Tag Archives: Blood Pressure

About prehypertension

Blood pressure is the force exerted on your artery walls as blood flows through your body. Slightly elevated blood pressure is known as prehypertension. Left untreated, prehypertension is likely to progress to definite high blood pressure. Both prehypertension and high blood pressure increase your risk of heart attack, stroke and heart failure.

A blood pressure reading has two numbers. The first, or upper, number measures the pressure in your arteries when your heart beats (systolic pressure). The second, or lower, number measures the pressure in your arteries between beats (diastolic pressure). Normal blood pressure is below 120 systolic/80 diastolic as measured in millimeters of mercury (mm Hg). Prehypertension is a systolic pressure from 120 to 139 or a diastolic pressure from 80 to 89.

When prehypertension was defined as a new category of blood pressure in 2003, many people who Continue reading About prehypertension

About Left Ventricular Hypertrophy

Left ventricular hypertrophy is enlargement (hypertrophy) of the muscle tissue that makes up the wall of your heart’s main pumping chamber (left ventricle).

Left ventricular hypertrophy develops in response to some factor, such as high blood pressure, that requires the left ventricle to work harder. As the workload increases, the walls of the chamber grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart.

If you have left ventricular hypertrophy, you’re at increased risk of heart disease, including heart attack, heart failure, irregular heartbeats (arrhythmia) and sudden cardiac arrest.

The incidence of left ventricular hypertrophy (LVH) increases with age and is more common in people who have high blood pressure or other heart problems.


Left ventricular hypertrophy usually develops gradually. You may experience no signs or symptoms, especially during the early stages of development. When signs or symptoms are present, they may include: Continue reading About Left Ventricular Hypertrophy

Drinking alcohol may boost blood pressure

Drinking alcohol, even moderate amounts, may boost blood pressure more than previously thought.

People with a genetic mutation that makes it difficult to consume alcohol had significantly lower blood pressure than regular or heavy drinkers, the researchers found.

People without the mutation who had about 3 drinks per day had “strikingly” higher blood pressure than people with the genetic change who tended to drink only small amounts or nothing at all.

The researchers said there was more than a two-fold risk for high blood pressure among drinkers and a 70 percent increased risk for “quite modest” drinkers compared to people with the genetic mutation.

High blood pressure, which affects more than a billion adults worldwide, can lead to stroke, heart failure, heart attack and kidney failure.

Previous studies have linked heavy drinking with high blood pressure while others have suggested that moderate alcohol intake provides health benefits such as lower cholesterol.

The genetic mutation is common in some Asian populations and discourages drinking because alcohol triggers facial flushing, nausea, drowsiness, headache and other unpleasant symptoms.

Salt and blood pressure in children

The relationship of dietary sodium to blood pressure in adults is well established by substantial epidemiological and clinical data as well as various pathophysiological studies. Not surprisingly, considerably less is known about the relationship in children.

In this issue researches analysed the salt to blood pressure link in a cross-sectional study of a large representative sample of British children. They found that, in children 4–18 years old, sodium, potassium, and energy intake, body mass index, arm circumference and all measures of blood pressure, increase with age. In the group as a whole, a significant direct relationship between salt intake and blood pressure was found, even after the adjustment for multiple potential confounders. Specifically, a difference in salt intake of 1 g was associated with a 0.4 mm Hg rise in blood pressure. However, the significance of this relationship disappeared after correction for energy intake. Stratification by 5-year age tertiles suggested a similar tendency towards a positive salt to blood pressure relation within each group. Interestingly, discretionary salt use, either at table or in cooking, was not associated with blood pressure in these youngsters.

The kidney, in normal circumstances, accommodates wide variations in sodium intake through compensatory excretion. In healthy humans, this occurs without change in systemic blood pressure. In practice, the short-term pressure response of individuals varies substantially with variations in sodium intake. Not surprisingly, therefore, it has been difficult in observational studies to demonstrate a meaningful or consistent link between dietary salt and blood pressure.

Nonetheless, these limitations of observational studies are of little moment since randomized clinical trials, the clearly preferred method to establish causality and draw clinical inferences, have defined the population impact of salt restriction. In fact, the link of blood pressure to dietary sodium is based on pretty strong stuff. More than 100 well designed and executed randomized clinical trials, and meta-analyses thereof, have unequivocally demonstrated, in adults, that a 75–100 mmol reduction in daily sodium intake can, on average reduce blood pressure by 3–4/<1 mm Hg—more in older, hypertensive, or black persons.

