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Critical Reviews in Clinical Laboratory... 2005This review focuses on the laboratory biochemical tests that are useful in the diagnostic approach to the hypertensive patient. A "minimal" diagnostic laboratory... (Review)
Review
This review focuses on the laboratory biochemical tests that are useful in the diagnostic approach to the hypertensive patient. A "minimal" diagnostic laboratory work-up, including a small number of tests that are simple and relatively inexpensive, is first described. Because these tests provide basic information on the presence of major cardiovascular (CV) risk factors and target organ damage, and might give some clues to the presence of a secondary form of hypertension (HT), they should be performed on all patients presenting with HT. Other tests that are aimed at assessing the overall CV risk, a major determinant of prognosis that dictates the therapeutic strategy in the individual HT patient, are then discussed. They allow identification of major CV risk factors and associated clinical conditions which, if present, lead to a substantial change of therapeutic strategy. The role of C-reactive protein as a marker of atherosclerosis and its predictive value for CV events are also discussed. Finally, a section is devoted to tests that are currently confined to research purposes, such as markers of endothelial function including endothelin-1, homocysteine and genetic analysis.
Topics: Animals; Biomarkers; Diagnostic Tests, Routine; Homocysteine; Humans; Hypertension; Kidney; Risk Factors
PubMed: 16390680
DOI: 10.1080/10408360500295600 -
Diabetes Research and Clinical Practice Apr 1998Almost two decades ago, the existence of a subset of essential hypertensive patients, who were sensitive (according to the increase in blood pressure levels) to the... (Review)
Review
Almost two decades ago, the existence of a subset of essential hypertensive patients, who were sensitive (according to the increase in blood pressure levels) to the intake of a diet with a high salt content, was described. These patients are characterized by an increase in blood pressure and in body weight when switched from a low to a high sodium intake. The increase in body weight is due to the incapacity of the kidneys to excrete the whole intake of sodium until renal perfusion pressure (mean blood pressure) attains a level that is able to restore pressure-natriuresis relationship to values that enable the kidney to excrete the salt ingested or administered intravenously. Salt sensitivity does not seem to depend on the existence of an intrinsic renal defect to handle sodium, but on the existence of subtle abnormalities in the regulation of the sympathetic nervous system, the renin-angiotensin system or endothelial function. It is also relevant that organ damage secondary to arterial hypertension, has been shown in animal models and in hypertensive humans sensitive to a high salt intake to be significantly higher when compared with that of salt-resistant animals or humans. Interestingly, in humans, salt sensitivity has been shown to correlate with microalbuminuria, an important predictor of cardiovascular morbidity and mortality, which correlates with most of the cardiovascular risk factors commonly associated with arterial hypertension. One of these factors is insulin resistance, that usually accompanies high blood pressure in overweight and obese hypertensives. Insulin resistance and hyperinsulinism are present in a significant percentage of hypertensive patients developing cardiovascular symptoms or death. For these reasons, therapy of arterial hypertension must be directed, not only to facilitate the lowering of BP level, but also, to halt the mechanisms underlying the increase in BP, when salt intake is increased. Furthermore, therapy must preferably improve the diminished insulin sensitivity present in salt-sensitive subjects that contribute independently to increased cardiovascular risk.
