Chest pain and ACS Flashcards
1
Q
what are the common causes of chest pain (order of most common to least)?
A
- atypical chest pain
- angina/CAD
- other cardiac causes (congestive cardiac failure, AF, dysrhythmia)
- non PE-pulmonary causes (pneumonia, pneumothorax)
- acute MI
2
Q
what are the signs and symptoms of acute coronary syndrome?
A
Central chest pain, squeezing, heaviness, radiation to jaw etc, nausea, vomiting, dyspnoea, dizziness, weakness, rest, normal examination?, jugular venous distension, S4 gallop, holosystolic murmur, bibasilar rales, hypotensive, tachycardic, bradycardic, hypoxic
3
Q
what conditions make up acute coronary syndrome?
A
unstable angina
NSTEMI
STEMI
4
Q
what investigations are performed in a patient with suspected acute coronary syndrome?
A
ECG-STEMI, NSTEMI, unstable angina
CXR-normal or signs of HF such as alveolar markings
Cardiac enzymes (troponins)-elevated in STEMI and NSTEMI but not unstable angina
BNP
Coronary angioplasty
5
Q
describe the coronary arteries?
A
The left coronary artery will divide into the circumflex and the left anterior descending artery. Subsequently, this will divide into much smaller branches. The right coronary will divide into smaller branches as well.
6
Q
what is unstable angina?
A
blood flow obstruction causing a lack of perfusion to the myocardium. Initial perfusion starts directly from the heart into the aorta and subsequently into the coronary arteries which supply their respective portions of the heart. Unstable angina results when the blood flow is impeded to the myocardium. Most commonly, this block can be from intraluminal plaque formation, intraluminal thrombosis, vasospasm, and elevated blood pressure. Often a combination of these is the provoking factor.
7
Q
what physiological factors can increase myocardial oxygen demand?
A
Arrhythmias Fever Hypertension Cocaine use Aortic stenosis AV shunts Anemia Thyrotoxicosis Pheochromocytoma CHF
8
Q
describe the pathophysiology of an NSTEMI?
A
NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion. Type 1 myocardial infarction (MI) is most commonly caused by a non-occlusive thrombus that develops in a disrupted atherosclerotic plaque, and leads to non-occlusive or near-complete thrombosis of a vessel supplying the myocardium. Plaque rupture with superimposed non-occlusive thrombus or embolic events leading to coronary vascular obstruction. Dynamic obstruction, such as in vasospasm. Progressive luminal narrowing (i.e., chronic arterial narrowing from restenosis). Inflammatory mechanisms (i.e., vasculitis).
9
Q
what extrinsic factors leads to poor coronary perfusion?
A
hypotension, hypovolaemia, or hypoxia
10
Q
what is the most common cause of NSTEMI and how does this relate to cardiac biomarkers?
A
plaque rupture or obstructive atherosclerotic disease. In this setting, the release of myocardial biomarkers in type 1 MI is thought to be due to atherosclerotic plaque fissuring or rupture with resulting intra-coronary thrombus or platelet emboli leading to diminished myocardial blood flow
11
Q
where does plaque rupture usually occur?
A
weakest and thinnest part of the atherosclerotic cap (often at shoulder region)
12
Q
what is contained within a ruptured plaque?
A
large numbers of inflammatory cells including monocytes, macrophages, and T lymphocytes.
13
Q
what proportion of occlusions occur at the sight with greatest stenosis?
A
one third of occlusions occur at a site with the greatest stenosis, most (66% to 78%) arise from lesions with <50% stenosis, and <5% arise from lesions exhibiting >70% stenosis. Approximately 25% of patients with a diagnosis of NSTEMI have a 100% occlusion of the affected artery on coronary angiography
14
Q
what is the severity of myocardial damage in NSTEMI dependent on?
A
Duration of ischaemia and time to reperfusion
Extent of underlying atherosclerosis
Presence of collateral blood flow to the affected region (reserve blood flow)
Diameter of affected coronary vessel
Degree of occlusion
Presence of other comorbidities (i.e., diabetes, renal failure, or hypertension).
15
Q
describe the pathophysiology of plaque formation?
