Coronary artery anatomy:-

Transcription

1 ISCHEMIC HEART DISEASE- CORONARY ARTERY REVASCULARIZATION We will talk about coronary artery bypass grafting from surgical aspects, since the subject is mainly medical, in cardiac surgery the patient come already diagnosed by the cardiologist.so the cardiac surgeon will not diagnose a patient with for example angina he will only do a surgical intervention. Coronary artery anatomy:- 1) Right coronary artery which mainly divides into: a- posterior descending artery "PDA" which gives off branches to supply the right and left ventricles and supplies branches to posteroinferior third of ventricular septum. b- LV branch. 2) Left coronary artery which mainly divides into: a- left anterior descending "LAD" the main and most important one because it gives the septal branches (branches to the ant. 2 thirds of the ventricular septum) and on it depends the left ventricular "LV" function which is the most important in prognosis.. b- Diagonal; diagonal1, and diagonal 2 c- Circumflex;Circumflex 1, circumflex 2 1 I wonder actually, its my first time to know that there's one coronary called (LV=left ventricular branch)!!!! However, I've googled for such one and from Wikipedia "The circumflex artery curves to the left around the heart within the coronary sulcus, giving rise to one or more diagonal or left marginal arteries (also called obtuse marginal branches (OM)) as it curves toward the posterior surface of the heart. It helps form the posterior left ventricular branch or posterolateral artery."

2 The most important prognostic wise of surgery is determined by the PDA and the LAD because they give the septal branches so those are the most important in revascularization. Now, Why stable, unstable angina or MI occur in patients? The base line is decreasing in the coronary blood flow but it depends on how much the limitation of blood going to the coronaries. ISCHEMIC HEART DISEASE. -DEFINITION- It is a stenosis of the CA by atherosclerosis which means narrowing of the lumen that limits the blood flow reserve to the myocardium and per se at the end the oxygen supply, the limitation occur in the blood flow reserve of coronary, so we may have a patient who has no symptoms but if we do angiogram we find for example 60% stenosis, and this because he has no symptoms in usual normal activity but if we do treadmill for him (is an exercise machine for walking or running while staying in the same place) we increase his activity and the limitation which we mean by the coronary flow reserve occurs,so the coronary reserve depends on the activity. In slides: Stenotic arteriosclerotic coronary artery disease is a narrowing of the coronary arteries caused by atherosclerosis that, when sufficiently severe, limits the flow of blood to the myocardium. Initially, the disease limits only the coronary flow reserve (the increase in flow that normally accompanies increased myocardial oxygen demands) but, when sufficiently advanced, it reduces the blood flow through the affected artery even at rest. In its most severe form, it occludes the coronary artery. Development of Coronary Artery Stenosis:- a. Focal intimal accumulations of lipids, complex carbohydrates, blood and blood products, fibrous tissue, and calcium deposits, associated with changes in the media. b. The lipoid foci are associated with or converted into plaques of fibrous or hyaline connective tissue, (as a cap so if we take it in size it will be larger ) although at least some atherosclerotic plaques may result from the organization of thrombi. c. The fibrolipoid plaques may become very thick and encroach upon the lumen of the artery to produce a stenotic lesion. Probably episodically, and at times 2