Topics: Animals; Blood Pressure; Humans; Hypertension; Insulin Resistance; Sodium, Dietary
PubMed: 9649956
DOI: 10.1016/s0168-8227(98)00018-7 -
The Primary Care Companion For CNS... May 2017
Topics: Adult; Diagnosis, Differential; Factitious Disorders; Humans; Hypertension; Male; Patient Compliance; Psychotherapy, Brief
PubMed: 28534598
DOI: 10.4088/PCC.16l02048 -
Journal of Human Hypertension Dec 2022Environmental temperature is now well known to have a U-shaped relationship with cardiovascular (CV) and all-cause mortality. Both heat and cold above and below an... (Review)
Review
Environmental temperature is now well known to have a U-shaped relationship with cardiovascular (CV) and all-cause mortality. Both heat and cold above and below an optimum temperature, respectively, are associated with adverse outcomes. However, cold in general and moderate cold specifically is predominantly responsible for much of temperature-attributable adversity. Importantly, hypertension-the most important CV risk factor-has seasonal variation such that BP is significantly higher in winter. Besides worsening BP control in established hypertensives, cold-induced BP increase also contributes to long-term BP variability among normotensive and pre-hypertensive patients, also a known CV risk factor. Disappointingly, despite the now well-stablished impact of temperature on BP and on CV mortality separately, direct linkage between seasonal BP change and CV outcomes remains preliminary. Proving or disproving this link is of immense clinical and public health importance because if seasonal BP variation contributes to seasonal adversity, this should be a modifiable risk. Mechanistically, existing evidence strongly suggests a central role of the sympathetic nervous system (SNS), and secondarily, the renin-angiotensin-aldosterone axis (RAAS) in mediating cold-induced BP increase. Though numerous other inflammatory, metabolic, and vascular perturbations likely also contribute, these may also well be secondary to cold-induced SNS/RAAS activation. This review aims to summarize the current evidence linking temperature, BP and CV outcomes. We also examine underlying mechanisms especially in regard to the SNS/RAAS axis, and highlight possible mitigation measures for clinicians.
Topics: Humans; Renin-Angiotensin System; Angiotensins; Hypertension; Blood Pressure
PubMed: 35618875
DOI: 10.1038/s41371-022-00707-8 -
Journal of Clinical Hypertension... Sep 2006The aim of this study was to evaluate ambulatory blood pressure monitoring in patients with essential hypertension and hypertension caused by adrenal pathology....
The aim of this study was to evaluate ambulatory blood pressure monitoring in patients with essential hypertension and hypertension caused by adrenal pathology. Sixty-six patients with primary aldosteronism, 37 with pheochromocytomas, and 45 with adrenal incidentalomas were included. These patients were compared with 152 essential hypertensive patients and 64 normotensive subjects. Ambulatory blood pressure monitoring evaluated daytime and nighttime systolic and diastolic blood pressure and heart rate. The authors found that the "nondipper" phenomenon was present in 51.5% of patients with primary aldosteronism, 43.2% with pheochromocytomas, 42.2% with incidentalomas, 34.2% with hypertension, and 15% of subjects who were normotensive. In 58% of primary aldosteronism patients with idiopathic adrenal hyperplasia, there was an absence of the physiologic blood pressure nocturnal fall (nondipper), which was statistically significant (P<.001) compared with nondipper primary aldosteronism patients with adrenocortical adenoma (38%). In conclusion, the prevalence of the nondipping pattern was higher in patients with adrenal hypertension compared with patients with essential hypertension, suggesting an independent cardiovascular risk factor.
Topics: Adrenal Gland Diseases; Blood Pressure Monitoring, Ambulatory; Circadian Rhythm; Female; Humans; Hypertension; Male; Middle Aged
PubMed: 16957426
DOI: 10.1111/j.1524-6175.2006.05712.x -
Polski Merkuriusz Lekarski : Organ... Aug 2021Hypertensive crisis is a sudden rise in blood pressure that is significantly above normal values. Depending on the severity of symptoms, hypertensive crisis can be... (Review)
Review
Hypertensive crisis is a sudden rise in blood pressure that is significantly above normal values. Depending on the severity of symptoms, hypertensive crisis can be classified as hypertensive urgency, i.e. severe arterial hypertension (AH) without organ failure and damage with nonspecific symptoms (pain, dizziness, nosebleeds, nausea, vomiting), and hypertensive emergency, i.e. severe AH with organ failure and/or acute organ damage. The most common causes of hypertensive crisis in neonates and infants are vascular diseases (thrombus or stenosis of the renal artery, coarctation of the aorta) or renal parenchymal diseases, in older children kidney diseases and renal artery stenosis, in adolescents also intoxications or pregnancy. In neonates and infants, nonspecific symptoms caused by acute heart failure predominate, and in older children, symptoms from the central nervous system are most typical. Fast- and short-acting medications are used in the treatment of hypertensive urgencies and emergencies; a gradual normalization of blood pressure within 36-48 hours is recommended. Hypertensive emergencies are treated with intravenous drugs (e.g., labetalol, hydralazine), and hypertensive urgencies with intravenous or oral drugs such as nifedipine, clonidine, and minoxidil. Hypertensive emergencies are treated with intravenous drugs (e.g., labetalol, hydralazine), and hypertensive urgencies with intravenous or oral drugs such as nifedipine, clonidine, and minoxidil. Emergency conditions are treated with intravenous drugs (e.g., labetalol, hydralazine), urgent conditions with intravenous or oral drugs such as nifedipine, clonidine, and minoxidil. Some causes of hypertensive crisis require different management, e.g. alpha-blockers in pheochromocytoma. In all patients, evaluation of target organ damage and extensive diagnostics for secondary forms of hypertension is necessary.
