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59 Cards in this Set
- Front
- Back
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Overview of Cardiac Pathology
4 Main parts of the heart associated with disease? Most common? |
*Coronary arteries
The heart valves The electrical conducting system The myocardium |
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Overview of Cardiac Pathology
What supplies the left ventricle with blood? |
The left main coronary artery branched into two major vessels: the left anterior descending artery (LAD) and the left circumflex (LCX). These vessels supply oxygen and nutrients to ~70% of the left ventricle. The right coronary artery (RCA) supplies the right ventricle and ~30% of the left ventricle.
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Overview of Cardiac Pathology
Coronary artery atherosclerotic changes result in what (2)? ___ million Americans affected. (M?F) |
Coronary artery disease - affected blood flow to the myocardium => angina and MIs
13.7 M>F |
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Overview of Cardiac Pathology
Are MIs acute or chronic narrowing? Tx (2)? |
Acute - thromboembolus, coronary artery disection
(with chronic, there is some enlargement of vessel and collateral circulation) CABG, Stenting |
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Overview of Cardiac Pathology
The most common valvular problem is ... The other common cardiac valve problem is ... The other significant complication of heart valves is ... Most significant involves which 2 valves? (younger) Rheumatic faver=> (older) HTN, smoking, male => |
...stenosis (thickening and calcification of the valve)
...regurgitation (blood flows in reverse through an incompetent valve. This can be the result of many different pathologies including aortic root dilatation and floppy mitral valve changes) ...endocarditis. This can be non-infectious or infectious (bacterial, fungal, etc.). Endocarditis is defined by plaques and vegetations on the heart valves which impact valve function. The vegetations are also at high risk to embolize to distant sites and block important arteries (think strokes) or spread infectious agents. Most serious: Mitral, aortic (left side) (younger) Rheumatic faver => Mitral stenosis (older) HTN, smoking, male => Calcific/degenerative aortic stenosis |
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Overview of Cardiac Pathology
Arrhythmias are the result of _________________ disturbances in the heart. There are numerous types of arrhythmias, some of which are relatively benign and some of which can be rapidly fatal. Patients at risk or arrhythmias can have ___________ or ___________ placed. |
electrical conductance
pacemakers, defibrillators to control the heart pacing or to reset a dangerous cardiac rhythm. |
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Overview of Cardiac Pathology
Three major myocardial diseases |
cardiomyopathies, myocarditis, ischemic injury
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Overview of Cardiac Pathology
There are 5 types of cardiomyopathies ... Most common? |
*dilated cardiomyopathy*
hypertrophic cardiomyopathy restrictive cardiomyopathy (rare - secondary) arrhythmogenic right ventricular dysplasia (ARVD) Endomyocardial fibrosis (EMF) obliterative cardiomyopathy |
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Overview of Cardiac Pathology
Most restrictive cardiomyopathy is secondary to an ____________. |
infiltrative process such as amyloid or sarcoidosis
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Overview of Cardiac Pathology
Myocarditis is inflammation of the heart. Most cases of myocarditis are the result of _________. Some patients recover fully, but many go on to develop ___________ cardiomyopathy and heart failure. Giant cell myocarditis is an unusual form of severe myocarditis of unknown etiology. |
a viral infection (Coxsakie B)
- Less common parasite (Chagas disease) dilated - lower ejection fraction |
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Overview of Cardiac Pathology
Myocardial infarctions (MIs) are the result of ___________ injury to the heart. Most MIs are secondary to _____________, but ___________ or ____________ can also result in a MI. Myocardial cells die secondary to ________________. Over a period of 4-24 hours __________, then later ___________ infiltrate the area of infarction and these inflammatory cells remove the dead myocyte cell debris. If a patient survives a MI, a _____________ usually replaces the area of infarction. |
ischemic
coronary artery occlusion general hypotension or anemia an inadequate oxygen and nutrient supply neutrophils, then macrophages scar of collagen |
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Overview of Cardiac Pathology
Transplanted hearts ultimately fail secondary to a process of ..... % survival at 10 years? |
medial vascular smooth muscle cell hyperplasia known as transplant vasculopathy in which the coronary vessels become narrowed. This process differs from atherosclerotic coronary artery disease.
