Exercise as it relates to Disease/What type of stress causes the increased risk of episodes occurring in Long QT syndrome

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The article that is being critically appraised is 'The response of the QT interval to mental and physical stress in types LQTS1 and LQTS2 of the long QT syndrome', researched by K J Paavonen, H Swan, K Piippo, L Hokkanen, P Laitinen, M Viitasalo, L Toivonen, K Kontula [1].

What is the background to this research?[edit | edit source]

The article looks into a minor population of inherited long QT syndrome type 1 and 2 to understand what type of stress either mental or physical can cause an episode. Long QT syndrome is "characterised by prolongation of the QT interval"[1] . The prolonged QT interval in the cardiac contraction is a serious condition that causes serve symptoms of sudden fainting, seizures or sudden death. The study has 3 groups of participants long QT syndrome 1 (LQTS1), long QT syndrome 2 (LQTS2), a control group without any heart conditions. LQTS1 is caused by KCNQ1 gene which influences potassium channels and LQTS2 is caused by HERG mutations which is a protein that affects the potassium ion channel.

This research was attempting to understand what causes episodes in long QT syndrome sufferers, whether it is an increased effect from either mental or physical stress. This research is important to understand what can cause an episode in long QT syndrome sufferers and can increase research into management of the disease as they cannot be cured.

Where is the research from?[edit | edit source]

The group used in this study was important to share as the non-infectious disease is a rare disease and is not very common. Long QT syndrome doesn't have lots of research in regards to what causes the cardiac abnormality to occur and how to prevent serious symptoms occurring.

The author K J Paavonen has a high reputation in the medical world of research especially in studies around the heart. She has conducted lots of study into long QT syndrome and how that condition occurs and what it is caused by. K J Paavonen was sponsored by University of Helsinki where most of her studies occurred. This could potentially cause concern for conflict of interest however there are lots of study completed by K J Paavonen on long QT syndrome, meaning that there is less likely to be biases on the study. However they did create the bias of only asymptomatic participants because of ethical objections and avoid any episodes occurring[1].

What kind of research was this?[edit | edit source]

The study was a case-control study where there were 16 participants with LQTS1, 14 participants with LQTS2 where the participants are both asymptomatic and there was 14 control subjects with no health conditions [1].

Research completed by K Takenaka and research crew found that exercise in LQTS1 had significant affect to the Tpec during exercise and there was a decrease in the Tpec response[2]. Showing a similar response as the study by K J Paavonen having LQTS1 patients showing beneficial results. The studies are both case-control study type.

What did the research involve?[edit | edit source]

Before any test proceeded the participants had to produce baseline data where an intravenous cannula was inserted and they rested in a supine position for 30 minutes where an ECG was taken and a blood sample[1]. They also have the restrictions of only drinking water 4 hours before the study.

The study included the participants completing 3 mental tests being serial subtraction test, Stroop-colour word test, and serial addition test, where they were told that they were being compared to other people in the study in the first 2 tests and for the serial addition test they were told that the mistakes that they made were being compared [1]. There were no rest periods between the tests other than to explain the next test they were going to complete and the participants also got encouraged to increase the speed at which they answered to increase the stress level [1]. When the participants reached maximal heart for over 3 minutes a blood sample was taken.[1] The patients then were required to rest until heart rate and blood pressure recovered.

The next testing condition was a bicycle ergometer test which started at a workload of 30 W and an increase of 15 W with each minute thereafter[1] once maximal heart rate was achieved a third blood sample was taken[1].

The methodology of the study was appropriate for the order, as it allows the study to be conducted in a similar time period. Having the mental stress tests first allows for a smaller recovery duration compared to the physical stress test. A limitation of the study was that it could have shown more results if there was a continuous ECG over the duration of the patient at the study.

What were the basic results?[edit | edit source]

The results of the study found that during mental stress caused an increase in serum potassium concentrate in any of the groups and found an increase in serum potassium during exercise for all 3 groups[1]. The study also found QT intervals were longer at rest and both stressors for LQTS1 and LQTS2 compared to the control group, however LQTS1 and LQTS2 results didn't differ[1].

The researcher found they had an increase in heart rate compared to other studies, and the over-emphasis on the serum potassium release during physical stress due to muscle contraction.

What conclusions can we take from this research?[edit | edit source]

The conclusion from this study is that there are increased QT adaptations to physical stress than mental stress in LTQS1 and LQTS2.

In a more recent paper conduct in 2018 by K Takenaka into ' Type 1 long QT syndrome and psychological stress in a laboratory setting' found that there is minimal abnormality to reactions of stress when comparing asymptomatic and symptomatic LQTS1 patients[3].

Practical advice[edit | edit source]

This research helps to understand the impacts of stress whether mental or physical stress caused episodes. The results discovered that there are more health benefits from physical ativity on the heart helping to reduce health risks of long QT syndrome, especially during aerobic exercise.

It is best to refer to a doctor for diagnoses as it is a rare disease, however through exercise it can help decrease the health burden.

Further information/resources[edit | edit source]

Further reading on the subject around Long-QT syndrome from the researcher K Paavonen can be found in this link here and in references[4]. Additional reading that was interesting was referred in the critically acclaimed study by S G Priori and research crew about genetic and molecular basis or cardiac arrhythmias [5].

References[edit | edit source]

Add in the references using this code

  1. a b c d e f g h i j k l Paavonen KJ, Swan H, Piippo K, Hokkanen L, Laitinen P, Viitasalo M, Toivonen L, Kontula K. The response of the QT interval to mental and physical stress in types LQTS1 and LQTS2 of the long QT syndrome. Available at < https://heart.bmj.com/content/86/1/39> : BMJ Journals; 2001
  2. Takenaka K, Ai T, Shimizu W, Kobori A, Ninomiya T, Otani H, Kubota T, Takaki H, Kamakura S, Horie M. Exercise Stress Test Amplifies Genotype-Phenotype Correlation in the LQT1 and LQT2 Forms of the Long-QT Syndrome. Available at < https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000048142.85076.A2 > : Circulation; 2003
  3. Maattanen I, Ravaja N, Henttonen P, Puttonen S, Paavonen K, Swan H, Hintsa T. Type 1 long QT syndrome and psychological stress in a laboratory setting. Available at < https://www.researchgate.net/publication/322651407_Type_1_long_QT_syndrome_and_psychological_stress_in_a_laboratory_setting> :Journal of Health Psychology; 2018
  4. K J Paavonen. Kristian J Paavonen's research while affiliated with University of Helsinki and other places. Available at < https://www.researchgate.net/scientific-contributions/Kristian-J-Paavonen-39907502 > 1999- 2018
  5. Priori S G, Barhanin J, Hauer R N W, Haverkamp W, Jongsma H J, Kleber A G, McKenna W J, Roden D M, Rudy Y, Schwartz K, Schwartz P J, Towbin J A, Wilde A. Genetic and molecular basis of cardiac arrythmias: European Heart Journal; 1997

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