Coronary Artery Disease - Ischemic Heart Disease - Angina

now ischemic heart disease how do we define a skinny heart disease what is the basic concept related with the ischemic heart disease right first of all you must know that it's one of the most important condition a doctor must know the reason being that ischemic heart disease is presently the number one cause of death number one cause of death in males and females both in USA and other Western countries or industrialized country let me repeat it that ischemic heart disease is the number one cause of death in males and females and USA and other industrialized country right and how do we define ischemic heart disease ischemic heart disease is a group of clinical pathological syndrome it is not one condition there are many syndromes I will discuss into detail that is creamy heart disease is a group of clinical pathological syndrome group of clinical pathological syndromes right which result due to imbalance between oxygen supply and demand to the myocardium is the clinical pathological problems which result due to imbalance in oxygen supply and demand to the myocardium right usually oxygen supply is less and our oxygen demand is more and there's a relative schemee of the myocardium right do two again let me repeat it what is the screaming heart disease it's a group of Clicquot pathological conditions in which due to imbalance between oxygen supply and demand to the myocardium there is relative ischemia of the myocardium right so what is the real problem in this screaming heart disease look here problem is that normally in a healthy myocardium there is a balanced end-of-season supply and not only oxygen supply we can say other nutrient also oxygen supply and oxygen demand or nutrient demand now this balance should be maintained whenever oxygen supply is reduced and our oxygen demand is increased and myocardium develop relative ischemia we say that there is ischemic heart disease is chemic heart disease right so what is this chemical disease it's a group of clinical pathological conditions characterized by imbalance in between oxygen supply and oxygen demand by the myocardium in which the result is relative Kamiya is that right to the myocardium now there are so many conditions in which oxygen supply is reduced and there are other conditions in which oxygen demand to the myocardium is increased but before we deal this area in detail that what are the causes which lead to reduce oxygen supply I would like to clear your concept related with concept of ischemia and concept of isolated hypoxemia isolated hypoxemia either two slightly different conditions both can lead to screaming heart disease let me explain let's suppose this is your left ventricle and he the coronary artery which is supplying the blood now ischemia mean there's reduced blood flow let's suppose that here is a throttle or notic block there's a fixed obstruction so naturally when there is a thorough signal erotic plaque here at the blood flow to distill to this plaque is reduced right when perfusion to distal dependent myocardium is reduced we say there is this Kimia and ischemia has three features number one this reduced oxygen supply but not only oxygen supply is reduced to the dependent area but there's also reduced other nutrients which are required by the myocardium schemas three component number one of course when blood supply is reduced this reduced oxygen supply number two there is reduced other nutrients right that other nutrients are also reduce other than oxygen right and not only other nutrients are reduced it is one more problem yes what is the third problem in patient with its skinny or hyper perfume there is another serious problem again suppose there is a fixed obstruction here due to a specific erotic block not only oxygen supply is reduced but other nutrients like fatty acid then glucose and other important substances which are required by the myocardium for the healthy function they are also reduced but there is one more problem with their dependent myocardium yes what is that problem please let me know what is their problem there is yes only very good doctors no answer to this there is impaired washout of metabolic wastes because this is one more function of the blood flow the reduced reduced washout off washout off yes metabolic waste metabolic waste right now opposite to that schema has three problem if I say a piece of myocardium is under ischemia it means perfusion has been relatively reduced is that right and due to that not only oxygen is less but other nutrients are also deficient along with that there is impaired washout off reduced washout off you can say metabolic waste from this area so this is a double problem oxygen and nutrients reduced and accumulation of waste product right so skinny is more dangerous than simple hypoxemia in case of simple hypoxemia in case of isolated hypoxemia hypoxemia what is the real problem in case of isolated hypoxemia yes only oxygen supply is reduced only oxygen supply is reduced but other nutrients are being supplied to the myocardium well and removal of the waste metabolites is also okay right due to this reason now what are the conditions in which there is isolated oxygen deficiency of course there must be some conditions in which blood flow to the myocardium is relatively normal but the oxygen carried by the myocardium is very very less the classical example here we can put yes yes so we are anemia if some patient has very very severe anemia mo globin may be only 3 grams per DL blood flow may be normal blood flow may be normal other nutrients coming to the myocardium may be normal removal of the waste product may be normal