50% |
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Myocardial disease may be due to a variety of processes, including (4).
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HTN
Ischemic heart disease Myocarditis Cardiomyopathy |
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_________ is heart muscle disease characterized by leukocytic infiltrate and necrosis of myocytes.
Theoretically, this would include _________, but this it is not included. |
Myocarditis
MI - not included |
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Pathology of Myocarditis
Myocarditis can be due to: (7) |
Viral
Bacterial Rheumatic Fever Fungal Parasitic Drug reaction Giant cell or Sarcoid myocarditis |
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Pathology of Myocarditis
Occurs at what age? How does it present? Any preceding symptoms? Labs? LV function? Ejection fraction? Gross appearance? Microscopic appearance? |
Any age
Acute - HF, arrhythmia, death Preceding virus-like illness Elevated Erythrocyte sedimentation rate, serum creatinine kinase, WBC Low LV function, decreased ejection fraction (40% will improve spontaneously) Gross: Pale, flabby Microscopic: leukocyte infiltrate, myocyte necrosis. Often edema. |
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Pathology of Myocarditis
Causes 1/7: Viral Name 2-3 viruses. Histology? Proposed mechanisms (2)? |
Coxsackie A, B (small RNA - picoronaviruses - fecal/oral)
HIV-1 Lymphocytic infiltrate, myocyte necrosis. Molecular mimicry, exposure of endogenous antigens (myocardial constituents) |
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Pathology of Myocarditis
Causes 2/7: Bacterial Name 2-5 bacteria. Histology? |
Staphylococci, Streptococci, Pneumococci, Meningococci, Diphtheria-toxin, TB (rare!)
PMNs in the myocardium! |
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Pathology of Myocarditis
Causes 3/7: Rheumatic fever Follows what? What is the acute rheumatic fever like? Histology? Proposed mechanism (1)? |
Pharyngeal infection with Group A beta hemolytic Streptococci.
(=> myocarditis, or recall -glomerulonephritis) Acute - Fever, migrating polyarthritis, pancarditis, cutaneous nodules, erythema marginatum, Sydenham's chorea Perivascular fibrinoid necrosis surrounded by lymphocytes and m0 = Aschoff's bodies (Anitschkow cells = modified histiocytes). Bacteria and cardiac myosin share and epitope |
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Pathology of Myocarditis
Causes 4/7: fungal Name 2 fungi. When might you see this? Histology? |
Aspergillus, cryptococcal
Immunocompromised patient Chronic inflammatory response - but may be minimal inn immunocompromised patient |
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Pathology of Myocarditis
Causes 5/7: Parasitic Name 2 parasites. Histology? Proposed mechanisms (2)? |
1 - Trypanosoma cruzi - Chagas (chronic phase includes progressive HF)
2 - Trichinosis - helminth in undercooked meat - multisystem, can infect heart. Eosinophilic infiltrate |
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Pathology of Myocarditis
Causes 6/7: Drugs Name 1 drug. Reactions to this drug? |
Cocaine
(also mentioned - hypersensitivity and eosinophils can affect heart) Sudden death syndrome, ischemic heart disease, myocarditis, contraction band necrosis (spasm - no flow - reperfusion) |
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Pathology of Myocarditis
Causes 7/7: Myocarditis with Giant Cells Name 2 causes. Histology? Outlook? Proposed mechanisms (2)? |
Sarcoidosis and Giant Cell myocarditis
Giant cell myocarditis - 'serpiginous areas of necrosis lined by giant cells,' limited to the heart Sarcoid - much more well defined Giant cell - rapidly fatal. |
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Pathology of Cardiomyopathy
Define Cardiomyopathy. Main categories (3)? |
Non-inflammatory heart muscle disease, excluding coronary heart disease, HTN, and valvular disease.
Dilated Hypertrophic Restrictive |
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Pathology of Cardiomyopathy
Category 1/3: Dilated cardiomyopathy Clincal? **Pathology (gross/microscopic)? Subcategories (~5)? Can myocarditis lead to dilated cardiomyopathy? |
Clinical: 4-chamber dilation and chronic progressive heart failure (may also have arrhythmias, embolism, mitral regurg, tricuspid regrug). Pts 20-50, M>F.
