Exercise stress test

 

As a followup on my previous stress echocardiogram last year, I took a treadmill stress ECG on 11 January 2024.  The procedure is much like the stress echocardiogram, except that they only record ECG traces and there is no lying down immediately after exercise to do the echocardiogram.  The echocardiogram limits how much exercise stress can be applied, because the technician does not want you breathing too hard while they apply the ultrasound probe.  Without the echocardiogram, the stress test gives less information, but the exercise level can be somewhat higher (it is also cheaper to do the test without the echocardiogram).

They used the BRUCE protocol for the stress test, which uses a standard stepwise increment in speed and incline on a treadmill.  I had decided ahead of time to go for maximal effort or at least getting to Step 6 of the protocol, whichever came first. 

Because my aerobic exercise has almost all been bicycling, I was not sure that I would be able to do maximum effort on a treadmill—hill-walking muscles are different from bicycling muscles. As it turned out, my legs were not my limiting factor. I had no trouble getting to Step 6, but I felt a little light-headed so I stopped the test at that point, even though I did not feel I was at maximum effort yet.

FINDINGS: The patient was stressed according to the BRUCE protocol for 15:15 min’s, achieving a work level of Max. METS: 17.50. The resting heart rate of 58 bpm changed to a maximal heart rate of 169 bpm during stress. This value represents 111 % of the maximal, age-predicted heart rate. The resting blood pressure of 126/81 mmHg, changed to a maximum blood pressure of 209/85 mmHg during stress. The Stress test was stopped due to fatigue and lightheadedness. 3-3 1/2 mm horizonal ST depression anterolateral leads at peak exercise

According to  “Age-Specific Exercise Capacity Threshold for Mortality Risk Assessment in Male Veterans” [Circulation. 2014;130:653–658 https://doi.org/10.1161/CIRCULATIONAHA.114.009666] this level of fitness reduces my chance of dying in the next 10 years by about a factor of 2, compared to “normal” MET levels (though the median for their measured cohort was below the level that they used as a reference).

My “resting” heart rate was higher than usual for me, as was the resting blood pressure—probably because I had not yet fully recovered from my bike ride to the clinic.  I find it interesting that they reported my METS as 17.50, when the BRUCE protocol calculators on the web that I tried all gave me only 16.03 METS—I wonder what the difference in calculation is.  Were they using more information (blood pressure? heart rate?) or just a different set of formulas?

Although the test shows me to be fit, the ST depression of 0.3–0.35mV is rather large (more than 0.1mV is considered abnormal), and it might indicate some ischemia, though it could just be the left ventricular hypertrophy that was diagnosed last year via echocardiogram.  Most of the studies that look at diagnosing coronary artery disease from ECGs exclude test patients with left ventricular hypertrophy, because it provides misleading signals. The rise in blood pressure at peak exercise is also large, though just below the level that is considered to be concerning.

Interestingly, there were no ectopic beats (neither PVCs nor SVT), which had been my initial problem that lead to the annual cardiology checkup. This change/improvement was unexpected, but I’ll take it as a sign that my heart condition (whatever it is—the tests seem to give different results every year) is not getting any worse. 

I originally had an appointment with my cardiologist to discuss my results (scheduled a year ago) on Feb 1, but it conflicted with my class at Cabrillo, so I rescheduled to the next available 20-minute appointment with the cardiologist: July 30.  It is a little ridiculous that there are so few cardiologists in the area that they are fully booked over 6 months in advance.

 

Stress echocardiogram

I have previously reported on my PVCs (premature ventricular complexes) mysteriously turning into SVT (superventricular tachycardia) in Holter monitor results. But when I had an echocardiogram done in January 2023, there were no SVT episodes. The reuslts were that things were pretty much normal:

