Cardio Path Flashcards
1
Q
Most common sites for cardiac atherosclerotic disease
A
LAD > RCA > LCX > LCA
2
Q
Leading cause of death in the US
A
Coronary artery disease (ischemic heart disease)
Most commonly caused by atherosclerosis (>90%)
3
Q
Coronary artery disease risk factors
A
Age, male, HTN, hyperlipidemia (especially LDL), smoking, diabetes
4
Q
Crushing, substernal chest pain (crushing/stabbing/squeezing)
Radiates to neck, shoulder or jaw
Rapid, weak pulse
Profuse sweating (diaphoresis)
A
Clinical features of MI
*may also present with dyspnea, N/V, or be asymptomatic
5
Q
Key events in ischemic cardiac myocytes
A
Hypoxia leads to ATP depletion
Loss of contractility occurs within 2 minutes
Irriversible cell injury occurs within 20-40 minutes
6
Q
Most sensitive and specific cardiac biomarkers
A
Troponin T and I
cTnT and cTnI
7
Q
Biomarker that is sensitive but not specific for cardiac myocyte injury
A
Creatine Kinase MB (CK-MB)
sensitive so negative CK-MB is likely a true negative for MI
8
Q
CK-MB and cTnT, cTnI time to peak
A
3-12 hours
9
Q
CK-MB normalizes after how long?
A
2-3 days (48-72 hours)
10
Q
Troponins (cTnT and cTnI) normalize after how long?
A
> 5 days (about a week)
11
Q
Occlusion of the LAD leads to infarct of which region(s) of the heart?
A
LAD occlusion => apex and anterior LV wall infarct
12
Q
Occlusion of the LCX leads to infarct of which region(s) of the heart?
A
LCX occlusion => lateral LV wall
13
Q
Occlusion of the RCA leads to infarct of which region(s) of the heart?
A
RCA occlusion => RV free wall, posterior 1/3 of septum and posterior LV wall (if right dominant)
RCA divides into PDA most commonly (right dominant heart)
14
Q
Subendocardial infarct can occur after (2)
A
- Reperfusion of a transmural infarct (will be in same region as initial infarct)
- Global hypotension (diffuse subendocardial infarct)
* subendocardium is furthest from blood supply, dies first, reperfusion saves more superficial myocytes, hypotension diffusely starves subendocardium
15
Q
Gross morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days* 3 - 7 days 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = none 4 - 12 hours = Dark mottling 12 -24 hours = Dark mottling 1 - 3 days = yellow coloration* 3 - 7 days = hyperemic border with yellowing 7 - 10 days = depressed red margins, maximally yellow and soft 10 - 14 days = depressed red margins 2 - 8 weeks = gray/white scar > 2 months = complete scarring
16
Q
Gross morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days 3 - 7 days* 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = none 4 - 12 hours = Dark mottling 12 -24 hours = Dark mottling 1 - 3 days = yellow coloration 3 - 7 days = hyperemic border with yellowing* 7 - 10 days = depressed red margins, maximally yellow and soft 10 - 14 days = depressed red margins 2 - 8 weeks = gray/white scar > 2 months = complete scarring
17
Q
Gross morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days 3 - 7 days 7 - 10 days* 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = none 4 - 12 hours = Dark mottling 12 -24 hours = Dark mottling 1 - 3 days = yellow coloration 3 - 7 days = hyperemic border with yellowing 7 - 10 days = depressed red margins, maximally yellow and soft* 10 - 14 days = depressed red margins 2 - 8 weeks = gray/white scar > 2 months = complete scarring
18
Q
Gross morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days 3 - 7 days 7 - 10 days 10 - 14 days* 2 - 8 weeks > 2 months
A
0.5 - 4 hours = none 4 - 12 hours = Dark mottling 12 -24 hours = Dark mottling 1 - 3 days = yellow coloration 3 - 7 days = hyperemic border with yellowing 7 - 10 days = depressed red margins, maximally yellow and soft 10 - 14 days = depressed red margins* 2 - 8 weeks = gray/white scar > 2 months = complete scarring
19
Q
Microscopic morphologic changes in MI