Hearts are hypertrophied (more than 400-500 grams) and dilated. Myocytes are hypertrophied with large, hyperchomatic, 'boxcar' nuclei. Subcategories: Alcoholic cardiomyopathy, Peripartum cardiomyopathy, Adriamycin - dose-related injury, Beer drinker's (cobalt), *Inherited (20%): Cardiac energy metabolism d/o, structural/contractile proteins, TFs for other cardiac myocyte genes (e.g. CREB) Looks that way, not proven. |
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Pathology of Cardiomyopathy
Category 2/3: Hypertrophic cardiomyopathy Characterized by (5)? Who is affected? Inheritance? **Molecular basis for some cases? |
Asymmetric septal hypertrophy
Systolic anterior motion of the anterior leaflet of the mitral valve Catenoidal configuration of the interventricular septum Presence or endomyocardial plaque on the outflow tract of the left ventricle Disarray of the myocytes Young adults - athletes Autosomal dominant Beta cardiac myosin heavy chain gene mutation |
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Pathology of Cardiomyopathy
Category 3/3: Restrictive cardiomyopathy What's wrong? Two forms? |
diastolic LV filling is impeded.
The contractile function of the LV is normal, but the wall is abnormally rigid. 1. Endomyocardial fibrosis - kids and young adults in Africa. 2. Loffer's syndrome - foci of myocyte necroses + eosinophilic infiltrate +/- mural thrombi. (Infiltrative - amyloid, hemochromatosis, Gaucher's disease discussed on different card) |
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Pathology of Infiltrative processes
Usually present as what type of cardiomyopathy? Name 3. |
Restrictive
Amyloid, hemochromatosis, Gaucher's disease (storage disease) |
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Heart transplantation
Matching? Immunosuppression? Two main short term complications? Long term complication? |
ABO blood type (expressed on endothelial cells!)
High dose - CsA Acute - infection or rejection (looks like viral myocarditis) Long - accelerated atherosclerosis, diffuse and concentric narrowing of the coronary arteries (CMV and immune rxn=>endothelial injury speed this up) |
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Endomyocardial bx
Uses (2)? |
1 - monitor heart transplants for rejection
2 - diagnose myocarditis in patients with new onset HF (Dallas criteria - myocarditis, borderline myocarditis (inflam without necrosis), & no myocarditis) |
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#1 cause of mortality in men?
Women? What is the trend? |
Cardiovascular disease is the #1 cause of mortality in the US today, for both males and females.
[Ischemic heart disease is the most common cause of death from cardiovascular disease, accounting for >50% of cardiovascular deaths] Deaths from heart disease, most of which are due to ischemic heart disease, have increased steadily from 1900, when it was a relatively uncommon cause of death, to 1970, but since 1970, the death rate from heart disease has stopped rising, and actually declined if the increase in population is taken into consideration. This is in part due to the creation of Coronary Care Units, and partly due to the development of defibrillators. |
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Abbreviations
IHD CHD CAD ASHD |
Ischemic Heart Disease (IHD)
Coronary Heart Disease (CHD) Coronary Artery Disease (CAD) Atherosclerotic Heart Disease (ASHD) |
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What are the four major ischemic heart disease syndromes?
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Angina Pectoris
Myocardial Infarction Sudden Cardiac Death Ischemic Cardiomyopathy (Chronic congestive heart failure) |
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Prevalence of Ischemic Heart Disease?
