the cardiovascular changes could be inferred. However, whether surgery or pharmacological blockade of the mineralocorticoid receptor (MR) warrant cure of high BP and regression of cardiovascular damage, and of cardiac remodeling, at long term remains unclear because limited data exist. 3,4 The adaption of the left ventricle (LV) to the increased afterload of patients with high BP involves development of hypertrophy (LVH), which predicts cardiovascular events and death, 5 and when regressed improved prognosis. 6 In the complex interplay of hemodynamic, genetic, and endocrine-paracrine factors that underlie development of LVH aldosterone plays a pivotal role. [7][8][9] In the setting of a high sodium intake, this major effector of the system causes LVH, transcription of collagen type I and III genes, 10 and promotes fibroblasts proliferation, oxidative stress, and inflammation, 11 in part, by potentiating the effects of angiotensin II on AT-1 receptors.12-15 These actions, alongside the effects of the steroid on pre-and after-load, are held to cause inflammation and fibrosis, which contribute to worsening prognosis of patients with hyperaldosteronism, 8,16 and can explain the survival benefit conferred by MR antagonists to optimally treated patients with LV systolic dysfunction. 17,18 Compared with BP-matched primary (essential) hypertensive patients, those with PA have an excess LVH and a LV mass inappropriately high for the degree of LV workload and BP elevation. [2][3][4]9,[19][20][21][22][23][24][25][26][27][28] Cardiac fibrosis with ensuing altered LV diastolic dysfunction can lead to left atrium dilatation and increased risk of atrial fibrillation (AF) 7,8,29 ; whether these changes regress with specific treatment for PA remains uncertain. 3,4,19,20,26 We, therefore, set out to prospectively investigate the long-term effects of correction of hyperaldosteronism on BP, LV mass, and cardiovascular events in a large cohort of patients with PA.Abstract-Primary aldosteronism (PA), a common cause of high blood pressure (BP), induces left ventricular (LV) hypertrophy and an excess rate of cardiovascular events. Whether its treatment provides long-term cure of hypertension and regression of cardiovascular damage remains uncertain. To the aim of assessing the effect of treatment of PA on BP and LV changes, we prospectively recruited 323 patients in a long-term follow-up study entailing serial echocardiography evaluations. Of them, 180 had PA and were assigned to either adrenalectomy (n=110) or medical therapy (n=70)

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confidence: 99%

Long-Term Control of Arterial Hypertension and Regression of Left Ventricular Hypertrophy With Treatment of Primary Aldosteronism

et al. 2013

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“…35) In previous studies, aldosterone levels were found to be high in essential hypertension patients with concentric hypertrophy as well, yet higher values were found in patients with concentric remodeling of the left ventricle and eccentric hypertrophy. 28) In our study, both in patients with eccentric and concentric hypertrophy, plasma aldosterone levels were observed to be higher, however; this only reached the limit of statistical significance in patients with concentric hypertrophy.…”

Section: Discussionmentioning

confidence: 89%

“…Independent of the effects of the factors increasing blood pressure, aldosterone might play a role in cardiac hypertrophy. Although eccentric LVH is more commonly seen in primary aldosteronism which is characterized by volume loading, 35) etiology is multifactorial in cases of essential hypertension and the geometry of the left ventricle might change depending on the degree of neurohumoral activity. Thus, further controlled studies are required in order to support the independent relationship that we have identified between aldosterone and concentric hypertrophy of the left ventricle in our study.…”

Section: Discussionmentioning

confidence: 99%

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The Influence of Aldosterone on the Development of Left Ventricular Geometry and Hypertrophy in Patients With Essential Hypertension

et al. 2004

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SUMMARYThe identification of risk factors for the initiation of left ventricle hypertrophy (LVH), which is an independent risk factor for cardiovascular mortality and morbidity in hypertensive patients, is very important. The objective of the present study was to identify the relationship of aldosterone with LVH and different geometrical patterns of left ventricle that develop in patients with essential hypertension.A total of 83 patients with essential hypertension (44 females, mean age, 51 ± 8 years, 39 males, mean age, 57 ± 10 years) were included in this study. Thirty-two had LVH. When evaluated according to the geometrical patterns of LVH, 18 patients had concentric LVH, 14 had eccentric LVH, and 17 had concentric remodeling. Thirty-four patients had normal left ventricle geometry. Two weeks after the cessation of antihypertensive medications, sodium, potassium, and proteinuria in 24-hour urine samples and plasma aldosterone levels and plasma renin activity were measured. Plasma aldosterone levels of the patients with LVH were found to be significantly higher (9.92 ± 6.34 ng/dL versus 5.83 ± 3.5 ng/dL, P < 0.01). The difference between plasma renin activities was not statistically significant. Linear regression analysis revealed that plasma aldosterone level and age were independent parameters increasing left ventricle mass index. The plasma aldosterone levels of patients with concentric hypertrophy of the left ventricle were significantly higher than those of patients with normal geometry and concentric remodeling. There was no significant difference between plasma renin activities. Twenty-four hour urine protein concentrations of the patients with LVH were found to be significantly higher and sodium to be significantly lower.Plasma aldosterone levels seem to be correlated with LVH especially with concentric hypertrophy of the left ventricle in patients with essential hypertension. (Jpn Heart J 2004; 45: 807-821)

