Case 1: Angina Pectoris and
Atrial Fibrillation
ANGINA PECTORIS
What?
Non-permanent myocardial ischemia, often due to CAD/atherosclerosis which gives a discrepancy
between O2 demand and supply. Episodes are short, 5-15 minutes. Risk of 1-2% death and 3% MI.
Ischemia causes the release of substances such as adenosine and bradykinin, which cause pain.
Classification angina NYHA I-IV
Stable angina: Caused by increased demand: emotions, stress, exertion, weather change. Male, age,
postmenopauzal women. Atherosclerotic abnormalities.
Unstable angina: Part of ACS (acute coronary syndrome), progressive pain due to worse CAD or
large plaque. Risk for MI.
ACS = collective name for unstable angina, STEMI and NSTEMI. The last two are types of myocardial
infarction. STEMI = st elevation, transmural ischemia and complete coronary artery occlusion.
NSTEMI = partial occlusion causing subendocardial ischemia and no ST elevation. The consequences
of an MI can be: contraction/relaxation disturbance, ischemic mitral insufficiency, arrythmia (atrial
and ventricular), thromboembolism, rupture LV wall or septum, psychosocial (depression). Fibrous
cap loss from the plaque exposes something and then platelets aggregate on the wound area
forming thrombus.
Diagnosis
To confirm the diagnosis of MI, laboratory tests are needed together with a clinical history, physical
examination and an ECG. Cardiac Troponin I and T (cTnI, cTnT)are specific and sensitive biomarkers
of myocardial injury. Also measure CK, CK-MB and liver enzymes. Echocardiography to exclude acute
valve problems and perfusion/ischemia.
Treatment:
In case of a STEMI, there are two procedures that can be performed when the patient arrives at the
hospital: PCI (Percutaneous Coronary Intervention) or fibrinolysis, with PCI being preferred within
the indicated time frames:
If we take the STEMI diagnosis: the preferred intervention is PCI if the delay between the
diagnosis and the intervention itself is <120 min.
, If the delay is >120 min, fibrinolysis is considered. If we take the onset of symptoms as
reference, in the next 12 hours the preferred intervention is PCI (must be done within the
120 min from diagnosis still), while fibrinolysis is indicated only if PCI cannot be performed.
Up until 48 hours, primary PCI is still indicated in patients with symptoms, hemodynamic
instability or arrhythmias. It may be considered in asymptomatic stable patients.
No matter the reperfusion modality chosen, patients presenting with an acute myocardial infarction
require adjunctive therapies in the absence of contraindications, these include:
a loading dose of Aspirin
a platelet aggregation inhibitor (for example, clopidogrel or ticagrelor – P2Y12 inhibitor)
anticoagulant (such as unfractionated heparin, enoxaparin or fondaparinux).
Specific drugs may depend on local availability and preferences as determined in consultation with
specialty backup. Complications potentially associated with myocardial infarction, such as
bradycardia, hypotension and dysrhythmia, are best treated according to standard Advanced Cardiac
Life Support (ACLS) protocols.
Cause:
Cardiac
1. Ischemic:
a. Atherosclerotic narrowing
b. Vasospastic angina: Prinzmental or cocaine, not related to any type of increase in
HR, BP or physical activity – transmural ischemia STEMI
c. Cardiac syndrome X: chest pain with normal coronary arteries, small vessel disease
so you do not see narrowing. However there is positive ECG exertion test. Can be
hereditary, not congenital.
d. Aortic valve stenosis: obstruction of blood flow across aortic valve. 50% mortality at
2 years. Latent period of 10-20y without symtpoms. Triad: angina pectoris by
exertion, heart failure (dyspnea night, orthopnea), syncope (vasodilation causes SYS
BP decline). Can be together with SYS hypertension but usually below 200mmHg.
Crescendo-decrescendo coarse systolic murmur.
e. Decrease in coronary circulation: tumors, congenital malformed coronary vessels,
Raynaud’s disease, thromboangiitis oliterans involving coronary tree.
