sf5272: okay so we're going to start off talking about hypertension okay so 
blood pressure is a biological variable that is characteristic to each 
individual and er within a population the B-P is distributed around a mean 
level but it does produce an asymmetrical curve because more individuals have 
high blood pressure than a low one and factors that determine the levels of B-P 
within a population are things like age and ethnicity er the classification of 
hypertension is sort of a controversial issue but the W-H-O has said it's about 
a hundred and sixty over ninety-five millimetres of mercury but i think U-S 
guidelines have said that it's a hundred and forty over ninety er despite these 
different values it is known that the risk of mortality and morbidity does rise 
progressively with increase in systolic and diastolic pressures er if someone 
does come in with a high blood pressure it's important that you er take 
subsequent readings and just ta-, and don't take the first one and they should 
be at least a week apart okay so our case study is Mr G and he's a forty-eight 
year old male who presented with a two week history of neck stiffness and one 
episode of vomiting and when his B-P was taken it was found to be two-hundred 
and twenty-two over a hundred and forty-six and he was an unknown hypertensive 
okay so the history of the presenting complaint was neck stiffness on waking 
which was getting progressively worse over the last two weeks and he was having 
pain on movement which was limiting this er he had no associated nausea er no 
rash or photosensitivity no headaches blurring of vision or loss of 
consciousness he had no significant past medical history and he'd had no 
operations he was on no medication and had no known drug allergies however 
there was a history of heart disease er he lives alone and he's an electrician 
his hobbies are walking and he smokes approximately ten a day for the last 
twenty thirty years and he does drink in excess of forty sixty units a week of 
alcohol okay so the systems review was unremarkable except for occasional 
indigestion cramp that he experiences er in either leg usually in the morning 
and palpitations that were due to anxiety and he had complained of 
approximately six-month history of slight fatigue that he thought was age-
related er on physi-, physical examination o-, on admission his B-P was two 
hundred and twenty-two over forty-si a hundred and forty-six and even after 
treatment when we ex-, we examined him it was still a hundred and eighty-four 
over a hundred and five er on fundoscopy there was found to be bilateral A-V 
nipping which i'll talk about later and there was no other significant findings 
okay so fundoscopy is an essential part of an examination on a hypertensive 
patient er and the abnormalities can be graded as follows so grade one it shows 
tortuous arteries within er with thick shiny walls grade two is A-V nipping 
plus er grade one and grade three is flame haemorrhages and cotton wool spots 
plus grade two and grade four is papilloedema plus grade three okay and i'm 
just going to show you a picture now of A-V nipping and so this is looking at 
the artery and the vein within the back of the eye and as you can see here just 
a slight kinking and narrowing where the artery and the vein cross over okay so 
now i'm just going to talk about causes of hypertension er there it's either 
like primary or secondary hypertension and primary otherwise known as essential 
hypertension counts for ninety per cent of causes of hypertension and it's a 
multifactorial etiology but recognised factors include genetic factors er 
foetal factors such as low birth weight and environmental factors such as 
obesity alcohol high sodium intake and possibly stress er it-, it's known that 
diabetes and hypertension are linked but just recently er a syndrome X has been 
linked with er hypertension although the mechanism underlying this is not known 
but syndrome X includes hyperinsulinemia glucose intolerance a reduced H-D-L 
cholesterol hypertriglyceridemia and central obesity and it is known that this 
is a major risk factor for er vascular disease so secondary hypertension needs 
to be considered er even though it counts for approximately ten per cent of 
causes of hypertension because you can possibly treat these er and renal causes 
that count for about eighty per cent of secondary hypertension and the reason 
it does this is it causes an elevation in the B-P due to the sodium and water 
retention causes include diabetic retinopathy chronic glomerulonephritis 
polycystic polycystic disease tubulo-interstitial nephritis and reno-vascular 
er disease and endocrine causes include Cohn's syndrome which is er results in 
an excess of er aldosterone there's adrenal hyperplasia pheochromocytoma which 
er results in sort of noradrenalin adrenaline secreting tumours and Cushing's 
syndrome okay other causes er are sort of drug causes such as oral 
contraceptive pill and steroids and in pregnant women they can develop 
something called pre-eclampsia which is hypertension in pregnancy with 
proteinuria and this is a medical emergency so now Andy is going to carry on 
talking about Mr G and talk about the investigations that took place
sm5277: okay er right so the investigations were carried out in order to 
uncover er any treatable causes of secondary er hypertension so got the full 
blood count urine analysis for protein and red cell casts U's and E's 
creatinine er blood glucose is important because er diabetes er is associated 
with er renal vascular disease and atherosclerosis er which may contribute to 
hypertension serum cholesterol er a chest X-ray looking for enlarged hearts and 
the E-C-G which er acts as a screen for er left ventricular hypertrophy er 
which may be a complication of er hypertension right er so in the case of Mr G 
there was a number of er abnormal results his potassium was er lowered which er 
may be indicative of hyperaldosteronism er since like the excess aldosterone 
causes er hypokalemia as well as sodium retention so er that needs to be 
investigated the urea and creatinine were levels were high which may indicate 
renal so on further investigation creatinine clearance was found to be low it's 
normally in the range of about a hundred and ten to a hundred and fifty er mils 
per minute and renal ultrasound however found er no obvious pathologies so this 
wasn't really in keeping with the er disease theory so er the cholesterol was 
in the normal range so he didn't have this additional risk factor for er heart 
disease E-C-G showed sinus tachycardia no left ventricular hypertrophy and 
there was no other significant findings okay so differential diagnosis it's 
likely to be essential hypertension due to the asymptomatic presentation er 
significant factors to consider in the case of Mr G were his excessive alcohol 
intake er er and alcohol is one of the most common causes of secondary 
hypertension and it's thought to cause this by raising cardia-, cardiac output 
and heart rates er by er a rapid rise in er epinephrine and cortisol levels 
okay er it's also important to consider er other causes of secondary 
hypertension and in the case of Mr G the most relevant ones were renal 
dysfunction and adrenal hypoplasia er but er it's it's also important to 
consider the fact that er the renal dysfunction could have been caused by the 
hypertension er itself er and so it's er it's it's sort of the converse theory 
really er and this this when this occurs when you get sort of er damage to end 
organs er this is due to er s-, sustained hypertension so i'm just going to 
talk a little bit about that so the most common sort of organs to be damaged 
are the brain and the heart so in the brain there's risk of throm- er 
thrombotic or haemorrhagic strokes er in the heart er left ventricular 
hypertrophy is a compensatory response to chronically elevated blood pressure 
er and heart failure may relate to left ventricular hypertrophy or to premature 
coronary disease er renal failure may also result er and this is caused by reno-
vascular damage and glomerulo loss okay so in terms of treatment for er Mr G 
the aims are to gradually reduce the blood pressure to er under a hundred and 
forty over eighty-five er and the emphasis was on a gradual reduction because 
er a rapid reduction in blood er pressure er can be fatal like in the context 
of er a stroke for example er lifestyle changes are important so a low fat diet 
weight reduction exercise smoking cessation and most importantly for mister G 
er reduced alcohol intake er and there's a number of pharmacological measures 
which can be er used to treat patients er and in the case of Mr G it was 
decided to use combination therapy so he was er treated with er the following 
drugs so diuretic bendrofluazide er calcium channel blocker er amlodipine and 
which er acts as a vasodilator er two different types of beta-blocker plus one 
atenolol er the second one labetalol has an additional arteriolar vasodilating 
action which lowers the er peripheral resistance an alpha blocker er which acts 
as a vasodilator as well doxazosin er and that was it thank you
su: namex
sm5277: any questions yeah
su: what about his neck pain