A
Atherosclerotic plaques form gradually over years. They begin with the accumulation of low-density lipoprotein cholesterol and saturated fat in the intima (the inner layer) of blood vessels. This is followed by the adhesion of leukocytes to endothelium, then diapedesis and entry into the intima, where they accumulate lipids and become foam cells. Foam cells are a rich source of proinflammatory mediators. The lesion up to this point is referred to as a fatty streak, and may be reversible to a certain extent. Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibres.Some of the smooth muscle cells in advanced plaques exhibit apoptosis. Plaques often develop areas of calcification as they evolve. The plaque initially evolves with the artery remodelling outwards, followed by encroachment on the arterial lumen. Eventually the stenosis can limit flow under conditions of increased demand, causing angina.
16
Q
when does a STEMI usually occur?
A
STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque
17
Q
how does a STEMI occur after abrupt disruption of cholesterol laden plaque?
A
exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial cell necrosis follows. On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work. Early hyperkinesis of the non-infarcted zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic activity and Frank-Starling mechanism
18
Q
what causes infarction expansion following STEMI?
A
As necrotic myocytes slip past each other, the infarction zone thins and elongates, especially in anterior infarction
19
Q
what happens if a sufficient quanity of myocardium undergoes ischaemic injury?
A
left ventricular (LV) pump function becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end diastolic pressure give rise to diastolic dysfunction.
20
Q
what are the signs and symptoms of stable angina?
A
Chest discomfort on exertion, relieved by GTN or rest, no change in intensity, frequency or duration, no associated diaphoresis, nausea/vomiting or SOB
21
Q
what investigations would be considered if a patient has suspected stable angina?
A
ECG-no acute changes-evidence of previous infarction (Q waves) CXR-Norma or cardiomegaly Cardiac biomarkers-not elevated Stress testing Coronary angiography CT coronary angiography
22
Q
what causes angina symptoms?
A
imbalance between myocardial oxygen supply and demand
23
Q
what determines myocardial oxygen supply?
A
determined by coronary blood flow and arterial oxygen content.
24
Q
how much stenosis is required to result in stable angina?
A
In the absence of collateral coronary circulation, stenoses of >70% of the cross-sectional area (equivalent to 50% of the lumen diameter by angiography) can result in stable effort angina due to inability to adequately increase coronary blood flow with exercise
25
what other conditions can precipitate angina?
mental and emotional stress, sexual activity, tachycardia from any cause, or the metabolic demands of fever, thyrotoxicosis, and hypoglycaemia
26
what is prinzmental variant angina syndrome X?
Rarely, patients may have severe coronary vasospasm in the absence of atherosclerotic plaque, resulting in angina (Prinzmetal variant angina), or angina in the presence of normal coronary arteries (syndrome X).
27
what are the signs and symptoms of pneumonia?
Productive or dry cough, fever, pleuritic pain associated with SOB, may have rigors, myalgias, arthralgias, recent history of travel
Decreased breath sounds, rales, wheezing, bronchial breath sounds, dullness to percussion, increased tactile fremitus
28
what investigations are needed in a patient with suspected pneumonia?
CXR-pulmonary infiltration, air bronchograms, pleural effusion
WBC count-elevated with left shift (increased neutrophil count)
Sputum culture
Blood culture
29
what is the pathophysiology of pneumonia?
Infection to the lung causing an inflammatory response to be initiated and alveolar oedema and exudate formation, alveoli and respiratory bronchioles fill with serous exudate, blood cells, fibrin, bacteria leading to consolidation of lung tissues
30
what are the signs and symptoms of viral pleuritis?
Pleural friction rub with or without low grade fever, sometimes reproducible tenderness to palpation of chest when perichondritis or pleurodynia accompanies pleuritis
31
what is the pathophysiology of viral pleuritis?
Infection/inflammation or trauma causes inflammation of pleura, irritate the sensory fibres of parietal pleura. During respiration (intensified on inspiration), the pleural membrane rub together the result is severe, sharp, knifelike pain
32
what investigations would be needed if a patient had suspected viral pleuritis?
CXR-usually normal
| FBC-normal or leucocytosis with lymphocytic predominance
33
what are the signs and symptoms of GORD?
Chest pain, retrosternal burning with eating fatty meals that can be reproduced when lying supine and relieved on sitting up, relieved by antacids
No specific physical findings
34
what investigations would be needed if a patient had suspected GORD?
