缺血性心脏病和动脉瘤课件

Ischemic heart disease and aortic aneurysms Cardiovascular lab #1 Ischemic heart disease general concepts Ischemic heart disease- Designation of a group of disorders that all cause ischemia to the myocardium Ischemia results from an imbalance of supply and demand Decreased coronary blood flow ( 90% of myocardial ischemic dz) Most commonly due to atherosclerosis with superimposed thrombus, vasospasm or both Uncommon causes of decreased supply are arteritis, emboli, cocaine-vasospasm and systemic hypotension Normal flow but not enough oxygen (increased demand or hypoxia) Tachycardia, and hypertrophy Cyanosis due to congenital heart disese (rt-lt shunts), smoking, carbon monoxide poisoning, lung disease. Myocardial ischemic syndromes Four basic ischemic syndromes- Angina pectoris- chest pain resulting from ischemia without frank infarction (reversible ischemia) Three clinical patterns of angina Stable-underlying path is usually stenosis of major coronary vessel (6 weeks- white tough fibrous scar will be present Common sites of coronary artery disease, and the distribution of myocardial necrosis with blockage of each respective vessel (listed in order of frequency, with the top being most frequent) Gross section of left ventricle myocardium showing a transmural infarction. Normal myocardium is to the left, the infarcted areas are thinned and alternating pallor and hemorrhage. Myocardial infarction Pathologic microscopic features- Atherosclerotic plaques- Eccentric thickening of intimal layer that contains variable amounts of smooth muscle, lipid-laden macrophages, fibrous connective tissue, and cholesterol clefts (angulated empty spaces, the cholesterol gets washed out in processing) Myocardial changes- Remember all the way back to summer Coagulative type necrosis of the cardiac myocytes- “Red is dead” the myocytes appear more red and lose their nuclei Time course of microscopic changes after a MI 1 hour- edema, some wavy myocytes (dead fibers getting stretched by adjacent viable myocytes) 12-72 hours- PMNs move in 3-7 days- Clean-up starts with increased numbers of macrophages 7-10 days- Granulation tissue is present ( the start of scar formation) 6 weeks- Scarring- collagenous scar (a good scar is bad for pumpng blood but protects the heart from the structural disasters of aneurysmal dilatation and rupture) Coagulative necrosis of myoctyes New cappilaries Fibroblasts and new collagen Micrograph of infarcted myocardium undergoing early organization with granulation tissue, and early fibroblastic proliferation. All the dead myocardium has not been removed, the necrotic myocardium here shows the typical hyper-eosinophilia, loss of cross striations and absence of nuclei that is associated with coagulative necrosis. Acute complications of myocardial infarction Arrhythmias (75-95% of complicated cases) All types of arrythmias- PVCs, sinus brady or tachy, v-tach , v-fib ,or asystole Congestive left sided heart faiure (60%) Cardiogenic shock (10-15%) Associated with large area of infarction (40% of ventricle) Large mortality rate (70%) Mural thrombosis and systemic thromboembolism (10-15%) Ventricular rupture (1-5%) Free wall rupture- pericardial hemorrhage and possible tamponade Septal rupture- acquired VSD (less common) Papillary muscle infarction and possible rupture (1-5%) Mitral valve dysfunction Fibrinous pericarditis (common but not clinically significant) Develops 2-3 days post MI- localized to the pericardial area over the infarct and resolves completely as the infarct heals (you hear a friction rub ) Deformation of heart wall expansion-aneurysm General considerations on complications of acute MIs Complications are present in 80-90% of cases of acute MI The type and severity of complication depends on the size, site and transmural extent of the infarct Large transmural infarct in general- More likely to have cardiogenic shock (70% mortality), arrhythmias, and late congestive heart failure Anterior transmural infarcts have the worst prognosis- Greater risk of regioal dilatation (ie. Aneurysm), mural thrombi and rupture Posterior transmural infarcts- More likely to develop conduction blocks, right ventricular involvement or both Subendocardial infarcts have far less complications- May develop mural thrombi (damage to endocardium makes it thrombogenic), but pericarditis, rupture, and ventricular aneurysm rarely occur. Left heart failure is very common after an acute MI, here is an example of pulmonary edema, one of the common manifestations of congestive heart failure. This gross change is best appreciated in the fresh state, as the lungs will be markedly heavy, boggy, and exude frothy substance with manipulation. Passive congestion of the liver, the so- called “nut-meg” liver that can be seen grossly. This is a manifestation of right heart failure, which is often seen after left heart failure associated with acute MI. The passively congested liver shows retained hepatic architecture with a distended central vein (arrow) and adjacent sinusoids congested with red blood cells. This is an example of mural thrombosis, which is commonly seen in both transmural (as in this case) and subendocardial infarcts. The are a result of a combination of stasis, and endocardial damage, both thrombogenic factors. The presence of mural thrombosis of the left ventricle gives the possibility of systemic thrombo-embolic disease. This is a massive embolic infarction (stroke) of the brain due to embolic occlusion of basilar artery. The embolus originated from the left ventricle of a patient