Risk Factor For Cardiovascular Mortality Research Articles

Risk factors for cardiovascular mortality and melanoma-specific mortality among patients with melanoma: a SEER based study.

This study aims to identify the risk factors for cardiovascular mortality in melanoma patients. Data of melanoma patients were obtained from the Surveillance, Epidemiology, and End Results database. We used Person's chi-square test to assess the relationships between categorical variables. We used Kaplan-Meier test in the univariate analysis and Cox regression test for the multivariate analysis. Analyses were conducted using the SPSS software. We analyzed data of 194 503 melanoma patients. Among them, 28 818 (14.8 %) died due to cardiovascular diseases. Cardiovascular-specific survival was higher in younger patients, women, married, localized disease, superficial spreading melanoma and in patients who had surgery. It was lower in patients who received chemotherapy or radiotherapy. The multivariate analysis revealed a higher risk of cardiovascular mortality in patients aged 50-64 years [hazard ratio (HR), 7.297; 95% confidence interval (CI), 6.68-7.97], patients aged ≥65 years (HR, 43.309; 95% CI, 39.706-47.240), men (HR, 1.535; 95% CI, 1.475-1.597), Blacks (HR, 1.29; 95% CI, 1.044-1.594), separated (HR, 1.286; 95% CI, 1.058-1.562), widowed (HR, 1.829; 95% CI, 1.706-1.961), patients with no or unknown history of chemotherapy (HR, 1.302; 95% CI, 1.071-1.583) or radiotherapy (HR, 1.477; 95% CI, 1.217-1.793) and patients with no surgery (HR, 1.468; 95% CI, 1.264-1.706). In patients with melanoma, the risk of cardiovascular death is higher in older patients, men, Blacks, separated, widowed and patients with nodular or lentigo maligna melanoma. The risk is lower in married, patients with superficial spreading or acral lentiginous melanoma, and patients who had chemotherapy, radiotherapy or surgery.

Magnesium Disorders and Prognosis in Heart Failure: A Systematic Review.

Magnesium is an essential mineral for the human body and plays an important role in cardiovascular health. Hypomagnesaemia has been linked with increased cardiovascular mortality in heart failure; however, previous studies have yielded conflicting results. Even fewer studies have addressed the association between hypermagnesemia and prognosis in heart failure. The aim of the present systematic review was to investigate the association of serum magnesium levels with cardiovascular and all-cause mortality in patients with heart failure and reduced ejection fraction (HFrEF). Cardiovascular morbidity, referring to heart failure rehospitalizations and ventricular arrhythmias, was also investigated. Eligible studies were identified by searching PubMed and Scopus. The Quality in Prognosis (QUIPS) tool was used to assess the quality of included studies. Eight studies (total of 13,539 patients with HFrEF) that assessed the effects of serum magnesium levels on cardiovascular mortality, all-cause mortality, and cardiovascular morbidity met inclusion criteria. In half of the studies, hypomagnesemia was found to be an independent risk factor for cardiovascular mortality, including sudden cardiac death. Only 1 study reported that hypermagnesemia (serum magnesium levels above 2.4 mg/dL) is a prognostic factor for noncardiac mortality suggesting that hypermagnesemia is more likely an indicator of comorbidities rather than a true independent prognostic marker. Finally, low serum magnesium levels were not associated with readmissions for heart failure or ventricular arrhythmias in patients with HFrEF.

Reduction in Monocyte Isolevuglandins Associated with High Interstitial Sodium Mirrors Salt‐Sensitivity of Blood Pressure in Patients with Essential Hypertension