Try PPI to see if pain relieved
| Oesophagogastrodeodenoscopy
35
what are the signs and symptoms of costochondritis?
Focal chest wall pain, precipitating injury, aggravated by sneezing, coughing, deep inspiration or twisting of the chest. Reproducible pain on chest wall palpation
36
what is the pathophysiology of costochondritis?
The pathophysiology is not clear, but results in inflammation of the costal cartilage.
Cartilage has a relatively poor blood supply, and use of antibiotics is usually ineffective in treating infective costochondritis.
37
what would CXR show in a patient with suspected costochondritis?
no specific findings
38
what are the signs and symptoms of anxiety/panic disorder?
Sharp chest pain with anxiety, dizziness, faintness, palpitations, sweating, trembling, fear of dying, chills, hot flushes, hyperventilation, examination normal
39
what investigations should be considered in a patient with suspected anxiety/panic disorder?
ECG-normal
CXR-normal
HADS (hospital anxiety and depression scale) score->11
40
what is an aneurysm?
True arterial aneurysms are defined as a 50% increase in the normal diameter of a blood vessel. Any artery may be affected. Commonest are the abdominal aorta and iliac arteries, with popliteal, femoral and carotid arteries less commonly affected
41
what are the symptoms of aneurysm?
Often few initially, so present late. First presentation is often rupture, thrombosis or distal embolization. Many picked up incidentally on ultrasound/CT performed for some other indication
42
what are the causes of abdominal aortic aneurysm?
Traditionally believed to be solely atherosclerotic. Although they tend to develop in older men, with a smoking history, and concomitant atherosclerosis, their aetiology is unknown. Current theories include; genetic predisposition (there is an increased familial risk of aneurysms), proteolytic (matrix metalloproteinase enzymes degrading elastin in the arterial wall), infective, auto-immune.
43
what are the treatment options for AAA?
Choice between conventional open surgery or endovascular aneurysm repair
44
describe open surgical repair?
Clamps are placed above and below the AAA, the aneurysm is opened, and a synthetic graft is sutured to the normal cuff of arterial wall. The aneurysm wall is then sutured over the graft
45
describe endovascular aneurysm repair?
```
A stentgraft (combined metal and fabric device) is placed inside the arteries (endovascularly) via the common femoral arteries at the groin. Most have at least 2 components that fit together (described as modular). It is manipulated using x-ray control, endovascularly to lie in the infrarenal aorta, and deployed to exclude the AAA from the circulation.
Patient prepared, and under spinal anaesthesia both common femoral arteries (CFA’s) are exposed at the groin. A measuring angiogram is performed via the left CFA, and measurements checked. The main body of the device is introduced via the left CFA and deployed infrarenally. The position of the stentgraft, as close to the renal artery origins, without occluding them is vital. The limb extension is prepared and deployed, to extend the stengraft into the common iliac arteries. The completion angiogram shows a satisfactory position of the stent graft device, with perfusion of the renal arteries. The aneurysm is excluded from the circulation, with no leakage of blood between the aortic wall and the stentgraft (called an endoleak). Both CFA’s are repaired by clamping the arteries temporarily and suturing the defects caused by passage of the stentgraft. The groin wounds are then closed, and dressings applied
```
46
describe AAA screening?
Level 1 evidence for AAA screening. Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. 42% risk reduction in screened population. Improved technology may increase proportion of AAA suitable for EVAR. Mechanism of expansion and rupture of AAA currently unknown, but intensive research into this. Possibly drug therapy in future may stop expansion/prevent rupture, allowing conservative management of small screen-detected AAA’s
47
what are the consequences of MI?
- loss of viable myocardium impairs cardiac output and cardiogenic shock
- systolic and diastolic dysfunction-ischaemic myocardium
- abnormal cardiac rhythms
- baroreceptor reflexes leading to activation of neurohormonal compensatory mechanisms
- sympathetic nervous system activation-systemic vasoconstriction and cardiac stimulation, increase myocardial oxygen demand, sweating, renal hypoperfusion, renin release
48
what are the symptoms of MI?
include intense chest pain that may radiate into the neck, jaw or arms (i.e., referred pain), a sense of substernal heaviness, squeezing or pressure, shortness of breath (dyspnea), fatigue, fainting (syncope), nausea, sweating (diaphoresis), anxiety, sleeplessness, hypertension or hypotension (depending in part on the extent of cardiac damage), tachycardia and arrhythmias.
