Re: Re: stats on long-term follow-up of PA patients who opt for meds

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You can limit your search to free full text or reviews which might help.Not many with more than 5 years that I can find. This is where we can lead the way as our longest followup is about 25 years if I am not mistaken. CE Grim MDThat helped, thanks - I always forget to also search "Conn's syndrome" since my healthcare team all seems to refer to it as hyperaldosteronism or primary aldosteronism.I found a lot of interesting abstracts but few full-text articles. Most, though, mentioned long-term follow-up after adrenalectomy (which I'm also interested in reading about). I'm going to have to see if some of my academic-type friends can access the full-texts...> > > On this board the lack of studies of long-term follow-up of patients > > after adrenalectomy is often mentioned. I got curious and started to > > look for studies of long-term follow-up of patients who manage their > > PA medically.> >> > I don't have access to full-text databases, so I'm probably missing > > a good chunk of literature. However, all I could find was this:> > http://www.annals.org/content/131/2/105.full.pdf+html> >> > If anyone here can point me to similar full-text links, I'd > > appreciate it. I didn't find this article to be especially positive > > - it's as if we really don't have any one good option, be it surgery > > or meds!> >> >> >>

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Not a randomized study in which half had surgery and 1/2 did not. Until such a study is done we will not know if surgery is better or worse than diet medical therapy. Note there is no mention of DASH or low sodium intake in "Medical Treatment". One of the most important correlates of heart size LVH is salt intake. Therefore they are only half treating by using only MCB.We are still leading the way.CE Grim MD Search: Advanced SearchHypertension HomeSubscriptionsArchivesFeedbackAuthorsHelpAHA Journals Home« Previous Article | Table of Contents | Next Article »Hypertension. 2007;50:911-918Published online before print September 24, 2007, doi: 10.1161/HYPERTENSIONAHA.107.095448This ArticleAbstract Full Text (PDF)CME: Take the course for this article:Hypertension: November 2007, Volume 50, Number 5All Versions of this Article:50/5/911 most recentHYPERTENSIONAHA.107.095448v1Alert me when this article is citedAlert me if a correction is postedCitation MapServicesEmail this article to a friendSimilar articles in this journalSimilar articles in PubMedAlert me to new issues of the journalDownload to citation managerRequest PermissionsCiting ArticlesCiting Articles via HighWireCiting Articles via Google ScholarGoogle ScholarArticles by Catena, C.Articles by Sechi, L. A.Search for Related ContentPubMedPubMed CitationArticles by Catena, C.Articles by Sechi, L. A.Pubmed/NCBI databasesCompound via MeSHSubstance via MeSHMedline Plus Health InformationAdrenal Gland CancerBenign TumorsHigh Blood PressureHazardous Substances DBPOTASSIUMSPIRONOLACTONERelated CollectionsHypertrophy Clinical Studies Other TreatmentRelated Article(Hypertension. 2007;50:911.)© 2007 American Heart Association, Inc. Original ArticlesLong-Term Cardiac Effects of Adrenalectomy or Mineralocorticoid Antagonists inPatients With Primary AldosteronismCristiana Catena; GianLuca Colussi; a Lapenna; Nadalini; Alessandra Chiuch; Pasquale Gianfagna; Leonardo A. Sechi From the Division of Internal Medicine, Hypertension and Cardiovascular Unit (C.C., G.C., R.L., E.N., A.C., L.A.S.), and Divisionof Cardiology (P.G.), Department of Experimental and Clinical Pathology and Medicine, University of Udine, Udine, Italy.Correspondence to Leonardo A. Sechi, Clinica Medica, Università di Udine, Department of Experimental and Clinical Pathology and Medicine, Piazzale S. della Misericordia, 1, 33100 Udine, Italy. E-mail sechi@... AbstractTopAbstractIntroductionMethodsResultsDiscussionReferences Exposure to excess aldosterone results in cardiac damage in hypertensive states. We evaluated the long-term cardiac structural and functional evolution in patients with primary aldosteronismafter surgical or medical treatment. Fifty-four patients with primary aldosteronism were enrolled in a prospective study and were followed for a mean of 6.4 years after treatment withadrenalectomy (n=24) or spironolactone (n=30). At baseline, echocardiographic measurements of patients with primary aldosteronism were compared with those of 274 patients with essential hypertension. Patients with primary aldosteronism had greater left ventricular mass, more prevalent left ventricular hypertrophy, lower early:late-wave diastolic filling velocities ratio, and longer deceleration time than patients with essential hypertension but no differences in relative wall thickness and systolic function. During follow-up, average blood pressure was 135/82 and 137/82 mm Hg in patients treated with adrenalectomy and spironolactone, respectively. In the initial 1-year period, left ventricular mass decreased significantly only in adrenalectomized patients. Subsequent changes in left ventricular mass were greater in patients treated with spironolactone, with an overall change from baseline to the end of follow-upthat was comparable in the 2 groups. Prevalence of hypertrophy decreased in both treatment groups, whereas diastolic parameters had only mild and nonsignificant improvement. Changes in blood pressure and pretreatment plasma aldosterone were independent predictors of left ventricular mass decrease in both treatment groups. Thus, in the long-term, both adrenalectomy and spironolactone are effective in reducing left ventricular mass in patients with primary aldosteronism, with effects that are partially independent of blood pressure changes.Key Words: adrenalectomy • echocardiography • left ventricular hypertrophy • spironolactone • diastolic filling IntroductionTopAbstractIntroductionMethodsResultsDiscussionReferences For many decades, aldosterone has been seen as a hormone almost exclusively involved in the regulation of body fluids, maintenance of electrolyte balance, and blood pressure homeostasis.1More recent views, however, indicate that aldosterone can contribute to cardiac damage independent of blood pressure.2 In animal studies, exposure to excess aldosterone levels has been associated with collagen deposition, myocardial fibrosis, and ventricular remodeling,3 and 2 large clinical trials have reported a significant decrease in the mortality rate of patients with heart failure who were treated with aldosterone antagonists.4,5Primary aldosteronism is a disease associated with hypertension that offers an important clinical opportunity for assessing the effects of excess aldosterone on the cardiovascular systembecause, in this condition, its effects are isolated from those of the renin-angiotensin axis. The widespread use of the aldosterone:renin ratio as a screening test has led to more efficient identification of this endocrine disorder.6,7 Cardiac structural and functional changes are common consequences of hypertensive states and have been demonstrated also in patients with primary aldosteronism, along with some additional surrogate cardiovascular end points (reviewed in Reference 2). Many cross-sectional echocardiographic evaluations and a few short-termfollow-up studies have reported variable results,8–20 with excess left ventricular (LV) hypertrophy and diastolic dysfunction being the most common,8–15 although not uniformly detected,16–20 abnormalities. Wehave further explored the relationship between aldosterone and the heart by assessing, in the long term, cardiac anatomic and functional evolution of patients with primary aldosteronism after treatment withadrenalectomy or aldosterone antagonists. MethodsTopAbstractIntroductionMethodsResultsDiscussionReferences PatientsFifty-four consecutive patients with primary aldosteronism were included in a prospective study. Recruitment of patients, diagnostic criteria, and follow-up have been described in detail in previous publications.21,22 Patients were referred to the hypertension clinic of our university for evaluation of their hypertensive state: 36 patients had persistent hypokalemia, and 27 had hypertension resistant to a triple-drug regimen. Blood pressure was measured by sphygmomanometry, and hypertension was diagnosed according to established guidelines.23 All of thepatients seen at the clinic are screened with extensive testing to define the cause of hypertension. Seven percent of patients with primary aldosteronism were taking no antihypertensive drug, 9% were on monotherapy, and the remaining 84% had multiple-drug treatment with an average of 2.9 drugs per patient. Patients treated with antihypertensive drugs were withdrawn from treatment a minimum of 2 weeks before diagnostic assessment. ß-Blockers, lipophilic calcium antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers were withdrawn for 3 weeks. No patient was taking mineralocorticoid receptor antagonists before the study.Primary aldosteronism was screened by the demonstration of an increased plasma aldosterone:active renin ratio (20)21,24 in the presence of a plasma aldosterone of >150 pg/mL, and the diagnosis was confirmed by the lack of aldosterone suppression (values of 50 pg/mL) after an intravenous saline load (2 L of 0.9% saline infused over 4 hours).25 This test has been shown to be highly effective in the distinction of both tumoral and idiopathic aldosteronism from low-renin essential hypertension.26 Measurements were performed under a normal sodium diet, and 24-hour urinary sodium excretion was checked in all of the patients. Plasma potassium concentration of 3.5 mmol/L was corrected by oral supplementation before the assessment of the plasma aldosterone:active renin ratio and saline suppression test. Differentiation between adrenal adenoma and idiopathic aldosteronism was obtained by high-resolution computed tomography scan, followed by selective adrenal vein sampling (n=14) and/or adrenal scintigraphy with iodocholesterol (n=47), which was performed under dexamethasone suppression. In patients who underwent adrenal vein sampling, adrenal vein cannulation was considered successful if the adrenal vein/inferior vena cava cortisol gradient was 2, and lateralization was defined by measurement of an aldosterone:cortisol ratio in 1 adrenal vein that was 4 times the ratio in the other adrenal vein.7 In all of the patients who underwent