Influence of plasma aldosterone on left ventricular geometry and diastolic function in treated essential hypertension.

Since aldosterone is known to promote interstitial fibrosis in cardiac tissues, it is possible that aldosterone may influence cardiac structure and function. In the present study, we investigated whether plasma aldosterone concentration (PAC) is related to the distinct patterns of left ventricular (LV) geometry and LV diastolic function in treated essential hypertension. In 92 patients with chronically treated essential hypertension, two-dimensional and Doppler echocardiographic examinations were performed and LV inflow velocities were measured for evaluation of LV diastolic function. When patients were divided into four groups by the different LV geometric patterns, PAC in patients with eccentric hypertrophy was significantly higher than in those with concentric hypertrophy (15.2+/-2.1 vs. 10.0+/-0.7 ng/dl, p<0.01). However, the ratio of the peak velocity of early diastolic filling to that of atrial filling (EIA), an index of LV diastolic function, was significantly decreased in patients with concentric hypertrophy compared with those showing normal geometry. In the relationship between PAC and LV diastolic function, PAC was negatively correlated with EIA (r=-0.35, p<0.05) only in the subgroup with normal relative wall thickness (i.e., without the concentric change in LV geometry). A multiple linear regression analysis showed that PAC was one of the independent determinants of E/A in the overall subject group. These observations indicate that PAC is associated with the eccentric change in LV geometry in patients with treated essential hypertension and also suggest that the increase in PAC participates in the impairment of LV diastolic function apart from the concentric change in LV geometry, although concentric hypertrophy clearly impairs LV diastolic function.

[1]  B. Pitt “Escape” of aldosterone production in patients with left ventricular dysfunction treated with an angiotensin converting enzyme inhibitor: Implications for therapy , 1995, Cardiovascular Drugs and Therapy.

[2]  T. Saruta,et al.  Aldosterone Escape during Angiotensinconverting Enzyme Inhibitor Therapy in Essential Hypertensive Patients with Left Ventricular Hypertrophy , 2001, The Journal of international medical research.

[3]  K. Arakawa,et al.  The regression of left ventricular hypertrophy by imidapril and the reduction of serum procollagen type III amino-terminal peptide in hypertensive patients. , 2000, Hypertension research : official journal of the Japanese Society of Hypertension.

[4]  B. Pitt,et al.  The Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure , 2000 .

[5]  C. Brilla Aldosterone and Myocardial Fibrosis in Heart Failure , 2000, Herz.

[6]  T. Saruta,et al.  Plasma aldosterone concentrations are not related to the degree of angiotensin-converting enzyme inhibition in essential hypertensive patients. , 2000, Hypertension research : official journal of the Japanese Society of Hypertension.

[7]  B. Pitt,et al.  The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. , 1999, The New England journal of medicine.

[8]  T. Saruta,et al.  Effects of spironolactone and angiotensin-converting enzyme inhibitor on left ventricular hypertrophy in patients with essential hypertension. , 1999, Hypertension research : official journal of the Japanese Society of Hypertension.

[9]  R. Fagard,et al.  Opposite associations of circulating aldosterone and atrial natriuretic peptide with left ventricular diastolic function in essential hypertension , 1998, Journal of Human Hypertension.

[10]  H. Schunkert,et al.  Neurohormonal activity and left ventricular geometry in patients with essential arterial hypertension. , 1998, American heart journal.

[11]  P. Palatini,et al.  Remodeling of the left ventricle in primary aldosteronism due to Conn's adenoma. , 1997, Circulation.

[12]  T. Nishikimi,et al.  Left ventricular systolic and diastolic function and mass before and after antihypertensive treatment in patients with essential hypertension. , 1997, Hypertension research : official journal of the Japanese Society of Hypertension.

[13]  L. Lind,et al.  Left ventricular hypertrophy and geometry in a population sample of elderly males. , 1996, European heart journal.

[14]  R. Schmieder,et al.  Angiotensin II related to sodium excretion modulates left ventricular structure in human essential hypertension. , 1996, Circulation.

[15]  Randolph P. Martin,et al.  Canadian consensus recommendations for the measurement and reporting of diastolic dysfunction by echocardiography: from the Investigators of Consensus on Diastolic Dysfunction by Echocardiography. , 1996, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[16]  T. Nishikimi,et al.  Comparison of changes in cardiac structure after treatment in secondary hypertension. , 1996, Hypertension.

[17]  K. Thygesen,et al.  Influence of humoral and neurohormonal factors on cardiovascular hypertrophy in untreated essential hypertensives. , 1996, American journal of hypertension.

