| How is atherosclerosis initiation? | Extracellular lipid accumulation, then leukocyte recruitment and retention, then focality of lesion formation, then intracellular lipid accumulation (foam cell formation)
Evolution (innate and adaptive immunity, smooth muscle cell migration and proliferation, then smooth muscle cell death during atherogenesis, then arterial ECM, angiogenesis in plaques and finally plaque mineralization.
Clinical complications of atherosclerosis traditionally used to be exponential, nowadays it became random and faster) |
| What is thrombosis and atheroma complication? | Thrombosis due to erosion (fibrous cap thick and intact, white fibrin rich thrombus, smooth muscle cells prominent, often sessile nonocclusive thrombus, less remodeled outwards, NETs involved more in NSTEMI)
Thrombosis due to rupture (thin cap, red fibirn rich thrombus, tissue factor trigger, prominent macrophages, occlusive thrombus, expansively remodeled, less NET and more STEMI) |
| How is thrombosis and healing in progression of atheroma? | Repetitive cycles of plaque disruption, thrombosis in situ, and healing probably contribute to lesion evolution and plaque growth.
These constitute one type of crisis in the history of a plaque may cause burst of SMC proliferation, migration and matrix synthesis.
Determinants of plaque (fluid phase: tissue factor microparticles, plasma, PAI-1, fibrinogen. Solid state: thrombomodulin, macrophages, tissue factors) |
| Give some special cases of arteriosclerosis? | Restenosis after arterial intervention (post balloon negative remodeling, post stent intimal thickening)
Aneurysmal disease, infection, accelerated arteriosclerosis after transplantation [arterial hyperplastic disease by immunosuprressive therapy long-term] |
| What is difference between typical and graft atherosclerosis? | Typical (eccentric, lipid deposits, focal distribution)
Graft (concentric lesion, no lipid core, diffuse distribution) |
| What are the criteria for MI? | Clinical (AMI detected by abnormal cardiac markers in setting of acute myocardial ischemia)
Myocardial injury (detection of elevated cTn value above 99th percentile URL, if there is a rise or fall of cTn values) |
| What is troponin cardiac biomarker? | group of proteins in striated muscle fibers, crucial in muscle contraction interacting btw actin and myosin.
Three subunits (TnC [binds calcium triggers contraction], TnI [inhibits interaction btw actin and myosin], TnT [anchors troponin complex to tropomyosin and helps positioning troponin on actin filament])
Clinical evidence of AMI includes increased TnC and one of anemia, V.Tach, HF, kidney disease, hypotension, hypoxemia. |
| What are reasons for troponin elevation? | Myocardiac injury AMI (atherosclerotic plaque/thrombossi)
Myocardial injury due to ischemia from O2 decreased (coronary artery spasm, coronary embolism, bradyarrhythmia, respiratory failure, anemia)
Other causes of MI (cardiac conditions [carditis, HF, cath, defibrillator...] systemic [sepsis, CKD, stroke, PE, infiltrative disease, chemo, strenous exercise]) |
| How is plaque formation and disruption? | Plaques causing ACS provoke thrombi caused by fibrous cap rupture, superficial erosion, or vasospasm/disruption by calcified nodule. Some cases lack culprit thrombosis.
Acute coronary syndrome (Plaque disruption exposes thrombogenic substances produce thrombus infarct, collateral, asymptomatic, and occlusive) |
| What is criteria for Type 1 MI? | Detection of rise/fall of TnC 99th percentile and one of (symptoms of AMI, new ECG changes, pathological Q, imaging loss of viable myocardium, coronary thrombus on angio seen)
It is plaque rupture/erosion that may be occlusive or non-occlusive. |
| What is criteria for Type 2 MI? | Rise/fall of TnC 99th percentile and evidence of imbalance O2 supply and demand unrelated to coronary athero-thrombus, and one of (symptoms of AMI, new ECG changes, pathological Q, loss of viable myocardium on imaging)
It is atherosclerosis, vasospasm, non atherosclerotic dissection or imbalance O2 alone. |
| What are criteria for Type 3 MI? | Cardiac death with symptoms suggestive of MI and ECG changes, die before blood samples for biomarkers obtained/before increase in biomarkers seen in autopsy |
| What are criteria for PCI-related MI <48 hrs type 4a MI? | TnC elevated 5 times 99th percentile, pre and post procedure (increases post procedure) and one of ECG changes, Pathological Q, imaging evidence, or angio flow limiting |
| What are criteria for CABG-related MI (type 5 MI)? | Elevated 10 times 99th percentile TnC post procedure + one of ECG Q wave, angio occlusion or imaging death of cells |
| What are criteria for prior or silent/unrecognized MI? | Any one of patho Q, imaging death of cells, or pathological findings of a prior MI. |
| Give algorithm of classification of MI? | . |
| Where are areas of necrosis following occlusion of each part of coronary artery? | LAD (anterior wall)
Left Circumflex (lateral wall)
RCA (posterior wall)
Some collaterals may compensate the blood occlusion |
| What are the potential outcomes of ischemia? | 40-60 minutes starts infarction, 3-6 hours lead to extensive necrosis |
| What is MI with non obstructive coronary arteries (MINOCA)? | Evidence of MI with normal angio or near normal coronary arteries and no other explanation for the presentation.
