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Kuwait is a small country located on the northeastern part of the Arabian Peninsula. The most recent data on hypertension show: (a) a prevalence rate of 26.3%, (b) awareness of the disorder in only 23% of affected persons, (c) mild to moderate hypertension in 86% of subjects, (d) increased proportion of hypertensive patients at older age, (e) high prevalence in diabetics at age > 35 years and (f) high association with obesity. Most patients still use beta-blockers with a recent surge in calcium channel-blockers (except for immediate-release nifedipine) and angiotensin converting enzyme inhibitors. Hypertension was responsible for 935 hospital admissions in 1997. Its related co-morbid conditions such as ischemic heart disease, cerebrovascular accidents, congestive heart failure and chronic renal failure were responsible for 4111, 791, 690 and 978, hospital admissions, respectively, during the same year. Hypertension is the fourth common cause of end-stage renal disease. The most disturbing observation is the lack of disease awareness and the persistently high mortality rate of the disease and its co-morbid conditions. Efforts should be directed towards increase of awareness of this important risk factor for cardiovascular disease.
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PMID:Hypertension in kuwait: the past, present and future. 1821 46

Treatment with different antihypertensive drug classes has varied effects on glucose metabolism. Thiazide diuretic use in hypertensives has been associated with the development of glucose intolerance and diabetes. Some findings suggest that the probability of worsening glucose metabolism and the development of new diabetes after thiazide initiation is associated with increasing body mass index. Nonselective or beta(1) selective beta-blockers may also lead to decreased insulin sensitivity in hypertensive patients. Newer beta-blockers that cause vasodilatation and beta-blockers that have intrinsic sympathomimetic activity may not have these deleterious effects on insulin sensitivity and glucose metabolism. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers may exert beneficial effects on glycemic control through a variety of mechanisms related to the inhibition of angiotensin II. These agents may be particularly useful in patients with microalbuminuria to slow the progression of renal disease. While there may be some small differences among different classes of calcium channel blockers, there is little net effect of these agents on glucose metabolism. The prevalence of obesity, hypertension, and type 2 diabetes mellitus is increasing in the US. In this setting, it is important to individualize antihypertensive therapy and to monitor its metabolic consequences so that potential adverse effects that would negate some of the benefits of blood-pressure lowering are minimized.
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PMID:Effects of antihypertensives on glucose metabolism. 1837 Jul 75

The prevalence of left ventricular hypertrophy (LVH) rises with severity of hypertension (HT), age, and obesity. Its prevalence ranges from 20% in mildly hypertensive patients to almost 100% in those with severe or complicated HT. However, the diagnosis of LVH is not straightforward, and the definitions and criteria used in clinical studies lack consistency. While many factors play a role in the onset and progression of LVH, blood pressure (BP) is recognized as a central factor. Twenty-four-hour BP measurements are more closely related to LVH than conventional BP readings taken in the clinician's office. Increased renin-angiotensin system (RAS) activity also plays an important role in the development of LVH, and various studies show a correlation between plasma renin activity and left ventricular mass (LVM). LVH is a recognized marker of HT-related target organ damage, and a strong and independent risk factor for adverse cardiovascular (CV) outcomes. CV risk increases with increasing LVM, and decreases with regression of LVH in response to antihypertensive treatment. Therefore the detection, prevention, and reversal of LVH are important goals in HT management. Most antihypertensive drugs can attenuate BP and LVH. However, each drug class may induce LVH regression to a different extent and these extents seldom correlate with the degree of BP reduction achieved. Data from the few large comparative studies in this area suggest that certain classes of antihypertensive drugs and/or their combinations are more effective than others. In particular, calcium channel blockers and drugs that target the RAS, such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), appear to have a specific effect on LVH, independent of BP reduction. Guidelines, therefore, have recommended these drug classes for the treatment of hypertensive patients with LVH.
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PMID:Left ventricular hypertrophy and clinical outcomes in hypertensive patients. 1843 40

