Rapid Rise in Systolic BP Midlife Predicts Greater LVMI

CHICAGO – The rate of increase in systolic blood pressure during an adult’s 30s, 40s, and 50s is a stronger predictor of later structural heart damage than is their absolute blood pressure.

This finding from the longest-running birth cohort study in the United Kingdom – now entering its 66th year of follow-up – has major implications for how high blood pressure is approached, according to Dr. Arjun K. Ghosh, a cardiologist at the National Heart and Lung Institute, Imperial College London.

"At the moment, if patients don’t reach that certain magic level of high blood pressure, they’re often not treated. They’re asked to come back, and a watch-and-wait policy is instituted," he noted at the annual meeting of the American College of Cardiology. "What we found in our study, in measuring people’s blood pressure from their 30s on, was that those with a faster rise in blood pressure had a heavier heart, or increased left ventricular mass, when they were 60-64 years of age. And this was true for any level of blood pressure, high or low. It actually wasn’t how high the blood pressure became as it was how quickly the blood pressure was rising."

A second key finding was that left ventricular hypertrophy was not reversed among hypertensive study participants whose blood pressure was normalized via medication. These patients had a significantly greater left ventricular mass indexed to body surface area (LVMI) as did their peers who had the same normal-range blood pressure but had never been treated for hypertension.

"This policy of watching and waiting for the blood pressure to cross a certain threshold before starting antihypertensive therapy may be waiting too long. The irreversible damage has already been done," Dr. Ghosh continued. "A new approach may be required. We need to identify those individuals whose blood pressure rises the fastest and target them with the most effective treatment."

His analysis involved 1,653 participants who were in the Medical Research Council National Survey of Health and Development and were born in Britain in a single week in March 1946. Subjects were followed serially, and underwent echocardiography and LVMI measurement at age 60-64.

The higher a subject’s systolic blood pressure at age 36, 43, 53, or 60-64, the greater the LVMI at age 60-64.

Moreover, individuals with well controlled blood pressure on antihypertensive therapy at age 60-64 had a mean LVMI that was 8.6 g/m² greater than that of subjects not on treatment. Participants on antihypertensive therapy at age 53 had a mean LVMI that was 7.3 g/m² higher than in those who weren’t, and individuals on treatment at age 43 had a mean LVMI at age 60-64 that was 11.5 g/m² more than in those not on treatment at age 43.

A sharp increase in blood pressure between ages 43 and 53 was particularly detrimental for LV size at age 60-64. An increase of 1 standard deviation in systolic blood pressure during that time period was associated with a 4 g/m² higher LVMI, whereas an increase of 1 standard deviation between ages 36 and 43 was associated with a 1 g/m² increase.

As this was an observational study, a clinical trial needs to be conducted before the findings can be translated into a change in practice. This study would compare the watch-and-wait strategy of threshold-based antihypertensive therapy with this novel approach stressing early identification and treatment of patients with rapidly increased systolic blood pressure, Dr. Ghosh said. Such a study is eminently feasible and could yield results in about 5 years using as the end point change in left ventricular size, which is well-established as a key driver of heart failure.

This new concept that the trajectory at which blood pressure rises has an irreversible adverse impact on cardiac structure is quite plausible, according to Dr. Joanne Foody.

"I think the real kernel is there needs to be more ongoing monitoring, particularly in young adults, so we don’t miss that window," she said in an interview.

The challenge is that young people leave their pediatricians and, except for injuries or acute illnesses, may not see a physician again until they’re in their 40s, observed Dr. Foody, medical director of the cardiovascular wellness program at Brigham and Women’s Hospital, Boston.

"We need to do more for people and do it earlier. People don’t really start thinking about preventive health until they’re in their 40s and 50s," she said.

The study was sponsored by the U.K.’s Medical Research Council. Dr. Ghosh and Dr. Foody reported having no financial conflicts.

CHICAGO – The rate of increase in systolic blood pressure during an adult’s 30s, 40s, and 50s is a stronger predictor of later structural heart damage than is their absolute blood pressure.

This finding from the longest-running birth cohort study in the United Kingdom – now entering its 66th year of follow-up – has major implications for how high blood pressure is approached, according to Dr. Arjun K. Ghosh, a cardiologist at the National Heart and Lung Institute, Imperial College London.

"At the moment, if patients don’t reach that certain magic level of high blood pressure, they’re often not treated. They’re asked to come back, and a watch-and-wait policy is instituted," he noted at the annual meeting of the American College of Cardiology. "What we found in our study, in measuring people’s blood pressure from their 30s on, was that those with a faster rise in blood pressure had a heavier heart, or increased left ventricular mass, when they were 60-64 years of age. And this was true for any level of blood pressure, high or low. It actually wasn’t how high the blood pressure became as it was how quickly the blood pressure was rising."

A second key finding was that left ventricular hypertrophy was not reversed among hypertensive study participants whose blood pressure was normalized via medication. These patients had a significantly greater left ventricular mass indexed to body surface area (LVMI) as did their peers who had the same normal-range blood pressure but had never been treated for hypertension.

"This policy of watching and waiting for the blood pressure to cross a certain threshold before starting antihypertensive therapy may be waiting too long. The irreversible damage has already been done," Dr. Ghosh continued. "A new approach may be required. We need to identify those individuals whose blood pressure rises the fastest and target them with the most effective treatment."

His analysis involved 1,653 participants who were in the Medical Research Council National Survey of Health and Development and were born in Britain in a single week in March 1946. Subjects were followed serially, and underwent echocardiography and LVMI measurement at age 60-64.

The higher a subject’s systolic blood pressure at age 36, 43, 53, or 60-64, the greater the LVMI at age 60-64.