adrenalectomy, adenomawas confirmed by histology and normalization of plasma aldosterone concentrations. Primary aldosteronism was treated by either unilateral adrenalectomy or spironolactone (range: 50 to 300 mg/d; average dose: 121 mg/d), and treatment was followed by normalization of blood pressure or significant improvement of hypertension in all of the patients.A total of 274 patients with essential hypertension served as control subjects for baseline comparisons. These patients were recruited at our hypertension clinic and were selected by frequency matching afterspecification of inclusion criteria to avoid age, gender, body mass index, and estimated duration of hypertension as potential confounding variables. In these patients, secondary causes of hypertension were excludedafter an appropriate drug washout. Among patients with essential hypertension, 11% were taking no antihypertensive drug, 16% were on monotherapy, and 73% had multiple-drug treatment with a mean of 2.3 antihypertensive agents per patient. Informed consent was obtained from all of the patients, and the protocol was approved by the local ethics committee.Echocardiographic ExaminationEchocardiography was performed by the same investigators who were unaware of patient diagnosis.27 Measurements of LV internal dimensions and wall thickness were obtained with commercial machines (Sonos HP1000, Hewlett-Packard or Aplio CV, Toshiba Medical Systems) and a 2.5-MHz transducer under bidimensional cross-sectional control, with the patients in the partial left decubitus position. The LV geometric pattern was defined by the ratio of the posterior LV wall thickness to one half of the LV internal dimension, and a value of >0.44 was used to define LV concentric geometry.28 The LV mass index (LVMI) was calculated by the Penn Convention formula29 and adjusted for body height with a cutoff value of 51 g/m2.7 that was used to define LV hypertrophy in both sexes.30 Systolic function was estimated by the ejection fraction and both endocardial and midwall fractional shortening (FS), with the latter taking into account epicardial migration of the midwall during systole.31 Endocardial FS was expressed as a percentage of the value predicted in normal subjects for meridional end-systolic stress.32 Circumferential end-systolic stress was calculated at the midwall,33 and the equation of de Simone et al34 was used to predict expected midwallshortening. The observed:predicted midwall shortening ratio was used as an index of LV systolic performance.35 Pulsed Doppler recordings at the level of the mitral valve tips were obtained from apical 4-chamber scans to measure early and late-wave diastolic filling velocities, their ratio (E/A ratio), and the early wave deceleration time.36Follow-UpAll 54 of the patients with primary aldosteronism were prospectively followed up.21 Twenty four of 29 patients with adrenal adenoma underwent adrenalectomy; among the remaining 5 patients, 2 had bilateral adenoma, and 3 refused surgery and were treated with spironolactone. Treatment with spironolactone was started with a dose of 100 mg/d that was titrated to reach the target blood pressure. Clinical assessment and laboratory tests were repeated 1, 3, and 6 months after enrollment and every 12 months thereafter. At each visit, antihypertensive therapy was adjusted according to the physician's judgment to reach a target of<140/90 mm Hg. The use of all antihypertensive agents was permitted. Echocardiography was repeated after 1 year and after an average follow-up of 6.4 years (range: 3 to 11 years) in all of the patients with primary aldosteronism and in 108 of 274 patients with essential hypertension who were matched for age, gender, body mass index, and estimated duration of hypertension.Statistical AnalysisThis study had a statistical power of >95% to detect 20% differences between patients with primary aldosteronism and essential hypertension, with an -value of 0.05. Variables are expressed as mean±SD unless otherwise indicated. Continuous variables were compared by Student's t test. Variables with skewed distribution were analyzed after logarithmic transformation. Categorical variables were compared by the Pearson's 2 test. The relationships between different variables were examined by linear regression analysis, and the correlation was expressed by the correlation coefficient. Changes from the baseline of echocardiographic parameters were assessed by 2-way ANOVA. Multivariate discriminant analysis was performed to identify variables independently associated with changes in echocardiographic parameters after treatment. All of the tests for significance and resulting P values were 2 sided, with a level of significance of 0.05. ResultsTopAbstractIntroductionMethodsResultsDiscussionReferences Adrenal adenoma was demonstrated in 29 (54%) of 54 patients with primary aldosteronism, whereas the remaining 25 (46%) had no evidence of adrenal masses. As shown in Table 1,patients with primary aldosteronism and essential hypertension had comparable heart rates, blood pressure levels, estimated durations of hypertension, plasma glucose, and plasma lipid profiles. As expected, patients with primary aldosteronism had significantly higher plasma aldosterone and lower plasma potassium and active renin levels than patients with essential hypertension.View this table:[in this window][in a new window] Table 1. Baseline Characteristics of the Study PopulationBaseline echocardiographic parameters are summarized in Table 2. The average LV internal dimensions and wall thickness had nonsignificant trends to higher values, and the LV mass and LVMI were significantlygreater in patients with primary aldosteronism as compared with patients with essential hypertension. The left atrial diameter and the ratio of the posterior LV wall thickness to one half of the LV internal dimension were comparable in the 2 groups. The prevalence of LV hypertrophy and LV concentric geometry was, respectively, 33% and 26% in primary aldosteronism and 21% (P<0.05) and 24% (P=0.73) in essential hypertension, respectively. No significant differences of ejection fraction, endocardial FS, and midwall FS were observed between patients with primary aldosteronism and essential hypertension, indicatingcomparable systolic function. Both the ratio of E/A velocities and the deceleration time were significantly different in the 2 groups, indicating the presence of more severe diastolic dysfunction in primary aldosteronism. In primary aldosteronism, linear regression analysis showed that LVMI, but not the ratio of the posterior LV wall thickness to one half of the LV internal dimension, had a significant relationship with mean blood pressure measured both before (r=0.362; P<0.01) and after (r=0.319; P<0.05) drug washout, duration of hypertension (r=0.375; P<0.01), and plasma aldosterone concentrations (r=0.294; P<0.05); the ratio of E/A velocities was inversely related with duration of hypertension (r=0.391; P<0.01), LVMI (r=0.323; P<0.05), and plasma aldosterone (r=0.304; P<0.05) but not with blood pressure levels. In essential hypertension, LVMI had a statistically significant relationship with mean blood pressure (r=0.194; P<0.01), duration of hypertension (r=0.249; P<0.01), E/A ratio (r=–0.233; P<0.01), and plasma aldosterone (r=0.134; P<0.05). No significant differences in echocardiographic parameters were observed between primary aldosteronism patients with or without computed tomography evidence of adrenal masses.View this table:[in this window][in a new window] Table 2. Baseline Echocardiographic Parameters of the Study PopulationFollow-UpPatients with primary aldosteronism were reassessed with echocardiography after treatment (adrenalectomy: n=24; spironolactone: n=30), at 1 year, and after an the average follow-up of 6.4 years.Antihypertensive medications used during the study are shown in Table 3. The frequency of the use of specific types of drugs was comparable in patients treated with adrenalectomy or spironolactone. Blood pressure declined significantly during the first year, with average values that, during the entire course of the study, were of 135/82 and 137/82 mm Hg in patients who were treated with adrenalectomy and spironolactone, respectively. Treatment was followed by normalization of blood pressure in 21 patients with primary aldosteronism (39%; adrenalectomy: n=10; spironolactone: n=11) and by significant improvement in the remaining 33 (61%; adrenalectomy: n=14; spironolactone: n=19; P=0.71). In the first year, plasma potassium increased significantly from baseline levels (from 3.2±0.4 to 4.2±0.3 mmol/L;P<0.001) and remained stable thereafter. Markers of volume change, such as body weight (from 79.4±10.3 to 78.6±9.3 kg), packed cell volume (from 44±3 to 44±3%), and serum albumin (from 41±2 to 42±3 g/dL), did not change significantly during follow-up.View this table:[in this window][in a new window] Table 3. Antihypertensive Medications Used at Baseline and at End of Follow-UpTable 4 summarizes the echocardiographic measurements obtained at follow-up in patients with primary aldosteronism. During the initial 1-year period, average LV internal dimensions and wall thickness had a nonsignificant trend to decrease in all of the patients with primary aldosteronism. This trend was more evident in patients who were treated with adrenalectomy as compared with patients treated with spironolactone and resulted in a decrease of the LV mass and LVMI that was significant only in the former group at this time point (Figure). Subsequent average changes in LV dimensions and wall thickness were greater in patients treated with spironolactone than in those who had adrenalectomy, with an overall change, from baseline to the end of follow-up, that tended to be greater, although nonsignificantly, in adrenalectomized patients. At the end of follow-up, the prevalence of LV hypertrophy and LV concentric geometry changed from 38% to 8% (P<0.05) and from 29% to 21% (P=0.44), respectively, in adrenalectomizedpatients, and from 30% to 7% (P<0.05) and from 23% to 20% (P=0.75), respectively, in patients treated with spironolactone. The E/A ratio and the deceleration time had nonsignificant trends to change after bothadrenalectomy and spironolactone treatment, suggesting only partial recovery of the diastolic dysfunction after removal of the effects of excess aldosterone. The ratio of the posterior LV wall thickness to one half ofthe LV internal dimension and parameters of systolic