(From Path book and lecture, 17 Jan 2001, by Brian Buschman)
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In accordance with the Frank-Starling law of the heart when EDV is higher than contractibility is higher up to a point. After that contractibility decreases. The decrease is uncompensated heart failure and is bad.
With left heart failure fluid spills out to cause pulmonary edema. Increased pressure bursts smaller capillaries, macrophages pick up the red blood cells (these macrophages are called heart failure cells). If this becomes chronic venous congestion you will see fibrosis of the walls and accumulation of hemosiderin called brown induration of the lungs.
Right heart failure leads to chronic passive congestion of the viscera (epically the liver) and other soft tissues. This causes nutmeg liver.
Clinically left heart failure will usually present with dyspnea (breathlessness). At night you may see paroxysmal nocturnal dyspnea (waking up from breathlessness and cough). You may also hear S3 (the 3rd heart sound) and find mitral murmurs from excess right heart hypertrophy.
Right sided heart failure is usually caused by left heart failure and shows chronic passive congestion of viscera, neck and feet. Ascites and pleural effusions are very low protein.
If heart failures are not treated patients will quickly become cyanotic, acidotic and develop arrhythmias.
IHD is the leading cause of death in the developed world. Depending on severity it leads to:
1) Angina pectoris
2) Acute MI
3) Sudden cardiac death
4) Chronic ischemic heart disease with congestive heart failure
Things that worsen/trigger IHD include:
1) Acute changes in the morphology of atherosclerotic plaques. This may be enlargement or change in shape of the given plaques.
2) Local platelet aggregation
3) Coronary artery thrombosis is usually associated with a plaque.
4) Coronary artery spasm can be triggered by TxA2 or endothelial dysfunction. Adrenergic activity and smoking can also cause it. Prinzmetal’s (variant) angina is associated with coronary artery spasm.
There are three types of angina and any given patient may experience more then one at a time.
1) Typical angina pectoris or stable angina is caused by excess demand in relation to work due to a stable size plaque. It is relieved by rest and nitro. The rest reduces work and the nitro is a vasodilator reducing venous return therefore further reducing workload and O2 demand.
2) Prinzmetal’s or variant angina is related to coronary arterospasm and is the type that might awaken a patient at night (angina during rest).
3) Unstable crescendo) angina differs from stable angina in that it requires less workload and it gets progressively worse and lasts longer. It is caused by plaques and either a superimposed thrombus or spasm.
Most MIs are caused by coronary artery thrombosis, often from a dislodges plaque. The infarct will usually reach it’s full size within 6 hours and necrosis will begin in the myocardium in the subendocardial portion. The subendocardium is predisposed to being first because it is both further from the epicardial blood supply and has increased pressure making it harder for blood to make it in.
The LAD supplies the anterior side and apex. The right coronary supplies the posterior/base of the heart. All three major arteries (LAD, right coronary and left circumflex) supply part of the left ventricular wall.
Morphologically the initial chance is coagulation necrosis and inflammation as it produces a fibrous scar. The artery that is blocked obviously dictates the location of the infarct. Most transmural infarcts involve the left ventricle.
Timeline:
|
0-12 hours |
There are no morphological changes yet. |
|
12-28 hours |
Coagulation necrosis begins with eosinophilia, loss of cross striations, pyknosis and karyorrhexis. |
|
18-24 hours |
Neutrophils begin to show up and the area shows a slight pallor. The neutrophils peak about 5-6 days. Hemmhorage is rare because MIs are ischemic by definition. |
|
4-5 days |
The infarct will appear pale with a hyperemic (extra blood) boarder. Macrophages and fibroblasts begin to migrate in. |
|
10 days |
Collagen fibers are seen and many macrophages with remnants of myocytes are seen. |
|
4-8 weeks |
Vascularity diminishes and fibrosis is near completion. |
Contraction bands appear on the periphery of the infracted area. This is from hypercontraction of dying cells with a Ca++ influx. If reperfusion is quick there are more contraction bands. These cells will not become normal again but will get a vacuolated appearance called myocytolysis from H2O that rushes in across damaged membranes.
In the first few days one change you will see if the constantly increasing numbers of macrophages. It helps tell how long after the MI the patient died.
1) Papillary muscle dysfunction may occur in some MIs. Most commonly in the left causing mitral valve insufficiency.
2) External rupture usually towards the end of the week 1 as blood dissects through the myocardium. It causes hemopericardium and cardiac tamponade. It can also dissect through the IV septum.
3) Mural thrombi formation that may detach and cause problems. A mural thrombus is a thrombus on the side of a heart chamber.
4) Acute pericarditis is inflammation of the pericardium.
5) Ventricular aneurysms may appear on the ventricular wall.