but still oxygen supply is less is that right so patient will develop and severe cases some of the manifestations of ischemic heart disease right or yes so we are pulmonary diseases you know and severe pulmonary diseases if blood is not getting oxygenated well the blood is not getting oxygenated well then again there is hypoxemia right carried by the blood is less in case of anemia oxygen carrying capacity of the blood is reduced and in case of severe pulmonary diseases oxygen carried by the blood is reduced this is the right and another condition which is related like this and that is due to cyanotic heart disease cyanotic heart disease and cyanotic heart disease for example when there are shunting of the blood within the heart and right-to-left Shanter so I'm not so generated blood goes to the left side and mixes with the oxygenated blood then in arterial tree oxygenation level of the blood will be reduced now look what I'm saying that this is a piece of myocardium right this is a piece of myocardium now this piece of myocardium if there is some reduced blood flow it will develop a true ischemia with three problems or if blood flow is going normal but either oxygen carrying capacity of the blood is reduced or oxygenation in the blood is reduced partial pressure of oxygen right then patients will develop only deficiency of oxygen so what is the difference between condition number one and condition number two condition number one is more dangerous of condition number two is more dangerous yeah what did you think role condition number one is more dangerous or condition number two of course this is more dangerous that is why when someone has reduced perfusion his Heat well as more serious ischemic heart disease complications right but someone with isolated hypoxemia usually this has less deleterious effects less dangerous effects so this concept clear right that it's not a matter of only oxygen supply it's a matter of oxygen supply plus other nutrient supply plus matter of removal of waste product is that right so that is why ischemia is more dangerous than the isolated hypoxemia emmaclaire now after developing these two concepts let come let us discuss why a piece of my Guardium may be ischemic what could be the reason right what could be the possible mechanisms and reasons and causes off skinnier to a piece of myocardium we have already discussed that phase of the problem is what either there is reduced oxygen supply and if there is a schema of course problem is not only just reduced oxygen supply but this reduced other nutrients plus this reduced washout of the metabolic waste and with that it may be coupled with another problem and that is increased oxygen demand this is that right now first we will deal with this ring what are the conditions which lead to reduce blood flow to the Mayo Cardale right so let's suppose I draw the left heart here okay tell me one thing that is commit heart disease more commonly involved our right heart or left heart ischemic heart disease more commonly involved left ventricular right when cheater every good doctor should answer without thinking it must be left please right if you read it 30 time and you don't know it's very bad write it down to spare a full page and then go to the other page on one full page only right this thing ischemic heart disease mainly 99 percent cases involve the left ventricle why okay we'll go into causes late this concept should be very bit concept that schema card these 98 99 percent of the cases mainly involve the left ventricle while affronti will suffer more why left ventricle suffer more there multiple reasons for that number one Larrin Chico has thickness of about one point five centimeter and right ventricle has sickness off point 3 2 point 5 centimeter so this is one thing their right ventricle has reduced oxygen needs it is less thick never entacle has increased oxygen needs or blood profil needs this should be very clear left ventricle why because right ventricle is thin left ventricle is thick then even right ventricle you know when ventricle is contracting it squeezes its own capital raise look here let's suppose this is the left ventricle here and let's suppose here is the right ventricle here now listen there are capillaries in the left ventricle eople is in the left ventricle and there is a Triple E network in the right ventricle of course now left ventricle has to build the pressure from 0 up to 125 millimeter of mercury and right ventricle has to build the pressure up to maybe 0 to 25 millimeter of mercury so which ventricle is working more hard left so it means when left ventricle will contact strongly it will secrete its own capillaries and it will squeeze its own people in network or it will squeeze its own micro circulation very strongly and right ventricle when it will contract at the peak of contraction it will squeeze its own micro circulation less severely are you understanding that when both ventricles contract left ventricle has to generate higher pressure so there's higher tension produced in the left ventricular wall and there is less tension produced in the right went into a wall so left ventricle muscles suppose these are the muscles of the left ventricle and this green is the capillary so naturally there's more tension produced by the left ventricle of muscle so left ventricle Kapil is the sorriest for more strongly disagrees so strongly that during systole no blood flows practically no blood flows through the left anterior this is very important concept because all the body tissues are receiving the blood during systole all the body tissue receive more blood during systole but left ventricle itself which is