_% of adult population have IHD (angina vs. previous MI?) _% of U.S. deaths? (how many of these IHD deaths are 'premature'?) _% of IHD deaths are due to M.I. complications _% are sudden cardiac deaths.... in _%, death is the first symptom. |
13.5 MILLION AMERICANS (7% OF ADULT POPULATION) HAVE IHD EVIDENCED BY:
ANGINA PECTORIS (50% OF IHD) PREVIOUS MYOCARDIAL INFARCTION (>50% OF IHD) OR BOTH 500,000 DEATHS/YEAR (ONE THIRD OF ALL U.S. DEATHS) ONE THIRD OF THESE ARE "PREMATURE" DEATHS, I.E. DEATHS BEFORE AGE 75 50% ARE DEATHS FROM COMPLICATIONS OF M.I. 50% ARE SUDDEN CARDIAC DEATHS (SCD) >50% OF SUDDEN CARDIAC DEATHS OCCUR IN PATIENTS FOR WHOM DEATH WAS THE FIRST SYMPTOM OF IHD |
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IHD: Sudden Cardiac Death
Electrophysiology? Anatomic findings? (3 possible) |
VENTRICULAR FIBRILLATION
1. ACUTE CORONARY PLAQUE RUPTURE OR THROMBOSIS (MINORITY OF CASES) 2. ACUTE OR ORGANIZING (CLINICALLY SILENT?) MYOCARDIAL INFARCT (MINORITY OF CASES) 3. NO ACUTE LESION ("PRIMARY VENTRICULAR FIBRILLATION") - SUPERIMPOSED ON CHRONIC ATHEROSCLEROSIS |
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Acute coronary occlusion and myocardial infarction
Cause? |
Cause:
[ACUTE ARTERIAL OCCLUSION COMPLICATING ATHEROSCLEROSIS] MOST COMMON CAUSE: THROMBUS SUPERIMPOSED ON A RUPTURED PLAQUE [FACTORS PROMOTING VULNERABILITY TO PLAQUE RUPTURE: -LARGE ATHEROMATOUS CORE THIN FIBROUS CAP/INCREASED CAP TENSION -INCREASED # OF MACROPHAGES IN FIBROUS CAP (METALLOPROTEINASE DEGRADATION OF COLLAGEN ETC.) -LOSS OF SMOOTH MUSCLE CELLS (REDUCED COLLAGEN SYNTHESIS)] |
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Clinical diagnosis of myocardial infarction?
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1. Chest pain that persists despite therapy such as nitroglycerin
2. Presence of heart-specific proteins in the blood, such as CK-MB and cardiac troponins |
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Myocardial Ischemia Pathology
Is ischemic injury reversible? When does damage start? Metabolic effects? Functional effects? Electrolyte imbalances? Cell swelling? Contraction bands? |
Myocardial ischemia is initially reversible if the tissue is reperfused promptly, but the consequences of ischemia begin immediately, and are progressive, eventually leading to cell death.
I. Metabolic effects of myocardial ischemia 1.Impaired oxygen and substrate delivery -Cessation of oxidative phosphorylation as a means to generate ATP -Conversion to anaerobic glycolysis as a means to generate ATP -Glycogen is consumed -Fall in creatine phosphate and ATP levels; increase in inorganic phosphate 2.Decreased removal of metabolic endproducts -Decreased intracellular pH -Lactate accumulation II. Functional effects of myocardial ischemia 1.Rapid loss of contractility 2.Slowly reversible contractile dysfunction persisting during reperfusion (stunning) III. Electrolyte imbalances developing during myocardial ischemia 1.Potassium efflux and decreased membrane potential 2.Rise in intracellular sodium 3.Rise in cytosolic free ionized calcium concentration IV. Cell swelling during ischemia 1.Increase in intracellular sodium results in water influx 2.Tissue osmolality increases due to cellular catabolism V. Morphologic changes during myocardial ischemia 1.Routine histology generally is not very useful for assessing early ischemic injury. Although cell swelling and nuclear chromatin margination are seen during early ischemia, these changes are seen in reversibly injured cardiac myocytes and for many hours after the cells have lost viability. 2.Often no gross evidence of ischemic injury is seen for many hours after coronary occlusion, although sometimes there is patchy hemorrhage within the infarct if there is some blood flow into the infarcted tissue. 3.Electron microscopy provides the earliest morphologic evidence of cell death, disruption of the plasma membrane. 4.The time course of ischemic injury and the timing of the transition from reversible to irreversible injury is provided by experimental studies of transient coronary occlusion and reperfusion, and clinical studies based on autopsy findings in patients with a good clinical history that provides a time of onset of ischemia. 5.Disruption of the plasma membrane is thought to be due to cytoskeletal injury combined with stress on the membrane, due to intrinsic cell swelling and/or contraction from adjacent non-ischemic myocardium. 