Hypertensive heart disease is diagnosed by LV hypertrophy resulting from hypertension. In hypertensive heart disease the LV hypertrophies causing increased demand for O2 in the myocardium. At the same time it caused decreased compliance, lower stroke volume and a greater distance across which blood must diffuse.
Pulmonary heart disease is a disease of the right sided chambers. It does not include right heart failure secondary to left heart failure.
Acute cor pulmonale is caused by embolism blocking up to 50% of the pulmonary vascular bed. The RV does not dilate/hypertrophy due to short duration.
Chronic cor pulmonale is caused by COPD and the duration leads to RV hypertrophy. It causes decrease in cardiac output and the backup into systemic circulation that is seen with CHF.
1) Things that block up the lungs like COPD, interstitial fibrosis, CF and atelectasis.
2) Things that block the vessels like pulmonary embolism, pulmonary arteriitis, pulmonary vascular stenosis.
3) Disorders of chest movement like obesity or kyphoscoliosis.
4) Disorders related to pulmonary artery constriction.
Rheumatic fever is an immune mediated disease that follows group A strep. It begins as fibrinoid necrosis that elicits an inflammatory response. Fibrosis is very common in the heart in chronic rheumatic heart disease.
Acute rheumatic carditis has the change in all three layers (pancarditis). It has Aschoff bodies that are points of inflammation. They have a necrotic center surrounded by mononuclear inflammation and large basophilic histocytes called Anitschkow cells.
Aschoff bodies may be found anywhere on the CT of the heart.
The inflammation will often involve both the pericardium and endocardium. This leads to fibrous pericarditis and mitral/aortic valve problems. The valves do not get many Aschoff nodules but do have focal fibroid spots.
Other changes include arthritis of large joints. Pulmonary involvement is rare but can happen. Skin changes take place as subcutaneous nodules/erythema marginatum.
Chronic rheumatic heart disease has irreversible damages to a valve usually mitral or aortic. It leads to either stenosis or regurgitation or both. Either causes increased workload of the ventricle and predisposes to future infective endocarditis.
Mitral valvulitis usually cause stenosis rather then regurg are more common in females and are described as having a “fish-mouth appearance.” They have thickened valves and chordae tendineae and led to L.A. hypertrophy/dilation.
Aortic valvulitis is most common in men because of partial fusion of the cusps. It leads to L.V. hypertrophy. If fibrosis is a factor then it leads to regurg.
Clinically patients are usually 5-15 and usually present as arthritis and carditis. The carditis tends to cause friction rubs, weak heart sounds, tachycardia and arrhythmias.
Calcification of the valves is a normal part of aging but it can go to the point of causing pathologic stenosis. The Ca++ builds up behind the valves (down stream) in the sinus of Valsalva. Unlike rheumatic valvulitis calcific stenosis does not fuse the cusps. It does have fibrosis leading to stenosis.
DCAS (degenerative calcific aortic stenosis) will cause angina, syncope and CHF. They show a crescendo-decrescendo systolic murmur and L.V. hypertrophy.
Mitral valve prolapse is very common among adults as a C.T. disorder leading to valvular incompetence. It is usually an isolated problem but may be related to Marfan or such.
It is related to enlarges chordae tendineae and stretchey valves cause the proapse. Most are asymptomatic but some have palpitations and fatigue. On ascultation you will hear a mid-systolic click with a late systolic murmur.
NBTE is a sterile endocarditis from deposits of fibrin, platelets or other blood components. It is usually found on normal valves.
The aortic valve is usually involved with eosinophilic material. It does not show inflammation or fibrosis and tends to resolve spontaneously. It is a symptomatic but may cause a thrombus to break loose or damage a valve to give opportunity for infective endocarditis.
Infective endocarditis is usually caused by bacteria, often acute endocarditis from Staph a or subacute by Strep v. High risk groups are infected by different organisms and include:
1) People with cardiac abnormalities get those subacute Strep v. infections.
2) IV drug abusers tend to get acute endocarditis from Staph a.
3) Prostatic valve patients tend to get HACEK infections. (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella.)
It can be tough to treat because of the avascularity of the valves.
The left is usually involved except for the Strep a that the IV drug abusers get.
The acute are worse and more damaging than the subacute. They can produce a thrombi that can lodge in the systemic circulation and produce an abscess at the given site of infarct. Granulation tissue is produced at the valvular site.
Clinically you see fever, clubbing of the digits, splenic enlargement or any of the many things that would be expected of a bacterial infection. Be sure to test with repeated blood cultures because it can hide for a while in the vasculature.
Valves may be mechanical or bioprosthetic (made of animal parts). Bioprosthetis are specifically prone to mechanical deterioration, stiffening and stenosis.
Mechanical valves are prone to thrombi formation and hemolysis from shear forces of blood flow.
Myocarditis is usually caused by Coxsackie virus A or B or by CMV or HIV. It may also be of Trypanosoma cruzi.
