Prognostic value of secondary hyperaldosteronism in patients with chronic heart failure with preserved ejection fraction

Purpose: to investigate the prognostic value of secondary hyperaldosteronism patients with heart failure with preserved ejection fraction. Materials and methods: prospective cohort study included 158 patients with hyperaldosteronism and heart failure with preserved ejection fraction. Baseline blood aldosterone levels were determined in all patients. Hyperaldosteronemia was diagnosed when the plasma aldosterone level was > 160 pg/ml. The primary endpoint was all-cause mortality. Results: at baseline, hyperaldosteronemia was detected in 59 of 158 patients (37.3%). Hyperaldosteronemic patients were younger, had higher functional class and NT-proBNP level, and a higher rate of comorbidity (all Ps <0.05). Over a median follow‐up of 32 (28-38) months, a total of 50 (37.6%) patients died. Cardiovascular death occurred in 32 (20.3%) cases, non-cardiovascular – in 18 (11.4%) cases. A total of 65 (41.1%) patients were hospitalized for HF. High aldosterone levels were associated with a significant (p <0.05) increase in the risk of hospitalization for HF (adjusted odds ratio (OR) 2.14, 95% confidence interval (CI) 1.34-9.68), all-cause death (OR 1.64; 95% CI 1.23-7.65, P = 0.033) and HF death (OR 1.56; 95 % CI 1.14-11.3, P = 0.021). Conclusion: Hyperaldosteronism in patients with heart failure with preserved ejection fraction secondary hyperaldosteronism is an independent predictor of hospitalization for heart failure, all-cause, and cardiovascular mortality. The inclusion of plasma aldosterone level in the existing prognosis models of heart failure with preserved ejection fraction will help improve their predictive value and optimize the management of high-risk patients.

Association Between Hyperaldosteronemia and Electrophysiological Myocardial Activity in Heart Failure with Preserved Ejection Fraction

Background. Sudden cardiac death, one of the most common types of cardiac death, is most often triggered by ventricular arrhythmia. Plasma aldosterone level has been shown to be an independent risk factor of life-threatening ventricular arrhythmia in patients with left ventricular systolic dysfunction following acute myocardial infarction. Whether either effect also occurs in patients with heart failure and preserved ejection fraction is currently unknown. Purpose. The study aims to investigate the relationship between plasma aldosterone level and ventricular arrhythmias in longterm heart failure with preserved ejection fraction. Methods. A cross-sectional study included 158 patients (58 men and 100 women, mean age 62.3±7.4 years) with heart failure with preserved ejection fraction (> 50%). Patients had no history of primary aldosteronism and did not use the mineralocorticoid receptor antagonists during the last 6 weeks. Aldosterone plasma level was measured and 24-hour electrocardiographic monitoring was performed. Results. According to laboratory results 99 patients (62.7%, 95% confidence interval 55.0-70.0%) had normal (40-160 pg/ml) aldosterone plasma level (nAld) and 59 patients (37.3%, 95% CI 30.0-45.0%) had high (> 160 pg/ml) aldosterone level (hAld). hAld patients more often had QTc prolongation (44.1% versus 18.2%) and ventricular arrhythmias (83.1% vs 61.6%) compared to nAld patients (all Ps <0.001). The number of ventricular premature complexes in 24 hours were higher in hAld group (median 214, range 64-758) compared to nAld (median 52, range 16-198, P < 0.003). hAld patients more often occurred bigemy, couple ventricular ectopy and nonsustained ventricular tachycardia (39.0% vs 19.0%, р=0.01). In Cox regression model’s high aldosterone plasma level was the independent risk factors of QTc prolongation (odds ratio 1.6, 95% confidence interval 1.1-5.7, p=0.034) and prognostically unfavorable ventricular arrhythmias (odds ratio 1.8, 95% confidence interval 1.2-6.8, p=0.024). Conclusion. In long-term HFpEF plasma aldosterone level is significantly related to QTc prolongation as well as ventricular arrhythmias.

P1391Plasma aldosterone level in different forms of atrial fibrillation

Background. Hyperactivation of the renin-angiotensin-aldosterone system plays a key role in the development of structural remodeling underlying the atrial fibrillation (AF). Nevertheless, the role of excessive aldosterone production in AF development has not been studied. Purpose. The study aims to evaluate the aldosterone levels in different forms of AF and sinus rhythm. Methods. The study included 130 patients (the main group) with non-valvular AF. Of these, 40 (30.8%) patients had permanent, 50 (38.4%) – persistent and 40 (30.8%) – paroxysmal AF. The control group consisted of 40 patients with cardiovascular pathology, who did not have a history of AF episodes. Plasma aldosterone levels were measured by immunoenzyme method. In patients with paroxysmal and persistent AF measurement was perfomed during AF episode before restoration of sinus rhythm. Aldosterone reference values was considered as 40-160 pg/ml. Results. Aldosterone levels were significantly higher in patients of the main group compared to the control (141.5 ± 41.8 pg/ml vs 105.0 ± 33.1 pg/ml, P &lt; 0.001). It was the highest in paroxysmal and persistent AF and lower – in permanent AF. Hyperaldosteronemia (&gt;160 pg/ml) prevalence was significantly higher among all patients of AF group compared to the control (32.3% vs 7.5%, respectively, P = 0.004), however multiple comparisons showed significant differences between paroxysmal AF (47.5%) and sinus rhythm only. Conclusion. Plasma aldosterone level is significantly higher in AF compared to sinus rhythm. In patients with paroxysmal and persistent AF it’s concentration is higher than in patients with permanent AF.

