“Hypertension is responsible for more deaths worldwide than any other medical disease known to man.”1 This quote from a renowned authority on medical epidemiology is startling and evocative, as I doubt one in 100— if not one in 1,000–health-care providers would have identified hypertension as the single greatest risk for future morbidity and mortality in their patient population.

Right now, 25% of the world’s adult population is hypertensive (BP 140+/90+ mm Hg) as defined by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7).2 In the United States, an estimated 30% of persons older than age 20 have hypertension.3 Many, if not most, of these individuals are undiagnosed, and of those who are formally diagnosed, only one in three is effectively treated, i.e., average BP <140/90. Framingham data show that 90% of participants with normal BP at age 55 were hypertensive before death.4 More than smoking, more than dyslipidemia, more than diabetes mellitus (DM), hypertension is by far the No. 1 risk factor for MI and stroke, the two most common causes of mortality.5-7 According to the World Health Organization, hypertension is easily the No. 1 preventable cause of death worldwide, far outpacing even such notables as tobacco, dyslipidemia, unsafe sex, obesity, physical inactivity, and alcohol abuse.

Advantages to effective treatment

The benefits of returning BP to “normal” (or at least <140/90) have been established repeatedly in studies conducted over the past 10 years. Hypertension is a silent, lurking killer, often requiring decades before its implications for morbidity and mortality are fully realized. Even though most recent studies encompassed time periods shorter than 10 years, virtually every one has confirmed significant improvements in overall mortality in cardiac and stroke events and from 30%-60% reduction in rates of congestive heart failure.7-9

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Behind the failure to recognize and treat

Despite ever-increasing knowledge regarding the threat of untreated hypertension, control rates in the United States have changed little in the past two decades. Lack of access to health care would be an obvious explanation for this failure, except for the fact that control of hypertension in this country (estimated to be 30% of the patient population) is significantly better than in other countries with universal health-care systems (i.e., Canada, England, Italy, Germany, Sweden).

The high cost of medicines is another convenient excuse. However, many generic formularies provide a drug regimen that would meet the needs of most Americans with high BP (enalapril 20 mg/day, carvedilol 6.25 mg b.i.d., hydrochlorothiazide [HCTZ] 12.5 mg/day, pravastatin 40 mg/day, and aspirin 81 mg/day) for approximately $15 per month. Cost of medication seems an unlikely explanation for our failure to identify and effectively treat hypertension.

The primary problem appears to be the failure of clinicians to consider a poor BP measurement on initial examination a snapshot of the patient’s BP status. Far too many abnormal BP readings are written off as white-coat hypertension. Abnormal BP readings should always be rechecked at the end of the visit. Patients thought to be at risk should use a simple home BP monitoring device to regularly measure morning and evening BP readings and record them for future office visits. Finally, far too few health-care practitioners know the Medicare requirements for 24-hour ambulatory monitoring of BP, which I liken to being the hemoglobin A1c of BP readings.

The etiology of hypertension

Although there seems to be a general consensus that the epidemic of hypertension is related to excessive sodium consumption, the really interesting observation regarding etiology is the relationship of potassium to sodium consumption. Twenty-first century humans have kidneys adapted through evolution to the diets of pre-18th century humans, in which the ratio of potassium and sodium in non-processed foods was roughly 1:1. The kidney is well-designed to retain sodium and excrete potassium. As the world’s diet has gradually changed to a near-total consumption of processed food, the ratio of potassium and sodium has changed dramatically. The ratio of potassium-to-sodium in processed foods is now 1:20, compared with the 1:1 ratio the kidney is engineered to handle. The kidney continues doing what it has always done; resorb sodium. Compelling evidence exists that the relative lack of potassium in our diets is as important as the amount of sodium intake.

It should be noted that total-body potassium stores are not reflected in a serum potassium determination. The efficacy of the thiazide diuretics chlorthalidone and HCTZ, especially as compared with other stronger diuretics (including the loop diuretics), lies not in the sodium excreted but much more likely in the change in potassium-to-sodium ionic composition of the vascular wall, leading to decreased systemic vascular resistance.

Compounding the problem of dietary potassium deficiency is the general ignorance regarding potassium-rich foods. For instance, bananas rank well below at least 30-40 other foods in providing potassium. And interestingly, the one form of potassium that fails to address the issue of potassium-to-sodium imbalance is potassium chloride, virtually the only form of supplemental potassium commonly prescribed by health-care providers. (The reasons for this are biochemical and deal with the difficulty a positively charged potassium ion has in crossing into an endothelial cell without something to accommodate the negatively charged chloride ion left behind). Health-food stores sell potassium gluconate tablets, but the amount required to correct the potassium (4.7 g/day10) requires ingestion of five of these large and bulky tablets four times daily. A compounding pharmacist can provide the same amount of potassium in the form of potassium bicarbonate, which requires ingestion of only two smaller capsules three times daily. Random checks for changes in serum potassium on this regimen revealed no change in serum potassium levels. Clearly, these recommendations will not apply to patients with known kidney disease.

Defining hypertension and need for therapy

The JNC 7 guidelines of 2003 define the threshold for pharmacologic intervention as a BP of 140/90 in the vast majority of patients. Exceptions are persons with DM or chronic kidney disease, where a BP of 130/80 was felt to be the threshold for justifying pharmacologic intervention. However, there is considerable evidence that a BP of 135/85, still “prehypertensive” by JNC 7 guidelines, doubles cardiovascular morbidity and mortality compared with a BP <120/70. As of 2007, the American Heart Association has recommended changing the threshold for initiating pharmacologic therapy to >130/70 not only for patients with DM or chronic kidney disease, but also for those with already established coronary artery disease (CAD), atherosclerotic peripheral vascular disease, abdominal aortic aneurysm, and/or carotid bruits and for persons without CAD who are considered high-risk. The threshold is lowered to >120/70 for any person with a current or remote history of congestive heart failure (CHF).

The now-accepted final word on the significance of BP readings comes from a nearly 14-year study of 29,829 subjects who did not have coronary heart disease (CHD) and were not taking medication for hypertension.11 This study found that in Caucasians, diastolic BP is the best predictor of CHD mortality in persons younger than age 40, whereas systolic BP (SBP) is the best predictor in persons aged 40 years and older. In African Americans, SBP is the best predictor for all age groups.