Ischaemic Heart Disease Flashcards
1
Q
What are the three layers of the heart muscle?
A
Endocardium, Myocardium, Epicardium
Endocardium resembles endothelial cells; myocardium is the thickest layer formed of cardiomyocytes; epicardium forms the visceral layer of the pericardium.
2
Q
What is hs-CTN and its significance?
A
High-sensitivity cardiac troponin, either troponin I (hs-cTnI) or troponin T (hs-cTnT)
It has high sensitivity and specificity for measuring sub-clinical cardiac damage.
3
Q
What is the normal range for troponin T?
A
14 ng/L
Levels above this indicate myocardial damage or infarction.
4
Q
What characterizes atherosclerosis?
A
Thickening of the tunica intima due to hypercholesterolemia, LDL infiltration, and inflammation
This process leads to foam cell formation, necrotic core development, and possible plaque complications.
5
Q
What is aortic dissection?
A
Aortic dissection is a life-threatening condition caused by tearing of the tunica intimia wall of the aorta, causing blood to acccumulate between the intima and media which creates a false lumen that compromises blood flow to vital organs. It tends to affect the very young with connective tissue disorders or elderly
Anterograde dissection affects the lower branches such as the iliac arteries
Retrograde move back towards the aortic valve at the root of the aorta, resulting in bleeding into pericardium and cardiac tamponade.
6
Q
What are the two types of aortic dissection
A
It is more common in individuals with connective tissue disorders
It is classified based on the Stanford classification into:
Type A: involves the ascending aorta- THIS IS A MEDICAL EMERGENCY
Type B: occurs in the aortic arch or descending aorta
Type A involves the ascending aorta and is a medical emergency; Type B occurs in the aortic arch or descending aorta.
7
Q
What is presentation of aortic dissection?
A
It presents with a tearing chest pain radiating to the back between the shoulder blades, most severe at onset.
Because thrombolysis may be fatal if incorrectly diagnosed, it is important to assess for history of signs of dissection like car accident, falls, pregnancy, vascular disorders, connective tissue disorders and hypertension.
8
Q
What is the clinical signs of of aortic dissection?
A
Common clinical signs include
Unequal pulses and BP on separate arms
tachycardia
hypotension
signs of end organ hypoperfusion such as acute limb ischaemia, abdominal pain, renal failure, stroke and MI.
9
Q
What are common risk factors for aortic dissection?
A
- Hypertension
- Atherosclerotic disease
- Male sex
- Connective tissue disorders
- Bicuspid aortic valve
10
Q
What is the features of atherosclerosis?
A
Athoersclerosis is characterised by thickening of the tunica intima, when there is a hypercholesterolaemia state where LDL infiltrates the endothelial wall and become oxidised, creating an inflammatory state which causes recruitment of macrophages and T lymphocytes resulting in foam cells forming. This is intnially protective however LDL accumualation. Macrophage cell death is triggered, contributing to further inflammation and development of necrotic core of soft unstable atheroma. This core can become hypoxic which stimulates angiogenesis and can lead to intra-plaque haemorrhage.
Vascular smooth muscle proliferates can differentiate to forms a fibrous cap and release calcifying extracellular deposits which create microcalcifications. The death of the cells like monocytes as they become foam cells contributes to calcification. calcified plaques are least likely to rupture and form over time.
Low density non calcified plaques are made up of fat and connective tissue and most likely to rupture.
Plaque inflammation triggers loss of smooth muscle and produces matrix metallo-proteinases that weaken the fibrous cap
11
Q
What are common clinical signs of aortic dissection?
A
- Tearing chest pain radiating to the back
- Tachycardia
- Hypotension
- Signs of end-organ hypoperfusion
12
Q
What ae the complications of aortic dissection?
A
Aortic rupture, aortic, regurgitation, myocardial ischaemia, cardiac tamponade and stroke.
Sign is high BP, unequal pulses, new diastolic murmur and pericardial friction rub.
13
Q
What is pericarditis?
A
Inflammation of the pericardial sac surrounding the heart typically presents with central chest pain that is pleuritic, relieved by sitting forward and associated with breathlessness and tachycardia.
On examination, there may be a pericardial friction rub and an ECG may show an initial ST elevation with T wave inversion but there is always ST depression in avR .
Pericarditis may result in fluid accumulation and pericardial effusion which can become severe.
It typically presents with pleuritic chest pain that is relieved by sitting forward and may be associated with symptoms like fever and cough.
14
Q
What is the presentation of pericarditis?
A
Pain relieved by sitting up. Or leaning forward
Pain worsened with PALPATION, exertion and positions
Precipitated by viral infection
-> Symptoms such as fever, cough, dizziness and rash secondary to the pain that is linked to the underlying disease.
