Do We Really Need a New Definition of Hypertension?

In the September issue of The Journal of Clinical Hypertension (JCH) that announced that the JCH had become an official journal of the American Society of Hypertension, a position paper entitled “Expanding the Definition and Classification of Hypertension” ¹ was published. There were two accompanying editorials. ² , ³ The crux of the argument, with which no one would disagree, is that there is more to hypertension than just high blood pressure (BP), or to put it another way, two patients with the same level of BP may have very different levels of cardiovascular (CV) risk, and hence different needs for treatment. This fact was recognized by JNC VI, ⁴ where for any given value of BP, patients were classified in one of three risk groups according to the presence or absence of target organ damage. The idea was dropped by JNC 7, ⁵ where treatment recommendations are based solely on BP.

While the concept is virtuous, the devil is in the details. The proposed new definition of hypertension from the Hypertension Writing Group (HWG) reads as follows:

Hypertension is a progressive cardiovascular syndrome arising from complex and interrelated etiologies. Early markers of the syndrome are often present before blood pressure elevation is observed; therefore, hypertension cannot be classified solely by discrete blood pressure thresholds. Progression is strongly associated with functional and structural cardiac and vascular abnormalities that damage the heart, kidneys, brain, vasculature, and other organs, and lead to premature morbidity and death.

According to the Oxford English Dictionary, the word “definition” can mean “the setting of bounds or limits,” or “the action of defining, or stating exactly what a thing is, or what a word means.” The old definition of hypertension was clear: a BP >140/90 mm Hg. While one might quibble about how the BP was measured, it was a definition that was easily understood by professionals and lay people alike, and had a huge public health impact. So what does the new definition mean, and how would we explain it to our patients? It has three sentences. The first one may be paraphrased that the causes of hypertension are complicated. The second one says that it is not just defined by BP, and the third that it is bad for you. So how do we decide whether a patient has hypertension or not?

The idea that factors other than BP should be used to classify the CV disease risk in individual patients is not a new one, and as the HWG paper acknowledges, several tools have been developed to give a quantitative estimate of risk of coronary heart disease events, of which the best known in the United States is the Framingham risk score, which has recently been updated by the American Heart Association/American College of Cardiology. ⁶ The proposed new definition of hypertension uses four categories of variables to classify patients: BP, CV risk factors, early disease markers, and target organ disease. There are four levels of hypertension, as in JNC 7, although their definition is very different. HWG stage 1 hypertension is defined by a number of factors: “occasional or intermittent BP elevations”; a possible BP range of 120‐160 mm Hg systolic, and 80‐100 mm Hg diastolic; one or more risk factors; zero or one early disease markers; and no target organ damage. One of the stated goals of the new HWG classification is to break up the JNC 7 “prehypertension” category into those who are at genuinely high risk, and those at low risk. But does it achieve this? Let us look at two hypothetical patients and see how the new and the old systems would classify them.

Patient 1 is a 60‐year‐old man with a systolic pressure of 124 mm Hg, who has a sedentary lifestyle, but is otherwise healthy. Patient 2 is a 50‐year‐old man with a systolic pressure of 158 mm Hg and an elevated total cholesterol (240 mg/dL) and serum creatinine. Patient 1 has a systolic pressure that puts him in either the normal or stage 1 category, but he also has two HWG risk factors (increasing age and sedentary lifestyle), so he is classified as having stage 1 hypertension. By JNC 7 criteria, he would be a prehypertensive (and hence not require drug treatment), and his Framingham score would be 5 (five points for his age, but no others). This gives him an absolute risk of 8% for a CVD event over 10 years, and he is classified as being below average risk for his age.

Patient 2 has a BP that puts him in the stage 1 or 2 HWG range, and he has two HWG risk factors (BP ≥140/90 mm Hg and elevated low‐density lipoprotein cholesterol [LDL‐C]) and one early disease marker (elevated serum creatinine), so he is also classified as HWG stage 1 hypertension. JNC 7 would put him in stage 1 hypertension (and hence recommend antihypertensive treatment), and his Framingham score is 7 (three points for his age, two for his cholesterol, and two for his BP). This puts him in the average risk group for his age, and at an absolute risk of 13% over 10 years. Thus these two patients with very different risk profiles by conventional criteria are classified in the same risk group by the HWG criteria. But who among us would treat Patient 1, and who would not treat Patient 2? The proposed new classification would make much more sense if stage 1 hypertension were limited to individuals whose BP is in the prehypertensive range of JNC 7 (120/80 mm Hg to <140/90 mm Hg).

The implication of the HWG classification is that patients (if we should really call them that) with stage 1 hypertension are sick, or as the HWG paper states: “Identifying hypertension in persons with high risk profiles but with BP levels <140/90 mm Hg offers the advantage of helping both providers and patients to recognize that a disease state already exists.”