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“…But in most patients the septum is only slightly thicker than the left ventricular posterior wall (3-5). Regarding secondary hypertension (6)(7)(8), such as renovascular hypertension, pheochromocytoma and primary aldo steronism, asymmetrical septal hypertrophy is more unusual. The present 3 cases showed asymmetrical septal hypertrophy on the echocardiographic examinations.…”

Section: Discussionmentioning

confidence: 99%

Disproportionate Hypertrophy of the Interventricular Septum and its Regression in Cushing's Syndrome. Report of Three Cases.

Sugihara

Shimizu

et al. 1992

Intern. Med.

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Three patients of Cushing's syndrome with severe disproportionate hypertrophy of the interventricular septum are reported. All three underwent adrenalectomy and the diagnosis of Cushing's syndrome was confirmed by the presence of adrenal adenoma. All three showed hypertension before the adrenalectomy and two remained hypertensive following adrenalectomy. Before the operations the electrocardiograms revealed inverted T waves in broad leads, and mechanocardiogram systolic and diastolic dysfunction. After the adrenalectomies, abnormal findings on electrocardiograms were normalized and septal hypertrophy was completely regressed. It appears that not only high aortic pressure but also excessive plasma cortisol may be an etiologic factor of the left ventricular hypertrophy in Cushing's syndrome. (Internal Medicine 31: 407-413, 1992) Key words: gluococorticoid, hypertension, left ventricular hypertrophy, regression of hypertrophy, asymmetrical septal hypertrophy, hypertrophic cardiomyopathy Intr oductionCushing's syndrome is frequently associated with hypertension and left ventricular hypertrophy, and it can be complicated with congestive heart (1, 2). How ever there are no detailed reports of left ventricular hypertrophy and postoperative course. Here, we report here three cases of Cushing's syndrome associated with asymmetrical septal hypertrophy and its regression. Case ReportsPatient 1 A 38-year-old woman was admitted to Kanazawa University Hospital on October 28, 1988 for a check-up for hypertension. On October 10, 1988 her hypertension was first noted at a level of 208/126mmHg. Physical examination showed central obesity and a moon face. The patient was 154cm tall and weighed 55kg. Her blood pressure was 196/120mmHg on ad mission and averaged 160/70mmHg during hospitaliz ation. Auscultation of the heart and lungs revealed no abnormalities. The serum potassium was 3.7mEq/l. Elevated baseline levels of urinary 17-hydroxycorticosteroids could not be suppressed with administration of 2 and 8 mg dexamethasone. Gortisol secretion increased and plasma ACTH levels were below lOpg/ml. In ad dition, the normal circadian rhythm in the levels of plasma cortisol and ACTH was absent. Venous sampling for plasma cortisol levels revealed remarkable gradients between the left adrenal vein and other sites. Abdominal ultrasonography and computerized tomography sug gested a left adrenal tumor, while 131I-adosterol scinti graphy confirmed a functioning left adrenal tumor. The diagnosis of Cushing's syndrome was thus confirmed due to presence of the left adrenal tumor.The electrocardiogram showed inverted T waves in leads I, aVL and Vl-6 (Fig. 1). The chest X-ray film showed a slight cardiac enlargement with a cardio thoracic ratio of 51%. On echocardiogram there was an increased thickness of the interventricular septum of 17mm, a posterior wall thickness of llmm and an in creased thickness of interventricular septum to thickness of posterior wall ratio (IVST/PWT ratio) of 1.55 (Fig. 2). The mechanocardiogram showed an increase in ...

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Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism

Cited by 46 publications

References 25 publications

Long-Term Control of Arterial Hypertension and Regression of Left Ventricular Hypertrophy With Treatment of Primary Aldosteronism

Long-Term Control of Arterial Hypertension and Regression of Left Ventricular Hypertrophy With Treatment of Primary Aldosteronism

The Influence of Aldosterone on the Development of Left Ventricular Geometry and Hypertrophy in Patients With Essential Hypertension

Disproportionate Hypertrophy of the Interventricular Septum and its Regression in Cushing's Syndrome. Report of Three Cases.

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