Pain may radiate to the trapezius if the phrenic nerve is damaged.
Suspicion of oesopagitis or acute pancreatitis should be had if it is assoicated with food intake.
15
Q
What are the causes of pericarditis?
A
- Infection (bacterial, tuberculosis, HIV)
- Malignancy
- Autoimmune conditions (lupus, rheumatoid arthritis)
- Dressler syndrome
16
Q
What is Dressler syndrome?
A
Dressler syndrome, an immune response where pericarditis, fever and pleuritic pain occurs after an MI, when there is damage to the heart muscle which can lead to the formation of anti-myocardial antibodies
17
Q
What is the presentation of musculoskeletal pain?
A
sharp and localised pain, which has tenderness over chest wall
It is not affected by exertion
Worsened with palpation, movements like coughing and heavy breathing
18
Q
What is oesophageal spasm?
A
Oesophageal spasm are painful contractions that can prevent food and liquids travelling through the oesophagus and there are two types:
Hyppercontractile oesophageal spasm in absence of regurgitation
Diffuse oesophageal spasm in the lower region causing regurgitatoin
19
Q
How does oesophageal spasm present?
A
It is characterised by squeezing chest pain, with difficulty swallowing solids and liquids, feeling of object stuck in the throat and regurgitation. There is water brash, where excessive saliva mixes with stomach acids in the throat causes a foul mouth taste typically at night, increasing the risk of oesophageal cancer. It is ore likely in women and people in their 60s
20
Q
What is cardiac tamponade?
A
Build-up of fluid in the pericardial sac causing cardiac compression
It presents with sharp pain, breathlessness, and signs similar to pericarditis.
21
Q
How does cardiac tamponade present?
A
Sharp pain that worsens when deep breathing or coughing and lying flat or on the left side, breathlessness, dysphagia and hoarseness. It has the same signs as pericarditis with decreased palpable pulse, tachycardia,hypotension, shockmuffled heart sounds and JVP distention.
22
Q
What are the signs of cardiac tamponade?
A
- Pulsus paradoxus: Decreased palpable pulse
-> Pain relieved by sitting forward - Tachycardia
- Hypotension
- Muffled heart sounds
- JVP distention
Management involves the drainage of pericardial fluid, and supportive therapy with IV colloids to expand the intravascular volume to prevent shock and adrenaline.
23
Q
How does pleuritic chest pain present?
A
Pleuritic chest pain is inflammation of the pleura lining that causes chest pain which worsens when breathing a dn coughing, shortness of breath and the pain may radiate to the shoulders or back.
It can be caused by an infection or injury
24
Q
How does oesophageal rupture?
A
Oesophageal rupture can result in sudden retrosternal chest pain, along with respiratory distress, severe vomiting/retching and subcutaneous emphysema. On examination, patient will have dullness to percussion, reduced air entry and oelural effusion.
There is a high risk of sepsis and low BP regulation, so acute management is fluid resuscitation with high flow oxygen, broad spectrum antibiotics and antifungals. Definitive management is removal of contamination in the mediastinum, Decompression of the oesophagus and nutritional support
25
How does pulmonary embolism present?
Pulmonary embolism chest pain presents with
Worsening pain when breathing with sudden shortness of breath, anxiety, dizziness, coughing blood, diaophoresis and hypotension. Symptoms of DVT may be associated such as pain, swelling, redness and soreness in the leg.
26
What are the non-modifiable risk factors for myocardial infarction (MI)?
* Elderly
* Male sex
* Family history
27
What are the modifiable risk factors for myocardial infarction (MI)?
* Diabetes
* Poor diet
* Hypertension
* Dyslipidemia
* Sedentary lifestyle
28
What are the parameters for haemodynamic stability?
Blood pressure
Heart rate
Urine output
Respiratory rate
29
What are the investigations for stable angina?
FBC or U&Es, fasting lipid prolife anad blood glucose
Contrast-enhanced CT angiography which shows coronary artery narrowing
12 lead ECG- may show T wave inversion and ST depression indicate ischaemia
Chest x ray for suspicion of heart failure or associated respiratory symptoms- NORMAL or CARDIOMEGALY
Cardiac enzymes- NO CHANGE
## Footnote
It is caused by increased myocardial oxygen demand due to ischemia.
30
What increases myocardial oxygen demand?
Arrhythmias, Fever, Hypertension, Cocaine use, Aortic stenosis, Arteriovenous shunts, Anemia, thyrotoxicosis, phaechromocytoma and congestive heart failure.
31
What is an indicator for ACS?
Infarction causes coagulation necrosis of cardio myocyte and results in the release of troponin that rises rapidly which can be used as an indicator for Acute coronary syndrome..