Spasm, plaque erosion/rupture, coronary dissection are common etiologies of MINOCA.
Pt survived STEMI w/out evidence of CAD better outlook than atherosclerotic mediated STEMI, in hospital mortality 60% lower and 1 year mortality 40% lower.
cardiac MRI recommended to exclude myocarditis w/out clear cause of MINOCA. |
| How is MINOCA dx? | Step 1 cath lab (hx, PE, ECG, angio, IV US, assessing coronary artery)
Step 2 ward (hx, CMRI, PE, ECG, echo, blood tests)
Step 3 post discharge (followup, CMRI, cardiac rehab)
Causes (coronary [embolism, spasm, thrombus, bridging, rupture/erosion, dissection], non-coronary [trauma, myopathy, toxins, myocarditis, takutsubo, transplant rejection], non cardiac causes [ARDS, HS, inflammation, PE, stroke, sepsis]) |
| What is stress takutsubo cardiomyopathy? | Acute stress cardiomyopathy, also termed transient LV apical ballooning syndrome or takotsubo cardiomyopathy, typically involves transient wall moTon abnormaliTes involving the LV apex and mid-ventricle
• This syndrome occurs in the absence of obstrucTve epicardial CAD and can mimic STEMI.
• IniTal ECGs demonstrate substanTal and oXen diffuse ST-segment elevaTon, prompTng, when coupled with the typical (frequently severe) chest discomfort, the appropriate immediate referral for coronary angiography. |
| What is the spectrum of acute cardiogenic shock? | Clinical spectrum (asymptomatic to chest pain to persistent pain to cardiogenic shock to death)
ECG (normal to ST depression to ST elevation to arrhythmia)
TnC elevated in last phases of ACS, final dx if asymptomatic unstable angina, in middle NSTEMI and in arrest final STEMI.
ACS: Abnormal ECG, Clinical context, Stable pt exam. |
| How is algorithm of action for pt sus of NSTEMI w/out angio need? | . |
| How is management of ACS? | Aspirin, control of cardiac pain (analgesics, nitrates, b blockers, oxygen), Anticoagulants (Heparin, LMWH, Bivalirudin), Reperfusion therapy |
| What is cardiac cath? | all forms of invasive and cath based assessments of the heart, distiction between it and coronary angiography.
Left heart cath (we should weigh risks and benifits, contraindications [known anaphylactoid rxn, kidney impairment, decompensated HF, pulmonary edema, uncontrolled HTN, active infection, coagulopathy, GI bleed.]
Risks [mortality, MI, CVA, arrhythmia, vascular, contrast agent rxn, hemodynamic complication, heart chamber perforation, others] |
| How is arterial access for cath? | radial/ulnar artery/femoral , there are many types of sheet. |
| What is FFR? | FFR is the raTo of maximal myocardial perfusion behind a stenoTc lesion divided by maximal hyperemic flow in that same region in the hypotheTcal case that the lesion was not present. |
| What is reperfusion therapy? | Timely reperfusion of jeopardized myocardium most effective way of restoring balance between oxygen supply and demand.
The dependence of myocardial salvage on the Tme elapsed unTl treatment pertains to paTents treated with either fibrinolysis or PCI |
| What is pathophysiology of myocardial reperfusion? | • Prevention of cell death by restoration of blood flow depends on the severity and duration of the preexisting ischemia
• Earlier blood flow is restored, the more favorable the recovery of LV systolic function, improvement in diastolic function, and reduction in overall mortality.