Topics: Adolescent; Antihypertensive Agents; Blood Pressure; Child; Emergencies; Female; Heart Failure; Humans; Hypertension; Infant; Infant, Newborn; Pregnancy
PubMed: 34464374
DOI: No ID Found -
Japanese Journal of Medicine Feb 1985Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension,...
Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension, renovascular hypertension, primary aldosteronism, Cushing syndrome, pheochromocytoma and malignant hypertension. In both normal subjects and the normal renin essential hypertensives, plasma prolactin was significantly higher in females than in males. Plasma prolactin was also significantly higher in the normal renin essential hypertensives than in normal subjects of both sexes, while no significant difference was found between the low renin group and normal subjects of either sex. A significantly positive correlation was observed between plasma renin activity and the plasma prolactin level in male essential hypertensives, but not in females. Although no significant difference in plasma prolactin level could be detected between patients with secondary hypertension and normal subjects, this level was significantly higher in malignant hypertensives than in normotensives. From these results, it was shown that significant differences of plasma prolactin levels exist between normal renin essential hypertensives, and low renin essential hypertensives or normal subjects, and that these differences may partly depend on renin status which might be related to the central dopaminergic activity. In malignant hypertensives, the high level of plasma prolactin may be caused by diminished renal function, but the suppression of central dopaminergic activity cannot be excluded in the mechanism of plasma prolactin increment.
Topics: Adolescent; Adrenal Gland Neoplasms; Adult; Cushing Syndrome; Female; Humans; Hyperaldosteronism; Hypertension; Hypertension, Malignant; Hypertension, Renal; Male; Middle Aged; Pheochromocytoma; Prolactin; Renin
PubMed: 3889434
DOI: 10.2169/internalmedicine1962.24.19 -
Recent Patents on Cardiovascular Drug... Jun 2008The beneficial effects of statins in hypertension stem from their effects on endothelial function, their interactions with the renin-angiotensin system, and their... (Review)
Review
The beneficial effects of statins in hypertension stem from their effects on endothelial function, their interactions with the renin-angiotensin system, and their influence on large artery compliance. Substantial evidence has recently accumulated showing that statins exert pleiotropic effects in vascular function. These include an increase in the synthesis of NO, inhibition of vascular smooth muscle cell proliferation and migration, anti-inflammatory actions, downregulation of angiotensin II type 1 receptor expression, and anti-oxidative effects. These effects occur before reduction of cholesterolemia. Available data support only a modest BP-lowering effect of statins which is most prominent in those patients with poorly controlled hypertension. Even though they only cause a minor reduction in BP, they may play a role in the prevention of cardiovascular disease. Statins may be useful therapeutic agents in hypertensives with high serum total cholesterol, in patients with poorly controlled hypertension even without hypercholesterolemia, in normocholesterolemic well-controlled hypertensive subjects with high C reactive protein levels, and in those subjects who need secondary prevention. Future research is needed to further characterize the impact of statins alone or in combination with antihypertensive agents to prevent or delay the development of stage 1 hypertension. This review article also includes relevant patents.
