Download Exercise Training and the Ischemic Patient

Exercise Training and the Ischemic Patient
Robert Bertelink, Paul Oh, Cardiac Rehabilitation and Secondary Prevention Program,
Toronto Rehabilitation Institute
Health care providers are commonly advised to proceed with
caution when prescribing exercise for individuals with coronary
artery disease (CAD) who are known to develop myocardial
ischemia. For example, guidelines from the American College
of Sports Medicine recommend that any such individual
exercise at a heart rate no greater than 10 bpm–1 below the
ischemic threshold (determined by –1.0mm of horizontal or
down sloping ST segmental depression).1 Providers are also
cautioned against exercise training individuals to the point at
which patients develop signs or symptoms of angina.
“Is it time to reassess these guidelines and
see if providers can train our patients more
aggressively so that they can realize their
functional goals, optimally improve risk factors
and derive prognostic benefits associated with
higher fitness without any adverse effects?”
Are the current guidelines appropriate for all individuals?
How effectively can an ischemic patient or one who develops
angina be trained following these guidelines? Is it time to
reassess these guidelines and see if providers can train our
patients more aggressively so that they can realize their
functional goals, optimally improve risk factors and derive
prognostic benefits associated with higher fitness without
any adverse effects? This article touches on this important
issue and we present here two case studies as illustrations of
potential training models and their outcomes.
Case #1 – Silent Ischemia
Mr. PA is a 51-year-old man referred for cardiac rehabilitation.
His past history includes posterior circulation myocardial
infarction four years ago. He has a resting ejection fraction
of 40%, but no symptoms of heart failure. He describes
occasional chest pressure with activity.
Past history includes: smoking (30 pack years), diet
controlled diabetes, and elevated cholesterol.
Current medications include ASA, atenolol 50 mg,
OD, ramipril 5 mg, OD, atorvastatin 20 mg, OD, and
nitroglycerine PRN.
An exercise perfusion study demonstrated reversible
changes in the apex, inferior, and lateral walls. A coronary
angiogram was performed, which demonstrated occlusion
of the right coronary artery and a diffuse 70% lesion in the
circumflex. The left main was normal, and the left anterior
descending artery had only minor disease in the mid portion.
Left to right flow through collaterals was visible. A decision
was made not to have any interventional procedure and to
continue with medical therapy only. As part of this, he was
referred for exercise rehabilitation.
A cardiopulmonary assessment with direct VO2 measure­
ment was carried out. The results are shown in the table
below. The ECG tracings showed significant ST depression
at peak of exercise although the patient did not report
symptoms of angina.
Table: Case 1 – Initial Cardiopulmonary
Assessment
Baseline
Peak
67
115
Blood Pressure
(mmHg)
130/70
160/70
ST Depression
(lead CM5)
–0.5 mm
–2.75 mm
Heart Rate
(bpm–1)
Rate Pressure
Product
18,400
VO2
(mL/kg/min)
18.3 (5.2 METs)
Respiratory
Exchange Ratio
(RER)
1.24
The assessment lasted 7 minutes and was terminated when a
VO2 plateau was achieved.
Current Issues in Cardiac Rehabilitation and Prevention
17
Exercise Prescription
Before embarking on an exercise program, we had very
careful and detailed discussions about his situation. The
importance of recognizing angina, modifying activity if
chest pain occurred, appropriate use of nitroglycerine,
medication adherence and timing of exercise in relation to
type and peak action of medication (especially beta-blockers)
and good communication with staff were emphasized.
Long warm-up and cool-down sessions to facilitate gradual
increases and decreases in heart rate and blood pressure were
also incorporated into his program. These principles meshed
well with the key considerations outlined in the CACR 2004
guidelines.2
The initial exercise prescription was set at 1 mile in
20 minutes, 5 times weekly, with an upper training heart
rate limit of 96 bpm–1. This HR limit corresponded to a
1.0mm ST segment change on the ECG (lead CM5) and
also correlated with 60% of the heart rate reserve and 75%
of the peak V02. When the patient was walking at this pace
his actual training heart rate averaged 88 bpm–1, which was
about 10 beats below the 1.0 mm ischemic threshold that
was identified by ECG; this level of activity was consistent
with parameters from the ACSM Guidelines.1 His exercise
prescription and training program progressed well and
he did not report any symptoms. In two weeks he was
walking 2 miles in 37 minutes, at one month 2.5 miles in
45 minutes, at two months 3 miles in 54 minutes, at three
months 3 miles in 51 minutes, and at four months 3 miles
in 49.5 minutes (all with a frequency of 5 days per week).