3 over a period of years, new layers develop on the luminal side of the plaque, resulting in further narrowing and sometimes complete coronary occlusion. If someone made a catheterization at this stage and they found that he has 30% occlusion then after 2 months he came with total occlusion, this because he entered directly from the stages A,B,C to the complications of stenosis and one of them is the rupture of the plaque which made total occlusion or increase the degree of stenosis. d. Newly formed very small blood vessels from around and within the atheroma. Hemorrhage may occur suddenly within a plaque, and occasionally this may suddenly increase the degree of coronary stenosis and precipitate acute myocardial infarction or unstable angina pectoris, or the complication occur as a rupture instead of hemorrhage which also increase the severity of stenosis, if not entered the complications there will be something like a scar and healing of the plaque which is the next stage(d). e. Gradual regression of plaque swelling seen clinically as regression of stenosis in a few patients and the development of collateral coronary blood flow can result in at least partial spontaneous restoration of regional myocardial blood flow. (This is a physiological response so if this stage is not found then all atherosclerosis will reach to the end in its result). f. Thrombosis (on of the end stage complication but may occur earlier) occasionally complicates the coronary arteriosclerotic process, generally when there is luminal narrowing. Sudden complete obstruction may result, and it's generally now agreed that acute thrombotic occlusion is the genesis of acute MI in most patients. Rapid recanalization frequently follows this process. So as a summary the complications of atherosclerosis which make a sudden increase in CA dis. :- 1. Rupture. 2. Newly formed BV that cause bleeding and hemorrhage around. 3. Thrombosis. When the atherosclerotic becomes will formed it will act as a nest that cause Platelet aggregation within the lumen of an already narrowed coronary artery which may induce the thrombosis or may per se suddenly narrow the lumen and provoke an acute MI or unstable angina. Platelet aggregation may play a role in the development of the atherosclerotic plaque itself. So this is the targeting of cardiologist (platelet aggregations because the platelets play a role in the acceleration or deceleration of the process) in conservative management to prevent the progression of atherosclerosis which is already found, so we give the 3

4 patient aspirin and plavix (clopidogrel) which is more important than aspirin. (Moreover, platelet aggregation releases thromboxane A2 and extremely potent vasoconstrictor). Atherosclerosis is a generalized progressive problem that may be found in carotid in abdominal aorta in lower limb and it does not stop in a limit but is progressive during the yrs. IF the patient developed a significant CA stenosis this will decrease the oxygen supply so the result will be either ischemia which is reversible or MI which is irreversible, and the prognosis depends on which result. The healing process of MI-or what we call post MI remodeling- ends with fibrosis and scars which leads to left ventricular aneurysm because the fibrous scar is weak area in the heart, so when the heart goes into systole this area will be seen by ECHO.while during the diastole there will be paradoxical movement.

5 NOTE: the following slides were skipped by the doctor only saying what is written above so it's up to u whether to skip or to read Myocardial Infarction and Its Morphologic Sequelae:- *When myocardial blood flow is sufficiently impaired in relationship to myocardial oxygen demands, myocardial necrosis occurs. The resultant infarction may be subendocardial and not involve the entire thickness of the ventricular wall. In its most extreme form, subendocardial infarction may be diffuse and result from triple- vessel disease, but more often subendocardial infarcts are regional and result primarily from the stenotic lesion in one or two vessels. *A transmural myocardial infarction involves the entire thickness of the ventricular wall. It is usually the result of a sudden increase in luminal narrowing or the complete obstruction of the artery supplying that area, or a sudden generalized increase in myocardial oxygen demand in the presence of a severely stenotic coronary artery. (Most so- called transmural MI are not homogenous but contain islands of viable muscle of varying number and size). *The process of MI is complex. Animal studies indicate that some myocardial cells die after 20 minutes of complete coronary occlusion and that after 60 minutes there is extensive myocardial cell death.. (Controversial). However, probably within minutes of the onset of the episode of acute ischemia, some reperfusion occurs within the ischemic area of myocardium, particularly in the border zone. If this spontaneous reperfusion occurs within 3 to 4 hours, the amount of necrosis is restricted; infarct size is reduced; and mortality is decreased. Spontaneous reperfusion can lead to hemorrhage, edema, and ventricular electrical instability. Healing of the acute MI leaves a scarred area of myocardium. In most cases, this scarred area is a mixture of fibrous tissue and viable myocardial cells in varying proportions. When the scar is virtually all fibrous tissue, it is usually large and termed a left ventricle aneurysm. These morphologic changes may be self- aggravating because of their effect on the circulation to the subendocardial layers; repeated infarctions may occur and add still more scarring. In aggregate, myocardial scarring leads to LV systolic and diastolic dysfunction and, ultimately, if the patient survives long enough, to the syndrome of chronic congestive heart failure with elevated right atrial and jugular venous pressure, hepatomegaly, and fluid retention. (Patients with severe LV dysfunction commonly die of another infarction or of sudden ventricular fibrillation).