Topics: Animals; Antihypertensive Agents; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Cardiovascular Diseases; Clinical Trials as Topic; Comorbidity; Drug Therapy, Combination; Evidence-Based Medicine; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertension; Meta-Analysis as Topic; Patents as Topic; Research Design; Treatment Outcome
PubMed: 18537759
DOI: 10.2174/157489008784705331 -
Biomedicine & Pharmacotherapy =... Sep 2017Bone metastases are the most frequent cause of cancer-induced bone pain (CIBP). Although palliative radiotherapy and pharmacotherapy conducted according to World Health... (Review)
Review
Bone metastases are the most frequent cause of cancer-induced bone pain (CIBP). Although palliative radiotherapy and pharmacotherapy conducted according to World Health Organization (WHO) analgesic ladder are the treatment of choice for CIBP reduction, these methods are not always successful, especially with regard to alleviation of incidental pain. Antiresorptive drugs (bisphosphonates) are able to inhibit bone destruction (loss), proliferation of cancer cells and angiogenesis, but their prolonged use may lead to a spectrum of adverse effects. In this paper, types of bone metastases, their complications, as well as diagnostic and therapeutic implications are presented. Moreover, the paper discusses presently used CIBP treatment methods and research directions for future methods, with special focus on bone metastases.
Topics: Bone Density Conservation Agents; Bone Neoplasms; Cancer Pain; Diphosphonates; Humans; Neoplasm Metastasis
PubMed: 28747002
DOI: 10.1016/j.biopha.2017.07.023 -
Clinical Hemorheology and... 1999During essential and secondary arterial hypertension it is possible to observe changes in microcirculation perfusion associated with a reduction in tissue oxygenation...
During essential and secondary arterial hypertension it is possible to observe changes in microcirculation perfusion associated with a reduction in tissue oxygenation due in part to hemorheological changes such as an increase in blood viscosity or the formation of the red blood cell "rouleaux" which favour an increase in peripheral resistance and can cause or worsen arterial hypertension. We studied 21 healthy subjects (11 male and 10 female aged 42 +/- 4) and 26 hypertensive subjects (14 male and 12 female aged 49 +/- 3). The patients were non smokers and non suffering from respiratory or haemathological pathologies. They were not undergoing antihypertensive or vasodilatory pharmaceutical treatment. The patients suffered from mild hypertension (II WHO) with Peripheral Occlusive Arterial Disease (POAD II "a" acc. to Leriche-Fontaine class.). The patients showed an increase in cholesterolaemia (6.42 +/- 0.81 mmol/l) and trygliceridaemia (2.73 +/- 0.09 mmol/l) at an average level. The patients were studied in standard conditions with a constant temperature of 22 degrees C. We measured SBP, DBP, MBP, and the HR. We also measured the elongation index (EI) (with shear stress range 0.30 to 30 pascals) using LORCA, acc. to Hardeman method (1994), in order to study the erythrocyte deformability and aggregation kinetics in dynamic condition. To evaluate deformability in static conditions we calculated the Erythrocyte Morphologic Index (EMI), acc. to Forconi method, via the bowl/discocyte ratio (for 100 red blood cells fixed in glutaraldehyde at 0.3% and observed with an optical microscope under immersion in glycerol). Peripheral oxygenation was taken transcutaneously (TcpO2). To establish the level of vascular disease we used the Regional Perfusion Index (RPI = TcpO2 foot/TcpO2 subclavean) and doppler guided Winsor Index (WI). The Student "t" test and linear regression were used for the statistical analysis. Our data confirm a reduction in peripheral tissue oxygenation in hypertensives especially if suffering from vascular disease which correlates significantly (p < 0.01) with a reduction in red blood cell deformability. This itself can increase peripheral resistances and favour the onset of hemorheological complications, at a cerebral-vascular level, which are frequent in hypertensives.
Topics: Adult; Blood Viscosity; Erythrocyte Aggregation; Female; Hemorheology; Humans; Hypertension; Lipoid Proteinosis of Urbach and Wiethe; Lung Diseases; Male; Microcirculation; Middle Aged; Pulsatile Flow; Vascular Resistance
PubMed: 10711762
DOI: No ID Found