32
What is the first line pharmacological treatment for stable angina?
Beta Blockers- reduce heart rate to increase diastolic filling time which increases myocardial oxygen supply
Calcium channel blockers- vasodilators effect to increase oxygenated blood supply to the heart
33
What is the management for stable angina?
Short acting nitrates for periods of angina
Aspirin can be given to reduce progression to ACS
Management of present hypertension with ACE or ARBs
Statins for high cholesterol
Follow up should occur 2-4 weeks after commencing treatment and changing treatment
34
What are the investigations for coronary artery disease?
ECG
Echocardiogram to detect wall motion, any valvular regurgitation, chamber size indicating hypertrophy and lesions from infection or autoimmunity
Stress test (should be stopped if angina symtpoms develop, hypotension, hypertension or abnormal ECG changes occur)
Serum markers for creatine kinase and troponin
C-reactive protein and ESR for inflammation from acute pericarditis
Liver function test
35
Why is LFT tested in CAD?
For haemachromatosis, where iron builds up over time in the liver and cause dilated cardiomyopathy with low left ventricular ejection
To test liver functioning prior to drug administration
36
What is the first line treatment for diabetics with stable angina?
ACE inhibitors, to manage potential impact on kidney.
37
What are the prinzmetal angina?
Transient coronary artery spasm which can be triggered by vasoconstriction stimuli smoking or cocaine. Patients respond to nitrates and there is a greater risk with metabolic disorder like insulin resistance. It can be precipitated by cold water, hyperventilation, and recreational drugs like cocaine, alcohol, marijuana and amphetamines.
38
What is the presentation of prinzmetal angina?
Patients present with chronic chest pain for 5 to 15 minutes which is worse at midnight and wakes them up
Relieved with nitrates,
ST segment elevation during chest pain.
39
How can prinzmetal angina be tested?
Adminstering acetylcholine or Ergonovine which reproduce coronary spasm
40
What is syndrome X?
Syndrome X- angina-like chest discomfort which is induced by exercise and radiates to the left arm followed by 20 minutes of dull discomfort, with nitrates ineffective in relieving the pain. There transientis ST depression but normal epicardial coronary arteries on CT angiography and no spasm in the absence of cardiac systemic disease. It has an unknown pathogeneiss but may be related to myocardial ischaemia or increased cardiac pain sensitivity.
41
What is acute coronary syndrome (ACS)?
A group of conditions describing acute sudden loss of blood flow to the heart
## Footnote
This includes STEMI, non-STEMI, and unstable angina.
42
What is the presentation of STEMI?
STEMI is a myocardial infarction which has has ST elevation on ECG due to complete occlusion of blood supply that can cause transmural infarction(from endocardium to epicardium) which occurs distally and proggrsses proximally, with an onset of 12 hours, where T wave inversion may occur and Q waves. Therefore it is important to assess for complications such as
New left bundle branch block
Papillary muscle damage
Mitral valve prolapse or regurgitation
43
How does STEMI present on ECG?
Over time, untreated STEMI will result in coagulation necrosis of cardiomyocyte as neutrophils and macrophageinfiltrate the area which progresses to fibrosis. ECG will show:
->ST elevation and T wave peak/hyperacute T waves on ECG and left bundle branch block. ->Coronary angiography may show critical occlusion.
->The location of ST elevation on the lead can indicate area of ischaemia.
Both STEMI and non-STEMI have an elevation of cardiac enzyme markers.
44
What is an indicator for myocardial cellular injury?
Creatine kinase
## Footnote
It serves as an important indicator for acute coronary syndrome.
45
What are the complications of aortic dissection?
* Aortic rupture
* Aortic regurgitation
* Myocardial ischemia
* Cardiac tamponade
* Stroke
46
What is the significance of GRACE scoring system?
Estimates the risk of death from myocardial infarction 6 months following initial acute coronary syndrome. This’s is based on:
AGE
PULSE
SYSTOLIC BP
CREATININE
47
What are the characteristics of Prinzmetal angina?
Transient coronary artery spasm triggered by vasoconstriction stimuli transient coronary artery spasm which can be triggered by vasoconstriction stimuli smoking or cocaine. Patients respond to nitrates and there is a greater risk with metabolic disorder like insulin resistance. It is identificed by 3 factors: response to nitrates during angina, evidence of coronary vasospasm during angiography and transient electrocardiograph changes
It can be precipitated by cold water, hyperventilation, and recreational drugs like cocaine, alcohol, marijuana and amphetamines. Patients present with chronic chest pain for 5 to 15 minutes which is worse at midnight, relieved with nitrates, with ST segment during chest pain. The patient is typically young with no cardiovascular risk factors.