Several factors have been incriminated in the genesis of diabetic nephropathy. To elucidate their interplay, we have used a hypertensive, obese, diabetic rat model with nephropathy (SHR/NDmcr-cp) that mimics human type 2 diabetes. This model is characterized by hypertension, obesity with the metabolic syndrome, diabetes with insulin resistance, and intrarenal advanced glycation end product (AGE) accumulation. In order to achieve renoprotection, which was evaluated by histology and albuminuria, various therapeutic approaches were used: caloric restriction, antihypertensive agents (angiotensin II receptor blocker [ARB] and calcium channel blocker), lipid- (bezafibrate) or glucose-lowering (insulin and pioglitazone) agents, and cobalt chloride (a hypoxia-inducible factor activator). Altogether, renoprotection is not necessarily associated with blood pressure or glycemic control. By contrast, it is almost always associated with decreased AGE formation, with the exception of insulin, which induces hyperinsulinemia, eventually leading to an overproduction of transforming growth factor-beta. AGE formation is reduced directly by in vitro active compounds (e.g., ARBs) or indirectly by in vitro inactive compounds (e.g., pioglitazone and cobalt). In the latter cases, AGE reduction may reflect a decreased oxidative stress as it is concomitant with a marked reduction of oxidative stress markers. It remains to be seen whether the renoprotection offered by these various approaches may be additive.
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PMID:Inhibition of advanced glycation end products: an implicit goal in clinical medicine for the treatment of diabetic nephropathy? 1844 8

Blacks have the highest rates of hypertension and cardiovascular disease, with earlier onset, greater severity, and more target organ damage including coronary disease, heart failure, stroke, and end-stage renal disease. A major reason is the greater prevalence of other cardiovascular disease risk factors, particularly obesity, inactivity, and diabetes mellitus, along with socioeconomic differences, adherence, and achievement of goals. This review focuses on the burden of cardiovascular disease in blacks. Therapeutic lifestyle changes and pharmacologic interventions to decrease clinical events in this high-risk group are described. Intensive blood pressure control is a primary means of "stopping the clock" in the progression of cardiovascular disease and renal disease. Thiazide diuretics remain primary first-step agents, especially for uncomplicated hypertension; calcium channel blockers are also efficacious. However, renin-angiotensin system modulators may also be beneficial, especially with a diuretic, considering the high prevalence in this group of patients of compelling indications for use of such agents.
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PMID:Cardiovascular disease in blacks: can we stop the clock? 1845 98

The epidemic of obesity in the United States and around the world is intensifying in severity and scope and has been implicated as an underlying mechanism in systemic hypertension. Obese hypertensive individuals characteristically exhibit volume congestion, relative elevation in heart rate, and high cardiac output with concomitant activation of the renin-angiotensin-aldosterone system. When the metabolic syndrome is present, insulin resistance and hyperinsulinemia may contribute to hypertension through diverse mechanisms. Blood pressure can be lowered when weight control measures are successful, using, for example, caloric restriction, aerobic exercise, weight loss drugs, or bariatric surgery. A major clinical challenge resides in converting short-term weight reduction into a sustained benefit. Pharmacotherapy for the obese hypertensive patient may require multiple agents, with an optimal regimen consisting of inhibitors of the renin-angiotensin-aldosterone system, thiazide diuretics, beta-blockers, and calcium channel blockers if needed to attain contemporary blood pressure treatment goals.
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PMID:Secondary hypertension: obesity and the metabolic syndrome. 1860 42

The metabolic syndrome considerably increases the risk of cardiovascular and renal events in hypertension. It has been associated with a wide range of classical and new cardiovascular risk factors as well as with early signs of subclinical cardiovascular and renal damage. Obesity and insulin resistance, beside a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with proinflammatory properties, have been implicated in the pathogenesis. The close relationships among the different components of the syndrome and their associated disturbances make it difficult to understand what the underlying causes and consequences are. At each of these key points, insulin resistance and obesity/proinflammatory molecules, interaction of demographics, lifestyle, genetic factors, and environmental fetal programming results in the final phenotype. High prevalence of end-organ damage and poor prognosis has been demonstrated in a large number of cross-sectional and a few number of prospective studies. The objective of treatment is both to reduce the high risk of a cardiovascular or a renal event and to prevent the much greater chance that metabolic syndrome patients have to develop type 2 diabetes or hypertension. Treatment consists in the opposition to the underlying mechanisms of the metabolic syndrome, adopting lifestyle interventions that effectively reduce visceral obesity with or without the use of drugs that oppose the development of insulin resistance or body weight gain. Treatment of the individual components of the syndrome is also necessary. Concerning blood pressure control, it should be based on lifestyle changes, diet, and physical exercise, which allows for weight reduction and improves muscular blood flow. When antihypertensive drugs are necessary, angiotensin-converting enzyme inhibitors, angiotensin II-AT1 receptor blockers, or even calcium channel blockers are preferable over diuretics and classical beta-blockers in monotherapy, if no compelling indications are present for its use. If a combination of drugs is required, low-dose diuretics can be used. A combination of thiazide diuretics and beta-blockers should be avoided.
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PMID:The metabolic syndrome in hypertension: European society of hypertension position statement. 1880 11