sm5277: his neck pain er it sort of disappeared yeah [laughter] 
sf5272: when er on examination his neck pain had gone
sm5277: yeah
sf5272: so he didn't actually have any neck pain so they don't know if it was 
like a musculoskeletal thing and then when he actually came in that's when they 
just discovered that he was hypertensive but on examination his range of movem-,
movement was fine and he wasn't complaining of any neck pain
sf5274: what was the first sort of grade of that retinopathy thing
sf5272: what was the first grade
sm5277: i'll go back to it if you want
sf5272: it was like tortuous arteries an increase in blood pressure basically 
which is then obviously going in any artery which goes into the eye
sm5278: can i just see the drug list again for a moment please
sm5277: yeah
sm5279: just tell me you've put it on the web and then 
su: why is it necessary for him to be on atenolol and labetalol
sf5272: er when he was in there his blood pressure would not come down it it 
started to come down and then it would just shoot back up again so they 
initially started him off only on i think it was thiazide and a beta blocker 
the atenanol er but then because it kept going back up again they started to 
use more combination therapy and they thought because it has the arteriolar 
vasodilating action they thought it might be helpful so they didn't actually 
put him on labetalol until later on
sf5273: okay right er more hypertension basically Neema and i are going to talk 
about that so er not just a straightforward case of hypertension this one it's 
something a little more over and above so Judy's already mentioned a few things 
about hypertension basically it is impossible to define exactly where you're 
going to cut off these people are hypertensive and these people aren't but er 
patients who have been given a diagnosis of hypertension it usually has been 
based on values that have been selected in trials and so on er where above that 
above that blood pressure there is actually proven health benefit to treatment 
versus the costs or because a B-P above that level is actually going to give 
you a significantly increased er level of er risk of adverse events basically 
so there have been some British guidelines published on this and so treatment 
basically is recommended for anyone with malignant hypertension which is sort 
of a sudden increased risk in B-P er patients who have sustained pressures over 
a hundred and sixty over a hundred which would be on the sort of three 
subsequent measurements er for patients who fall in the range slightly below 
that a hundred and forty over ninety and so on er then you have to make the 
decisions based upon co-morbidities er risk of coronary events from other 
things such as other risk factors like atherosclerosis and things that we all 
know about and also concurrent diabetes or end organ damage the presence of 
those kind of things so er our case study is Mr P-S i'm going to talk about 
this in a bit of a slightly roundabout fashion rather than talking about his 
presentation to begin with just to give you some of the background because it 
kind of makes more sense once you actually know what his history is so 
background to Mr P-S he's a male aged sixty-six a retired engineer who lives 
with his wife he's a non-smoker and only drinks occasional alcohol and he 
doesn't seem to have very many risk factors for hypertension there but in his 
past medical history he actually has been diagnosed with hypertension since 
sort of roughly nine years ago and his B-P is usually around the level of a 
hundred and fifty over ninety so not dra-, dramatically elevated like we've 
just seen but still high enough to warrant treatment er for about three or four 
years he's been suffering er periods of super ventricular arrhythmias which 
i'll come to in a moment and also peripheral vascular disease suffering 
intermittent claudication on on walking and so on and other slightly less 
relevant things cholecyst-, systectomy and appendicectomy some years ago so his 
drug history and treatment includes what you can see here his atrial 
fibrillation was treated with a couple of episodes of er DC cardioversion to 
put him back into sinus rhythm er which was successful for a time but usually 
tended to relapse and eventually it converted itself into an atrial flutter in 
two-thousand-two so he was sent for er a procedure at the Queen Elizabeth in 
Birmingham which is a radio-frequency ablation which i don't think i know much 
about so i won't try and explain that to you er the drugs that he was taking on 
presentation were an A-C-E inhibitor a beta-blocker and an anti-platelet drug 
aspirin like most people seem to be so his presentation he was actually 
admitted by ambulance his presenting complaint was that he'd lost the use of 
both legs very suddenly and also had lost all sensation below the waist and 
this had happened about three or four hours before presenting in the morning er 
to sort of describe how the onset actually happened it was very sudden he des-, 
er described a sort of a dramatic pain suddenly radiating from his face down 
his whole body towards his legs and particularly noted chest and back pain 
which he described as a ripping quality you might be able to see where i'm 
going here but er anyway it resulted in loss of sensation and movement in both 
legs er so on examination his Glasgow coma scale was fifteen out of fifteen so 
he was alert and talkative and he was quite with it er but basically was in a 
lot of pain and quite ill at the same time notably er his chest was clear his 
abdomen was soft and tender and he described this back pain but that wasn't 
tender no sort of musculoskeletal element there and there had been no history 
of previous trauma or anything to suggest that but basically the warning signs 
came when you examined his cardiovascular system he had no femoral pulses and 
actually no pulses in the lower limbs at all on either side and er his 
neurological assessment showed that sensation was absent in the right and left 
lower leg from the knee down and also much diminished in the lateral thighs as 
well er movement and reflexes were absent in both legs so obviously quite a 
worrying picture fairly dramatic the impression that was recorded at 
presentation was that this was probably an acute vascular event er an occlusion 
and they originally suspected that it might be a saddle embolus sitting over 
the bifurcation of the aortas and obviously blocking off er both of the sort of 
common iliac vessels and everything below that level er differential really the 
only other thing that's included is aortic dissection so for some reason they 
didn't actually assess him any further until the following day which seems a 
bit odd in the circumstances but at that time on examination his leg sensation 
had returned actually so that's a good thing er his foot pulses were weak but 
palpable legs were cold with poor capillary refill er his radial pulses the 
left pulse was found to be stronger than the right which er we might be able to 
explain when we come to what was found subsequently and his heart sounds were 
soft er but er heart sounds one and two were both audible and with a soft early 
diastolic murmur
su: had he had any treatment sorry
sf5273: sorry
su: had he had any treatment
sf5273: no not at this point quite bizarrely so the next thing that happened is 
he was sent for a C-T scan and er i'm not sure what they were expecting to find 
but what they did find was a type A aortic dissection extending right from the 
very root of his aorta down to the bifurcations so pretty drastic kind of 
dissection there er it's a DeBakey type one Neema's going to mention later on 
what that actually means so when you look at the anatomy you can see that a d-, 
dissection of that extent's actually going to involve a lot of branches of the 
aorta obviously it involved the right coronary origin so obviously affecting 
the blood supply to the heart itself the left common carotid the left 
subclavian origin and the brachiocephalic trunk and coeliac origin and it 
extended along the superior mesenteric artery but that wasn't actually majorly 
compromised and involved the left renal origin and the inferior me-, mesenteric 
artery and he did actually suffer some subsequent kidney failure so in of the 
left kidney so we'll see about that in a moment er the distal aorta obviously 
severely compromised no blood flow having got to his legs at the initial 
presentation so they did actually commence treatment at this point g-, gave him 
some heparin thank god and basically rushed him for some emergency surgery to 
repair the dissection so the risks of this surgery basically it's very high if 
you're if you're not going to operate then it's pretty drastic and a lot of 
patients die i'm not entirely sure of the figures because obviously aortic 
dissections each to their own they all differ in their extent but for something 
that that drastic you really you are going to have to have surgery there's no 
two ways about it so the surgery itself mortality's approximately twenty per 
cent there's obviously a risk of stroke paraplegia and kidney failure as we 
said because ob-, obviously all this surgery involves clamping vessels and 
