Angina and ischemia Flashcards
Coronary perfusion gradient
aortic root pressure - LV pressure
perfused during diastole
Laplace’s equation
wall stress = r x p / (2h)
Left main CA
originate from left coronary sinus
travels between LA and pulmonary trunk to reach the AV groove, divides into
- LAD
- circumflex
LAD artery
anterior interventricular groove
diagonal branches: anterior surface of LV
septal branches: anterior 2/3 of the interventricular septum and the apical portion of the anterior papillary muscle
Circumflex CA
left AV groove and passes around the left border of the heart to reach the posterior surface
obtuse marginal branches: supplies lateral & posterior wall of the LV
Right main CA
originate from right coronary sinus
right AV groove, passing posterior to btw RA and RV
Marginal branches: RV, including SA and AV nodes
Right posterior descending: distal part of the right main CA, travels from the inferoposterior aspect of the heart to the apex, inferior & posterior walls of both ventricles and posterior 1/3 of interventricular septum
Conductance vessels
epicardial &myocardial penetrating
large in diameter
compressed by contracting cardiac muscle during diastole
Resistance vessels
Arterioles and capillaries
smaller in diameter
surrounded by smooth muscle, can change diameter in response to stimuli (NO, adenosine)
precapillary sphincters can vary flow through coronary capillaries
Coronary sinus
coronary veins accompany the coronary arteries and converge into here
posterior surface of the heart in the AV groove
empties into RA
Stable angina
usually due to atherosclerosis of CA chest pain on exertion arteries must be >75% occluded adenosine released locally in response to ischemia (dilates BV, chest pain) relieved by rest ST depression
Unstable angina
at rest or minimal exertion
artery may be >90% occluded
loss of predictability of anginal attacks
does not respond to NO
ST depression, T wave inversion/depression
Atypical angina
do not have chest pain
instead have other symptoms - weakness, faintness, sweating, nausea
more commonly seen in diabetic patients
same pathophysiology as stable angina
MI
death of myocardial tissue secondary to ischemia
begin after 15-20 minutes of severe ischemia
First 12 hours of MI - histo & gross
Micro
• EM changes in myocytes and their membranes within the first 15-20 min
• Wavy fibers – intracellular edema
• Coagulation necrosis – hypereosinophilic myocytes
• Contraction band necrosis – compaction of Z-lines of sarcomeres
Macro
• If no reperfusion of infracted area then pallor due to extrusion of erythrocytes from capillary bead
• If reperfused then hemorrhagic from blood vessel bursting
Vulnerable plaque
thin fibrous cap + large soft lipid cholesterol pool underneath
- prone to rupture
usual cause for sudden-onset MI
Progression of MI
Subendocardial –> epicardial
subendo more susceptible to ischemia
greater degree of systolic fiber shortening in subendo (high oxygen demand), more flow
greater dependence on diastolic coronary flow
poor collateral development
flow to the endocardium may be reduced by : CAD, LVH, HF with increased LVEDP
Determinants of infarct size
severity/duration of ischemia size of area at risk (CAD) Collateral Ischemic conditioning - e.g. hypertrophy Reperfusion (spontaneous lysis, therapy) Myocardial oxygen demand and supply
Stage of inflammation (12 hours - 5 days) post-MI
Micro
• Influx of PMNs
o If no reperfusion, then they collect at the borders of the infarct
o If reperfusion, then they are distributed diffusely
• Macrophages are seen after about 5 days
• Myocyte nuclei start to disappear and myocytes become attenuated and separated
o Phagocytosis of myocytes occur
Macro
• Yellow centre with hyperemic border (not reperfused)
• Prominent hemorrhage (reperfused)
Granulation tissue formation (1-3 weeks post-MI)
Micro
• Residual macrophages, revascularization, fibroblasts and early collagen formation
Macro
• Infarct turning from yellow to gray
Scar formation (2-8 weeks post-MI0
Micro