Salt Sensitivity (SS) of blood pressure (BP) is an independent risk factor for cardiovascular mortality. Sodium (Na+) is stored in skin and muscle interstitium. Antigen presenting cells are activated in response to elevated extracellular Na+ in an ENaC-dependent manner resulting in formation of (isolevuglandin) IsoLG-protein adducts. This leads to T-cell activation, release of inflammatory cytokines, kidney damage, endothelial dysfunction and an increase in BP. We aimed to determine the effect of tissue Na+ storage and immune cell activation on salt-sensitive hypertension. Five subjects with essential hypertension discontinued all anti-hypertensive therapy two weeks before the study. SS was assessed by a rapid inpatient protocol of salt loading (460 mmoL/24 hours) and salt depletion (10 mmoL/24 hours, plus furosemide 40 mg x 3). 23Sodium magnetic resonance imaging was used to measure muscle and skin Na+ contents at baseline (BA). Urine and serum electrolytes, glomerular filtration rate, plasma renin, aldosterone levels, plasma and urine EETs (8-9, 11-12 and 14-15 isoforms) and the percentage of IsoLG adduct-containing CD14+ monocytes via flow cytometry were measured at BA, after salt-loading (HI) and after salt-depletion (LO). All continuous data are displayed as median (interquartile range). Spearman's correlation was used to test associations. 60% of subjects were female, median age was 54 years (44-55), BMI was 35 kg/m2 (30-39), and screening BP was 140/88 mmHg (134-148 / 84-99). The range of the drop in systolic BP from HI to LO (salt-sensitivity index, SSI) was -13.8 to +1.8 mmHg. %isoLG+ CD14+ cells were 48 (27-65) at BA, 55 (31-56) at HI, and 70 (33-72) at LO (p=0.594, by the Kruskal-Wallis test). The correlation between SSI and delta (∆) %isoLGLO minus HI in CD14+ monocytes, was 0.86, [95% confidence interval (CI), -0.07-0.99] (Figure 1A). Skin Na+ content correlated with baseline % IsoLG+ CD14 (r=0.91; 95% CI, 0.12-0.99) (Figure 1B). Higher excretion of urine EETs associated with less IsoLG+ CD14+ cells whereas higher plasma aldosterone per unit urine EET, (a marker of net stimulation of ENaC) associated with a greater number of IsoLG-containing CD14+ cells. No such relationships were observed with plasma EETs. Finally, less stimulation of the aldosterone/urine EET ratio by salt depletion associated with a greater fall in IsoLG+ CD14+ cells (Figure 1C). The change in IsoLG-containing CD14+ monocytes in response to salt depletion appears to be associated with SSBP, which if confirmed in larger number of subjects could constitute a biomarker for SSBP in humans. The association between baseline % of IsoLG-containing CD14+ monocytes and skin Na+ suggests that activation of these cells is due to hyperosmolar Na+ exposure in some interstitial compartment of the body. Relationships between IsoLGs and urine but not plasma EETs suggest that this exposure could be occurring in the hyperosmolar renal medulla.

Causes of death and influencing factors of atrial fibrillation patients undergoing anticoagulation therapy

Objective: To investigate the causes of death and predictors in patients with nonvalvular atrial fibrillation (AF) undergoing anticoagulation therapy. Methods: Consecutive anticoagulated nonvalvular AF patients were recruited from the China Atrial Fibrillation Registry (China-AF) Study from August 2011 to December 2018. After exclusion of patients with hypertrophic cardiomyopathy, dilated cardiomyopathy, or loss of follow-up within 1 year, 2 248 patients were included in this analysis. Enrolled patients were followed up were followed up for 3 and 6 months, and then every 6 months. The primary endpoint was death, including cardiovascular death, non-cardiovascular death and undetermined death. The patients were divided into survival group and death group according to the survival status after follow-up. Clinical information such as age and sex was collected. Cox proportional hazards regression was performed to identify associated risk factors for all-cause mortality, and Fine-Gray competing risk model was used to identify associated risk factors for cardiovascular mortality. Results: A total of 2 248 patients with atrial fibrillation receiving anticoagulant therapy died over a mean follow-up of (42±24) months, mean age was (67±10) years old and 41.1% (923/2 248) patients were female. The mortality rate was 2.8 deaths per 100 patient-years. The most common cause of death was cardiovascular deaths, accounted for 55.0% (120/218). Worsening heart failure was the most common cause of cardiovascular deaths (18.3% (40/218)), followed by bleeding events (12.9% (28/218)) and ischemic stroke (8.7% (19/218)). Multivariate Cox regression analysis showed that age (HR = 1.05, 95%CI 1.04-1.07, P<0.001), anemia (HR = 1.81, 95%CI 1.02-3.18, P = 0.041), heart failure (HR=2.40, 95%CI 1.75-3.30, P<0.001), ischemic stroke/transient ischemic attack (TIA)(HR = 1.59, 95%CI 1.21-2.13, P = 0.001) and myocardial infarction (HR = 2.93, 95%CI 1.79-4.81, P<0.001) were independently associated with all-cause death. Fine-Gray competing risk model showed that age (HR=1.05, 95%CI 1.02-1.08, P<0.001), heart failure (HR=2.81, 95%CI 1.79-4.39, P<0.001), ischemic stroke/TIA (HR=1.50, 95%CI 1.02-2.22, P=0.041) and myocardial infarction (HR=3.31, 95%CI 1.72-6.37, P<0.001) were independently associated with cardiovascular death. Conclusions: In anticoagulated nonvalvular AF patients, ischemic stroke represents only a small subset of deaths, whereas worsening heart failure is the most common cause of cardiovascular deaths. Heart failure, ischemic stroke/TIA, and myocardial infarction are associated with increased mortality.

