Cardiovascular Organ Damage Research Articles

Arterial Hypertension, Metabolic Syndrome and Subclinical Cardiovascular Organ Damage in Patients with Asymptomatic Primary Hyperparathyroidism before and after Parathyroidectomy: Preliminary Results.

Background. Primary hyperparathyroidism (PHPT) is associated with high cardiovascular morbidity, and the role of calcium and parathyroid hormone is still controversial. Objective. To evaluate the prevalence and outcomes of metabolic syndrome, hypertension, and some cardiovascular alterations in asymptomatic PHPT, and specific changes after successful parathyroidectomy. Material and Methods. We examined 30 newly diagnosed PHPT patients (8 males, 22 females; mean age 56 ± 6 yrs), 30 patients with essential hypertension (EH) (9 males, 21 females; mean age 55 ± 4), and 30 normal subjects (NS) (9 males, 21 females: mean age 55 ± 6). All groups underwent evaluation with ambulatory monitoring blood pressure, echocardiography, and color-Doppler artery ultrasonography and were successively revaluated after one year from parathyroidectomy. Results. PHPT patients presented a higher prevalence of metabolic syndrome (38%) with respect to EH (28%). Prevalence of hypertension in PHPT was 81%, and 57% presented altered circadian rhythm of blood pressure, with respect to EH (35%) and NS (15%). PHPT showed an important myocardial and vascular remodelling. During follow-up in PHPT patients, we found significant reduction of prevalence of metabolic syndrome, blood pressure, and “non-dipping phenomenon.” Conclusions. Cardiovascular and metabolic alterations should be considered as added parameters in evaluation of patients with asymptomatic PHPT.

Physical activity is independently associated with multiple measures of arterial stiffness in adolescents and young adults

Physical activity (PA) is associated with decreased levels of arterial stiffness in adults, but the relationship between PA and multiple measures of arterial stiffness in adolescents and young adults is not clear. The objective of this study was to test the hypothesis that PA is an independent predictor of multiple measures of arterial stiffness in adolescents and young adults. A total of 548 participants were enrolled in a study of the cardiovascular effects of obesity and type 2 diabetes mellitus (T2DM) (lean, 201; obese, 191; T2DM, 156). Anthropometrics, blood pressure, central and peripheral measures of arterial stiffness (pulse wave velocity, brachial distensibility, and augmentation index), blood (lipids and metabolic tests), and accelerometry data were collected. General linear modeling was performed to test for the independent relationship of PA on arterial stiffness. The mean age of the participants was 17.9 years (standard deviation, 3.5 years). After adjusting for other cardiovascular disease risk factors such as age, sex, body size, mean arterial pressure, and the presence of obesity or T2DM, PA was an independent predictor of augmentation index and brachial distensibility (P < .001). A greater effect of PA on pulse wave velocity was found in participants with T2DM (P = .009) compared with participants in the lean or obese groups. Physical activity is significantly and independently associated with multiple measures of arterial stiffness in adolescents and young adults. The role of PA in the prevention of cardiovascular disease target organ damage in youth, independent of energy balance, merits further exploration.

English

Metabolic and humoral mechanisms have been known to be involved in the development and progression of cardiovascular-related sympathetic overdrive. Sympathetic overactivity in the genesis of major complications of cardiovascular system and associated organ damages has been reported as one of the major participant. Evidences has been provided that sympathetic neural mechanisms may participate in the development of cardiovascular -related target organ damage, such as left ventricular hypertrophy, diastolic dysfunction, impaired arterial compliance vascular atherosclerosis and renal failure. Renalase, a circulating FAD-dependent amine oxidase, has been reported as a secretion in blood form the kidney as well as from heart, skeletal muscle and small intestine and known to alter systemic blood pressure, cardiac & renal function in health and diseases. It has been identified in two isoforms of the human protein and is produced by alternative splicing. In vitro studies have demonstrated that Renalase triggers the release as well as degrades catecholamines such as dopamine, norepinephrine and epinephrine and thus has been claimed to have casual link between sympathetic overdrive and increase risk of cardiovascular dysfunction & related organ damage. This paper discussed the main features of physiological functions of renalase, including its sources of secretion, expression and circulating level and their relevance with adrenergic function in cardiovascular dysfunctions & related organ damage. The paper also reviewed the potential role of renalase in the diagnostic and /or therapeutic approach to cardiovascular disorders & renal diseases, aimed at regulation of sympathetic deactivation.

