Download Exercise and Ischemia

TABLE 2
Estimation of Relative Risk Reduction in All-Cause
Mortality in Patients with Coronary Artery Disease
– adapted from Iestra JA, et al.3
Intervention
Mortality Risk Reduction %
(95% Confidence Interval)
Pharmacologic
Low-dose aspirin
18 (1-30)
Statins
21 (14-28)
Beta-Blockers
23 (15-31
ACE Inhibitors
26 (16-35)
Non-Pharmacologic
Smoking Cessation 35 (CI not given)
Physical Activity
25 (2-41)
Moderate Alcohol
20 (17-22)
References:
1.Kelvin L. Lecture to the Institution of Civil Engineers; 3 May 1883;
Ireland.
2.Keys A, Aravanis C, Blackburn HW, et al. Epidemiological studies
related to coronary heart disease: characteristics of men aged 40-59 in
seven countries. Acta Med Scand Suppl 1966;460:1-392.
3.Iestra JA, Kromhout D, van der Schouw YT, et al. Effect size estimates
of lifestyle and dietary changes on all-cause mortality in coronary artery
disease patients: a systematic review. Circulation 2005;112:924-934.
4.De Backer G, Ambrosioni E, Borch-Johnsen K, et al. European
guidelines on cardiovascular disease prevention in clinical practice:
third joint task force of European and other societies on cardiovascular
disease prevention in clinical practice (constituted by representatives
of eight societies and by invited experts). Eur J Cardiovasc Prev Rehabil
2003;10:S1-S10.
5.Third Report of the National Cholesterol Education Program (NCEP)
Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult Treatment Panel III) final report.
Circulation 2002;106:3143-3421.
6.Wilson K, Gibson N, Willan A, et al. Effect of smoking cessation on
mortality after myocardial infarction: meta-analysis of cohort studies.
Arch Intern Med 2000;160:939-944.
7.Critchley JA, Capewell S. Mortality risk reduction associated with
smoking cessation in patients with coronary heart disease: a systematic
review. JAMA 2003;290:86-97.
8.Greenwood DC, Muir KR, Packham CJ, et al. Stress, social support,
and stopping smoking after myocardial infarction in England.
J Epidemiol Community Health 1995;49:583-587.
9.Capewell S, Livingston BM, MacIntyre K, et al. Trends in case-fatality
in 117,718 patients admitted with acute myocardial infarction in
Scotland. Eur Heart J 2000;21:1833-1840.
10.MacIntyre K, Capewell S, Stewart S, et al. Evidence of improving
prognosis in heart failure: trends in case fatality in 66,547 patients
hospitalized between 1986 and 1995. Circulation 2000;102:11261131.
11.Health effects of exposure to environmental tobacco smoke. California
Environmental Protection Agency. Tob Control 1997;6:346-353.
12.Brown AT, Noorani R, Stone H, Skidmore JB. Exercise-based Cardiac
Rehabilitation Programs for Coronary Artery Disease: A Systematic
Clinical and Economic Review. Ottawa: Canadian Coordinating Office
for Health Technology Assessment (CCOHTA); 2003.
13.Cooper HA, Exner DV, Domanski MJ. Light-to-moderate alcohol
consumption and prognosis in patients with left ventricular systolic
dysfunction. J Am Coll Cardiol 2000;35:1753-1759.
14.Witt BJ, Jacobsen SJ, Weston SA, et al. Cardiac rehabilitation
after myocardial infarction in the community. J Am Coll Cardiol
2004;44:988-996.
15.Cooper AF, Jackson G, Weinman J, et al. Factors associated with
cardiac rehabilitation attendance: a systematic review of the literature.
Clin Rehabil 2002;16:541-552.
Exercise and Ischemia
Rick Stene, BSPE, ACSM Program Director, Manager, Cardiac Rehabilitation and First Step
Programs, Saskatoon Health Region
“Confidence is that feeling we have before
we fully understand our situation.”
