Several studies have attempted to assess the effect of the heart rate on ca
rdiovascular and non-cardiovascular mortality. The best known of these, the
Framingham study, showed that an increased heart rate was associated with
an increased frequency of sudden death. This study also demonstrated that t
he role of the heart rate in cardiovascular complications, especially coron
ary artery disease, was even greater in hypertensive patients. Nevertheless
, in the other studies, when the results are corrected for other cardiovasc
ular risk factors, the heart rate becomes insignificant. The patients with
the highest heart rates often have other risk factors, especially hypertens
ion and hypercholesterolaemia.
The first large scale French trial was carried out on the data base of the
Centre of Preventive and Clinical Investigations. This Centre, recognised b
y the Ministry of Health and Social Security, carries out 25 000 check-ups
each year and has been working for the last 25 years. The check-up includes
clinical, biological and radiological investigations, A significant relati
onship was observed between the heart rate and most of the classical cardio
vascular risk factors in both sexes. Subjects with the highest heart rates
(> 85 beats/min) compared with those with the lowest heart rates (< 65 beat
s/min) had higher systolic blood pressures by 12 mmHg and diastolic blood p
ressures by 7 mmHg. Similarly, most of the patients with tachycardia had hi
gher plasma cholesterol, triglyceride and sugar levels. It was also demonst
rated that rapid heart rates in men were associated with increased cardiova
scular and non-cardiovascular mortality In women, a relationship between th
e heart rate and cardiovascular mortality was not demonstrated. On the othe
r hand, the heart rate was associated with non-cardiovascular mortality. Th
e association between heart rate and cardiovascular mortality in men was ma
inly explained by a large increase in coronary mortality in those with the
fastest heart rates. After adjustment for the other known risk factors, the
increase in risk corresponding to a heart rate 20 beats/min faster was 40%
for cardiovascular mortality.
These epidemiological findings may be explained by at least two mechanisms:
a) the increase in the number of heart beats increases the myocardial oxyge
n requirements, accelerate arterial fatigue and may provoke rupture of cons
tituted atheromatous plaques;
b) the increase in heart rate is a sign of increased sympathetic activation
which may have negative effects on the cardiovascular system, especially t
he coronary circulation.
In the light of these epidemiological and physiopathological data, the valu
e of lowering the heart rate in high risk patients, especially hypertensive
patients with rapid heart rates, remains to be demonstrated.