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unstable-angina-pathogenesis-and-clinical-findings
unstable-angina-pathogenesis-and-clinical-findings
![Unstable Angina/Unstable Angina Pectoris: Pathogenesis and clinical findings Primary cause:
Secondary causes:
Coronary artery vasospasm - primary or drug induced (Ex: cocaine, triptans)
Coagulopathy
(Ex: antiphospholipid antibody syndrome)
Vasculitic syndromes (Ex: Takayasu arteritis)
Authors: Marisa Vigna Ryan Wilkie Yan Yu* Reviewers: Julena Foglia Davis Maclean Mehul Gupta Andrew Grant* * MD at time of publication
Atherosclerosis
Fatty plaque accumulates inside the intimal walls of arteries Coronary arterial atherosclerotic plaque rupture or erosion
Plaque disruption exposes subendothelial components of damaged vessel wall to platelets, initiating the coagulation cascade and platelet adhesion
Aggregation of platelets results in the formation of a thrombus Thrombus partially occludes blood flow through a coronary artery âmyocardial blood supply
Congenital anomalies (Ex: myocardial bridge, anomalous coronary)
Spontaneous coronary artery dissection
Increased blood viscosity (Ex: polycythemia, thrombocytopenia)
Factors thatámyocardial (cardiac muscle) oxygen demand (Ex: tachycardia, hypotension, hypertension, anemia, exertion, stress)
Coronary embolism (Ex: A. Fib, endocarditis, prosthetic valve thrombus)
áheart rate, contractility, and/or wall tension ámyocardial oxygen demand
Myocardial ischemia due to imbalance between blood supply and oxygen demand (insufficient blood/oxygen supply)
Unstable Angina/Unstable Angina Pectoris
Can be new onset angina; typically progressive in frequency, severity, or duration; can occur at rest
Subtotal occlusion of a coronary arteryà
reduced, but continued, myocardial blood supply
Maintained perfusion means cardiomyocytes are still alive and thus do not leak troponin into bloodstream
Normal serum troponin
Diaphoresis
(sweating)
Since bloodflow occurs from epicardium to endocardium, myocardial ischemia is more
pronounced in the subendocardium (region furthest away from heart’s external surface)
Sufficient blood flow is maintained in regions superficial to the subendocardium, resulting in non-transmural (partial thickness) heart wall ischemia
Non-inferior wall ischemia triggers a predominantáin sympathetic nervous system activity, given the proximity of cardiac sympathetic nerve innervation
Ischemiaâ cardiomyocyte resting membrane potential andâ action potential duration
Voltage gradient between normal and subendocardial ischemic zones creates injury currents, shifting the ST- vector on ECG
ECG: ST depression
and/or T wave inversion
Cardiac sensory nerve fibres mix with somatic sensory nerve
fibres and enter the spinal cord via the T1-T4 nerve roots
Brain perceives increased cardiac sensory nerve signaling as nerve pain coming from the skin of T1-T4 dermatomes (“Referred Pain”)
Myocardial ischemia causes hypoxic stress on cardiomyocytesàâaerobic (requiring oxygen) metabolism,áanaerobic (not requiring oxygen) metabolism
áanerobic respirationálactic acid production,á[H+], andâcellular pH which impairs cardiomyocyte function
Cardiomyocyte dysfunction impairs myocardial relaxation in diastole and/orâ left ventricular contractility in systole
âleft ventricular cardiac output àbackup of blood in the left ventricle, atrium, and pulmonary vasculature
ápulmonary capillary pressures pushes fluid out of the capillaries into the alveoli in the lungs
Fluid filled alveoliâgas exchange andâ oxygenation, triggering harder and faster breathing in order to compensate
Dyspnea
Activation of sweat glands via acetylcholine release
Hormones bind to cardiac β1 receptors
Tachycardia
(áheart rate)
Epinephrine/ Norepinephrine hormone release from the adrenal medulla
Hormones bind to arterial smooth muscle α1 receptors ávascular tone (vasoconstriction)
Hypertension
The Vagus nerve sits in close physical proximity to the inferior wall of the heart àinferior wall ischemia triggers involuntary Vagus nerve activation
Since the Vagus nerve coordinates parasympathetic activity,áVagus nerve activity leads to a variety of parasympathetic nervous system responses:
Retrosternal discomfort: May present as pain, heaviness, tightness, aching, pressure, burning or squeezing
Pain radiation to T1-T4 dermatomes:
Left shoulder and arm, lower jaw, neck, abdomen, upper back
Syncope
(fainting)
Bradycardia
Nausea Hypotension
(âheart rate)
(âblood pressure)
(áblood pressure)
(shortness of breath)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Findings
Complications
