Aa
Stress test
Yesterday I had an exercise test with an ergometric bicycle. The test was stopped after 9 minutes because my legs became very tired. The test was OK with only a few extrasystoles. My capacity was even better than normal. But 1 min after the test I got supraventricular tachycardia (169 beats/min) and ST segment depression. At the same time I had a short period of hyperventilation. After two times valsalva maneuver the normal rhytm returned. After that there was also some lowering of the ST level.
My maximal heart rate was 157 (96%). The maximal load was 135 W. I am 65 y old. PEF was 420 (96%) and there was no bronchial compression after the test.
I had 12 mg Tenoblock (atenolol) in the morning and 25 + 25 mg on the previous day .
Why did my ST segment depress after the test?
My maximal heart rate was 157 (96%). The maximal load was 135 W. I am 65 y old. PEF was 420 (96%) and there was no bronchial compression after the test.
I had 12 mg Tenoblock (atenolol) in the morning and 25 + 25 mg on the previous day .
Why did my ST segment depress after the test?
Thank you for your answer.
I am thinking of these things because I'd like to have the best treatmnent to my heart problems and other health problems. The whole physiologic system should be taken into consideration (hormones, electrolytes, fluids kidneys etc.). Many doctors have a too narrow way of looking at things. I have to say that electrophysiology is not an easy thing to understand.
I think that the prominently abnormal extrasystoles in the EKG recording during the 2010 AF were aberrant complexes as follows (MediLexicon): Definitions: 1. an anomalous electrocardiographic complex, more specifically an abnormal ventricular complex caused by abnormal intraventricular conduction of a supraventricular impulse. I don't have the record paper any longer, but I remember the shape of the beats. I think that because during AF, the electric function of the atrium is disturbed, it may cause also increase of premature supraventricular impulses. As I can understand, the variable heart rate during AF could cause aberrant conduction of some premature supraventricular impulses in the bundle branches and Purkinje fibres in the ventricle walls. The conduction can be blocked, or its partial block (in the right bundle branch) can change the shape of the complex in EKG.
As to possible LQTS: I cannot use erythromycin or cisapride. Because my ionized calcium is slightly high, it may shorten QT. Possibly my beta blocker atenolol also shortens it (I do not know it surely). I am using magnesium suppelement, which can also shorten it. My corrected baseline QT was recently 460. I don't like to use such rhythm medications which could prolong QT.
When in 2010 I had AF, a doctor prescribed me amiodarone. I refused to take it. Amiodarone could prolong QT, and I had some precautions: I had pulmonary, liver and thyroid problems, which amiodarone could worsen. Later I used dronedarone. I got muscular dystonia and I was wondering whether dronedarone caused it.
Maybe doctors will think, after possible coronary artery scan, that I should use eg. flecainide or sotalol to prevent arrhythmias. I cannot use calcium channel blockers or many beta blockers. Verapamil has caused fever and diarrhea for me and a worse tachycardia than before its use. Dilmin caused dizziness and weakness during walking uphill. The same was with digitalis. Bisoprolol irritates my heart, Selectol and Spesicor have no effect on high heart rate.
I am thinking of these things because I'd like to have the best treatmnent to my heart problems and other health problems. The whole physiologic system should be taken into consideration (hormones, electrolytes, fluids kidneys etc.). Many doctors have a too narrow way of looking at things. I have to say that electrophysiology is not an easy thing to understand.
I think that the prominently abnormal extrasystoles in the EKG recording during the 2010 AF were aberrant complexes as follows (MediLexicon): Definitions: 1. an anomalous electrocardiographic complex, more specifically an abnormal ventricular complex caused by abnormal intraventricular conduction of a supraventricular impulse. I don't have the record paper any longer, but I remember the shape of the beats. I think that because during AF, the electric function of the atrium is disturbed, it may cause also increase of premature supraventricular impulses. As I can understand, the variable heart rate during AF could cause aberrant conduction of some premature supraventricular impulses in the bundle branches and Purkinje fibres in the ventricle walls. The conduction can be blocked, or its partial block (in the right bundle branch) can change the shape of the complex in EKG.