48
What are the symptoms of pulmonary embolism?
* Sudden shortness of breath
* Chest pain worsening with breathing
* Syncope
* Anxiety
* Haemoptysis
49
How is the risk of a pulmonary embolism scored?
Well’s score, where individual symptoms indicating a diagnosis of DVT are given a rating to necessity the use of an ultrasound, which includes:
->Active cancer
->Calf swelling compared to asymptomatic leg
->Previous DVT
50
What is a significant Well’s score?
A high Well’s score over 4 requires an urgent CT pulmonary angiogram to be performed.
For those with a score below 4, a D-dimer test should be performed
51
What is a D-dimer?
A d-dimer is one of the degradation products of a blood clots which can be used to indicate blood clotting disorders, such as DVT or pulmonary embolism, stroke or disseminated intravascular coagulation
52
What are the risk factors for a pulmonary embolism?
-> DVT, including family history
-> Recent surgery
-> Long haul flight or car journey
->Use of combined contraceptive pill
->Active cancer
->Recent myocardial infarction
->Pregnancy and 6 weeks post partum: decreased blood flow to the legs and increase in clotting factors in the blood
53
What is the management for suspected pulmonary embolism?
Anticoagulants and fibrinolytic therapy, until D-dimer result returns and discontinue if result is negative.
## Footnote
Occasionally, a pulmonary embolectomy may be performed.
54
What is the management of confirmaed pulmonary embolism?
Anticoagulant early with low molecular weight heparin and Thrombolytic therapy which can be systemic, through a peripheral vein or catheter-directed to the pulmonary arteries
55
What is the presentation of oesophageal rupture?
Typically triggered by severe vomiting, surgical procedures or excessive alcohol intake, causing a transmural tear that requires emergency treatment:
Sudden retrosternal chest pain
Respiratory distress
Severe vomiting
Subcutaneous emphysema- air bubbles trapped under the skin
## Footnote
May also present with subcutaneous emphysema.
56
What are the investigations for oesophageal rupture?
* FBC for inflammatory markers
* CT scan to show air or fluid in the thoracic cavity
57
What is a Mallory Weis syndrome?
oesophageal tear in the innermost layer due to rise in intra-abdominal pressure associated with excessive food or alcohol intake that causes
Vomit with blood or coffee grounds
Chest pain
Dysphagia
Hoarseness of voice
58
What are the key symptoms of acute myocardial infarction (MI)?
Symptoms include:
* Syncope
* Coma
* Dyssrhythmia
* Acute confusional state
* Hyperglycaemic crisis
## Footnote
These symptoms can vary in presentation among individuals.
59
What does ECG show in STEMI?
ECG shows:
* ST elevation
* T wave peak/hyperacute T waves
* Left bundle branch block
## Footnote
Location of ST elevation indicates area of ischaemia.
60
What are the complications of untreated myocardial infarction?
Complications include:
* Myocardial rupture
* Cardiac tamponade
* Papillary muscle damage
* Acute heart failure
* Pericarditis
* Pulmonary embolism
## Footnote
These complications can lead to severe consequences if not addressed promptly.
61
How is Non-STEMI diagnosed?
Non-STEMI is diagnosed by:
* Rise in cardiac enzymes
* Symptoms fitting acute coronary syndrome
* Absence of ST elevation on ECG
It is caused by a partial occlusion of the coronary artery, cuausing ischaemia of the subendocardium. It can present with:
->Angina at rest
->New-onset severe angina
->Pre-existing angina with increased frequency and duration
## Footnote
ST depression and T wave inversion may be present.
62
What is unstable angina?
Unstable angina is when chest pain occurs even at mild exertion/rest due to a plaque where there is ischaemia in the absence of infarction and pain is more severe. It is a medical emergency that requires immediate evaluation it forms part of acute coronary syndrome and due to risk of progression to a non-STEMI where there is a ruptured plaque that causes a subendocardial infarction in the area of infarction.There is no change in troponin or cardiac enzymes in stable or unstable angina Signs include JVP distention, mitral regurgitation murmur, hypotension, tachycardia and hypoxia. It is diagnosed based on the history
63
What is the initial management of MI?
MOAN which stands for:
* Morphine
* Oxygen therapy for patients with an O2 sat below 92%
* Aspirin to prevent platelet clot formation
* Nitrates for vasodilator effect and to relieve pain
## Footnote
This approach is aimed at pain relief and improving oxygenation.
64
Why is morphine provided?
Pain relief like morphine is ideal because it causes dilatation of the veins to reduce cardiac preload, alleviating ischaemia and any potential pulmonary oedema. Pain activates the sympathetic nervous system for vasoconstriciton, inotropy and HCO3 which increases heart workload.