going on p-, bypass and things like that so the outcome of the treatment itself 
the surgery whilst they were actually sending him into bypass he had his first 
cardiac arrest er but they did manage to pull him back from that one and 
continue with the operation long enough to give him a a knitted graft whatever 
er Gelscal triaxial graft i think Doctor Shiu could tell you more about that 
than i could er they only repaired actually the proximal aorta sort of in the 
ascending region which er would kind of cut out the bit the opening as it were 
to the dissection they didn't actually repair the entire length of the aorta 
because that would be very complicated with all the branches and so on so if 
you can imagine that in your head's er they had to re-suspend the aortic valve 
which is quite common when er the ascending aorta's involved because that can 
sort of either the root of the aorta can be dilated and so on which can 
compromise the valve function they also drained the pericardial effusion and 
took him to an I-C-U at which point he had his second cardiac arrest including 
a su-, sudden drop in blood pressure so they rapidly opened his chest and 
basically found that he had a huge clot in his right atrium which they 
extracted and after which he managed to sort of stabilise again er suffered 
some subsequent tachyarrhythmia which were treated with ad-, amiodarone and he 
also had a creatinine rise and was sub-, subsequently found to have had left 
kidney failure from probably resulting from the original dissection rather than 
the surgery er so the outcome happily in the end he for some reason it was a 
miracle seeing as he walked into our clinic and has no persistent neurological 
defects he has palpable femoral pulses and palpable foot pulses with a good 
perfusion and basically's very lucky to be alive i think but that's a rather 
dramatic presentation of hypertension for you so over to Neema
sm5280: okay so i'm just going to talk about er aortic dissection which the 
majority of you probably all know like a bit about it it's generally where 
there's er a tear in the intima and blood can blood can surge between the two 
layers or two of the three layers of the aortic wall and as a result when the 
blood goes between the layers you create a another lumen so you get a a true 
and a false lumen occurring and this can happen to a variable extent along the 
length of the aorta generally in an antrograde direction which is downwards to 
anyone who didn't know what antrograde is like me and so in this case it 
happened throughout the whole length of the aorta er it's also er well i'm not 
sure worthwhile to know but up to an eighth of cases there is no intimal tear 
in somebody with aortic dissection from the literature that i read and this can 
happen when er the vaso vasorum the the small vessels that supply nutrients to 
the wall of the aorta they can rupture and you can get an intramural haematoma 
so there was actually no insult to the er intima aortic dissections are three 
times more common in men than in women they're more common in black and less 
common in Asian people and about three-quarters of aortic dissection occur 
between the ages of forty and seventy okay as the dissection advanta-, advances 
down the down the length of the aorta it can occlude arteries that happen to 
branch off so consequences of this can include a stroke and a heart attack 
sudden abdominal pain lower back pain and nerve damage so factors that can 
predispose somebody to getting aortic dissections er er mainly hypertension 
which is found in the great majority of people with aortic dissection 
atherosclerosis er cystic medial necrosis which er i couldn't really tell you 
much about i think it's just a pathology of the er of the tunica media where 
you get a loss of elastin and weakness in fibres and you get some mucoid 
polysaccharide build up there but that's not important but you you see it in 
conditions such as Marfan's syndrome Ehlers-Danlos syndrome and something you 
will never need to know about but but there's some other causes as well aortic 
stenosis prosthetic aortic valve trauma pregnancy and there's a list of other 
causes as well so the types of dissection there's two different types of 
classification there's a DeBakey classification and there's the Stanford 
classification and as we've said th-, our case Mr P-S i think he was called er 
has had a DeBakey type one which involves the entire aorta type two just 
affects the ascending aorta and type three just the descending aorta the 
Stanford classification is a bit simpler whether it involves the ascending 
aorta or it doesn't so if it does then it has to be a type A if it doesn't it's 
a type B simple as that so what are the clinical presentations by far and away 
the most common presentation is that of chest pain the pain is sharp tearing 
intractable chest pain which is abrupt and of maximal intensity straight from 
the onset which is unlike what we learnt last week ischemic pain which has a 
crescendo quality to it two-thirds of patients have a murmur or a bruit of 
aortic regurgitation and this is where you get a circumferential er lesion 
basically from the dissection which alters the shape of the aortic valve 
causing aortic regurgitation and normally in people with aortic regurgitation 
they'll get er left ventricular dilatation in chronic cases but somebody like 
this where it's very sudden sudden and acute aortic regurgitation can cause 
left re-, er left ventricular failure other clinical presentations you should 
look for is somebody who is hypertensive i.e. somebody who's got a high 
predisposition to getting an aortic dissection who is now hypotensive and 
shocked on examination they may have asymmetrical pulses er because you can get 
pulse deficits where arteries are getting occluded basically which may appear 
and disappear over time they may have pulmonary oedema neurological deficits 
and cardiac tamponade so looking at imaging on chest X-rays you can see all 
those different stuff which to be honest i wouldn't be able to tell you what 
they look like on a chest X-ray apart from the picture on the far on the top 
right you can see mediastinal widening i can't really see anything else er M-R-
I you can see an intimal flap or a slow flow or clot in the false lumen which 
you can see on this next picture see round about here that's where the false 
lumen is and here you can see where the the intima has closed in and where you 
get accumulation of blood in the outer layer so the prognosis the long term 
survival of somebody who's survived an acute episode is sixty per cent over 
five years and it's forty per cent over a ten year period however that's if 
they manage to get through the acute ph-, the acute problem seventy five per 
cent of untreated people die within a fortnight a third of them er from late 
deaths of the complications of dissection and two-thirds are due to other 
diseases which i i'm not quite sure what they are because i couldn't find them 
but er before i go onto treatment er something to do with prognosis is that i 
read somewhere that for every hour you leave somebody with er a dissection 
untreated increase their mortality by one per cent so if you leave somebody for 
two days untreated they'll have a fifty per cent mortality so treatment if 
somebody's got a dissection and you're in A and E and you see somebody the 
initial treatment should always be medical sorry i had to laugh at that so er 
because mortality is highest in the first few hours following a dissection 
immediate er pharmacological intervention is needed you need drugs that will 
lower the blood pressure so a combination of sodium nitroprusside and a beta 
blocker are needed er the sodium nitroprusside is a vasodilator and will reduce 
er vascular resistance and the beta blocker will reduce cardiac output and i've 
put down some doses of what you'd typ-, typically give er to somebody but i 
won't leave that on it's not too important except for on here i've put 
propranolol a lot of doctors would probably disagree with me and say 
labetalol's probably a better one because it's a non-specific alpha and beta 
blocker so what about surgery well surgery is generally reserved for those who 
have dissections in the first few inches of the aorta as it comes out of the 
heart and it's pretty much done always in this case unless there are 
complications which will make surgery too risky however dissections that are 
further away from the heart it should always be medically treated and they 
probably treat it for the rest of their life er however there are some 
indications where you'll need to do surgery whenever there's a a leakage of 
blood a clot or they've got something like Marfan's syndrome er i haven't read 
this er the surgical mortality in major medical centres with interest in aortic 
dissection is about fifteen per cent and somewhat higher for distal dissections 
as i said before all patients er including those treated surgically should be 
treated medically with beta blockers calcium channel blockers and A-C-E 
inhibitors the most important late complications you'll get with aortic 
dissections is re-dissection formation of localised aneurysms er this is 
probably a pseudo aneurysm where you get a hole in the aorta and blood can seep 