6.Mitochondrial amorphous matrix densities are another finding that is associated with irreversible injury 7.Contraction-band necrosis is a form of cell death that is seen in reperfused infarcts and on the periphery of non-reperfused infarcts, and occurs in the setting of recent cell death with sufficient mitochondrial integrity that some ATP synthesis is possible when oxygen becomes available, such as during reperfusion. Contraction-band necrosis can be seen by routine histology and can help to establish that an infarct has occurred and to suggest the extent of the infarct since it is most likely to occur on the periphery of an infarct. |
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Myocardial Ischemia Pathology
Infarct size as a prognostic factor? Determinants of infarct size? |
Larger infarct => Higher frequency of arrhythmias, Higher frequency of hemodynamic complications, Higher short-term mortality
Cardiogenic shock (ie, global hypoperfusion) is usually associated with infacts occupying > 30% (mean = 40%) of the LV Infarct size... (1) Vascular territory at risk (2) Magnitude of residual anterograde flow or collateral blood flow (3) Duration of ischemia (4) Metabolic rate of myocardium during ischemia (hemodynamic - HR, systolic LV pressure, contractility. Myocardial temperature) |
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MI pathology:
Anatomy 1.Coronary anatomy a. LAD supplies what? b. Left circumflex coronary artery supplies what? c. PDA (posterior descending artery, typically arising from Right Coronary Artery) supplies what? 2. Flow favors which layer? 3. Collateral flow favors which layer? 4. Wavefront concept of infarct development? 5. Collateral vessels are best developed in healthy patient or in patients with chronic angina? |
1 -LAD supplies anterior wall of LV and anterior two-thirds of septum
-Left circumflex coronary artery supplies lateral wall of LV -PDA supplies posteroseptal LV 2 -Arterial blood flow favors subepicardium over subendocardium (though Subendocardial rim of myocytes that typically survives ischemic injury) 3 -Collateral flow often provides some blood flow into an ischemic zone, even with proximal coronary occlusion, but collateral flow primarily supplies subepicardium 4 -Wavefront concept of infarct development: infarction occurs as a wavefront from subendocardium to subepicardium, as a function of duration of ischemia; the transmural progression is limited by the amount of collateral flow; transmural infarcts occur when there is little or no collateral flow (data obtained from in vivo experimental dog studies, and may be somewhat slower in humans) 5 -Collateral vessels are rudimentary in the absence of coronary artery disease, but will develop in patients with chronic angina, and can provide enough blood flow to prevent infarction |
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Morphological Stages of Myocardial Infarction, Inflammatory Response, and Repair
0-6 HOURS 6-24 HOURS 1-4 DAYS 5-7 DAYS 7-10 DAYS 1-6 WEEKS 1-3 MONTHS |
0-6 HOURS - No change (gross or microscopic)
6-24 HOURS - "Wavy-fiber change" - Early features of coagulation necrosis (cytoplasmic eosinophilia; nuclear pyknosis followed by karyolysis) 1-4 DAYS - Coagulation necrosis with acute inflammatory response (primarily neutophils) maximum influx at 2-3 days; Neutrophils intact at first, disintegrating by 3-4 days. 5-7 DAYS - Macrophage activity - phagocytosis of dead myocytes 7-10 DAYS - Developing peripheral rim of granulation tissue 1-6 WEEKS - Progressive organization of the infarct 1-3 MONTHS - Progressive collagen deposition |
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Effect of reperfusion of ischemic myocardium
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1. ACCELERATES DISINTEGRATION OF IRREVERSIBLY INJURED MYOCYTES (CAUSES CONTRACTION-BAND NECROSIS)
2.MAY ACCENTUATE HEMORRHAGE INTO AREAS OF MICROVASCULAR INJURY (RESULTS IN HEMORRHAGIC INFARCTS) 3.MAY OR MAY NOT CAUSE LETHAL REPERFUSION INJURY 4.LIMITS MYOCARDIAL INFARCT SIZE 5.SUPPORTS SLOW METABOLIC AND CONTRACTILE RECOVERY OF VIABLE MYOCYTES |
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MI pathology
1. When do you see coagulation necrosis? 2. When do you see contraction-band necrosis? |
1.