0.5 - 4 hours* 4 - 12 hours 12 -24 hours 1 - 3 days 3 - 7 days 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = waviness of fibers at border*
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
20
Q
Microscopic morphologic changes in MI
0.5 - 4 hours 4 - 12 hours* 12 -24 hours 1 - 3 days 3 - 7 days 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema*
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
21
Q
Microscopic morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours* 1 - 3 days 3 - 7 days 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis*
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
22
Q
Microscopic morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days* 3 - 7 days 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate*
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
23
Q
Microscopic morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days 3 - 7 days* 7 - 10 days 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages*
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
24
Q
Microscopic morphologic changes in MI
0.5 - 4 hours 4 - 12 hours 12 -24 hours 1 - 3 days 3 - 7 days 7 - 10 days* 10 - 14 days 2 - 8 weeks > 2 months
A
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue*
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
25
Microscopic morphologic changes in MI
```
0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days*
2 - 8 weeks
> 2 months
```
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition*
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar
26
Microscopic morphologic changes in MI
```
0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks*
> 2 months
```
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition*
> 2 months = dense collagenous scar
27
Microscopic morphologic changes in MI
```
0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months*
```
0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar*
28
General gross morphologic progression of MI
- dark mottling during the first day
- yellowing of infarct over the first few days
- hyperemic border develops over 1 week - 10 days
- scarring from 2 weeks onward
29
General microscopic progression of MI
- waviness of fibers in the first 4 hours
- coagulative necrosis over the first few days w/ neutrophils
- macrophages after neutrophils up until 1 week
- granulation tissue at 7-10 days
- collagen deposition over the next several weeks
- dense collagenous scar after 2 months
30
Early (within 24 hours) MI complications (2)
Arrhythmia: #1 cause of death, can occur within 1 hour
Contractile dysfunction: can lead to cardiogenic shock
31
Intermediate (within 2-4 days) MI complications (2)
Myocardial rupture: septal, free wall, papillary
Acute pericarditis: fibrinous or serofibrinous (tamponade)
32
Late (after 2 weeks) MI complications (3)
Dressler syndrome: febrile, autoimmune fibrinous pericarditis
Ventricular aneurysm: thin walled scar leads to dilation (remodeling can also cause arrhythmia)
Risk of CHF and life threatening arrhythmia
33
Angina induced by activity, stress
Stable angina
34
Episodic angina unrelated to physical activity, HR, or BP
Prinzmetal angina
35
Angina present at rest with a "cresendo" pattern (increasing in severity and duration)
Unstable angina
36
ECG and troponins in stable angina
Normal ECG and Troponins
37
ECG and troponins in unstable angina
ECG: Normal, inverted T-waves or ST depression
Troponins: Normal
38
ECG and troponins in NSTEMI
ECG: Normal, inverted T-waves or ST depression
Troponins: Elevated
39
ECG and troponins in STEMI
ECG: ST elevation
Troponins: Elevated
40
How long before troponins become elevated?
Approximately 3 hours
*important! STEMI presentation (ECG changes, chest pain and radiations etc.) for less than 3 hours should be assumed to be a transmural acute MI!!!
