Prevalence, Biochemical and Clinical Characteristics of Resistant Hypertension

2018 ◽  
Vol 69 (10) ◽  
pp. 2845-2849
Author(s):  
Daniela Gurgus ◽  
Elena Ardeleanu ◽  
Carmen Gadau ◽  
Roxana Folescu ◽  
Ioan Tilea ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Resistant Hypertension ◽  
Clinical Characteristics ◽  
Salt Intake ◽  
Target Organ Damage ◽  
Multivariate Logistic Regression Analysis ◽  
Organ Damage ◽  
Left Ventricular ◽  
High Salt Intake

The objectives of the present study were to evaluate the prevalence of resistant hypertension (RH) in primary care setting and to analyse its biochemical and clinical characteristics. After 3 months of treatment and evaluation, 721 (14.01%) of 5,146 patients with hypertension did not reach target office blood pressure of [ 140/90 mmHg. After exclusion of �white-coat effect� with ambulatory blood pressure, of secondary and pseudo- resistant hypertension, prevalence of RH was 6.74%. Lifestyle factors associated with RH were physical inactivity, obesity, high salt intake, smoking and excessive alcohol ingestion. Compared to controlled hypertension, RH patients presented higher incidence of family history of cardiovascular disease (38.90% vs 25.94%), diabetes mellitus (34.87% vs 19.01%), impaired fasting glucose (21.91% vs 19.07%), target organ damage (29.1% vs 15.95%), and cardiovascular disease (27.09% vs 17.06%). Dyslipidaemia (52.90% vs 42.03%), fasting plasma glucose (116.10�38.9 vs 107.80�37.2), HbA1c (6.41�1.42 vs 5.96�0.94), serum creatinine (1.09�0.27 vs 1.03�0.24) and microalbuminuria (21.90% vs 10.95%) were significantly higher in RH. Predictors of RH, determined by a multivariate logistic regression analysis were left ventricular hypertrophy (OD 2.14, 95% CI 1.32-3.69), renal impairment expressed as eGFR [ 60 ml/min/1.73m2 (OD 1.62, 95% CI 1.21-2.21) and the presence of cardiovascular disease (OD 1.48, 95% CI 1.02-2.16).

Abstract P150: Aldosterone Dysregulation Increases Cardiovascular Risk in African-American Youth

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Gregory A Harshfield ◽  
Evan Mulloy ◽  
Melinda Beavers
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
African American ◽  
African Americans ◽  
Early Development ◽  
Salt Intake ◽  
Target Organ Damage ◽  
Target Organ ◽  
High Salt ◽  
High Salt Intake

Background: The prevalence of hypertension and blood pressure-related target organ damage in African-Americans is among the highest in the world. We hypothesize that this is in part due to aldosterone dysregulation among African-Americans beginning in youth and leading to the early development of cardiovascular disease in this population. To begin to test this hypothesis, we examined ethnic differences in aldosterone regulation in normal, healthy adolescents. Methods: The subjects in this study were 145 (60 Caucasian, 85 African-American) healthy, normotensive youth aged 15–19 years. Testing was performed following 72 hours on a controlled sodium diet. Testing consisted of the collection of aldosterone, systolic blood pressure (SBP), and urinary sodium excretion (U Na V) during continuous water intake (400 ml total) over a 2 hour period. An echocardiogram was also performed to measure target organ changes. Log transformations were performed on aldosterone levels prior to analyses. Results: African-American compared to Caucasian subjects had higher casual SBP (109±10 v 104±10; p=.006) and relative wall thickness (0.32±.03 v 0.34±.04; p=.003). During the testing procedure African-Americans also had lower levels of aldosterone (4.78±.6 v 4.35±.6 pg/ml; p =.001). In the Caucasian subjects only, aldosterone was inversely correlated with U Na V (r=−0.427; p=.001) and U Na V was positively correlated with SBP (r=0.356; p=.001). The subjects were divided into those in the upper and lower quartiles of salt intake for further analysis. The interaction between race and salt intake was significant for aldosterone (F=7.173; p=.008). Caucasian subjects with high salt intake had lower aldosterone (4.56±.59 v 5.02±0.59 pg/ml). However, aldosterone levels did not differ by salt intake in African-Americans. Summary and Conclusion: African-American subjects did not show the expected associations between aldosterone and the pressure natriuresis relation. Furthermore, African-Americans on the high salt intake failed to suppress aldosterone. These findings are consistent with our hypothesis that aldosterone dysregulation in youth may lead to the early development of cardiovascular disease in Africans-Americans.