shortly after a transmural MI. Hemorrhagic infarction has destroyed much of the brain stem (arrow), and much of the cerebellum and left meso-temporal lobe. Other systemic embolic infarcts with less tragic consequences can happen after an MI. The kidney is very commonly infarcted (arrow), unlike the CNS embolic infarcts, the kidney usually has anemic infarcts, as it has fairly solid parenchyma and no dual blood supply. A wedge shaped subcapsular splenic infarct. The spleen is also a commonly infarcted organ in thromboembolic disease emanating from left ventricular mural thrombi. Like the kidney this tends to be an anemic infarct. Left ventricular aneurysm Etiology- Transmural death of a large portion of myocardium that becomes deformed outward- more often seen in large anterior and anteroseptal infarcts Starts as an expansion, then heals into a fibrous aneurysm Possible outcomes of ventricular aneurysms- Pump failure- heart wastes useful cardiac output into the non-contractile aneurysm. Pulmonary edema- secondary to left heart failure (above) Mural thrombus formation- stasis of blood in the aneurysm, and thrombogenic surface due to underlying infarct leads to clot- parts of clot can then embolize into systemic circulation Dysrhythmias- fibrous aneurysmal wall may make for conduction problems Clinical features- All the above complications may occur Pathologic findings- Gross outpouching of thinned fibrous portion of ventricular wall Micro thinned remnant of myocardium with variable amounts of fibrous tissue admixed Cardiac aneurysms often causes left heart failure, as the ventricle, even with good force, isnt able to put out the same volume of blood due to unloading into the aneurysmal wall. Another common complication shown here is mural thrombus formation which gives potential for thromboembolisation. Only rarely will an aneurysm rupture. Gross photo of a chronic left ventricular aneurysm (arrow), which is located in the anterior wall (typical location). This aneurysm appears fibrotic and thus would likely not have the paradoxical systolic out pouching seen with aneurysm walls with more viable ( and thus stretchable) myocardium. Mural thrombus formation is often seen after myocardial infarctions, especially when a ventricular aneurysm has formed. Parts of this thrombus may embolize and cause ischemic damage, most commonly going to the brain, kidney, spleen, and the extremities. Rupture of left ventricular free wall Incidence-Uncommon (1-5% of complicated MIs) Etiology- Extensive thinning and destruction of myocardium. Seen in transmural infarcts at there weakest point in healing (1 week post MI, when the clean-up starts, but no good scar has started forming) Risk factors- Female sex, sustained hypertension (htn), Age80, First MI Size of MI: Large area of ventricle involved by MI (20%) Site of MI: Anterior and anterolateral portion most susceptible to rupture Time post MI: 4-7 days after MI the highest risk (grossly MIs are soft at this point) Clinical features- Cardiac tamponade with resultant compression of the heart-impaired diastolic filling- decreased cardiac output- cardiac arrest Path features: Gross- Hole through left ventricular wall; may be very small (but doesnt take much to give tamponade so even a small hole will be bad news) Micro- Simple hole defect will be seen in area of destroyed myocardium Diagram of left ventricular free wall rupture, which usually occurs 4-7 days after an acute MI when the wall is weakest. Often having catastrophic results by causing bleeding into the pericardial space (hemopericardium) resulting in cardiac tamponade. Gross photo of a left ventricular free wall rupture (pericardium has been removed). This anterior location is typical for ruptures as it is for aneurysms, for this reason anterior wall MIs in general have a worse prognosis Hemopericardium Hemopericardium occurs most commonly with ventricular wall rupture in the early convalescence of an MI, and proximal extension of an aortic dissection. papillary muscle damage Etiology- Infarction of one or more of the papillary muscles of the left ventricle which leads to- Papillary muscle dysfunction- ( presents as mitral insufficiency) Acutely- due to ischemia of the muscle Chronically- due to fibrous scarring of the damage muscle Papillary muscle rupture- (very rare, less common than both free wall and septal wall rupture) Ruptures of one head of papillary muscle leads to acute severe mitral insuffiency, (more common), produces a prolapsing mitral valve. Rupture of the entire trunk of the papillary muscle leads to sudden death Clinical presentation- Signs and symptoms (sxs) of mitral insufficiency- Murmur- Mid-late systolic murmur Pulmonary edema (hear rales ) Pathologic features- Gross Infarcted papillary muscle is discolored, just like infarcted myocardium, has different appearance depending on the stage of resolution. Ruptured papillary muscle will be free-floating in the ventricular cavity Most often only part of the papillary muscle ruptures causing insufficiency, but if the entire muscle trunk tears (as shown in this diagram) sudden death results. Partial tear of a papillary muscle after infarction. Partial tears will result in mitral insufficiency and produce a mid-late systolic click due to prolapse of the valve. Acquired ventricular-septal defect Rupture of the septal wall of the left ventricle (less common than rupture of the free wall) Clinical findings- Pansystolic murmur with associated palpable thrill (findings seen in all VSDs, acquired or congenital) Produces a left to right