Changes in extracellular water and left ventricular mass in peritoneal dialysis patients.

BackgroundIncreasing number of peritoneal dialysis (PD) patients are reported to have increased left ventricular hypertrophy (LVH), a major risk factor for cardiovascular mortality. We wished to determine which factors were most associated with changes in left ventricular mass index (LVMI).MethodsWe reviewed patient and treatment factors in prevalent PD patients with repeat echocardiograms 18 to 24 months apart, with corresponding bioimpedance measurements of extracellular water (ECW) and serum N-terminal pro-brain natriuretic peptide (NT-proBNP).ResultsWe studied 60 patients (34 males, 35 with diabetes) who were treated with PD for a median of 14 months (2.5–26.3 months). All but one had LVH; on repeat echocardiography, there was no overall change in LVMI (106 [84–127] g/m2 vs. 108 [91–122] g/m2) despite a loss of residual renal function. Left ventricular mass increased in 34 (56.7%), and the percent change in LVMI was associated with percent change in NT-proBNP (r = 0.51, p = 0.017) and ECW/height (r = 0.32, p = 0.029), but not with ECW/total body water or changes in systolic or mean arterial pressure, urine output, 24-hour PD ultrafiltration, or net sodium balance. Only ECW/height remained independently associated with the percent change in LVMI in a multivariable model (odds ratio, 1.25; 95% confidence interval, 1.08–1.36; p = 0.007). ConclusionIn this observational longitudinal report, a reduction in ECW/height was associated with regression of LVMI, whereas an increased ECW/height was associated with increased LVMI. As there was no corresponding association with systolic or mean arterial pressure, then volume expansion would appear to be a more significant factor in determining LVH than blood pressure.

Angiopoietin-like proteins 8 knockout reduces intermittent hypoxia-induced vascular remodeling in a murine model of obstructive sleep apnea

ObjectiveObstructive sleep apnea (OSA) is a major risk factor for cardiovascular mortality. Apnea-induced chronic intermittent hypoxia (CIH) is a primary pathophysiological manifestation of OSA that promotes various cardiovascular alterations, such as aortic vascular remodeling. In this study, we investigated the association between angiopoietin-like proteins 8 (ANGPTL8) and CIH-induced aortic vascular remodeling in mice. MethodsC57BL/6J male mice were divided into four groups: Normoxia group, ANGPTL8−/− group, CIH group, CIH + ANGPTL8−/− group. Mice in the normoxia group and ANGPTL8−/− group received no treatment, while mice in the CIH and CIH + ANGPTL8−/− group were subjected to CIH (21%–5% O2, 180 s/cycle, 10 h/day) for 6 weeks. At the end of the experiments, intima-media thickness (IMT), elastin disorganization, and aortic wall collagen abundance were assessed in vivo. Immunohistochemistry and Western-blot were used to detect endoplasmic reticulum stress (ERS) and aortic vascular smooth muscle cell proliferation. ANGPTL8 shRNA and ANGPL8 overexpression were used in aortic vascular smooth muscle cells to investigate the mechanism of ANGPTL8 in CIH. ResultsCompared to the control group, CIH exposure significantly increased intima-media thickness (IMT), elastic fibers disorganization, and aortic wall collagen abundance. CIH also significantly increased blood pressure, induced hyperlipidemia, as well as the expression of ERS protein activating transcription factor-6 (ATF6) and aortic vascular smooth muscle cell proliferation. Contrary, ANGPTL8−/− significantly mitigated the CIH-induced vascular remodeling; ANGPTL8−/− decreased CIH-induced hypertension and hyperlipidemia, inhibited the protein expression of ATF6, and aortic vascular smooth muscle cell proliferation. Moreover, our in vitro study suggested that CIH could induce ANGPTL8 expression via hypoxia-inducible factor (HIF-1α); ANGPTL8 induced proliferation of aortic vascular smooth muscle cells via the ERS pathway. ConclusionANGPTL8−/− can prevent CIH-induced aortic vascular remodeling, probably through the inhibition of the ERS pathway. Therefore, ANGPTL8 might be a potential target in CIH-induced aortic vascular remodeling.