As to possible LQTS: I cannot use erythromycin or cisapride. Because my ionized calcium is slightly high, it may shorten QT. Possibly my beta blocker atenolol also shortens it (I do not know it surely). I am using magnesium suppelement, which can also shorten it. My corrected baseline QT was recently 460. I don't like to use such rhythm medications which could prolong QT.
When in 2010 I had AF, a doctor prescribed me amiodarone. I refused to take it. Amiodarone could prolong QT, and I had some precautions: I had pulmonary, liver and thyroid problems, which amiodarone could worsen. Later I used dronedarone. I got muscular dystonia and I was wondering whether dronedarone caused it.
Maybe doctors will think, after possible coronary artery scan, that I should use eg. flecainide or sotalol to prevent arrhythmias. I cannot use calcium channel blockers or many beta blockers. Verapamil has caused fever and diarrhea for me and a worse tachycardia than before its use. Dilmin caused dizziness and weakness during walking uphill. The same was with digitalis. Bisoprolol irritates my heart, Selectol and Spesicor have no effect on high heart rate.
You're very welcome. I will try to answer your new questions.
1 a). Yes, they are the same as PACs. In Norway we use the name SVES (supraventricular extrasystoles)
1 b) Atrial fibrillation is sort of starting a fire, you'll need both a spark and wood. Wrong timed extrasystoles are triggers a variety of arrhythmias (the "spark"), however, for an arrhythmia to persist certain changes must have happened in the heart (the "wood"). In the setting of atrial fibrillation, it's quite uncommon for PACs to occur "early" enough in the heart rhythm cycle to trigger fibrillation (which will occur when an impulse spreads through semi-recharged cardiac tissue, causing multiple re-entry patterns). However, in the pulmonary veins, a PAC may in theory trigger too early, causing this to happen. The phenomenon can happen in the ventricles too, though much less likely to happen and if it happens, ventricular fibrillation is (luckily) rarely triggered. In this case, the name for it is "R on T PVCs" but I don't think a similar name exists for PACs.
2. a) Much is not known about the cause for atherosclerosis, but as far as I know (I'm not a doctor though), blood calcium levels have little impact on buildups in arteries. The problem is not the calcium, calcification happens when the body is trying to repair damages (and when so happens, the plaque often reduces some, and gains more stability.) However, high Ca may be a risk factor, most often due to increased blood pressure, which happens from the polarization between extracellular and intracellular calcium, causing muscles to contract stronger and blood vessels to constrict. Which is why Ca blockers often are used as treatment for high blood pressure.
2 b) ST depression during recovery is mostly a marker for CAD if it happens when in supine position, because lying down will increase ventricular preload and increasing the blood pressure and cardiac work load. Often, "hidden" ST depression is revealed during recovery. I think in general ST depression (or ventricular arrhythmias) during recovery may be significant too, but I'm not completely sure.
3. You may have had PVCs, and you may have had aberrant PACs. It's hard to tell from a Holter test. PVCs can not trigger atrial fibrillation.
4. It's hard to say if you have LQTS or not. Still, a QT time of 460 is extremely unlikely to trigger any arrhythmias, the problem is when the QT time goes above 500 msec (often severe risk will not be present before uncorrected QT time is close to 600 msec). The problem is that QT time may vary throughout the day (and night) and during bradycardia, the uncorrected QT interval may get dangerously long if "baseline" QT is prolonged. 460 is sort of borderline but not in any way diagnostic of LQTS. LQTS will not manifest with atrial fibrillation (though people with LQTS of course ALSO may have atrial fibrillation). The risk is "R on T PVCs" (see above), and their ability to trigger a dangerous rhythm known as Torsades de Pointes. If you during 65 years never have had events of fainting due to arrhythmias, I would guess your risk is low regarding this. Still, with a slightly long QT, it's wise to avoid medications which prolong QT (full list at www.torsades.org), the most common are certain antidepressants (especially tricyclics and tetracyclics), antipsychotics, macrolid antibiotics (erythromycine, clarithromycine), and certain allergy remedies. You probably know this already. And it's a good idea to avoid hypokalemia and hypocalcemia (though the latter probably is of little concern in your case).