Published Oct 18, 2015, updated Aug 29, 2021 on www.thecalgaryguide.com](https://calgaryguide.ucalgary.ca/wp-content/uploads/2015/10/Unstable-Angina-2021.jpg "Unstable Angina/Unstable Angina Pectoris: Pathogenesis and clinical findings Primary cause:
Secondary causes:
Coronary artery vasospasm - primary or drug induced (Ex: cocaine, triptans)
Coagulopathy
(Ex: antiphospholipid antibody syndrome)
Vasculitic syndromes (Ex: Takayasu arteritis)
Authors: Marisa Vigna Ryan Wilkie Yan Yu* Reviewers: Julena Foglia Davis Maclean Mehul Gupta Andrew Grant* * MD at time of publication
Atherosclerosis
Fatty plaque accumulates inside the intimal walls of arteries Coronary arterial atherosclerotic plaque rupture or erosion
Plaque disruption exposes subendothelial components of damaged vessel wall to platelets, initiating the coagulation cascade and platelet adhesion
Aggregation of platelets results in the formation of a thrombus Thrombus partially occludes blood flow through a coronary artery âmyocardial blood supply
Congenital anomalies (Ex: myocardial bridge, anomalous coronary)
Spontaneous coronary artery dissection
Increased blood viscosity (Ex: polycythemia, thrombocytopenia)
Factors thatámyocardial (cardiac muscle) oxygen demand (Ex: tachycardia, hypotension, hypertension, anemia, exertion, stress)
Coronary embolism (Ex: A. Fib, endocarditis, prosthetic valve thrombus)
áheart rate, contractility, and/or wall tension ámyocardial oxygen demand
Myocardial ischemia due to imbalance between blood supply and oxygen demand (insufficient blood/oxygen supply)
Unstable Angina/Unstable Angina Pectoris
Can be new onset angina; typically progressive in frequency, severity, or duration; can occur at rest
Subtotal occlusion of a coronary arteryà
reduced, but continued, myocardial blood supply
Maintained perfusion means cardiomyocytes are still alive and thus do not leak troponin into bloodstream
Normal serum troponin
Diaphoresis
(sweating)
Since bloodflow occurs from epicardium to endocardium, myocardial ischemia is more
pronounced in the subendocardium (region furthest away from heart’s external surface)
Sufficient blood flow is maintained in regions superficial to the subendocardium, resulting in non-transmural (partial thickness) heart wall ischemia
Non-inferior wall ischemia triggers a predominantáin sympathetic nervous system activity, given the proximity of cardiac sympathetic nerve innervation
Ischemiaâ cardiomyocyte resting membrane potential andâ action potential duration
Voltage gradient between normal and subendocardial ischemic zones creates injury currents, shifting the ST- vector on ECG
ECG: ST depression
and/or T wave inversion
Cardiac sensory nerve fibres mix with somatic sensory nerve
fibres and enter the spinal cord via the T1-T4 nerve roots
Brain perceives increased cardiac sensory nerve signaling as nerve pain coming from the skin of T1-T4 dermatomes (“Referred Pain”)
Myocardial ischemia causes hypoxic stress on cardiomyocytesàâaerobic (requiring oxygen) metabolism,áanaerobic (not requiring oxygen) metabolism
áanerobic respirationálactic acid production,á[H+], andâcellular pH which impairs cardiomyocyte function
Cardiomyocyte dysfunction impairs myocardial relaxation in diastole and/orâ left ventricular contractility in systole
âleft ventricular cardiac output àbackup of blood in the left ventricle, atrium, and pulmonary vasculature
ápulmonary capillary pressures pushes fluid out of the capillaries into the alveoli in the lungs
Fluid filled alveoliâgas exchange andâ oxygenation, triggering harder and faster breathing in order to compensate
Dyspnea
Activation of sweat glands via acetylcholine release
Hormones bind to cardiac β1 receptors
Tachycardia
(áheart rate)
Epinephrine/ Norepinephrine hormone release from the adrenal medulla
Hormones bind to arterial smooth muscle α1 receptors ávascular tone (vasoconstriction)
Hypertension
The Vagus nerve sits in close physical proximity to the inferior wall of the heart àinferior wall ischemia triggers involuntary Vagus nerve activation
Since the Vagus nerve coordinates parasympathetic activity,áVagus nerve activity leads to a variety of parasympathetic nervous system responses:
Retrosternal discomfort: May present as pain, heaviness, tightness, aching, pressure, burning or squeezing
Pain radiation to T1-T4 dermatomes:
Left shoulder and arm, lower jaw, neck, abdomen, upper back
Syncope
(fainting)
Bradycardia
Nausea Hypotension
(âheart rate)
(âblood pressure)
(áblood pressure)
(shortness of breath)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Findings
Complications
Published Oct 18, 2015, updated Aug 29, 2021 on www.thecalgaryguide.com")