Correlation of staging and risk factors with cardiovascular autonomic neuropathy in patients with type II diabetes mellitus

The impairment of cardiovascular autonomic control among the underdiagnosed complication of diabetes mellitus (DM) with a high prevalence rate of up to 60% in type 2 DM (T2DM). Cardiac autonomic neuropathy (CAN) is an independent risk factor for cardiovascular mortality, arrhythmia, silent ischemia, any major cardiovascular event, and heart failure. We aimed to evaluate cardiovascular autonomic activity by different physiological maneuvers, study risk factors for diabetic CAN including age, gender, duration of diabetes, body mass index (BMI), and glycemic control, and correlate CAN stage with risk factors. One hundred and forty-two T2DM patients consisted of 62 males and 80 females and 100 volunteers as a control sample. Cardiac autonomic functions were assessed by Ewing's tests. Glycated hemoglobin (HbA1c), body weight, height, body mass index (BMI), and waist-hip ratio (WHR) were also measured. Cardiovascular autonomic functions and Ewing scores were significantly different in people with diabetes when compared with control healthy subjects. Ewings test values and Ewing scores were significantly different between diabetics with and without CAN and within patients with different CAN staging. People with diabetes with CAN have a significantly longer duration of disease when compared to those without CAN. A strong association has been found between CAN severity and patient age, duration of disease, HbA1c severity, and the WHR (P < 0.001) but not with BMI. The duration of disease and HbA1c level appear to be associated with the development of CAN (P = 0.001 and P = 0.008, respectively). The poorer glycemic control and the longer the duration of the disease, the higher the prevalence of CAN in T2DM. Age, duration of disease, WHR, and HbA1c are well correlated with the severity of CAN. Parasympathetic impairment is more sensitive to the detection of autonomic dysfunctions than do sympathetic impairment.

For Massive Obesity: What is the Metabolic Risk Gradient?

Background: Obesity with BMI body mass index = 40kg / m² is called Massive obesity (MO) according to the WHO, is a recognized risk factor of cardiovascular mortality. It is not known whether there is a metabolic risk gradient (MRC) above the threshold of 40kg / m². Objective: To classify metabolic abnormalities based on higher BMI. Methods: This is a cross-sectional study involving 230 patients followed for MO. These patients were divided into 3 groups (G) according to their BMI (G1: 40 <BMI <44.9; G2: 45 <BMI <49.9; G3: BMI> 50). The assessment focused on the age, gender, blood pressure (TAs and TAd), dyslipidemia (HDL = 0.4 g / l and / or TG = 1.5 g / l) treated or no, glycemic control (fasting glycemia and / or OGTT 75). Results: The mean age was 46 years with no differences between the 3 G. This is 76% women. The prevalence of an abnormality in carbohydrate tolerance was not different between the 3 G (p = 0.49). Apart from a known HTA, the BPs differed between the 3 G (in mm Hg G1: 122 ± 11; G2: 128 ± 15; G3: 133 ± 10, p = 0.028), unlike the BP (G1: 67 ± 10; G2: 70 ± 10; G3 73 ± 12, NS).

Prevalence of Severe Anemia (Hb ≤ 5 g/dl) in Non-Dialyzed Chronic Renal Failure Patients in the Nephrology and Hemodialysis Department of Point G University Hospital