Atorvastatin reduces sympathetic activity in patients with chronic kidney disease

Hypertensive chronic kidney disease (CKD) patients often have sympathetic hyperactivity, which appears to contribute to the pathogenesis of hypertension and cardiovascular organ damage. Experimental studies and some clinical studies have shown that statin therapy can reduce central sympathetic activity. Blockade of the renin-angiotensin system (RAS), which is standard treatment for CKD, is known to lower sympathetic activity. We hypothesized that adding a statin for 6 weeks to RAS blockade would further lower sympathetic activity in hypertensive stage 2-4 CKD patients. In 10 stable CKD patients (eight men, aged 45 ± 11 years, estimated glomerular filtration rate 56 ± 22 ml/min per 1.73 m2), who were on chronic treatment with aliskiren 300 mg, blood pressure and sympathetic activity (quantified by assessment of muscle sympathetic nerve activity, MSNA) were assessed at baseline and 6 weeks after atorvastatin 20 mg/day was added. Ten other CKD patients served as time control and were studied twice with an interval of 6 weeks without any change in medication, to quantify within participant reproducibility. Mean arterial blood pressure remained stable throughout the study (93 ± 5 versus 94 ± 5 mmHg). MSNA was reduced from 28 ± 8 to 20 ± 6 bursts/min (P = 0.01), while heart rate remained stable during the study. In the control CKD group, MSNA did not change: 26 ± 5 to 25 ± 6 bursts/min. Atorvastatin reduced total and low-density lipoprotein cholesterol. Atorvastatin has a further sympatholytic effect in CKD patients, who are on chronic aliskiren, which is independent of blood pressure and heart rate.

M-006 EFFECTS OF EPLERENONE VERSUS HYDROCHLOROTHIAZIDE IN PATIENTS WITH ESSENTIAL HYPERTENSION UNCONTROLLED WITH ANGIOTENSIN II RECEPTOR BLOCKERS

Background Eplerenone, a highly selective aldosterone blocker, has been shown to prevent cardiovascular and renal organ damage. The aim of this study was to investigate the efficacy of eplerenone add-on therapy on end-organ protection in patients with hypertension uncontrolled with angiotensin II receptor blockers (ARBs) therapy in comparison with hydrochlorothiazide (HCTZ). Methods We reviewed fifty-seven treated hypertensive outpatients who did not achieve the target blood pressure (BP) on standard-dose of ARBs therapy. These patients were added to 25–50 mg eplerenone or 6.25–12.5 mg HCTZ (ARBs/eplerenone, group E; n = 25 or ARBs/HCTZ, group H; n = 32). Baseline and follow-up measurements of BP, heart rate, general biochemical values, plasma brain natriuretic peptide (BNP) and estimated glomerular filtration rate (eGFR) were examined. Results The average follow-up duration was 5.65 ± 3.52 months. There was no difference in the baseline characteristics between two groups. These add-on therapy resulted in significant decreases in systolic and diastolic BP in both groups (group E: 159.4 ± 11.9/88.0 ± 13.9 to 132.1 ± 14.2/74.6 ± 12.2mmHg, group H: 164.6 ± 19.9/93.7 ± 14.7 to 138.0 ± 17.6/82.2 ± 11.7mmHg, p < 0.05vs. baseline, respectively). Mean BP after add-on therapy in group E was reduced more than group N (93.8 ± 10.9vs100.8 ± 12.2mmHg, p < 0.05). Plasma BNP levels were significantly decreased in group E after add-on therapy (117.4 ± 166.2vs69.9 ± 123.0pg/ml, p < 0.05), but not changed in group N. eGFR did not change after therapy in both groups. There was no significant difference in incidence of electrolyte, lipid and glucose metabolic disorder between two groups. Uric acid levels in group H were significantly increased after therapy (5.80 ± 1.50vs6.67 ± 1.48 mg/dl, p < 0.05). There was no major adverse event in both groups. Conclusions ARBs/eplerenone or HCTZ combination therapy provided additional BP control. Eplerenone was more beneficial in the cardioprotective effect compared to HCTZ with reduction of mean BP. Selective aldosterone blockade with eplerenone may be useful for add-on therapy in hypertensive patients inadequately controlled on ARBs.