49
what are the differences between MI symptoms in men and women?
Recent clinical research indicates that the symptoms may be very different between men and women. Chest pain is less common in women. Instead, their most common symptoms are weakness, fatigue and dyspnea.
50
what is MI?
myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand. This is usually caused by occlusion in the coronary arteries.
51
when is STEMI suspected?
ST-elevation myocardial infarction (STEMI) is suspected when a patient presents with persistent ST-segment elevation in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history.
52
describe the role of cardiac biomarkers in diagnosis and prognosis of MI?
highly specific for myocardial damage and will be elevated around 4 to 6 hours after injury. They remain elevated for around 10 days, which can make it difficult to determine the time of myocardial injury. Patients with elevated troponin levels have a worse prognosis than those with normal troponin
53
describe glucose levels in patients with acute MI?
Hyperglycaemia is common in the setting of acute MI, with or without a history of diabetes
54
describe serum lipid levels in patients with MI?
Cholesterol levels may be lowered by high catecholamine levels produced by the myocardial infarction in its early phases, and serum lipids should therefore be repeated in 30 to 60 days
55
what is an NSTEMI?
Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischaemic event causing myocyte necrosis. NSTEMI encompasses a broad spectrum of ischaemic injury to the myocardium, which is detected by elevation of troponin
56
what will an ECG show in patients with NSTEMI?
The initial ECG may show ischaemic changes such as ST depressions, T-wave inversions, or transient ST elevations; however, it may also be normal or show non-specific changes. If persistent ST elevation, evidence of posterior MI, or a new left bundle-branch block is present, then the patient should be evaluated as an ST-elevation myocardial infarction
57
how can NSTEMI be distinguished from unstable angina?
It can be distinguished from unstable angina pectoris by normal serial troponin
58
describe the role of cardiac troponins in diagnossis and prognosis of NSTEMI?
Troponin levels confirm the diagnosis of infarction. Test is more specific than CK-MB or myoglobin and is the best marker for musculoskeletal injury, small myocardial infarction (MI), or late (>2-3 days) MI.
The 99th percentile is the cut-off value used to determine acute MI. Troponins rise 4-6 hours after onset of infarction, peak at 18-24 hours, and may persist for 14 days or longer. Infarct size can be estimated from the troponin value measured at 72 hours. Point-of-care testing can provide quantitative results in as little as 10 minutes.
Patients with negative cardiac biomarkers within 6 hours of the onset of symptoms consistent with acute coronary syndrome should have biomarkers remeasured in the time frame of 8-12 hours after symptom onset.
59
what other conditions can cause raised cardiac biomarkers?
trauma, renal failure, congestive heart failure, surgery, inflammatory states, pulmonary embolism, sepsis, burns, rhabdomyolysis, and drug toxicity.
60
what investigations should be performed in patients with suspected MI?
```
creatinine kinase
CK-MB
FBC
urea and serum creatinine
electrolytes
liver function tests
blood glucose
CXR.
```
61
describe the use of creatinine kinase in diagnosing MI?
not as selective as troponins
62
describe the use of CK-MB in diagnosing MI?
takes upto 72 hours to return to normal so can detect early infarction. Useful for secondary increases
63
describe the use of FBC in diagnosing MI?
Hb and haematocrit evaluate secondary cause of NSTEMI and evaluate thrombocytopenia
64
describe the use of urea and serum creatinine in diagnosing MI?
to know if renally cleared drugs should be adjusted
65
describe the use of electrolytes in diagnosing MI?
electrolyte abnormalities may predispose to arrythmias
66
describe the role of Echo in diagnosis of NSTEMI?
Cardiac ultrasound can demonstrate ischaemic changes even before ECG changes appear. The presence of regional wall motion abnormalities and decreased LV function provide evidence for acute coronary syndrome. Cardiac ultrasound is also useful to evaluate ischaemic complications and other causes of chest pain (i.e., pulmonary embolism, effusion, or acute valvular pathology).
regional wall motion abnormality, depressed left ventricular (LV) function, or decreased ejection fraction
67
describe the role of Echo in diagnosing STEMI?