41
Blunt force to the heart in a MVA can cause
Cardiac contusion
If full thickness can cause rupture and blood filling into the pericardial space, causing cardiac tamponade
42
Most common aortic injury due to rapid deceleration in a MVA
Tearing of the aorta at the ligamentum arteriosum
*rapid deceleration can rip the ligamentum arteriosum from the aorta, causing massive hemorrhage
43
Most common cause of arrhythmia
Ischemic heart disease
*Almost any structural alteration to the heart can cause arrhythmia. others include cardiomyopathies, amyloidosis, sarcoidosis, myocarditis (autoimmune or infectious), congenital heart disease
44
Arrhythmia due to a damaged SA node, presents as bradycardia
Sick sinus syndrome
45
Arrhythmia due to independent and sporadic myocyte depolarization with variable AV node transmission, leading to an irregularly irregular HR
Atrial fibrillation
*can cause thrombus formation and thromboembolism
46
Arrhythmia due to dysfunctional AV node: prolonged PR interval
First degree heart block
47
Arrhythmia due to dysfunctional AV node: dropped beats (no QRS following some P waves)
Second degree heart block
* Type 1: progressive PR lengthening leading to eventual dropped QRS
* Type 2: Dropped QRS with normal PR
48
Arrhythmia due to dysfunctional AV node: P waves and QRS complexes are completely out of synch; independent beating of artia and ventricles
Third degree heart block
49
Hereditary channelopathy (Na or K channel dysfunction) that causes problems conducting electrical impulses throughout the heart
Long QT syndrome
*may progress to Torsades de Pointes
50
Most common cause of ischemia induced arrhythmia that leads to death
Coronary artery disease
51
Pressure overload on the heart (HTN, aortic stenosis) leads to
Hypertrophic cardiomyopathy
*cardiac myocytes grow in size in response to the need to increase contractile strength, the heart is now able to pump with more force but less volume
52
Pathologic vs Physiologic hypertrophic cardiomyopathy
Physiologic hypertrophic cardiomyopathy (due to exercise) leads to increased capillaries supplying the heart
Pathologic hypertrophic cardiomyopathy does not, leads to ischemia in severe cases
53
Volume overload on the heart leads to
Dilated cardiomyopathy
*increased volume stretches the chambers, decreasing the ability to pump blood
54
The inability of the heart to pump blood to meet the body's demand for oxygen
Congestive heart failure
55
CHF can result from diastolic dysfunction, which is
an inability to fill the ventricles during diatole
56
CHF can result from systolic dysfunction, which is
an inability to sufficiently contract the ventricles during systole
57
Systolic left sided heart failure causes (4)
- Ischemic heart disease
- HTN
- Aortic stenosis
- Dilated cardiomyopathy
58
Systolic left sided heart failure leads to
decreased ejection fraction
59
Diastolic left sided heart failure causes (4)
- HTN
- Aortic stenosis
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
60
Diastolic left sided heart failure leads to
normal ejection fraction but lower volume output due to less filling
61
Right sided heart failure causes (2)
- Left sided heart failure (most common)
| - Cor pulmonale (lung dysfunction)
62
Diagnosis?
Paroxsymal nocturnal dyspnea
Pulmonary congestion (cough, crackles, wheezes, tachypnea)
Orthopnea
Tachycardia
Exertional dyspnea
Cyanosis
Kerley B lines on CXR (interstitial pulm edema)
Left heart failure
*inability of the LV to pump leads to pulmonary edema/congestion, decreased tissue perfusion (including brain and kidneys)
63
Diagnosis?
```
Exertional dyspnea
Ascites
Hepatomegaly
Splenomegaly
Jugular venous distension
```
Right heart failure
*inability of the RV to pump causes the blood/fluid to back up into the venous system
64
Chronic, slowly accumulating pericardial effusion
Typically asymptomatic
Appears as enlarged heart on CXR
Serous effusion
*from CHF
65
Acute (<1 week) rapidly accumulating pericardial effusion
Symptomatic (hypotension, death)
Cardiac tamponade
Hemopericardium
*from trauma, ruptured MI, aortic dissection
66
Clinical signs of what diagnosis?