SEEN IN AREAS OF PERSISTENT MYOCARDIAL ISCHEMIA (ineffective reperfusion) 2. ISCHEMIA FOLLOWED BY REPERFUSION-- -CORONARY OCCLUSION FOLLOWED BY SPONTANEOUS OR THERAPEUTIC THROMBOLYSIS -ISCHEMIC CARDIAC ARREST AND REPERFUSION IN CARDIAC SURGERY, HYPOTENSION OR CARDIORESPIRATORY ARREST FOLLOWED BY SUCCESSFUL RESUSCITATION -CATECHOLAMINE TOXICITY-- IATROGENIC, BRAIN TRAUMA, PHEOCHROMOCYTOMA ELECTRICAL SHOCK OR MECHANICAL TRAUMA -ANY LETHAL INSULT TO MYOCYTES WHICH OCCURS IN A SETTING OF INTACT PERFUSION |
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MI pathology
Interventions to limit myocardial infarct size: 1- Restore myocardial perfusion? (2 ways) 2- Adjunctive therapy? |
1- Thrombolytics, Emergency coronary angioplasty
2- None yet. Ideas- can we delay myocyte injury until reperfusion is achieved? can we reduced reperfusion injury? |
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Complications & mortality in myocardial infarction
Acute in-hospital mortality? One-year mortality? Arrythmias - what percent of deaths? Pump failure - what percent of deaths? Other complications? |
In hospital - 7%
One-year - 35% Arrythmias= 40-50% of deaths Pump Failure= 40-45% of deaths - Cardiogenic shock, congestive heart failure (20% of MI survivors develop chronic HF) Complications: Ruptures (LV free wall, septum, papillary mm), mitral valve insufficiency, ventricular aneurysm, mural thrombosis |
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Valve Pathology
The heart valve pathologies can be divided into roughly 4 main groups ... |
stenotic valve disease, regurgitant valve disease, endocarditis and miscellaneous valve disease.
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Valve Pathology
Stenosis results from_______ and ___________ of a heart valve. Stenosis predominantly affects the ____ valve, then ____ valve. Stenosis results in a pressure __________ across the valve. How much? |
fibrosis and calcification
aortic then mitral pressure gradient -- The pressure difference between the left ventricle and aorta can be as great as 100 mm Hg with a severely stenotic aortic valve. |
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Valve Pathology
What does bicuspid aortic valve predispose? When does it happen? |
(1-2% of population) have a high risk of developing a stenosis requiring valve replacement.
earlier age (50-60s) than patients with normal tricuspid aortic valves that develop stenosis later in life (age = 70s-80s). The normal cross sectional diameter of an aortic valve is 3-4 cm2. Critical stenosis occurs when the diameter is reduced to 0.75 cm2, although symptoms can start earlier. |
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Valve Pathology
What is the primary cause of mitral valve stenosis? What are valve diameters for 'normal,' symptomatic, and 'critical'? |
Most mitral valve stenosis is secondary to chronic rheumatic heart disease (declining in incidence in the West)
normal cross sectional diameter: 4-6 cm2 symptoms: 2 cm2 Critical stenosis: 0.75 cm2 |
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Valve Pathology
What is the most common cause of right-sided stenosis? How does it happen and is the left side involved? |
(maybe congenital, but lecture said ...) carcinoid heart disease - carcinoid tumor in the intestine (pulmonic and tricuspid stenosis is quite rare)
Carcinoid tumors secrete vasoactive substances (serotonin is the most important). These cause the buildup of plaques on the right sided valves, but the vasoactive substances are neutralized in the lungs, sparing the left heart valves. |
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Valve Pathology
Regurgitant valve disease is when a valve is __________ and allows a _____ flow of blood. This can be the result of a disease affecting the valve or an expansion in the _____ of the valve. |
incompetent, back flow, root of the valve
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Valve Pathology
Diseases that can cause aortic regurgitation? (many) |
Bacterial endocarditis (deposits on the valves impact proper closure or destruction => holes in the valve)
chronic rheumatoid heart disease, lupus and congenital bicuspid valves. Also, root dilation from causes such as: syphilis, ankylosing spondylitis, old age and Marfan disease. |
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Valve Pathology
The primary cause of regurgitation of the mitral valve is _________. What is the frequency of this? Do they all get regurgitation? Pathologic features? |
floppy mitral valve - FMV - (mitral valve prolapse)
2-5% of people- only a subset get regurg [Pathologically, prolapse is defined as extension of the mitral valve leaflet or leaflets above the mitral annulus into the left atrium during systole. Pathologic changes include thinning and stretching of the chordae tendineae secondary to a disjunction of the mitral annulus fibrosus and a thickening and redundancy of the leaflets. Despite thickening, the valves remain soft without increased rigidity or commissural fusion.] |
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Valve Pathology
After MVP (aka FMV), what are the 3 next important causes of mitral regurgitation? |
Chronic rheumatic mitral valve disease can cause regurgitation in addition to stenosis. This happens when the chordae become thickened and shortened preventing the valve from fully closing.