Because he was feeling so well, his training heart rates were
titrated closer to the ECG ischemic threshold and were kept
between 90 and 96 bpm–1.
A second cardiopulmonary test was performed at six months
in order to monitor his exercise capacity and cardiac status.
Table: Six Month Cardiopulmonary Assessment
Baseline
Peak
67
155
Blood Pressure
(mmHg)
110/65
174/74
ST Depression
(CM5)
–0.5 mm
–2.50 mm
Heart Rate
(bpm–1)
Rate Pressure
Product
26,970
VO2
(mls/kg/min)
24.6 (7.0 METs)
RER
18
1.31
The assessment lasted for 8 minutes and was terminated
when a VO2 plateau was achieved.
This test showed a large improvement his VO2 maximum
by 34% in 6 months. He still demonstrated ST segmental
depression of –2.50 mm at the peak of exercise, but it now
occurred at a higher Rate Pressure Product (RPP), i.e.,
–2.75 mm at a RPP of 18,400 on the initial test compared
with –2.5 mm at a RPP of 26,970 6 months after exercise
training.
This case illustrates a positive outcome with training
following standard guidelines for exercise rehabilitation
in a man with silent ischemia. Could the patient have
further improved his fitness, exercise capacity and ischemic
threshold by exercising at a higher intensity, i.e. one that
actually brought on a degree of ischemia? This is explored
in the next case.
Case #2 – Ischemia
Mr. RC is a 53-year-old man referred for cardiac rehabilitation.
His past history includes anterior wall infarction 6 years ago
followed by PCI with stent to his LAD. The patient was left
with mild to moderate left ventricular dysfunction.
Recently, the patient began to experience exertional
chest discomfort again (when climbing stairs). He under­
went exercise testing which was positive for symptoms and
suggestive of inferior wall ischemia. A subsequent catheter­ization demonstrated an occluded RCA (new lesion) not
amenable to angioplasty with minimal restenosis in the
stented portion of his LAD and minor irregularities in the
circumflex.
Medications included metoprolol 50 mg bid, ramipril
10 mg OD, ASA 325 mg, rosuvastatin 40 mg OD, and
nitroglycerine PRN.
The patient was referred for cardiac rehabilitation. How
do we proceed with exercise training in this patient with
prior anterior MI, LV dysfunction and now exercise induced
chest pain? Initial exercise test data are shown in the table.
Current Issues in Cardiac Rehabilitation and Prevention
Initial Cardiopulmonary Assessment
Baseline
Peak
46
111
Blood Pressure
(mmHg)
120/70
170/85
ST Depression
(CM5)
–0.1mm
–1.4mm
Heart Rate
(bpm–1)
Rate Pressure
Product
18,870
VO2
(mL/kg/min)
28.8 (8.2 METs)
RER
At week eleven, his prescription was progressed to
include 100 m of jogging every 300 m and at week fifteen,
to alternate 100 m of jogging with 100 m of walking. On
each increase in exercise intensity, the patient reported an
initial increase in frequency of chest tightness, gradually
decreasing as time progressed. By week fifteen, his exercising
heart rates were reported to be in the 110-120 bpm–1 range
and he wasn’t experiencing any angina.
He was monitored closely with periodic telemetry
sessions and stress tests. At the end of one year the patient
underwent a final cardiopulmonary assessment with the
following results.