shunt- Right heart failure- overload of right side as blood moves in through the defect dilated neck veins hepatomegaly peripheral edema, and ascites Outcome- Can be fatal depends on the size of the defect. If it is small it might be stable enough to be corrected surgically. Septal rupture after an MI may be fatal but not in all cases, it depends on the size of the defect. Fibrinous pericarditis is often seen after myocardial infarctions. Here is shown the classic “bread and butter” appearance (close up is above). Pericarditis after an MI, unlike some of the other complications is not usually problematic and resolves without sequelae. A “friction rub” is often heard with chest auscultation. Aneurysms Definitions- Aneurysm: Localized abnormal dilatations of vessels True aneurysm: Aneurysm bounded by a complete vessel wall (although it usually is not a normal wall as it is often attenuated) False aneurysm: Not really a dilatation of a vessel, but a hematoma that communicates with the vessel lumen, better terms are “pulsating hematoma”, or “pseudo aneurysm”. Why are aneurysms bad? ( whats their morbidity?) Rupture Impingement on adjacent structures Occlusion of nearby vessels by overlying thrombus formation, or by extrinsic pressure Ebolism from their mural thrombi Main Causes of aneurysms- Atherosclerosis ( especially AAA) and Cystic medial degeneration (dissecting aneurysm) Other less common causes- Syphilis, Trauma, PAN, Congenital defects, Infections (“mycotic aneurysms”) False aneurysm (aneurysm spurium) Dissecting aneurysm Arteriovenous aneurysm Cirsoid aneurysm Saccular aneurysm Fusiform (Spindle) aneurysm Medial necrosis Arteriosclerosis Erosion in TB or ulceration Abdominal aortic aneurysms (AAA) Etiology- Almost all due to atherosclerosis- damage to aortic wall and subsequent dilatation Ulceration and thrombus formation occur (just like in other sites of endothelial damage) Clinical features- Typically in men 50 years of age Often asymptomatic with acute, usually fatal hemorrhage; Risk of rupture increases with the diameter of the aneurysm 5 cm associated with risk of rupture 5-10% per year Enlargement of aorta can cause local compression and damage adjacent structures Local extension of aneurysm distally to iliac arteries to lower extremities Signs and symptoms Pulsating abdominal mass (dont push too hard!) Bruit heard over aorta (due to turbulent flow) Abdominal aortic aneurysms (AAA) Pathologic features Gross Characteristically fusiform Usually located between the renal arteries and the iliac bifurcation Most of the aneurysm is filled with clot- the vessel lumen at the level of the aneurysm may be only as big or even smaller than normal surrounding aorta. Microscopic features Laminated thrombus atheroslcerotic debris (macrophages, cholesterol clefts) Outlook- Operative mortality- 5% before rupture 50% after rupture (I.e. emergent surgery) This diagram demonstrates the typical appearance of abdominal aortic aneurysm. The shape is usually fusiform (circumferential), and located between the renal arteries and the iliac bifurcation. Syphilitic Aneurysms Very uncommon today, associated with tertiary syphilis Unusual distribution- Affects the ascending aorta Pathogenesis- Begins with adventitial inflammation, knocks out vasa vasorum causing ischemia in the aortic media- weak vessel wall Associated morbidity/mortality- Left heart failure: Aneurysm may extend down into aortic valve ring- the widened ring causes aortic stenosis and subsequent left heart failure over time Impingement adjacent thoracic structures Ruptures only RARELY Gross- Distribution is usually limited to the ascending and transverse aorta Shape is variable may be saccular, fusiform or cylindrical Intimal surface shows linear folds giving it a tree bark-like appearance Microscopic- Inflammation of the adventitia and medial vaso-vasorum Syphilitic aneurysm with its characteristic ascending aorta location. This diagram clearly shows how an aneurysm here would cause a hoarse voice as it stretches the recurrent laryngeal nerve. Sandritter, W.: Color Atlas and Textbook of Macropathology (Yearbook Medical Publishers, Inc. 1972). Syphilitic aorta with aortic dilatation limited to the ascending aorta. The damage to the vessel wall often extends to the aortic valve ring, causing severe aortic valve insufficiency. Dissecting Aortic Aneurysms AKA “dissecting aortic hematoma”, since there is no dilatation of the aorta Incidence- Primarily occurs in two distinct populations- Middle aged men (age 40-60 years) with hypertension ( accounts for 90% of pts) Younger people with connective tissue defect of Aorta (e.g. Marfans syndrome) Can also be iatrogenic- arterial cannulation (catheter) diagnostic or therapeutic Other risk factors- Pregnancy, bicuspid aortic valve, aortic coarctation Etiology- Both hypertensive and genectic causes of dissection are a result of aortic media damage, more severe in the latter. Clinical presentation and course- Sudden onset of excruciating pain with a “tearing” quality in the anterior chest and extending into the back. Pain extends lower as dissection progresses Clinical signs- Signs of ischemia- with involvement of carotids, or vertebrals see CNS ischemic sxs, MI if coronaries involved. Diminished carotid or upper extremity pulses Aortic insufficiency murmur Dissecting Aortic Aneurysms Classification- ( types A and B) Type A- Proximal dissection (ie. Involving the ascending aorta) More common and more dangerous than type B Type B- Distal desection (ie. Not involving ascending aorta, usually starts af