As Kostis et al. ² point out in their editorial accompanying the HWG paper, two people with a BP in the JNC 7 prehypertensive range (125/85 mm Hg) may have very different levels of risk. They cite a healthy 26‐year‐old woman and a 70‐year‐old man who is also a smoker and has high cholesterol and blood sugar levels. The latter is clearly at much higher risk, and our management of these two individuals would be very different. But here's the crux: would we treat their BP differently? The HWG paper is actually very vague about treatment recommendations, but the implication is that people with stage 1 hypertension should be treated. Clearly, the appropriate first‐line treatment of the 70‐year‐old diabetic smoker with a BP of 125/85 mm Hg is not to start him on antihypertensive drugs.

This brings me to the most critical deficit of the HWG paper—what happened to the BP? As hypertension is traditionally defined, the only way of determining whether someone has hypertension is to measure his or her BP. The HWG paper does acknowledge that BP is “dynamic and variable,” but its description of BP levels in the proposed stages of hypertension is vague. Thus in the table summarizing the different categories of hypertension, stage 1 is described as “Occasional or intermittent BP elevations,” stage 2 as “Sustained elevations,” and stage 3 as “Marked and sustained elevations.” What do these mean? Unfortunately, we are left in the dark. BP measurement should be about numbers, not about words. For the past 50 years or so, the definition of hypertension based on BP levels (usually 140/90 mm Hg) has served us very well. All of the many clinical trials that have shown that treating hypertension lowers CV risk have relied on precise BP criteria for inclusion in the trials, and it is these trials that justify our existence as hypertension specialists. The treatments that we prescribe for our patients are primarily focused on lowering the BP (and hence risk), and once again we rely on numbers to tell us whether we are doing a good job. All physicians, and most patients, know that the BP is supposed to be less than 140/90 mm Hg. This simple message seems to have been lost in the new HWG definition of hypertension, which does not specify any BP level.

We can all agree that the time has come to go beyond BP in our evaluation and treatment of hypertensive patients, and to treat on the basis of “global risk,” but this should be done without losing sight of the primacy of BP. BP is actually a very potent predictor of risk, despite the now well recognized fact that, as conventionally measured, the estimation of an individual's true BP is very imprecise. The HWG paper pays little attention to the potential improvements in risk that can be obtained using modern techniques of BP measurement such as self‐ and ambulatory monitoring. This may be particularly true in the case of prehypertension. Some years ago, we showed that a subgroup of subjects with normal clinic BP (<140/90 mm Hg) had increased “early markers” of CV disease as assessed by increased left ventricular mass and carotid plaque. ⁷ These individuals also had ambulatory BPs that were above the normal range, leading us to coin the term “masked” hypertension. There is emerging evidence (T.G.P., unpublished data, 2005) that these individuals can also be identified using self‐monitoring, and we have found that an elevated home BP in clinically normotensive individuals predicts increased left ventricular mass better than a single 24‐hour recording.

There are, in principle, at least three ways in which we might be able to improve the prediction of risk in our patients. The first is to make more extensive use of newer methods of BP measurement. Second, we can evaluate early markers of hypertensive CV disease (as proposed in the HWG paper) which, if present, may indicate that the BP has been higher than would be thought from the measured level (although this may be less likely to occur if we use out‐of‐office monitoring), with the implication that antihypertensive treatment should be more aggressive than it would otherwise be. The third evaluation is to identify concomitant conditions that are not directly the consequence of high BP, but which add to the CV risk. Examples are a high LDLC and smoking, where there are specific treatments that can lower the risk, but do not involve lowering the BP. There are certain other conditions that come into this second category where there is evidence that setting a lower target for the BP may lower risk, such as diabetes, renal disease and, possibly, patients with established coronary artery disease.

The goal of any new definition and classification of hypertension should be to improve the evaluation and treatment of patients, and it should be evidencebased. If we believe that the damage resulting from hypertension is from the BP itself, the first task should be to promote more accurate measurement of BP. Ambulatory and home BP monitoring are well established, and there is a rapidly growing database showing their value in predicting risk in individual patients. Improved methods of measuring clinic BP using automated recorders that can take multiple readings in the absence of a physician, thus avoiding the white coat effect, also have great promise. The relationship between BP and other risk factors with clinical events is quantitative and continuous, and classifying all hypertensive patients into four rather arbitrary groups may ultimately do them a disservice. What we urgently need are better algorithms based on a few well‐established risk markers that we can add to the prediction based on BP. If we do need a new definition of hypertension, it should be based on improved measures of BP, and should be separate from a new definition of risk.