65
When is oxygen provided?
Oxygen should only be provided if saturation is below 90%, unless patient has pulmonary oedema, heart failure or mechanical implications.
66
What is assessed in FBC for heart disease?
FBC
-> Lactate dehydrogenase for signs of hypoxia
-> Cardiac enzymes for troponin and creatine kinase
-> U& Es for K+ levels and electrolyte imbalances
-> Lipid profile and glucose levels for diabetic emergency
-> Cardiac enzymes Troponin I and T
67
What are the signs of hypercholesterolaemia?
Signs of hypercholesterolaemia is xanthelasma plaques around the eyes, corneal arcus rings around the iris and xanthelasma plaques on the skin or tendons.
68
How are the coronary arteries assessed with suspected MI?
Coronary artery calcium scoring is used to:
* Assess degree of calcification in coronary artery disease
* Identify significant plaque burden with a score over 400
## Footnote
It involves low radiation scanning techniques.
69
What are the NICE guidelines for early management of STEMI?
NICE guidelines include:
* Offer aspirin as soon as possible
* Assess eligibility for reperfusion therapy
* Dual anti-platelet therapy
* Angiography with PCI if presenting within 12 hours
* Fibrinolytic therapy as an alternative
## Footnote
Proper adherence to guidelines can improve outcomes.
70
What is the gold standard for treating STEMI?
The gold standard is:
* Percutaneous coronary intervention (PCI) is performed by using an angiogram to image the area of occlusion with a balloon for all patients with chest pain and ST elevation. It is a more cost-effective method in the long-term and is the gold standard, consisting of:
Balloon angioplasty inserted into the arm and used to squish the fatty tissue for coronary blood flow and stunting to prevent re-narrowing.
Access for introducer needle is typically through radial or femoral artery, but radial artery is preferred because it can easily be compressed against the radial bone which reduces the risk of access site bleeding. Prior t PCI, antiplatelet therapy is given with dual therapy or heparin. A balloon is inflated at the location of stenosis to open the artery for stent implantation.
## Footnote
PCI involves angiography and balloon angioplasty to restore blood flow.
71
What are the phases of cardiac rehabilitation?
The phases of cardiac rehabilitation are:
* Phase 1: Acute phase
* Phase 2: Subacute phase
* Phase 3: Intensive outpatient therapy
* Phase 4: Independent ongoing conditioning
## Footnote
Each phase focuses on different aspects of recovery and rehabilitation.
72
What are common signs pointing to acute coronary syndrome?
Signs include:
* Elevated JVP
* Hypotension
* S3 or S4 heart sounds
* Uncoordinated apex beat
## Footnote
These signs indicate possible ventricular dysfunction.
73
What does the acronym ABCD represent in pharmacological management?
ABCD stands for:
* ACE inhibitors
* Beta blockers
* Calcium channel blockers
* Diuretics
## Footnote
Each medication class plays a role in managing heart function and symptoms.
74
What is Dressler’s syndrome?
Dressler’s syndrome is characterized by:
* Pericarditis
* Fever
* Pleuritic pain
* Pericardial effusion
## Footnote
It can increase the risk of cardiac tamponade and constrictive pericarditis.
75
How does STEMI present on ECG?
Over time, untreated STEMI will result in coagulation necrosis of cardiomyocyte as neutrophils and macrophageinfiltrate the area which progresses to fibrosis. ECG will show:
ST elevation and T wave peak/hyperacute T waves on ECG and left bundle branch block. Coronary angiography may show critical occlusion.
The location of ST elevation on the lead can indicate area of ischaemia.
Both STEMI and non-STEMI have an elevation of cardiac enzyme markers.
76
How does non STEMI present on ECG?
Non-STEMI is diagnostic by a rise in cardiac enzymes and symptoms fitting with the profile of acute coronary syndrome, in the absence of ECG changes that cause an ST elevation. ST depression and T wave inversion may be present which is specific to myocardial ischaemia, however area cannot be localised. This differentiates it from STEMI and unstable angina. It is caused by a partial occlusion of the coronary artery, cuausing ischaemia of the subendocardium.
77
What are the NICE guidelines for non STEMI management?
Provide loading dose of aspirin
Provide antithrombin
Risk score system is GRACE to manage patients into either low risk or intermediate/high risk
-> Low risk patients are managed conservatively with dual platelet therapy and consider angiography with PCI if ischaemia develops or shown on testing
->High risk [patients are managed with immediate angiography and PCI and dual aspirin therapy
Assess left ventricular function and progress to cardiac rehabilitation
78
What are the high risk patients for non-STEMI?