Gender and hypertension management: A sub-analysis of the I-inSYST survey

Hypertension is a major risk factor for cardiovascular disease, which is the leading cause of death in women. Aim. To evaluate blood pressure control, prevalence of concomitant cardiovascular risk factors, subclinical and clinical organ damage, and treatment according to gender. Methods. 11,562 patients (49% women) from the cross-sectional I-inSyst survey in primary care were included. Results. Blood pressure control in women (21.8%) and men (21.2%) was similar, despite a slightly older age (64.9 vs 63 years, p<0.0001). Women had less concomitant cardiovascular risk factors and organ damage, with the exception of diabetes, cerebrovascular and renal disease, than men. They received more antihypertensive drugs than men (1.7 ± 0.9 vs 1.5 ± 0.9, p<0.0001). Diuretics were more (45% vs 36.5%, p<0.0001), calcium-channel blockers (26% vs 29%, p<0.003) and angiotensin-converting enzyme inhibitors (20% vs 22%, p<0.02) were less commonly prescribed in women than in men. Different clinical factors (i.e. age, duration of hypertension, smoking) in women and men were associated with blood pressure control, but gender itself was not. Conclusions. In this group of treated hypertensive patients, blood pressure control in women and men was not different. Women had a lower prevalence of most cardiovascular risk factors, subclinical and clinical organ damage. Antihypertensive drug treatment varied according to gender.

Aldosterone and cardiovascular disease

The renin-angiotensin-aldosterone system is a co-ordinated hormonal cascade of major importance in the control of fluid and electrolyte homeostasis and blood pressure. During the past decade, the scientific community has realized that this system is also of paramount importance in pathophysiology of cardiovascular and renal target organ damage. In particular, inappropriately elevated aldosterone levels in the face of body sodium expansion have been incriminated in cardiac and vascular inflammation and fibrosis leading to remodeling and disease. Substantial advances on the role and mechanisms of aldosterone-induced tissue damage and novel findings on the genetic control of aldosterone secretion have been reported during the past year, and these are the subjects of this brief review. A novel control mechanism for aldosterone secretion may be circadian clock genes, disruption of which leads to increased aldosterone secretion and hypertension. Animal models for human idiopathic hyperaldosteronism have been reported for the first time. Glucocorticoids have now been found to activate cardiac mineralocorticoid receptors during certain cardiovascular disease states. Crosstalk between mineralocorticoid and angiotensin AT1 receptors contributes to target organ damage. Endogenous cardiotonic steroids may explain at least some of the tissue damage during sodium loading previously attributed to aldosterone. Insights on aldosterone and cardiovascular disease gained during the past year provide new avenues for research and applications for treatment in the future.

Sympathetic activity in chronic kidney disease patients is related to left ventricular mass despite antihypertensive treatment

Chronic kidney disease (CKD) patients often have sympathetic hyperactivity, which contributes to the pathogenesis of hypertension and cardiovascular organ damage. Angiotensin-converting enzyme (ACE) inhibitors (ACEi) and angiotensin II receptor blockers (ARB) reduce sympathetic hyperactivity. Ideally, treatment should eliminate the relation between sympathetic activity and organ damage. The aim of the present study is firstly to compare left ventricular mass (LVM) of CKD patients using chronic ACEi or an ARB with LVM of controls. Secondly, we determine whether previously found muscle sympathetic nerve activity (MSNA) and arterial blood pressure during follow-up are predictive for the presence of increased LVM. Methods. We restudied 20 CKD patients and 30 healthy volunteers matched for age. Sympathetic nerve activity was quantified by the microneurography (MSNA). Arterial blood pressure was the mean of office blood pressure measurements. LVM was quantified by magnetic resonance imaging (MRI) without contrast. The period between MSNA and MRI measurements was 9 ± 3 years. All patients were treated according to guidelines with an ACEi or an ARB. In CKD patients, mean systolic and diastolic arterial pressure were 129 ± 10 and 84 ± 5 mmHg, respectively, during follow-up. In patients, as compared to controls, LVM was 93 ± 16 versus 76 ± 18 g, LVM index 30 ± 5 versus 24 ± 4 g/m(2.7) and mean wall thickness 11 ± 2 versus 9.0 ± 1 mm (all P < 0.01). Moreover, MSNA was related to LVM (r = 0.65, P < 0.002), LVM index (r = 0.46, P < 0.03) and LV mean wall thickness (r = 0.84, P < 0.001). Conclusions. In conclusion, the present study demonstrates that measures of LVM in CKD patients are greater than in healthy controls, despite a well-controlled blood pressure in the patients. Moreover, there is a positive relationship between these measures of LVM and MSNA, assessed years before, despite a standard antihypertensive treatment. These results support the notion that additional sympatholytic therapy could be beneficial.

