[Football] Tom Lockyer

[Swimboy64]

Fabulous. Long may it continue (you are awful, etc. )

I thought why has Harry said that and then saw my picture Honky Tonks

 

[Harry Wilson's tackle]

Here is a quick guide to terminology:

Atrial fibrillation (AF): this is where the two small heart chambers, the atria, have an electrical storm. Instead of the electrical depolarization (that starts in the pacemaker, the sinoatrial node) moving smoothly like a wave across that atria, down through the atrioventricular (AV) node to the ventricles (the main pumping chambers), the atria experience multiple electrical waves at once, so they don't beat they quiver. This will not affect the ventricles the same way because the AV node is a high pass filter and allows only some of the electrical waves to pass through to the ventricles. The ventricles will then beat irregularly and the patient may feel faint, but many people can live with this for long periods. The cure is electrical defibrillation.
Wolf Parkinson White (WPW) syndrome: This is extremely rare. Here there is an extra bit of tissue connecting the atria to the ventricles (called the bundle of Kent). This allows the electrical wave to bypass the AV note. This means if you get AF (or atrial tachycardia - AT, also known as supraventricular tachycardia - SVT), the ventricles may 'follow' because the AV node is being bypassed and can no longer act as a high frequency filter. If you have WPW this means that if you get AF or AT, the condition can be very dangerous beacuse the ventricles will beat in time with the atria - very fast. Why is this bad? When ventricles beat fast (and I mean > 200 beats/min) they have insufficient time to fill with blood (ventricles fill and eject blood every heart beat). This lowers 'cardiac output' and the body and brain receives less oxygenated blood per unit time. So you will feel feint, and may faint.
Ventricular fibrillation (VF): here the disease is in the ventricles (not atria or bundle of Kent - see above). This is electrical storm in the ventricles. It is commonly caused by a heart attack (acute block of a coronary artery - the heart's own blood supply - acute myocardial ischaemia). Acute block is typically sudden thrombosis (clot) on top of an atheroma (atherosclerosis - a lump of fat in the artery) that has fissured (surface split, exposing thrombogenic innards). So you feel fine, then suddenly you lose blood supply to part of the ventricles and then 5 minutes later you get electrical storm. You will faint in around 10 seconds. Out cold. And if the electrical storm is not defibrillated quickly or CPR is not done well (we are talking minutes) irreversible brain damage and death are on the cards. This is now about ensuring oxygenated blood gets to the brain, because the heart is no longer pumping any blood. This is the single largest cause of death in the UK, and is my research area.
Heart attack: This is a lay term for the events around acute myocardial ischaemia, which can include anything from feeling suddenly weak through to sudden chest pain (acute angina) followed by VF (collapse) and death. The treatment is to keep the patient alive (defibrillation, CPR as needed), treat the chest pain (morphine) and open the artery (get to hospital fast and get thrombolysis (clot busting drugs like streptokinase) and/or a stent (a tube inside the coronary artery to open it and keep it open) or a bypass graft (a bit of your own leg vein is sewn into the coronary artery after surgical removal of the atherosclerotic bit). A big syndrome, in other words.
Cardiac arrest: this is when the heart 'stops'. Also known as asystole. In fact this term is badly misused, and people who have gone into VF may be described by lay people and the media as having 'arrest'. The ventricles are not beating in a co-ordinated way die to storm, or due to asystole, but the treatments are different. The heart does not usually 'stop', i.e., the sinoatrial node go to sleep, unless the patient has been dead for 30 plus minutes. So we are talking about a different scenario to a heart attack. I don't like the term (too vague) and never use it, and get cross when I read or hear others using it.
Hypertrophy: This is muscle enlargement. This occurs naturally with exercise. Cardiac hypertrophy is common in footballers. It can be dangerous in those who have underlying genetic heart conditions, some of which can make the hypertrophy extra massive (so the heart pumps inefficiently due to the law of LaPlace - no need to look that up), and some of which affect the electrical properties of heart cells - channelopathy.
Channelopathy: like WPW this is rare. Unlike heart attacks which are common, but in the older population, not in footballers. Here we have a mutation in a gene that codes for a bit of kit called an ion channel. These are tiny pores that selectively 'see' ions like sodium potassium and calcium. If the ion channel structure is changed due to the mutated gene that codes for it, the function may be altered and this can increase the risk of a cardiac arrhythmia. This can include VF. The chance if VF is low but given we have thirty one and a half million heart beats a year, if there is a one in a six hundred million chance the channelopathy may trigger VF, then over 20 years it is ods on the person will go into VF. This is why it is a killer in younger people. But it is very rare.