Indicated for all patients with acute MI after reperfusion therapy, to assess left ventricular function.
Useful for further risk stratification in patients with an atypical presentation.
Echocardiography is carried out in patients with acute decompensation after acute MI, to evaluate for complications such as mitral regurgitation, ventricular septal rupture, or ventricular free wall rupture.
hypokinesis, dyskinesis, or akinesis
68
what are the goals of echocardiography?
- ventricular function, morphological abnormalities (thrombus)
- inducible ischaemia
- myocardial viability
69
what are the strengths and weaknesses of using echo to assess ventricular function?
strengths:
-high spatial and temporal resolution, can be used everywhere, at anytime, low cost
weaknesses:
-quality of images and data varies depending on operator skills and patient characteristics
70
what are the strengths and weaknesses of using echo to test for inducible ischaemia?
strengths:
-slightly more specific than nuclear imaging
weaknesses
-operator dependent, less sensitive than nuclear imaging and MRI
71
what is coronary angiography?
procedure that uses a special dye and x-rays to see how blood flows through the arteries in the heart
72
how is coronary angiography performed?
- often done along with cardiac catheterisation
- measures pressures in heart chambers
- mild sedative given
- local anaesthetic given to arm or groin and a catheter is passed through the artery to the heart
- X-rays used to help doctor position the catheter
- when the catheter is in place a contrast material is injected through the catheter
- X-rays are taken to see how dye moves through the artery and shows any blockages
- procedure lasts 30-60 mins
73
what are the indications for angiography?
recurrent symptoms (refractory angina), ischaemia despite adequate medical treatment, high risk (e.g., congestive heart failure, malignant ventricular arrhythmias), or non-invasive test findings (significant left ventricular dysfunction, ejection fraction <0.35, large anterior or multiple perfusion defects)
74
what are the potential contraindications for angiography?
Renal failure is a relative contraindication and patients with contrast allergy must be pre-medicated prior to angiography.
75
describe the features of stable angina?
- episodic
- crescendo-decrescendo pattern
- on exertion and relieved at rest
- 2-5 mins
- retrosternal pressure, heaviness, burning, radiate to arms, neck, jaw
- related to effort
- predictable
- long term symptoms
76
what is the basic pathophysiology of stable angina?
fixed stenosis
stable fibrous plaque
significant stenosis of the coronary artery
77
describe the features of unstable angina?
- severe and new onset
- crescendo pattern
- occurs at rest
- lasts >10 minutes
- same as stable but more severe and prolonged
- thrombi that project into but do not completely occlude lumen
78
describe the basic pathophysiology of acute coronary syndrome?
dynamic stenosis
| ruptured or inflamed plaque
79
what assessments would be performed in a patient with stable angina?
- exercise testing (duration, degree of ECG changes, BP response)
- CT coronary angiogram
80
what assessments would be carried out in a patient with suspected acute coronary syndrome?
ECG changes at rest, with symptoms
| troponin elevation
81
what is the prognosis for stable angina?
1.7% a year
| CV mortality 1% during 9 year follow up
82
what scoring systems are used for assessing prognosis of acute coronary syndrome?
- TIMI score (identifies high risk patients in NSTEMI)
- GRACE (global registry of acute coronary events)-mortality risk after MI
- killip class-30 day mortality post MI
83
what factors are used as part of the TIMI score system?
- age>65
- >3risk factors for CAD
- use of ASA within 7 days
- known CAD
- >1 episode rest angina
- ST segment deviation
- elevated cardiac markers
84
what factors are considered in the GRACE in hospital risk score?
```
age
heart rate
systolic bp
serum creatinine
killip class
cardiac arrest at admission
elevated cardiac markers
st segment deviation
```
85
what factors are considered in the GRACE 6 month risk score?