The peroxisome proliferator-activated receptor gamma agonist pioglitazone improves cardiometabolic risk and renal inflammation in murine lupus.

Individuals with systemic lupus erythematosus (SLE) have a striking increase in the risk of premature atherosclerosis, a complication preceded by significant subclinical vascular damage. A proposed mechanism leading to accelerated vascular disease in SLE is an imbalance between vascular damage and repair, as patients with this disease display significant abnormalities in phenotype and function of endothelial progenitor cells. In addition, individuals with SLE have a higher incidence of insulin resistance which may further contribute to the increased cardiovascular risk. This study examined the role of the peroxisome proliferator activated receptor gamma agonist pioglitazone in improving endothelial function, endothelial progenitor cell numbers and functional capacity, metabolic parameters, and disease activity in the lupus-prone murine model New Zealand Black/New Zealand White (NZB x NZW)F(1). Ten-week-old prenephritic female NZB/NZW F(1) mice were exposed to 10 or 25 mg/kg/day of oral pioglitazone or vehicle for 15 or 24 wk. Mice exposed to pioglitazone exhibited pronounced enhancement in endothelial-dependent vasorelaxation of thoracic aortas and in endothelial progenitor cell function, as assessed by the capacity of bone marrow-derived endothelial progenitor cells to differentiate into mature endothelial cells. Pioglitazone-treated mice showed improvement in insulin resistance, adipokine, and lipid profile. Kidneys from pioglitazone-treated mice showed significant decreases in immune complex deposition, renal inflammation, T cell glomerular infiltration, and intrarenal synthesis of TNF-alpha, IL-1beta, and VCAM-1. These results indicate that peroxisome proliferator-activated receptor gamma agonists could serve as important tools in the prevention of premature cardiovascular disease and organ damage in SLE.

Hypertension artérielle du sujet âgé : particularités et précautions d’usage

Hypertension is very common and inadequately controlled among the elderly. The HYVET study showed that antihypertensive therapy significantly reduces total mortality and cardiovascular events in people aged 80 years and older. The therapeutic goal for patients aged from 60 to 80 years is systolic blood pressure (SBP) less than 140 mmHg and a diastolic blood pressure (DBP) less than 90 mmHg, without orthostatic hypotension. For patients older than 80 years, the aim is keep SBP < 150 mmHg. This goal also depends on comorbidities, iatrogenic risk, and life expectancy. The choice of treatment must be adapted to the patient's clinical situation, taking into account any cardiovascular diseases, organ damage, and comorbidities. All of the principal antihypertensive drugs can be used in the elderly, with a preference for thiazide diuretics or calcium channel blockers for those with systolic hypertension. Generally, no more than three antihypertensive drugs should be prescribed for octogenarians (including a thiazide diuretic). Particular attention must be paid to the renal risk (estimated by glomerular filtration rate), especially for nephrotoxic and multiple drugs. Blood levels of potassium, sodium, and creatinine must be monitored in patients receiving diuretics or renin angiotensin system blockers, particularly during acute events (e.g., fever, infection, dehydration, and diarrhea). Cognitive function should be assessed in patients with hypertension older than 80 years, with the MMSE (Mini-Mental-State-Examination) to assess the risk of poor adherence, in view of the increased risk of dementia.

Staging of Hypertension and Total Cardiovascular Risk Assessment: Related but Not the Same—Challenge for the Hypertension Specialist

Staging of Hypertension and Total Cardiovascular Risk Assessment: Related but Not the Same—Challenge for the Hypertension Specialist

High heart rate: More than a risk factor. Lessons from a clinical practice survey

Several epidemiological studies have reported that an elevated heart rate (HR) is associated with coronary atherosclerosis independently of other risk factors. Nevertheless, it is still unclear whether HR is itself the cause or there is merely an association between HR and mortality in this population. A total of 1686 patients with hypertension and chronic ischemic heart disease were included in this study. According to the resting HR, the patients were distributed in 3 groups (group 1: HR < 63 bpm; group 2: 63-82 bpm; group 3: > 82 bpm). 580 patients (34.4%) belonged to group 1; 936 (55.5%) to group 2 and 170 (10.1%) to group 3. Patients with high HR exhibited a poorer prognosis not only due to a worse clinical profile (more concomitant cardiovascular risk factors and organ damage), but suggestively because despite the use of a similar number of drugs, patients with higher HR were associated with lesser risk control rates in daily clinical practice. Despite current guidelines that do not still recognize HR as a cardiovascular risk factor, it appears that physicians should pay more attention to it in clinical practice since high HR is warning about an increased risk.