P480Aldosterone plasma level as risk factor of ventricular arrhythmias in heart failure with preserved ejection fraction

Background. Sudden cardiac death, one of the most common types of cardiac death, is most often triggered by ventricular arrhythmia. Plasma aldosterone level has been shown to be an independent risk factor of life-threatening ventricular arrhythmia in patients with left ventricular systolic dysfunction following acute myocardial infarction. Whether either effect also occurs in patients with heart failure and preserved ejection fraction (HFpEF) is currently unknown. Purpose. The study aims to investigate the relationship between plasma aldosterone level and ventricular arrhythmias in long-term HFpEF. Methods. The study included 158 patients (58 men and 100 women, mean age 62.3 ± 7.4 years) with HFpEF (&gt; 50%). All patients had a history of hospitalization due to HFpEF during the last 12 months, left ventricular diastolic dysfunction and / or elevated NT-proBNP level. Median confirmed HFpEF duration was 5 (range 4-8) years. Patients had no history of primary aldosteronism and did not use the mineralocorticoid receptor antagonists during the last 6 weeks. Aldosterone plasma level was measured and 24-hour electrocardiographic monitoring was performed. Results. According to laboratory results 99 patients (67.1%, 95% confidence interval (CI) 59.6-74.2%) had normal (40-160 pg/ml) aldosterone plasma level (nAld) and 59 patients (37.3%, 95% CI 30.0-45.0%) had high (&gt; 160 pg/ml) aldosterone level (hAld). hAld patients more often had QTc prolongation (44.1% versus 18.2%) and ventricular arrhythmias (83.1% vs 61.6%) compared to nAld patients (all Ps &lt; 0.001). The number of ventricular premature complexes in 24 hours was higher in hAld group (median 214, range 64-758) compared to nAld (median 52, range 16-198, P &lt; 0.003). hAld patients more often occurred bigemy, couple ventricular ectopy and nonsustained ventricular tachycardia (39.0% vs 19.0%, P = 0.01). In Cox regression models high aldosterone plasma level was the independent risk factors of QTc prolongation (odds ratio (OR) 1.6, 95% CI 1.1-5.7, P = 0.034) and prognostically unfavorable ventricular arrhythmias (OR 1.8, 95% CI 1.2-6.8, P = 0.024). Conclusion. In long-term HFpEF plasma aldosterone level is significantly related to QTc prolongation as well as ventricular arrhythmias.

Aldosterone levels and the -344t/C aldosterone synthase in individuals with a family history of hypertension

Background: Genetic factors play an important role in the determination of hypertensive disease in a family. The -344T/C the aldosterone synthase gene has been reported in various populations closely related to hypertension. The aim of this study was to determine the presence of the -344T/C polymorphism of the aldosterone synthase gene and the levels of plasma aldosterone in individuals with and without a family history of hypertension.Methods: This study was a case control design, with healthy individuals with a family history of hypertension as cases (n-42) and those without a family history of hypertension as controls (n=41). The subjects’ plasma aldosterone levels were analysed by enzyme-link immunosorbent assay (ELISA) and the gene polymorphism was analysed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The data were analysed by an independent sample T-test and Chi square test, and the significance level was set at P<0.05.Result: The frequency of the TT + TC genotype was higher in cases, and this increase was significant different compared to the controls (P<0.046). The frequency of the TT + TC genotype was 2.56 higher in cases than controls. The frequency of the C allele in cases was also significantly different compared to the controls (P = 0.039) and 2.29 more frequent in cases than the controls (P = 0.039). The plasma aldosterone level was 42.35 pg/dL in cases and 34.9 pg/dL in controls (P = 0.616). Plasma aldosterone level in cases with the CC, TC and TT genotypes were 48.29, 40.8 and 35.2 pg/dL, respectively (P = 0.774). Our study concludes that individuals with a family history of hypertension are at a higher risk of developing hypertension. Follow-up studies are required to determine the incidence of hypertension in a person with a family history of hypertension and who is a carrier of genetic risk factors.Bangladesh Journal of Medical Science Vol.15(3) 2016 p.435-440