responsible to produce the systolic pressure so queasy the strangulate so its own blood supply and when it is producing such a high tension units of all right even though it's providing the blood to the whole body it stimulates its own blood supply and makes it very very very vulnerable to ischemia opposite to that it's strangulated blood supply less strongly if it's strangulation its blood supply less strongly it means right when turtle is going to be risk less this is that right so another reason is that it produces less tension in its wall less tension involved and voila right ventricle I mean there's more tension generate state pension generated in left ventricular wall now what are the importance of this tension if there's less tension in the right ventricular wall it is Julie zero to twenty five millimeter of mercury and tension which is generated in left ventricular wall that is 0 to 125 millimeter of mercury am i clear to you is it right now listen if there's less tension produced on this there is less work there is less work if there's less work it means it needs less oxygen right when there's less tension in the wall of the right ventricle right so this is doing less work so it's oxygen requirements are less and when we go to the left side what really happens the cause on the left side tension generated in the left ventricular wall is more so there is more work and if there is more work that will lead to what more oxygen needs more oxygen needs am i clear so now look at the very basic thing requirement of oxygen on the right side are less and of a requirement of sisian on the left side up more at the top another tragedy right side it squeeze it squeeze is so qui this it's on micro circulation micro circulation with less tension with less tension right so it appeared this own blood flow less but when we talk about the left side what really happened that left front recall during systole during systole it impedes and beads its own its own micro circulation micro circulation with more yes plays with more tension so it means that during the systole here there is less oxygen sub there is as compared to the left as compared to the left during systole right side has more oxygen supply because they're less strangulation of micro circulation and here there is less oxygen supply now you look at the basic formula the left side has to work it is thicker side if it is thick it needs more oxygen number two it has to build more tension again it needs more oxygen at the top it's aqueous blood supply so do two so Queens on its own blood supply that will lead to what type of problem reduce blood supply so left side has more demand of oxygen as compared to the right side and it impedes its blood supply more then as compared to the right side so left heart is far more vulnerable to skim it heart disease as compared to the right side rather here is the very important point we should remember that blood flow through the left ventricle is mainly during die why because when larren Lyttle relaxes right and during the - li pressure is about 80 millimeter of mercury in the aorta you know during systole pressure here is 120 and during - Li it is 18 but doon in Sicily when aortic pressure the high during systole when aortic pressure the high these vessels are too much constructed microcirculation so in spite of high pressure in yoga and high perfume pressure and coronary system higher filling pressure in coronary system you can say micro circulation of left is so much wheezed that it cannot really serve the ventricle that is why left ventricle write it down from an earthly left ventricle receives its blood supply only during - ghastly but right ventricle the seals blood supply during diastole as well as Sicily because systolic pressure in aorta is really very high and still during systole and diastole both right when she token get some blood her left ventricle needs more oxygen but unfortunately it impedes its circulation more effectively and due to their freedom left ventricle is more vulnerable to skin make heart disease that is why in 98 99 percent of the cases when we are talking about this gimmick heart disease we are talking about the myocardium of the left ventricle only one to two percent of cases right ventricular Escamilla may occur especially when there is right ventricular hypertrophy for example in cor pulmonale pulmonary hypertension and right when it'll become really very much hypertrophied then it also depends develops the risk for ischemic heart disease hugely ischemia to the right ventricle occurs when right ventricle is hypertrophic and Julie it occurs when blood flows right coronary artery is reduced because right coronary artery supplies the right ventricle right so this is the basic thing that now next time if someone asked you that when we are talking about ischemic heart disease it more often involved left ventricular right ventricle what will be your answer it is left ventricle right now I will discuss that what are the conditions right which can lead to reduced blood flow to when Chiklis pose here is your coronary artery ostium and this is coronary artery which is supplying the ventricular tissue is the right this is coronary artery with its branches now I will draw this artery in a big way here and we'll see how the blood flow through this can be reduced and how the oxygen supply within this can be reduced so I will draw it outside next suppose this is coronary artery ostium and this is yes now you imagine this is a big coronary artery area which we have removed from the heart this is coronary vessel now we have to see this is supplying the myocardium all around it has myocardium we have to see