Any more words anyone want explaining, fire away. But I really am going out now.

Edit: I seem to keep confusing fainting footballers with feinting footballers. <doh!>

 

[Poyningsgull]

Here is a quick guide to terminology:

Atrial fibrillation (AF): this is where the two small heart chambers, the atria, have an electrical storm. Instead of the electrical depolarization (that starts in the pacemaker, the sinoatrial node) moving smoothly like a wave across that atria, down through the atrioventricular (AV) node to the ventricles (the main pumping chambers), the atria experience multiple electrical waves at once, so they don't beat they quiver. This will not affect the ventricles the same way because the AV node is a high pass filter and allows only some of the electrical waves to pass through to the ventricles. The ventricles will then beat irregularly and the patient may feel faint, but many people can live with this for long periods. The cure is electrical defibrillation.
Wolf Parkinson White (WPW) syndrome: This is extremely rare. Here there is an extra bit of tissue connecting the atria to the ventricles (called the bundle of Kent). This allows the electrical wave to bypass the AV note. This means if you get AF (or atrial tachycardia - AT, also known as supraventricular tachycardia - SVT), the ventricles may 'follow' because the AV node is being bypassed and can no longer act as a high frequency filter. If you have WPW this means that if you get AF or AT, the condition can be very dangerous beacuse the ventricles will beat in time with the atria - very fast. Why is this bad? When ventricles beat fast (and I mean > 200 beats/min) they have insufficient time to fill with blood (ventricles fill and eject blood every heart beat). This lowers 'cardiac output' and the body and brain receives less oxygenated blood per unit time. So you will feel feint, and may faint.
Ventricular fibrillation (VF): here the disease is in the ventricles (not atria or bundle of Kent - see above). This is electrical storm in the ventricles. It is commonly caused by a heart attack (acute block of a coronary artery - the heart's own blood supply - acute myocardial ischaemia). Acute block is typically sudden thrombosis (clot) on top of an atheroma (atherosclerosis - a lump of fat in the artery) that has fissured (surface split, exposing thrombogenic innards). So you feel fine, then suddenly you lose blood supply to part of the ventricles and then 5 minutes later you get electrical storm. You will faint in around 10 seconds. Out cold. And if the electrical storm is not defibrillated quickly or CPR is not done well (we are talking minutes) irreversible brain damage and death are on the cards. This is now about ensuring oxygenated blood gets to the brain, because the heart is no longer pumping any blood. This is the single largest cause of death in the UK, and is my research area.
Heart attack: This is a lay term for the events around acute myocardial ischaemia, which can include anything from feeling suddenly weak through to sudden chest pain (acute angina) followed by VF (collapse) and death. The treatment is to keep the patient alive (defibrillation, CPR as needed), treat the chest pain (morphine) and open the artery (get to hospital fast and get thrombolysis (clot busting drugs like streptokinase) and/or a stent (a tube inside the coronary artery to open it and keep it open) or a bypass graft (a bit of your own leg vein is sewn into the coronary artery after surgical removal of the atherosclerotic bit). A big syndrome, in other words.
Cardiac arrest: this is when the heart 'stops'. Also known as asystole. In fact this term is badly misused, and people who have gone into VF may be described by lay people and the media as having 'arrest'. The ventricles are not beating in a co-ordinated way die to storm, or due to asystole, but the treatments are different. The heart does not usually 'stop', i.e., the sinoatrial node go to sleep, unless the patient has been dead for 30 plus minutes. So we are talking about a different scenario to a heart attack. I don't like the term (too vague) and never use it, and get cross when I read or hear others using it.
Hypertrophy: This is muscle enlargement. This occurs naturally with exercise. Cardiac hypertrophy is common in footballers. It can be dangerous in those who have underlying genetic heart conditions, some of which can make the hypertrophy extra massive (so the heart pumps inefficiently due to the law of LaPlace - no need to look that up), and some of which affect the electrical properties of heart cells - channelopathy.
Channelopathy: like WPW this is rare. Unlike heart attacks which are common, but in the older population, not in footballers. Here we have a mutation in a gene that codes for a bit of kit called an ion channel. These are tiny pores that selectively 'see' ions like sodium potassium and calcium. If the ion channel structure is changed due to the mutated gene that codes for it, the function may be altered and this can increase the risk of a cardiac arrhythmia. This can include VF. The chance if VF is low but given we have thirty one and a half million heart beats a year, if there is a one in a six hundred million chance the channelopathy may trigger VF, then over 20 years it is ods on the person will go into VF. This is why it is a killer in younger people. But it is very rare.