Cilnidipine in management of patients with uncontrolled hypertension and white-coat effect

Introduction: Hypertension is a major public health problem worldwide. It is an established risk factor in the prognosis of cardiovascular diseases and organ damage [1]. Cilnidipine is a long-acting antihypertensive agent that lowers blood pressure by inhibiting L-type calcium channels directly associated with vascular tone, and N-type calcium channels related to sympathetic nervous activity [2]. Because it acts specifically on N-type calcium channels, cilnidipine is expected to achieve better reduction in morning blood pressure than other classes of calcium channel blockers, and to attenuate the white-coat effect caused by sympathetic nerve hyperactivity. Incomplete drug-regimen compliance (DRC) and white-coat hypertension are two of several possible causes of uncontrolled hypertension. Therefore, in this study, cilnidipine was evaluated in reducing morning blood pressure at home and in ameliorating the white-coat effect.

Cardiac structure and function and arterial circulation in hypertensive patients with and without metabolic syndrome

High blood pressure (BP) is one of the crucial determinants of the metabolic syndrome (MS). The extent to which MS, diagnosed according to the criteria of the International Federation of Diabetes, impacts on cardiovascular organ damage, independently of BP, is debated. Three hundred and forty hypertensive patients and 100 normotensive controls underwent the following procedures: (1) physical examination and resting BP measurements, (2) 24 h ambulatory BP monitoring, (3) laboratory routine examination, (4) echocardiography, (5) carotid ultrasonography and (6) ankle-brachial BP index. The syndrome was found in 104 of the 340 hypertensive patients (30.6). In comparison to those without MS, those with MS had significantly higher prevalence of left ventricular (LV) hypertrophy by mass/height(2.7) criteria (46 vs 42%, P<0.01) but not by LV mass/body surface criteria (30 vs 31%); the ratio between early-to-late peak velocities of the LV filling waves (E/A) was higher (E/A=0.99+/-0.14 vs 0.89+/-0.15, P<0.01) and left atrium was larger (3.8+/-0.3 vs 3.5+/-0.5 cm, P<0.01). Both hypertensive groups had significantly greater LVM and carotid intima-media thickness than normotensives, without between-group-difference. In this hypertension outpatient clinic almost one-third hypertensive patients have MS. They show a deterioration in structure and function of the heart in comparison to hypertensive patients without MS, but no difference was detected in the carotid and peripheral arterial circulation.

Renal resistive index and cardiovascular organ damage in a large population of hypertensive patients

We evaluated the relationship between renal resistive index (RRI) of the intrarenal vasculature and cardiovascular (CV) organ damage such as left ventricular hypertrophy (LVH), diastolic dysfunction and carotid atherosclerosis in a large sample of hypertensive patients. 566 hypertensive patients underwent echocardiography with conventional Doppler and Doppler tissue imaging (DTI), carotid and renal ultrasonography. In addition, lipids profile, creatinine in serum, and urinary albumin concentrations were determined. The patients were divided according to their RRI values in 2 groups: <70 and >or=70. Subjects with high RRI were older, had higher systolic and pulse pressure (PP) and more years of hypertension, compared to those with low RRI (P<0.0001). Patients with the higher RRI showed an increased left ventricular mass index (LVMI) and carotid intima-media thickness (IMT) with a higher prevalence of LVH, carotid plaques and microalbuminuria (P<0.001). There were differences in overall diastolic parameters, in particular when evaluated by DTI (P<0.001). A positive correlation was found between RRI and age, PP, carotid IMT, LVMI, SBP and a negative correlation was found with DTI diastolic parameters (P<0.001). Age, PP, carotid IMT and LVMI were independently related to RRI. While, RRI was independently related to IMT and IVRT. RRI, especially the higher values, are positively correlated with target organ damage in hypertensive patients, indicating that renal vascular resistance is related to morphologic and hemodynamic alteration of the CV system. The evaluation of RRI could predict the presence of early CV damage and provide an accurate estimate of overall risk.