The patient was in normal sinus rhythm during the exam. The patient had occasional PACs during the exam. The patient had occasional PVCs during the exam.
Left Ventricle: The left ventricle is normal in size. There is mild concentric left ventricular hypertrophy. The left ventricular ejection fraction is normal. The left ventricular ejection fraction calculated by 3D echo is 65%. The left ventricular wall motion is normal. Assessment of diastolic parameters suggests a pseudonormalization pattern, consistent with elevated filling pressures.
Right Ventricle: The right ventricle is normal in size and function.
Atria: The left atrium is mildly dilated. 3D LAVI: 36 ml/m2.
Mitral Valve: The mitral valve leaflets appear to be normal, and opens well. There is no mitral valve stenosis. There is trivial mitral regurgitation.
Aortic Valve: The aortic valve is trileaflet. The aortic valve is sclerotic, but shows no functional abnormality. There is no aortic valve stenosis. No aortic regurgitation is present.
Tricuspid Valve: The tricuspid valve leaflets are thin and pliable. There is no tricuspid stenosis. There is trace tricuspid regurgitation. Unable to estimate PA systolic pressure due to poor TR signal.
Pulmonic Valve: The pulmonic valve is normal in structure and function. There is no pulmonic valvular stenosis. There is no pulmonic valvular regurgitation.
Great Vessels: The aortic root is normal size. The ascending aorta is normal in size. Atherosclerotic changes can be seen in the abdominal aorta. The inferior vena cava appeared normal.
Pericardium/ Pleural: There is no pericardial effusion. There is no pleural effusion.

In discussing the results with the cardiologist, I pointed out that the Zio monitor results (with 2161 SVT episodes in 329 hours, about 6.66/hour) showed clusters of episodes when my heart rate was high, suggesting that they were triggered by exercise.  The cardiologist ordered a stress echocardiogram, to see whether we could catch the SVTs that way.

Today I had the stress echocardiogram test. Here are the stress results:

Protocol Name	BRUCE
Max Work Load (METS*10)	165
Time In Exercise Phase	00:13:38
Max. Systolic BP	196 mmHg
Max Diastolic BP	72 mmHg
Max Heart Rate	166 BPM
Max Predicted Heart Rate	152 BPM

The resting blood pressure was 122/70 mmHg.

We stopped the test because they wanted only about 80% effort, not maximum effort, as they didn’t want me breathing too hard for the echocardiogram at the end of the test. They reported the termination condition as “dyspnea (shortness of breath)”, but I was still able to talk fairly comfortably when we stopped, so it definitely wasn’t maximum effort. When I was wearing the Zio monitor, I got up to 176bpm (though that was with an SVT episode—my highest sinus rate was only 160 bpm). Still, 16.5 METS is not too shabby for a 68-year-old man.  If I do another stress test in future, I’ll probably push for a higher level of exertion.

Here are the main observations from the test:

No ischemia with good tolerance and normal LVEF
PVCs, PACs, short runs of SVT

———————————

Normal BP response to exercise.
Resting ECG Sinus rhythm @ 56 bpm.
Stress ECG: No ischemic ST changes. Rare PVCs during stress. Rare PACs during exercise and recovery. Short runs of PAT.
Left Ventricle: Normal global systolic function. There are no wall motion abnormalities.
Immediate Post Stress Echocardiogram: There is appropriate exercise augmentation of the ejection fraction. There are no exercise-induced wall-motion abnormalities.

Note: PAT stands for paroxysmal atrial tachycardia—a type of paroxysmal supraventricular tachycardia (PSVT). So we did manage to trigger an SVT episode, but there doesn’t seem to be much more information—everything looks pretty normal. 

I guess in cardiology, having arrhythmias be hard to catch is probably good news, but I don’t know why they were so common when I had the Zio monitor on, but so rare now, just a few months later.

Holter monitor results

I got back the results from wearing the Holter monitor for 14 days today, and they were not what I expected.  I was expecting to see frequent PVCs, particularly when I was resting or sleeping. Instead the report had almost no PVCs but frequent PACs (premature atrial contractions) with runs of supraventricular tachycardia (runs of more than 3 PACs without normal beats in between).  “Isolated SVEs [supraventricular ectopy] were frequent (10.3%, 114645).” “2161 Supraventricular Tachycardia runs occurred, the run with the fastest interval lasting 6 beats with a max rate of 176 bpm, the longest lasting 26.7 secs with an avg rate of 133 bpm.”

Asymptomatic PACs (like asymptomatic PVCs) do not generally call for any treatment, but “many idiopathic PACs are relatively benign in the short term, although they can be associated with an increased risk of cardiac and all-cause mortality if they occur frequently.” [https://www.ncbi.nlm.nih.gov/books/NBK559204/] Most of the medical treatments seem to be focussed on lowering heart rate or blood pressure, neither of which seem appropriate for me (I have normal blood pressure and a low heart rate). The followup recommended for frequent PACs is an echo cardiogram, which I have now scheduled for mid-January (the soonest date that the clinic had available).

