Project description:BackgroundTreatment of severe inpatient hypertension (HTN) that develops during hospitalization is not informed by guidelines. Intravenous (i.v.) antihypertensives are used to manage severe HTN even in the absence of acute target organ damage; however they may result in unpredictable blood pressure (BP) reduction and cardiovascular events. Our goal was to assess the association between i.v. antihypertensives and clinical outcomes in this population.MethodsThis is a multihospital retrospective study of adults admitted for reasons other than HTN who develop severe HTN during hospitalization without acute target end organ damage. We defined severe HTN as BP elevation of systolic >180 or diastolic >110 mmHg. Treatment was defined as receiving i.v. antihypertensives within 3 h of BP elevation. We used overlap propensity score weighted Cox models to study the association between treatment and clinical outcomes during index hospitalization.ResultsOf 224 265 unique, nonintensive care unit hospitalizations, 20 383 (9%) developed severe HTN, of which 5% received i.v. antihypertensives and 79% were untreated within 3 h of severe BP elevation. In the overlap propensity weighted population, patients who received i.v. antihypertensives were more likely to develop myocardial injury (5.9% in treated versus 3.6% in untreated; hazard ratio [HR]: 1.6 [1.13, 2.24]). Treatment was not associated with increased risk of stroke (HR: 0.7 [0.3, 1.62]), acute kidney injury (HR: 0.97 [0.81, 1.17]), or death (HR: 0.86 [0.49, 1.51]).ConclusionsIntravenous antihypertensives were associated with increased risk of myocardial injury in patients who develop severe HTN during hospitalization. These results suggest that i.v. antihypertensives should be used with caution in patients without acute target organ damage.
Project description:Apolipoprotein L1 (APOL1) gene association studies and results of the African American Study of Kidney Disease and Hypertension are disproving the longstanding concept that mild to moderate essential hypertension contributes substantially to end-stage renal disease susceptibility in African Americans. APOL1 coding variants underlie a spectrum of kidney diseases, including that attributed to hypertension (labeled arteriolar or hypertensive nephrosclerosis), focal segmental glomerulosclerosis, and HIV-associated nephropathy. APOL1 nephropathy risk variants persist because of protection afforded from the parasite that causes African sleeping sickness. This breakthrough will lead to novel treatments for hypertensive African Americans with low-level proteinuria, for whom effective therapies are lacking. Furthermore, APOL1 nephropathy risk variants contribute to racially variable allograft survival rates after kidney transplantation and assist in detecting nondiabetic forms of nephropathy in African Americans with diabetes. Discovery of APOL1-associated nephropathy was a major success of the genetics revolution, demonstrating that secondary hypertension is typically present in nondiabetic African Americans with nephropathy.
Project description:BackgroundIsolated diastolic hypertension (IDH) is defined as diastolic blood pressure (DBP) ≥80 mmHg and systolic blood pressure (SBP) <130 mmHg according to 2017 ACC/AHA guidelines. The effective cardiovascular risk linked to IDH is debated.HypothesisIDH might contribute marginally to hypertension-related target organ damage (TOD) development.MethodsIn this cross-sectional analysis 1605 subjects from the STANISLAS cohort, a large familiar longitudinal study from Eastern France, were included. Participants were categorized according to average values at 24-h ABP recording as having normal BP (SBP < 130/DBP < 80 mmHg); combined hypertension (SBP ≥130/DBP ≥80 mmHg or on antihypertensive treatment); IDH (SBP <130/DBP >80 mmHg); isolated systolic hypertension (ISH: SBP ≥130/DBP <80 mmHg). The association between hypertension status and TOD was assessed by multivariable-adjusted logistic models.ResultsUsing normotension as reference, IDH was not significantly associated with NTproBNP levels (adjusted odds ratio [OR] 1.04 [95%CI 0.82;1.32], p = .750), microalbuminuria (OR 0.99 [0.69; 1.42], p = .960), diastolic dysfunction (OR 1.53 [0.88; 2.68], p = .130), left ventricular (LV) mass index (OR per 10 g/m2 increase 1.07 [0.95; 1.21], p = .250), LV longitudinal strain (global: OR 1.07 [0.99; 1.14], p = .054; subendocardial: OR 1.06 [0.99; 1.13], p = .087), carotid intima media thickness (OR 1.27 [0.79; 2.06], p = .320), reduced ankle-brachial index (<0.9; OR 1.59 [0.19; 13.55], p = .670) and pulse wave velocity (PWV; OR 1.07 [0.93; 1.23], p = .360). In contrast, combined hypertension and ISH were independently associated with LV mass index and PWV increase (all p ≤ .01).ConclusionsIDH was not significantly associated with TOD. Further studies are needed to clarify the clinical role of IDH. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01391442.