function did not change significantly during the study. After 1 year, plasma renin levels increased significantly in both patients who were treated withadrenalectomy (from 4.6±6.0 to 9.3±5.8 pg/mL; P<0.01) and spironolactone (from 5.0±6.6 to 8.8±5.6 pg/mL; P<0.02); at the end of follow-up, renin levels were comparable in the 2 treatment groups (8.9±5.8 and 8.6±5.7 pg/mL, respectively; P=0.85). In both adrenalectomized and spironolactone-treated patients, the reduction of LVMI was directly correlated with changes in mean blood pressure (respectively: r=0.509, P<0.01and r=0.427, P<0.05) and pretreatment plasma aldosterone concentrations (respectively: r=0.413, P<0.05 and r=0.391, P<0.05) but not with pretreatment plasma potassium and active renin. Multivariate analysis showed that changes in mean blood pressure (P<0.05) and pretreatment aldosterone levels (P<0.05) were both independent predictors of LVMI decrease after treatment, and their respective contributions were 47% and 24%. In 108 patients with essential hypertension, the average blood pressure during follow-up was 137/81 mm Hg, and the decrease in LVMI (–11.8%) was significantly smaller than in patients with primary aldosteronism (–17.4%; P<0.05), whereas the frequency of reversal of LV hypertrophy (essential hypertension: from 22% to 8%; primary aldosteronism: from 33% to 7%) did not differ significantly between the groups (P=0.19).View this table:[in this window][in a new window] Table 4. Echocardiographic Parameters of Patients With Primary Aldosteronism Who Were Treated With Adrenalectomy (n=24) or Spironolactone (n=30) at Baseline, After 1 Year, and at the End of Follow-UpView larger version (22K):[in this window][in a new window] Figure. Percentage changes of LVMI in the short- and long-term follow-up in patients with primary aldosteronism who were treated with adrenalectomy(n=24) or spironolactone (n=30). Short-term and long-term follow-up measurements were done after 1 year and after an average period of 6.4 years, respectively. *P<0.05 vs baseline; P<0.01 vs baseline. DiscussionTopAbstractIntroductionMethodsResultsDiscussionReferences Increased LV mass and impaired LV diastolic filling have been reported in patients with primary aldosteronism and might predispose these patients to cardiac complications. Our study has examined the long-term echocardiographic evolution in a large cohort of patients with primary aldosteronism after treatment. Results demonstrate that adrenalectomy and spironolactone are both effective in decreasing the LV mass, although this effect occurs earlier after surgical treatment. In both treatment groups, the LV diastolic filling pattern had only mild and nonsignificant improvement. Pretreatment plasma aldosterone concentrations predict LVMI decrease during follow-up, independent of treatment-related blood pressure changes.A growing body of evidence links aldosterone to development and/or progression of cardiovascular disease, seemingly separate from its effects on blood pressure. In fact, animal and humanstudies support the contention that cardiac damage in aldosteronism is not just the result of a pressure-volume overload but might involve additional endocrine and paracrine mechanisms.2,3Many cross-sectional echocardiographic evaluations have reported an excess increase of LV mass in patients with primary aldosteronism as compared with other types of hypertensive disease,8–15 although this finding has not been confirmed in other studies.16–20 Disparity of the findings could be ascribed to the limited sample size of some studies and differences in the severity and duration of hypertension in selected patients and respective control subjects. The present study has been conducted in a large cohort of patients with primary aldosteronism who were diagnosed usingstandardized procedures that were homogeneously applied by the same physicians.21 This practice, together with the collection of data in a single database, should have limited any possible selection bias. Moreover,patients with primary aldosteronism have been compared with patients with essential hypertension who were appropriately matched for age, sex, severity, and estimated duration of hypertension and who had comparable cardiovascular risk profiles. Our results confirm the presence of greater LV mass and more prevalent LV hypertrophy in patients with primary aldosteronism that is associated with evidence of an abnormal pattern of LV diastolic filling, such as that reported in previous studies,10,11 but not with changes of LV geometry and systolic function.Measurement of increased LV mass in patients with primary aldosteronism might reflect the increased circulating volume resulting from the renal effects of the hormone. However, we have observed greater differences in wall thickness than ventricular volumes between patients with primary aldosteronism and essential hypertension at baseline and greater changes in wall thickness than ventricular volumes after both surgical and medical treatment of primary aldosteronism. This would suggest that the contribution of volume factors is not predominant over other factors and that cardiac changes, in this condition, could not simply be explained by the salt- and water-retaining effects of aldosterone. The cardiac hemodynamic overload is not the only determinant of LV hypertrophy, and various hormones can play specific roles in different subsets ofhypertension. The renin-angiotensin-aldosterone system is an important contributor to the pathogenesis of LV hypertrophy,37 and primary aldosteronism permits evaluation of the cardiac effects of elevated aldosterone independent from those of angiotensin. LV hypertrophy is an important independent predictor of major cardiovascular events38 in hypertension, and increased LV mass in patients with primary aldosteronism might be associated with worse cardiovascular outcome in comparison with other hypertensive groups. Relevant to this point, a recent retrospective study of a large cohort of patients with adrenal adenoma or idiopathic aldosteronism has reported an excess rate of cardiovascular complications and LV hypertrophy in comparison with properly matched patients with essential hypertension.39Cross-sectional evidence of associations between cardiac phenotypes and possible causative factors is of limited value, and findings should be confirmed in longitudinal evaluations. The few echocardiographicobservations of cardiac changes after treatment of aldosteronism are confined to short-term follow-up studies, mostly after removal of an adrenal adenoma.9,10,18 The present study is the first to provide data of a long-term echocardiographic follow-up in a substantial cohort of patients with primary aldosteronism after either surgical or medical treatment. Our 11-year study demonstrates that patients treated with eitheradrenalectomy or spironolactone have significant decrease of LVMI, a response that occurs within the first year only after surgical treatment. In both treatment groups, baseline LVMI was directly correlated with plasma aldosterone concentration, and this concentration was an independent predictor of changes of LVMI after treatment. Data demonstrate that the decrease of LVMI is only partially explained by blood pressure changes, suggesting a role of aldosterone that is independent from the hemodynamic overload. This possibility would also be supported by the observation that, in patients with essential hypertension, the decrease ofLVMI that occurred during follow-up in the presence of very similar blood pressure values was significantly smaller than in patients with primary aldosteronism.Mineralocorticoid receptors have been demonstrated in human cardiomyocytes,40 and their activation might play a role in myocardial hypertrophy and cardiac remodeling41 in patients with primary aldosteronism via mechanisms that include modulation of ionic movements42 and accelerated fibrosis.43 The latter mechanism might, in turn, result from interactions of aldosterone with angiotensin, endothelin, and bradykinin; activation of inflammatory cells; and stimulation of fibroblast proliferation and collagen synthesis (reviewed in References 41 and 43). Interruption of these receptor-mediated mechanisms might explain why, in the long term, treatment of primary aldosteronism with aldosterone receptor antagonists has comparable effects to the removal of an aldosterone-secreting adenoma in reducing LV mass, although this response occurs later than after the removal of excess circulating aldosterone by adrenalectomy. From a pathophysiological point of view, persistent hyperaldosteronemia with possible involvement of nongenomic effects ofaldosterone2,3 might hypothetically explain why regression of LV hypertrophy requires a longer time to occur in patients treated with spironolactone than in those treated with surgery. Consistent with our findings, favorable effects of mineralocorticoid antagonists on reduction of LV mass have been reported in patients with essential hypertension and LV hypertrophy.44 In these patients, effects of aldosterone antagonists resulted to be additive with those of angiotensin-converting enzyme inhibitors and, therefore, independent from the renin-angiotensin axis. In the present study, no patient in the essential hypertension group was treated with spironolactone.Some limitations of our study need to be highlighted. First, given that we performed selective adrenal vein sampling in only 14 of our patients and, instead, mainly relied on computed tomography and adrenal scintigraphy for subtype differentiation, it is possible that we have misclassified some patients with aldosterone-producing adenoma as idiopathic hyperplasia or vice versa. More accurate detection of truly unilateral forms of primary aldosteronism may have resulted in better blood pressure and echocardiographic responses to adrenalectomy than were seen in this study. Second, the majority of patients were on treatment at the time of study, and the use of certain antihypertensive medications during follow-up might have influenced the echocardiographic evolution. For instance, angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers could be more effective than other agents in reducing the LV mass,45 but frequency of the use of these drugs was comparable in patients treated with adrenalectomy or spironolactone. Nonetheless,differences in the pretreatment status and in drugs used at baseline and during follow-up might have had significant impact