My sinus heart rate was about what I expected with “a min HR of 36 bpm, max HR of 160 bpm, and avg HR of 55 bpm”, though the 36 bpm minimum was a little lower than the 40bpm I expected—my sinus rate drops a little lower when I sleep than I expected. The recording of the 36bpm period does not look like my normal sinus rhythm—it looks like a series of ectopic beats with really tiny QRS complexes to me, but it did occur when I was asleep (in the middle of a period of very low heart rate). On another day, there was a recording of 37 bpm which showed normal QRS complexes, so my sinus rate does indeed drop that low.

The max of 160 bpm occurred when I was exercising fairly hard—pushing myself a bit on bicycling uphill to campus.  It is probably not my real maximum heart rate (I was not doing an all-out effort).  I looked up estimates of maximum heart rate and found three formulas: (220 – age), (207 – 0.7 age), and (211 – 0.64 age).  The first is very common, but clearly wrong for me, the second is adjusted for people over 40 years old and pretty accurately matches the observed maximum on the Holter monitor, and the third is adjusted for active people and may slightly overestimate my max heart rate.  If I ever need to take a stress ECG or stress echocardiogram, I’ll argue for them using the second formula rather than the first in estimating my max heart rate, so that the stress level is appropriately set.

One thing I wanted to know that is not reported in the short summary report from the Holter monitor is whether there was any correlation between the sinus rhythm and the ectopic beats—in particular, I wanted to know whether the ectopic beats occurred primarily when my sinus rhythm was very low.  If that is the case, then a pacemaker set to maintain a minimum sinus rhythm might be a possible treatment, should treatment ever be needed.  I downloaded the full report, which shows when the SVT runs occurred, and they seem to be primarily when I’m awake and active, which is the opposite of what I expected based on my observations of PVCs earlier in the year.

I wasn’t sure how one distinguishes a PAC from a PVC on a one-lead Holter monitor, so I watched a video (https://www.youtube.com/watch?v=7Vz8olVnGgU) from “Catalyst University”, which showed the difference between PVCs and PACs on a one-lead ECG. The crucial differences are whether the P-wave (from atrial depolarization) is observed and whether the resulting QRS complex is more or less normal or much longer duration that usual.  If the P-wave is observed and the QRS spike is normal duration and shape (though usually lower amplitude), then you have a premature atrial contraction.  If there is no P-wave and the QRS complex is much longer than usual, you have a PVC.  By these criteria, the observations I made earlier (see PVC again, for example) were clearly PVCs, and the examples of SVT runs shown in the report were indeed PACs. My most recent home ECG recordings have not shown me PVCs, but if I now have PACs instead, my inability to find PVCs may represent a change in what my heart is doing, rather than a failure in my rather crude code for detecting them.

I looked for genetic causes of PACs, but have not found much. Deletion of the STK11 gene is the only thing I’ve found so far, and there is no hint of that in my genome—I do have a SNP in an intron of a gene whose protein that interacts with it: STK11IP, as well as some SNPs in the intergenic region upstream of STK11.  None of these SNPs seem likely to be a major cause of problems.

Holter monitor

For the past 10 days, I’ve been wearing a Holter monitor made by Zio, in order to determine the real frequency of my premature ventricular complexes (PVCs).

I’ve checked the PVCs myself with my own home-made ECG starting about a year ago, but my ECG can only be used when I’m awake and generally sitting in one place, so it does not catch the full range of my heart activity. Because the amplifier board had to be connected to PteroDAQ running on a breadboard connected to a laptop, the ECG setup is not very portable, and I had to sit still to avoid disturbing the circuitry. I couldn’t even use the laptop to browse the web or read email while recording, since changing my contact with the laptop changed the bias voltage on my body, which the amplifier took a second or two to recover from.  So I only recorded about 5–10 minutes at a time.

Some of my recordings got a lot of PVCs, and some got almost none. I did notice that raising my heart rate through exercise seemed to abolish the PVCs. So I think that my PVCs are “slow-rate-dependent” PVCs—that is, that I only get the extra ventricular contractions when my sinoatrial node does not start frequent enough contractions.  Because my heart rate is most likely lowest when I’m sleeping, the ECGs that I did myself probably missed most of the PVCs.

I mentioned my curiosity about what my real PVC burden was at my annual checkup, so my doctor ordered a 14-day recording with a Holter monitor.

Holter monitors have gotten quite small. This Zio monitor has electrodes about 9cm apart and just sticks onto the chest.

Here is a closeup of the Zio Holter monitor.

