Is it important to treat mild or moderate essential hypertension?

Yes. There is good evidence that a reduction in diastolic blood pressure decreases the relative risk for cerebrovascular and cardiovascular events. The data are most convincing with regard to the incidence of cerebrovascular accidents, where the diastolic blood pressure correlates with the risk of cerebrovascular accident. Therefore, patients with diastolic blood pressure 60 mmHg fare better than patients with diastolic pressure 80 mmHg with regard to risk for cerebrovascular accident.

What is the cause of hypertension?

It is multifactorial. There are good epidemiologic data of a genetic influence in offspring of hypertensive parents as well as offspring of parents with extremely low blood pressure, accounting for approximately 25% of the variability of patients’ blood pressure measurements. The genetic influences are most likely polygenic and include sodium sensitivity, renal kallikrein excretion, and adrenal sensitivity to angiotensin II and intracellular calcium levels.

Interacting with the genetic contribution are lifestyle and environmental influences. Alcohol intake in men and oral contraceptive use in women are the two leading causes of nonessential hypertension. Other factors known to affect blood pressure include caffeine intake, cigarette smoking, dietary potassium, sodium, and calcium intake, as well as obesity.

Can essential hypertension be classified?

Yes. The most useful classification system was developed by Dr. Laragh’s group, who performed sodium-renin profiling in a large number of hypertensive patients. In sodium-renin profiling, the patient’s plasma renin activity is determined in the sitting position without antihypertensive medication while a 24-hour urine collection is obtained to determine the patient’s sodium intake. Because sodium intake, postural position, and blood pressure medication all affect plasma renin activity, all variables must be accounted for. Most hypertensive patients demonstrate normal plasma renin activities for a given sodium intake, but approximately 35% have low-renin hypertension and 15% have high-renin hypertension. Importantly, patients with high-renin hypertension have a greater vasoconstrictor profile than those with low-renin hypertension, who tend to have increased circulating blood volume and a suppressed renin-angiotensin-aldosterone axis.

Why is this differentiation important?

Prospective studies have shown that patients with high-renin hypertension are at increased risk for cerebrovascular accidents and there is a trend toward an increased risk for cardiovascular accidents, especially young white men. Not only is renin-sodium profiling important from a prognostic standpoint, but it also allows the physician to choose an antihypertensive medication that will best treat the patient’s hypertension. For example, diuretics are most likely an effective antihypertensive agent in patients with low-renin hypertension (most commonly black or elderly) in whom intravascular volume expansion is present. In contrast, in patients with high-renin hypertension (young white men), converting enzyme inhibitors or sympathetic blocking agents are most effective. Clearly, to do renin-sodium profiling, it is necessary to take the patient off antihypertensive medication, which is often impossible to do. As well, the sample must be handled properly for measurement of plasma renin activity.

What are some indications that a patient’s blood pressure has been poorly controlled for some time?

The three organ systems bear the brunt of end-organ damage in hypertension:

Eyes: The two major circulatory systems involving the optic nerve are the retinal and choroidal vascular systems. Increased vascular reactivity in both is best promoted by the pressor angiotensin II, leading to neuroretinopathy being observed more often in high angiotensin II states.

Kidney: Essential hypertension is the second leading cause of renal failure in the United States. Blacks appear to have an increased renal sensitivity to the effects of hypertension independent of socioeconomic factors. Serum creatinine elevations and proteinuria are clinical markers for end-organ renal damage due to hypertension.

Heart: Left ventricular (LV) hypertrophy and increased LV mass are consequences of the increased cardiac workload imposed by the hypertensive process. M-mode echocardiography is more sensitive than electrocardiography or chest x-ray in demonstrating the presence of LV hypertrophy. The severity of the hypertensive state often correlates with LV mass, which is an early marker of risk for myocardial infarction or sudden death due to hypertension. Patients with LV hypertrophy are at 2- to 5-fold higher risk of sudden cardiac death than patients with normal LV mass (even when accounting for other risk factors). Both systolic and diastolic dysfunction as determined by LV compliance and filling are also markers of end-organ damage due to hypertension.

What guidelines are useful in the treatment of hypertension?

The most noninvasive way of treating hypertension should be attempted first:

‚ Dietary sodium restriction and calcium or potassium supplementation

‚ Removal of alcohol or cigarette use

‚ Increased physical activity and weight loss in obese patients

‚ Reduction in dietary saturated fats and cholesterol More often than not, medication is required.


What are the current recommendations for the medical treatment of uncomplicated mild essential hypertension?

At present, diuretics and sympathetic blocking agents should be used as first-line agents in the treatment of hypertension, due to their lower cost and proven efficacy. Other agents have not been shown to be less effective, but extended testing has not been performed to demonstrate equal benefit. Clearly, some patients may benefit from first-line treatment with calcium channel blockers, converting enzyme inhibitors, as well as alpha or alpha-beta blocking agents.

Is there a problem with treating patients’ blood pressure too low?

Some investigators seriously believe mortality and blood pressure in treated hypertensive patients are related in a J-shaped curve. In other words, at a certain point, a lower diastolic pressure represents a group of patients who are likely to do worse than their more hypertensive counterparts. Unfortunately, the data to support this view were not collected in a prospective double-blinded fashion and may represent those patients with other medical conditions, such as malignancy or infection.

If hypertensive patients with increased LV mass are treated aggressively, will they reduce heart size, return function to normal, or reduce the risk of a fatal arrhythmia or infarction?

Many prospective, blinded antihypertensive trials have demonstrated reversal of LV hypertrophy by echocardiographic measurement. However, whether the increased risk of fatal myocardial infarction is reduced by reversing LV hypertrophy is unknown and debated. Recent work in animal models or hypertension induced by angiotensin II or aldosterone shows an early increase in collagen II levels and induction of myocardial fibrosis that may not be reversible. As well, the increase in collagen synthesis and myocardial fibrosis demonstrated in these studies was inhibited by early application of angiotensin-converting enzyme inhibitors and high doses of spironolactone. Clearly, more work is needed including long-term follow-up studies of cardiovascular mortality in patients with treated and reversed LV hypertrophy.

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