– Unknown
Past: Angina Pectoris was first described by William Heberden
in the 1770’s. The physical symptoms he described were later
found to be the result of ischemic heart muscle. Myocardial
ischemia occurs when oxygen supply to the heart muscle is not
sufficient to meet the oxygen demand. In the past it was believed
that ischemia occurred due to a fixed narrowing (atherosclerosis,
plaque) in the artery, which would restrict blood flow, not
allowing enough blood through to meet the demand. This was
reproducible; occurring at a consistent fixed work load.
The work load at which ischemia occurs can be measured
10
and quantified by using the Rate Pressure Product (Heart
Rate x Systolic Blood Pressure). Generally, ischemia was
felt to be represented by ST depression on an ECG. This
is usually defined as 1 mm of ST depression from baseline,
flat or down sloping, at 80msec from the j point, lasting
more than 1 min., in 1 or more leads. It was believed that
the ischemic threshold would only change if and when the
plaque progressed. It was also believed that angina occurred
with all ischemic events. Those individuals who denied any
symptoms with the ischemia denied symptoms leading up
to, and during, a heart attack.
Based on this knowledge an exercise prescription for
patients with angina was developed, and is still in use today. The
American College of Sports Medicine (ACSM) guideline for
exercise prescription in patients with Ischemia/angina states:
Current Issues in Cardiac Rehabilitation and Prevention
“Because symptomatic or silent ischemia may be
arrhythmogenic, the THR (training heart rate) for endurance
exercise should be set safely below (>10 beats/min) the
ischemic ECG or anginal threshold. Alternately, the upper
heart level can be set as the highest non ischemic workload
from a Graded Exercise Tolerance (GXT).”1
Typically a patient would undergo a GXT and the point,
(heart rate/rate pressure product), at which they developed
1mm of ST depression (as defined above) would be deemed
the ischemic threshold. From this the exercise prescription
would be developed as 10 beats below that ischemic heart
rate. The primary purpose behind this was to avoid having
patients exercising while they are experiencing ischemia, and
the resulting risk of arrhythmias and sudden cardiac death.
Unfortunately, the early concepts of ischemia/angina,
were based on assumptions that were simplistic in their
understanding of ischemia and angina. The frequency of
“silent” ischemia was not fully appreciated. The importance
of vascular smooth muscle control of lumen diameter was
unknown and the role endothelium plays in vascular disease
was yet to be discovered.
The Ischemic Cascade:
The ischemic cascade refers to a sequence of events that
appear to take place during an ischemic episode.10 This
sequence is outlined below and includes the percentage of
times during an ischemic event each step is likely to be
detected (Berger et al.)1,5
1.Imbalance in the myocardium between
supply of oxygen and the demand. (100%)
2. Changes in diastolic and systolic function. (80%)
3. ECG changes may occur.
(50%)
4. Patient may experience angina.
(30%)
Examples of some factors that are currently
believed to influence ischemic episodes:
•Circadian rhythms: the influence of diurnal variation
on the frequency of ischemia, angina and MIs is well
documented.11 There is a tendency for a disproportionate
number of events to occur during the first few hours of
the morning. Ischemic episodes are more common in the
first waking hours of the day.
•Endothelial function: it is believed that a dysfunctional
endothelium does not produce sufficient Nitric Oxide
to stimulate smooth muscle relaxation.18,20 In contrast,
the direct effect of catecholamines on smooth muscle
is vasoconstriction. This may cause “warm up” induced
angina/ischemia.12,14
•Effects of smooth muscle constriction:12,20 patients with
variant angina which is caused by smooth muscle spasm
or constriction.