on the cardiac outcome of the study patients. Third, the doses of spironolactone that have been used in this study are higher than those that are currently recommended for medical treatment of primary aldosteronism, and, therefore, extrapolation of the results to a more general context should be done with caution. With regard to this issue, further investigation of the cardiac effects of the newer aldosterone-receptor antagonists, such as eplerenone, which offer the opportunity to use relatively higher doses without antiandrogenic effects, is warranted. Last, our study might have underestimated the impact of blood pressure on cardiac structure, because we did not include measurements of the 24-hour blood pressure profile, which is superior to clinic blood pressure for the prediction of LV mass.46 Results of previous studies with ambulatory blood pressure monitoring in primary aldosteronism are controversial, with some studies reporting significant differences with essential hypertension47,48 and others not supporting this contention.11,15 In our hands, comparison of ambulatory blood pressure profiles in subsets of the primary aldosteronism (n=32) and essential hypertension (n=153) group did not show significant differences.PerspectivesRecovery of cardiac anatomic and/or functional abnormalities and prevention of cardiovascular events are primary goals of treatment in hypertensive patients. Primary aldosteronism was once considered to account for <1% of all forms of hypertension, but recent work suggests that it might be the most common curable cause, worth screening for in patients with high blood pressure and an index of suspicion, including those with hypokalemia and/or resistance to treatment. This study presents evidence that primary aldosteronism is associated with LV hypertrophy out of proportion to blood pressure levels that benefits substantially from treatment in the long term. In this view, adrenalectomy and mineralocorticoid receptor blockade appear to be of considerable therapeutic value inasmuch as they significantly reduce LV mass, whereas their beneficial effect on the LV diastolic filling pattern is only partial. These findings underscore the importance of a timely identification of this endocrine disorder to obtain regression of cardiac abnormalities. Future studies will have to address the potential benefits of the newest mineralocorticoid receptor antagonists on cardiac structural and functional abnormalities of primary aldosteronism and to clarify whether these therapeuticinterventions can effectively prevent late cardiovascular complications. Acknowledgments Sources of FundingThis work was supported by research grants from the Italian Ministry of the University and Scientific and Technologic Research (to L.A.S. and C.C.) and by research grants from the Italian Society of Hypertension (to G.L.C. and E.N.).DisclosuresNone. Footnotes Continuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz.Received May 28, 2007; first decision June 25, 2007; accepted September 4, 2007. ReferencesTopAbstractIntroductionMethodsResultsDiscussionReferences 1 Freel EM, Connell JM. Mechanisms of hypertension: the expanding role of aldosterone. J Am Soc Nephrol. 2004; 15: 1993–2001.[Abstract/Free Full Text]2 Rossi GP, Boscaro M, Ronconi V, Funder JW. Aldosterone as a cardiovascular risk factor. Trends Endocrinol Metab. 2005; 16: 104–107.[CrossRef][Medline] [Order article via Infotrieve]3 Rocha R, Funder JW. The pathophysiology of aldosterone in the cardiovascular system. Ann N Y Acad Sci. 2002; 970: 89–100.[Medline] [Order article via Infotrieve]4 Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, A, Palensky J, Wittes J. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999; 341: 709–717.[CrossRef][Medline] [Order article via Infotrieve]5 Pitt B, Remme W, Zannad F, Neaton J, ez F, Roniker B, Bittman R, Hurley S, Kleiman J, Gatlin M. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. 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Left ventricular mass and geometry before and after etiologic treatment in renovascular hypertension, aldosterone-producing adenoma, and pheochromocytoma. Am J Hypertens. 1993; 6: 907–913.[Medline] [Order article via Infotrieve]10 Rossi GP, Sacchetto A, Visentin P, Canali C, Graniero GR, Palatini P, Pessina AC. Changes in left ventricular anatomy and function in hypertension and primary aldosteronism. Hypertension. 1996; 27: 1039–1045.[Abstract/Free Full Text]11 Rossi GP, Sacchetto A, Pavan E, Palatini P, Graniero GR, Canali C, Pessina AC. Remodeling of the left ventricle in primary aldosteronism due to Conn's adenoma. Circulation. 1997; 95: 1471–1478.[Abstract/Free Full Text]12 Shigematsu Y, Mareomi H, Hideki O, Hara Y, Hayashi Y, Kodama K, Katsuhiko K, Hiwada K. Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism. 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J Am Coll Cardiol. 1992; 20: 1251–1260.[Abstract]31 Devereux RB, Roman MJ. Evaluation of cardiac and vascular structure by echocardiography and other noninvasive techniques. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, Treatment. 2nd ed. New York, NY: Raven Press; 1995: 1969–1985.32 Reichek N, J, St Sutton M, Piappert PA, Goidberg S, Hirshfeld JW. Noninvasive determination of left ventricular end-systolic stress: validation of the method and initial application. Circulation. 1982; 65: 99–109.[Free Full Text]33 Gaasch WH, Zile MR, Hosino PK, Apstein CS, Blaustein AS. Stress-shortening relations and myocardial blood flow in compensated and failing canine hearts with pressure-overload hypertrophy. Circulation. 1989; 79: 872–883.[Abstract/Free Full Text]34 de Simone G, Devereux RB, Roman MJ, Ganau A, Saba PS, Alderman MH, Laragh JH. Assessment of left ventricular function by the midwall fractional shortening/end-systolic stress relation in human hypertension. J Am Coll Cardiol. 1994; 23: 1444–1451.[Abstract]35 Devereux RB, de Simone G, Pickering TG, Schwartz JE, Roman MJ. Relation of left ventricular midwall function to cardiovascular risk factors and arterial structure and function. Hypertension. 1998; 31: 929–936.[Abstract/Free Full Text]36 Quinones MA, Otto C, Stoddard M, Waggoner A, Zoghbi W. Recommendations for quantifications of Doppler echocardiography: a report from the Doppler quantification Task Force for the Nomenclature and Standards Committee of the American Society of Echocardiography. J Am Soc Echocardiogr. 2002; 15: 167–184.[CrossRef][Medline] [Order article via Infotrieve]37 HE, Baker KM. Cardiac hypertrophy: mechanical, neural, and endocrine dependence. Circulation. 1991; 83: 13–25.[Free Full Text]38 Casale PN, Devereux RB, Milner M, Zullo G, Harshfield GA, Pickering TG, Laragh JH. Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Ann Intern Med. 1986; 105: 173–176.[Abstract/Free Full Text]39 Milliez P, Girerd X, Plouin PF, Blacher J, Safar ME, Mourad JJ. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. J Am Coll Cardiol. 2005; 45: 1243–1248.[Abstract/Free Full Text]40 Lombes M, Alfaidy N, Eugene E, Lessana A, Farman N, Bonvalet JP. Prerequisite for cardiac aldosterone action: mineralocorticoid receptor and 11--hydroxysteroid dehydrogenase in the human heart. Circulation.1995; 92: 175–182.[Abstract/Free Full Text]41 Schmidt BMW, Schmieder RE. Aldosterone-induced cardiac damage: focus on blood pressure independent effects. Am J Hypertens. 2003; 16: 80–86.[CrossRef][Medline] [Order article via Infotrieve]42 Kometiani P, Gnudi L, Kahn BB, Askari A, Xie Z. Multiple signal transduction pathways link Na/K-ATPase to growth-related genes in cardiac myocytes. The role of Ras and mitogen-activated protein kinases. J Biol Chem. 1998; 273: 15249–15256.[Abstract/Free Full Text]43 Funder J. Mineralocorticoids and cardiac fibrosis: the decade in review. Clin Exp Pharmacol Physiol. 2001; 28: 1002–1006.[CrossRef][Medline] [Order article via Infotrieve]44 Pitt B, Reichek N, Willenbrock R, Zannad F, RA, Roniker B, Kleiman J, Krause S, Burns D, GH. Effects of eplerenone, enalapril, and eplerenone/enalapril in patients with essential hypertension and left ventricular hypertrophy: the 4E-left ventricular hypertrophy study. Circulation. 2003; 108: 1831–1838.[Abstract/Free Full Text]45 Devereux RB. Therapeutic options in minimizing left ventricular hypertrophy. Am Heart J. 2000; 139: S9–S14.[CrossRef][Medline] [Order article via Infotrieve]46 Mancia G, Zanchetti A, Agabiti-Rosei E, Benemio G, De Cesaris R, Fogari R, Pessina A, Porcellati C, Rappelli A, Salvetti A, Trimarco B. Ambulatory blood pressure is superior to clinic blood pressure in predicting treatment-induced regression of left ventricular hypertrophy. Circulation. 1997; 95: 1464–1470.[Abstract/Free Full Text]47 Ceruti M, Petramala L, Cotesta D, Cerci S, Serra V, Caliumi C, Iorio M, De Toma G, Ciardi A, Vitolo D, Letizia C. Ambulatory blood pressure monitoring in secondary arterial hypertension due to adrenal diseases. J Clin Hypertens. 2006; 8: 642–648.[CrossRef]48 El-Gharbawy AH, Nadig VS, Kotchen JM, Grim CE, Sagar KB, Kaldunski M, Hamet P, Pausova Z, Gaudet D, Gossard F, Kotchen TA. Arterial pressure, left ventricular mass, and aldosterone in essential hypertension. Hypertension. 2001; 37: 845–850.[Abstract/Free Full Text]Related Article:Will the Lessons From Primary Aldosteronism Change the Treatment of Hypertension and Left Ventricular Hypertrophy? J. Auchus and Mark H. DraznerHypertension 2007 50: 837-839. [Extract] [Full Text] [PDF]This article has been cited by other articles:Y.-H. Lin, K.-H. Huang, J.-K. Lee, S.-M. Wang, R.-F. Yen, V.-C. Wu, S.-D. Chung, K.-L. Liu, S.-C. Chueh, L.-Y. Lin, et al.Factors influencing left ventricular mass regression inpatients with primary aldosteronism postadrenalectomyJournal of Renin-Angiotensin-Aldosterone System, March 1, 2011; 12(1): 48 - 53. [Abstract] [PDF] L. A. Sechi, G. Colussi, and C. CatenaHyperaldosteronism and Left Ventricular HypertrophyHypertension, September 1, 2010; 56(3): e26 - e26. [Full Text] [PDF] N. Sukor, C. Kogovsek, R. D. Gordon, D. Robson, and M. StowasserImproved Quality of Life, Blood Pressure, and Biochemical Status Following LaparoscopicAdrenalectomy for Unilateral Primary AldosteronismJ. Clin. Endocrinol. Metab., March 1, 2010; 95(3): 1360 - 1364. [Abstract] [Full Text] [PDF] P. Mulatero, C. Bertello, N. Sukor, R. Gordon, D. Rossato, N. Daunt, D. Leggett, G. Mengozzi, F. Veglio, and M. StowasserImpact of Different Diagnostic Criteria During Adrenal Vein Sampling on Reproducibility of Subtype Diagnosis in Patients With Primary AldosteronismHypertension, March 1, 2010; 55(3): 667 - 673. [Abstract] [Full Text] [PDF] B. A. Maron and J. A. LeopoldAldosterone Receptor Antagonists: Effective but Often ForgottenCirculation, February 23, 2010; 121(7): 934 - 939. [Full Text] [PDF] M. StowasserUpdate in Primary AldosteronismJ. Clin. Endocrinol. Metab., October 1, 2009; 94(10): 3623 - 3630. [Abstract] [Full Text] [PDF] R.