Say “No” to Drugs … For Cardiac Stress Testing

And “Yes” to Exercise

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The standard exercise stress test has gotten a bad rap and has been replaced in many cardiac stress labs by nuclear and echocardiographic imaging stress tests, often using regadenoson for the nuclear and dobutamine for the echocardiographic studies.  The shift from exercise, non-imaging stress tests occurred for multiple reasons including diagnostic accuracy and the ease of the procedure. 

I have argued against the diagnostic accuracy claim because most of these studies compared the accuracy of ECG ST-segment shifts with cardiac imaging.  But the standard exercise test provides a knowledgeable clinician with much more information than the ST segment alone.  I totally get the superiority of the imaging stress tests when the patient “cannot” exercise on the treadmill, but even this group of patients can often exercise if given a modified protocol such as the Naughton exercise protocol.  Labs don’t like to use gradual protocols like the Naughton because it takes time.  The Naughton starts with a 0% grade at 1 MPH for 1 minute (min), increases to 2 MPH for 2 min and then maintains a 2 MPH speed but increases the grade 3.5% every 2 min for 6 stages.  Many patients who cannot perform the much more difficult Bruce Protocol can do the Naughton. But if the patient cannot perform enough exercise using  the Naughton protocol, starting with low level exercise and switching to pharmacologic stress is still more valuable than pharmacologic stress testing alone.

Why do I push to do some exercise, any exercise, with cardiac stress testing? Two reasons:

1.     It is more physiologic and gives an indication of what the patient can do in real life.  (Most people have to do some waddling around just to survive, but nobody has to inject themselves with regadenoson or dobutamine on a daily basis.)

2.     Exercise gives you an indication of the individual’s maximal “internal” and “external” work rates.

The concept of “internal” and “external” work rates is a key concept for cardiologists.  I do not hear it used much, but to my knowledge it was first proposed by Ezra Amsterdam, MD, and colleagues at the University of California at Davis in 1974. (1)  I have used this concept often including in a Circulation paper on the role of exercise training in atherosclerotic cardiovascular disease.  (2)

The external work rate is how much work the patient can perform on their environment.  How far did they walk on the treadmill or how many watts did they do on the stationary bicycle?  This is their total exercise performance and measures their maximal exercise capacity.  Maximal exercise capacity can also be measured by collecting exhaled gases and measuring the patient’s maximal exercise oxygen uptake (O2) or VO2max, during a “cardiopulmonary exercise test” or PET.  VO2max is the product of maximal heart rate X maximal stroke volume X the maximal arterial-venous oxygen difference (A-V O2 diff).  Maximal heart rate will be obvious from the ECG tracings so you can readily see problems there.  Maximal A-V O2 diff is not measured routinely but won’t differ enormously among patients.  So, what you get when you measure maximal exercise capacity is an estimate of maximal stroke volume.  Any great endurance athlete has a big maximal stroke volume, and how far a patient can go on a stress test gives an indication as to how good their heart is as a pump.

This is an important concept: exercise capacity is an indirect measure of cardiac stroke volume.

But even more important, maximal exercise capacity, or cardiorespiratory fitness, is one of the absolute best predictors of survival.  If someone can perform a lot of aerobic exercise, their cardiac capacity must be good, and they are capable of surviving many of the vicissitudes of life such as pneumonia, COVID-19, a heart attack, etc.  Like the Timex watch commercial from the 1950s, a  heart with a good maximum stroke volume can “take a licking and keep on ticking.” You don’t get total exercise capacity from a pharmacologic stress test.

(I should point out that you only get an accurate measurement of treadmill exercise capacity if the patient is not allowed to hang onto the treadmill’s front bar for dear life.  It’s a maximal treadmill test; not a maximal handgrip test, although handgrip does also predict survival. (3)   So, if you are a cardiologist interested in cardiac health and not in handgrip strength, make the patient use their open hand for balance and not their grip for survival.)

In addition to the “external work rate”, exercise testing gives an indication of the “internal” or cardiac work rate.  Myocardial oxygen demand (MVO2) can be estimated by the heart rate (HR) times the systolic blood pressure (SBP) times the left ventricular ejection time (LVET).  I think of this like weight lifting: how much weight did the heart lift (SBP), how many times per minute and how long did it hold the contraction (LVET).  LVET is closely related to HR, so LVET can be ignored because it’s already considered in the HR.  SBP is important to MVO2, but not that important.  The key determinant of MVO2 is HR so by measuring HR during exercise you get an assessment of the state of the patient’s coronaries.  If they can get to a high HR without symptoms or ST segment shifts, their coronaries can supply a lot of blood to the heart and you can be reassured that the coronary pipes are probably in decent shape. 

Furthermore, ST-segment changes at a high exercise HR without symptoms are often a “false positive” result.  This is especially true if the ST changes resolve within the first 2 minutes or so after exercise.  Even if the ST-segment changes are real and even if the patient is symptomatic, a high exercise HR suggest that the coronary stenoses are not very tight because the patient reached a high “internal” work rate.

There is also much more you get from an exercise stress test.  You can detect symptoms.  You can observe for arrhythmia.  You can see if there is exercise hypertension, which indicates failure to vasodilate and is a predictor of subsequent hypertension.  You get so much more than you can get from a drug stress test.  And it’s faster and cheaper.

So, here are the rules:

·      Say “No” to drugs.  Say “Yes’ to exercise.

·      An exercise stress test gives you the “external work rate” or total exercise capacity.  Total exercise capacity is an indirect measure of cardiac stroke volume and a strong predictor of survival.  

·      An exercise stress test also gives you the “internal work rate” or exercise HR, an indicator of cardiac oxygen demand.  Being able to reach a high exercise HR without symptoms or ECG changes suggests that the coronary pipes are free of tight disease.

·      Resolution of ST-segment shifts in the first 2 minutes after exercise suggests that the ECG changes were a false positive response.

·      Don’t let the patients hang on for dear life during their exercise test.  They can use their hands for balance, but it’s an exercise test and not a hand-grip measurement.

1.     Amsterdam EA, Hughes JL, DeMaria AN, Zelis R, Mason DT. Indirect assessment of myocardial oxygen consumption in the evaluation of mechanisms and therapy of angina pectoris. Am J Cardiol. 1974 May 20;33(6):737-43. PMID: 4151042 

2.     Thompson PD. Exercise prescription and proscription for patients with coronary artery disease. Circulation. 2005 Oct 11;112(15):2354-63. PMID: 16216979

3.     López-Bueno R, Andersen LL, Koyanagi A, Núñez-Cortés R, Calatayud J, Casaña J, Del Pozo Cruz B. Thresholds of handgrip strength for all-cause, cancer, and cardiovascular mortality: A systematic review with dose-response meta-analysis. Ageing Res Rev. 2022 Dec;82:101778. PMID: 36332759 

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