in and get trapped by the soft tissues around it and also progressive aortic 
valve insufficiency and that's me done
sf5281: i was just wondering you know when it actually er tears and the sort of 
dissection evolves does it literally happen like a tear or is it gradual
sm5280: it happens like a tear
sf5281: so it can go literally right down
sm5280: well no it's well it depends on the people if somebody's got a cystic 
medial necrosis where there's actual pathology of the the media then you're 
bound to get it a lot quicker than somebody who's who's got normal aorta like 
the tissue's fine but hypertensive because the actual integrity of the tissue 
is there
sf5273: i sort of think it sort of pushes itself it's way through under 
pressure from like you know beating of the heart basically so it won't just 
sort of be instant but it will sort of push it's way through
sm5280: so hence the need for the the beta blocker and like something to reduce 
vascular resistance
su: how could they repair it if they only repaired the top bit and it was all 
the way down did they just sort of leave it and hope for the best
sf5273: well if you if you imagine that the a-, aorta's sort of you know like 
that the entrance to the dissection as it were is in the ascending aorta but 
there's no sort of entry or exit of blood through the rest of it so by 
repairing the entrance to the dissection the rest of it's just going to be cut 
off from the main lumen
sf5275: when he bled did he just bleed into the mediastinum is that why he 
didn't vascular collapse
sm5280: well that that's more of a rupture it because when blood goes in 
between the two layers they can either it can either break back in to the lumen 
of the the vessel in which case no blood will be lost because it's just going 
out into between the layers and then back in it can also go out of which in 
that case it's effectively an aortic rupture and so will probably go to the 
retroperitoneal space now if blood happened to escape the retroperitoneal space 
into the peritoneum they're pretty much going to die if it stays in the 
retroperitoneum the prognosis is a lot better it holds a lot less blood
sf5273: but in that case it just it sort stayed within the rather than like 
actually leaking out of the aorta itself
sm5282: okay er our talk is actually on left ventricular failure it may not 
sound like that at the beginning but er bear with us we think it is er it's Mrs 
W she's a seventy-three year old female and she presented with chest pain and 
shortness of breath the chest pain was sudden onset she was actually asleep at 
night and woke with this chest pain and breathlessness and she described the 
pain as retrosternal radiating to the back it was a dull ache she described the 
intensity as six out of ten and it lasted for approximately thirty minutes it 
wasn't relieved by her G-T-N spray and er she did say it was associated with 
sweating breathlessness which was at rest and a wheeze she had no palpitations 
no nausea and no vomiting before this episode she did have er three pillow 
orthopnoea P-N-D she described her exercise being limited to thirty yards er 
but felt that the limiting factor in that case was actually her arthritis in 
her knees and hips she had mild pedal oedema er and important negatives she had 
no dizziness no peripheral vascular disease no cough no sputum and no history 
of any respiratory conditions C-O-P-D asthma her past medical history in two 
two-thousand-two she was admitted to hospital with what she described as fluid 
on her lungs she's had hypertension i think it was for approximately twenty 
years her angina she's had since nineteen-seventy-five in nineteen-sixty-eight 
she had a thyroidectomy and er she's had osteoarthritis in her lower back knees 
and hips she's no history of diabetes rheumatic fever or stroke social history 
she lives at home with her husband er her husband is severely limited with his 
daily tasks due to breathing problems and unfortunately for them both they live 
in an upstairs council maisonette they can cope with their their normal 
activities of daily living and er last year they sold the car and they now use 
taxis and share a mobility scooter to go to the shops taking it in turns to 
ride on the back of course er she stopped smoking twenty-five years ago er and 
she currently drinks slightly more than she possibly should at er twenty-one to 
twenty-eight units of alcohol a week family history er her father died of an M-
I when he was sixty-five mother died of breast cancer aged eighty-four one 
brother has an angiogram she doesn't speak to the brother so doesn't really 
know the history behind any of that and her other two brothers are both well 
she has no other family history of note her drug history pre-admission er 
aspirin anti-platelet a hundred and fi-, well i'll let you read the doses 
prazosin again for her high blood pressure her sustained release nifedipine for 
high blood pressure angina her loop diuretic simvastatin and her G-T-N spray 
and will go through the rest of it
sm5283: the salient points on examination er she was slightly bradycardic but 
er that's probably due to the medication she was on at the time when we 
examined her er she still had moderately high blood pressure er J-V-P wasn't 
raised she had mild sort of pitting ankle oedema but she had varicosities so i 
put it down to poor venus return er J-V-P wasn't raised so er she was a rather 
great big obese lady so er it was quite difficult to palpate her apex beat er 
couldn't palpate it heart sounds one and two were present but they were quite 
soft again probably due to her obesity she had a late systolic murmur er 
probably suggesting mitral reflux and la-, late systolic prolapse er she had oh 
that that should read right-sided carotid br-, bruits not bilateral and a 
slight expiratory wheeze when we listened to her lungs but on admission she had 
bibasal crackles okay the investigations that were done er chest X-ray 
unfortunately was an A-P view but the heart looked fairly big but you can't be 
sure more importantly er lung fields were clear but she had er had frusemide by 
that time er E-C-G showed S-T depression and also there was a positive troponin 
T so that indicates she's had a non S-T elevation myocardial infarction er all 
other bloods were normal apart from potassium which was slightly low er again 
that's because she was on diuretics and her echo actually showed reasonable 
left ventricular function and right ventricular function so i'm starting to 
think that maybe this is er diastolic left-sided failure rather than systolic 
so basically she can squeeze the blood out okay it's just not there's a problem 
with filling okay so impressions she's had a N-S-T-E-M-I er acute left 
ventricular failure secondary to the N-S-T-E-M-I and there her sort of other 
risks er in order of importance systemic hypertension er long standing ischemic 
heart disease er mitral prolapse er she's possibly alcoholic and 
atherosclerosis and obesity okay this is the acute treatment er you'd sort of 
do this in this order sit the patient upright but the oedema usually resolves 
itself in about ten to thirty minutes so she might be okay by the time you get 
there hundred per cent oxygen er I-V frusemide er put the cannula in so you've 
got diamorphine next also reassure the patient and keep them calm and then er 
rather than sublingual again that shouldn't be there I-V er isosorbide 
mononitrate and also monitor the B-P while you're doing this er so this was 
done in this patient and also her drugs were reviewed er she was put on a more 
appropriate sort of A-C-E inhibitor and given a beta blocker er only a 
cardiologist in this circumstance can initiate the beta blocker because he 
might worsen the cardiac failure by giving her that but in the long term er 
especially that one metoprolol er has produced good results it reduces symptoms 
rather than mortality A-C-E inhibitor itself reduces mortality and symptoms 
also various lifestyle changes er reducing her alcohol low sodium diet you 
don't need to restrict fluid until heart failure's a lot more severe than this 
and that's about it it's a common condition ten per cent of over seventy-five 
year olds er one-point-eight per cent of twenty-five to seventy-five year olds 
in the West Midlands okay thanks
nm5271: the retinal appearance show that of hypertensive changes i don't 
suppose you showed any actual pictures you did what sort of changes did he have 
in his 
su: sort of A-V nipping
nm5271: A-V nipping er you discussed the so called secondary and primary 
hypertension in this case you decided it was due to any particular cause
sf5272: alcohol excess alcohol that he drank
nm5271: yes how many units was he taking
sf5272: about forty to sixty units a week
nm5271: right pretty average for Coventry folk as it happens it's very 
difficult to prove that that caused the hypertension but there's certainly a 
lot of studies showing that if you are hypertensive that amount of alcohol will 
make your hypertension harder to treat of course there are other illnesses from 
alcohol on the heart we can address that later did he respond to therapy
sf5272: er in the end he did initially he didn't his hyperten-, his blood 