Any more words anyone want explaining, fire away. But I really am going out now.

Edit: I seem to keep confusing fainting footballers with feinting footballers. <doh!>

That's easy for you to say.

 

[ozspike]

Apologies for chipping in with speculation, but I'd like to respond to some of the comments above. Last time this player collapsed it was said to be atrial fibrillation. This is itself odd since AF can make a person feel faint, but the ventricles will continue to receive electrical signals, albeit irregularly (not typically extra fast, paradoxically), via the AV node. I met a bloke on a train some years ago who had been in continuous AF for 2 years. He was largely symptomless. I'm surprised this was sufficient to cause 'collapse' last time, let alone a much more protracted episode this time. If his ventricles follow his atria more closely when in AF than one would expect, he may have a 'bundle of kent' which presumably was ablated during his first surgery. This 'bundle' is a bit of tissue that makes a fast electical connection between atria and ventricles, bypassing the AV node (a high pass filter) and gives rise to WPW syndrome (https://www.bhf.org.uk/informationsupport/conditions/wolff-parkinson-white-syndrome).

Unless it is an electrophysiologist speaking (medic who specializes in arrhythmias) I suspect there may be a bit of communication 'miss-spokenry' here. If you can follow all that above it may be of some interest, however.

You are correct, I have Paroxysmal Afib (atrial fabulation) and have had 6 episodes each time lasting few hours until returning to normal sinus rhythm, not everyone is the same but at worst I feel weak and fatigued(HR 130+), If Tom had Ventricular fibrillation then that can be life threatening and requires immediate medical attention.

 

[Harry Wilson's tackle]

Very good phone in on the topic on radio 5 right now.

 

[Arthritic Toe]

He'll obviously be making his future career decisions based on the advice from football forums. Why bother with all those medical experts.

 

[Peacehaven Wild Kids]

He'll obviously be making his future career decisions based on the advice from football forums. Why bother with all those medical experts.

Well you say that but something similar was said about the Covid advice.

I think with hindsight we’d have been better off listening to ENREST rather than the UK government

 

[Commander]

I had this in October as well. Got to have another one in the next few months. This is what Lockyer had for his Atrial Fibulation, I read about him when I was reading about the surgery to decide if I was going to get it.

A lot of heart issues you are born with and don’t know about till they become an issue, that’s what was the issue with mine. A lot of things flare up in adulthood that are fine in childhood.

It is amazing the amount of people who wanted to blame mine on the Covid vaccine, despite my telling them I was born with my heart issue. It’s mad.

I have also had two of these. Difficult not to feel concern when you read about what happened to this guy, but it does feel like there is some 'miss-speak' going on somewhere.

 

[hans kraay fan club]

Not related directly to Tom Lockyer, obviously - but an interview with Connor Goldson, about his issues, raising money for the BHF, and encouraging learning CPR:

MSN

 

[ManOfSussex]

He's been released from hospital.

 

[TomandJerry]

Luton Town captain Tom Lockyer had a "successful procedure" on Tuesday to fit an implantable cardioverter defibrillator (ICD) device to "prevent a repeat of Saturday's incident"

 

[pasty]

Tom Lockyer: Luton Town captain discharged from hospital following cardiac arrest https://www.bbc.co.uk/sport/football/67789549

 

[Weststander]

Tom Lockyer: Luton Town captain discharged from hospital following cardiac arrest https://www.bbc.co.uk/sport/football/67789549

Is Cardiac on remamd?