what can go wrong with the SCARA artery and blood supply it to the myocardium can be reduced is that right first of all we'll talk about the most important cause most important causes atherosclerosis in the coronary artery at Roma formation and coronary artery you know at four miles what I throw my eyes fibro fatty plaque farmed in intima is that right so in the intima of coronary artery fibro fatty fatty plaque may be made right and these plaques are called at from us and this disease is called atherosclerosis this is the most important and most common cause of ischemic heart disease the other causes also I will discuss them of course now what really happens number one a trauma may be a simple look here this is an okay here let's suppose in the intima this is fibro fat accumulation this is the trauma now truly speaking you know the structure of a trauma that it should have of course dysfunctional and the thulium on it and atheneum which is there at the top of the trauma is disturbed so it has dysfunctional endothelium on it number one number two it is having a fibrous cap and this fibrous cap right this fibrous cap consists of smooth muscles right this fibrous cap consists of yes plays smooth muscles right and with these smooth muscles yes what else it has it has lot of collagen right this is the collagen this is the fibrous cap so move muscles and macrophages may also be there and some collagen is there right now this is a fibrous cap under this there are forms health foam cells are just large some smooth muscle which are eaten up lot of so lot of lipids these are typically thrown one drying so these are the smooth muscle and macrophages which are present in this area and the smooth muscle the macrophages have engulfed a lot of lipids and this is lipid core inside extracellular lipid and connective tissue and here is some new vascularization new vessels develop at the shoulder of the block now this is a typical block does it right sometimes what happen in some patients blocks keep on going over here the years and years and years in coronary artery v the precursor lesions like fatty dots and fatty streaks they start forming very early around the ten year of age and almost all $1 cents have some fatty streaks in their coronary arteries is that right but clinically they become they start manifesting the problem in the age of 40 and plus usually now this is block one way the problem will start then this plaque will keep on growing right and this they will offer an obstruction to the blood flow and if these plaques are offering an obstruction to the blood flow such blocks are called stable because they are not rupturing they are not fitting these are not undergoing any complication we say these plaques are stable but they are offering a fixed obstruction to the flow why I call it fits obstruction because when there's arteriolar dilatation can this point of the plaque can dilate which is fibrotic now so we could say that a truly this block may be a stable uncomplicated stable thrown through meters block and this a--throw metastable aromatisse block is acting as a fixed obstruction fixed obstruction is there right now this fixed obstruction is at early stages does not produce ischemia fixed obstruction does not produce ischemia in the beginning when you start producing ischemia to produce a schema it has to block the lumen up to 70% if up to more than 70% luminal obstruction luminal obstruction is there right it will lead to look for example if one person coronary artery is almost 70% obstructed and 30% blood flow is going this 30% blood or 25% blood which is moving through this unobstructed area is enough to meet the requirement of myocardium during rest so this person will not develop this Kimia during rest scheme iya will develop only during increase demand so tsukimiya will develop usually this is angina pain right so scheme iya will be there this Kimia and it's related syndrome are only during yes increased demand of oxygen when oxygen demand is increased when person is having Achrekar dia is right when person is having hypertension for example or person is exerting let's suppose this person who has more than about 70 percent of the luminal obstruction this person who has 70% of the luminal obstruction if you go upstairs normally what happened when you do some physical exercise for example you go upstairs or you walk or some other physical exertion what really happens heart needs more oxygen hardest work more right cardiac output will increase during the insertion if cardiac output will increase it means ventricular myocardium has to work more if ventricular myocardium has to work more what does it mean it will produce whether dilators in healthy heart and coronary vessels will dilate to provide extra blood but a person who has obstruction like this can he die late at this point no so when he will Doozer Chien increase demand will not be met by just 30 percent unobstructed area and person will develop relative ischemia and this is kim IAM a clinically manifest as angina this is the right we'll talk about later in detail what is in China but what I'm saying is skimming skimming problem will develop whenever this person has increased demand right but during the rest phase you may not have any problem but if someone has obstruction about 90 percent luminal obstruction it's the fixed obstruction someone has up to 90 percent of the vessel caliber obstructed then what will happen he will develop ischemia even during the rest ischemia even during rest right so bouts of it's fixed obstruction you must remember two points that there's a stable block and it is progressively becoming more and more fibrotic and