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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 3, May/June 2021
124
AFRICA
ventricular ejection fraction 30%, pericarditis, cardiomyopathy,
ST-segment depression > 2 mm at rest, uncontrolled tachycardia,
exercise-induced malignant ventricular arrhythmia, acute
systemic illness, skeletal vascular disease, or acute metabolic
disorders. Patients who refused to provide informed consent for
the exercise programme were excluded from both groups.
Each patient completed a six-month CR programme that
began with an out-patient CR session, which was held within two
weeks of the index PCI. The exercise training programme and
CR comprised two stages as follows: the first stage consisted of
six weeks of prescribed supervised exercise and the second stage
of community-based and self-managed exercise for the remaining
28 weeks. Patients were required to visit the cardiac rehabilitation
clinic at least twice a month. The second stage could be extended
to six months depending on medical judgement or at the patient’s
request.
Cardiorespiratory capacity was measured twice using a
symptom-limited exercise-tolerance treadmill test (ETT). The
measurements were performed before the commencement, and at
the end of the first six weeks of supervised exercise training. The
ETT was conducted on the first day that the patient visited the
CR clinic after discharge, using a modified Bruce protocol: we
measured oxygen uptake during peak exercise (VO
2peak
), exercise
time, resting heart rate (HR), peak HR, resting blood pressure
(BP), peak BP, rate pressure product (RPP), peak respiratory
exchange ratio (RER: the ratio of VCO
2
over VO
2
; the magnitude
of the peak RER roughly reflects the effort expended by the
patient at peak exercise), and the rate of perceived exertion (RPE).
The exercise test was supervised by experienced physicians.
A real-time recording 12-channel electrocardiograph (Q4500;
Quinton Instrument Co, Boston, MA, USA), respiratory gas
analyser TrueOne 2400 metabolic measurement system (Parvo
Medics Inc, East Sandy, UT, USA), an automatic blood pressure
and pulse monitor Model 412 (Quinton Instrument Co), and a
treadmill MedTrack ST55 (Quinton Instrument Co) were used
for the ETT.
All tests were terminated according to the American Heart
Association (AHA) termination criteria and the patients were
instructed about the termination of the ETT before the test.
When the test was close to the end, patients were encouraged to
endure the test and to stop only when experiencing intolerable
dyspnoea, unless there was an event that met the ETT termination
criteria in the AHA guidelines.
The patients initially participated in six weeks of prescribed,
supervised exercise. Exercise intensities of 40 and 85% HR
reserve were calculated using the Karvonen formula: [(maximal
HR – resting HR × % intensity) + resting HR], based on the
results obtained during the first ETT.
The CR programme was composed of 10 minutes of warm
up (stretching), 40 minutes of main aerobic exercise, and 10
minutes of cool down, three times a week for six weeks, for a
total of 18 sessions. Following the completion of the six-week
CR programme, the ETT was performed again. The VO
2peak
, ETT
time, resting HR, peak HR, resting BP, peak BP, RER, RPP and
RPE were measured again during the second ETT.
After the six-week supervised exercise period, the community-
based, self-managed exercise was performed based on the results
of the reassessed cardiorespiratory capacity for the remaining
period. The patients were required to exercise at a local fitness
centre and maintain aerobic exercise on a treadmill or bicycle
ergometer. Every exercise training session was required to be one
hour in length and was to be performed three times per week.
The FMD was measured within two weeks of the PCI,
and was followed up at six months after the initiation of the
CR programme. Endothelial function (endothelium-dependent
brachial artery FMD) was measured as previously described.
10,12,13
Briefly, each patient arrived at the laboratory at a similar time of
day (8:00–9:00). Patients were required to fast, avoid exercise and
smoking, and to avoid consumption of alcohol or anti-oxidant
vitamins, for at least 12 hours before the test.
The FMD was measured by a single ultrasonographer who
was blinded to the subject’s clinical status. After a 10-minute
equilibration period, the measurement was taken in the right arm
while the patient was in the recumbent position in a temperature-
controlled room (22°C). Using an 11–3-MHz linear array
(L11-3) transducer connected to a Philips iE33 (Philips Medical
Systems, Andover, MA, USA) echocardiography machine, the
brachial artery was longitudinally imaged approximately 5 cm
proximal to the antecubital crease, at the point at which the
clearest image was visible. The skin surface was marked when
a reasonable image was obtained. The arm and the ultrasound
probe were kept in the same position by the ultrasonographer
throughout the study.
A pneumatic cuff was placed distal to the imaged artery, and
baseline scans for the assessment of the resting vessel diameter
and flow were recorded. The occluding cuff was then inflated
to > 50 mm Hg above the systolic blood pressure value for five
minutes, and the diameter was measured 30 seconds before cuff
deflation. After deflation, the arterial diameter was measured
at 60 and 90 seconds in order to determine the maximum post-
occlusive reactive hyperaemia diameter. An electrocardiogram
was monitored continuously and blood pressure was recorded
each minute in the left arm throughout the test.
Statistical analysis
Depending on the distribution, the data are expressed as mean
and standard deviation (SD) values or as median values with
interquartile ranges. Categorical variables were compared using
the
χ
2
test. Continuous variable data were compared within
groups using the paired Student’s
t
-test, and between groups
using the unpaired Student’s
t
-test. A two-tailed
p
-value < 0.05
was considered to indicate a statistically significant result. All
clinical and laboratory data were analysed using SPSS software
(version 25.0).
Results
Of the 119 patients, 69 presented with ACS and 50 with stable
angina. Table 1 presents a summary of the results of the subjects’
clinical characteristics. The mean age of the patients was 54.9 ± 9.1
years, and the patients in the ACS group were slightly younger than
those in the stable-angina group (52.9 ± 9.1 vs 57.6 ± 8.5 years,
respectively,
p
= 0.050). There were no between-group differences in
the distributions of males, hypertension, diabetes, dyslipidaemia or
smoking. A greater percentage of patients in the ACS group took
angiotensin converting enzyme inhibitors (ACEIs) or angiotensin
II receptor blockers (ARBs), and beta-blockers, compared to
the stable-angina group patients. All the patients in both groups
received statin and dual anti-platelet therapy.