I hope this helps, and I apologize if the answer was a bit technical. But you seem to know very much about the heart :-)
1 a). Yes, they are the same as PACs. In Norway we use the name SVES (supraventricular extrasystoles)
1 b) Atrial fibrillation is sort of starting a fire, you'll need both a spark and wood. Wrong timed extrasystoles are triggers a variety of arrhythmias (the "spark"), however, for an arrhythmia to persist certain changes must have happened in the heart (the "wood"). In the setting of atrial fibrillation, it's quite uncommon for PACs to occur "early" enough in the heart rhythm cycle to trigger fibrillation (which will occur when an impulse spreads through semi-recharged cardiac tissue, causing multiple re-entry patterns). However, in the pulmonary veins, a PAC may in theory trigger too early, causing this to happen. The phenomenon can happen in the ventricles too, though much less likely to happen and if it happens, ventricular fibrillation is (luckily) rarely triggered. In this case, the name for it is "R on T PVCs" but I don't think a similar name exists for PACs.
2. a) Much is not known about the cause for atherosclerosis, but as far as I know (I'm not a doctor though), blood calcium levels have little impact on buildups in arteries. The problem is not the calcium, calcification happens when the body is trying to repair damages (and when so happens, the plaque often reduces some, and gains more stability.) However, high Ca may be a risk factor, most often due to increased blood pressure, which happens from the polarization between extracellular and intracellular calcium, causing muscles to contract stronger and blood vessels to constrict. Which is why Ca blockers often are used as treatment for high blood pressure.
2 b) ST depression during recovery is mostly a marker for CAD if it happens when in supine position, because lying down will increase ventricular preload and increasing the blood pressure and cardiac work load. Often, "hidden" ST depression is revealed during recovery. I think in general ST depression (or ventricular arrhythmias) during recovery may be significant too, but I'm not completely sure.
3. You may have had PVCs, and you may have had aberrant PACs. It's hard to tell from a Holter test. PVCs can not trigger atrial fibrillation.
4. It's hard to say if you have LQTS or not. Still, a QT time of 460 is extremely unlikely to trigger any arrhythmias, the problem is when the QT time goes above 500 msec (often severe risk will not be present before uncorrected QT time is close to 600 msec). The problem is that QT time may vary throughout the day (and night) and during bradycardia, the uncorrected QT interval may get dangerously long if "baseline" QT is prolonged. 460 is sort of borderline but not in any way diagnostic of LQTS. LQTS will not manifest with atrial fibrillation (though people with LQTS of course ALSO may have atrial fibrillation). The risk is "R on T PVCs" (see above), and their ability to trigger a dangerous rhythm known as Torsades de Pointes. If you during 65 years never have had events of fainting due to arrhythmias, I would guess your risk is low regarding this. Still, with a slightly long QT, it's wise to avoid medications which prolong QT (full list at www.torsades.org), the most common are certain antidepressants (especially tricyclics and tetracyclics), antipsychotics, macrolid antibiotics (erythromycine, clarithromycine), and certain allergy remedies. You probably know this already. And it's a good idea to avoid hypokalemia and hypocalcemia (though the latter probably is of little concern in your case).
I hope this helps, and I apologize if the answer was a bit technical. But you seem to know very much about the heart :-)
Thank you for your profound answer.
1. In 2010 when I had AF, an EKG showed many aberrant premature complexes. I don't remember whether they were atrial or ventricular. Possibly atrial contractions conducted aberrantly to ventricles. Are they the same as you mark with PAC? Does AF predispose to them or do they only coexist with AF ?
2. I may have real calcification in my blood vessels because I have slight hypercalcemia (hyperparathyroidism). My cholesterol level is not high. Nowadays it has been thought that high cholesterol may not be a cause for arteriosclerosis. An inflammation may be a cause.
I did not have much ST depression during the exercise, but during the recovery it became more prominent. During the SVT, the depression was ad 1.5 mm, and after the SVT there was slight down-sloping ST segment depression. In an earlier stress test, in 1997, there was also slight down-sloping ST depression during recovery. A gallop rhythm started and was left prevailing.
3. In a 24-h holter recording in 2011 (with 75 mg atenolol, and Multaq) I have also had ventricular ectopic beats (92 single and 10 pairs).