Rat chromosome 19 transfer from SHR ameliorates hypertension, salt-sensitivity, cardiovascular and renal organ damage in salt-sensitive Dahl rats

Unlike Dahl salt-sensitive (SS) rats, some strains of spontaneously hypertensive (SHR) rats develop only minor organ damage even when exposed to high-salt diet. In previous linkage studies, we identified quantitative trait loci on rat chromosome 19 (RNO19) linked to the SHR allele suggesting a protective effect against salt-induced hypertensive organ damage in SS. To test the relevance of this finding, we generated and characterized a consomic strain SS-19SHR in which RNO19 from SHR was introgressed into the susceptible background of SS. We compared the effects of low-salt (0.2% NaCl) and high-salt (4% NaCl) diet exposure for 8 weeks on the development of hypertension and target organ damage in male consomic and SS animals (n=14-20, each). Systolic blood pressure, relative left ventricular weight and urinary protein excretion were significantly lower in SS-19SHR compared to SS under both low-salt and high-salt diet (P < 0.05, respectively). Left ventricular atrial natriuretic peptide mRNA expression showed a more pronounced 4.5-fold increase in SS compared to SS-19 (two-fold) after high-salt (P < 0.05). In comparison to low diet, high-salt exposure induced a significant increase in vascular aortic hypertrophy index, left ventricular interstitial fibrosis (+210%) and perivascular fibrosis (+195%) in SS but not in consomic SS-19SHR (P < 0.05, respectively). These results demonstrate a strong protective effect of RNO19 from SHR on the development of hypertension, salt-sensitivity, cardiovascular and renal organ damage in SS. In particular, we demonstrate a genetic effect protecting against the development of cardiac fibrosis in salt-sensitive hypertension.

2007 Guidelines for the management of arterial hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC)

For several years the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC) decided not to produce their own guidelines on the diagnosis and treatment of hypertension but to endorse the guidelines on hypertension issued by the World Health Organization (WHO) and International Society of Hypertension (ISH)1,2 with some adaptation to reflect the situation in Europe. However, in 2003 the decision was taken to publish ESH/ESC specific guidelines3 based on the fact that, because the WHO/ISH Guidelines address countries widely varying in the extent of their health care and availability of economic resource, they contain diagnostic and therapeutic recommendations that may be not totally appropriate for European countries. In Europe care provisions may often allow a more in-depth diagnostic assessment of cardiovascular risk and organ damage of hypertensive individuals as well as a wider choice of antihypertensive treatment. The 2003 ESH/ESC Guidelines3 were well received by the clinical world and have been the most widely quoted paper in the medical literature in the last two years.4 However, since 2003 considerable additional evidence on important issues related to diagnostic and treatment approaches to hypertension has become available and therefore updating of the previous guidelines has been found advisable. In preparing the new guidelines the Committee established by the ESH and ESC has agreed to adhere to the principles informing the 2003 Guidelines, namely 1) to try to offer the best available and most balanced recommendation to all health care providers involved in the management of hypertension, 2) to address this aim again by an extensive and critical review of the data accompanied by a series of boxes where specific recommendations are given, as well as by a concise set of practice recommendations to be published soon thereafter as already done in 2003; …

The Emergent Cardiovascular Risk Factors and Organ Damage in Arterial Hypertension

Correction of cardiovascular risk factors is a mainstay of the treatment of hypertensive patients that have developed or might develop target organ damage. In addition to traditional risk factors, such as smoking, diabetes, obesity, and dyslipidemia, clinical research has identified additional conditions that put patients at a greater risk of developing cardiovascular disease and that might achieve particular relevance in the hypertensive state. Over the last decades, effective intervention in the treatment of traditional risk factors has reduced remarkably cardiovascular morbidity and mortality, but the incidence of coronary artery disease, stroke, and renal failure remains unacceptably high. Emerging cardiovascular risk factors are likely to contribute substantially to this picture and it could be anticipated that their contribution will become increasingly evident in the future. Physicians involved in the field of hypertension and dealing with problems concerning cardiovascular prevention should be aware of these new risk factors, give them an appropriate consideration, and correct them whenever possible. This review will consider the literature supporting the role of lipoprotein(a), homocysteine, and fibrinogen as contributors to cardiovascular risk in the general population and, more specifically, to the development and progression of target organ damage in hypertensive patients. The impact of early impairment of renal function on these factors will be analyzed in relation to the progression of renal disease as found in patients with hypertensive nephrosclerosis.