One-Year Cardiopulmonary Assessment
1.32
The patient developed chest tightness in the 10th minute
of exercise (on a 100 kpm/min incremental bicycle protocol;
corresponding to about one minute into stage 3 of a Bruce
protocol). The pain was rated at 2/10, and occurred at a
heart rate of 102 bpm–1 and VO2 of 23.8 mL/kg/min. The
tightness cleared after one minute of recovery. The test was
terminated when a VO2 plateau was achieved.
Exercise Prescription
Despite his cardiac status, this man was quite active,
walking 3.5 miles 2 to 3 times per week, sometimes with
chest discomfort. His goal was to become much more
active to meet the needs of his work and home life. His
initial exercise prescription was therefore set at 3 miles in
45 minutes, 5 times weekly, with an upper training heart rate
limit of 102 bpm–1. This corresponded with a -0.65 mm ST
segmental change on the ECG (lead CM5), 63% of VO2
peak, and the level of exertion at which the patient first began
to experience his symptoms.
When the patient was walking at the prescribed pace, his
heart rate was found to be approximately 90 bpm–1 and he
experienced chest tightness on a regular basis. The patient
was advised to lengthen his cardiovascular warm-up and to
continue exercising as long as the chest tightness remained
“mild” (pain rating 2/10 or less). After exercising at this level
for 2-3 weeks, the patient reported a reduced frequency
of chest tightness. After three weeks, his prescription
was increased to 4 miles walking in 60 minutes without
discomfort. The patient remained mostly symptom free.
At week seven, his prescription was increased to include
100 m of jogging every 700 m at a pace of 12 minutes per
mile. The patient reported a recurrence of chest tightness
with the increased intensity (pain rating 2/10) for the first
2-3 weeks at the higher intensity, followed by a decrease in
frequency over the next 2 weeks.
Baseline
Peak
57
130
Blood Pressure
(mmHg)
110/70
180/60
ST Depression
(CM5)
–0.2 mm
–2.0 mm**
Heart Rate
(bpm­)
Rate Pressure
Product
23,400
VO2
(mL/kg/min)
41.8
(11.9 METs)
RER
1.25
On this test, the patient developed chest tightness in
the 9th minute of exercise on a treadmill using a Bruce
protocol (pain rating 2/10, at heart rate of 120 bpm–1 and
VO2 of 34.3 mL/kg/min). This threshold was at a much
higher intensity than the baseline test. The tightness cleared
after 4 minutes of recovery. The test was terminated due to
increasing ST segmental depression and thus underestimated
his true maximal fitness.
The patient was able to improve his VO2 peak by 45% in
one year. He was also able to push back his anginal threshold
and thus engage in a higher level of activity, which was the
main reason the patient wished to participate in a cardiac
rehabilitation program. This case illustrates a successful
outcome associated with training at or slightly above the
ischemic threshold. Had the patient been trained more
intensely, could his anginal threshold have been pushed
back even further or his ST segmental changes improved?
These situations happen in real life every day. People
with CAD will participate in activities until they get pain
or even more commonly, while they are experiencing silent
ischemia. Previous teaching would have excluded individuals
with exertional ST-depression (_> 1 mm) without symptoms
Current Issues in Cardiac Rehabilitation and Prevention
19
or those recovering from a large MI from vigorous exercise
training.3 Concerns were raised about deleterious effects on
the myocardium, increasing risk of cardiac arrest, or worsening
LV function post anterior MI associated with exercise.4-6 More
recent studies, however, have demonstrated typical positive
outcomes associated with exercise training under ischemic
conditions.7-8 Perhaps in the controlled environment provided
by cardiac rehabilitation, carefully selected and monitored
individuals can be pushed a little harder and receive greater
benefits. This topic should be explored in future studies.
References:
1.ACSM’s Guidelines for Exercise Testing and Prescription. Seventh
Edition, p. 180.
2.Canadian Guidelines for Cardiac Rehabilitation and Cardiovascular
Disease Prevention. Enhancing the Science, Refining the Art. Canadian
Association of Cardiac Rehabilitation, Winnipeg, 2004. p. 262.
3.Myers J, Froelicher VF. Predicting outcome in cardiac rehabilitation.
J Am Coll Cardiol 1990;15:983-985.