pressure kept going back up again so they just tried different combinations of 
er medication
nm5271: okay er the standard approach is really just focus on the history for a 
primary cause of hypertension usually that really virtually el-, eliminates the 
majority of so-called secondary hypertension i.e. this primary disease in other 
words if a patient present with kidney failure present with er chronic urinary 
tract infection and a history of paranephritis or something like that you know 
there's a renal cause there are patients who present with other medical 
conditions such as Cushing's disease so in the course of your other medical 
conditions you find hypertension you're not surprised but when you first 
diagnose the hypertension taking a history such as this one with actually no 
background chances are you're dealing with essential hypertension er now i 
think it's quite interesting to contrast this patient with the heart failure 
patient in various ways i mean the interesting thing about medicine is that 
given any particular disease diagnosis you want to know what is a patient's 
perception of his condition and how is he he's how he's going to respond to 
treatment or a psychological response if you think of hypertension and heart 
failure you can't be more contrastive the hypertensive usually don't know what 
the fuss is about that's a problem he has the condition but a lot of the time 
you have to convince him that he has it and therefore he will accept your 
treatment with the heart failure patient it is quite the opposite by the time 
you diagnose it the patient's usually symptomatic that's the case isn't it in 
your patient with heart failure i think it does illustrate a lot because it 
influences how you counsel the patient and how likely he is to comply with his 
medications i say that interestingly hypertensive patients are the least likely 
to comply with medications if you actually do surveys something like forty to 
sixty per cent of patients do not take their the medications according to 
instructions but by the time you consider heart failure then you have a much 
higher percentage and the reasons are very obvious in the hypertension they're 
not symptomatic the patient sometimes never quite convinced that he has to take 
these nasty medications so i think that you have a job to do there now back to 
er i i put up this slide and if you if you like i'll fo-, show some prepared 
pictures that one shows one of the more common conditions which is really renal 
artery disease however that's very much age-related the older the patient the 
more evidence of artery disease elsewhere the more likely you'll find artery 
disease causing renal artery cyanosis thereby causing hypertension but of 
course in medical student tex-, text books that's high up on the lists of all 
various causes yes it is if you look at the elderly people and it is not often 
that it requires any attention so it's i think it's accepted as one of the 
causes but usually there's evidence of widespread artery disease so probability 
wise again the history taking will help you if somebody has evidence of artery 
disease elsewhere any suggestion how it might show up in the history hands up 
evidence of artery disease elsewhere
nm5271: yes i think that's one of the best ones right if you've got low 
intermittent claudication chances are you've got disease in your aorta and 
really the kidneys arteries are not far away er of course patients with er 
coronary artery disease and severe hypertension so i think the point is we look 
for is where patients do not respond now of on first presentation of course you 
would do various tests and the simplest one is really simply electrolyte and 
urea and that's pretty good pointer to any chronic renal problem in the young 
for example younger populations you look for evidence of kidney infection in 
particular in females why females because cystitis and pyelonephritis is far 
more common in female gender because of a urinary tract tendency to get 
infected so that's the kidney side definition is difficult you will find again 
again when you come across patients with high blood pressure you ask them they 
say oh my doctor last checked my blood pressure he tells me it's usually 
alright it is very difficult to establish whether somebody in fact one has had 
hypertension not treated or hasn't had hypertension and never had it checked 
the government is really trying a big drive in making sure that there are so-
called well men clinics well women clinics that there is so-called 
opportunistic checking of high blood pressure i stress this because 
hypertension is one of those conditions that's more often diagnosed 
opportunistically in other words the patient goes and seek advice for something 
totally different check picked up er patient will seek advice for for example 
contraceptive pill that's definitely an indication to check the high bl-, check 
the B-P of course if that's high then it's relative contraindication and a lot 
of the time the patient comes in for hip operations hernia operations so all 
these opportunities are for us to pick the diagnosis now what is normal what is 
abnormal strangely you will have thought that this is a condition that nobody 
will argue about but physicians or cardiologists themselves have been moving 
the goal posts so we can't blame other specialists not to be up to date and if 
you look at this it's pretty severe definition of normal versus abnormal and 
you might wonder why we're moving the goal posts if you look at this now er 
adults eighteen years and older so it doesn't apply to most of you here optimal 
one twenty systolic diastolic eighty normal up to one thirty in fact i bet you 
one or two of you sitting here will have that kind of reading so go home get it 
checked er we begin to run into real problem with the elderly and partly like 
all other conditions British physicians have been reluctant to inc-, how should 
i say it include more patients as it were in other words they are very very 
prone to see a patient with say age seventy-five with blood pressure one eighty 
over ninety a lot a lot of primary care physicians and G-P's will just say oh 
well it's alright for your age or is it i'll show you the evidence it is not 
alright so therefore regardless of age we now recognise that blood pressure 
below one forty systolic is preferred and i sorry should be really not above 
ninety what sort of problem do we raise we may diagnose a lot of hypertension 
does it matter if we diagnose a lot of hypertension it doesn't why at least you 
will keep checking you may not treat after the first reading you may not even 
treat after the second reading but you will begin to at least counsel the 
patient and look for risk factors such as what we just discussed because 
hypertension's a condition a a best example of what we call preventive 
treatment heart failure isn't and we can talk about that later hypertension 
definitely is okay so we're very strict we have moved the goal posts and i will 
put this on the net if you want but it is of course in the text books er so 
it's quite severe and i'll explain to you the reasons now A-V nipping i hope 
you did explain what causes A-V nipping
sf5272: it's the hardening of the arteries
nm5271: that's right it's hardening normally the arteries and veins are quite 
soft in fact right so really very mild grade one most people won't be able to 
diagnose that unless you are very very good at looking at it right and this is 
where great tool moderate sclerosis is increased light reflex and compression 
of veins at crossings this is what we mean and this is a good example there 
it's very simply the bigger veins the smaller ones are arteries and the 
crossover is so i won't dwell on that and of course the increasing stages where 
there are so-called high exudates and haemorrhages and of cause papilloedema 
and this is when patients begin to have visual symptoms and that's quite severe 
and you will see this in so really so-called hypertensive encephalopathy we 
very very rarely see that now fortunately partly because of this drive to pick 
up hypertension when it's mild and treat and it is quite interesting when i was 
a medical student really an acute take often includes the hypertensive crisis 
it is now very rare so i think the primary care system has helped left 
ventricular hypertrophy a lot of people worry about this and you know including 
very seasoned doctors how do you diagnose left ventricular hypertrophy on the E-
C-G the answer is if it's overt it's very easy if it's subtle you just have to 
again go back to square one no don't read the history and look at the patient 
if somebody gives me an E-C-G and say look tell me where the left ventricular 
hypertrophy i just won't give the answer at all why because it the the chap's 
history and even the physical form influences the E-C-G and the best example 
would be amongst some of you i bet i will find the so-called text book 
measurement of left ventricular hypertrophy why louder hands up
sm5280: is is because of just the difference in people's body shape
nm5271: alright
sm5280: like short fat people might have a displaced apex
nm5271: not so much displaced subcutaneous fat is very good at er reducing 