Reccurrent angina and ECG changes despite treatment
Elevated troponin
New ST segment depression
Chest pain with features of heart failure
Poor left ventricle systoli function
Co-morbidities like malignancy, liver or renal where revascularisation would increase the risk of bleeding and out weigh the benefits
79
What are the risk factors for myocardial infarction?
Risk factors include:
* Atherosclerosis
* Smoking
* High triglyceride count
* Low HDL
* Sedentary lifestyle
* Family history of coronary artery disease
## Footnote
Addressing these factors can help prevent MI.
80
What are poor prognostic factors for MI treatment?
Poor prognostic factors include:
* Old age
* Diabetes
* Low left ventricular ejection fraction
* Smoking
* Low socioeconomic status
## Footnote
These factors can complicate recovery and increase mortality risk.
81
What cardiac markers confirm a diagnosis of myocardial infarction?
Cardiac markers include:
* Troponin T and I
* Creatine kinase-MB
## Footnote
Troponin is the most sensitive and specific marker.
82
What is the significance of the ischaemic penumbra zone?
The ischaemic penumbra zone refers to:
* Area around the umbra zone where many myocardial cells are alive
* Potential for recovery if blood flow is restored
## Footnote
This zone can recover with timely intervention.
83
What is the recommended agent for thrombolysis in STEMI?
The recommended agent is:
* Alteplase and streptokinase which is a recombinant human form of plasminogen, a pro-enzyme that breaks down the fibrin in blood clots.
## Footnote
It is a recombinant form of human tissue plasminogen.
84
What should be avoided in patients with significant left ventricular dysfunction?
Patients should avoid:
* Calcium channel blockers because it depresses cardiac function and worsens symptoms.
## Footnote
These can worsen heart function in such cases.
85
What are the complications of STEMI?
* Systolic murmur
* Fever (peaks 3-4 days post MI with raised WCC and CRP)
* Pulmonary thromboembolism
* Continuing chest pain post-MI- this should be treated with cardiac catheterisation and revascularisation
* Dysrhythmia such as AV block and bradycardia
* Pump failure leading to heart failure and cardiogenic shock
* Pericarditis is more common with STEMI
* Pericardial effusion
86
What is a stable plaque?
A stable plaque has a small lipid core, thick fibrous cap and few macrophages and lymphocytes which may bukdge into the lumen and reduce coronary flow and produce stable angina. It has macrocalcification calcification
87
What type of plaque causes ACS?
Only an unstable plaques can cause ACS, where there is a large lipid core, thin fibrous cap and macrophages and lymphocytes which can burst anytime and result in platelet recruitment and reduce the lumen space and result in a STEMI.Therefore, treating with anticoagulant is importantly and statins to shrink the lipid core.
88
What is stunned myocardium?
The damage where many myocardial cells are alive but inactive.
89
What does an echocardiogram show immediately after a myocardial infarction (MI)?
A regional wall motion of inactivity, indicating absent or abnormal contractility of the myocardium.
90
What are the risks associated with myocardial stunning?
Heart failure, myocardial necrosis, and mitral regurgitation due to papillary muscle dysfunction.
91
What happens to the penumbra zone after successful PCI/thrombolysis after 3 months?
The penumbra zone overtakes the umbra zone, showing little regional wall abnormalities on echocardiogram. Ischaemic penumbra zone at the peripheral of the damage where many myocardial cells are alive, called stunned myocardium
92
What is chronic ischemia characterized by on an echocardiogram?
Immediately after a MI, the myocardial cells are in a state of inactivity. An echocardiogram of the heart will show a regional wall motion of inactivity, indicating absent or abnormal contractility of the myocardium. There is a risk of heart failure due to myocardial stunning, necrosis of the cells and mitral regurgitation due to papillary muscle regurgitation.
93
How is chronic ischemia managed?
With revascularizing techniques through PCI or CABG surgery.
94
What causes Type 1 myocardial infarction (MI)?
Spontaneous atherosclerotic plaque rupture and thrombosis typically assoicated with coronary artery disease. There is myocardial necrosis indicated by a rise in the has-CTN1 concentration in the contex of suspected ACS and signs of myocardial ischaemia on ECG..
95
What indicates myocardial necrosis in Type 1 MI?
A rise in the hs-CTN1 concentration in the context of suspected ACS and signs of myocardial ischemia on ECG.
96
What triggers Type 2 myocardial infarction (MI)?
A mismatch between demand and supply of oxygen due to conditions like tachyarrhythmia or severe anemia.
97
What are the diagnostic criteria for myocardial infarction?
Evidence of myocardial necrosis, rise and/or fall in biomarkers, new ST segment and T wave changes, new left bundle branch block, development of Q waves, imaging showing regional wall motion abnormality, and identification of intracoronary thrombosis.