-F. Yen, V.-C. Wu, K.-L. Liu, M.-F. Cheng, Y.-W. Wu, S.-C. Chueh, W.-C. Lin, K.-D. Wu, K.-Y. Tzen, C.-C. Lu, et al.131I-6{beta}-Iodomethyl-19-Norcholesterol SPECT/CT for Primary Aldosteronism Patients with Inconclusive Adrenal Venous Sampling and CT ResultsJ. Nucl. Med., October 1, 2009; 50(10): 1631 - 1637. [Abstract] [Full Text] [PDF] N. C. , R. P. Steeds, P. M. , C. J. Ferro, and J. N. TownendEffect of spironolactone on left ventricular mass and aortic stiffness in early-stage chronic kidney disease: a randomized controlled trial.J. Am. Coll. Cardiol., August 4, 2009; 54(6): 505 - 512. [Abstract] [Full Text] [PDF] L. A. Sechi, A. Di Fabio, M. Bazzocchi, A. Uzzau, and C. CatenaIntrarenal Hemodynamics in Primary Aldosteronism before and after TreatmentJ. Clin. Endocrinol. Metab., April 1, 2009; 94(4): 1191 - 1197. [Abstract] [Full Text] [PDF] E. Born-Frontsberg, M. Reincke, L. C. Rump, S. Hahner, S. Diederich, R. Lorenz, B. Allolio, J. Seufert, C. Schirpenbach, F. Beuschlein, et al.Cardiovascular and Cerebrovascular Comorbidities ofHypokalemic and Normokalemic Primary Aldosteronism: Results of the German Conn's RegistryJ. Clin. Endocrinol. Metab., April 1, 2009; 94(4): 1125 - 1130. [Abstract] [Full Text] [PDF] M. L. Muiesan, M. Salvetti, A. Paini, C. Agabiti-Rosei, C. Monteduro, G. Galbassini, E. Belotti, C. Aggiusti, D. Rizzoni, M. Castellano, et al.Inappropriate Left Ventricular Mass in Patients With Primary AldosteronismHypertension, September 1, 2008; 52(3): 529 - 534. [Abstract] [Full Text] [PDF] B RaynerPrimary aldosteronism and aldosterone-associated hypertensionJ. Clin. Pathol., July 1, 2008; 61(7): 825 - 831. [Abstract] [Full Text] [PDF] G. P. Rossi, M. Bolognesi, D. Rizzoni, T. M. Seccia, A. Piva, E. Porteri, G. A.M. Tiberio, S. M. Giulini, E. Agabiti-Rosei, and A. C. PessinaVascular Remodeling and Duration of Hypertension Predict Outcome of Adrenalectomy in Primary Aldosteronism PatientsHypertension, May 1, 2008; 51(5): 1366 - 1371. [Abstract] [Full Text] [PDF] N. M. KaplanResponse to More Fuel to the Debate on the "Epidemicof Primary Aldosteronism"Hypertension, January 1, 2008; 51(1): e3 - e3. [Full Text] [PDF] R. J. Auchus and M. H. DraznerWill the Lessons From Primary Aldosteronism Change the Treatment of Hypertension and Left Ventricular Hypertrophy?Hypertension, November 1, 2007; 50(5): 837 - 839. [Full Text] [PDF] This ArticleAbstract Full Text (PDF)CME: Take the course for this article:Hypertension: November 2007, Volume 50, Number 5All Versions of this Article:50/5/911 most recentHYPERTENSIONAHA.107.095448v1Alert me when this article is citedAlert me if a correction is postedCitation MapServicesEmail this article to a friendSimilar articles in this journalSimilar articles in PubMedAlert me to new issues of the journalDownload to citation managerRequest PermissionsCiting ArticlesCiting Articles via HighWireCiting Articles via Google ScholarGoogle ScholarArticles by Catena, C.Articles by Sechi, L. A.Search for Related ContentPubMedPubMed CitationArticles by Catena, C.Articles by Sechi, L. A.Related CollectionsHypertrophy Clinical Studies Other TreatmentRelated ArticleHypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | SearchCopyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.> > >> > > > On this board the lack of studies of long-term follow-up of > > patients> > > > after adrenalectomy is often mentioned. I got curious and > > started to> > > > look for studies of long-term follow-up of patients who manage > > their> > > > PA medically.> > > >> > > > I don't have access to full-text databases, so I'm probably > > missing> > > > a good chunk of literature. However, all I could find was this:> > > > http://www.annals.org/content/131/2/105.full.pdf+html> > > >> > > > If anyone here can point me to similar full-text links, I'd> > > > appreciate it. I didn't find this article to be especially > > positive> > > > - it's as if we really don't have any one good option, be it > > surgery> > > > or meds!> > > >> > > >> > > >> > >> >> >> >>

[Guest guest]

Thats what we are here for. You are part of the cure.CE Grim MDSaw that one, thanks.I'm actually most interested in quality-of-life issues, which I suspect will not be addressed in medical journals. Things like development of side effects, need to increase dosage or add other meds, etc. particularly as compared with adrenalectomy patients.> > > >> > > > > On this board the lack of studies of long-term follow-up of> > > patients> > > > > after adrenalectomy is often mentioned. I got curious and> > > started to> > > > > look for studies of long-term follow-up of patients who manage> > > their> > > > > PA medically.> > > > >> > > > > I don't have access to full-text databases, so I'm probably> > > missing> > > > > a good chunk of literature. However, all I could find was this:> > > > > http://www.annals.org/content/131/2/105.full.pdf+html> > > > >> > > > > If anyone here can point me to similar full-text links, I'd> > > > > appreciate it. I didn't find this article to be especially> > > positive> > > > > - it's as if we really don't have any one good option, be it> > > surgery> > > > > or meds!> > > > >> > > > >> > > > >> > > >> > >> > >> > >> >>

[Guest guest]

Not a randomized study in which half had surgery and 1/2 did not. Until such a study is done we will not know if surgery is better or worse than diet medical therapy. Note there is no mention of DASH or low sodium intake in "Medical Treatment". One of the most important correlates of heart size LVH is salt intake. Therefore they are only half treating by using only MCB.We are still leading the way.CE Grim MD Search: Advanced SearchHypertension HomeSubscriptionsArchivesFeedbackAuthorsHelpAHA Journals Home« Previous Article | Table of Contents | Next Article »Hypertension. 2007;50:911-918Published online before print September 24, 2007, doi: 10.1161/HYPERTENSIONAHA.107.095448This ArticleAbstract Full Text (PDF)CME: Take the course for this article:Hypertension: November 2007, Volume 50, Number 5All Versions of this Article:50/5/911 most recentHYPERTENSIONAHA.107.095448v1Alert me when this article is citedAlert me if a correction is postedCitation MapServicesEmail this article to a friendSimilar articles in this journalSimilar articles in PubMedAlert me to new issues of the journalDownload to citation managerRequest PermissionsCiting ArticlesCiting Articles via HighWireCiting Articles via Google ScholarGoogle ScholarArticles by Catena, C.Articles by Sechi, L. A.Search for Related ContentPubMedPubMed CitationArticles by Catena, C.Articles by Sechi, L. A.Pubmed/NCBI databasesCompound via MeSHSubstance via MeSHMedline Plus Health InformationAdrenal Gland CancerBenign TumorsHigh Blood PressureHazardous Substances DBPOTASSIUMSPIRONOLACTONERelated CollectionsHypertrophy Clinical Studies Other TreatmentRelated Article(Hypertension. 2007;50:911.)© 2007 American Heart Association, Inc. Original ArticlesLong-Term Cardiac Effects of Adrenalectomy or Mineralocorticoid Antagonists inPatients With Primary AldosteronismCristiana Catena; GianLuca Colussi; a Lapenna; Nadalini; Alessandra Chiuch; Pasquale Gianfagna; Leonardo A. Sechi From the Division of Internal Medicine, Hypertension and Cardiovascular Unit (C.C., G.C., R.L., E.N., A.C., L.A.S.), and Divisionof Cardiology (P.G.), Department of Experimental and Clinical Pathology and Medicine, University of Udine, Udine, Italy.Correspondence to Leonardo A. Sechi, Clinica Medica, Università di Udine, Department of Experimental and Clinical Pathology and Medicine, Piazzale S. della Misericordia, 1, 33100 Udine, Italy. E-mail sechi@... AbstractTopAbstractIntroductionMethodsResultsDiscussionReferences Exposure to excess aldosterone results in cardiac damage in hypertensive states. We evaluated the long-term cardiac structural and functional evolution in patients with primary aldosteronismafter surgical or medical treatment. Fifty-four patients with primary aldosteronism were enrolled in a prospective study and were followed for a mean of 6.4 years after treatment withadrenalectomy (n=24) or spironolactone (n=30). At baseline, echocardiographic measurements of patients with primary aldosteronism were compared with those of 274 patients with essential hypertension. Patients with primary aldosteronism had greater left ventricular mass, more prevalent left ventricular hypertrophy, lower early:late-wave diastolic filling velocities ratio, and longer deceleration time than patients with essential hypertension but no differences in relative wall thickness and systolic function. During follow-up, average blood pressure was 135/82 and 137/82 mm Hg in patients treated with adrenalectomy and spironolactone, respectively. In the initial 1-year period, left ventricular mass decreased significantly only in adrenalectomized patients. Subsequent changes in left ventricular mass were greater in patients treated with spironolactone, with an overall change from baseline to the end of follow-upthat was comparable in the 2 groups. Prevalence of hypertrophy decreased in both treatment groups, whereas diastolic parameters had only mild and nonsignificant improvement. Changes in blood pressure and pretreatment plasma aldosterone were independent predictors of left ventricular mass decrease in both treatment groups. Thus, in the long-term, both adrenalectomy and spironolactone are effective in reducing left ventricular mass in patients with primary aldosteronism, with effects that are partially independent of blood pressure changes.Key Words: adrenalectomy • echocardiography • left ventricular hypertrophy • spironolactone • diastolic filling IntroductionTopAbstractIntroductionMethodsResultsDiscussionReferences For many decades, aldosterone has been seen as a hormone almost exclusively involved in the regulation of body fluids, maintenance of electrolyte balance, and blood pressure homeostasis.1More recent views, however, indicate that aldosterone can contribute to cardiac damage independent of blood pressure.2 In animal studies, exposure to excess aldosterone levels has been associated with collagen