Patients usually have cardiac dilation and their hearts also appear pale and flabby. In viral myocarditis it has an inflammatory infiltrate. With parasites, Trypanosoma, it directly infects myocytes as in Chagas’ disease.
Cardiac transplant rejection can show the same pattern of lymphocytes and myocytes degeneration.
Giant cell myocarditis is an inflammatory disease with giant multinucleated cells.
They appear anywhere from asymptomatic to CHF and arrhythmias.
Cardiomyopathies are 1o diseases of the myocardium.
Dilated cardiomyopathy is a disease of hypertrophy of the myocardium from reasons other then hypertension, usually toxic insults of one type (virus, chemical, etc.). More frequently in men from 20 to 60 years old.
The heart grows in excess of 900gm and all chambers are dilated. This leads to stasis and mural thrombi. Patients end up with ejection fractions as low as 25% leading to CHF.
It can occur transiently with pregnancy but usually goes away postpartum.
Hypertrophic cardiomyopathy is also called asymetheric septal hypertrophy or idiopathic hypertrophic subaortic stenosis. It has a hypertrophy of the myocardium, specifically of the IV septum of the L.V., abnormal filing and outflow obstructions. Despite the hypertrophy it has increased power.
The IV septum tends to be thicker then the LV’s free wall. The hypertrophies is without dilation.
Clinically they will have a harsh ejection murmur from turbulence. This leads to ischema because of the small CO. It also leads to angina, ventricular arrhythmias and sudden death.
Restrictive cardiomyopathy has a low ventricular compliance that leads to impaired filling. Loffler’s syndromes is an eosinophilic endomyocardial fibrosis causing proteins to be released from eosinophils. This decreases compliance. It can also be caused by cardiac amyloidosis, hemochromatosis and radiation injury.
Depending on the cause of the restriction the appearance varies. With Loffler’s syndrome the atria are dilated but the ventricles are normal.
It has poor filling like hypertrophic cardiomyopathy but it lacks the forceful ejection.
These include atrial septal defects (ASD), ventral septal defects (VSD) and patient ductus arteriosus (PDA). Cyanosis is not an early feature since pulmonary circulation is not bypassed.
ASD is a failure of proper fusion of the endocardial cushions. It may be a patient foramen ovale, foremen primum or a bigger hole. It can lead to increased resistance and heart failure.
VSD develops between weeks 4-6 and VSD is the most common congenital heart defect. They may be asymptomatic or lead to cardiac failure.
PDA is a high pressure left to right shunt creating a “machinery” murmur. IT leads to pulmonary hypertension.
It is the most common cyanotic congenital heart disease. It involves:
1) VSD
2) Overriding aorta
3) Pulmonary A. stenosis
4) R.V. hypertrophy
If the patient can survive the pulmonary A usually does not grow with the rest of the heart. This causes an effective worsening of the pulmonary stenosis.
This has a complete isolation of the pulmonary and systemic circulations. If no shunt exists and surgery is not begun immediately it means death.
Coarctation of the aorta is the most common congenital cardiac abnormality. It can be pre-ductal or post-ductal referring to the ductus arteriosus.
Pre-ductal is detected early because it causes a patient’s ductus arteriosus to shunt blood right-to-left. This leads to peripheral cyanosis from pumping of poorly oxygenated blood.
Post-ductal is not detected until later because collateral circulation develops via the sub-clavian and brachiocephalic A’s (which are pre-ductal). This causes decreased perfusion of the kidneys leading to U.L. hypertension.
Infection of the pericardium is usually viral and often has myocardial involvement. It is often related to uremia, SLE or metastatic malignancies. It can lead to:
1) Immediate hemodynamic complications
2) Resolve without sequelae
3) Progress to a fribrosing process.
It often appears fibrinous, a “bread and butter” pericarditis. If it’s of tuberculin it has caseous material.
Clinically patients come in with a high-pitched friction rub and atypical chest pain. They may show sings of cardiac tamponade like distended neck, veins, shock and declining CO.
Fluid that accumulates pericardially comes from a variety of sources. If it accumulates slowly then large amounts can be tolerated. Sources may include:
1) Serous fluid from CHF or hypoalbumenia.
2) Serosanguineous (serum and blood) from blunt chest trauma and malignancy.
3) Chylous (fluid that is taken up by lymph nodes that appears milky white from chylomicrons) from mediastinal lymphatic obstruction.
The worst is hemopericardium which is a direct pericardial bleed that will lead to cardiac tamponade.
Most cardiac malignancies are metastatic. The most common are from the lungs, breast, malignant melanomas and hematopoietic malignanies.
Primary tumors are rare but include:
1) Mytomas are benign neoplasms of the L.A. near the fossa ovalis. They are of the myocardium and may obstruct the valves if not removed.
2) Cardiac rhabdomyomas are common in very young and can obstruct a valve.
3) Lipomas can also grow and kill.
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