Pleuritic chest pain (worsens with breathing)
Position dependent chest pain
Pericardial friction rub on auscultation
Pericarditis
67
Fibrinous/ serofibrinous pericarditis causes (3)
* increased fibrin = fibrinous
* increased fibrin and fluid = serofibrinous
- Acute MI (inflammation post-MI)
- Dresslers syndrome (autoimmune 1-3d post MI)
- Uremia (CKD pt who presents w/ pericarditis)
68
Pericarditis caused by viral or noninfectious inflammatory diseases
Serous pericarditis
69
Pericarditis caused by active microbial infection
Purulent/suppurative pericarditis
70
Pericarditis caused by Tuberculosis, sometimes fungal
Caseous pericarditis
71
Pericarditis caused by the spread of a malignant neoplasm or trauma
Hemorrhagic pericarditis
72
Pericarditis where the heart is encased in a dense fibrous scar that limits diastolic expansion; mimics restrictive cardiomyopathy
Constrictive pericarditis
73
Most common primary cardiac tumor in adults (benign)
Mesenchymal origin
Arise in the LA, in the septal region of the fossa ovalis
Pedunculated, moves like wrecking ball
Can embolize
Secretes IL-6 (fever and malaise)
Cardiac Myxoma
74
Cardiac tumor comprised of fat (benign)
Cardiac lipoma
75
Cardiac tumor that looks like a sea anemone
| Resemble a larger version of Lambl excrescences (thrombi on valves of old people)
Papillary fibroelastoma
76
Most common tumor of the pediatric heart (benign)
Hamartoma of developing cardiac myocytes
50% due to mutations in tuberous sclerosis genes (TSC1 or TSC2)
Cardiac rhabdomyoma
77
Malignant endothelial neoplasm that primarily affects older adults
Angiosarcoma
78
Heart transplant rejection in the first month
- Cell mediated rejection (T-cells)
- Antibody mediated rejection
*both due to immune response to foreign heart HLA Ags
79
Most significant long term limitation to survival post heart transplant
Allograft vasculopathy
*immune response induces growth factors that eventually lead to occlusion and stenosis of coronary arteries
80
How may allograft vasculopathy present?
Silent MI
(at +/- 10 years)
*no angina due to denervated heart
81
Chronic immunosuppression in heart transplant patients put pts at risk for
- Increased risk of skin cancers
| - EBV positive lymphoproliferative disorder
82
General effect of aging on the heart
Decreased compliance and elasticity of the heart and vessels
*fibrotic valves, calcific deposits, LV cavity size decrease, atrial dilation, atherosclerosis induced stenosis
83
Shunt type in ASD, VSD and PDA
| Typically asymptomatic unless large
Left to right shunt
* oxygenated blood can move back to the right heart
* ASD/VSD lead to increased RV outflow and pulm bloodflow
* PDA increases only pulmonary bloodflow
84
Shunt type in tetrology of fallot, transposition of the great vessels and tricuspid atresia
Right to left shunt
*deoxygenated blood bypasses the lungs
85
Failure of the septum secundum to close
Asymptomatic until adulthood
Systolic ejection murmur
Ostium secundum ASD
* L to R shunt
* most common ASD
86
Most common form of congenital heart disease
Malformation of the membranous part of the interventricular septum
Asymptomatic until adulthood
Holosystolic murmur
VSD
* L to R shunt
* Symptomatic VSD associated with other cardiac anomalies
* Membranous type most common
87
Failure of the ductus arteriosus to close after birth due to hypoxia or other heart defects
Increased pulmonary vascular resistance
Harsh machine like murmur
Typically asymptomatic
PDA
*L to R shunt
88
Explain Eisenmenger Syndrome
- Longstanding L to R shunt causes pulmonary HTN -Pulm vascular remodeling increases resistance
- Shunt reversal (L to R becomes R to L)
- Blood bypasses lungs
- Hypoxia (cyanosis) and extreme dyspnea leads to death
89
Patent foramen ovale in pt with a DVT can lead to
Paradoxical embolism
* venous thrombosis => arterial thrombosis => end organ effects/stroke
* paradoxical embolism due to PDA would lead to LE arterial occlusion
90
Four features of Tetrology of Fallot
- VSD
- RVH
- Subpulmonic stenosis
- Overriding aorta (entrance to aorta centered over VSD)
91
Clinical presentation of what diagnosis?
