Organ damage (OD) is an indicator of increased cardiovascular risk. Blood pressure variability (BPV) is related to greater incidence of events, regardless of the severity of hypertension. We ...investigated the relationship between ambulatory blood pressure monitoring (ABPM)-derived indices of BPV and the presence of multiple OD in primary hypertension (PH). One hundred and sixty-nine untreated patients with PH were evaluated. Systolic (SBP) and diastolic blood pressure (DBP) variability were assessed as the crude and weighted (w.) standard deviation (s.d.), and average real variability (ARV) of the mean value of 24-h, awake and asleep ABPM recordings. Left ventricular mass index, intima-media thickness, estimated-glomerular filtration rate and urinary albumin excretion were assessed as indices of cardiac, vascular and renal damage, respectively. Risk profile progressively increased starting from patients without OD to patients with only one sign of OD, and then to those with multiple OD. In addition to greater severity of the organ involvement, the only variables that were found to significantly differ between subjects with multiple and single OD were office SBP (160 ± 14 vs 154 ± 11 mm Hg, P=0.0423) and DBP (101 ± 7 vs 97 ± 8 mm Hg, P=0.0291), ambulatory arterial stiffness index (AASI) (0.60 ± 0.10 vs 0.50 ± 0.17, P=0.0158) and indices of BPV (24-h SBP s.d., 23 ± 5 vs 20 ± 6 mm Hg, P=0.0300; awake SBP s.d., 22 ± 6 vs 19 ± 6 mm Hg, P=0.0366; 24-h SBP w.s.d., 20 ± 5 vs 17 ± 5 mm Hg, P=0.0385; and 24-h SBP ARV, 18 ± 4 vs 15 ± 5 mm Hg, P=0.0420). All the above mentioned BPV parameters turned out to be determinants of multiple OD, regardless of several confounding variables, including BP levels. Therefore, in hypertensive patients increased SBP variability is associated with multiple signs of OD, regardless of BP values.
The aim of the study was to review the literature on clinical pharmacology of lercanidipine and experimental and clinical evidence and evaluate its ability to reduce proteinuria and preserve renal ...function when used as monotherapy or in combination with the angiotensin-converting enzyme (ACE) inhibitor enalapril.
MEDLINE/PubMed was searched for appropriate keywords.
Lercanidipine, a third-generation calcium channel blocker, has been shown to have a unique pharmacological and clinical profile, which translates into favorable renal hemodynamic changes. The fixed-dose combination lercanidipine/enalapril has been proposed to overcome unmet therapeutic needs, often as the initial treatment in the high-risk patient.
Lercanidipine may be regarded as an ideal antihypertensive drug for patients at renal risk and possibly the preferred choice among calcium channel blocker drugs.
The actual reference range of serum uric acid has been assessed according to its variations among healthy individuals. i.e. those without clinical evidence of gout. By this approach, serum uric acid ...values between 3.5 and 7.2 mg/dL in adult males and postmenopausal women and between 2.6 and 6.0 mg/dL in premenopausal women have been identified as normal in many countries. However, this definition of normal range of serum uric acid in the general population is inevitably influenced by what we consider as "normal", since the absence of gout flares does not necessarily imply the absence of uric acid-related damage. Indeed, a growing body of evidence indicates that silent deposition of monosodium urate crystals as a result of hyperuricaemia may occur and lead to early destructive skeletal changes. In addition, a growing body of evidences demonstrates that uric acid might play a pathophysiological role in many "cardio-nephro-metabolic" disorders, which seems to be independent of the deposition of monosodium urate crystals, since it is evident also for serum uric acid concentrations below the saturation point for monosodium urate. Taken together, these findings strongly suggest to carefully reconsider the concept of "asymptomaticity" for chronic hyperuricemia and to consequently revise the normal range of serum uric acid levels also considering the progressive worldwide increase of circulating levels of uric acid, which could lead to a "shift to right" (i.e. toward higher values) of normal range. In the light of the new scientific knowledge on the pathophysiological role of uric acid in human disease, a threshold value < 6.0 mg/dL (< 360 µmol/L) seems to better identify true "healthy subjects" and should reasonably be considered for all subjects.
This analysis is aimed to determine blood pressure (BP) levels and BP control rates in a large population of hypertensive patients in Italy. Data were taken from two large and inclusive ...cross-sectional surveys, which covered two distinct and subsequent time periods (2000-2005 and 2005-2011, respectively). Observational clinical studies and surveys, which reported average systolic/diastolic clinic BP levels, proportions of treated/untreated and controlled/uncontrolled patients, and prevalence of cardiovascular risk factors in hypertensive patients followed in either outpatient clinics, hypertension centres or general practice, were considered for the analyses. The overall sample included 211 591 hypertensive patients (119 997 (56.7%) women, age 57.0±10.0 years, body mass index 26.9±4.0 kg m(-2), BP levels 146.9±16.7/88.7±9.6 mm Hg). BP levels were 148.2±15.4/87.5±9.3 mm Hg in patients followed by general practitioners (n=168 313, 79.5%), 148.1±17.3/90.1±9.7 mm Hg in those followed by hypertension centres (n=28 180, 13.3%), and 142.4±17.6/86.6±9.8 mm Hg in those followed by outpatient clinics and hospital divisions (n=15 098, 7.1%). Among treated hypertensive patients (n=128 079; 60.5%), 43 008 (33.6%) were reported to have controlled BP levels. Over one decade of observation, we reported that ~60% of hypertensive patients were treated and among these only 33% achieved effective BP control. These findings highlight the need for more effective interventions to improve management of hypertension in Italy.