[18]  C. Delcayre,et al.  Biological determinants of aldosterone-induced cardiac fibrosis in rats. , 1995, Hypertension.

[19]  D. Levy,et al.  Prognosis of left ventricular geometric patterns in the Framingham Heart Study. , 1995, Journal of the American College of Cardiology.

[20]  H. Matsuoka,et al.  Clinical evidence for an association between left ventricular geometric adaptation and extracardiac target organ damage in essential hypertension , 1995, Journal of hypertension.

[21]  T. Ogihara,et al.  Association between a deletion polymorphism of the angiotensin-converting-enzyme gene and left ventricular hypertrophy. , 1994, The New England journal of medicine.

[22]  C. Delcayre,et al.  Increased cardiac types I and III collagen mRNAs in aldosterone-salt hypertension. , 1994, Hypertension.

[23]  R. Dilley,et al.  Mineralocorticoids, hypertension, and cardiac fibrosis. , 1994, The Journal of clinical investigation.

[24]  J. Parameshwar,et al.  The role of calcium antagonists in the treatment of chronic heart failure. , 1993, European heart journal.

[25]  A. de la Sierra,et al.  Left ventricular hypertrophy in asymptomatic essential hypertension: its relationship with aldosterone and the increase in sodium-proton exchanger activity. , 1993, European heart journal.

[26]  J. Laragh,et al.  Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. , 1992, Journal of the American College of Cardiology.

[27]  J. Kaufman,et al.  Influence of the arterial blood pressure and nonhemodynamic factors on left ventricular hypertrophy in moderate essential hypertension. , 1991, The American journal of cardiology.

[28]  J S Janicki,et al.  Impaired diastolic function and coronary reserve in genetic hypertension. Role of interstitial fibrosis and medial thickening of intramyocardial coronary arteries. , 1991, Circulation research.

[29]  K. Weber,et al.  Pathological Hypertrophy and Cardiac Interstitium: Fibrosis and Renin‐Angiotensin‐Aldosterone System , 1991, Circulation.

[30]  K Lindpaintner,et al.  The cardiac renin-angiotensin system. An appraisal of present experimental and clinical evidence. , 1991, Circulation research.

[31]  J. Laragh,et al.  Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. , 1991, Annals of internal medicine.

[32]  A. Labovitz,et al.  Echocardiographic evaluation of cardiac structure and function in elderly subjects with isolated systolic hypertension. , 1991, Journal of the American College of Cardiology.

[33]  K. Baker,et al.  Cardiac Hypertrophy: Mechanical, Neural, and Endocrine Dependence , 1991 .

[34]  D. Levy,et al.  Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. , 1990, The New England journal of medicine.

[35]  P. Granier,et al.  Correlations between M-mode markers of left ventricular hypertrophy and radionuclide angiographic indices of left ventricular diastolic function in mild to moderate hypertension. , 1989, Journal of hypertension. Supplement : official journal of the International Society of Hypertension.

[36]  D. Bonaduce,et al.  Myocardial hypertrophy and left ventricular diastolic function in hypertensive patients: an echo Doppler evaluation. , 1989, European heart journal.

[37]  M. Kuramochi,et al.  Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism. , 1988, The American journal of cardiology.

[38]  R. Schmieder,et al.  Does the renin-angiotensin-aldosterone system modify cardiac structure and function in essential hypertension? , 1988, The American journal of medicine.

[39]  W. White,et al.  Echocardiographic Assessment of Left Ventricular Diastolic Performance in Hypertensive Subjects Correlation with Changes in Left Ventricular Mass , 1987, Hypertension.

[40]  R. Devereux Detection of Left Ventricular Hypertrophy by M‐Mode Echocardiography: Anatomic Validation, Standardization, and Comparison to Other Methods , 1987, Hypertension.

[41]  R. Tarazi,et al.  Left ventricular diastolic function in hypertension: relation to left ventricular mass and systolic function. , 1984, Journal of the American College of Cardiology.

[42]  B. Massie,et al.  Abnormal left ventricular filling: an early finding in mild to moderate systemic hypertension. , 1984, The American journal of cardiology.

[43]  J. Staessen,et al.  Increase in plasma aldosterone during prolonged captopril treatment. , 1982, The American journal of cardiology.

[44]  R. Tarazi,et al.  The multifactorial role of catecholamines in hypertensive cardiac hypertrophy. , 1982, European heart journal.

[45]  J. Staessen,et al.  Rise in plasma concentration of aldosterone during long-term angiotensin II suppression. , 1981, The Journal of endocrinology.

[46]  N Reichek,et al.  Echocardiographic Determination of Left Ventricular Mass in Man: Anatomic Validation of the Method , 1977, Circulation.