Standard Bruce protocol exercise testing will overestimate the ischemic threshold (rate pressure product) as
compared to longer endurance training of activities of daily
living.16 Studies have demonstrated that ischemia routinely
occurs at lower rate pressure products when patients engage
in longer sustained aerobic exercise than what would have
been estimated from standard exercise testing. Ischemic
episodes vary with the type of activity being done. Different
aerobic exercises cause ischemia in patients at different rate
pressure products.1
Incidence of silent ischemia:
•Silent ischemic episodes are more common that first
believed9,15
•Perhaps as many as 9 episodes of silent ischemia for every
episode of angina17,19
•20%-30% of all individuals with diabetes experience silent
ischemia6,7,8
•About 20% of all elderly people have episodes of silent
ischemia4
Conclusion:
Lumen diameter is a dynamic construct. Ischemic events
during exercise and activities of daily living are far more
common and less predictable than we once thought. These
episodes are fairly common in people with diabetes and in
cardiac patients. The guideline for exercise prescription
in patients with angina was written prior to our current
understanding of angina and ischemia. Concern for the
development of arrhythmias and sudden cardiac death are
well founded. It is also known that regular endurance exercise
is protective against sudden cardiac death.2,3
“Ischemic events during exercise and activities
of daily living are far more common and less
predictable than we once thought.”
It is important, and perhaps unsettling, to realize the
extent at which ischemic episodes occur during exercise and
activities of daily living. There is clear evidence outlining the
shortcomings of our current approach for exercise prescription
at limiting these occurrences. Clinical experience has shown
that after millions of patient-hours of exercise within Cardiac
Rehabilitation programs, this approach to prescribing exercise
is safe. This begs the question, are these episodes of ischemia
as dangerous as we have thought? If they are, then a new
approach to prescribing exercise is needed. If these episodes
are not as concerning and are to be ignored, then the current
Current Issues in Cardiac Rehabilitation and Prevention
11
approach to exercise prescription is adequate. More study is
needed to address these questions.
References:
1.American College of Sports Medicine: ACSM’s Guidelines for Exercise
Testing and Prescription 5th Ed., 2005.
2.Franklin BA: Cardiovascular Events Associated with Exercise: The
Risk-Protection Paradox. Journal of Cardiopulmonary Rehabilitation
189-194, 2005.
3.Canadian Guidelines for Cardiac Rehabilitation and Cardiovascular
Disease Prevention. 2nd Edition, 2004.
4.Saiadieh A, Nielsen OW, Rasmussen V, Hein HO, Hansen JF.
Prevalence and prognostic significance of daily-life silent myocardial
ischemia in middle-aged and elderly subjects with no apparent heart
disease. Eur Heart J 2005;26:1402-9.
5.Berger HJ, Reduto LA, Johnstone DE, Borkowski H, Sands JM, Cohen
LS, Langou RA, Gottschalk A, Zaret BL, Pytlik L. Global and regional
left ventricular response to bicycle exercise in coronary artery disease.
Assessment by quantitative radionuclide angiocardiography. Am J Med
1979;66:13-21
6.DeLuca A J, Sulle LN, Arunow WS, Ruvinu G, Weiss MB. Prevalence
of silent myocardial ischemia in persons with diabetes mellitus or
impaired glucose tolerance and association of hemoglobin A1c with
prevalence of silent myocardial ischemia. Am J Cardiol 15;95:1472-4,
2005.
7.Valensi P. Silent coronary artery disease in diabetic patients. New
guidelines. Rev Med Liege 2005;60:531-5.
8.Negrusz-Kawecka M, et al. Frequency of silent ischemic heart disease
in patients with diabetes mellitus. Pub Med Pol Merkuriuaz Lek
1997;3:53-6.
9.Causse C, Marcoutoni JA, Allaert FA, Wolf JE. Frequency of silent and
painful ischemia in patients with treated stable coronary insufficiency.
Pub Med Ann Cardiol Angeiol (Paris) 2000;49:277-86.
10.Nesto RW, Kowalchuk GJ: The ischemic cascade: temporal sequence
of hemodynamic, electrocardiographic and symptomatic expressions of
ischemia. 1987;59:23C-30C.
11.Zarich S, Waxman S, Freeman RT, Mittleman M, Hegarry P, Nesto RW.
Effect of autonomic nervous system dysfunction on the circadian
pattern of myocardial ischemia in diabetes mellitus. J Am Coll Cardiol
1994;24:956-62.