it is progressively becoming larger over the years and years and years usually patient will develop symptomatic problem when more than 70% of the lumen is blocked around that time person will develop ischemic problems when hard demands more oxygen for example during emotional crisis you know Rena lien is released heart rate is up and you need more oxygen or during desertion but if this obstruction comes near around 90% then even patient during the rest may feel what problem Kamiya and he may develop chest pain is that right is it clear now so some patient have ischemic heart disease due to stable aromatase block in the coronary which are acting as fixed obstruction now I will talk about more dangerous situation in which obstruction is not fixed fifths obstruction makin word into dynamic obstruction fixed obstruction may convert into dynamic obstruction and these are the people you have to be very careful of later on I will tell you this fixed obstruction is a hallmark lien of typical angina because the definition of typical angina is that in general like symptom occur with exertion generalized symptoms develop when there is tachycardia or when after the meal right we'll talk about that in detail so in classical angina or in typical angina or in stable angina the underlying leonis yes plays stable Lian's is that right now this was stable block stable block now we'll talk about stable block leading to yes fixed obstruction now we'll go to the one next step fixed obstruction sometimes what happen that in some patient block is not stable block is not stable what really happens there look for example again this is another block okay even if it may not be as much of struct in this is very wrong concept among the doctors you know some young doctors think if stenosis is more it is more dangerous block but research has told even the plaques which are moderately obstructive may be very very dangerous because these plots may be having a composition like they have less fibrous less and thin fibrous cap right and this type of block undergo dynamic changes and dangerous changes rapidly these plugs are not stable so this is a wrong concept doctors jung-hoon think that the plug is producing nine eighty percent obstruction it is very dangerous actually some plaques which are producing only forty percent obstruction can be very dangerous because they undergo dynamic alteration now let me tell you how they can undergo dynamic alteration look one thing is first of all let me tell you which plots are not stable the plots which have lot of extracellular fat number 1 number 2 we can say dangerous blocks you make ahead in dangerous plants or vulnerable plants right plus not to be trusted trusted at all right this plot can be trusted to some degree this cannot be why the reason means it has lot of extra solar matrix it has lot of foam cells look here it has lot of foam cells but fibrous cap is very thin fibrous cap is fibrous cap is very thin this is one problem number two it is more foam cells number three it has more macrophages it has more these are the naughty happy but making trouble for us what are these yes macrophages the plaques with more lipid plaques with more foam cells and plots with more macrophages are highly unstable plugs right and these plaques are vulnerable to severe disruptions these plaques are vulnerable to severe disruption let's compare the block number one with the block number two the plot number one has a very thick fibrous cap it is a very thin fibrous cap it has less what is this foam cells it has more foam cells it is less macro features this has more macrophages is that right and this is having less fat and that is having more fat right so what is really happening that this type of block is vulnerable bloc vulnerable to what vulnerable to disruptions versa vulnerable bloc vulnerable block main vulnerable to what to disruptions acute disruptions it may undergo at any time never to be trusted acute disruptions is that right now what type of a cube disruption can occur there right what kind of acute disruptions can be their number one block may undergo I will make this block here lock may undergo fishing okay simple thing erosions and ulcerations rahman irr GUI revisions or alterations or more dangerous complication as that it may be disrupted so much that it may undergo fishing fishing and rupture and let me tell you what is the difference in these two group of problem erosion and alteration are different problem fish ring and rupture is more dangerous problem let me tell you exactly you know this is the basement membrane and over this what is this this is endothelium which is dysfunctional and this is the normal address area now and this is that let's suppose lipid material is that right if and the trinium is damaged and removed from here and underlined thrombogenic basement membrane is exposed then it is a rayon or alteration if endothelium is shaved off removed of course there's no raiser there it is removed right and if endothelium is lost from here and underlying basement membrane of intima exposed is the right and this basement membrane is highly thrombogenic right it will attract the platelets and platelets will start sticking over there late lead will develop at hands we will talk about this particular problem later but it is so much an exposure of sub endothelial collagen of the basement membrane then it is a rayon that alteration but if problem becomes so severe that damage goes deeper and this is sub what is expose now highly thrombogenic intra plaque lipid material when within the plaque lipid like material is exposed is the right to the blood this is called fresh ring if it is very