2. Non-ischemic
a. Endocarditis, pericarditis, myocarditis
b. Tachycardia, abnormal rhythms
Non-cardiac
1. Anaemia
2. Lungs: pneumothorax, embolism
3. Esophagus: rupture (Boerhaaves), heartburn
4. Panic disorder, hyperventilation syndromes
5. Muscle ache
6. Aortic dissection type A: Tear in the wall of the aorta ascendens (blood enters the ‘false
lumen’ in the media between intima and adventitia layer, there are two lumens since blood
runs in both, however blood always stays intravescular, no rupture no haemmorhage and a
lot of pain. Stops when it reaches a bifurcation or a branch) can cause full rupture of it,
medical emergency -> surgery.BP, bicuspid aortic valve, heart surgery, trauma, smoking,
pregnancy, aortic aneurysm, high lipids, male, most above 63 years old. Very rare, no
treatment means 50% death in 3 days. Connective tissue disease (marfan) associated with
aortic dissection, first they get an ascending aorta aneurysm/valve issue and then we get wall
weakening and dissection usually triggered by hypertension even if there is no connective
tissue disease:
, o Marfan syndrome. Most prevalent. Fibrillin 1 mutation. Marfan syndrome affects the
bones, ligaments, eyes, heart, and blood vessels. People with Marfan syndrome tend
to be tall and have extremely long bones and thin "spider-like" fingers and toes, are
hypermobile. A lot of patients do not know that they have marfan.
o Loeys-Dietz syndrome
o Ehlers-Danlos syndrome (EDS). Difficulty processing collagen (ECM). Pretty rare, not
all forms are vascular.
We treat type A immediately due to risk for cardiac tamponade and coronary vessel rupture
(massive infarct and death). All other types we leave be and see what happens, it can keep
dilating and remain biluminal, it can heal for some part or later if critical we can do surgery.
Diabetes mellitus
T1DM is characterized by an absolute insulin deficiency caused by T-cell mediated autoimmune
destruction of pancreatic B-cells. The key pathophysiology is decreased insulin secretory capacity.
CVD is a long term complication of T1DM.
Higher risk CAD, earlier in life
Have smaller vessels, due to calcification wall diabetic arteries, so worse prognosis in
treatment. Long term mortality is higher. Also multiple vessels, more severe stenosis, higher
risk of restenosis after CABG, more distal disease.
Parallel with cardiac patients with diabetes and peripheral patients with diabetes: silent
ischemia. Signs of ischemia on testing without actually having angina.
Survival rates after CABG is significantly lower for diabetic patients than for non diabetic
patients. Graft survival is lower as well.
Diagnosis:
Key to distinguish condition from others that are in the DD. Rule out deadly conditions like acute MI,
myocarditis/pericarditis/pericardial effusion, aortic dissection, pulmonary embolism, pneumothorax,
Esophagus rupture (Boerhaave’s).
, Anamnesis:
History of chief complaint: chest pain
o Duration, amount of episodes - progression
o Context
o Type (pressure, tightness, elephant sitting on your chest, stabbing)
o Location and radiation (retrosternal, arms/shoulder, neck/jaw, back, epigastrio)
o How bad 1-10, worsening or better or same upon: coughing, position, touch chest
wall, exercise, emotional stress, weather change, wind, drug use AND relieving
factors.
o Similar to any previous angina or MI?
o Associated symptoms
Other signs
o Sweating
o Sickness
o Signs of onset shock (pale/blue/grey) in emergency setting
o Dyspnea
Personal history: IHD, surgery, treatment, medication, comorbidities (COPD-any less ox
disease), allergies (aspirin and other heart medication)
Family hisotry: heart diseases (especially first grade family members under 60y)
Lifestyle: intox/smoking/drugs, nutrition (cholesterol), sports and movement
Physical examination
Heart examination
Lung examination
If needed ABCDE or rescucitation
Further examination:
Hart enzymes (hs-TnT etc.)and other relevant lab data. In the laboratory we test for cardiac
biomarkers which are released when muscle cells are damaged, this in order to differentiate angina
from heart attack. We look at:
Troponin: cardiac-specific marker, elevated hours up to two weeks after a heart attack
CK-MB: creatinine kinase, elevated after troponin, not cardiac-specific when total CK, CK-MB
is most cardiac specific
hs-TnT: high sensitivity troponin, detects troponin as well but at much lower levels, may help
detect heart injury and ACS earlier than standard test, can also be positive in people with
stable angina and asymptomatic people
Myoglobin: skeletal muscle injury marker
BNP or NT-proBNP: released by the body as a natural response to heart failure, not
diagnostic for heart attack but indicates increased risk for cardiac problems in people with
ACS.
ECG, heart rhythm (principles, value and limitations, connection with clinical practice).
Normally, an ECG does not rule out ACS. However the ECG does have value of some sort. We want to
see on the ECG weather there is an ST-segment elevation, this would indicate STEMI. In the case of
NSTEMI we might see ST-depression, T-top inversion or aspecific abnormalities or the ECG could be
normal. It is important to see whether there is a STEMI/NSTEMI because this means emergency. ECG
and blood work combined give a good diagnostic tool.
Exertion tolerance test ECG (principles): called treadmill test or exercise test helps a doctor find out
how well the heart handles work. Patient is hooked up to HR, breathing, BP, ECG or EKG monitors