deposition, myocardial fibrosis, and ventricular remodeling,3 and 2 large clinical trials have reported a significant decrease in the mortality rate of patients with heart failure who were treated with aldosterone antagonists.4,5Primary aldosteronism is a disease associated with hypertension that offers an important clinical opportunity for assessing the effects of excess aldosterone on the cardiovascular systembecause, in this condition, its effects are isolated from those of the renin-angiotensin axis. The widespread use of the aldosterone:renin ratio as a screening test has led to more efficient identification of this endocrine disorder.6,7 Cardiac structural and functional changes are common consequences of hypertensive states and have been demonstrated also in patients with primary aldosteronism, along with some additional surrogate cardiovascular end points (reviewed in Reference 2). Many cross-sectional echocardiographic evaluations and a few short-termfollow-up studies have reported variable results,8–20 with excess left ventricular (LV) hypertrophy and diastolic dysfunction being the most common,8–15 although not uniformly detected,16–20 abnormalities. Wehave further explored the relationship between aldosterone and the heart by assessing, in the long term, cardiac anatomic and functional evolution of patients with primary aldosteronism after treatment withadrenalectomy or aldosterone antagonists. MethodsTopAbstractIntroductionMethodsResultsDiscussionReferences PatientsFifty-four consecutive patients with primary aldosteronism were included in a prospective study. Recruitment of patients, diagnostic criteria, and follow-up have been described in detail in previous publications.21,22 Patients were referred to the hypertension clinic of our university for evaluation of their hypertensive state: 36 patients had persistent hypokalemia, and 27 had hypertension resistant to a triple-drug regimen. Blood pressure was measured by sphygmomanometry, and hypertension was diagnosed according to established guidelines.23 All of thepatients seen at the clinic are screened with extensive testing to define the cause of hypertension. Seven percent of patients with primary aldosteronism were taking no antihypertensive drug, 9% were on monotherapy, and the remaining 84% had multiple-drug treatment with an average of 2.9 drugs per patient. Patients treated with antihypertensive drugs were withdrawn from treatment a minimum of 2 weeks before diagnostic assessment. ß-Blockers, lipophilic calcium antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers were withdrawn for 3 weeks. No patient was taking mineralocorticoid receptor antagonists before the study.Primary aldosteronism was screened by the demonstration of an increased plasma aldosterone:active renin ratio (20)21,24 in the presence of a plasma aldosterone of >150 pg/mL, and the diagnosis was confirmed by the lack of aldosterone suppression (values of 50 pg/mL) after an intravenous saline load (2 L of 0.9% saline infused over 4 hours).25 This test has been shown to be highly effective in the distinction of both tumoral and idiopathic aldosteronism from low-renin essential hypertension.26 Measurements were performed under a normal sodium diet, and 24-hour urinary sodium excretion was checked in all of the patients. Plasma potassium concentration of 3.5 mmol/L was corrected by oral supplementation before the assessment of the plasma aldosterone:active renin ratio and saline suppression test. Differentiation between adrenal adenoma and idiopathic aldosteronism was obtained by high-resolution computed tomography scan, followed by selective adrenal vein sampling (n=14) and/or adrenal scintigraphy with iodocholesterol (n=47), which was performed under dexamethasone suppression. In patients who underwent adrenal vein sampling, adrenal vein cannulation was considered successful if the adrenal vein/inferior vena cava cortisol gradient was 2, and lateralization was defined by measurement of an aldosterone:cortisol ratio in 1 adrenal vein that was 4 times the ratio in the other adrenal vein.7 In all of the patients who underwent adrenalectomy, adenomawas confirmed by histology and normalization of plasma aldosterone concentrations. Primary aldosteronism was treated by either unilateral adrenalectomy or spironolactone (range: 50 to 300 mg/d; average dose: 121 mg/d), and treatment was followed by normalization of blood pressure or significant improvement of hypertension in all of the patients.A total of 274 patients with essential hypertension served as control subjects for baseline comparisons. These patients were recruited at our hypertension clinic and were selected by frequency matching afterspecification of inclusion criteria to avoid age, gender, body mass index, and estimated duration of hypertension as potential confounding variables. In these patients, secondary causes of hypertension were excludedafter an appropriate drug washout. Among patients with essential hypertension, 11% were taking no antihypertensive drug, 16% were on monotherapy, and 73% had multiple-drug treatment with a mean of 2.3 antihypertensive agents per patient. Informed consent was obtained from all of the patients, and the protocol was approved by the local ethics committee.Echocardiographic ExaminationEchocardiography was performed by the same investigators who were unaware of patient diagnosis.27 Measurements of LV internal dimensions and wall thickness were obtained with commercial machines (Sonos HP1000, Hewlett-Packard or Aplio CV, Toshiba Medical Systems) and a 2.5-MHz transducer under bidimensional cross-sectional control, with the patients in the partial left decubitus position. The LV geometric pattern was defined by the ratio of the posterior LV wall thickness to one half of the LV internal dimension, and a value of >0.44 was used to define LV concentric geometry.28 The LV mass index (LVMI) was calculated by the Penn Convention formula29 and adjusted for body height with a cutoff value of 51 g/m2.7 that was used to define LV hypertrophy in both sexes.30 Systolic function was estimated by the ejection fraction and both endocardial and midwall fractional shortening (FS), with the latter taking into account epicardial migration of the midwall during systole.31 Endocardial FS was expressed as a percentage of the value predicted in normal subjects for meridional end-systolic stress.32 Circumferential end-systolic stress was calculated at the midwall,33 and the equation of de Simone et al34 was used to predict expected midwallshortening. The observed:predicted midwall shortening ratio was used as an index of LV systolic performance.35 Pulsed Doppler recordings at the level of the mitral valve tips were obtained from apical 4-chamber scans to measure early and late-wave diastolic filling velocities, their ratio (E/A ratio), and the early wave deceleration time.36Follow-UpAll 54 of the patients with primary aldosteronism were prospectively followed up.21 Twenty four of 29 patients with adrenal adenoma underwent adrenalectomy; among the remaining 5 patients, 2 had bilateral adenoma, and 3 refused surgery and were treated with spironolactone. Treatment with spironolactone was started with a dose of 100 mg/d that was titrated to reach the target blood pressure. Clinical assessment and laboratory tests were repeated 1, 3, and 6 months after enrollment and every 12 months thereafter. At each visit, antihypertensive therapy was adjusted according to the physician's judgment to reach a target of<140/90 mm Hg. The use of all antihypertensive agents was permitted. Echocardiography was repeated after 1 year and after an average follow-up of 6.4 years (range: 3 to 11 years) in all of the patients with primary aldosteronism and in 108 of 274 patients with essential hypertension who were matched for age, gender, body mass index, and estimated duration of hypertension.Statistical AnalysisThis study had a statistical power of >95% to detect 20% differences between patients with primary aldosteronism and essential hypertension, with an -value of 0.05. Variables are expressed as mean±SD unless otherwise indicated. Continuous variables were compared by Student's t test. Variables with skewed distribution were analyzed after logarithmic transformation. Categorical variables were compared by the Pearson's 2 test. The relationships between different variables were examined by linear regression analysis, and the correlation was expressed by the correlation coefficient. Changes from the baseline of echocardiographic parameters were assessed by 2-way ANOVA. Multivariate discriminant analysis was performed to identify variables independently associated with changes in echocardiographic parameters after treatment. All of the tests for significance and resulting P values were 2 sided, with a level of significance of 0.05. ResultsTopAbstractIntroductionMethodsResultsDiscussionReferences Adrenal adenoma was demonstrated in 29 (54%) of 54 patients with primary aldosteronism, whereas the remaining 25 (46%) had no evidence of adrenal masses. As shown in Table 1,patients with primary aldosteronism and essential hypertension had comparable heart rates, blood pressure levels, estimated durations of hypertension, plasma glucose, and plasma lipid profiles. As expected, patients with primary aldosteronism had significantly higher plasma aldosterone and lower plasma potassium and active renin levels than patients with essential hypertension.View this table:[in this window][in a new window] Table 1. Baseline Characteristics of the Study PopulationBaseline echocardiographic parameters are summarized in Table 2. The average LV internal dimensions and wall thickness had nonsignificant trends to higher values, and the LV mass and LVMI were significantlygreater in patients with primary aldosteronism as compared with patients with essential hypertension. The left atrial diameter and the ratio of the posterior LV wall thickness to one half of the LV internal dimension were comparable in the 2 groups. The prevalence of LV hypertrophy and LV concentric geometry was, respectively, 33% and 26% in primary aldosteronism and 21% (P<0.05) and 24% (P=0.73) in essential hypertension, respectively. No significant differences of ejection fraction, endocardial FS, and midwall FS were observed between patients with primary aldosteronism and essential hypertension, indicatingcomparable systolic function. Both the ratio of E/A velocities and the deceleration time were significantly