• Decrease in inflammatory cells with increasing collagen deposition and prominent capillary vessels
Macro
• Infarct changing from gray to white as collagenization becomes complete
Complications of MI
Death: 50% due to ventricular arrhythmia
Arrhythmia; major determinant of post-discharge mortality, ischemic tissue at border zone
Ventricular dysfunction
Cardiogenic shock: infarction >40%
Recurrent infarction: 2-10 days post-MI
Infarct expansion
Myocardial rupture: first few days or 2nd week after MI, at the border
RV infarction: associated with transmural inferior LV MI
Pericarditis: requires transmural infarct
Mural thrombus
Ventricular aneurysm: transmural MI, >2 CAD
NSTEMI
subendocardial tissue ischemia + necrosis
ST depression, T wave inversion/depression
test for troponin I or T or CK MB in blood
STEMI
full occlusion
transmural tissue necrosis
ST elevation
Common causes of chest pain
Cariac: angina, acute MI, pericarditis
Vascular: aortic dissection, PE, Pulmonary HTN
Pulmonary: pleuritis/pneumonia, tracheobronchitis, spontaneous pneumothorax
GI: reflux, peptic ulcer, gallbladder disease, pancreatitis
MSK: costochondritis, cervical disc disease, trauma/strain
Infectious: Herpes zoster
Psychological: panic disorder
Stable angina Tx
Pharmaco: sublingual nitro
organic nitrates, b-blockers, Ca blockers
Prevention of MI: aspirin, lipid-regulation, ACEi
Invasive: revascularization: PCI, coronary stents, drug-eluting stents, bypass graft
Unstable angina/NSTEMI Tx
Additional to stable angina: heparin
use invasive techniques earlier in patients with high-risk features (ST deviation, elevated Trop-I, multiple CV risk factors)
STEMI tx
administer same as stable angina IMMEDIATELY
fibrinolytics
Primary PCI: immediate angioplasty and usually stenting
Percutaneou coronary intervention/PC transluminal coronary angioplasty
Under fluoscopy
balloon-tipped catheter inserted through peripheral artery
inflate in CA
1/3 patients redevelop symptoms within 6 months
Coronary stents
Thrombogenic –> give oral antiplatelets
larger luminal diameter than PTI, decreased restenosis rate, reduced need for repeated angioplasties
risk of restenosis due to neointimal proliferation
Drug-eluting stents
antiproliferative medication released over 2-4 weeks
Coronary artery bypass graft
requies a bypassable lesion
>50% stenosis in left main coronary artery or 2-3 vessel disease with diabetes
preferable to angioplasty when there is significant disease of >2 vessels
Nitrate
Stimulates release of NO (venodilates, reduce return and dilate CA)
Indications: symptomatic acute ischemia
CI: preload-dependent patients: aortic stenosis, RV dysfunction, viagra users
SE: lightheadedness, headache, palpitations
b-blockers
indications: CAD
CI: obstructive airway disease, LV dysfunction, marker bradycardia/heart block, insulin-treated patients
SE: fatigue, sexual dysfunction
Ca channel blockers
non-DHPs: verapamil and diltiazem
antagonize V-gated L-type Ca channels
reduce inotropy and slow HR, minor vasodilatory
Indications: ischemia persistent despite b-blocker/nitrate therapies, or for those with CI to b-blockers
CI: LV systolic dysfunction
Lipid lowering agents
Statins, niacin, fibric acid derivatives, cholesterol intestinal absorption inhibitors, bile acid binding agents
HMG-CoA synthase inhibitors (reduce cholesterol synthesis)
ASA
Irreversible COX inhibition –> inhibit synthesis of thromboxane A2
Indications: CAD
CIs: gastric bleeding, allergies
Heparin
bind and increase potency of antithrombin III
inhibit coagulation factor Xa
Indications: standard therapy for UA and NSTEMI
adjunctive after fibrinolysis or PCI in STEMI
Fibrinolytics
alteplase tPA, reteplase rPA, tenecteplase TNK-tPA
stimulate natural fibrinolytic system; transform inactive precursor plasminogen into active protease plasmins –> lyses fibrin clots
Indications: fibrinolytic therapy in STEMI (ONLY STEMI)
CI: underlying bleeding disorders, active peptic ulcer disease, recent stroke, recovering from recent surgery, pregnancy, intracranial tumour/AVM, suspected aortic dissection or pericarditis
