CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 4, May 2012
AFRICA
233
Cardiff in the United Kingdom asked the
question whether there is potential for
harm from too much exercise. Troponin
is released after prolonged exercise. After
the London Marathon, 56% of athletes
have troponin levels above the cut-off for
myocardial infarction. He concluded that
troponin release was ‘physiological and
not related to any functional abnormality
of the heart’.
After endurance exercise, such as a
marathon or a 100-miler, the pressure in
the right ventricle was increased, while
there was a reduction in strain, strain
rate and diastolic function in the right
ventricle. Speckle tracking confirmed an
abnormality of radial strain in the septum
with septal flattening. The intense duration
caused acute dysfunction of the right
ventricle and although the right ventricular
function had usually normalised by the
end of the first week, chronic structural
changes, as demonstrated on MRI, with
reduced right ventricular function were
found in some of the most practiced
athletes.
Beta-adrenergic receptor desensitisa-
tion has been found after exercise and
this attenuates cardiac function because
of reduced chronotropic and inotropic
response. Furthermore, changes in
loading conditions did not explain the
reduced function of the right ventricle.
Highly trained athletes differ
from amateur athletes in that cardiac
remodelling is more profound and may
persist despite detraining. Cardiac MRI
has shown myocardial fibrosis in athletes
with an extensive history of competition
in endurance sport. The long-term clinical
significance of the fibrosis is unknown
and warrants further study.
Prof Neil Poulter discussed the
ASCOT trial, which has influenced the
newest set of NICE/BHS guidelines. In
these guidelines, patients under the age
of 55 years should be given an ACE
inhibitor as first-line therapy, whereas
older or black patients should start initial
therapy with a calcium channel blocker. If
the blood pressure remains uncontrolled,
the next step would be the combination
of an ACE inhibitor and calcium channel
blocker. This combination was associated
with a more favorable outcome than
the beta-blocker and thiazide–diuretic
combination. Blood pressure variability
was much less using the former
combination and was associated with
an improved cardiovascular outcome.
The ACE inhibitor–CCB combination
was better even in those patients with a
relative tachycardia.
Cardiovascular risk in
obstructive sleep apnea
Obstructive sleep apnea (OSA) is found
in 25% of heart failure patients, 60% of
patients who have had a stroke, 85% of
patients with resistant hypertension, 50%
of hypertensives and 30% of patients with
acute coronary syndrome. About 30% of
obese patients have unrecognised OSA.
Patients with hypertension, OSA and
obesity are at increased risk of atrial
fibrillation, sudden cardiac death, reduced
cardiac function, coronary disease and
atrio-ventricular block. There is a nine-
fold increase of developing the metabolic
syndrome and more silent cerebrovascular
lesions.
There is much more blood pressure
and heart rate variability in patients
with OSA. Alternating bradycardia and
tachycardia at night on 24-hour ECG
monitoring is another clue to the presence
of OSA.
Clues to the diagnosis of OSA include
excessive daytime sleepiness, choking at
night, night sweats, nocturnal diuresis,
motor activity during sleep, headaches,
dry mouth, impotence and cognitive
impairment. Clinical signs relate
to the waist and neck circumference,
hypertrophy of the tonsils, adenoids,
the soft palate and even the uvula.
Contributing lifestyle parameters include
excessive alcohol consumption, smoking,
sedatives, as well as sleeping in a supine
position.
Avoiding these factors is key to
management. Continuous positive airway
pressure via a nasal mask should be
administered for five to six hours per
night to improve outcome.
Prof Somers then discussed sleep,
obesity and cardiovascular disease. In
1910, the average sleep duration was
nine hours per night and in 2005 it was
6.5 hours per night. A third of people are
sleep deprived on a daily or regular basis.
In an elegant experiment conducted at the
Mayo Clinic, it was shown that less sleep
was associated with higher caloric intake
(500 calories a day) and this translated
into 3 kg of extra fat accumulation in one
month.
Normally, leptin levels increase at night
during sleep and this tells the brain to stop
eating. Patients who have less sleep have
lower leptin but higher ghrelin levels. The
latter is produced by the stomach and
causes the sensation of hunger. Sleep-
deprived people had no difference in
energy expenditure versus those who
were not sleep deprived. Obese patients
report less sleep than lean patients and
this has been linked to the pathogenesis
of obesity. In the Nurses Health study,
those who slept less than five versus more
than seven hours per night had a 1.5-fold
increased risk of developing obesity.
Another study conducted by Somers
evaluated subjects sleeping less or more
than seven hours per night. In those who
were sleep deprived, 50% snored, 45%
fell asleep in the day for no reason and
5% fell asleep while driving in the last 30
days of observation.
If subjects sleep less and have a
disrupted sleep cycle, less insulin is
secreted by the pancreas, even though
blood glucose levels are higher after
meals than in those who are not sleep
deprived. The metabolic rate is reduced
and the subjects have higher nighttime
and daytime blood pressure. Chronic
sleep deprivation (< five hours per night)
was associated with a two-fold increase in
incidence of acute coronary syndrome in
the Nurses Health study.
Hypertension in the elderly
The VALISH trial enrolled patients with
isolated systolic hypertension (age range
70–84 years). These patients were divided
into two groups. In one group, target
systolic blood pressure was < 140 mmHg
whereas in the second group the target
systolic blood pressure was between 140
and 149 mmHg. They found no difference
in outcome with strict versus less strict
blood pressure control (< 140 vs 140–149
mmHg).
There was some discussion about the
J-shaped curve regarding diastolic blood
pressure in elderly patients. The data
suggest that if diastolic blood pressure
is lowered to < 80 mgHg in patients who
have coronary heart disease at baseline,
there is an increase in cardiovascular
mortality.
Prior to blood pressure measurement,
patients must have rested for at least five
minutes and the readings are repeated. In
the elderly, particular emphasis should be
placed on standing blood pressure.
The HYVET trial recruited patients
