Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of 19 000 men in the Whitehall study

In
their estimation of the life expectancy in the Whitehall cohort, Clarke et al
claimed that the decline in cardiovascular mortality that has occurred in the UK
population was partly attributable to changes in cholesterol concentrations.¹
This statement can be questioned. Since a meta-analysis of the randomised and
controlled cholesterol lowering trials performed up to 1992 did not find any
effect on cardiovascular mortality,² the alleged influence of
cholesterol lowering must have been caused by the statins introduced a few years
later. However, according to the mortality curves in their paper the decrease of
vascular mortality started already in the sixties, and the slopes are unchanged
from about 1980 up to today.
     The authors’ conclusion that more intensive cholesterol lowering can
result in further improvement in life expectancy is dubious as well.Recently
Sachdeva et al. reported that the mean LDL cholesterol in 136,905 patients
admitted because of an acute myocardial infarction was lower than normally.³
These authors also concluded that cholesterol lowering should be intensified, as
did Al-Mallah et al. who came up with similar results.⁴ However, at a
three-year follow-up, all cause mortality for those whose LDL cholesterol was
below 105 mg/dl at admission was almost twice as high as those whose LDL
cholesterol was higher.⁴
     From the above we suggest
that the observed reduction of cardiovascular mortality is rather the result of
the increasing numbers of and quality of revascularization procedures than
cholesterol lowering. 

1. Clarke
   R, Emberson J, Fletcher A, Breeze E, Marmot M, Shipley MJ. Life expectancy
   in relation to cardiovascular risk factors: 38 year follow-up of 19 000 men
   in the Whitehall study. BMJ 2009;339:b3513. doi: 10.1136/bmj.b3513.

2. Ravnskov
   U. Cholesterol lowering trials in coronary heart disease: frequency of
   citation and outcome. BMJ 1992;305:15-9.

3. Sachdeva
   A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, et al. Lipid
   levels in patients hospitalized with coronary artery disease: an analysis of
   136,905 hospitalizations in Get With The Guidelines. Am Heart J
   2009;157:111-7

4. Al-Mallah
   MH, Hatahet H, Cavalcante JL, Khanal S. Low admission LDL-cholesterol is
   associated with increased 3-year all-cause mortality in patients with non ST
   segment elevation myocardial infarction. Cardiol J 2009;16:227-33.

Competing interests:
None declared

Robert Clarke et. al. (BMJ 17 Sept. 2009) found that in middle age
people, the cardiovascular risk factors like hypertension, cholesterol,
smoking and others, like diabetes and body mass index, can shorten life
expectancy (LE) by 10 to 15 years after age 50, and they recommend public
health strategies to lower the levels of the main risk factors, together
with more intensive medical treatment for ‘high risk’ sub-groups,
including the use of medication that have proven efficacy and could
improve life expectancy.

Their findings agree with the known reduction of ca. 5 year LE in
untreated hypertension and ca. 8 to 10 years in type 2 diabetes, morbid
obesity, smoking or depression.

At the other hand, the preventive measures and improved treatments
have resulted in reduced mortality, longer life expectancy and more years
with quality of life. Though some trends like increased number of obese
population and younger persons with hypertension or diabetes, threatens to
stop or even reverse the great advances already achieved.

It is therefore of the highest importance to identify the younger
patients, in their twenties or thirties, who are hypertensive or pre-
hypertensive, diabetics or with metabolic syndrome, that could benefit
with more aggressive preventive measures or appropriate medications, as
well as cessation of cigarette smoking at age 30 years or earlier, which
adds about 10 years of life expectancy that they would lose if they
continued to smoke.

Ten years ago (Lancet, 13 March 1999), we published that the Pulse
Mass Index is a simple way for the preliminary identification of young
patient with a high cardiovascular risk, when their Pulse Mass Index is
over 1.2 and specially if over 1.3

The Pulse Mass Index is calculated as follows:
Pulse or Resting Heart Rate (after at least 2 hours fasting) multiplied by
the Body Mass Index and divided by 1730 as common denominator. Normal is a
Pulse Mass Index of 1.0 or less (0.7 to 1.0).

A Pulse Mass Index over 1.2 or 1.3 has a correlation with the
Framingham Risk Score of 95% in people over 40 years old, but is more
sensitive in younger persons, despite their Framingham RS being apparently
normal because of their young age.

The practical usefulness of the Pulse Mass Index helps us to identify
the persons with high risk that could need more intensive preventive
measures or appropriate drugs, after confirmation with the Framingham Risk
Score and other appropriate tests.

The Pulse Mass Index can also help us to identify younger patients
with pre-hypertension or metabolic syndrome that could also benefit from
intensive prevention, including medication. There is a close association
of the PMI with the Metabolic Syndrome and it is also frequently elevated
in overweigth or obese persons with hypertension in initial stadiums or in
pre-hypertensive.

The Pulse Mass Index is also the most simple and economical first
clinical approach, followed by the Framingham RS for the risk evaluation
in a large population of both men and women, and more so in the developing
countries, where around 80% of all cardiovascular deaths occurs.

In the last few years, almost a decade after our original
publication, several studies have confirmed the importance of the pulse or
resting heart rate, as well as the body mass index, the two components of
the Pulse Mass Index, as cardiovascular risk factors of first range. Among
others the studies: BEAUTIFUL, EUROPA, QRISK, Women Health Initiative
(WHI), the Framingham Heart Study and the Framingham Offspring Study.

The Pulse Mass Index is useful in two ways:
1.- For a preliminary, rapid, inexpensive, clinical evaluation of the
cardiovascular risk, especially practical in younger people that could
require an early prevention or medications, and

2.- To predict the potential benefit or risks of new cardiovascular,
metabolic or other drugs.

Lately, we are studying the idea to improve the Pulse Mass Index to
form the Pulse Mass Pressure Product (PMPP), an extension of both, the
Pulse Mass Index and the Pulse Pressure Product, which I think could give
us as clinicians, a more exact initial evaluation of the global
cardiovascular risk, of hypertension in early stadiums, pre-hypertension,
metabolic syndrome and which patients should be treated early, either with
intensive lifestyle interventions, or appropriate drugs, according to the
patients’ characteristics, to prevent cardiovascular events or
complications of hypertension in young or pre-hypertensive people.

For instance, the Pulse Mass Pressure Product (PMPP) can be:
72 (RHR) x 24 (BMI) x 115 (SBP), which totals 198720 or round 200000 or
(200 k) as normal or basic values.

In the case of a young pre-hypertensive patient, if he had a PMPP of
round 240 k (PMPP x 1.2), he could be a candidate for intensive lifestyle
interventions.

If he had a PMPP of round 260k (PMPP x 1.3), he could be a serious
candidate for prevention with appropriate drugs.

If he had a PMPP of round 300k (PMPP x 1.5), he could be a definite
candidate for treatment with appropriate antihypertensive drugs.

Something similar could apply for the metabolic syndrome and global
cardiovascular risk.

I invite interested colleagues to evaluate this idea and contact with
me to collaborate in this study.

Prof. Enrique Sánchez-Delgado, MD

Internist-Clinical Pharmacologist

Director of Medical Education

Hospital Metropolitano Vivian Pellas

Managua, Nicaragua

Competing interests:
None declared