 

[mejonaNO12 aka riskit]

So he's good for my FPL this week, yeah?

 

[dazzer6666]

Here is a quick guide to terminology:

Atrial fibrillation (AF): this is where the two small heart chambers, the atria, have an electrical storm. Instead of the electrical depolarization (that starts in the pacemaker, the sinoatrial node) moving smoothly like a wave across that atria, down through the atrioventricular (AV) node to the ventricles (the main pumping chambers), the atria experience multiple electrical waves at once, so they don't beat they quiver. This will not affect the ventricles the same way because the AV node is a high pass filter and allows only some of the electrical waves to pass through to the ventricles. The ventricles will then beat irregularly and the patient may feel faint, but many people can live with this for long periods. The cure is electrical defibrillation.
Wolf Parkinson White (WPW) syndrome: This is extremely rare. Here there is an extra bit of tissue connecting the atria to the ventricles (called the bundle of Kent). This allows the electrical wave to bypass the AV note. This means if you get AF (or atrial tachycardia - AT, also known as supraventricular tachycardia - SVT), the ventricles may 'follow' because the AV node is being bypassed and can no longer act as a high frequency filter. If you have WPW this means that if you get AF or AT, the condition can be very dangerous beacuse the ventricles will beat in time with the atria - very fast. Why is this bad? When ventricles beat fast (and I mean > 200 beats/min) they have insufficient time to fill with blood (ventricles fill and eject blood every heart beat). This lowers 'cardiac output' and the body and brain receives less oxygenated blood per unit time. So you will feel feint, and may faint.
Ventricular fibrillation (VF): here the disease is in the ventricles (not atria or bundle of Kent - see above). This is electrical storm in the ventricles. It is commonly caused by a heart attack (acute block of a coronary artery - the heart's own blood supply - acute myocardial ischaemia). Acute block is typically sudden thrombosis (clot) on top of an atheroma (atherosclerosis - a lump of fat in the artery) that has fissured (surface split, exposing thrombogenic innards). So you feel fine, then suddenly you lose blood supply to part of the ventricles and then 5 minutes later you get electrical storm. You will faint in around 10 seconds. Out cold. And if the electrical storm is not defibrillated quickly or CPR is not done well (we are talking minutes) irreversible brain damage and death are on the cards. This is now about ensuring oxygenated blood gets to the brain, because the heart is no longer pumping any blood. This is the single largest cause of death in the UK, and is my research area.
Heart attack: This is a lay term for the events around acute myocardial ischaemia, which can include anything from feeling suddenly weak through to sudden chest pain (acute angina) followed by VF (collapse) and death. The treatment is to keep the patient alive (defibrillation, CPR as needed), treat the chest pain (morphine) and open the artery (get to hospital fast and get thrombolysis (clot busting drugs like streptokinase) and/or a stent (a tube inside the coronary artery to open it and keep it open) or a bypass graft (a bit of your own leg vein is sewn into the coronary artery after surgical removal of the atherosclerotic bit). A big syndrome, in other words.
Cardiac arrest: this is when the heart 'stops'. Also known as asystole. In fact this term is badly misused, and people who have gone into VF may be described by lay people and the media as having 'arrest'. The ventricles are not beating in a co-ordinated way die to storm, or due to asystole, but the treatments are different. The heart does not usually 'stop', i.e., the sinoatrial node go to sleep, unless the patient has been dead for 30 plus minutes. So we are talking about a different scenario to a heart attack. I don't like the term (too vague) and never use it, and get cross when I read or hear others using it.
Hypertrophy: This is muscle enlargement. This occurs naturally with exercise. Cardiac hypertrophy is common in footballers. It can be dangerous in those who have underlying genetic heart conditions, some of which can make the hypertrophy extra massive (so the heart pumps inefficiently due to the law of LaPlace - no need to look that up), and some of which affect the electrical properties of heart cells - channelopathy.
Channelopathy: like WPW this is rare. Unlike heart attacks which are common, but in the older population, not in footballers. Here we have a mutation in a gene that codes for a bit of kit called an ion channel. These are tiny pores that selectively 'see' ions like sodium potassium and calcium. If the ion channel structure is changed due to the mutated gene that codes for it, the function may be altered and this can increase the risk of a cardiac arrhythmia. This can include VF. The chance if VF is low but given we have thirty one and a half million heart beats a year, if there is a one in a six hundred million chance the channelopathy may trigger VF, then over 20 years it is ods on the person will go into VF. This is why it is a killer in younger people. But it is very rare.