voltage and vice versa if we are dealing a very thin patient you have increased 
voltage don't forget E-C-G is taken on the surface you're trying to draw a 
conclusion deduction about the heart that's one er another reason why some of 
you sitting here may have significant left ventricular hypertrophy on the E-C-G
su: level of fitness
nm5271: yes level of fitness so physiological left ventricular hypertrophy in 
other words what people know about is the slowing down of the heart rate but in 
addition it is of course a a physiological response to exercise that you have 
got left ventricular hypertrophy of course you won't reach this stage i use 
this slide to show that really if you are going to a gym regularly and you have 
an E-C-G like this i'd worry because you're not supposed to reach this stage 
and what you see here is apart from an increased voltage which is pretty 
obvious there is also abnormal T waves especially in V-four to V-six er it is 
in fact very difficult to understand why the T waves behave like that but take 
it from me it is a feature of very se-, severe left ventricular hypertrophy it 
is doubtful whether that's reversible now but if it's not reversible that means 
there's something structurally wrong while you undergo physiology training 
you've got left ventricular hypertrophy if you train the voltage will go down 
in other words the er heart is quite capable of hypertrophy and then become 
thinner what's the difference between hypertrophy and hyperplasia
nm5271: and when do you get hyperplasia in the heart
nm5271: well done no never the heart muscle cells do not duplicate any more 
after the person's mature so all you get is hyper-, hypertrophy in other words 
increase in cell size rather than increase in cell number anyway so much for 
that er a much more specific way if one of you come to my clinic and say your G-
P's picked up your E-C-G's quite abnormal a lot of voltage i take a history you 
do go to the gym er but perhaps the E-C-G's a little too much for what it is so 
the next test is a echocardiogram er i'm not sure whether i have included i was 
going to put an echo there but i didn't anyway so where various investigations 
will be according to how how much you want to assess the patient the 
echocardiogram is a superb tool for establishing left ventricular hypertrophy 
don't look at this slide just yet it is also very good for assessing whether 
there are so-called end stage sorry not not end organ damage alright these are 
these are the terms that you want to pick up when you deal with hypertension if 
it's picked up early and no damage in the organ we really only refer to three 
serious organs the brain the heart and the kidney alright the eye is part of 
the brain if you like by the time you've got all the eye changes really that is 
end organ damage er this patient as far as i know had no renal damage and h-, 
has no er is that right no kidney disease
sf5272: he didn't have any disease but his creatinine and urea was up but we 
thought that was due to the hypertension damaging it
nm5271: right who was going to present the aortic dissection or was that 
presented
su: yep
nm5271: it was in that case was there a history
sf5273: er his medical history included er hypertension for about nine years 
super ventricular arrhythmias and intermittent cau-, claudication
nm5271: was that the adequately investigated and treated do you think
sf5273: his arterial disease i don't
nm5271: or hypertension
sf5273: er he was on an ACE inhibitor and a beta blocker and an anti-platelet
nm5271: so he was quite vigorously treated so this come to this is the next 
slide alright so you have two examples where really one is early presenting 
minimal signs of hypertension and you have somebody who is now one into one of 
the really most serious complications of hypertension er but it is not unheard 
of put it the other way it is exceedingly rare to have aortic dissection if you 
weren't hypertensive so you can look at it the other way you can have a stroke 
you can have a heart attack you get kidney trouble without hypertension but 
aortic dissection would be very rare unless you have specific conditions 
affecting the aorta now this is a very busy slide so on the whole i don't like 
busy slides but it says that i've been trying to look for a slide like this for 
a long time i've it's only in preparing this lecture i found it and i want you 
to take note of it it teaches you so much on the on the horizontal axis 
obviously you will find that the high the blood pressure of increasing degree 
just look at this first column first systolic blood pressure up to one nine 
five cholesterol like that glucose tolerance normal no cigarette smoking E-C-G 
is normal so in other words this patient may take the worst case patient with a 
systolic B-P of over one is normal it's very good now move to the next category 
and take this the middle category instead now same sort of blood pressure 
ranges one o five to one nine five instead now this is American reading and 
cholesterol three three five that is something like er sixty per cent above 
normal so it would be something like seven cholesterol or seven instead upper 
limit normal in this country's five and there is now mild there is now glucose 
intolerance in other words the patient is a diabetic but otherwise doesn't 
smoke and no evidence of E-C-G or rate but what it shows here this is an eight 
year probability per one thousand patient you are now moving from something 
like a hundred er events to four-hundred events per thousand in other words in 
eight years roughly half of those patients will have a significant 
cardiovascular event what does that tell you hypertension per se is not so bad 
but if you've got all these other risk factors in the worst case really scary 
if you've got that kind of blood pressure systolic of one-hundred and ninety-
five and what i said earlier on there are patients out there walking around 
aged seventy with systolic hypertension like that untreated and you have almost 
a certainty that within eight years you have a major cardiovascular event and 
of course this group has got all these but then it is not difficult to find 
cigarette smoking non-insulin dependant diabetes and high cholesterol some 
people have put a name to this condition they call it syndrome X to me it's 
it's very confusing i think calling it insulin resistance is probably much more 
er if you like specific it is suspected that this is a group of patients who 
otherwise er are no by self no major single risk but by the time you put it all 
together mild hypertension glucose intolerance usually some obesity and you 
have a very major cardiovascular risk what that tells you is so-called the 
multiplying effect of m-, of coronary risk factors in other words by the time 
you add things together they multiply rather than just addition as it happens 
there are very few patients in this category it seems as if really things can 
be grouped together in this fashion there by the time you look at if there are 
hypertensives in fact most of them are from this column to the right which goes 
back to the concept of so-called glu- glucose intolerance may be a grouped 
condition are they inherited together or affecting the genes together and this 
is now the most fashionable hypothesis now it's quite important for you to know 
this can now be called now the Barker hypothesis that among the peasant Western 
population i stress that for the moment there there is an increasing prevalence 
of people with this particular syndrome by themselves each of the risk factors 
don't seem very severe but they are lumped together as a group anybody ever 
read the Barker hypothesis as to what is causing this upsurge of group risk and 
ischemic heart disease in the Western population
su: is it low birth weight
nm5271: yes very good low birth weight so it was a very interesting 
epidemiological study somebody happened while Doctor Barker happened to be 
reviewing some records that were about to be chucked out in East Anglia fifty 
years ago somebody housed in some sort of barn or something and er apparently 
the East Anglians don't move around very much so he was able to correlate sort 
of fifty years on people's birth weight birth weight with cardiovascular risk 
apart from birth weight there were other measures er which is really skull size 
versus length now what is behind the hypothesis let's see whether you read 
beyond that did you what is the hypothesis behind the birth weight because this 
is now the most interesting aspect of this condition i would say speak up
sf5276: was it developmental risk factors er du-, in during pregnancy
nm5271: no i don't think it's necessary injury it's very hard to prove injury
sm5280: is it something to do with it's supposed to reflect like the life 
course of the parents or you know 
nm5271: yes i'm sure it does yeah yeah yeah i in other words possibly 
relatively under nutrition of the maternal mother well sorry of the mother 
alright and there is a very good evolutionary explanation to this who can come 
up with a plausible evolutionary explanation
sm5280: you try and retain sodium if you don't have it in your diet or something
nm5271: yeah may not may not be just with sodium right this the hypothesis is 