```
age
H/o congestive heart failure
heart rate
systolic BP
ST segment depression
serum creatinine
elevated cardiac markers
no in hospital PCI
```
86
describe characteristics and mortality rate for class IA killip-kimball class?
no heart failure
no rales or S3
6% mortality
87
describe characteristics and mortality rate for class II B killip-kimball class?
heart failure
rales (<50% lungs), s3 and venous hypertension
17% mortality
88
describe characteristics and mortality rate for class III C killip-kimball class?
severe heart failure; frank pulmonary oedema
rales (>50% lungs)
38% mortality
89
describe characteristics and mortality rate for class IV D killip-kimball class?
```
cariogenic shocks (signs-hypotension, peripheral vasoconstriction, oliguria, cyanosis, diaphoresis, heart failure, pulmonary oedema
81% mortality
```
90
what is thrombolysis/fibrinolytic therapy?
breakdown (lysis) of blood clots formed in blood vessels, using medication
91
when is thrombolysis/fibrinolytic therapy indicated?
T elevation myocardial infarction, stroke, and very large pulmonary embolisms. Thrombolysis therapy uses thrombolytic drugs that dissolve blood clots
92
give examples of fibrinolytics?
Streptokinase (Kabikinase), Anistreplase (Eminase), Recombinant tissue plasminogen activators (rtPA), Alteplase (Activase or Actilyse), Reteplase (Retavase), Tenecteplase, Urokinase
93
what is percutaneous coronary intervention?
on-surgical procedure used to treat narrowing (stenosis) of the coronary arteries of the heart found in coronary artery disease.
94
describe the process of percutaneous coronary intervention?
After accessing the blood stream through the femoral or radial artery, the procedure uses coronary catheterization to visualise the blood vessels on X-ray imaging. After this, an interventional cardiologist can perform a coronary angioplasty, using a balloon catheter in which a deflated balloon is advanced into the obstructed artery and inflated to relieve the narrowing; certain devices such as stents can be deployed to keep the blood vessel open.
95
what us primary percutaneous coronary intervention?
urgent use of PCI in people with acute myocardial infarction (heart attack), especially where there is evidence of heart damage on the electrocardiogram (ST elevation MI). PCI is also used in people after other forms of myocardial infarction or unstable angina where there is a high risk of further events.
96
what treatment is an alternative to PCI?
coronary artery bypass graft (bypasses stenotic arteries by grafting vessels from elsewhere in the body
97
in what situations may CABG be superior to PCI?
patients with extensive blockages or with a background of diabetes
98
what is endarterectomy?
surgical procedure, where the intima and inner media are removed, leaving the residual media and adventia. It removes the atherosclerotic material, relieving stenosis, or tissue that promotes embolization. It can be performed in any artery but mainly in carotid (embolic disease) or femoral artery (stenotic disease)
99
what are the indications for carotid endarterectomy in symptomatic disease?
>70% stenosis in symptomatic internal carotid artery
Symptoms are carotid tertiary TIA, amaurosis fugax or stroke
Symptoms due to embolization, rather than hypoperfusion
Prophylactic operation (reduces the risk of future strokes)
USS used to quantify degrees of narrowing in the arteries
Evidence base-NASCET and ECST. Risk of future strokes declines so early surgery is important. Currently the aim is for surgery to be with 2 weeks of symptom onset
100
what are the indications for carotid endarterectomy in asymptomatic carotid disease?
ACST published 2004 (10 year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis). If the carotid artery narrowing remains asymptomatic (no strokes etc), successful carotid endarterectomy reduces stroke incidence
RCT, asymptomatic 60-99% stenosis allocated to surgery or BMT
5yr stroke risk 11.8% for BMT, 6.4% for surgery (2.8% operative stroke risk)
ARR (absolute risk reduction) at 5 yrs of 5.4% (RRR 46%)
Often an increase in symptomatic patients
Plaque morphology (grey scale imaging)
101
describe the use of angioplasty?
RCT shows only equivalent to ‘poor surgery’
Rarely in UK
Recently reports show poor results
102
describe the procedure of carotid endarterectomy?
- A longitudinal incision is made along the anterior border of sternocleidomastoid
- The incision is deepened, with the sternocleidomastoid muscle, then the internal jugular vein retracted laterally
- The common carotid (CCA), internal caroitd (ICA) and external carotid (ECA) arteries are dissected and controlled. The carotid bifurcation, the site of the disease is left untouched, to avoid embolisationl. The 10th and 12th cranial nerves are identified and preserved.