• Even after successful reperfusion and despite the absence of irreversible myocardial damage, a period of postischemic contractile dysfunction can occur—a phenomenon called myocardial stunning. |
| What is reperfusion injury? | Lethal reperfusion injury, which refers to reperfusion-induced death of cells that
were s5ll viable at restora5on of coronary blood flow
• Vascular reperfusion injury, which is progressive damage to the microvasculature such that there is an expanding area of no-reflow and loss of coronary vasodilatory
reserve
• Stunned myocardium, in which salvaged myocytes display a prolonged period of contrac5le dysfunc5on aCer restora5on of blood flow because of abnormali5es in
intracellular metabolism, leading to reduced energy produc5on
• Reperfusion arrhythmias, which refer to bursts of VT (and occasionally VF) that occur within seconds of reperfusion. |
| What are reperfusion arrhythmias? | Transient sinus bradycardia, PVCs, accelerated idioventricular rhythm, nonsustained VT |
| What is fibrinolysis tx? | • Fibrinolysis can recanalize the thrombotic occlusion associated with STEMI, and when achieved, restoration of coronary flow reduces infarct size and improves myocardial function and survival over both the short and the long term
• Patients treated within the first 1 to 2 hours after the onset of symptoms seem to have the greatest potential for long-term improvement in survival with fibrinolysis
• Electrocardiographic ST-segment resolution, when present, has a high positive predictive value (PPV) of greater than 90% for infarct artery patency with, but persistent ST-segment elevation (i.e., lack of ST-segment resolution) is a poor predictor of infarct-related artery occlusion, with a negative predictive value (NPV) of approximately 50%
• All fibrinolytic agents exert their effect by converting the proenzyme plasminogen to the active enzyme plasmin. |
| What are complications and contraindications of fibrinolytic therapy? | Bleeding (intracranial hemorrhage, nonintracranial bleed)
Contraindication (absolute [previous intracranial hemorrhage, ischemic stroke 6months, CNS neoplasm, recent head injury/trauma, GI bleed past month, known bleeding disorder/ aortic dissection/puncutres], relative [Oral AG, pregnancy, HTN, peptic ulcer...] |
| What are complications of STEMI? | LV failure (mechanical [wall rupture, pseudoaneursym, papillary muscle rupture])
Cardiac arrhythmias (electrical instability, pump failure and bradyarrhythmias)
Recurrent chest discomfort, pericardial effusions, LV thrombus and arterial thrombus, pericarditis (Day 1-8 weeks after MI, Dressler syndrome (day 1-8 week after MI, malaise, fever, leukocytosis, effusion))
RV failure (clinical features from RV dysfunction to CS, 1/3 inferior LV infarct, hemodynamics elevated filling pressure and decreased RV pressure and CO. |
| What is ECG finding for STEMI? | • ST-segment elevation in lead V4R (right precordial lead in the V4 position)
• Transient elevation of the ST segment in any of the right precordial leads can occur with RV MI
• ST-segment elevation of 0.1 mV or greater in any one or a combination of leads V4R, V5R, and V6R in patients with the clinical picture of acute MI |
| How is management of STEMI and NSTE? | . |
| What is long term tx for ACS? | healthy lifestyle choices, continue optimal pharmacologic and cardioprotective tx, sustain risk factor tx targets bp, LDL, HbA1c |
| What are types of chest pain? | Typical (constricting discomfort of front of chest or neck/jaw/shoulder/arm, precipitated by exertion, relieved by rest/nitrates w/in 5 min)
Atypical (meets two of charaterstics above)
non-anginal (one or none of the characteristics) |
| What are types of angina? | . |
| What are etiologies of myocardial ischemia? | Inflammation, platelets and coagulation, vasospasm, microvascular dysfunction, endothelial dysfunction, coronary stenosis |
| How is unstable angina? | Unstable angina 1 of 3 (rest angina, new onset angina, crescendo angina) |
| What are tx options of chest pain | • Before any tesTng is considered, one must assess
• the paUent’s general health
• comorbidiUes
• quality of life
• If revascularizaTon is unlikely to be an acceptable opTon
• further tesUng may be reduced to a clinically indicated minimum and
• appropriate therapy should be insUtuted, which may include a trial of anUanginal medicaUon even if a
diagnosis of CAD has not been fully demonstrated.
• Non-invasive funcUonal imaging for ischaemia may be an opUon if there is need to verify the diagnosis
• If the pain is clearly non-anginal, other diagnosTc tesTng may be indicated to idenTfy gastrointesTnal, pulmonary, or musculoskeletal causes of chest pain |
| What are basic biochem tests done for angina? | CBC, creatinine for renal function, lipid profile, screen T2DM, thyroid function |