During a few years I have been thinking that could I have long QT syndrome. I cannot use some medications which are not good for those who have LQTS. In the latest stress test in last week, before the exercise, my QTc was 460. This may be at the upper limit of normal(?) My father had often some kind of rhythm disorders. He told sometimes that his heart beating was totally disturbed. I have not heard the words atrial fibrillation in that connection. Myabe he had short episodes of AF, I don't know. My brother's son has long QT. It could be genetic.
1. In 2010 when I had AF, an EKG showed many aberrant premature complexes. I don't remember whether they were atrial or ventricular. Possibly atrial contractions conducted aberrantly to ventricles. Are they the same as you mark with PAC? Does AF predispose to them or do they only coexist with AF ?
2. I may have real calcification in my blood vessels because I have slight hypercalcemia (hyperparathyroidism). My cholesterol level is not high. Nowadays it has been thought that high cholesterol may not be a cause for arteriosclerosis. An inflammation may be a cause.
I did not have much ST depression during the exercise, but during the recovery it became more prominent. During the SVT, the depression was ad 1.5 mm, and after the SVT there was slight down-sloping ST segment depression. In an earlier stress test, in 1997, there was also slight down-sloping ST depression during recovery. A gallop rhythm started and was left prevailing.
3. In a 24-h holter recording in 2011 (with 75 mg atenolol, and Multaq) I have also had ventricular ectopic beats (92 single and 10 pairs).
During a few years I have been thinking that could I have long QT syndrome. I cannot use some medications which are not good for those who have LQTS. In the latest stress test in last week, before the exercise, my QTc was 460. This may be at the upper limit of normal(?) My father had often some kind of rhythm disorders. He told sometimes that his heart beating was totally disturbed. I have not heard the words atrial fibrillation in that connection. Myabe he had short episodes of AF, I don't know. My brother's son has long QT. It could be genetic.
To help you understand:
Your SVT was triggered by an extrasystole with RBBB morphology. Meaning you had an early PAC (so early in the heart rhythm cycle that the right bundle branch was still refractory and could not conduct). Those are known for triggering supraventricular tachycardias.
You ask why you got ST depression after the test, during the supraventricular tachycardia. In general there are three possible answers.
1. Depending on the tachycardia (atrial tachycardia vs AVRT vs AVNRT), some supraventricular tachycardias are causing ST depression because the atrial depolarization happens after the ventricular depolarization and happens "backwards" (from bottom to top), so the ST depression in fact is just an inverted and abnormally timed P wave. Also, it's fairly common, even without any arrhythmias, that the atrial repolarization happens after the QRS complex, causing ST depression.
2. Even with completely clean coronary arteries, all of us may develop ischemia if the heart rate is high enough. If I had a supraventricular tachycardia at 280 bpm, I would likely develop ischemia, because 1) oxygen demand is extremely high, 2) cardiac output is diminished, and 3) blood pressure (and coronary perfusion pressure) drops. Which is why we don't tolerate extremely rapid heart rates; an engine will eventually fail if we're stepping on the gas pedal without having the car in gear. I assume you didn't have ST depression during the exercise test (when you had a heart rate of 157 at max work load).
3. You may have mild calcifications in your coronary arteries. But if your exercise tolerance was great, they are likely not very serious. At age 65, most of us will have developed some calcifications, it's sort of a normal process. Which is interesting, because our maximum heart rate slows with age (I wonder if this is one of nature's tricks to prevent us from getting a too rapid heart rate when we have some coronary artery narrowings). If someone at age 65 had a heart rate of 205 (my maximum), likely all of them would get chest discomfort and angina symptoms.
Radiation exposure from CT's and angiography is fairly low and doctors always weigh risk against benefits. If your doctor recommends it, I would consider following his advice. I did not know that an MRI would provide any information about the coronary arteries, as far as I know it's used to examine the heart muscle itself and any structural abnormalities.
Can series of PACs trigger atrial fibrillation? Yes and no. Yes, because series and runs of PACs most often precede atrial fibrillation. Such PACs often origin from the pulmonary arteries, which also contain atrial tissue which may gain electrical independence from the rest of the heart and fire misplaced PACs with the ability of triggering AF. Still, to maintain atrial fibrillation, changes must usually have happened in the left atrium. And most often, by far, PACs are benign. But you already know they are able to trigger SVT in your case, so maybe a referral to an EP isn't a bad idea, especially if you along with your SVT have signs of CAD.