Introduction: Chronic renal failure (CRF) is defined as glomerular filtration rate (GFR) less than 60 ml/min/1.73m2 for at least three (3) months. Anemia is one of its most common complications. Anemia increases the risk factor for cardiovascular mortality by 18% per gram of hemoglobin loss. Objectives: To determine the prevalence and characteristics of this severe anemia, to determine the indications for transfusion, the complications related to this anemia, the evolution and the prognosis of these patients. Materials and Methods: This was a descriptive study with retrospective data collection over 18 months (January 1, 2017 to June 30, 2018) that included hospitalized CRF patients. Were included, non-dialyzed chronic renal failure patients with Hb ≤ 5 g/dl hospitalized during the said period. Not included were chronic renal failure patients with an Hb level ≥ 5 g/dl, those followed up and/or hospitalized outside the study period. Results: Among 1176 patients, 26 had severe anemia (Hb level ≤ 5 g/dl) on CRF, a prevalence of 2.21%. The mean age was 40 years ± 32.62 with extremes of 15 and 67 years. Seventeen women and 9 men. The etiology of chronic renal failure (CRF) was hypertensive vascular nephropathy in 50% of cases. CRF was end-stage in 18 patients (69.2%). The mean hemoglobin level was 4.10 g/dl ± 0.64 with extremes of 2 and 5 g/dl. The anemia was microcytic hypochromic in 50% and aregenerative (96.2%). The main symptoms were asthenia in 20 cases (76.9%), dizziness in 20 cases (76.9%), exertional dyspnea in 19 cases (73.1%). Signs of cardiac decompensation (n = 12) were jugular turgor 10 cases (38.5%), hepato-jugular reflux 06 cases (23.1%), mitral insufficiency murmur 06 cases (23.1%). The main complication was left ventricular hypertrophy 17 cases (77.3%). There was no correlation between anemia and sex (p = 0.291), age (p = 0.778), malaria (p = 0.158), etiology of CRF (p = 0.26). The evolution after treatment of anemia was favorable in 19 patients (73.1%), unfavorable in 02 patients (7.7%) and 05 deaths (19.2%). The deaths were of cardiovascular cause: left ventricular insufficiency 04 cases, stroke 01 case. Conclusion: Anemia is frequent in patients with chronic renal failure and remains an important risk factor for cardiovascular disease and poor general condition.

ДИАГНОСТИКА ДИАБЕТИЧЕСКОЙ КАРДИАЛЬНОЙ АВТОНОМНОЙ НЕЙРОПАТИИ

Diabetes mellitus is a severe disease that leads to an early disability and premature death. Diabetic cardiac autonomic neuropathy (DCAN) is a serious and frequent complication of diabetes mellitus with a poor prognosis. Timely diagnosis of DCAN can have important clinical implications, since DCAN is an independent risk factor for cardiovascular mortality, arrhythmias, painless ischemia, and other cardiovascular disorders. Despite this, until now, in clinical practice, they are rarely engaged in an active search for the symptoms of DCAN and it remains a poorly studied and rarely diagnosed complication of diabetes mellitus. The article discusses the methods of detecting and assessing DACN in clinical practice, including the assessment of clinical manifestations, the use of reflex cardiovagal tests and common instrument6al diagnostic methods.

Volume status and arterial stiffness evaluation in peritoneal dialysis patients.

Arterial stiffness represents an independent risk factor for cardiovascular mortality in dialysis patients and is strongly connected to hypervolemia. The aim of the study was to evaluate different methods for fluid status assessment and their association with arterial stiffness parameters in peritoneal dialysis patients. In 16 peritoneal dialysis patients (53 ± 18 years, 9/16 men) fluid status was determined by clinical examination, lung ultrasound (number of B-lines, normal up to 4), overhydration degree by bioimpedance monitor device, estimation of central venous pressure by ultrasound measurement of vena cava inferior, measurement of serum N-terminal pro b-type natriuretic peptide (NT-proBNP), and albumin level. Pulse wave velocity and augmentation index were measured non-invasively with an oscillometric device to indirectly assess arterial stiffness, blood pressure (BP) was obtained by the same device. Clinical evaluation (BP 136 ± 15/93 ± 15 mmHg, edema in 2/16 patients) and lung ultrasound (on average 3 ± 6 B-lines) showed mostly normal fluid status of patients. Patients had slightly lower albumin values (37 ± 4 g/L), slightly elevated central venous pressure (10 ± 4 mmHg), and elevated NT-proBNP (11,596 ± 13,635 ng/L). Body composition evaluation showed mild overhydration (1.5 ± 2 L), which significantly correlated with central venous pressure (p = 0.046) and NT-proBNP (p = 0.004). Lung ultrasound significantly negatively correlated with albumin (r = -0.82, p < 0.001) and positively with NT-proBNP (r = 0.62, p = 0.011). Augmentation index (22 ± 11%) and augmentation pressure correlated with lung ultrasound (r = 0.54, p = 0.032 and r = 0.67, p = 0.004, respectively), although pulse wave velocity (8.4 ± 2.5 m/s) showed no significant correlation with fluid status parameters. The multivariate model showed that lung ultrasound B-lines were an independent determinant of augmentation pressure (β = 0.58, p = 0.043). Fluid status evaluated with lung ultrasound showed good correlation with augmentation index and augmentation pressure, which are markers of arterial stiffness. The lung ultrasound B-lines were found to be an independent determinant of augmentation pressure. Overall arterial stiffness evaluated with pulse wave velocity and augmentation index was not markedly elevated in our patients, which could be due to a good euvolemic status. We conclude that different methods for fluid status evaluation are complementary, with lung ultrasound as a beneficial tool in routine clinical practice in peritoneal dialysis patients.