4.Hess OM, Schneider J, Nonogi H, et al. Myocardial structure in
patients with exercise-induced ischemia. Circulation 1988;77:967977.
5.Hoberg E, Schuler G, Kunze B, et al. Silent myocardial ischemia as a
potential link between lack of pre-monitoring symptoms and increased
risk of cardiac arrest during physical stress. Am J Cardiol 1990;65:583589.
6.Jugdutt BI, Michorowski BL, Kappagoda CT. Exercise training after
anterior Q wave myocardial infarction: importance of regional left
ventricular function and topography. J Am Coll Cardiol 1988;12:362372.
7.Mark DB, Hlatky MA, Califf RM et al. Painless exercise ST deviation
on the treadmill: long-term prognosis. J Am Coll Cardiol 1989;14:885892.
8.Schuler G, Shlierf G, Wirth A, et al. Low fat diet and regular supervised
physical exercise in patients with symptomatic coronary artery
disease: reduction of stress-induced myocardial ischemia. Circulation
1988;77:172-181.
References and Reviews
Lea Carlyle, BKin, RCPT(C), Faculty of Physical Education and Recreation, University of Alberta
John Lester, BSc, Exercise Specialist, Northern Alberta Cardiac Rehabilitation Program,
Edmonton, Alberta
REVIEWS
Percutaneous Coronary Intervention versus
Conservative Therapy in Non-acute Coronary
Artery Disease: A Meta-Analysis
Katritsis DG, Ioannidis JPA.
Circulation 2005; 111:2906-12.
Although percutaneous coronary intervention (PCI) has
been shown to improve symptoms of ischemic heart disease
(IHD) compared with conservative medical treatment, there
is limited evidence on the effect of PCI on the risk of death,
myocardial infarction (MI), and future revascularization.
This meta-analysis report results from 11 studies in 2950
patients (1476 received PCI, and 1474 received conservative
treatment) with angiographically documented coronary
stenoses in non-acute settings. The results of this metaanalysis revealed that PCI does not decrease mortality or the
risk of MI during follow-up of patients with chronic stable
coronary artery disease (CAD). However, PCI was found to
be advantageous early after an MI. The authors note several
limitations of the meta-analysis, but conclude that many
percutaneous interventions performed in patients with
stable CAD may not be warranted since PCI was not found
to provide long-term benefits in hard clinical outcomes
compared to conservative medical treatment.
20
Long-Term Outcomes of Coronary Artery Bypass
Grafting versus Stent Implantation
Hannan EL, et al. N Engl J Med 2005;352:2174-83.
This observational study sought to determine whether longterm mortality differed significantly among 37,212 patients
who underwent coronary artery bypass grafting and 22,102
patients who underwent stenting. The endpoints included
revascularization (coronary artery bypass grafting [CABG]
or percutaneous coronary intervention [PCI]) or death at
any time before the completion of the 3-year follow-up. The
authors found that the risk-adjusted rates of survival were
significantly higher among patients who received CABG
than among those who received a stent. This was evident in
CABG patients with two-vessel disease with non-proximal
left anterior descending (LAD) artery involvement (adjusted
hazard ratio [HR] = 0.76) and in CABG patients with
three-vessel disease with involvement of the proximal LAD
(adjusted HR = 0.64). Revascularization rates were found
to be considerably higher after stenting than after CABG
(7.8% vs. 0.3% for subsequent CABG and 27.3% vs. 4.6 %
for subsequent stenting). The results of this study show that
CABG is associated with higher adjusted rates of long-term
survival than stenting in patients with two or more diseased
coronary arteries. However, the authors note that many
factors need to be taken into consideration when choosing
an intervention for patients with ischemic heart disease.
Current Issues in Cardiac Rehabilitation and Prevention
Copyright © 2006 Canadian Association of Cardiac Rehabilitation.
All rights reserved
The materials contained in the publication are the views/findings of the author(s) and do not
represent the views/findings of CACR. The information is of a general nature and should not be
used for any purpose other than to provide readers with current knowledge in the area.
For more information please contact:
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