```
Cyanosis present since birth
Holosystolic murmur
Systolic ejection murmur
Cyanosis, syncope during emotional distress, excitement or activity
Compensatory squatting
Boot shaped heart on CXR
```
Tetrology of Fallot
* Holosystolic murmur (VSD)
* Systolic ejection murmur (subpulmonic stenosis)
* Cyanosis, syncope during emotional distress, excitement or activity (Tet spell)
* Compensatory squatting (increases systemic pressure)
92
Aorta and pulmonary artery are switched
Incompatible with life
Cyanosis at birth
Transposition of the Great vessels
*Must keep PDA open or death (give PGE1), surgery necessary
93
Complete absence of the tricuspid valve
Severe immediate cyanosis
Oxygenation maintained by ASD/PFO and VSD, otherwise incompatible with life
Severe immediate cyanosis
Tricuspid atresia
* LV pumps to lungs and systemic circulation simultaneously
* surgical correction necessary
94
Infantile vs adult type of coarctation of the aorta (focal narrowing of the aorta)
- Infantile form has PDA (creates shunt that bypasses lungs)
| - Adult form without PDA
95
Coarctation of the aorta is associated with what genetic abnormality in females?
Turner syndrome (45, X)
96
Clinical presentation diagnosis?
- Baby with cyanosis of lower half of body only
- Adult with upper body HTN and lower body hypotension, rib notching
Coarctation of the aorta
*closure of the PDA leads to no cyanosis in adult form
97
Clinical presentation diagnosis?
Cyanotic baby with left ventricular hypertrophy
Congenital aortic stenosis
98
Most common septal defects in down syndrome (trisomy 21)
AVSD > VSD > ASD
99
Marfan syndrome (tall, thin, lanky, Fibrillin-1 mutation) is at risk for what cardiovascular complication?
Aortic aneurysm/dissection
*Fibrillin-1 mutation leads to excessive TGF-B activity, increasing metalloproteases, leading to degradation of elastin
100
DiGeorge syndrome is associated with what cardiac defect?
Conotruncal abnormalities (TOF, transposition, ASD, VSD)
*CATCH-22
101
Hypertensive heart disease can lead to
CHF due to diastolic or systolic heart failure
* HTN => LV hypertrophy
* diastolic failure due to concentric LV hypertrophy, systolic failure due to increased O2 demand
102
Pulmonary HTN due to pulmonary vessel diseases causes RV dilation then hypertrophy, eventually leading to right heart failure
Cor pulmonale
103
Wear and tear of the aortic valve associated with HTN and hyperlipidemia
Calcific aortic stenosis
*chronic progressive injury leads to calcification of valve
104
Bicuspid aortic valve is associated with what complications (3)
- Accelerated onset of calcific aortic stenosis
- Aortic valve prolapse
- Infective endocarditis more likely
105
Mitral annular calcification is associated with what complications (2)
- Arrhythmia (heart block)
- Infective endocarditis
*most common in elderly females with MVP
106
Mitral valve prolapse can rarely occur in what genetic condition?
Marfan syndrome
*MVP is typically absent of an underlying cause
107
Clinical presentation diagnosis?
Midsystolic click on auscultation
Mitral regurgitation
Dyspnea in chronic cases
Mitral valve prolapse
*may lead to arrhythmia (afib with atrial dilation) or infective endocarditis in severe cases
108
```
GAS
JONES criteria
M streptococcal antigen
Dx confirmed with Ab to Streptolysin O and DNase B
Valves affected = MAT
```
Rheumatic fever
109
Acute infectious endocarditis presentation
Fever and chills that develop rapidy
110
Subacute infectious endocarditis presentation
Low grade fever (<101F) and fatigue
111
Organism that causes acute infectious endocarditis, specifically tricuspid valve in IVDU
S aureus
*can also infect prosthetic valves
112
Organism that causes subacute infectious endocarditis after dental procedure/ poor dentition
S viridans, HACEK group
*Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella
113
Organism that causes subacute infectious endocarditis, specifically prosthetic valves
S epidermidis
114
Sterile, non-inflammatory valvular thrombi caused by hypercoagulable states like cancer, antiphospholipid syndrome, SLE
Nonbacterial Thrombotic Endocarditis
* Cancer = mucinous adenocarcinomas
* APS and SLE create anti-endothelial Ab, which is procoagulant
115
What side of the heart can be affected in carcinoid heart disease and why?