6 Arteriosclerotic Plaque Rupture and Thrombosis(the dr. skipped saying he talked about previously) Relatively new information has emphasized the dynamic nature of the coronary arteriosclerotic plaque as a fundamental feature of coronary artery disease. Fissuring, or rupture, of arteriosclerotic plaques is probably the genesis of the acute ischemic episodes termed unstable angina and acute MI. When this phenomenon develops, mural or occlusive coronary thrombi often coexist and contribute further to the development of the unstable states. Coronary stenosis that produce less than 50% reduction in diameter are commonly the site of the atherosclerotic plaque rupture that precipitates unstable angina or acute MI. This may be the explanation for the infrequent need for PTCA(Percutaneous Transluminal Coronary Angioplasty) or CABG (Coronary Artery Bypass Grafting) soon after successful thrombolytic therapy for acute MI, thrombolysis leaving the vessel with a noncritical stenosis Certain arteriosclerotic plaques appear to have a higher prevalence of plaque rupture than others. They are characterized by relative softness and contain a high concentration of cholesterol and cholesterol esters, and their lipid pool tends to be situated eccentrically. Rupture is though the cap of the plaque, and areas in which the cap lacks underlying collagen support seem particularly vulnerable; So If a patient comes with unstable angina and was diagnosed to have CA disease, patient might ask why to do surgery? Is to cure completely? No since the atherosclerotic process is progressive even those vessels transplanted can become diseased, so what are the surgical indications for CA revascularization???

7 Surgical Indications for Coronary Revascularization:- To do intervention (surgery or stinting) means we have significant stenosis ((in surgery significant means 50% +" 50% or more" of the diameter that you see by eyes)) 1. to protect the myocardium from MI because the patient is with stable angina so if we left him he will have in the end stage massive MI or what so called killer MI, he will die. 2. To preserve the left ventricular (LV), if the patient has a good LV function with stable, unstable angina or acute MI that still does not affect the main bulk of the myocardium, we have to do revascularization quickly to protect the other parts of the myocardium. 3. To improve the quality of the patient from the pain (improve exercise tolerance). 4. to relieve ischemia and the symptoms of angina, prolong survival. The conflicts now between surgeons and cardiologists is which is better to do surgery or do stinting??!!!!!! Several studies have examined the relationship between the extent of CAD, the relief of angina, and improvement in survival, to determine the relative benefits of medical, percutaneous therapeutic, or surgical management. Results of these studies are used to determine which patients are appropriate candidates for bypass surgery. Factors That Must Be Evaluated In Patients Being Considered For Any Form of Management:- 1. The degree of symptoms. 2. The presence of associated medical problems to see the prognosis and mortality (in cardiac surgery in the operation we are talking about 2 major things stroke and mortality,we have straightforward 3% mortality which is not a small percent,in stroke depending on age may reach 8% ). 3. A determination of the physiologic significance of coronary disease (evidence of reversible ischemia.).