Any more words anyone want explaining, fire away. But I really am going out now.

Edit: I seem to keep confusing fainting footballers with feinting footballers. <doh!>

Thanks for this. Finding this fascinating and slightly scary at the same time - I had an ‘abnormality’ detected on a routine ECG (annual company healthcheck) 4 years or so ago which ended up with me being sent to a consultant cardiologist. I was doing a lot of long distance running at the time and he thought it was ‘probably‘ related to that and mentioned ‘athlete’s heart’ (it was either that or ‘myopathic’ apparently), but wanted to be sure so he said I either needed to ‘de-train’ for 6 months (ie stop running) or go and have a perfusion scan (? MRI with dye in my blood and an artificially stressed heart). Opted for the latter which took about 2.5 hours and was pretty unpleasant. I had all that done privately under my company plan…..then he recently wrote to me and suggested a follow-up check which was done under the NHS (I’m no longer insured). Abnormality is still there (despite cutting back on my exercise significantly) and it (quote) ‘shows sinus rhythm, borderline first-degree AV block, resting HR below 60 with a hint of right bundle-branch delay and very clear T-wave inversion in V1 to V3. BP 115/70’.

He still thinks it’s down to ‘extreme’ (LOL, was just a bit of jogging) levels of exercise and hasn’t suggested anything needs doing……..but it’s always at the back of my mind when I see what can happen to proper athletes like Lockyer.

 

[Gazwag]

So he's good for my FPL this week, yeah?

Bloody owes me after I captained Solanke last week

 

[Harry Wilson's tackle]

Thanks for this. Finding this fascinating and slightly scary at the same time - I had an ‘abnormality’ detected on a routine ECG (annual company healthcheck) 4 years or so ago which ended up with me being sent to a consultant cardiologist. I was doing a lot of long distance running at the time and he thought it was ‘probably‘ related to that and mentioned ‘athlete’s heart’ (it was either that or ‘myopathic’ apparently), but wanted to be sure so he said I either needed to ‘de-train’ for 6 months (ie stop running) or go and have a perfusion scan (? MRI with dye in my blood and an artificially stressed heart). Opted for the latter which took about 2.5 hours and was pretty unpleasant. I had all that done privately under my company plan…..then he recently wrote to me and suggested a follow-up check which was done under the NHS (I’m no longer insured). Abnormality is still there (despite cutting back on my exercise significantly) and it (quote) ‘shows sinus rhythm, borderline first-degree AV block, resting HR below 60 with a hint of right bundle-branch delay and very clear T-wave inversion in V1 to V3. BP 115/70’.

He still thinks it’s down to ‘extreme’ (LOL, was just a bit of jogging) levels of exercise and hasn’t suggested anything needs doing……..but it’s always at the back of my mind when I see what can happen to proper athletes like Lockyer.

I'll PM you.

 

[Seagull on the Hill]

Great to see Tom Lockyer looking well, and talking about Atrial Fibrillation, on Good Morning Britain .
He managed to get a little dig at Susannah Reid when she admitted she was a Palace fan.

 

[dazzer6666]

Great to see Tom Lockyer looking well, and talking about Atrial Fibrillation, on Good Morning Britain .
He managed to get a little dig at Susannah Reid when she admitted she was a Palace fan.

Brilliant interview with him (with Chapman who is always excellent) here......

Football Daily - Monday Night Club: Lockyer LIVE & where’s Sheffield? - BBC Sounds

Mark Chapman is with Luton’s Tom Lockyer, Chris Sutton & The New York Times' Rory Smith.

www.bbc.co.uk

 

[LamieRobertson]

Brilliant interview with him (with Chapman who is always excellent) here......

Football Daily - Monday Night Club: Lockyer LIVE & where’s Sheffield? - BBC Sounds

Mark Chapman is with Luton’s Tom Lockyer, Chris Sutton & The New York Times' Rory Smith.

www.bbc.co.uk

Meant to post this myself …..great listen, not just about his health but other stuff throughout the program