- The arteries are clamped, and then the artery is opened. The atherosclerotic plaque is teased away, leaving as smooth a surface as possible.
- The artery is closed using a synthetic patch, to prevent narrowing, and reduce the risk of thrombosis and stroke. The clamps are removed, and flow restored
- The wound is closed over a drain, and the patient is monitored carefully. Most patients are discharged home the following day.
103
what anaesthetic is used for carotid endarterectomy?
- General or local
- Local-able to awake test patient, detect cerebral ischaemia and shunt selectively
- A shunt is a plastic tube, inserted temporarily into CCA and ICA to allow flow into ICA preoperatively
- No reliable method for detecting cerebral ischaemia intraoperatively under general, allowing selection for shunting
- GALA is a RCT to address the issue
104
describe the management pathway for a patient presenting with acute chest pain?
1. assessment and immediate management of suspected ACS
2. early management of unstable angina and non ST segment elevation MI
OR
NICE pathway on STEMI
3. NICE pathway on MI: rehabilitation and preventing further CVD
105
describe the management pathway for a patient presenting with stable chest pain?
1. assess and diagnose stable angina
| 2. manage stable angina
106
describe the management pathway for a patient who has had MI?
1. cardiological assessment for coronary revascularisation
2. drug treatment
3. cardiac rehabilitation
4. discharge summary
5. lifestyle changes
107
what drug treatment is given to patients to manage MI?
1. ACE inhibitors
2. antiplatelets and anticoagulants
3. beta blockers
4. lipid modification therapy
5. potassium channel activators and calcium channel blockers
6. treat left ventricular systolic dysfunction and heart failure after MI
7. cardiac rehabilitation
108
describe cardiac rehabilitation in patients following MI?
1. advice and encourage to attend the programme
2. health education and advice on work, travel and physical activity
3. psychological and social support
4. advice on sexual activity
5. discharge summary
109
what should be part of the discharge summary for a patient after MI?
```
confirmation of diagnosis
results of investigations
incomplete drug titrations
future management plans
advice on secondary prevention
copy of discharge summary to patient
```
110
what lifestyle changes should be advised following MI?
```
physical activity
diet
safe alcohol consumption
stop smoking
weight management
```
111
what information should be given to a patient when discussing management plan for stable angina?
- info and support-explain diagnosis, provoking factors, long term course of disease, management
- encourage patient questions
- address any misconceptions such as implications for daily activities, MI risk, life expectancy
- advice to seek medical help if sudden worsening
- discuss reasons for treatment
112
what investigations should be done on a patient with suspected stable angina?
- resting ECG
- haemoglobin
- fasting lipid profile
- fasting blood glucose
- thyroid stimulating hormone
- stress exercise ECG without imaging
- stress single photon emission computed tomography,
- stress echo
- stress cardiac magnetic resonance
- stress positron emission tomography
- cardiac computed iomographic angiography
- invasive coronary angiography
113
what would resting ECG show in a patient with stable angina?
often normal, but may reveal ST-T changes suggestive of ischaemia or Q waves indicative of prior infarction
114
describe the role of stress exercise ECG without imaging in investigating stable angina, what scoring systems are used, who is it unsuitable for and what are the recomendations in the UK?
- ECG before, during, and in recovery from exercise
- exercise capacity and heart rate achieved, symptoms, and haemodynamic response during and after exercise.
- Scores such as the Duke treadmill score -cardiac risk. moderate in sensitivity and specificity, used for diagnosis and prognosis in many patients at intermediate risk of SIHD. Risks are primarily related to inducing cardiac stress.
- Not routinely recommended in UK guidelines]. -Inappropriate for patients with baseline ECGs that make interpretation of exercise ST-segment changes difficult (left bundle branch block, baseline ST depression >1 mm, paced rhythm, digitalis use, pre-excitation). Inappropriate for patients who have limited exercise capacity (i.e., <4-5 METS) due to poor conditioning, obesity, physical impairments, or co-existing illness.