8 4. Documentation of the angiographic abnormalities of the CA. 5. Assessment of left ventricular function which is the alarm of the prognosis. How to diagnose a patient with unstable angina, or MI medically?? 1- ECG. 2- Cardiac enzymes and the most important is Troponin T (within 3-4 hrs it starts to increase, so if you suspect MI and in first hr it is not elevated then CCU care and measure it again after 4 hrs, it should be started to increase, its peak is after 6 hrs). If patient comes stable with not significant chest pain we do:- 1. Treadmill 2.ECHO Now if we have a patient with poor LV function (poor ejection fraction) we have to know whether it is due to ischemia or MI, because if it was due to ischemia then those are the best for surgery or stinting since we will improve the ejection fraction then better prognosis, nowadays we do Radionuclide studies and PET (positron emission tomography) only for those with poor LV function because those are at high risk and high mortality, to determine whether the myocardium is viable and might improve or dead because always even when PET showed that most parts of heart are dead,still there are some viable islands of viable tissue between the scars, if we do revascularization will improve, but if it was dead then no need to surgery since we will no improve the ejection fraction. AGIN THOSE WERE SKIPPED, SINCE WE WILL TAKE THEM IN INTERNAL. So JUST FOR THOSE INTERESTED... Severity of Symptoms:- The majority of patients with CAD come to medical attention because of angina. It should be determined whether the patient has stable or unstable angina, two conditions that have a different prognosis with medical treatment. Chronic stable angina refers to a pain pattern that has been stable for 4 to 6 weeks without significant change. The severity of symptoms should be classified into the Canadian Cardiovascular Society categories I- IV. CCSC (Canadian Cardiovascular Society categories):- *Class I angina - occurs only with strenuous or prolonged exertion at work or recreation and does not occur with ordinary physical activity. *Class II angina occurs with rapid walking on level ground or climbing stairs. Walking at a normal pace for less than two blocks on level ground or climbing one flight of stairs does not cause angina, except when walking occurs during the first few hours after awakening, after meals, under emotional stress, in 7

9 the wind, or in cold weather. Class II angina implies slight limitation of ordinary activity. *Class III angina occurs when walking less than two blocks on level ground, at a normal pace, under normal conditions, or when climbing one flight of stairs. This implies marked limitation of ordinary physical activity. *Class IV angina occurs with even mild activity and may occur at rest, but must be brief, i.e., less than 15 min. If the angina is of longer duration, it is called UNSTABLE ANGINA. This implies the inability to carry out even mild physical activity. Unstable angina refers to a variety of clinical conditions of varying significance. It has been defined as the new onset of severe angina within the past 2 mo, acceleration of a previously stable pattern, or angina occurring at rest. For patients with rest angina, it is important to note whether it is occurring in the early post infarction period (within 2 weeks of an MI), within the last 48 hours, and whether angina is associated with ECG changes. In any event, unstable angina is taken as clear evidence of important reversible myocardial ischemia. Documentation of Myocardial Ischemia: -Includes radionuclide exercise testing: A radioactive substance is injected into the patient and the perfusion of the heart tissue is visualized; the perfusion pictures are done both in rest and exercise. An abnormal amount of thallium will be seen in those areas of the heart that have decrease blood supply. Compared to the regular stress test, the nuclear tests have more sensitivity (92%) and specificity (95%). Also these tests are not affected by baseline changes in the ECG. -In acute MI, the newly occluded vessel often does not have a pre- existing stenotic lesion, which is consistent with the idea that the myocardium supplied by the diseased vessel is usually devoid of important collateral vessels. -Current available information suggests that rupture of an unstable atheromatous plaque is the genesis of the acute reduction in luminal diameter often accompanied by thrombosis and platelet aggregation. How to diagnose a patient with CAD? Those coming with chest pain which may be atypical sometimes, but the classical one we know is central to the left side, jaw, neck, the other side and epigastric area, so some patients are diagnosed to have biliary colic then it appears to be MI, so patients sometimes come with sever epigastric pain, then how to know that it is MI????? 1. Symptoms (hx, exam). 2. ECG (here in Jordan for any patient more than 30yrs). 3. Cardiac enzymes (in Australia it is a routine in emergency for any patient with epigastric pain). 8

