Ischemic Heart Disease, Angina, and Myocardial Infarction Flashcards
(86 cards)
1
Q
Ischemic heart disease physiology
A
–Coronary blood demand exceeds coronary blood flow
•Decreased supply vs. Increased demand
•Myocardial metabolism is aerobic!
2
Q
Ischemic heart disease physiology
A
–Coronary blood demand exceeds coronary blood flow
•Decreased supply vs. Increased demand
•Myocardial metabolism is aerobic!
3
Q
Ischemic heart disease etiology
A
–Atherosclerosis
–Hyperthyroidism
–Anemia
–Emotional stress
–Variant angina
•Prinzmetal’s -vasospasm in etiology, associated with other vasospastic phenomena
4
Q
Ischemic heart disease physical presentation
A
–Retrosternal, aching or squeezing, may radiate to neck, shoulder (usually left), back, teeth, epigastrium
msk you can pinpoint bc it is innervated heavily heart is not so they cant pinpoint
5
Q
Ischemic equivalents/Associated symptoms
A
–Shortness of breath –Diaphoresis –Nausea and/or vomiting –Dizziness –Weakness
due to visceral overlap
6
Q
IHD risk factors Framingham
A
after WWII
–1948 –5209 men and women ages 30-62 –Return every two years –Second generation 1971 with 5124 patients –Third generation 2002 –Omni cohorts in 1994 (blacks too)
7
Q
IHD risk factors
A
- Increasing age
- Male
•Smoking
–Dose-response relationship
–2-3 fold increase risk of dying form cardiovascular disease
–Rapid risk reduction in 2 years after quitting
- Hypertension
- Diabetes
- High cholesterol/Dyslipidemia –the most powerful modifiable risk factor
•Family history
–Premature heart disease in a first-degree relative
•Male
8
Q
IHD risk factors metabolic syndrome
A
–Clustering of risk factors with a two fold increase in CAD risk
- Insulin Resistance
- Hyperglycemia
- Hypertension
- Elevated Triglycerides
- Low HDL cholesterol
- Obesity
–Nearly doubles the risk of cardiovascular disease
9
Q
IHD risk factors Conditional
A
lack validation and/or used to supplement clinical judgment
–Homocysteine (an intermediate amino acid in methionine metabolism)
–Lipoprotein(a)
–hsCRP -(High-sensitivity C-reactive protein)
–LDL particle size
–Antioxidant therapies (vitamins E &C and beta-carotene) (largely disproven)
–Omega-3-fatty acids intake has been shown to reduce cardiovascular risk but direct study of supplementation is not well-defined
10
Q
–Homocysteine (an intermediate amino acid in methionine metabolism)
A
Cardiac risk not improved with folate supplementation
b12 folate
11
Q
–Lipoprotein(a)
A
- Resembles LDL with an added glycoprotein
- Few pharmacological agents lower Lipoprotein(a) [Niacin can reduce levels]
- No research has demonstrated efficacy in CV risk reduction by lowering Lipoprotein(a)
12
Q
–hsCRP -(High-sensitivity C-reactive protein)
A
Useful in assessing patients with intermediate Framingham risk scores, reclassifies up to 30% into either low or high risk
association between inflammation and heart disease
13
Q
–LDL particle size
A
Inconclusive and needs further study
14
Q
Cardiovascular Inflammation Reduction Trial (CIRT)
A
- directly test the inflammatory hypothesis of atherothrombosis
- determine whether the common anti-inflammatory drug low-dose methotrexate (LDM, target dose of 15 to 20 mg po weekly) will reduce rates of recurrent myocardial infarction, stroke, or cardiovascular death among patients with established coronary artery disease and either type 2 diabetes or metabolic syndrome
- determine whether LDM will reduce the rate of new onset type 2 diabetesamong those with metabolic syndrome at study entry
15
Q
IHD low risk
A
16
Q
IHD intermediate risk
A
10-20% 10-year Framingham risk
–Further evaluation
17
Q
Reynolds risk score
A
Sex specific tool that accounts for family history and high sensitivity C-reactive protein
most accurate one
18
Q
Reynolds risk score
A
Sex specific tool that accounts for family history and high sensitivity C-reactive protein
most accurate one
19
Q
Ischemic heart disease etiology
A
–Atherosclerosis
–Hyperthyroidism
–Anemia
–Emotional stress
–Variant angina
•Prinzmetal’s -vasospasm in etiology, associated with other vasospastic phenomena
20
Q
risk factors from greatest odds to least odds
A
cholesterol
current smoking
psychosocial stressors
diabetes mellitus
htn
abdominal obesity
moderate alcohol intake
exercise
veggies and fruit daily
21
Q
Ischemic equivalents/Associated symptoms
A
–Shortness of breath –Diaphoresis –Nausea and/or vomiting –Dizziness –Weakness