narrow or if a big area then it is called rupture is that right so it means one thing will be common in fishing and rupture that whenever fishing and rupture is their problem has gone beyond the basement membrane and even underlying what is exposed a fat cholesterol material and other intra this area so if again let me repeat this is endothelium which is dysfunctional if only dysfunctional endothelium is a last this is erosion then alterations and if with the endothelium basement membrane is also lost and even this material is exposed then it is fishing and rupture but both conditions are something common in both conditions platelets will stick on that this is the right and when platelet will stick what will happen let me tell you let's suppose this is the area this is exposed now these are the platelets which will stick and when platelet are sticking to this exposed area we call this a deplete let adhere in reaction reaction number one is yes what is happening to this platelet platelet are becoming adherent should I make a larger diagram so that you can understand okay platelet at here when platelets stick to non platelet surface the is called platelet adhere and late let's stick to non planar surface this is called platelet at here already and ruthenium was dysfunctional dysfunctional endothelium on the block does not produce nitric oxide it means it does not repeal the platelet and now what really happens platelet will stick after platelets stick over here these platelet will start releasing these platelets which are sticking there they will start early in yes please can you tell me what will they release they will release more platelet aggregating factor they will release ADH which will call more platelet they will release 500 slipped amine they will release yes epinephrine they will release procoagulant substances Pro coagulant some of the coagulation factors and they will expose and not release but expose you can say platelet factor 3 & 4 which help in coagulation now look when platelets stick to Nam plate red surface they undergo what is this reaction a DM reaction and it here will lead to release reaction release reaction will produce the product which will attract more platelet which will attract more platelet then next line of platelet will undergo release reaction and more platelet will come now platelet are sticking to the platelet when platelets stick to the platelet this is called platelet aggregation please focus here that when this first layer of platelet this one this first layer of platelets stick to the non platelet surface and this layer is shown at here but second and third layer are sticking with the platelet where platelets stick with each other the term uses platelet aggregation so it means wherever there Aronian the ulcerations or whenever there efficient or rupture there will be platelet adhesion platelet release reaction platelet aggregation and eventually a platelet aggregate will be formed what are this platelet aggregate or they form so it means that this vulnerable plaque may undergo what type of complications this vulnerable plaque may undergo yes erosions and alteration or they may undergo fishing and rupture right these are two group of complications or disruptions and this and after this disruption one more problem occur there is in addition to that there is platelet later let Eddie hand release reaction and aggregation so platelet plug platelet aggregate is form agree gate is formed you think it's a good development of bad development they had develop and now this stable clock is totally unstable now the stable clock is becoming what type of block disrupted block and this acute change in the block or disruption in the block that has led to ruins or alterations of fitting or rupture that is leading to platelet adhesion and release reaction and plated aggregate formation is that right some people develop only platelet aggregation and some unfortunate people the tissue factors are released and at the top of platelet aggregate what is this process College what is deposited fibrin is deposited and fibrin deposition result from what process of coagulation now let me tell you there's a difference in platelet aggregation and there's difference in coagulation many people confuse that let's settle it once for ever platelet aggregation main plate let's stick to each other and make a small mass this is platelet aggregation and let's define coagulation write it down coagulation is conversion of coagulation processes the conversion of soluble fiber Imogen soluble fibrinogen and two insoluble fibrin you must be knowing coagulation cascade is it right intrinsic pathway of coagulation and extrinsic pathway of coagulation all those paths wait in the end have common thing what is the common that all coagulation pathway in the end convert the insoluble fiber Nina Jane sorry soluble fiber Imogen they convert the blood soluble fiber Imogen into insoluble fibrin strands right and when these fibrin strand deposit on the platelet plug we say now coagulation has occurred at the top of platelet plug so it's the two different thing one is platelet plug other is coagulation so in some patients is only platelet plug formation and in some unfortunate patient at the top of the platelet plug this deposition of fibrin and we see at the top of platelet plug there's coagulation process also and when platelet plus platelet plug plus coagulation both things are there we call this situation from bus and both of them are there we call it thrombus so what we'll write here that there may be trumbo from bus as well from bus as well right now look at these dynamic changes now look at these dynamic changes which