It has been suggested that increased dietary calcium intake can attenuate obesity. Calcium antagonists, such as benidipine, also have been shown to have an anti-obesity effect. However, the mechanism for calcium-related anti-obesity effect has not yet been established. A defective brown adipose tissue thermogenesis has been shown in obese rodents. This study was designed to examine the direct effects of calcium channel blocker benidipine and calmodulin antagonist W7 administration on the adaptive thermogenesis in brown adipose tissue taken from the genetically obese mice and their lean controls. The GDP binding to brown-fat cell mitochondria was used as a brown adipose tissue thermogenic index. The results show that benidipine treatment had no marked effect on brown-fat cell GDP-binding capacities in both obese and lean mice. However, GDP-binding capacities were significantly reduced in both obese and lean mice after the W7 administration. The results of this study support the previous finding that benidipine did not have direct thermogenic effect on brown adipose tissue and suggest that the change in intracellular calmodulin availability might contribute to the adaptive thermogenesis in brown adipose tissue.
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PMID:The effects of calcium channel blocker benidipine and calmodulin antagonist W7 on GDP-binding capacity of brown adipose tissue in mice. 1895 5

Several factors are incriminated in the genesis of diabetic nephropathy (DN). To elucidate their interplays, we utilized a diabetic rat model with nephropathy (SHR/NDmcr-cp). This model is characterized by hypertension, obesity with the metabolic syndrome, diabetes with insulin resistance, and intrarenal AGE accumulation. Various therapeutic approaches were used to achieve renoprotection. Caloric restriction corrects metabolic abnormalities and protects the kidney without correcting hypertension. Anti-hypertensive agents, angiotensin II receptor blocker (ARB) and calcium channel blocker, lower blood pressure to the same extent, but only ARBs protect the kidney without changes in metabolic abnormalities. Glycemic control is better with insulin than with pioglitazone. The plasma insulin level is increased by insulin but decreased by pioglitazone which worsens the obesity. Nevertheless, pioglitazone provides renoprotection unlike insulin, perhaps as a result of the up-regulation of TGF-beta by hyperinsulinemia. Cobalt up-regulates the expression of a hypoxia-inducible factor (HIF) and its downstream genes (erythropoietin, VEGF, HO-1). It protects the kidney without correcting hypertension and metabolic abnormalities. Altogether, renoprotection is not necessarily associated with blood pressure or glycemic control. By contrast, it is almost always associated with a decreased AGE formation. AGE reduction may reflect a decreased oxidative stress as it is concomitant with a marked reduction of oxidative stress markers.
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PMID:Inhibition of advanced glycation end products (AGEs): an implicit goal in clinical medicine for the treatment of diabetic nephropathy? 1895 18

Of the more than 5 million Americans who have heart failure (HF), 30% to 50% have HF with preserved ejection fraction (HF-PEF). HF-PEF commonly occurs in elderly patients, especially women, with comorbidities of hypertension, left ventricular hypertrophy, diabetes, myocardial ischemia, and obesity. HF-PEF is associated with high morbidity and mortality. Although two large multicenter randomized, placebo-controlled trials evaluating an angiotensin-converting enzyme inhibitor (ACEI) and an angiotensin receptor blocker (ARB) in patients with HF-PEF did not demonstrate any statistically significant benefit in their primary end points, they did suggest that these agents may have a modest role in reducing HF hospitalizations. Although calcium channel blockers and beta-blockers may be of benefit in patients with HF-PEF, large clinical trial data are not available to support their routine use in all patients with HF-PEF. Subgroup analysis does not support the use of digoxin in patients with HF-PEF in sinus rhythm. Current therapeutic recommendations for HF-PEF are aimed at 1) management of HF symptoms with sodium and fluid restriction along with diuretics for volume overload and 2) treatment of concomitant comorbidities, especially hypertension, rate and possibly rhythm control of atrial fibrillation, and evaluation and treatment of myocardial ischemia and anemia. ACEIs, ARBs, calcium channel blockers, and beta-blockers are recommended for HF-PEF patients who have other established indications for their use. Results are awaited from ongoing clinical trials with another ARB, irbesartan, and an aldosterone blocker, spironolactone.
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PMID:Treatment of patients with heart failure and preserved ejection fraction. 1902 82


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