that this is maladaptation right it seems that evolution takes c-, cares of our 
i-, if our if you like er survival in a very slow way but society is changing 
in a fast way if you look at it like that it's fine in other words it seems and 
it is now being shown again and again in other emerging populations and that's 
why it's very important to understand if you starve a population of mice let's 
not talk about people for the moment starve a population of mice the next 
generation of mice if you keep them starved they're alright but if you now feed 
the next generation very well that generation will suffer tremendous er high er 
cholesterol problems so it is very easy to understand it could be that genetic 
or or according to Darwinian explanation this is really how genes are supposed 
to work if you've got a population exposed to relative malnutrition the next 
generation is prepared for hardship but then there's the then the environment 
changes very fast instead of hardship you get Western lifestyle hamburgers and 
all that it's very bad news now although it may seem you know very cute as it 
happens it's seriously worrying all the emerging under developed countries 
which are becoming wealthy and China is a very good good example and even more 
worrying is the whole of the African continent and South America as well 
there's an explosion of coronary artery disease diabetes hypertension so i 
think this is no longer just a cute observation it's a very good animal 
experiment data very good and in time i'm sure we will establish something 
about the switching on and off of genes now because it's getting late we 
haven't got a lot of time i'm going to switch straight over to talk about how 
heart failure also brings in very interesting evolutionary ideas of 
maladaptation i'll just briefly hear from your heart failure stories first 
though
nm5271: summarise in five sentences
sm5283: Mrs W a seventy-three year old er presented with shortness of breath 
and chest pain
nm5271: how old
sm5283: seventy-three year old
nm5271: seventy-three year old
sm5283: er she was found to have a N-S-T-E-M-I precipitated the pulmonary 
oedema and so and so i think the echo didn't find anything wrong with the left 
ventricular function so it must be query diastolic and left ventricular 
dysfunction 
nm5271: mm yeah
sm5283: systolic
nm5271: yeah and
sm5283: on examination there was no evidence of cardiomegaly and couldn't feel 
the 
nm5271: okay and this is a lady who eventually was found to have coronary 
artery disease as well
sm5283: she had a 
nm5271: and she's waiting for emergency surgery i think i'm pretty sure
sm5283: we had examined her before that stage
nm5271: yeah she is right so er that patient then has surprisingly at age 
seventy something presented for the first time with heart failure and it is in 
through that route that we find that she has coronary artery disease alright 
there's no previous warning that she has angina or heart attack correct
sm5283: er she had a twenty-five year old history of angina she said it was 
being managed by her G-P
nm5271: right no M-I good now what are the learning points there er i could use 
the slide but i i feel i'd rather just i don't think i'll talk about drug 
treatment it'll be too much let's see how if i open my heart failure meanwhile 
how do i get out of this sorry i should be able to close this and open if any 
of you attended my heart failure lecture some of the slides you may have seen 
if you have okay it's too long that's even worse that one so i think that this 
may be even if if somebody present with angina or N-S-T-E-M-I and immediately 
complains of shortness of breath we'd worry same thing in a clinic patient with 
just angina should not seriously have shortness of breath unless they confuse 
the chest pain with shortness of breath you have to immediate suspect heart 
failure as well as angina if you don't suspect that you-, you're never to 
diagnose it you're never going get a patient on the right treatment in other 
words every time you hear somebody with angina you ask them apart from the 
chest pain do you get shortness of breath as well why is it so important 
because angina should not cause shortness of breath angina means just 
restriction of blood vessels in the myocardium not necessarily damaging the 
heart and by the time patients have genuine shortness of breath symptoms that 
means they have damaged the heart ischemic damage there are two ways coronary 
artery disease damages the heart the overt way of course having an M-I how 
would a patient with-, without an M-I damage the myocardium any suggestion
sf5281: compensatory hypertrophy
nm5271: that's an interesting one but i think that comes later compensatory 
hypertrophy i'm going to touch on in a minute but why should somebody just 
suffering from angina for the last twelve years now have got heart failure with 
echo evidence of enlargement of the heart 
su: have they got something like aortic stenosis
nm5271: no let's not bring in other things coronary artery disease itself is 
quite sufficient to cause trouble interestingly if you were to do surveys of 
heart failure er especially in the older age group and in fact coronary artery 
disease is the single most common explanation hypertension is the second most 
common i think so your explanation of secondary failure to hypertension is 
related with hypertension but let's keep things pure and simple for the moment 
coronary artery disease sorry angina well what i'm trying to illustrate is that 
angina is only what the patient feels what we worry about is ongoing damage of 
the myocardium without infarct trouble is there are many ways they do it and 
sometimes they are more a silent infarct even silent infarct is too narrow a 
definition in other words silent infarct really is an event it's just the 
patient doesn't have pain but it is usually an event either documented 
incidentally with an E-C-G or patient come in with real heart failure and then 
you then document silent infarct unfortunately coronary disease can quietly 
cause myocardial damage nobody quite understands it could be that each time 
there is really severe angina maybe the patient just treat it like another 
episode of bad angina on the golf course in fact there's a bit of myocardial 
damage why do we posture for that the reason we do is that by the time you 
examine an old patient with angina many years never had an infarct they die of 
another cause you look at the heart it's got various bits which is necrosed or 
scarred and that really is a worry about coronary artery disease that there can 
be ongoing damage i'm sure with our if you like more specific means of 
diagnosing small infarcts reminding the population remind the caring 
practioners to send this patient with so-called unstable angina then we're done 
using more of these now why do i use the words so-called unstable angina er i'm 
going to come to that slide later i want to use this opportunity to clarify one 
point about the word angina it causes confusion in medical students in doctors 
in students sorry in er in patients alright we should really eliminate the term 
angina or unstable angina from the text books now the confusion it has caused 
is that the patient never understands what angina means if the doctors confuse 
m-, small myocardial infarcts with angina angina as a term should be restricted 
in very very narrow usage of patients with chest pain with exception which goes 
away with rest very simple that's a classical text book desc-, desc-, 
description who first described it in the literature
su: Heberden Heberden
nm5271: Heberden well done and er he described it very very well as well 
alright you know definitely associated with severe gripping pain with 
instruction which is relieved by rest unfortunately for some years it's the 
cardiologist's fault they come across patients who come in with same pain no E-
C-G evidence of a infarct so many years we call this unstable angina then the 
patients that get very confused and the other doctors get confused and they 
begin to use the word angina very loosely infarcts are infarcts angina's 
fortunately we now have very specific cardiac markers called troponin T er C-K 
is not bad the so-called creatinine kinase in especially the but anyway soon as 
the introduction of these very sensitive markers we now know in a patient of 
chest pain at rest they have a small infarct in other words we can get rid of 
the term unstable angina we might as well call a spade a spade it's a small 
infarct and chances are unless you pick these up the patient will keep on doing 
these small infarcts that's how they damage the heart and that's quite worrying 
it's almost like kidney disease isn't it if somebody has kidney disease the 
kidneys are losing nephron and i think we have to begin to look at the heart as 
losing myocytes they're not difficult concept but in medicine it seems that 
certain concepts are much harder to introduce than others really er possibly 
because kidneys easy to measure we measure kidney function with a blood test so 
there you are one group coronary artery disease lose muscle now i'll come back 
to the concept of hy-, hypertrophy can you enlarge on what you said
sf5281: i've been thinking about that