different in the 2 groups, indicating the presence of more severe diastolic dysfunction in primary aldosteronism. In primary aldosteronism, linear regression analysis showed that LVMI, but not the ratio of the posterior LV wall thickness to one half of the LV internal dimension, had a significant relationship with mean blood pressure measured both before (r=0.362; P<0.01) and after (r=0.319; P<0.05) drug washout, duration of hypertension (r=0.375; P<0.01), and plasma aldosterone concentrations (r=0.294; P<0.05); the ratio of E/A velocities was inversely related with duration of hypertension (r=0.391; P<0.01), LVMI (r=0.323; P<0.05), and plasma aldosterone (r=0.304; P<0.05) but not with blood pressure levels. In essential hypertension, LVMI had a statistically significant relationship with mean blood pressure (r=0.194; P<0.01), duration of hypertension (r=0.249; P<0.01), E/A ratio (r=–0.233; P<0.01), and plasma aldosterone (r=0.134; P<0.05). No significant differences in echocardiographic parameters were observed between primary aldosteronism patients with or without computed tomography evidence of adrenal masses.View this table:[in this window][in a new window] Table 2. Baseline Echocardiographic Parameters of the Study PopulationFollow-UpPatients with primary aldosteronism were reassessed with echocardiography after treatment (adrenalectomy: n=24; spironolactone: n=30), at 1 year, and after an the average follow-up of 6.4 years.Antihypertensive medications used during the study are shown in Table 3. The frequency of the use of specific types of drugs was comparable in patients treated with adrenalectomy or spironolactone. Blood pressure declined significantly during the first year, with average values that, during the entire course of the study, were of 135/82 and 137/82 mm Hg in patients who were treated with adrenalectomy and spironolactone, respectively. Treatment was followed by normalization of blood pressure in 21 patients with primary aldosteronism (39%; adrenalectomy: n=10; spironolactone: n=11) and by significant improvement in the remaining 33 (61%; adrenalectomy: n=14; spironolactone: n=19; P=0.71). In the first year, plasma potassium increased significantly from baseline levels (from 3.2±0.4 to 4.2±0.3 mmol/L;P<0.001) and remained stable thereafter. Markers of volume change, such as body weight (from 79.4±10.3 to 78.6±9.3 kg), packed cell volume (from 44±3 to 44±3%), and serum albumin (from 41±2 to 42±3 g/dL), did not change significantly during follow-up.View this table:[in this window][in a new window] Table 3. Antihypertensive Medications Used at Baseline and at End of Follow-UpTable 4 summarizes the echocardiographic measurements obtained at follow-up in patients with primary aldosteronism. During the initial 1-year period, average LV internal dimensions and wall thickness had a nonsignificant trend to decrease in all of the patients with primary aldosteronism. This trend was more evident in patients who were treated with adrenalectomy as compared with patients treated with spironolactone and resulted in a decrease of the LV mass and LVMI that was significant only in the former group at this time point (Figure). Subsequent average changes in LV dimensions and wall thickness were greater in patients treated with spironolactone than in those who had adrenalectomy, with an overall change, from baseline to the end of follow-up, that tended to be greater, although nonsignificantly, in adrenalectomized patients. At the end of follow-up, the prevalence of LV hypertrophy and LV concentric geometry changed from 38% to 8% (P<0.05) and from 29% to 21% (P=0.44), respectively, in adrenalectomizedpatients, and from 30% to 7% (P<0.05) and from 23% to 20% (P=0.75), respectively, in patients treated with spironolactone. The E/A ratio and the deceleration time had nonsignificant trends to change after bothadrenalectomy and spironolactone treatment, suggesting only partial recovery of the diastolic dysfunction after removal of the effects of excess aldosterone. The ratio of the posterior LV wall thickness to one half ofthe LV internal dimension and parameters of systolic function did not change significantly during the study. After 1 year, plasma renin levels increased significantly in both patients who were treated withadrenalectomy (from 4.6±6.0 to 9.3±5.8 pg/mL; P<0.01) and spironolactone (from 5.0±6.6 to 8.8±5.6 pg/mL; P<0.02); at the end of follow-up, renin levels were comparable in the 2 treatment groups (8.9±5.8 and 8.6±5.7 pg/mL, respectively; P=0.85). In both adrenalectomized and spironolactone-treated patients, the reduction of LVMI was directly correlated with changes in mean blood pressure (respectively: r=0.509, P<0.01and r=0.427, P<0.05) and pretreatment plasma aldosterone concentrations (respectively: r=0.413, P<0.05 and r=0.391, P<0.05) but not with pretreatment plasma potassium and active renin. Multivariate analysis showed that changes in mean blood pressure (P<0.05) and pretreatment aldosterone levels (P<0.05) were both independent predictors of LVMI decrease after treatment, and their respective contributions were 47% and 24%. In 108 patients with essential hypertension, the average blood pressure during follow-up was 137/81 mm Hg, and the decrease in LVMI (–11.8%) was significantly smaller than in patients with primary aldosteronism (–17.4%; P<0.05), whereas the frequency of reversal of LV hypertrophy (essential hypertension: from 22% to 8%; primary aldosteronism: from 33% to 7%) did not differ significantly between the groups (P=0.19).View this table:[in this window][in a new window] Table 4. Echocardiographic Parameters of Patients With Primary Aldosteronism Who Were Treated With Adrenalectomy (n=24) or Spironolactone (n=30) at Baseline, After 1 Year, and at the End of Follow-UpView larger version (22K):[in this window][in a new window] Figure. Percentage changes of LVMI in the short- and long-term follow-up in patients with primary aldosteronism who were treated with adrenalectomy(n=24) or spironolactone (n=30). Short-term and long-term follow-up measurements were done after 1 year and after an average period of 6.4 years, respectively. *P<0.05 vs baseline; P<0.01 vs baseline. DiscussionTopAbstractIntroductionMethodsResultsDiscussionReferences Increased LV mass and impaired LV diastolic filling have been reported in patients with primary aldosteronism and might predispose these patients to cardiac complications. Our study has examined the long-term echocardiographic evolution in a large cohort of patients with primary aldosteronism after treatment. Results demonstrate that adrenalectomy and spironolactone are both effective in decreasing the LV mass, although this effect occurs earlier after surgical treatment. In both treatment groups, the LV diastolic filling pattern had only mild and nonsignificant improvement. Pretreatment plasma aldosterone concentrations predict LVMI decrease during follow-up, independent of treatment-related blood pressure changes.A growing body of evidence links aldosterone to development and/or progression of cardiovascular disease, seemingly separate from its effects on blood pressure. In fact, animal and humanstudies support the contention that cardiac damage in aldosteronism is not just the result of a pressure-volume overload but might involve additional endocrine and paracrine mechanisms.2,3Many cross-sectional echocardiographic evaluations have reported an excess increase of LV mass in patients with primary aldosteronism as compared with other types of hypertensive disease,8–15 although this finding has not been confirmed in other studies.16–20 Disparity of the findings could be ascribed to the limited sample size of some studies and differences in the severity and duration of hypertension in selected patients and respective control subjects. The present study has been conducted in a large cohort of patients with primary aldosteronism who were diagnosed usingstandardized procedures that were homogeneously applied by the same physicians.21 This practice, together with the collection of data in a single database, should have limited any possible selection bias. Moreover,patients with primary aldosteronism have been compared with patients with essential hypertension who were appropriately matched for age, sex, severity, and estimated duration of hypertension and who had comparable cardiovascular risk profiles. Our results confirm the presence of greater LV mass and more prevalent LV hypertrophy in patients with primary aldosteronism that is associated with evidence of an abnormal pattern of LV diastolic filling, such as that reported in previous studies,10,11 but not with changes of LV geometry and systolic function.Measurement of increased LV mass in patients with primary aldosteronism might reflect the increased circulating volume resulting from the renal effects of the hormone. However, we have observed greater differences in wall thickness than ventricular volumes between patients with primary aldosteronism and essential hypertension at baseline and greater changes in wall thickness than ventricular volumes after both surgical and medical treatment of primary aldosteronism. This would suggest that the contribution of volume factors is not predominant over other factors and that cardiac changes, in this condition, could not simply be explained by the salt- and water-retaining effects of aldosterone. The cardiac hemodynamic overload is not the only determinant of LV hypertrophy, and various hormones can play specific roles in different subsets ofhypertension. The renin-angiotensin-aldosterone system is an important contributor to the pathogenesis of LV hypertrophy,37 and primary aldosteronism permits evaluation of the cardiac effects of elevated aldosterone independent from those of angiotensin. LV hypertrophy is an important independent predictor of major cardiovascular events38 in hypertension, and increased LV mass in patients with primary aldosteronism might be associated with worse cardiovascular outcome in comparison with other hypertensive groups. Relevant to this point, a recent retrospective study of a large cohort of patients with adrenal adenoma or idiopathic aldosteronism has reported an excess rate of cardiovascular complications and LV hypertrophy in comparison with properly matched patients with essential hypertension.39Cross-sectional evidence of associations between cardiac phenotypes and possible causative factors is of limited value, and findings should be confirmed in