It should also be noted that blood pressure response to dietary change in sodium is hardly consistent. In some, blood pressure actually rises, and in most, a change in pressure is undetectable. Moreover, the blood pressure effect of substantial and sustained decrease in sodium consumption tends to attenuate over time and, in a 3-year randomized trial, virtually disappeared at the end of the study. In short, and with some caveats, there can be no quibble with the claim that sodium intake contributes to variation in blood pressure, and that this relationship is modulated by genetics, behaviour and environment. The findings here are consistent with this settled dogma.

The study has the strength of size, representativeness and multiple daily dietary records to estimate sodium intake. Its muted findings reflect the difficulty, in cross-sectional study, of identifying a robust association of sodium intake to blood pressure. For example, the strong correlation of energy intake and sodium has made separating the impact of these (like almost all other nutrients) factors difficult if not impossible. Interestingly, the 1980 clinical study by Cooper on 73 black and white school children in Chicago detected what the authors described as a ‘quantitatively weak’ (although their findings of a 1 mm Hg per gram of sodium increase was greater than seen here) but significant (P=0.045) relation of sodium to blood pressure. In Chicago, as opposed to the current study, urine collection replaced dietary recall as the basis of estimating sodium intake. Because the earlier study did not capture energy intake and could not assess its potentially confounding effect. On the other hand, creatinine excretion was available. Its inclusion in the analysis eliminated the significance of the relationship between sodium and blood pressure in these children.

Regrettably, the current report provides little information regarding other associations to blood pressure or variations in other characteristics that might be associated with variations in sodium intake. For example, stature and physical maturation are associated with blood pressure. Bigger children may be muscular or pudgy. Children who exercise vigorously may have large energy (and sodium) intakes, and be taller and leaner than youngsters who have the same body mass index and different life styles.
Perhaps, the best measure of growth and development available here is mid-arm circumference. The strong arm to blood pressure correlation may reflect muscle mass and suggests that diets high in energy (and therefore, among other things, sodium) may be conducive to physical maturation, along with a slightly higher blood pressure. In short, if this were the causal pathway, then higher pressure might even be a desirable sign in children.

Dietary intake is complex, and to characterize it on the basis of one element may well oversimplify any assessment of its value. For example, given the high correlation of energy with virtually all other nutrients, it is possible that those consuming more sodium (and energy) had more satisfactory consumption of other important dietary elements—both known and unknown. In any event, blood pressure is not the only measure of the health of children. The British Survey of Young People probably includes, in addition to physical and physiological data, information on other social, economic and developmental characteristics whose explanation might well inform our understanding of the relation of blood pressure, diet, health and development in these youngsters. For example, researches note that 18-year-old British residents, in 1997, were consuming approx2.6-g of sodium per day. That was similar to levels found in Chicago a decade earlier, and falls within the range of adult sodium intake seen world-wide in most countries and suggests that, a decade and 2 ago, these near adults were within that range.

It is also interesting to note that measures of discretionary sodium use did not correlate with blood pressure. This supports the Cochrane Collaboration conclusion that there was not sufficient evidence for a general dietary recommendation to reduce sodium intake. Parenthetically, it is interesting to note that in countries where most sodium intake is discretionary, as parts of East Asia, sodium intake is much higher than in Britain, where most sodium is not discretionary, but consumed in our foods!

Guess is that the findings in adults—namely, that a large drop in sodium could produce a detectable fall in pressure—is probably true for youngsters as well. But, it is also true that randomized clinical trials in adults have shown that lowering sodium intake increases sympathetic nerve activity, reduces insulin sensitivity, increases the activity of the renin–angiotensin system, and increases aldosterone secretion.

Taking Blood Pressure Pills at Night

For certain people, it may be better to take high blood pressure medications at night instead of in the morning , says study.
The researchers concluded that this simple change may help normalize blood pressure patterns in people at increased risk from heart and kidney disease.

In healthy people, blood pressure drops by 10 percent to 20 percent during sleep. Scientists suspect that this may occur in order to give arteries a bit of rest. People with hypertension who don’t experience this blood pressure dip at night are more likely to develop serious heart disease than other hypertension patients who do experience the dip.

People with chronic kidney disease are most likely to be “non-dippers,” which increases their risk of worsening kidney damage and heart disease.

In this study, 32 non-dippers with kidney disease started taking a high blood pressure drug at night instead of in the morning, the CP reported. Within two months, nearly 90 percent had turned into dippers, with an average seven-point drop in nighttime blood pressure. There were also signs of improved kidney function. The patients experienced no side effects or increases in daytime blood pressure.