kill so many people you see you see in USA every year how many people suffered with myocardial infarction 1.5 million people every year suffer with myocardial infarction and half million of them every year die half million people die due to such things so you must know as a good doctor what really really happened at Salander level molecular level at block level and vascular level which really kills the patient so commonly you know in the world every minute one person died with myocardial function every minute not one rather not more than one right so again let's come back so what is happening I told you that plaque may be stable at throw meters plaque may be classified as stable plaque or these may be plaque with acute changes acute changes or we call it acute disruptions and of course of them like the word of dynamic that it has become a dynamic block and dynamic block is like a dynamite o'clock it's like a dynamite it will really kill many of the patients right why this dynamic plaque which is undergoing acute changes what are the cube changes we have already discussed yes first there was erroneous and ulceration other group was yes pressuring and yes rupture right there is another acute change I did not discuss I think it's worth discussing another of Q changes that sometimes the vessel at the margin of the plop I told you they're new vessels formation at the margin o clock these new vessels why these are forming these new vessels are formed because platelets are releasing growth factors smooth muscles are releasing growth factors macrophages in the plaque are releasing growth factor and those who sell the releasing growth factor so all the cellular player in the plaque are releasing growth factors and these growth factor lead to growth of the endothelial tubes from small ways of Azzurri and these endothelial tube which grow towards the plaque is a very bad news these endothelial tubes are not well supported by collagen these are not mature blood vessels this newer neovascularization is a very weak was polarization with the little irritation they are with little stress these vessels can rupture and if these vessels rupture they will lead to what trap lock hemorrhage they will lead to entrap lock hemorrhage and flock will simply balloon up do you think it's a happy news this is one balloon you should be afraid of as they write that sometimes in the plaque there's in crop block hemorrhage and when intra plaque hemorrhage occur plaque simply Atromitos block simply swell up and when it will swell up it may produce severe acute obstruction of the coronary artery this is the right now why intra Plock hemorrhage occur please write it here there is one more complication and which you should not forget intra yes block hemorrhage youth this is also cute change you never know at what time in your life one of the block and coronary artery undergo hemorrhage and if I block undergoes hemorrhage it's a very very bad news so what are the bad news here erosion then ulcerations fissures and ruptures and intra plaque hemorrhages these are the three group of acute changes in the block right now erosions and erosions and fissures they can lead to platelet plug at the top platelet plug or if person is really unfortunate there may be our full thrombus formation thrombus formation and it will these two platelet plug formation or thrombus formation will dynamically obstruct the lumen very rapidly does that right they will rapidly reduce the lemon size secondly why we call them dynamic changes look here why we call them dynamic changes why because when platelets are binding there they may be less platelet there may be more quiet lat just the right sometimes in the beginning they are less with the time they become more or if you have given some fibrinolytic drug or antiplatelet drug maybe thrombus or the platelet may wash away does it right so when you can give no listen why we call them dynamic changes because these are not stable either they spontaneously change platelet plug my form and disperse or they even thrombus sometimes in some lucky guy's even thrombus may go into thrombolytic process naturally this is it right so this is a dynamic change or in some unfortunate platelet plug may convert into thrombus and thrombus grow more and more and become occlusive thrombus is that right or thrombus made attached and may lead to embolization it is quite possible this thrombus which has been made here look here this was a thrombus right okay let me draw it this is the thrombus this is quite possible the thrombus may detach and may go to smaller vessel and block it here very happy to it has traveled something but it may produce fear problem right this thrombus so it is there dynamic changes which are occurring that later plug may form and dynamically obstruct plate thrombus form dynamically obstruct are become truly dynamic that it become detached embolize and this thromboembolism may block some other this distal part of the artery is the right and then of course intra proc hemorrhage is also dynamic do you think a plaque which has hemorrhage inside it it is stable clock no it is dynamically ballooning up another point to remember that dynamic intra plaque hemorrhage may be from within the plaque or sometimes after some fish ring some fish ring here blood may enter from this area and if blood is entering from this area intra plaque am bridges occurring from the luminal side so intra plaque hemorrhage may occur within the plaque or blood may seep from the liberal fissure into that under both condition it is good or bad it's very bad another point which I would love to highlight is that what is the point in the block where the