scholarly journals Correlation among high salt intake, blood pressure variability, and target organ damage in patients with essential hypertension

Medicine ◽  
2020 ◽  
Vol 99 (14) ◽  
pp. e19548
Author(s):  
Wei Cai ◽  
MingJian Lang ◽  
XiaoBo Jiang ◽  
Qian Yu ◽  
Congliang Zhou ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Blood Pressure Variability ◽  
Salt Intake ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ ◽  
High Salt ◽  
High Salt Intake

AT1receptor antagonism attenuates target organ effects of salt excess in SHRs without affecting pressure

2008 ◽  
Vol 294 (2) ◽  
pp. H853-H858 ◽  
Author(s):  
Jasmina Varagic ◽  
Edward D. Frohlich ◽  
Dinko Susic ◽  
Jwari Ahn ◽  
Luis Matavelli ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Myocardial Fibrosis ◽  
Salt Intake ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Dietary Salt ◽  
High Salt Intake

Our recent studies have demonstrated that salt excess in the spontaneously hypertensive rat (SHR) produces a modestly increased arterial pressure while promoting marked myocardial fibrosis and structural damage associated with altered coronary hemodynamics and ventricular function. The present study was designed to determine the efficacy of an angiotensin II type 1 (AT1) receptor blocker (ARB) in the prevention of pressure increase and development of target organ damage from high dietary salt intake. Eight-week-old SHRs were given an 8% salt diet for 8 wk; their age- and gender-matched controls received standard chow. Some of the salt-loaded rats were treated concomitantly with ARB (candesartan; 10 mg·kg−1·day−1). The ARB failed to reduce the salt-induced rise in pressure, whereas it significantly attenuated left ventricular (LV) remodeling (mass and wall thicknesses), myocardial fibrosis (hydroxyproline concentration and collagen volume fraction), and the development of LV diastolic dysfunction, as shown by longer isovolumic relaxation time, decreased ratio of peak velocity of early to late diastolic waves, and slower LV relaxation (minimum first derivative of pressure over time/maximal LV pressure). Without affecting the increased pulse pressure by high salt intake, the ARB prevented the salt-induced deterioration of coronary and renal hemodynamics but not the arterial stiffening or hypertrophy (pulse wave velocity and aortic mass index). Additionally, candesartan prevented the salt-induced increase in kidney mass index and proteinuria. In conclusion, the ARB given concomitantly with dietary salt excess ameliorated salt-related structural and functional cardiac and renal abnormalities in SHRs without reducing arterial pressure. These data clearly demonstrated that angiotensin II (via AT1receptors), at least in part, participated importantly in the pressure-independent effects of salt excess on target organ damage of hypertension.

Abstract 117: Preclinical Target Organ Damage Changes in Patients with Resistant Hypertension Randomized to Renal Denervation or Spironolactone as Add-on Therapy. Results From the DENERVHTA Study

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Anna Oliveras ◽  
Pedro Armario ◽  
Laia Sans ◽  
Albert Clarà ◽  
Susana Vázquez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistant Hypertension ◽  
Renal Denervation ◽  
Linear Models ◽  
Antihypertensive Drugs ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Group Differences