Project description:BackgroundBlood pressure (BP) elevations are commonly treated in hospitalized patients; however, treatment is not guideline directed. Our objective was to assess BP response to commonly prescribed antihypertensives after the development of severe inpatient hypertension (HTN).MethodsThis is a cohort study of adults, excluding intensive care unit patients, within a single healthcare system admitted for reasons other than HTN who developed severe HTN (systolic BP>180 or diastolic BP >110 mmHg at least 1 hour after admission). We identified the most commonly administered antihypertensives given within 6 hours of severe HTN (given to >10% of treated patients). We studied the association of treatment with each antihypertensive vs. no treatment on BP change in the 6 hours following severe HTN development using mixed-effects model after adjusting for demographics and clinical characteristics.ResultsAmong 23,147 patients who developed severe HTN, 9,166 received antihypertensive treatment. The most common antihypertensives given were oral metoprolol (n = 1991), oral amlodipine (n = 1812), oral carvedilol (n = 1116), IV hydralazine (n = 1069) and oral hydralazine (n = 953). In the fully adjusted model, treatment with IV hydralazine led to 13 [-15.9, -10.1], 18 [-22.2, -14] and 11 [-14.1, -8.3] mmHg lower MAP, SBP, and DBP in the 6 hours following severe HTN development compared to no treatment. Treatment with oral hydralazine and oral carvedilol also resulted in significantly lower BPs in the 6 hours following severe HTN development (6 [-9.1, -2.1 and -7 [-9.1, -4.2] lower MAP, respectively) compared to no treatment. Receiving metoprolol and amlodipine did not result in a drop in BP compared to no treatment.ConclusionAmong commonly used antihypertensives, IV hydralazine resulted in the most significant drop in BP following severe HTN, while metoprolol and amlodipine did not lower BP. Further research to assess the effect of treatment on clinical outcomes and if needed which antihypertensives to administer are necessary.
Project description:A recent study reported that morning hypertension is associated with poor cardiovascular outcomes in hypertensive patients. However, it is unclear whether morning hypertension associated with sustained nocturnal hypertension and that associated with morning blood pressure (BP) surge differ in terms of their effects on cardiovascular target organ damage and clinical outcomes. The present study aimed to determine the association of morning hypertension with/without nocturnal hypertension with vascular target organ damage and central hemodynamics in patients at high risk for cardiovascular disease. Ambulatory BP monitoring was performed and central BP was measured in 1070 consecutive patients with high cardiovascular risk. We grouped morning hypertension into the following 3 subtypes: (I) morning normotension; (II) morning hypertension without nocturnal hypertension; and (III) morning hypertension with nocturnal hypertension. Morning hypertension was noted in 469 (43.8%) patients and morning hypertension with nocturnal hypertension was noted in 374 (34.9%) patients. The central systolic/diastolic BP and carotid to femoral pulse wave velocity were significantly higher in the subtype III group than in the subtype I and II groups (all P<0.001). Subtype III (versus subtype I) was an independent predictor of central hypertension and high-risk arterial stiffness (P<0.001 and P=0.018, respectively) but not vascular damage in a fully adjusted model (model Y). Morning hypertension, especially that associated with nocturnal hypertension, is related to high central BP and increased arterial stiffness. Further studies on whether morning hypertension with or without nocturnal hypertension is related to clinical outcomes should be performed. URL: http://www.clinicaltrials.gov. Unique identifier: NCT02003781.