Deacetylation of cGAS by HDAC1 regulates vascular calcification by promoting autophagy.

Vascular calcification is a major risk factor for cardiovascular mortality accompanied by DNA damage. Cyclic GMP-AMP synthase (cGAS) is a DNA sensor that is activated by genomic DNA damage. Here, we investigated the molecular mechanisms linking cGAS to vascular calcification. Diabetic arteriosclerotic model and vascular calcification of primary vascular smooth muscle cells (VSMCs) were induced. Calcification was visualized with Alizarin red staining. Calcium deposition and alkaline phosphatase activity were analyzed by respectively kits. Deacetylation of cGAS was investigated using co-immunoprecipitation assay. Protein, but not mRNA, expression of cGAS is down-regulated in VSMCs and animal models of calcification. Overexpression of cGAS attenuated high-Pi induced calcification, calcium content and ALP activity. In addition, cGAS regulated VSMCs phenotype as overexpression of cGAS increased expression of contractile markers α-SMA and SM22α and decreased the expression of osteogenic markers RUNX2 and BMP2. The LC3II/LC3I ratio and Atg5 level were upregulated by cGAS overexpression. Under calcification-inducing conditions, HDAC1 deacetylates cGAS and inactivates it. HDAC1 knockdown by short hairpin HDAC1 reversed the cGAS-induced reduction in vascular calcification, as well as in autophagy. HDAC1-induced cGAS deacetylation enhances vascular calcification and may therefore be a potential therapeutic target.

Evaluation of heart rate variability using 24-hour Holter electrocardiography in hypertensive patients.

BackgroundHypertension (HTN) remains a serious risk factor for cardiovascular mortality across the world. Hypertensive state has been shown to be associated with autonomic nervous function. This study aimed to explore the association between autonomic nervous impairment assessed by heart rate variability (HRV) and HTN.MethodsA total of 52 hypertensive and 55 non‐hypertensive patients were consecutively studied using 24‐hour Holter. The hypertensive patients were grouped into controlled blood pressure (BP) and uncontrolled BP. This study compared HRV in non‐hypertensive and hypertensive patients; and hypertensive patients with controlled and uncontrolled BP. HRV parameters include time and frequency domain.ResultsMean age for hypertensive and non‐hypertensive patients were 53.58 ± 14.31 and 44.89 ± 16.63 years old, respectively. Median (IQR) SDNN for hypertensive and non‐hypertensive group were 109.00 (90.00‐145.00) and 129.00 (107.00‐169.00), respectively. SDNN, ASDNN, rMSSD, pNN50, BB50, VLF, and HF values were significantly lower in the hypertensive group compared to non‐hypertensive group (all P < .05). A multiple regression analysis showed that HRV parameters: SDANN, ASDNN, rMSSD, and LF values were independent risk factors of HTN. SDNN, SDANN, ASDNN, VLF, LF, and HF values were significantly lower in the uncontrolled BP compared to controlled BP group (all P < .05). A multiple regression analysis showed that HRV parameters: SDNN, SDANN, rMSSD, and HF values were independent risk factors of uncontrolled BP in hypertensive patients.ConclusionsOur study showed that cardiac autonomic nervous impairment, as demonstrated by reduced HRV, is significantly associated with HTN. Decreased HRV was more evident in uncontrolled BP than in controlled BP group.

Recent advances in managing primary hypertension.

Hypertension remains a leading risk factor for cardiovascular mortality and morbidity globally despite the availability of effective and well-tolerated antihypertensive medications. Accumulating evidence suggests a more aggressive blood pressure regulation aimed at lower targets, particularly for selected patient groups. Our concepts of the optimal method for blood pressure measurement have radically changed, maintaining appropriate standard office measurements for initial assessment but relying on out-of-office measurement to better guide our decisions. Thorough risk stratification provides guidance in decision making; however, an individualized approach is highly recommended to prevent overtreatment. Undertreatment, on the other hand, remains a major concern and is mainly attributed to poor adherence and resistant or difficult-to-control forms of the disease. This review aims to present modern perspectives, novel treatment options, including innovative technological applications and developing interventional and pharmaceutical therapies, and the major concerns emerging from several years of research and epidemiological observations related to hypertension management.