10 So if a patient comes to you with sever neck pain or a spasm it is not wrong to do cardiac enzymes because it may be MI, so you will be lucky to save the patient if he came during the first 3 or 4 hrs and here we will see the importance of hx since this pain will not respond to voltaren. For any patient comes for general surgical procedures do chest x-ray and ECG as general investigation for general evaluation. So if we suspect MI from atypical symptoms do ECG and cardiac enzymes. Coronary Angiogram: Is something seen by naked eyes, it is a simple procedure, where the cardiologist enters with a catheter through the femoral artery to the aorta going to the roots injecting dyes to the right and left,then when seeing the dyes we know the degree of stenosis since there are no measurements by instruments. When we said that the significant stenosis is 50%+ we meant the diameter of the vessel which we see on x-ray in angiography, and this means 7o%+ of the luminal diameter from inside which we don't see (the dr. said stick to 50%+ the one which we see). -so 33% is no indication neither for surgery nor for stinting only medical, same as any percent less than 50%. In addition to the degree of stenosis in left and right CA, it is important to give the ejection fraction which we judge also by naked eyes, and if he didn't make it for example due to renal impairment because we have to give a large amount of dyes for ejection fraction, then we should do ECHO for the ejection fraction to detect the LV function. 9

11 SORRY OUT OF MY HANDS BUT ALSO SKIPPED:- Coronary arteriography is indicated for patients who have angina or anginal variants, a positive stress test, and those with previous documented MI. The number of major vessels involved, the location of the stenosis, and the status of the distal vessels must be assessed. A stenosis is important when it produces a 70% or greater reduction in the luminal diameter of the vessel. An exception is the left main coronary artery in which a greater than 50% reduction in luminal diameter is important. Functional status of the LV can be determined by ventriculography, echocardiography, or radionuclide ventriculography. EF greater than 50% is normal and an EF less than 35% reflects moderate to severe LV dysfunction. Whatever the techniques used for coronary arteriography, the methods of recording and analyzing the data are crucial. A 75% cross- sectional area loss (50% diameter loss) is considered a significant but moderate stenosis, while a 90% cross- sectional area (67% diameter) loss is considered severe. -the film of angiogram is a dynamic one (moving) This is a left angiogram The catheter is going to the left, this x-ray. This is the right system with no stenosis

12 This is a significant stenosis more than 50% (about70%) in proximal LAD which can be distinguished by lateral view. This is significant stenosis in the right(very long area) -99% stenosis in proximal LAD 11

13 Medical vs. Surgical Management (SKIPPED):- Major randomized trials of medical vs. surgical management of CAD were initiated in the early 1970s to determine whether there was any survival advantage to bypass surgery in patients with stable angina. These studies demonstrated that surgery proved superior relief of angina and improvement in functional capacity, a reduction in the incidence of fatal MI, but no difference in the incidence of late nonfatal MI. It was shown that patients with left main disease or three- vessel disease with moderate LV dysfunction also had survival advantage with surgery. The advantage diminished with time due to vein graft occlusion. Application of these studies to patients undergoing CABG today requires an understanding of the limitations and exclusion criteria of each study and appreciation of the changes in medical and surgical practice that have occurred during the past 25 years. If we have a patient who needs intervention which is better surgery or stinting?? THE CLASSICAL SCHOOL INDICATIONS FOR SURGERY:- 1. Failure of medical therapy. 2. Unstable angina but after proving that the patient has significant stenosis. 3. Left main CAD.(now they are trying to put a stint) 4. Symptomatic three vessels CAD (triple) with depressed LV function. 5. Postinfarction angina. 6. Acute myocardial infarction with cardiogenic shock. 7. Failed PTCA."'Percutaneous transluminal coronary angioplasty" (100% surgical) 8. Reoperation for recurrent symptoms (now stinting). 9. Congenital anomalies of coronary arteries (100% surgical). 10.Kawasaki's disease -This list has been changed nowadays because of improvement of stints and types of stinting in cardiology; nowadays we have what so called drug eluting stint in which the metal stints are covered with antiplatelets drug and this gives a better prognosis - So traditionally, any one of the above except (7, 9, 10) if it is stentable for the cardiologist he will put a stent -previously: if we have single stenosis then stenting if triple surgery but now this changed. -single short area segment; stinting is better. 12