due to visceral overlap
22
Q
IHD risk factors Framingham
A
after WWII
–1948 –5209 men and women ages 30-62 –Return every two years –Second generation 1971 with 5124 patients –Third generation 2002 –Omni cohorts in 1994 (blacks too)
23
Q
IHD risk factors
A
- Increasing age
- Male
•Smoking
–Dose-response relationship
–2-3 fold increase risk of dying form cardiovascular disease
–Rapid risk reduction in 2 years after quitting
- Hypertension
- Diabetes
- High cholesterol/Dyslipidemia –the most powerful modifiable risk factor
•Family history
–Premature heart disease in a first-degree relative
•Male
24
Q
IHD risk factors metabolic syndrome
A
–Clustering of risk factors with a two fold increase in CAD risk
- Insulin Resistance
- Hyperglycemia
- Hypertension
- Elevated Triglycerides
- Low HDL cholesterol
- Obesity
–Nearly doubles the risk of cardiovascular disease
25
IHD risk factors Conditional
lack validation and/or used to supplement clinical judgment
–Homocysteine (an intermediate amino acid in methionine metabolism)
–Lipoprotein(a)
–hsCRP -(High-sensitivity C-reactive protein)
–LDL particle size
–Antioxidant therapies (vitamins E &C and beta-carotene) (largely disproven)
–Omega-3-fatty acids intake has been shown to reduce cardiovascular risk but direct study of supplementation is not well-defined
26
–Homocysteine (an intermediate amino acid in methionine metabolism)
Cardiac risk not improved with folate supplementation
b12 folate
27
–Lipoprotein(a)
* Resembles LDL with an added glycoprotein
* Few pharmacological agents lower Lipoprotein(a) [Niacin can reduce levels]
* No research has demonstrated efficacy in CV risk reduction by lowering Lipoprotein(a)
28
–hsCRP -(High-sensitivity C-reactive protein)
Useful in assessing patients with intermediate Framingham risk scores, reclassifies up to 30% into either low or high risk
association between inflammation and heart disease
29
–LDL particle size
Inconclusive and needs further study
30
Cardiovascular Inflammation Reduction Trial (CIRT)
* directly test the inflammatory hypothesis of atherothrombosis
* determine whether the common anti-inflammatory drug low-dose methotrexate (LDM, target dose of 15 to 20 mg po weekly) will reduce rates of recurrent myocardial infarction, stroke, or cardiovascular death among patients with established coronary artery disease and either type 2 diabetes or metabolic syndrome
* determine whether LDM will reduce the rate of new onset type 2 diabetesamong those with metabolic syndrome at study entry
31
IHD low risk
32
IHD intermediate risk
10-20% 10-year Framingham risk
| –Further evaluation
33
IHD High risk
>20% 10-year Framingham risk
| –Aggressive risk modification
34
Reynolds risk score
Sex specific tool that accounts for family history and high sensitivity C-reactive protein
most accurate one
35
IHD reduction of risk factors
```
-Aspirin
•Risk vs. benefit
–Reduction of blood pressure
–Reduction of hyperlipidemia
–Smoking cessation
–Regular exercise
–Weight reduction and reduction of BMI (
```
36
Acute Coronary Syndromes
•History and Physical Exam
–Necessary to distinguish between syndromes that mimic acute coronary syndromes or may change the disease management
* Onset –timing of treatment
* Risk factor evaluation
* Recent medication use (aspirin etc)
* Aortic dissection
* Pericarditis
* Pulmonary embolism
* CHF –SOB, orthopnea
37
Aortic dissection
–in the back, often described as a tearing sensation (Type A dissection may extend into the right coronary artery and the presentation may be that of an actual inferior wall MI with the dissection, although the left coronary artery can be involved but less often)
–Widened mediastinum on chest X-Ray
38
Pericarditis
–recent viral illness, pleuritic chest pain, pulses paradoxus
39
Pulmonary embolism
–inactivity, malignancy/hypercoagulable state, pleuritic chest pain
–New onset of Atrial fibrillation
40
Troponin
can show up with just angina
41
mm
skeletal muscle
42
mb
heart
43
bb
brain
44
exercise stress test
–Bruce protocol
–HRmax= 220 − age
every 3 mintues it goes up in grade and speed until you hit max hr, if you hit it and ekg shows no changes your heart is in good shape
45
Pharmacological stress test
–Dobutamine (b agonist)
•Increase cardiac stress and oxygen demand
–Adenosine/Dipyridamole
•Vasodilation (work with coronary steal phenomenon)
46
Imaging
•Imaging
–Nuclear (dye that goes where its supposed to?)