Your SVT was triggered by an extrasystole with RBBB morphology. Meaning you had an early PAC (so early in the heart rhythm cycle that the right bundle branch was still refractory and could not conduct). Those are known for triggering supraventricular tachycardias.
You ask why you got ST depression after the test, during the supraventricular tachycardia. In general there are three possible answers.
1. Depending on the tachycardia (atrial tachycardia vs AVRT vs AVNRT), some supraventricular tachycardias are causing ST depression because the atrial depolarization happens after the ventricular depolarization and happens "backwards" (from bottom to top), so the ST depression in fact is just an inverted and abnormally timed P wave. Also, it's fairly common, even without any arrhythmias, that the atrial repolarization happens after the QRS complex, causing ST depression.
2. Even with completely clean coronary arteries, all of us may develop ischemia if the heart rate is high enough. If I had a supraventricular tachycardia at 280 bpm, I would likely develop ischemia, because 1) oxygen demand is extremely high, 2) cardiac output is diminished, and 3) blood pressure (and coronary perfusion pressure) drops. Which is why we don't tolerate extremely rapid heart rates; an engine will eventually fail if we're stepping on the gas pedal without having the car in gear. I assume you didn't have ST depression during the exercise test (when you had a heart rate of 157 at max work load).
3. You may have mild calcifications in your coronary arteries. But if your exercise tolerance was great, they are likely not very serious. At age 65, most of us will have developed some calcifications, it's sort of a normal process. Which is interesting, because our maximum heart rate slows with age (I wonder if this is one of nature's tricks to prevent us from getting a too rapid heart rate when we have some coronary artery narrowings). If someone at age 65 had a heart rate of 205 (my maximum), likely all of them would get chest discomfort and angina symptoms.
Radiation exposure from CT's and angiography is fairly low and doctors always weigh risk against benefits. If your doctor recommends it, I would consider following his advice. I did not know that an MRI would provide any information about the coronary arteries, as far as I know it's used to examine the heart muscle itself and any structural abnormalities.
Can series of PACs trigger atrial fibrillation? Yes and no. Yes, because series and runs of PACs most often precede atrial fibrillation. Such PACs often origin from the pulmonary arteries, which also contain atrial tissue which may gain electrical independence from the rest of the heart and fire misplaced PACs with the ability of triggering AF. Still, to maintain atrial fibrillation, changes must usually have happened in the left atrium. And most often, by far, PACs are benign. But you already know they are able to trigger SVT in your case, so maybe a referral to an EP isn't a bad idea, especially if you along with your SVT have signs of CAD.
It was not a nuclear stress test. I was on a "bicycle" (is it a treadmill?) and EKG was recorded all the time. The stress test showed that I got through the test better than persons of my age (65) normally do. I did not, however, reach my set maximun heart rate (160), I reached 157.
But problems (depression of the ST segment, and SVT tachycardia) began during the recovery. Because I have AF history and episodes of weakness and tachycardia during walking and now depression of ST segment was revealed during recovery, the doctor said that I should have a scan of my coronary arteries. The ST segment depression generally means that there is shortage of oxygen in the heart muscle.
The SVT tachycardia began after a RBBB type extrasystole. That is some bundle block. When I was yonger (at the eighties), I had often episodes of tachycardia. I don't know what was their cause. Many beta blockers and calcium channel blockers were then tested, and atenolol was selected for me.
When I am working in our garden, I often get series of extrasystoles, or tachycardia, and I am afraid that AF could originate from them. Should I avoid such working that causes extrasystoles or tachycardia? Sometimes leaning to foreward or gas in the intestines causes series of extrasystoles.
A CT scan of my coronary arteries has been discussed on. I have got many other CT scans and X-ray images within a few years, thus I don't want to have more radiation studies. I asked for an MRI. maybe I 'll get it, I'll see.
I was advised not to take atenolol on the morning of the test, or even on the day before. It is not easy. I had to take a bit of atenolol in the morning of the test, because my heart began to beat very rapidly when I left home to travel to the town. On the day before I took it normally.