Right heart (tricuspid, pulmonic, RV) because lungs catabolize serotonin, protecting the left heart
*Carcinoid tumor must mets to liver to affect heart
116
Complications of prosthetic heart valves (mechanical and bioprosthesis)
- Infectious endocarditis (both)
- Lifelong risk of thromboembolism (mech)
- Only last 10-15 years (bio)
- RBC shearing (both)
- Regurgitation (both)
117
Cardiomyopathy definition
Structurally and functionally abnormal heart with mechanical or electrical dysfunction in teh absence of CAD, HTN, valvular disease, congenital heart disease
118
Dilated cardiomyopathy with systolic dysfunction due to a mutation in TTN (Titin)
Familial dilated cardiomyopathy
119
Dilated cardiomyopathy with systolic dysfunction due to volume overload that occurs in late pregnancy
Peripartum cardiomyopathy
120
Dilated cardiomyopathy with systolic dysfunction due to direct cytotoxic effects of alcohol on cardiomyocytes, or thiamine deficiency (impaired cell metabolism)
Alcoholic cardiomyopathy
121
Dilated cardiomyopathy with systolic dysfunction due to antracyclines doxorubicin and daunorubicin
Drug induced dilated cardiomyopathy
122
Dilated cardiomyopathy with systolic dysfunction due to hemochromatosis
Iron overload dilated cardiomyopathy
123
Classic presentation:
Otherwise seemingly healthy athlete dies of sudden cardiac death
May present with systolic ejection murmur
Hypertrophic ventrcular septum
Hypertrophic cardiomyopathy (diastolic dysfunction)
* Mutations in sarcomere proteins, most commonly B-myosin heavy chain
* Myocyte hypertrophy and disarray with septal prominence
124
Myocardium of the right ventricular wall is replaced with adipose & fibrosis
Leads to Vtach, premature contractions, fibrillation
Sudden death
Arrythmogenic Right Ventricular Cardiomyopathy (ARVC)
125
ARVC with plantar and palmar hyperkeratosis, wooly hair
| Mutation in plakoglobin
Naxos syndrome
126
Cardiomyopathy caused by deposition of material (amyloid) in heart wall
Diastolic dysfunction leads to enlarged atria with normal sized ventricles
Restrictive cardiomyopathy
* AL amyloid from multiple myeloma
* AA amyloid released from liver in chronic inflammatory states
127
Most common myocarditis, seen in viral infection (most common) and autoimmune
Abundant lymphocytic infiltrate
Lymphocytic myocarditis
* Viral infection: Coxsackie B and COVID-19
* Coxsackie B presents as fever, headache, sore throat, GI distress, fatigue, chest pain, myalgias
128
Myocarditis can also be caused by Chagas disease
Trypansoma cruzi
129
Myocarditis after eating undercooked pork, also comes with myalgias and GI symptoms
Trichenella spiralis
130
Myocarditis after tick bite, erythema migrans, bells palsy, heart block
Lyme disease, Borriela burgderofi
131
Myocarditis with eosinophilia in the absence of parasitic infection
Caused by hypersensitivity to drug
Eosinophilic myocarditis
132
Idiopathic myocarditis that is aggressive and poor prognosis
| Enlarged multinucleated cells
Idiopathic giant cell myocarditis
133
Idiopathic myocarditis
| Giant cells with non-necrotizing granulomas
Myocardial sarcoidosis