Objective: To compare the effect of renal denervation (RDN) and spironolactone, two proposed therapeutic strategies for the treatment of patients with resistant hypertension (RH), on preclinical target organ damage (pTOD). Methods: Patients with office systolic blood pressure (SBP) ≥150 mmHg and 24h-SBP ≥140 mmHg despite receiving ≥3 full-dose antihypertensive drugs, one a diuretic, but none aldosterone antagonist, were randomized to receive RDN or spironolactone (50mg), as add-on therapy. Changes (Δ) in 24h-BP, as well as Δ in urinary albumin excretion (ΔUAE), carotid-femoral pulse-wave velocity (ΔcfPWV), carotid intima-media thickness (ΔIMT), left ventricular mass index (ΔLVMI) and E/e’ (ΔE/e’), a marker of hypertension-induced diastolic dysfunction, were evaluated at 6 months. Between-group comparisons of ΔUAE (after log transformation), ΔcfPWV, ΔIMT, ΔLVMI and ΔE/e’ were carried out by generalized linear models before and after adjusting by Δ24h-SBP and the corresponding baseline value. Results: Twenty-four patients (mean age 64±8 yr) were included. Mean baseline-adjusted difference (95% CI) between the two groups (Spironolactone vs.RDN) at 6 months in 24h-SBP (mmHg) was of-17.9 (-30.9 to -4.9), p=0.01. As shown in the table, there were no statistically significant between-group differences in Δ on pTOD. Conclusion: Changes at 6 months on pTOD as assessed by UAE, cfPWV, IMT, LVMI and E/e’, were not associated with the therapeutic add-on strategy used to reduce high blood pressure in RH patients. We cannot discard that the high variability of some of these markers, especially UAE, could account for this lack of statistically significant between-group differences.

Abstract 432: Race Differences in the Relationship between Urinary ET-1 and BP-related Target Organ Damage in Youth

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Gregory A Harshfield ◽  
Gregory A Harshfield ◽  
Jennifer Pollock ◽  
David Pollock
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Mass ◽  
Target Organ Damage ◽  
Albumin Excretion Rate ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Related Target ◽  
Ventricular Mass ◽  
Lv Mass

The overall goal of this study was to determine race/ethnic differences in the associations between renal ET-1 and indices of blood pressure-related target organ damage in healthy adolescents. The subjects ranged in age between 15-19 years, had no history of any disease, and were not on any prescription medications. The 92 subjects consisted of 48 Caucasians (CA) and 44 African-Americans (AA). The two groups were similar with respect to height, weight, body mass index, blood pressure, ET-1), albumin excretion rate (AER), and left ventricular mass). Results: The CA’s were slightly older 17±1 v 16±1 (p=.02). The protocol was preceded by a 3 day self-selected sodium controlled diet of 250 mEq/day day which the subject picked up each day. The test day began with an echocardiogram for the assessment of left ventricular mass. Next, the subjects were seated for 60 minutes of rest during which the subjects consumed 200 ml of water. This was followed by the collection of a urine sample for the measurement of ET-1 and AER. Overall, ET-1 excretion was correlated with AER (r=.278), LV mass/ht 2.7 (r=.341), and systolic blood pressure (SBP; r=.365; p=.01 for each). The significant overall correlations were the result of significant correlations in AAs for AER (r=.344; p=.05), LV mass/ht 2.7 (r=.520; p=.01), and SBP (r=.645; p=.01) which were not apparent in CA’s. These findings suggest urinary ET-1 contributes to the development of BP-related target organ damage in AA youths prior to the development of increases in blood pressure.

scholarly journals Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

2020 ◽  
Vol 17 (8) ◽  
pp. 2811 ◽  
Author(s):  
Federica Nista ◽  
Federico Gatto ◽  
Manuela Albertelli ◽  
Natale Musso
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Sodium Intake ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Main Role ◽  
Sodium Consumption

Salt intake is too high for safety nowadays. The main active ion in salt is sodium. The vast majority of scientific evidence points out the importance of sodium restriction for decreasing cardiovascular risk. International Guidelines recommend a large reduction in sodium consumption to help reduce blood pressure, organ damage, and cardiovascular risk. Regulatory authorities across the globe suggest a general restriction of sodium intake to prevent cardiovascular diseases. In spite of this seemingly unanimous consensus, some researchers claim to have evidence of the unhealthy effects of a reduction of sodium intake, and have data to support their claims. Evidence is against dissenting scientists, because prospective, observational, and basic research studies indicate that sodium is the real villain: actual sodium consumption around the globe is far higher than the safe range. Sodium intake is directly related to increased blood pressure, and independently to the enlargement of cardiac mass, with a possible independent role in inducing left ventricular hypertrophy. This may represent the basis of myocardial ischemia, congestive heart failure, and cardiac mortality. Although debated, a high sodium intake may induce initial renal damage and progression in both hypertensive and normotensive subjects. Conversely, there is general agreement about the adverse role of sodium in cerebrovascular disease. These factors point to the possible main role of sodium intake in target organ damage and cardiovascular events including mortality. This review will endeavor to outline the existing evidence.