12.Hasdai D, Gibbons RJ, Holmes DR Jr., Higano ST, Lerman A.
Coronary endothelial dysfunction in humans is associated with
myocardial perfusion defects. Circulation 1997;96:3390-5.
13.Shea MJ, Deanfield JE, deLandsheere CM, Wilson RA, Kensett M,
Selwyn AP. Asymptomatic myocardial ischemia following cold
provocation. Am Heart J 1987;114:469-76.
14.Dagianti A Jr., Arveri A, Sgorbini L, Penco M, Fedele F. Stress
echocardiography in the study of the warm-up phenomenon.
Cardiologia 1998;43:711-5.
15.Hinderliter A, Miller P, Bragdon E, Battenger M, Sheps D. Myocardial
ischemia during daily activities: the importance of increased myocardial
oxygen demand. J Am Coll Cardiol 1991;18:405-12.
16.Garber CE, Carleton RA, Camaione DN, Heller GV. The threshold
for myocardial ischemia varies in patients with coronary artery disease
depending on the exercise protocol. 1991;17:1256-62.
17.Caboni GP, Lahui A, Cashman PM, Raftery EB. Ambulatory heart
rate and ST-segment depression during painful and silent myocardial
ischemia in chronic stable angina pectoris. Am J Cardiol 1987;59:1029-34.
18.Landmesser U, Drexler H. The clinical significance of endothelial
dysfunction. Curr Opin Cardiol 2005;20:547-51.
19.Causse C, Allaert FA, Murcantoni JP, Wolf JE, Frequency and detection
rate of silent myocardial ischemia by Holter monitoring in patients
with stable coronary insufficiency under treatment. Study of 95,725
recorded hours. Arch Mal Coeur Vaiss 2001;94:779-84.
20.Kawano H, Ogawa H. Endothelial function and coronary spastic
angina. Intern Med 2005;44:91-9.
Saskatchewan Medication Assessment for Risk
Reduction Treatment Targets (SMART2 Study)
William Semchuk, MSc, PharmD, FCSHP, on behalf of the SMART2 Investigators,
Regina Qu’Appelle Health Region
Vascular diseases are the leading cause of increased morbidity and
mortality in North America. Together, cerebro- and cardiovascular
disease accounted for approximately 40% of all deaths in
Canada in 1996, were the leading cause of hospital days (18%
of the total) and constituted a significant economic impact both
directly and indirectly.1,2,3 As the population of Canada ages and
life expectancy increases, the incidence and cost of care for both
cerebro- and cardiovascular disease will continue to increase.
It is clear that the progression of vascular disease is most
often initiated by the presence of multiple risk factors.4,5 Aside
from age, sex, ethnicity, heredity, and previous history of
vascular events, most of the remaining risk factors, including
hypertension, diabetes mellitus, hyperlipidemia, atrial fibrilla­
tion, atherosclerosis, smoking and sedentary lifestyle, are
modifiable.4,5 Targeted risk factor management and/or reduction
as primary or secondary prevention measures have resulted in
significant decreases in both cerebro- and cardiovascular events
12
in large randomized clinical trials.6 –17 The use of anti-platelet
agents, agents used to alter blood pressure, agents used to lower
cholesterol, beta-blockers and others have all been shown to
be beneficial in both the acute and chronic settings.6,7,8,9,12–17
Data pertaining to the acute benefit of these agents generally
demonstrates improvement in outcome in the first several
days to weeks after an acute event, while the benefit seen in
the primary or secondary prevention setting demonstrates
significant improvement in outcome generally between 12 and
36 months after initiation with increasing benefit over time.
“Despite the availability of vast amounts of
clinical data and the proliferation of treatment
guidelines, a large proportion of patients are not
receiving optimal treatment.”
The benefits of aggressive disease management as demon­
strated by these and other studies18,19 has led to the publications of
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:
Executive Director CACR
1390 Taylor Avenue Winnipeg, MB R3M 3V8
Canada