Uric acid to high-density lipoprotein cholesterol ratio predicts cardiovascular mortality in patients on peritoneal dialysis

Background and aimsSerum uric acid (UA) and high-density lipoprotein cholesterol (HDL-C) disorders are both considered as risk factors of cardiovascular mortality. The predictive value of UA to HDL-C ratio (UHR) has been validated in diabetes. However, association of UHR with cardiovascular (CV) mortality is undetermined in peritoneal dialysis (PD) patients. Methods and resultsIn this retrospective cohort study, we enrolled 1953 eligible incident patients who commenced PD treatment on our hospital from January 1, 2006 to December 31, 2015, and followed up until December 31, 2019. Of the participants, 14.9% were older than 65 years (mean age 47.3 ± 15.2 years), 24.6% were diabetics, and 59.4% were male. Patients were categorized into quartiles according to baseline UHR level. Multivariate Cox Proportional Regression analysis was applied to explore the association of UHR with mortality. Overall, 567 patients died during a median follow-up period of 61.3 months, of which 274 (48.3%) were attributed to CV death. The mean baseline UHR was 16.4 ± 6.7%. Compared to quartile 2 UHR, hazard ratios (HRs) for the highest quartile UHR were 1.35 (95% confidence interval [CI] 1.06–1.78; P = 0.017) and 1.46 (95% CI 1.00–2.12; P = 0.047) for all-cause and CV mortality, respectively. Subgroup analysis showed that association of UHR with CV mortality was remarkable among PD patients with age ≥65 years, malnutrition (albumin <35 g/L), diabetes, and CVD history. ConclusionsAn elevated UHR predicted increased risk of all-cause and CV mortality in PD patients.

Association of double product and pulse pressure with cardiovascular and all‐cause mortality in the LURIC study

Systolic (SBP) and diastolic blood pressure (DBP) and mean arterial pressure (MAP) are risk factors for cardiovascular mortality (CVM). Pulse pressure (PP) is considered as an easily available marker of vascular stiffness and the double product (DP) as a marker of cardiac workload. Therefore, we have examined the predictive value of PP and DP in the Ludwigshafen Risk and Cardiovascular Health study, a monocentric cohort study of 3316 patients referred to coronary angiography. An increase of SBP or PP by 1mmHg increased the risk of CVM with hazard ratios of 1.009 (95% CI, 1.005-1.012) and 1.016 (1.012-1.020), respectively. Increasing DP by 100mmHg/min was associated with a 1.010 (1.007-1.013) higher risk of CVM. In patient subgroups with coronary artery disease (CAD) and heart failure (HF), PP and DP predicted CVM better than SBP or MAP. In a multivariate analysis adjusted for sex, BMI, diabetes, eGFR, hazard ratios for CVM for z-standardized PP, DP, SBP, and HR were 1.20, 1.16, 1.12, and 1.14. After adding age to the multivariate analysis, only DP and HR remained significant. We provide evidence that PP and DP are powerful predictors of CVM and all-cause mortality in a CV medium- to high-risk population, especially in patients with CAD and HF. While DP proved to be an independent predictor of cardiovascular and all-cause mortality also in multivariate analysis, PP was no independent predictor in our cohort with widespread antihypertensive treatment (>85%). PP is associated with age, presence of diabetes, obesity, and impaired renal function.

The effectiveness of Baduanjin exercise for hypertension: a systematic review and meta-analysis of randomized controlled trials

BackgroundHypertension, a major risk factor of cardiovascular mortality, is a critical issue for public health. Although Baduanjin (Eight Brocades, EB), a traditional Chinese exercise, might influence blood pressure, glucose, and lipid status, the magnitude of true effects and subgroup differences remains unclear. Therefore, we performed a systematic review of relevant randomized controlled trials (RCTs) to evaluate the effect of EB on patient-important outcomes.MethodsWe systematically searched PubMed, the Cochrane Library, Web of Science, and Chinese databases since inception until March 30, 2020. Meta-analysis was carried out using “meta” package in R 3.4.3 software. A prespecified subgroup analysis was done according to the type of comparisons between groups, and the credibility of significant subgroup effects (P < 0.05) were accessed using a five-criteria list. A GRADE evidence profile was constructed to illustrate the certainty of evidence.ResultsOur meta-analysis, including 14 eligible trials with 1058 patients, showed that compared with routine treatment or health education as control groups, the mean difference (MD) in systolic blood pressure (SBP) of the EB groups was − 8.52 mmHg (95%CI:[− 10.65, − 6.40], P < 0.01) and diastolic blood pressure (DBP) was − 4.65 mmHg (95%CI: [− 6.55, − 2.74], P < 0.01). For blood pressure, the evidence was, however, of low certainty because of risk of bias and inconsistency, and for the outcomes of most interest to patients (cardiovascular morbidity and mortality directly), of very low certainty (measurement of surrogate only). Subgroup analysis showed there was no significant interaction effect between different type of comparisons (SBP P = 0.15; DBP P = 0.37), so it could be easily attributed to chance.ConclusionRegularly EB exercising may be helpful to control blood pressure, but the evidence is only low certainty for blood pressure and very low certainty for cardiovascular morbidity and mortality. Rigorously designed RCTs that carry out longer follow-up and address patient-important outcomes remain warranted.Trial registrationPROSPERO Registration number: CRD42018095854.