plaque ruptures most often which is the point where the plaque ruptures most often first of all it's worth repeating which blocks are vulnerable which blocks are vulnerable blocks which are with moderate obstruction blocks with thin cap plots with more fat lipid and plaque with more foam cells and plaque with more macrophages because macrophages produce metalloprotein nez's with digestive either fibrous material and make the block weak and make the block more susceptible to hemodynamic stresses the intrinsic factor related with the block the structure of block is more vulnerable now question is that which part of the plaque is most vulnerable of course not the cap at the edge of the cap so easy to understand you need common sense you know tear the plaque with a camp right now gap is thinnest this is the cap of the block now you tell me where this cap is thinnest at the margin at the ends or it is thinner at the middle margin so that in a through circular block most often the rupture where the cap is meeting the normal arterial wall there are two reasons for this number one the minimum fibrous tissue here is the weakest point of the block at the top you need macrophages the entering from this point and these macrophages may be producing metalloprotein ages and digesting away at the top most sheer hemodynamic stresses also here blood is moving like this and here too thus obstruction it will love to a wealth it from here so next time if someone asked you that what is the point in the block which is most vulnerable to rupture the same most vulnerable point is the junction of the block with the normal arterial side it does not really rupture from the middle it ruptures from the ends where the plaque edges are meeting with the normal arterial wall why it is happening so because there the fibrous cap is very very 10 and macrophage activity is more and here I should give you some good news you know there are lipid lowering drugs statins they have wonderful drugs statins and put a tick mark with them the one thing which every good doctor knows other thing only a few good doctor know the thing which everyone knows is the statins reduce the cholesterol level everyone knows there's no fun in telling you people you are so intelligent everyone knows that statin reduce what cholesterol level and of course when statin are reducing the cholesterol level cholesterol entering in the plaques is less then foam cells are less so plug becomes stable I told you the plaque will become more vulnerable when they have more lipid and more foam cells and if you are taking statin if you are giving your patients statins regularly when his cholesterol levels are low then cholesterol supplied to the plaque is also low and if they're less cholesterol coming to the plaque then it's very natural to understand that intra plaque lipid will be less and of course intra plaque forms has will be also less this is what every doctor knows but only very good doctors know statins drug have and inflammatory reaction on the block write it down statin drugs have anti-inflammatory action on the clock what does it mean that if statins can inhibit the inflammatory activity in the block block will become more stable or less stable most ever there will be less inflamed because inflammation in the block made the block very vulnerable this is that right so straight in the wonderful drug not only they reduce the lipid and n help instability of the plaque but they also inhibit that and from michi process in the plaques and when macrophages in the plaque become less metalloprotein disease and other destructive enzymes will become less then fibrous cap is less destroyed and plaque will become more stable even this claim now that not only stated statins not only reduce the progression of plaque but now the believed that proper use of statin can even regress some of the plaques proper use of statins can even I will teach you these things in detail in pharmacology for a while to just trust me I'm right that stretching the so wonderful drug that not only they stabilize the plaque not only they reduce the further progression of the plaque rather taken yes regress the plaque also so very good news for those people who really know that they are in trouble and by the way look we can talk later but this is right now it came to my mind and it's again or should be written with the golden words you know platelets make the plaque very dynamic when platelets take plaque block will grow dynamically and it may remain platelet plug or made convert into thrombus is that right you know one of a very powerful factor which increases the chances of platelets to stick to the disrupted plaque one of the very important factor which may which make the platelet which favor the platelet to stick to the on to the disrupted plaque is smoking no tobacco smoke engines one of the major factor which favors the sticking of platelet with the block so if you smoke more players have more chance they will stick to their disrupted clock and you have more chances to develop more severe ischemic heart

Channel: Dr. Najeeb Lectures

Views: 330,522

Rating: 4.8863635 out of 5

Keywords: ihd, cad, ischemic heart disease, coronary artery disease, heart, myocardial infarction, heart failure, ischemia, heart attack, cardiology, heart disease, congestive heart failure, dr najeeb, dr najeeb lectures, medical lectures, armando hasudungan, usmle, usmle step 1, angina, cardiovascular disease, clinical medicine, medschool, medicine, medical school, chest pain, signs, symptoms, treatment, pathology, khan academy medicine, internal medicine

Id: oQ235E1gvrU

Length: 59min 20sec (3560 seconds)

Published: Thu Dec 06 2018