Bacterial endocarditis can cause regurgitation from either deposits on the valves impacting proper closure or from destruction and resultant holes in the valve, as seen in aortic disease. Myocardial infarctions that impact on the papillary muscles can cause severe regurgitation as the valve no longer moves. Rarely, a calcified mitral annulus can cause mitral regurgitation. |
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Valve Pathology
Endocarditis can be noninfectious or infectious. What is the common cause of noninfectious endocarditis (marantic)? What is a secondary risk? |
Hypercoagulable state - small thrombotic plaques develop on the heart valves. One well-known form is Libman-Sacks endocarditis, seen in 4% of patients with lupus. This form of endocarditis is at risk for secondary bacterial infection.
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Valve Pathology
What is Libman-Sacks endocarditis? |
A noninfectious endocarditis (marantic) seen in 4% of lupus patients - mall thrombotic plaques develop on the heart valves - at risk for secondary bacterial infection.
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Valve Pathology
What are three populations at risk for infective endocarditis? The most common and dangerous bacterial cause is ________, followed by _______ and other________ species. A rarer, but well-known group of bacteria that cause endocarditis are the ______ organisms. An aggressive endocarditis may cause valve destruction resulting in valvular regurgitation. Vegetations can also do what? Histologically, what do we see? |
IV drug users, the elderly and individuals with prosthetic heart valves
Staph. aureus, Streptococcus, Staphlococcus ... HACEK spontaneously break off and enter the circulation. These emboli can cause severe complications such as strokes and myocardial infarctions from left sided endocarditis and pulmonary emboli from right sided endocarditis. Histologically: adherent vegetation on the valve, valve ulceration, bacterial colonization and acute inflammatory cell (neutrophil) response. |
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Valve Pathology
Artificial Valve Disease The two types of artificial valves are _______ and ___________ valves. In addition to valve replacement, the mitral valve is routinely repaired. What is used to treat stenotic mitral valves? regurgitant (floppy) mitral valves.? |
mechanical, bioprosthetic
Balloon valvuloplasty Valve ring annuloplasty [Balloon valvuloplasty is associated with a small risk of embolization (1-3%) and annuloplasty rings are known to become infected similar to other foreign material.] |
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Valve Pathology
Artificial - what is the main disad? What were the original replacement valves, first used in the 1960s? What next? What is the current prominent artificial valve? How long does it last? What are bioprosthetic valves? Advantage? Disad? The biggest 3 complications of valve replacement are what? |
Disad: Life-long anticoagulation.
original: caged ball (Starr-Edwards) valves -- loud and were known to drive some recipients mad tilting disk valve, the Bjork-Shiley (engineering defect which can result in the catastrophic loss of a strut, and is no longer used) Current: bi-leaflet valve, the St. Jude valve was introduced in the early 1970s and has since become the prominent artificial valve. - Lasts 20-30 years bioprosthetic valves: cow and pig valves sown into a new annulus. Good: no anticoag. Bad: Only last 10-15 years leaks, obstructions and infections (+ Bioprosthetic valves often calcify and tear resulting in regurgitation by the end of their useful lives.) |