Moreover, individuals with well controlled blood pressure on antihypertensive therapy at age 60-64 had a mean LVMI that was 8.6 g/m² greater than that of subjects not on treatment. Participants on antihypertensive therapy at age 53 had a mean LVMI that was 7.3 g/m² higher than in those who weren’t, and individuals on treatment at age 43 had a mean LVMI at age 60-64 that was 11.5 g/m² more than in those not on treatment at age 43.

A sharp increase in blood pressure between ages 43 and 53 was particularly detrimental for LV size at age 60-64. An increase of 1 standard deviation in systolic blood pressure during that time period was associated with a 4 g/m² higher LVMI, whereas an increase of 1 standard deviation between ages 36 and 43 was associated with a 1 g/m² increase.

As this was an observational study, a clinical trial needs to be conducted before the findings can be translated into a change in practice. This study would compare the watch-and-wait strategy of threshold-based antihypertensive therapy with this novel approach stressing early identification and treatment of patients with rapidly increased systolic blood pressure, Dr. Ghosh said. Such a study is eminently feasible and could yield results in about 5 years using as the end point change in left ventricular size, which is well-established as a key driver of heart failure.

This new concept that the trajectory at which blood pressure rises has an irreversible adverse impact on cardiac structure is quite plausible, according to Dr. Joanne Foody.

"I think the real kernel is there needs to be more ongoing monitoring, particularly in young adults, so we don’t miss that window," she said in an interview.

The challenge is that young people leave their pediatricians and, except for injuries or acute illnesses, may not see a physician again until they’re in their 40s, observed Dr. Foody, medical director of the cardiovascular wellness program at Brigham and Women’s Hospital, Boston.

"We need to do more for people and do it earlier. People don’t really start thinking about preventive health until they’re in their 40s and 50s," she said.

The study was sponsored by the U.K.’s Medical Research Council. Dr. Ghosh and Dr. Foody reported having no financial conflicts.

CHICAGO – The rate of increase in systolic blood pressure during an adult’s 30s, 40s, and 50s is a stronger predictor of later structural heart damage than is their absolute blood pressure.

This finding from the longest-running birth cohort study in the United Kingdom – now entering its 66th year of follow-up – has major implications for how high blood pressure is approached, according to Dr. Arjun K. Ghosh, a cardiologist at the National Heart and Lung Institute, Imperial College London.

"At the moment, if patients don’t reach that certain magic level of high blood pressure, they’re often not treated. They’re asked to come back, and a watch-and-wait policy is instituted," he noted at the annual meeting of the American College of Cardiology. "What we found in our study, in measuring people’s blood pressure from their 30s on, was that those with a faster rise in blood pressure had a heavier heart, or increased left ventricular mass, when they were 60-64 years of age. And this was true for any level of blood pressure, high or low. It actually wasn’t how high the blood pressure became as it was how quickly the blood pressure was rising."

A second key finding was that left ventricular hypertrophy was not reversed among hypertensive study participants whose blood pressure was normalized via medication. These patients had a significantly greater left ventricular mass indexed to body surface area (LVMI) as did their peers who had the same normal-range blood pressure but had never been treated for hypertension.

"This policy of watching and waiting for the blood pressure to cross a certain threshold before starting antihypertensive therapy may be waiting too long. The irreversible damage has already been done," Dr. Ghosh continued. "A new approach may be required. We need to identify those individuals whose blood pressure rises the fastest and target them with the most effective treatment."

His analysis involved 1,653 participants who were in the Medical Research Council National Survey of Health and Development and were born in Britain in a single week in March 1946. Subjects were followed serially, and underwent echocardiography and LVMI measurement at age 60-64.

The higher a subject’s systolic blood pressure at age 36, 43, 53, or 60-64, the greater the LVMI at age 60-64.

Moreover, individuals with well controlled blood pressure on antihypertensive therapy at age 60-64 had a mean LVMI that was 8.6 g/m² greater than that of subjects not on treatment. Participants on antihypertensive therapy at age 53 had a mean LVMI that was 7.3 g/m² higher than in those who weren’t, and individuals on treatment at age 43 had a mean LVMI at age 60-64 that was 11.5 g/m² more than in those not on treatment at age 43.

A sharp increase in blood pressure between ages 43 and 53 was particularly detrimental for LV size at age 60-64. An increase of 1 standard deviation in systolic blood pressure during that time period was associated with a 4 g/m² higher LVMI, whereas an increase of 1 standard deviation between ages 36 and 43 was associated with a 1 g/m² increase.

As this was an observational study, a clinical trial needs to be conducted before the findings can be translated into a change in practice. This study would compare the watch-and-wait strategy of threshold-based antihypertensive therapy with this novel approach stressing early identification and treatment of patients with rapidly increased systolic blood pressure, Dr. Ghosh said. Such a study is eminently feasible and could yield results in about 5 years using as the end point change in left ventricular size, which is well-established as a key driver of heart failure.

This new concept that the trajectory at which blood pressure rises has an irreversible adverse impact on cardiac structure is quite plausible, according to Dr. Joanne Foody.

"I think the real kernel is there needs to be more ongoing monitoring, particularly in young adults, so we don’t miss that window," she said in an interview.

The challenge is that young people leave their pediatricians and, except for injuries or acute illnesses, may not see a physician again until they’re in their 40s, observed Dr. Foody, medical director of the cardiovascular wellness program at Brigham and Women’s Hospital, Boston.

"We need to do more for people and do it earlier. People don’t really start thinking about preventive health until they’re in their 40s and 50s," she said.

The study was sponsored by the U.K.’s Medical Research Council. Dr. Ghosh and Dr. Foody reported having no financial conflicts.