Improving Antihypertensive Agent Selection to Promote Nephroprotection

Introduction: Despite improved control rates of hypertension in the United States during the last twenty years, the rate of chronic kidney disease (CKD) and end-stage renal disease (ESRD) has steadily increased for the same time period. Purpose: The purpose for this review is to examine the evidence that the choice of antihypertensive therapy makes a difference in the promotion of nephroprotection. Method: A systematic comprehensive search of the National Library of Medicine utilizing Medline was conducted. Search terms included “antihypertensive therapy chronic kidney disease” and “nephropathy;” search limits were confined to randomized clinical trials. Results: Angiotensin receptor blockers (ARBs) and Angiotensin-converting enzyme inhibitors (ACEIs) are nephroprotective alone, and particularly in combination. Calcium channel blockers (CCBs) can be effective nephroprotective agents when combined with ACEIs and ARBs. Thiazide-type diuretics (TTDs) and beta-blockiers (BB) are not nephroprotective and TTDs may have nephrotoxic properties. Conclusion: Government sponsored guidelines that recommend TTDs as first line antihypertensive agents because of their lower acquisition costs may be contributing to the current epidemic of CKD and ESRD. ACEIs and ARBs are preferred first-line agents because they are effective in the prevention of renal as well as cardiovascular and cerebrovascular target organ damage associated with hypertension. When diuretic therapy is indicated for hypertension control, indapamide is preferred over TTDs for nephroprotection. Keywords: hypertension, nephroprotection, ace inhibitor, angiotensin receptor blocker

Arterial hypertension in chronic kidney disease: An ABPM study

ABPM is an accurate tool for estimating the relationship between true BP load and cardiovascular organ damage. Although cardiovascular morbidity is elevated in renal patients, few studies have used ABPM for BP assessment in patients with chronic kidney disease (CKD) before dialysis. Thus, we investigated 244 pts (164 men, aging 17-78 yrs) with CKD. Each patient had blood pressure (BP) assessed by 24 hrs ABPM, left ventricular mass index (LVMi) by M-Mode echocardiography, creatinine clearance (CrCl) by Cockroft formula, and hemoglobin (Hb), biochemical profile, and daily urinary protein excretion (UPROT) by routine methods. The values for 24 hr systolic (S), diastolic (D) BP and pulse pressure (PP) were 138±17 mmHg, 80±10, and 58±14 respectively; daytime SBP and DBP were 139±17 and 82±10 mmHg, while nighttime SBP and DBP 136±18 and 77±11. The prevalence of arterial hypertension (24 hr BP>130/80 mmHg) was 66%. Non dippers were 79%. CrCl was 36±27 ml/min, Hb 11.9± 2.0 g/dl and proteinuria 1.21±1.97 g/day. LVMi was 160±50 g/m2 bsa, and the prevalence of LVH (LVMi>125 g/m2 bsa) was 76%. A direct relationship was demonstrated between UPROT and 24 h SBP (p=0.0107), PP (p=0.0119), daytime SBP (p=0.0185), and nighttime SBP (p=0.0028), and an inverse relationship between CrCl and 24 h SBP (p=0.037), PP (p=0.0058), and nighttime SBP (p=0.0081). Additionally, a strict direct relationship was demonstrated between LVMi and 24 h SBP (p=0.0113), PP (p=0.0003), daytime SBP (p=0.0206) and nighttime SBP (p=0.0059). By multiple stepwise regression analysis PP was the only BP inversely associated with CrCl (p<0.0058), while nighttime SBP the only one directly associated with 24 h UPROT. Moreover, PP was the only significant predictor of LVMi (p=0.0003). Lastly, the prevalence of AH was significantly higher in patients with advanced CKD (stages 3 to 5) than early CKD (stages 1-2), (p=0.036, chi-square). In conclusion the prevalence of AH and non dipping is elevated in CKD patients and increases as renal function worsens. Moreover increased SBP is associated with proteinuria, and PP is the strongest predictor of LVH. ABPM is a reliable tool for identifying the link between BP load and CV damage in CKD, and AH is a powerful predictor of both the worsening of renal function and the development of cardiac damage much prior to the onset of ESRD.