Do you think that ST segment depression is a normal consequence of stress (exercise)? Could it cause my weakness episodes during walking? Great variation of my condition (generally good but sometimes poor) is odd.
I think that my heart problems (AF and others) may be caused by infections; I have some immune deficiency (low IgG3 and low lectin pathway of complement). I think that I am having an enterovirus infection now. Possibly had it also in last spring, or have it chronically. I have sore red blotches in the mucous membrane of my mouth. I have been diagnosed with CFS in 2007 but have had it possibly since the eighties. Its origin has often been attributed to (an) infection(s).
But problems (depression of the ST segment, and SVT tachycardia) began during the recovery. Because I have AF history and episodes of weakness and tachycardia during walking and now depression of ST segment was revealed during recovery, the doctor said that I should have a scan of my coronary arteries. The ST segment depression generally means that there is shortage of oxygen in the heart muscle.
The SVT tachycardia began after a RBBB type extrasystole. That is some bundle block. When I was yonger (at the eighties), I had often episodes of tachycardia. I don't know what was their cause. Many beta blockers and calcium channel blockers were then tested, and atenolol was selected for me.
When I am working in our garden, I often get series of extrasystoles, or tachycardia, and I am afraid that AF could originate from them. Should I avoid such working that causes extrasystoles or tachycardia? Sometimes leaning to foreward or gas in the intestines causes series of extrasystoles.
A CT scan of my coronary arteries has been discussed on. I have got many other CT scans and X-ray images within a few years, thus I don't want to have more radiation studies. I asked for an MRI. maybe I 'll get it, I'll see.
I was advised not to take atenolol on the morning of the test, or even on the day before. It is not easy. I had to take a bit of atenolol in the morning of the test, because my heart began to beat very rapidly when I left home to travel to the town. On the day before I took it normally.
Do you think that ST segment depression is a normal consequence of stress (exercise)? Could it cause my weakness episodes during walking? Great variation of my condition (generally good but sometimes poor) is odd.
I think that my heart problems (AF and others) may be caused by infections; I have some immune deficiency (low IgG3 and low lectin pathway of complement). I think that I am having an enterovirus infection now. Possibly had it also in last spring, or have it chronically. I have sore red blotches in the mucous membrane of my mouth. I have been diagnosed with CFS in 2007 but have had it possibly since the eighties. Its origin has often been attributed to (an) infection(s).
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I don't fully understand, are you saying your stress test was not conclusive, or not done? Was it a nuclear stress test?
I had a nuclear stress test a couple of month back and I was told no to take my beta blocker (now Atenolol) or calcium channel blocker that morning.. as it turns out I forgot to take it the night before too.. so my HR was high (I have AFib). Thus I wasn't on the tread mill very long before I hit my maximum HR, 135 is what I recall them setting.. so the just gave me a shot of the nuclear fluid at that point. Then the scans went on as normal... they didn't find any blocks. Nor MRI was even discussed - in fact the heart catheter is the normal (in my experience) test done if the stress test is not conclusive. This has been the case fo me in past years.
I had a nuclear stress test a couple of month back and I was told no to take my beta blocker (now Atenolol) or calcium channel blocker that morning.. as it turns out I forgot to take it the night before too.. so my HR was high (I have AFib). Thus I wasn't on the tread mill very long before I hit my maximum HR, 135 is what I recall them setting.. so the just gave me a shot of the nuclear fluid at that point. Then the scans went on as normal... they didn't find any blocks. Nor MRI was even discussed - in fact the heart catheter is the normal (in my experience) test done if the stress test is not conclusive. This has been the case fo me in past years.
Now I am waiting for a decision, whether I can have an MRI of my coronary arteries.
Today in the morning I was weak, slightly dizzy. I took an additional piece of atenolol tablet due to raising heart beating. Then in the afternoon I felt better. During the weakness my vision becomes foggy and eyes feel weird. Yesterday in the evening I had similar eye symptoms, too. I don't know what is the cause of these symptoms.
Today in the morning I was weak, slightly dizzy. I took an additional piece of atenolol tablet due to raising heart beating. Then in the afternoon I felt better. During the weakness my vision becomes foggy and eyes feel weird. Yesterday in the evening I had similar eye symptoms, too. I don't know what is the cause of these symptoms.
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