–Echocardiograph (us that shows wall motion abnormalities)
•Angiography
–Lower dose radiation
–Gold standard for defining coronary occlusion
•CT/MRI
–Good to estimate coronary artery calcium scoring and anatomy, but no functional information
47
IWMI is?
volume dependant so we treat it with volume
48
Coronary Artery Calcifications
incidental finding?
49
Acute Coronary Syndromes
•A spectrum of a single disease
•Unstable Angina ST-elevation MI
–Stratified based upon ECG and serum biomarkers (troponin and creatine kinase –CPK)
50
Typical chest pain clinical presentation
| •(Central, Visceral, Exertional)
1) Central substernal pain/discomfort –usually retrosternal
2) Exertional –Brought on or increased with activity/emotional stress
3) Relieved by nitrates or rest
51
1) Central substernal pain/discomfort –usually retrosternal
* May radiate to the shoulder, arms, jaw or back
| * Visceral –usually poorly located; associated with nausea, vomiting, diaphoresis and/or shortness of breath
52
2) Exertional –Brought on or increased with activity/emotional stress
•25% maybe silent ischemia
•25% atypical
–Woman, diabetics, elderly
53
Acute Coronary Syndromes
•History and Physical Exam
–Necessary to distinguish between syndromes that mimic acute coronary syndromes or may change the disease management
* Onset –timing of treatment
* Risk factor evaluation
* Recent medication use (aspirin etc)
* Aortic dissection
* Pericarditis
* Pulmonary embolism
* CHF –SOB, orthopnea
54
Aortic dissection
–in the back, often described as a tearing sensation (Type A dissection may extend into the right coronary artery and the presentation may be that of an actual inferior wall MI with the dissection, although the left coronary artery can be involved but less often)
–Widened mediastinum on chest X-Ray
55
Pericarditis
–recent viral illness, pleuritic chest pain, pulses paradoxus
56
Pulmonary embolism
–inactivity, malignancy/hypercoagulable state, pleuritic chest pain
–New onset of Atrial fibrillation
57
Acute Coronary Syndromes
ST-elevation myocardial infarction
–Early reperfusion indicated –time is muscle!
•Thrombolytic therapy versus rapid revascularization in the catheterization lab
–Most significant determining factor is “Door to Balloon” time (75)
tpa if cant get to cath lab
58
Absolute contraindications to thrombolytic therapy
»Intracranial Hemorrhage
»Ischemic CVA in the last 3 months
»Facial trauma in the last 3 months
»Bleeding diathesis
59
Relative contraindications to thrombolytic therapy
»Thrombolytic therapy does not has a clear benefit weighed against the risks beyond 12 hours
»Chronic, severe, poorly-controlled hypertension
»Severe uncontrolled hypertension on presentation
»Ischemic CVA > 3 months, known intracranial pathology
»Dementia
»Internal bleeding within the last 4 weeks
»Noncompressible vascular site
»Pregnancy
»Peptic Ulcer disease
»Current anticoagulant use
60
Myocardial Infarction Complications -Early
Early complications –immediate or first few hours
–Thrombolytics
–IWMI
–AWMI
61
Early complications
thrombolytics
* Bleeding (2-3 times higher incidence of hemorrhagic CVA in women)
* Reperfusion arrhythmias (be patient it will go back to normal)
62
Early complications
IWMI
* Bradycardia and AV block –AV nodal perfusion by the right coronary artery
* Right ventricular infarction, always think about RV infarct with inferior wall MI
* Hypotension for volume depletion
63
Coronary artery calcium (CT or MRI)
•Highly effective in negative predictive value, also used to evaluate patients with an intermediate Framingham score
64
IWMI is?