98
What defines Type 3 MI?
Cardiac death prior to measuring blood samples for cardiac biomarkers with symptoms indicating myocardial ischemia.
99
What characterizes Type 4a MI?
Caused by PCI, with a rise in cardiac troponin correlating to myocardial ischemia and new loss of viable myocardium on imaging.
100
What is Type 4B MI caused by?
Thrombosis with the use of a stent.
101
What causes Type 5 MI?
Coronary artery bypass grafting.
102
What is Ticagrelor?
A non-competitive P2Y12 antagonist that binds irreversibly and acts as an anti-platelet.
103
What is the impact of coronary artery disease on myocardial perfusion?
It can result in acute and chronic myocardial perfusion, decreasing myocardial contractility and left ventricular function.
104
What occurs during acute myocardial perfusion?
Stunned myocardium leading to transient reversible myocardial contractile dysfunction.
105
What is hibernating myocardium?
Chronic myocardial perfusion due to narrowed coronary artery causing chronic coronary contractile dysfunction.
106
What is a d-dimer?
A degradation product of blood clots that indicates blood clotting disorders.
107
What is the risk of pulmonary embolism?
Worsening chest pain when breathing, sudden shortness of breath, coughing blood
## Footnote
Symptoms of DVT may accompany it.
108
What are the modifiable risk factors for myocardial infarction?
* Diabetes
* Poor diet
* Hypertension
* Dyslipidemia
* Sedentary lifestyle
109
What is stable angina?
Chest pain occurring with exertion, relieved by rest
## Footnote
Caused by increased oxygen demand due to ischemia distal to atherosclerotic plaque.
110
What is acute coronary syndrome?
A group of conditions that describe acute sudden loss of blood flow to the heart
## Footnote
Includes STEMI, non-STEMI, and unstable angina.
111
What is the GRACE scoring system used for?
Estimating the risk of death from myocardial infarction following an initial acute coronary syndrome event.
112
What are the symptoms of oesophageal spasm?
Squeezing chest pain, difficulty swallowing, sensation of an object stuck in the throat.
113
What is the typical pain presentation in women experiencing angina?
Pain in the neck, jaw, throat, abdomen, or back, often accompanied by nausea and shortness of breath.
114
What is the consequence of untreated STEMI?
Coagulation necrosis of cardiomyocyte, infiltration by neutrophils and macrophages, progression to fibrosis.
115
What will the ECG show in STEMI?
ST elevation, T wave peak/hyperacute T waves, left bundle branch block.
116
What are the complications after an untreated myocardial infarction (MI)?
* Myocardial rupture
* Cardiac tamponade
* Papillary muscle damage
* Acute heart failure
* Pericarditis
* Pulmonary embolism
117
How is Non-STEMI diagnosed?
Rise in cardiac enzymes, symptoms fitting acute coronary syndrome, absence of ST elevation.
118
What symptoms may present in Non-STEMI?
* Angina at rest
* New-onset severe angina
* Increased frequency and duration of pre-existing angina
119
What does a Q wave on ECG indicate?
Negative deflection before QRS complex, indicating absence of electrical activity due to extensive infarction.
120
What are the signs of hypercholesterolaemia?
* Xanthelasma plaques around the eyes
* Corneal arcus rings
* Xanthelasma plaques on skin or tendons
121
What are signs pointing to acute coronary syndrome?
* Elevated JVP
* Hypotension
* S3 or S4 heart sounds
* Dyskinetic apex beat
122
True or False: In the initial stages of acute coronary syndrome, ECG may be normal in 20% of individuals.
True
123
What is a significant coronary artery calcium score?
Score over 400 indicates Significant plaque burden with atherosclerosis.
124
What is the recommended agent for thrombolysis in STEMI?
Alteplase, a recombinant form of human tissue plasminogen.
125
What are complications of primary PCI?
* Coronary artery dissection
* Bleeding from arterial puncture
* Increased thrombosis risk
* Stroke
* Need for emergency coronary artery bypass
* Renal failure
126
Fill in the blank: Patients with __________ should receive dual antiplatelet therapy regardless of risk.
NSTEMI
127
What lifestyle changes are recommended for ongoing management of cardiac health?
* Smoking cessation
* Alcohol reduction
* Dietary changes
* Exercise and weight loss focus
128
What is the risk score system used for managing patients with NSTEMI?
GRACE score.
129
What characterizes unstable plaques in relation to acute coronary syndrome (ACS)?
Large lipid core, thin fibrous cap, presence of macrophages and lymphocytes.
130
What are two zones of damage in myocardial infarction?