longitudinal evaluations. The few echocardiographicobservations of cardiac changes after treatment of aldosteronism are confined to short-term follow-up studies, mostly after removal of an adrenal adenoma.9,10,18 The present study is the first to provide data of a long-term echocardiographic follow-up in a substantial cohort of patients with primary aldosteronism after either surgical or medical treatment. Our 11-year study demonstrates that patients treated with eitheradrenalectomy or spironolactone have significant decrease of LVMI, a response that occurs within the first year only after surgical treatment. In both treatment groups, baseline LVMI was directly correlated with plasma aldosterone concentration, and this concentration was an independent predictor of changes of LVMI after treatment. Data demonstrate that the decrease of LVMI is only partially explained by blood pressure changes, suggesting a role of aldosterone that is independent from the hemodynamic overload. This possibility would also be supported by the observation that, in patients with essential hypertension, the decrease ofLVMI that occurred during follow-up in the presence of very similar blood pressure values was significantly smaller than in patients with primary aldosteronism.Mineralocorticoid receptors have been demonstrated in human cardiomyocytes,40 and their activation might play a role in myocardial hypertrophy and cardiac remodeling41 in patients with primary aldosteronism via mechanisms that include modulation of ionic movements42 and accelerated fibrosis.43 The latter mechanism might, in turn, result from interactions of aldosterone with angiotensin, endothelin, and bradykinin; activation of inflammatory cells; and stimulation of fibroblast proliferation and collagen synthesis (reviewed in References 41 and 43). Interruption of these receptor-mediated mechanisms might explain why, in the long term, treatment of primary aldosteronism with aldosterone receptor antagonists has comparable effects to the removal of an aldosterone-secreting adenoma in reducing LV mass, although this response occurs later than after the removal of excess circulating aldosterone by adrenalectomy. From a pathophysiological point of view, persistent hyperaldosteronemia with possible involvement of nongenomic effects ofaldosterone2,3 might hypothetically explain why regression of LV hypertrophy requires a longer time to occur in patients treated with spironolactone than in those treated with surgery. Consistent with our findings, favorable effects of mineralocorticoid antagonists on reduction of LV mass have been reported in patients with essential hypertension and LV hypertrophy.44 In these patients, effects of aldosterone antagonists resulted to be additive with those of angiotensin-converting enzyme inhibitors and, therefore, independent from the renin-angiotensin axis. In the present study, no patient in the essential hypertension group was treated with spironolactone.Some limitations of our study need to be highlighted. First, given that we performed selective adrenal vein sampling in only 14 of our patients and, instead, mainly relied on computed tomography and adrenal scintigraphy for subtype differentiation, it is possible that we have misclassified some patients with aldosterone-producing adenoma as idiopathic hyperplasia or vice versa. More accurate detection of truly unilateral forms of primary aldosteronism may have resulted in better blood pressure and echocardiographic responses to adrenalectomy than were seen in this study. Second, the majority of patients were on treatment at the time of study, and the use of certain antihypertensive medications during follow-up might have influenced the echocardiographic evolution. For instance, angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers could be more effective than other agents in reducing the LV mass,45 but frequency of the use of these drugs was comparable in patients treated with adrenalectomy or spironolactone. Nonetheless,differences in the pretreatment status and in drugs used at baseline and during follow-up might have had significant impact on the cardiac outcome of the study patients. Third, the doses of spironolactone that have been used in this study are higher than those that are currently recommended for medical treatment of primary aldosteronism, and, therefore, extrapolation of the results to a more general context should be done with caution. With regard to this issue, further investigation of the cardiac effects of the newer aldosterone-receptor antagonists, such as eplerenone, which offer the opportunity to use relatively higher doses without antiandrogenic effects, is warranted. Last, our study might have underestimated the impact of blood pressure on cardiac structure, because we did not include measurements of the 24-hour blood pressure profile, which is superior to clinic blood pressure for the prediction of LV mass.46 Results of previous studies with ambulatory blood pressure monitoring in primary aldosteronism are controversial, with some studies reporting significant differences with essential hypertension47,48 and others not supporting this contention.11,15 In our hands, comparison of ambulatory blood pressure profiles in subsets of the primary aldosteronism (n=32) and essential hypertension (n=153) group did not show significant differences.PerspectivesRecovery of cardiac anatomic and/or functional abnormalities and prevention of cardiovascular events are primary goals of treatment in hypertensive patients. Primary aldosteronism was once considered to account for <1% of all forms of hypertension, but recent work suggests that it might be the most common curable cause, worth screening for in patients with high blood pressure and an index of suspicion, including those with hypokalemia and/or resistance to treatment. This study presents evidence that primary aldosteronism is associated with LV hypertrophy out of proportion to blood pressure levels that benefits substantially from treatment in the long term. In this view, adrenalectomy and mineralocorticoid receptor blockade appear to be of considerable therapeutic value inasmuch as they significantly reduce LV mass, whereas their beneficial effect on the LV diastolic filling pattern is only partial. These findings underscore the importance of a timely identification of this endocrine disorder to obtain regression of cardiac abnormalities. Future studies will have to address the potential benefits of the newest mineralocorticoid receptor antagonists on cardiac structural and functional abnormalities of primary aldosteronism and to clarify whether these therapeuticinterventions can effectively prevent late cardiovascular complications. Acknowledgments Sources of FundingThis work was supported by research grants from the Italian Ministry of the University and Scientific and Technologic Research (to L.A.S. and C.C.) and by research grants from the Italian Society of Hypertension (to G.L.C. and E.N.).DisclosuresNone. Footnotes Continuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz.Received May 28, 2007; first decision June 25, 2007; accepted September 4, 2007. ReferencesTopAbstractIntroductionMethodsResultsDiscussionReferences 1 Freel EM, Connell JM. Mechanisms of hypertension: the expanding role of aldosterone. 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[Full Text] [PDF] This ArticleAbstract Full Text (PDF)CME: Take the course for this article:Hypertension: November 2007, Volume 50, Number 5All Versions of this Article:50/5/911 most recentHYPERTENSIONAHA.107.095448v1Alert me when this article is citedAlert me if a correction is postedCitation MapServicesEmail this article to a friendSimilar articles in this journalSimilar articles in PubMedAlert me to new issues of the journalDownload to citation managerRequest PermissionsCiting ArticlesCiting Articles via HighWireCiting Articles via Google ScholarGoogle ScholarArticles by Catena, C.Articles by Sechi, L. A.Search for Related ContentPubMedPubMed CitationArticles by Catena, C.Articles by Sechi, L. A.Related CollectionsHypertrophy Clinical Studies Other TreatmentRelated ArticleHypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | SearchCopyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.> > >> > > > On this board the lack of studies of long-term follow-up of > > patients> > > > after adrenalectomy is often mentioned. I got curious and > > started to> > > > look for studies of long-term follow-up of patients who manage > > their> > > > PA medically.> > > >> > > > I don't have access to full-text databases, so I'm probably > > missing> > > > a good chunk of literature. However, all I could find was this:> > > > http://www.annals.org/content/131/2/105.full.pdf+html> > > >> > > > If anyone here can point me to similar full-text links, I'd> > > > appreciate it. I didn't find this article to be especially > > positive> > > > - it's as if we really don't have any one good option, be it > > surgery> > > > or meds!> > > >> > > >> > > >> > >> >> >> >>

[Guest guest]

We need to set up our own file of interviews with pts which we can do with Skype I think. Anyone know how to do this? I can moderate.CE Grim MDYou may want to keep up with Flowerspy conn's blog. http://hyperaldosteronism.blogspot.com/--- In hyperaldosteronism , "msmith_1928" wrote:>> Saw that one, thanks.> > I'm actually most interested in quality-of-life issues, which I suspect will not be addressed in medical journals. Things like development of side effects, need to increase dosage or add other meds, etc. particularly as compared with adrenalectomy patients.> > > > > > >> > > > > > On this board the lack of studies of long-term follow-up of> > > > patients> > > > > > after adrenalectomy is often mentioned. I got curious and> > > > started to> > > > > > look for studies of long-term follow-up of patients who manage> > > > their> > > > > > PA medically.> > > > > >> > > > > > I don't have access to full-text databases, so I'm probably> > > > missing> > > > > > a good chunk of literature. However, all I could find was this:> > > > > > http://www.annals.org/content/131/2/105.full.pdf+html> > > > > >> > > > > > If anyone here can point me to similar full-text links, I'd> > > > > > appreciate it. I didn't find this article to be especially> > > > positive> > > > > > - it's as if we really don't have any one good option, be it> > > > surgery> > > > > > or meds!> > > > > >> > > > > >> > > > > >> > > > >> > > >> > > >> > > >> > >> >>