Project description:Objectives: To determine the association between morning hypertension and target organ damage (TOD) in patients with chronic kidney disease (CKD) and hypertension. Methods: In this cross-sectional study, 447 patients with CKD and hypertension from two centers were enrolled. Ambulatory blood pressure monitoring was conducted in all patients. Linear regression and logistic regression analysis were used to determine the association between morning hypertension and TOD in patients with CKD and hypertension, including assessments of estimated glomerular filtration rate (eGFR), left ventricular mass index (LVMI), urine protein/creatinine ratio (UPCR), and left ventricular hypertrophy (LVH). Results: Overall, 194 (43.4%) participants had morning hypertension. Morning hypertension was strongly correlated with LVH [odds ratio (OR), 2.14; 95% confidence interval (CI), 1.3-3.51; p < 0.01], lower level of eGFR (β = -0.51; 95%CI, -0.95--0.08; p < 0.05), higher LVMI (β = 0.06; 95%CI, 0.04-0.08, p < 0.001), and UPCR (β = 0.22; 95%CI, 0.06-0.38, p < 0.01), independent of nocturnal hypertension and elevated morning blood pressure surge. As a continuous variable, both morning systolic blood pressure (SBP) and diastolic blood pressure (DBP) were found to be associated with LVH and higher level of UPCR and LVMI (p < 0.05), whereas only morning SBP was negatively correlated with eGFR (p < 0.01). Conclusion: Morning hypertension was strongly correlated with cardiac damage and impaired kidney function in CKD patients with hypertension, independent of nocturnal hypertension and morning surge in blood pressure. Morning hypertension in CKD patients warrants further attention.
Project description:The aim of this study is to investigate the prevalence of metabolic disorders in patients with primary aldosteronism (PA) and target organ damage (TOD) in different subtypes of patients with PA with or without metabolic syndrome (MS). Patients with PA were screened out from those with secondary hypertension and then subtyped via adrenal venous sampling (AVS). Baseline clinical characteristics (blood pressure, blood glucose, abdominal circumference, and lipid profile) were collected for the diagnosis of MS. Organ damage was evaluated according to cardiac and carotid ultrasound and urine microalbumin measurements. In all 261 patients with PA, 113 patients had concomitant MS and experienced more severe cardiac hypertrophy and increased intima-media thickness (IMT). The incidence of MS and diabetes mellitus (DM) had no statistic difference between the two groups, moreover, the rates of TOD were not different except microalbuminuria. However, metabolic disorders caused more remarkable TOD in PA patients with unilateral hypersecretion. It showed that cardiac hypertrophy was associated with obesity while microalbuminuria was related to plasma aldosterone concentration (PAC) in PA patients. In this retrospective study, our findings suggest that the effect of metabolic disorders on organ damage is more remarkable in patients with unilateral PA.
Project description:High blood pressure or Primary Hypertension is associated with target organ damage (TOD) in both adults and youth, where TOD predicts the adverse cardiovscular (CV) events. The mechanisms involved in blood pressure mediated TOD are limitedly understood in onset of TOD. To understand this, first using RNA sequencing, we identified candidate differentially expressed genes in circulating PBMCs of study participants with and without hypertension and elevated left ventrivlar mass index . Next, through miRNA and whole genome bisulphite sequencing of circulating PBMCs we determined the epigenetic regulators of TOD. Also, using LCMS, serum proteomics, the key circulatory protein involved in advancing CV- TOD events was identified. In conclusion, multiomics approach was utilized to define the circulatory regulators involved in BP mediated CV-TOD.
Project description:Objective: The aim of this study was to confirm the potential role of testosterone in hypertension and target organ damage (TOD) in hypertensive postmenopausal women. Methods: A matched group study was conducted. One hundred sixty-one hypertensive postmenopausal women between 45 and 65 years of age were enrolled as group 1. Another 161 age-matched hypertensive men were enrolled as group 2. Ambulatory blood pressure monitoring, echocardiographic imaging, vascular function, sex hormones and clinical characteristics were evaluated. Quantitative data were analyzed using independent Student's t-test and multiple regression analysis. Results: The mean and load level of blood pressure were lower in women than in men (P<0.05), except for the mean level and load of the nocturnal systolic blood pressure (SBP) (123.77±15.72 mmHg vs 126.35±15.64 mmHg, and 50.43±30.31% vs 55.35±28.51%, P>0.05). However, the carotid-femoral pulse wave velocity (cf-PWV) in women was higher than that in men (9.68±2.23 m/s vs 8.03±2.82 m/s, P<0.05). The ratio of the early diastolic mitral peak flow velocity to early diastolic mitral annular velocity (E/Em) was obviously impaired (13.06±3.53 vs 12.05±3.68, P<0.05) in women. Furthermore, in women, a positive correlation was found between testosterone and cf-PWV (γ=0.157, P=0.046), and Cf-PWV was positively related to the mean level of nighttime SBP (γ=0.210, P=0.008). Moreover, nocturnal SBP was a risk factor for E/Em (γ=0.156, P=0.048, P<0.05). Conclusion: Testosterone may play a role in the correlation between hypertension and TOD in hypertensive postmenopausal women. Clinical Trial number: This research study was registered under the ClinicalTrials.gov PRS Website (NCT03451747).