14 -triple vessels dis. Still till now all studies Say surgery is better (long-term patency, and protection of the function) Triple vessels dis. Or any vessel with depressed LV function the indication is surgery. -coronary artery bypass grafting is 40% decreasing nowadays because the cardiologists become more aggressive with stinting, so most patients come to surgery in advance stage with very bad vessels. Opened heart operation:- 1- we are dealing with microscopic surgery, the diameter of the field through which the surgeon look about 5 cm not more. 2- The vessels we are dealing with are micron (1.3 or 1.5 mm). 3- It is a bypass grafting so where we have the stenosis we transplant after It but the vessels should be graftable (the best lumen is 1.5mm, less than 1mm is not graftable). 4- we have to stop the heart temporarily, we use heart lung machine (called pump in the picture), we take the venous blood from the heart, (So we put a canula in the right atrium to collect the venous blood), send it to a machine and the machine will return it to the rest of the body, oxygenated just like the lung, through a canula we put in the aorta, 5- But as the heart still receiving and giving blood the contractility is there so we should arrest the heart by putting a Cross clamp on the aorta but after the canula, so we kill the heart while the body still alive 13

15 6- But still we have to protect the heart, we myocardial protection solution which contain a lot of metabolic products plus the most important high potassium, so we put a canula Below the cross clamp and give the cardiogenic solution which comes either from the pump or the anesthesia, then goes down to the coronaries, also we put cold saline" ice" around the heart to increase the protection, then we do what we want and put what we want. 7- After we finish, we remove the clamp so the heart returns gradually functioning. - This vein graft on the left (Ur left hand), is connected to the PD then to the aorta. - the one on the right is connected to the circumflex then to the aorta. - for the LAD we use a conduit called LIMA (LEFT INTERNAL MAMARY ARTERY), which arises from the subclavian artery, and pass below the ant. Thoracic wall. It is called pedicle graft because it continues from the subclavian then the surgeon cut it distally after harvesting (bnazlo), and connects it to the LAD. While the venous grafts are called free grafts, because we take the saphenous vein and turn it so that the distal part connected to the aorta returning the valves non functioning. The best results for the mammary graft is when it is connected to the LAD (ya3ni if we connect it to the circumflex it will not give the same long patency rate) why is unknown but some say that because the blood flow in LAD will be more. 14

16 The arterial conduits have a better long patency rate than the venous ones, if we take them all after 10 yrs, we will find that 95% of the arterial ones are patent, whereas only 60% of the venous are patent and the rest are diseased and closed, because the vein's tolerance to the blood pressure of the aorta is not like the artery. CONDUITS FOR BYPASS GRAFTING 1. So we use as a conduit the saphenous vein (long or short but the long is more comfortable) 2. left mammary and sometimes the right mammary, but we avoid the bilateral mammary because it increase the incidence of infection. In slides:- -Saphenous Vein Grafts- 1-year patency rate for aortocoronary veins grafts is between 80 and 90%. 5-year patency was only 45%. -Internal Mammary Artery Grafts- Long term patency, significantly better than SVG at varying postoperative intervals: 95.7 versus 93.4 at 1 year, 87.9 versus 74.0 at 5 years, and 83.0 versus 41.0% at 10 years, respectively. WHY??? 1. Not completely understood- seems to be free of the progressive intimal thickening noted in coronary arteries with advancing age. 2. Preserved vasa vasora of the arterial graft may be a factor that contributes to its increased patency rate. 3. Prostacyclin production from the internal mammary artery endothelium, when compared to that of harvested SVG. ALTERNATE CONDUITS:- *Gastroepiploic Artery. (most commonly used by Japanese because they are small and short so their mammaries are small) *Inferior Epigastric Artery. *Radial Artery (better than the veins and is taken free). *Cryopreserved Homograft Vein. (50%- 7 mo. Patency rate).(completely failed nobody use it) - Any artery or vein you can take you can use as a graft

17 1. 2. Complications of cardiac surgery:- Mortality 3%. Stroke, the most common cause of it in cardiac surgery is; the aorta the main source of atherosclerosis. The end 3ola A. Krasneh