* Ischaemic umbra zone
* Ischaemic penumbra zone
131
What is the role of calcium channel blockers in cardiac management?
Should be avoided in significant left ventricular dysfunction.
132
What imaging technique is used to assess blood vessels for occlusion?
Coronary angiography.
133
What is the significance of early prominent T waves on ECG?
Early sign of acute myocardial infarction.
134
What should be monitored in patients with suspected acute myocardial infarction?
Cardiac troponin levels and continuous ECG monitoring.
135
What should be avoided in patients with suspected aortic dissection?
Thrombolysis.
136
What is stunned myocardium?
A state where many myocardial cells are alive but in a state of inactivity and causes transient reversible myocardial contractile dysfunction. This occurs in stable angina and acute myocardial infarction This is a feature of the Ischaemic penumbra zone at the peripheral of the damage where many myocardial cells are alive
137
What does an echocardiogram show immediately after a myocardial infarction (MI)?
Immediately after a MI, the myocardial cells are in a state of inactivity. An echocardiogram of the heart will show a regional wall motion of inactivity, indicating absent or abnormal contractility of the myocardium. There is a risk of heart failure due to myocardial stunning, necrosis of the cells and mitral regurgitation due to papillary muscle regurgitation.
138
What are the risks associated with myocardial stunning?
Heart failure, myocardial necrosis, and mitral regurgitation due to papillary muscle dysfunction.
139
What happens to the penumbra zone after 3 months of successful PCI/thrombolysis?
The penumbra zone overtakes the umbra zone, showing little regional wall abnormalities.
140
What characterizes chronic ischaemia in the myocardium?
Reduced activity and regional wall motion abnormality on echocardiogram without previous MI scars. results in hibernating myocardium that causes chronic coronary contractile dysfunction. The myocardium is still viable and function can be restored at least partially with timely vascularisation.
141
What are the causes of myocardial hibernation?
It is where ischemic myocardium supplied by a narrowed coronary artery in which ischemic cells remain viable, but contraction is chronically depressed. It is caused by chronic ischaemia and associated more with unstable angina. It is viable with reperfusion therapy.
142
How is chronic ischaemia managed?
Through revascularizing techniques such as PCI or CABG surgery.
143
What causes Type 1 myocardial infarction?
Spontaneous atherosclerotic plaque rupture and thrombosis, typically associated with coronary artery disease.
144
What indicates myocardial necrosis in Type 1 MI?
A rise in the hs-CTN1 concentration in the context of suspected ACS.
145
What is Type 2 myocardial infarction caused by?
Mismatch between demand and supply of oxygen due to factors like tachyarrhythmia or severe anemia.
146
What are the diagnostic criteria for myocardial infarction?
Evidence of myocardial necrosis, rise and/or fall in cardiac troponin, new ST segment and T wave changes, new left bundle branch block, development of Q waves, imaging showing regional wall motion abnormality, and identification of intracoronary thrombosis.
147
What is a Type 3 myocardial infarction?
Cardiac death prior to measuring blood samples for cardiac biomarkers with signs of myocardial ischaemia.
148
What characterizes Type 4a myocardial infarction?
Caused by PCI, indicated by rise in cardiac troponin and correlation to myocardial ischaemia.
149
What is Type 4B myocardial infarction associated with?
Thrombosis with the use of a stent.
150
What causes Type 5 myocardial infarction?
Coronary artery bypass grafting (CABG).
151
What is ticagrelor?
A non-competitive P2Y12 antagonist that binds irreversibly and acts as an anti-platelet.
152
What is the effect of stenosis over 70%-80% in coronary artery disease?
Reduces resting blood supply, diminishing contractile capacity and producing angina.
153
What is acute myocardial perfusion and its effect?
Results in a stunned myocardium causing transient reversible myocardial contractile dysfunction.
154
What is chronic myocardial perfusion and its effect?
Due to narrowed coronary artery, causing hibernating myocardium and chronic contractile dysfunction.
155
What investigations are used for coronary artery disease?
* ECG
* Echocardiogram
* Stress test
* Serum markers for creatine kinase and troponin
* C-reactive protein and ESR
* Liver function test
156
What can elevated BNP indicate?
Volume overload but can be falsely high in kidney disease and falsely low in obesity.
157
What are common complications of coronary artery disease?
* Arrhythmias
* Sinus bradycardia
* Tachycardia
* AV block
* Ventricular arrhythmia
* High-grade AV block
* Atrial fibrillation
158
What is a d-dimer?
A degradation product of blood clots used to indicate blood clotting disorders.
159
When should troponin be performed for ACS?
At least 3 hours after pain starts. It will need to be repeated after 6 hours to measure a toonin rise.
160
What is the