nm5271: you were waiting for me to come back to you
sf5281: er i guess if you're not if you're not perfusing the myocardium er 
there may be an el-, element where you're not your output is less so you get a 
larger end diastolic volume and so there is hypertrophy as a result of that
nm5271: good okay that's what cardiology have been trying to struggle with for 
some years yes trying to use the idea that left ventricular hypertrophy 
eventually runs out of it's blood supply er i think i was taught it when i was 
when i was medical student it's essentially rather naive idea because we do 
know that those of you again athletes listen er physiological hypertrophy of 
the same degree it's got no problem right so therefore if pure L-, L-V-H as 
such by itself is shouldn't be a problem and do not deal with blood supply it 
is to do really how should i put it it it has to do with why there is L-V-H in 
the first place it seemed that if you've got o-, overt pressure overall it's 
particularly bad for the myocardium if you've got er if you see in this 
physiological adaptation of the heart most mostly it's due to what we call er 
endurance exercise the endurance athletes those of you who are runners can feel 
relaxed because that's been shown again and again to be good left ventricular 
hypertrophy now by saying that it would imply that the other athletes are not 
so good in other words what's the opposite of the endurance athlete
nm5271: the weight lifters alright and the the the weight lifters will appear 
to cause more concentric inward thickening of the myocardium and this is a very 
good example that slide there shows it er that the heart has not enlarged 
upwards the cavity's interfered with and that wall thickness is thick that 
introduces a very difficult concept it seems there's some inward thickening of 
left ventricular hypertrophy due to pressure overload really the the weight 
lifters you will see that really increases systolic blood pressure like mad 
when they pump the iron and the runners don't the runners increase cardiac 
output so again think of evolution it seems that our body is adapted for 
endurance exercise and not adapted for weight lifting i suppose it's not 
difficult do you imagine evolutionary process of humans you know we were we 
were surviving on large plains running from tigers and lions and that's how 
they survived they don't spend all their time lifting rocks there's another 
cute story about evolution now because i only want to spend ten more minutes 
and then we're finished why do i bring in evolution what is wrong with heart 
failure that we seem to be struggling with okay so we've finished the story now 
that for some reason pathological left ventricular hypertrophy lead to changes 
we're beginning to understand now it is to do with the abnormal how should i 
say its not just blood supply it's obvious that the hypertensive heart has 
quite adequate blood supply if you do all sorts of checking of ischemia they 
don't have ischemia and yet the L-V-H lead to heart failure it is something to 
do with switching on some genes that causes your heart muscle to the the 
myocyte to fail we haven't got all the answers yet but interestingly it is to 
it will explained by certain genet-, er gene switching and somehow the thyroid 
hormone is involved not at body level but local mutilisation of thyroid hormone 
so it's very strange but we know we will get an answer there and this picture's 
to illustrate how patients can move from that phase to this phase to show 
tremendous [dilatation] of the left ventricle this these two slides illustrate 
the power of a really easy cheap non-invasive test echocardiogram so patients 
with hypertension patients with heart failure really must have these tests er 
kidney in heart failure go on then go on then and our list here then what i 
said earlier on potential causes of heart failure it is very good to have this 
kind of idea behind when you treat a patient of course ischemic heart disease 
as i mentioned the damage from coronary artery disease maybe actually 
environmental hypertension large unknown alcohol features quite high here 
diabetes systemic disease dilated cardiomyopathy there are known ones there is 
no history maybe the patient has been hypertensive er sorry the V-H-D valvular 
heart disease of course this changes a lot depending on what patient population 
if you are caught in the Far East valvular heart disease will overtake ischemic 
heart disease for the moment quite a lot of unknowns in fact will have some 
form of viral heart disease in the past a lot of them but you can't prove it 
alright right so that's give you an idea i think i will skip that it is largely 
a disease of old age and this is where i want to bring in the concept of 
evolution it seems that evolution hasn't taken care of us with respect to heart 
failure why if anything evolution i'll read it again seems to have caused us 
trouble in so far as in the treatment of heart failure we're constantly 
fighting the body's response to heart failure did you touch on that if so i 
will be brief in other words in treating heart failure what are we treating a 
lot of the time we can't make the heart beat stronger we're giving diuretics 
why are we giving diuretics because the body's retaining sodium right we 
remember not water sodium why does the body retain sodium
su: cardiac output increase circulating volume
nm5271: yeah and where's the heart rate
su: in the kidney
nm5271: kidney right so all the time the kidney is in fact driving the heart 
mad as it were the heart begins to fail the kidney makes it worse no question 
about it kidney makes it worse why who can give me a good evolutionary 
explanation why is there such a a hard wire condition as the heart fails the 
kidney does something crazy and makes things worse not just sodium retention 
what else does the kidney do wrong which causes the heart to fail more
ss: vasoconstriction
nm5271: vasoconstriction system now these two are powerful agents so there must 
be reason why the kidneys are doing that
sm5280: is it an attempt to try and increase loads which then
su: yeah it's a compensation
nm5271: okay i was waiting for that one alright don't take it personally alright
sm5284: because there is there is decreased er blood going to the kidneys
nm5271: yeah and i know that i know that and that's which is a sample of what 
he's saying attempt to increase the blood pressure in other words we're now 
ascribing some thinking process in kidneys now aren't we really the kidney 
wants blood as it were the kidney's very selfish it's i would much prefer the 
other way i would consider a lot of the if you like the cardiovascular control 
and responses to various injuries as you like it's hard wired in our genes that 
how our body's supposed to work hard wire in other words the kidney's not 
choosing the kidney doesn't say ah well i want a bit more blood now the kidney 
has got reflex acts built in with hypertension under perfusion then it secretes 
these why give me the best possible explanation why our body's so stupid
su: is it because we came from sea
nm5271: yeah it goes all the way back when we came from the sea first we're 
lying horizontal creeping around on the ground next we try to stand up it is a 
very pure concept the price we pay for for being biped is that we get 
haemorrhoids we get backache we get strokes we get heart failure we get 
hypertension it's worrying by having a it seems that really the price we pay 
for for standing on on two legs is pretty high why because in fact there's yet 
another worrying thing it depends how this thing on heart failure the kidneys 
doing this there's another major problem causing heart defects which al-, also 
goes back to evolutionary turn what causes a heart attack clot in artery 
coronary artery why would there be c-, clot in the coronary artery why should 
it be what triggers these very tiny if you like erosion of the coronary artery 
and need to clot this is crazy what for what's wrong in the homeostatic 
mechanism in our body has lead to such a catas-, catastrophic event that it 
leads to a death of the organism it doesn't seem right which part of our body 
is if you like functioning strangely
nm5271: it's a coping system yeah agreed it's a coping system if you cut your 
fingers the same reaction that stops the bleeding is actually happening inside 
your coronary artery when this tiny fracture in your endothelium now that's 
worrying but then which comes first the in the coronary artery or bleeding in 
the evolution in the human evolution bleeding running away from the tigers and 
lions getting scratched among the bushes this to the early human beings sorry 
you talk about mammals for the mammalian species bleeding to death was a big 
risk hence all this reaction in the hard wire it's quite interesting to look at 
that because really we're now trying to devote very important drugs to fight an 
e-, an evolutionary process the present conclusion is that human beings were 
never really meant to live to seventy eighty ninety we're meant to live to 
child bearing age bring up that child if we're lucky and die of e-, 
evolutionary if you like forces and the gene is propagated the species is 
maintained we're not meant to be grandparents that's all