Projecting the Prevalence of Hypertension in the Philippines: Its Impact and the Need for a Call-to-Action

Hypertension is a major risk factor for cardiovascular mortality, and the global numbers of affected individuals are increasing. Several health care strategies and reforms have been implemented by different countries to curb the prevalence of hypertension and the Philippines has also started to implement programs for non-communicable diseases, including hypertension. To determine the impact of hypertension in the country, this paper aims to project the hypertension prevalence by 2050 using published statistical data and plotting the data to linear regression model. Results showed hypertension prevalence will remain as high as 23% but the number of cases will double in 2050 given the population projection if no intervention will occur. Filipino males will have a higher prevalence rate, but the hypertension cases will doubly increase in females by 2050. However, because some interventions conducted by the government and medical societies, hypertension prevalence declined in 2018. If the downward trend continues, we see a reduced projected rate of hypertension prevalence and lower cardiovascular deaths. This trend will continue if government and medical programs on hypertension continue to strengthen. The need for continued proper diagnosis and management of hypertension needs to be implemented in the country. Funding Statement: The Philippine Society of Hypertension Declaration of Interests: No conflict of interest.

CME: Left Bundle Branch Block and Painful Left Bundle Branch Block Syndrome

CME: Left Bundle Branch Block and Painful Left Bundle Branch Block Syndrome Abstract. Left bundle branch block (LBBB) is the electrocardiographic correlate of a pathologic transmission of the electrical signals in the myocardium which can lead to a dyssynchronous left ventricular activation and thus to an inefficient contraction of the ventricles. It is usually the expression of an underlying cardiopathy and represents an independent risk factor of cardiovascular mortality, therefore further examination is indicated in each case. Besides the treatment of an underlying disease, a specific therapy has been available since the introduction of cardiac resynchronization therapy (CRT). A rarer phenomenon is the painful left bundle branch block in structurally healthy hearts.

SERUM URIC ACID AND TARGET ORGAN DAMAGE IN ESSENTIAL HYPERTENSION AT MEDICINE DEPARTMENT OF GMC, BETTIAH, BIHAR

Background Hypertension is a major risk factor for cardiovascular mortality, as it acts through its effects on target organs, such as the heart and kidneys. Hyperuricemia increases cardiovascular risk in patients with hypertension. Objective To assess the relationship between serum uric acid and target organ damage (left ventricular hypertrophy and microalbuminuria) in untreated patients with essential hypertension. Patients and methods: A cross-sectional study was carried out in 130 (85 females, 45 males) newly diagnosed, untreated patients with essential hypertension. Sixty-five healthy age- and sex-matched non-hypertensive individuals served as controls for comparison. Left ventricular hypertrophy was evaluated by cardiac ultrasound scan, and microalbuminuria was assessed in an early morning midstream urine sample by immunoturbidimetry. Blood samples were collected for assessing uric acid levels. Results Mean serum uric acid was significantly higher among the patients with hypertension (379.7±109.2 μmol/L) than in the controls (296.9±89.8 μmol/L; P&lt;0.001), and the prevalence of hyperuricemia was 46.9% among the hypertensive patients and 16.9% among the controls (P&lt;0.001). Among the hypertensive patients, microalbuminuria was present in 54.1% of those with hyperuricemia and in 24.6% of those with normal uric acid levels (P=0.001). Similarly, left ventricular hypertrophy was more common in the hypertensive patients with hyperuricemia (70.5% versus 42.0%, respectively; P=0.001). There was a significant linear relationship between mean uric acid levels and the number of target organ damage (none versus one versus two: P=0.012). Conclusion These results indicate that serum uric acid is associated with target organ damage in patients with hypertension, even at the time of diagnosis; thus, it is a reliable marker of cardiovascular damage in our patient population.