115
describe the role of imaging investigations in patients with stable angina?
maging identifies the extent and distribution of inducible ischaemia or irreversible infarct. The difference in summed scores for perfusion/wall motion from rest to stress adds prognostic information. The addition of imaging improves sensitivity and perhaps specificity over exercise ECG. Imaging is required when patients' baseline ECG precludes the detection of ischaemia or when a pharmacological rather than exercise stress is used. Stress testing with imaging is also used for prognosis or to guide revascularisation decisions in patients with known SIHD. Risks include inducing cardiac stress and (for SPECT and PET) the use of radiation. Choice of imaging modality may be influenced by patient factors, and the exact questions being asked, as well as local availability and expertise. Stress echocardiography and SPECT are the best studied and most available. Echocardiography provides more detailed information about cardiac anatomy but is more operator dependent.For patients at intermediate risk of SIHD (pre-test probability 15% to 85%), European guidelines recommend stress test with imaging when available; for patients at high-intermediate pre-test probability (65% to 85%), imaging is required. US guidelines recommend the addition of imaging to stress tests when stress ECG alone is contraindicated (baseline ECG abnormalities or pharmacological stress). British guidelines reserve stress imaging for patients with indeterminate cardiac CT angiography.
116
describe the role of cardiac compound tomographic angiography in patients with stable angina?
CCTA has high sensitivity and specificity and an increasing evidence base for prognosis and risk stratification. Severe coronary calcification can limit diagnostic quality. Risks are primarily related to contrast and radiation, although administration of beta-blockers or nitrates may also be required during the test.British guidelines recommend CCTA for initial diagnosis of SIHD, whereas US and European guidelines recommend functional testing for this purpose. Result-typically luminal narrowing of >50% is considered positive, although the presence of lesser lesions is prognostically relevant; identification of 'soft plaques' is also considered positive
117
describe the role of invasive coronary angiography in patients with stable angina?
Coronary angiography is the conventional reference standard for diagnosis of coronary artery disease. Angiography also provides details about the overall coronary anatomy. Fractional flow reserve (FFR) is increasingly used to clarify the functional significance of stenoses, particularly when intervention is being considered without prior functional testing.
Risks include the use of radiation and administration of contrast, as well as thrombosis or haemorrhage related to vascular access, arrhythmia, and atheroembolism.
Invasive angiography is not typically used for initial diagnosis of SIHD, although in patients with a high pre-test probability it may be used for confirmation of the diagnosis, risk stratification, and to identify appropriate candidates for revascularisation. It may also be used for diagnosis when initial non-invasive testing is inconclusive
118
what is cardiac rehabilitation?
Cardiac rehabilitation is a complex intervention offered to patients diagnosed with heart disease, which includes components of health education, advice on cardiovascular risk reduction, physical activity and stress management. Evidence that cardiac rehabilitation reduces mortality, morbidity, unplanned hospital admissions in addition to improvements in exercise capacity, quality of life and psychological well-being is increasing, and it is now recommended in international guidelines
119
describe cardiac rehabilitation programmes?
Various organisations and national bodies have defined cardiac rehabilitation, which is encompassed by: “Cardiac rehabilitation (and secondary prevention) services are comprehensive, long term programmes involving medical evaluation, prescribed exercise, cardiac risk factor modification, education, and counselling. These programmes are designed to limit the physiological and psychological effects of cardiac illness, reduce the risk for sudden death or re-infarction, control cardiac symptoms, stabilise or reverse the atherosclerotic process, and enhance the psychosocial and vocational status of selected patients.” Although exercise training is a core component, current practice guidelines consistently recommend “comprehensive rehabilitation” programmes that should include other components to optimise cardiovascular risk reduction, foster healthy behaviours and compliance to these behaviours, reduce disability, and promote an active lifestyle
120
what patient groups benefit from cardiac rehabilitation?
- patients with ACS
- patients with newly diagnosed chronic heart failure and chronic heart failure
- patients with heart transplant and ventricular assist device
- patients who have undergone surgery for implantation of defibrillator or resynchronisation device
- patients with heart valve replacements
- patients with exertional angina
121
what factors affect the severity of damage following NSTEMI?
1. Duration of ischaemia and time to reperfusion
2. Extent of underlying atherosclerosis
3. Presence of collateral blood flow to the affected region (reserve blood flow)
4. Diameter of affected coronary vessel
5. Degree of occlusion
6. Presence of other comorbidities (i.e., diabetes, renal failure, or hypertension).