The adhesive that holds the Zio on sticks well to dry skin (though it makes my skin itch a bit), but one day this week I got a bit sweaty cycling up to campus in my rain suit, and the monitor started to slide around. It seems to be firmly in place again after my skin dried, but I think it is slightly lower than its original placement.

I have to mail the Zio back to the manufacturer for them to unload the recorded data and send a report to the cardiology department.  I’m hoping that the cardiologist will provide me with the information I’m interested (things like what my minimum heart rate is when I’m sleeping, what the PVC burden is when I’m sleeping and overall, whether my PVCs are indeed slow-rate-dependent, whether there is a minimum heart rate for me above which very few PVCs are seen, … ).

Right now the PVCs are completely asymptomatic, which just means that I can’t tell when I have them without using an ECG. For asymptomatic PVCs, all the treatments are worse than the PVCs, so nothing needs to be done now, but if anything changes, I’ll want to know.  The treatments I’m aware of include ablation of the cells that trigger the premature complex, beta blockers to lower heart rate (not appropriate for slow-rate-dependent PVCs), and electrical pacemakers to start extra heartbeats at the sinoatrial node when the pacemaker cells fail to do so on their own.  I believe that my father had a pacemaker just for that purpose, and I suspect I may be getting one in a decade or so.

ECG: 2-electrode vs. 3-electrode

In Lower PVC frequency, I said “I did not do direct comparisons of the 2-electrode and 3-electrode configurations—I’ll have to try that sometime soon.” So I did that earlier this week, recording resting ECGs first with a 3-electrode configuration (with the bias electrode on my sternum, halfway between the LA and RA electrodes) and then with a 2-electrode configuration (with the bias wire clipped to the RA electrode).  The 60 Hz noise was slightly higher with the 2-electrode configuration, but after filtering and signal averaging the two recordings were almost identical:

The waveforms after signal averaging were remarkably similar. The PVC burden was also similar (20.1% for the 3-electrode recording and 20.5% for the 2-electrode recording).

The pulse rate from looking at time between spikes worked well for the resting recordings, but the autocorrelation method failed completely, so I did not plot it. The rapid fluctuation in heart rate within a narrow range is real, not an artifact of the algorithm—the heart beats are not perfectly periodic, and the PVCs may be making them even less periodic. The 2-electrode recording probably started a little after 400 seconds—PteroDAQ only time stamps when the file was saved, not what the t=0s time was. I should probably fix PteroDAQ to change that, recording both.

I tried recording a session on the exercise bike also. The PVCs are mainly during resting at the beginning of the session and at the end of a recovery at the end of the session—the PVC burden was only 1.4%.

For the exercise recording, the noise really disrupted the spike-based pulse detection, but did not interfere as much with the autocorrelation-based pulse detection. My peak pulse rate was about 151.5 bpm, by the autocorrelation measure. I’m not sure whether the sudden changes in pulse rate at 100s (when I started pedaling) and around 556s (about 130s into the recovery time) are real or not—the noise in the recording makes it a little difficult to determine the “correct” pulse rate.

The noise during exercise was not 60Hz noise and seemed to vary with whether I was inhaling or exhaling, so I think that it was probably caused by EMG signals from the pectoral muscles or perhaps the diaphragm. The spike detector was clearly missing a lot of the spikes, but making it more sensitive would probably result in false triggering on the EMG noise. I’m wondering whether putting the electrodes on my back, over the scapulae, would reduce the EMG noise, but placing those electrodes and clipping to them would be difficult without an assistant.

The autocorrelation-based pulse detection seems more reliable when exercising, as my pulse is more periodic and has few PVCs, and the autocorrelation method is less susceptible to aperiodic noise.  The spike-based pulse detection seems more reliable when resting, when the pulse is not as periodic and PVCs disrupt the pattern.

I’m also wondering whether a more strenuous exercise session would raise my pulse rate, or whether I’m getting close to my maximum heart rate.  The standard formula for maximum heart rate by age suggests that this may be close to my maximum, but the exercise does not seem all that strenuous, and a couple of years ago I could routinely push to 170 bpm (though perhaps on a device that was an unreliable reporter—it was built into a treadmill at the gym).  So sometime in the next few weeks I’ll try using a higher power output and seeing where my heartbeat tops out.  I’ll probably need to increase the cadence, rather than the resistance, as I’ve been using about 70rpm and 28Nm to get about 205W.  Raising that to 80rpm or even 90rpm is probably easier than increasing the torque.