volume dependant so we treat it with volume
65
Post ACS Mortality Risk Stratification
To determine level of intervention prior to hospital discharge
Angiography vs. Non-invasive testing
Angiography indications
66
Angiography vs. Non-invasive testing
* Used to identify high-risk patients -three vessel disease and left main disease require revascularization
* Patients should have evaluation of ejection fraction and a provocative ischemic test, if they hav
67
Angiography indications
•EF
68
Post Acute Coronary Syndrome Mortality Intervention
Mortality reduction
–Beta-blockers 20%
–Aspirin 33%
–Angiotensin-Converting Enzyme Inhibitors
–HMG-CoA Reductase Inhibitors 25-30%
–Intense management of hyperglycemia, maintaining blood sugars below 180 mg/dL, during the acute hospital stay
69
–Angiotensin-Converting Enzyme Inhibitors
* Normal EF 17%
| * Reduced EF 23%
70
–HMG-CoA Reductase Inhibitors 25-30%
* Proportional to the reduction in LDL levels
| * LDL goal
71
Post Acute Coronary Syndrome Mortality Intervention
Coronary Revascularization
–Percutaneous intervention (PCI)
–Coronary Artery Bypass Grafting
72
–Percutaneous intervention (PCI)
shown not to have improvement overall in survival or recurrent acute events, except those with silent ischemia by noninvasive stress testing. It is primarily reserved for those with positive stress tests, failure of medical therapy or poor surgical risk
angiopalsty cardiac cath are all synonymous terms
73
–Coronary Artery Bypass Grafting
in stable CAD is only indicated in patients with Left Main disease, Left Main equivalent (high grade stenosis >70% Proximal LAD and Circ), Three vessel disease, two vessels involving proximal LAD and EF
74
Chronic Coronary Artery Disease Stratification
Diagnostic evaluation
```
–Pretest probability
–Ability to exercise
–ECG findings
–Co-morbid diseases (pulmonary)
–Non-cardiac surgery risk stratification
–Assess exercise capacity
```
75
pretest probabilty
•Patients with high pretest probably may be treated empirically and then stressed tested in order to evaluate therapy
76
Chronic Coronary Artery Disease Stratification
Type of tests/indications
Exercise stress test
Chemical stress test
Coronary angiography –the gold standard
Coronary artery calcium (CT or MRI)
77
Exercise stress test
* Intermediate risk
| * Assess treatment (stable vs. unstable)
78
Chemical stress test
* Dobutamine, dipyridamole, adenosine
| * Inability to exercise/physical limitations due to lack of conditioning or co-morbidities
79
Coronary angiography –the gold standard
* Positive stress test
* Successfully resuscitated for cardiac arrest
* Life limiting angina despite medical therapy
* Unclear diagnostic evaluation
* ST segment elevation MI –interventional as well as diagnostic
80
Coronary artery calcium (CT or MRI)
•Highly effective in negative predictive value, also used to evaluate patients with an intermediate Framingham score
81
Females IHD
–Average age of diagnosis 10 years later than for males
•Originally thought to be an estrogen protective effect
•Results in more comorbidities and more complicated course of disease
•Due to alterations in pharmacokinetics of aging/volume of distribution, medications often dosed inappropriately
–Have more vasospastic presentation and therefore less obstructive coronary disease
•Lower specificity with higher false positive exercise ECG testing
–More non-cardiac chest pain syndromes
–More atypical presentations
•Shortness of breath, palpitations, dizziness, and syncope
–Hormone replacement
•Has not been shown to reduce CAD risk; has lead to increase venous thromboembolism and CVA
82
females have less collaterization bc
of the increase after menopause so they get more devastating mi they also have more false positive stress tests
83
estrogen is
not protective
84
Diabetics IHD
–Between two and eight times more likely to suffer from and die from cardiovascular diseases
–Patients typically have more advanced and higher grade disease and less collateralization at presentation
–Risk reduction
•Glycemic control
•Blood pressure control
85
Diabetics Diagnosis
* Often difficult due to autonomic neuropathy
* Fatigue, dyspnea, nausea and vomiting may predominate the presentation
* Silent ischemia
* Exercise stress testing has similar diagnostic value
* Some care with angiography, but not an absolute contraindication –contrast nephropathy
contrast is nephrotoxic
86
diabetics have no chest pain bc
diabetic neuropathy
