These guidelines have been written to provide a straightforward approach to managing hypertension in the community. We have intended that this brief curriculum and set of recommendations be useful not only for primary care physicians and medical students, but for all professionals who work as hands-on practitioners.We are aware that there is a great variability in access to medical care among communities. Even in so-called wealthy countries, there are sizable communities in which economic, logistic, and geographic issues put constraints on medical care. And, at the same time, we are been reminded that even in countries with highly limited resources, medical leaders have assigned the highest priority to supporting their colleagues in confronting the growing toll of devastating strokes, cardiovascular events, and kidney failure caused by hypertension.Our goal has been to give sufficient information to enable healthcare practitioners, wherever they are located, to provide professional care for people with hypertension. All the same, we recognize that it will often not be possible to carry out all of our suggestions for clinical evaluation, tests, and therapies. Indeed, there are situations in which the most simple and empirical care for hypertensionsimply distributing whatever antihypertensive drugs might be available to people with high blood pressure -is better than doing nothing at all. We hope that we have allowed sufficient flexibility in this statement to enable responsible clinicians to devise workable plans for providing the best possible care of hypertension in their communities.We have divided this brief document into the following sections:1. General introduction 2. Epidemiology 3. Special issues with black patients (African ancestry) 4. How is hypertension defined? 5. How is hypertension classified? 6. Causes of hypertension 7. Making the diagnosis of hypertension 8. Evaluating the patient 9. Physical examination 10. Tests

These guidelines have been written to provide a straightforward approach to managing hypertension in the community. We have intended that this brief curriculum and set of recommendations be useful not only for primary care physicians and medical students, but for all professionals who work as hands-on practitioners.We are aware that there is great variability in access to medical care among communities. Even in so-called wealthy countries there are sizable communities in which economic, logistic, and geographic issues put constraints on medical care. And, at the same time, we are been reminded that even in countries with highly limited resources, medical leaders have assigned the highest priority to supporting their colleagues in confronting the growing toll of devastating strokes, cardiovascular events, and kidney failure caused by hypertension.Our goal has been to give sufficient information to enable health care practitioners, wherever they are located, to provide professional care for people with hypertension. All the same, we recognize that it will often not be possible to carry out all of our suggestions for clinical evaluation, tests, and therapies. Indeed, there are situations where the most simple and empirical care for hypertension-simply distributing whatever antihypertensive drugs might be available to people with high blood pressure-is better than doing nothing at all. We hope that we have allowed sufficient flexibility in this statement to enable responsible clinicians to devise workable plans for providing the best possible care for patients with hypertension in their communities.We have divided this brief document into the following sections:

Despite the effects of sodium intake on blood pressure and on response to antihypertensive medication, sodium intake is rarely monitored in clinical practice. The current method, the 24-hour urine collection for sodium excretion, is cumbersome, often incorrectly performed, and not commonly ordered. Further, its results have limited meaning because of the substantial day-to-day variation in sodium intake. A spot urine test to enable convenient, inexpensive, and serial monitoring of sodium excretion would be desirable. In this study, the accuracy of predicting 24-hour sodium excretion from a spot urine sample was assessed. The urine sodium ⁄ creatinine ratio was determined from the following urine samples: an ''AM sample,'' submitted at the beginning of the 24-hour urine collection; a ''PM sample'' collected in the later afternoon ⁄ early evening before dinner, at roughly the midpoint of the collection; and a ''random sample,'' collected after its completion. The ratio was then corrected for 24-hour creatinine excretion. The strongest correlation between predicted and actual 24-hour sodium excretion was observed with the PM sample collected near the midpoint (r=0.86, P<.001). This sample also identified persons with sodium excretion <100 mEq ⁄ d with a sensitivity of 100% and specificity of 82%. The sodium ⁄ creatinine ratio from a spot urine sample collected in the late afternoon ⁄ early evening at roughly the midpoint of the 24-hour collection, and adjusted for 24-hour creatinine excretion, strongly correlated with 24-hour sodium excretion. Additional studies are merited to further evaluate the role of the spot urine sample in assessing sodium intake.

BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.

(Greenwich). 2008;10:477-484 . © 2008 Le Jacq C onsiderable attention is paid to the problem of thiazide-induced hypokalemia. Much less attention is paid to thiazide-induced hyponatremia (tih), which is seen with considerable frequency. tih occurs predominantly in the elderly.1-4 as a result, it is not encountered in the data of large drug treatment trials that involve predominantly younger patients. however, in the systolic hypertension in the Elderly program (shEp), which focused on older patients, hyponatremia (defined as a sodium level <130 mEq/L) was observed in 4.1% of patients treated with chlorthalidone vs 1.3% in the control group, while hypokalemia (potassium level <3.2 mEq/L) was observed in 3.9% of patients in the treatment group.5 thirty percent of patients were receiving 12.5 mg of chlorthalidone, and 60% were receiving 25 mg.5 in another study in the elderly, diuretic-induced hyponatremia, defined as a serum sodium concentration ≤130 mEq/L, was seen in 17% and hypokalemia in 6.6%.6 fiftythree percent of patients were receiving a thiazide diuretic and 24% a loop diuretic. 6 in patients with tih, an average daily hydrochlorothiazide dose of 35 mg has been reported, with 44% of patients having received ≥50 mg.7 however, in 10% of cases the dose was only 12.5 mg.8 the risk of tih is 3-fold higher in persons older than 70 years and is higher among women, possibly because of smaller body size or lower sodium intake.2,3 With the high prevalence of hypertension in the elderly and the routine use of thiazide diuretics to treat it, tih is clearly a prevalent problem.CLINICAL PRESENTATION tih can develop acutely or gradually. it can range from mild to severe and from asymptomatic to symptomatic. the onset is within 2 weeks of starting the diuretic in 50% to 90% of cases, but it can occur within a day or two or even after a single dose.3,7-9 hyponatremia can occur after months or years of taking a thiazide and is likely related to subsequent contributory factors such as reduction of R e v i e w P a p e r