scholarly journals Intrinsic and extrinsic epigenetic age acceleration are associated with hypertensive target organ damage in older African Americans

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Jennifer A. Smith ◽  
Jeremy Raisky ◽  
Scott M. Ratliff ◽  
Jiaxuan Liu ◽  
Sharon L. R. Kardia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Dna Methylation ◽  
African Americans ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Effect Modification ◽  
Target Organ ◽  
Epigenetic Age ◽  
Epigenetic Age Acceleration

Abstract Background Epigenetic age acceleration, a measure of biological aging based on DNA methylation, is associated with cardiovascular mortality. However, little is known about its relationship with hypertensive target organ damage to the heart, kidneys, brain, and peripheral arteries. Methods We investigated associations between intrinsic (IEAA) or extrinsic (EEAA) epigenetic age acceleration, blood pressure, and six types of organ damage in a primarily hypertensive cohort of 1390 African Americans from the Genetic Epidemiology Network of Arteriopathy (GENOA) study. DNA methylation from peripheral blood leukocytes was collected at baseline (1996–2000), and measures of target organ damage were assessed in a follow-up visit (2000–2004). Linear regression with generalized estimating equations was used to test for associations between epigenetic age acceleration and target organ damage, as well as effect modification of epigenetic age by blood pressure or sex. Sequential Oligogenic Linkage Analysis Routines (SOLAR) was used to test for evidence of shared genetic and/or environmental effects between epigenetic age acceleration and organ damage pairs that were significantly associated. Results After adjustment for sex, chronological age, and time between methylation and organ damage measures, higher IEAA was associated with higher urine albumin to creatinine ratio (UACR, p = 0.004), relative wall thickness (RWT, p = 0.022), and left ventricular mass index (LVMI, p = 0.007), and with lower ankle-brachial index (ABI, p = 0.014). EEAA was associated with higher LVMI (p = 0.005). Target organ damage associations for all but IEAA with LVMI remained significant after further adjustment for blood pressure and antihypertensive use (p < 0.05). Further adjustment for diabetes attenuated the IEAA associations with UACR and RWT, and adjustment for smoking attenuated the IEAA association with ABI. No effect modification by age or sex was observed. Conclusions Measures of epigenetic age acceleration may help to better characterize the functional mechanisms underlying organ damage from cellular aging and/or hypertension. These measures may act as subclinical biomarkers for damage to the kidney, heart, and peripheral vasculature; however more research is needed to determine whether these relationships remain independent of lifestyle factors and comorbidities.

scholarly journals Epigenetic loci for blood pressure are associated with hypertensive target organ damage in older African Americans from the genetic epidemiology network of Arteriopathy (GENOA) study

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Minjung Kho ◽  
Wei Zhao ◽  
Scott M. Ratliff ◽  
Farah Ammous ◽  
Thomas H. Mosley ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Dna Methylation ◽  
African Americans ◽  
Genetic Epidemiology ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Cpg Sites ◽  
Cell Counts