This review aims to describe the pathogenic role of triglycerides in cardiometabolic risk, and the potential role of omega-3 fatty acids in the management of hypertriglyceridemia and cardiovascular ...disease.
In epidemiological studies, hypertriglyceridemia correlates with an increased risk of cardiovascular disease, even after adjustment for low density lipoprotein cholesterol (LDL-C) levels. This has been further supported by Mendelian randomization studies where triglyceride-raising common single nucleotide polymorphisms confer an increased risk of developing cardiovascular disease. Although guidelines vary in their definition of hypertriglyceridemia, they consistently define a normal triglyceride level as <150 mg/dL (or <1.7 mmol/L). For patients with moderately elevated triglyceride levels, LDL-C remains the primary target for treatment in both European and US guidelines. However, since any triglyceride level in excess of normal increases the risk of cardiovascular disease, even in patients with optimally managed LDL-C levels, triglycerides are an important secondary target in both assessment and treatment. Dietary changes are a key element of first-line lifestyle intervention, but pharmacological treatment including omega-3 fatty acids may be indicated in people with persistently high triglyceride levels. Moreover, in patients with pre-existing cardiovascular disease, omega-3 supplements significantly reduce the risk of sudden death, cardiac death and myocardial infarction and are generally well tolerated.
Targeting resistant hypertriglyceridemia should be considered as a part of clinical management of cardiovascular risk. Omega-3 fatty acids may represent a valuable resource to this aim.
•Studies have shown a link between triglyceride levels and cardiovascular (CV) risk.•A normal triglyceride level is <150 mg/dL (or <1.7 mmol/L).•Treatment is indicated in patients with triglyceride levels >200 mg/dL (2.3 mmol/L).•Omega-3 supplements have been indicated in the treatment of hypertriglyceridemia.•Omega-3 supplements have proven benefit in secondary prevention of CV disease.
To develop and validate a model for predicting 5-year eGFR-loss in type 2 diabetes mellitus (T2DM) patients with preserved renal function at baseline.
A cohort of 504.532 T2DM outpatients ...participating to the Medical Associations of Diabetologists (AMD) Annals Initiative was splitted into the Learning and Validation cohorts, in which the predictive model was respectively developed and validated. A multivariate Cox proportional hazard regression model including all baseline characteristics was performed to identify predictors of eGFR-loss. A weight derived from regression coefficients was assigned to each variable and the overall sum of weights determined the 0 to 8-risk score.
A set of demographic, clinical and laboratory parameters entered the final model. The eGFR-loss score showed a good performance in the Validation cohort. Increasing score values progressively identified a higher risk of GFR loss: a score ≥ 8 was associated with a HR of 13.48 (12.96–14.01) in the Learning and a HR of 13.45 (12.93–13.99) in the Validation cohort.
The 5 years-probability of developing the study outcome was 55.9% higher in subjects with a score ≥ 8.
In the large AMD Annals Initiative cohort, we developed and validated an eGFR-loss prediction model to identify T2DM patients at risk of developing clinically meaningful renal complications within a 5-years time frame.
The increased atherothrombotic risk in patients with metabolic syndrome (MetS) has been classically explained by the multiplicative effect of systemic concomitant pro-atherosclerotic factors. In ...particular, centripetal obesity, dyslipidaemia, glucose intolerance, hypertension (differently combined in the diagnosis of the disease) would be expected to act as classical cardiovascular risk conditions underlying accelerated atherogenesis. In order to better understand specific atherosclerotic pathophysiology in MetS, emerging evidence focused on the alterations in different organs that could serve as both pathophysiological targets and active players in the disease. Abnormalities in adipose tissue, heart and arteries have been widely investigated in a variety of basic research and clinical studies in MetS. In this narrative review, we focus on pathophysiological activities of the liver and kidney. Considering its key role in metabolism and production of soluble inflammatory mediators (such as C-reactive protein CRP), the liver in MetS has been shown to be altered both in its structure and function. In particular, a relevant amount of the fat accumulated within this organ has been shown to be associated with different degrees of inflammation and potential insulin resistance. In humans, non-alcoholic fatty liver disease (NAFLD) has been described as the hepatic manifestation of MetS. In an analogous manner, epidemiological evidence strongly suggested a "guilty" association between MetS and chronic kidney disease (CKD). Some biomarkers of hepatic (such as C-reactive protein, TNF-alpha or other cytokines) and renal diseases (such as uric acid) associated with MetS might be particularly useful to better manage and prevent the atherothrombotic risk.
Abstract
Objectives:
In this article, the results of clinical and experimental studies that examine the association of hyperuricemia and gout with hypertension and kidney disease are presented and ...discussed.
Methods:
Key papers for inclusion were identified by a PubMed search, and articles were selected according to their relevance for the topic, according to the authors' judgment.
Results and conclusions:
Increasing evidence supports a causal role for Uric acid (UA) in hypertension. Further larger studies are needed to confirm the possible beneficial role of UA lowering drugs and/or xantine-oxidase (XO) inhibitors. Overall, clinical evidence suggests a relationship of UA level with incident chronic kidney disease (CKD). In addition, the results of clinical trials using urate lowering therapy provide some promising evidence that lowering UA levels may retard the progression of CKD. Reviewed data indicate the need for large, well designed studies in these patients to evaluate XO inhibitors or uricosuric drugs in cardio-renal diseases and further elucidate the role of UA in the development and progression of CKD.
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