Abstract Background Hypertension is a major modifiable risk factor for arteriosclerosis that can lead to target organ damage (TOD) of heart, kidneys, and peripheral arteries. A recent epigenome-wide association study for blood pressure (BP) identified 13 CpG sites, but it is not known whether DNA methylation at these sites is also associated with TOD. Methods In 1218 African Americans from the Genetic Epidemiology Network of Arteriopathy (GENOA) study, a cohort of hypertensive sibships, we evaluated the associations between methylation at these 13 CpG sites measured in peripheral blood leukocytes and five TOD traits assessed approximately 5 years later. Results Ten significant associations were found after adjustment for age, sex, blood cell counts, time difference between CpG and TOD measurement, and 10 genetic principal components (FDR q < 0.1): two with estimated glomerular filtration rate (eGFR, cg06690548, cg10601624), six with urinary albumin-to-creatinine ratio (UACR, cg16246545, cg14476101, cg19693031, cg06690548, cg00574958, cg22304262), and two with left ventricular mass indexed to height (LVMI, cg19693031, cg00574958). All associations with eGFR and four associations with UACR remained significant after further adjustment for body mass index (BMI), smoking status, and diabetes. We also found significant interactions between cg06690548 and BMI on UACR, and between 3 CpG sites (cg19693031, cg14476101, and cg06690548) and diabetes on UACR (FDR q < 0.1). Mediation analysis showed that 4.7% to 38.1% of the relationship between two CpG sites (cg19693031 and cg00574958) and two TOD measures (UACR and LVMI) was mediated by blood pressure (Bonferroni-corrected P < 0.05). Mendelian randomization analysis suggests that methylation at two sites (cg16246545 and cg14476101) in PHGDH may causally influence UACR. Conclusions In conclusion, we found compelling evidence for associations between arteriosclerotic traits of kidney and heart and previously identified blood pressure-associated DNA methylation sites. This study may lend insight into the role of DNA methylation in pathological mechanisms underlying target organ damage from hypertension.

P3833Low heart rate variability is associated with future arrhythmic events in hypertension

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Terentes-Printzios ◽  
C Vlachopoulos ◽  
L Korogiannis ◽  
G Christopoulou ◽  
P Xydis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Primary Endpoint ◽  
Target Organ Damage ◽  
Roc Curves ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Increased Risk

Abstract Background/Introduction Cardiac autonomic dysfunction and target organ damage are associated with increased cardiovascular mortality and arrhythmias. Purpose The aim of the study was to investigate the effect of heart rate variability (HRV) and markers of target organ damage in the prognosis of future arrhythmic events. Methods We studied 292 untreated at baseline hypertensives (mean age 53±13, 153 males). Cardiac autonomic function was evaluated by analysis of short-term HRV measures over 24-h using 24-h ambulatory blood pressure monitoring and the standard deviation of the measurements. Echocardiography was also performed and left ventricular mass index (LVMI) was estimated with the Demereux formula. Aortic stiffness was assessed with carotid-femoral pulse wave velocity (cfPWV) and wave reflections with aortic augmentation index corrected for heart rate (Alx@75). Patients were followed up for a median period of 13 years. The primary endpoint was a composite of atrial/ventricular tachycardias, symptomatic multiple premature ventricular contractions, second and third-degree heart blocks and pacemaker/defibrillator placement. Results In comparison without events, patients with the primary endpoint (n=37, 13%) had lower 24-h daytime HRV (9.6 beats per minute vs. 11.1 beats per minute, p=0.005), higher systolic blood pressure (168 mmHg vs. 163 mmHg, p=0.003), higher cfPWV (8.4 m/s vs. 7.7 m/s, p=0.005), higher LVMI (133 g/m2 vs. 122 g/m2, p=0.002) and higher AIx@75 (29.0% vs. 26.3%, p=0.043). In further analysis, receiver operating characteristic (ROC) curves were generated to evaluate the ability of HRV, cfPWV, LVMI and AIx@75 to discriminate subjects with arrhythmic events. The area under the curve (AUC) and 95% CIs of the ROC curves were AUC=0.35 (95% CI: 0.26–0.44, p=0.003) for HRV, AUC=0.64 (95% CI: 0.54–0.73, P<0.006) for cfPWV, AUC=0.67 (95% CI: 0.58–0.75, P=0.001) for LVMI and AUC=0.55 (95% CI: 0.47–0.64, P=0.298) for AIx@75 (Figure). In Cox regression analysis, only HRV was associated with increased risk of arrhythmic events (Hazard ratio per 1 unit =0.87, 95% Confidence intervals 0.76 to 0.995, p=0.043) when adjusted for age, gender, cfPWV, LVMI and AIx@75. ROC curves of HRV & target organ damage Conclusions Low heart rate variability is associated with increased risk of future arrhythmic events suggesting an early sympathovagal imbalance that could lead to future events in hypertension.

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