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Internal Medicine (IM platinum) > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

2 groups of Ischemic Heart Disease

A
  • Stable coronary artery disease (SCAD)
    • Stable chronic angina pectoris (CSAP)
  • Acute coronary syndrome (ACS), which are composed of:
    • Non-ST segment elevation acute coronary syndrome (NSTE-ACS), which includes:
      • Unstable angina(UA)
      • Non-ST-segment elevation myocardial infarction (NSTEMI)
    • ST-segment elevation acute myocardial infarction (STEMI)
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2
Q

Etiopathogenesis of Stable Coronary artery Disease

A
  • Inadequate supply of blood flow and oxygen to a portion of the myocardium causing inadequate perfusion of myocardium (ischemia) supplied by an involved coronary artery
  • Usually inducible by :
    • Stress
    • exercise
    • emotion
  • Most common cause:
    • Atherosclerotic disease of an epicardial coronary artery
  • Obesity, insulin resitance, and T2DM are increasing and powerful risk factors for IHD
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3
Q

Clinical Manifestation of Chronic Stable Angina Pectoris (CSAP)

A
  • Typical history involves a man >50 years old or woman >60 years old who complains of Chest discomfort:
    • Described as heaviness, pressure, squeezing, smothering, or choking
    • Crescendo-decrescendo in nature
    • Usually lasts 2-5 minutes
    • Associated with physical exertion on stress
    • Radiation to either or both shoulders/arms, but does not radiate to the trapezius muscles
    • Releived within 5-10 mins by rest and/or sublingual nitroglycerin
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4
Q

Hand placed over sternum with a clenched fist to indicate a squeezing, central, substernal discomfort

A

Levine’s sign

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5
Q

Canadian Cardiovascular Society Classification of Angina

A
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6
Q

Typical vs Atypical Angina

A
  • Substernal chest discomfort of characteristic quality and duration
  • Provoked by exertion or emotional stress
  • Releived by rest and/or nitrates within minutes

TYPICAL ANGINA : all 3

ATYPICAL ANGINA: Meets only 2 of the 3

NON-ANGINAL PAIN: Meets only one or none of the manifestions

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7
Q

Basic Laboratory Work-up for SCAD

A
  • CBC: Anemia may trigger ischemia
  • Fasting lipid profile and FBS/HbA1c: to identify risk factor such as dyslipidemia and diabetes
  • Baseline liver and kidney function prior to starting medications
  • Others:
    • Consider thyroid function tests, BNP/NT-proBNP
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8
Q

12-Lead Electrocardioogram for SCAD

A
  • May be normal at rest - but it does not exclude diagnosis of ischemia (stress testing may be needed)
  • May find ST-segment and T-wave changes, LV hypertrophy, Intraventricular conduction disturbances, arrythmias
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9
Q

Chest Radiograph for SCAD

A
  • Does not provide specific information for SCAD
  • May be useful to rule out other non-cardiac causes of chest pain
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10
Q

2D echo for SCAD

A
  • used to assess left ventricular function in patients with CSAP and patients with a history of a prior MI, pathologic Q waves, or clinical evidence of CHF
  • Assess for wall motion abnormalities, ejection fraction, presence of thrombus
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11
Q

Stress testing for SCAD

A
  • ECG exercise testing: most widely used for both diagnosis of IHD and estimating prognosis; involves recording the 12-Lead ECG before, during and after exercise
  • Stress imaging (stress echpcardiography, radionuclide perfusion or MPI, stress cardiac MRI) : preferred when the resting ECG is already abnormal
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12
Q

CT Angiography (CTA) and calcium score

A
  • CTA: imaging technique for anatomical diagnosis of obstructive coronary lesionsl used as an alternative to stress imaging to”rule out” SCAD, since it is a high sensitivity test
  • Calcium score: calcified lesions are quantified using the Agatston score
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13
Q

Indications for Coronary Angiography

A
  • Patients with CSAP who have survived cardiac arrest or life-threatening ventricular arrhythmia
  • Patients with CSAP with severe symptoms despite optimal medical therapy
  • Patients with high cardiac event risk (e.g., death, AMI) based on noninvasive testing, regardless of symptoms
  • Patients with troublesome symptoms that present diagmostic difficulties in whome there is a need to confirm or rule out the diagnosis of IHD
  • Patients with CSAP or evidence of ischemia on noninvasive on noninvasive testing with clinical or laboratory evidence of ventricular dysfunction
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14
Q

Control of Risk factors and Lifestyle medication for SCAD

A
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15
Q

3 drugs focus primarily on reducing acute thrombotic events and LV dysfunction in patients with SCAD

A
  • Aspirin
  • ACE-inhibitors
  • Statins
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16
Q

Drugs that is shown to reduce mortality in SCAD with LV dysfunction following Myocardial infarction

A
  • Beta Blockers
  • ACE-inhibitors
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17
Q

DRUGS USED IN SCAD (prevention of mortality and morbidity)

A
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18
Q

Pharmacologic Treatment for relief of angina (ANTI-ISCHEMIC DRUG)

A
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19
Q

Other Anti-Ischemic Drugs for SCAD

A
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20
Q

Percutaneous Coronary Intervention (PCI)

A
  • Balloon dilatation usually accompanied by coronary stenting
  • Most common indication is persistent or symptom-limiting angina pectoris, despite medical therapy, accompanied by evidence of ischemia during a Stress test
  • Patients who have received a drug eluting stent will need:
    • Dual antiplatelets for 1 year (Aspirin +ADP-P2Y12-Inhibitor), then
    • SIngle antiplatelet indefinitely (usually aspirin)
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21
Q

Cronary Artery Bypass Grafting

A
  • Done to Achieve complete revascularization by grafting all coronary arteries of sufficient caliber that have significant proximal stenoses
  • Preferred approach for:
    • Left main CAD
    • 3 vessel CAD, especially if with LV dysfunction
    • 2 vessel CAD with significant proximal left anterior descending artery disease with LV dysfunction or high risk findings on non-invasive tests
    • Patients with multi-vessel CAD and Diabetes
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22
Q

Operational term that refers to a pectrum of conditions compatible with acute myocardial ischemia and/or infarction due to an abrupt reduction in coronary blood flow

A

Acute Coronary Syndrome

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23
Q

Hallmark of Acute Coronary Syndrome (ACS)

A

Sudden imbalance between myocardial oxygen consumption (MVO2) and demand usually due to coronary obstruction

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24
Q

Patients with ACS are composed of..

A
  • Non-ST segment elevation ACS (NSTE-ACS) divided according to presence of necrosis biomarker:
    • Non-ST segment elevation myocardial infarction (NSTEMI)
    • Unstable angina (UA)
  • ST-segment elevation myocardial infarction (STEMI)
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25
Q

Criteria for Acute Myocardial Infarction

A
  • “Acute MI” should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia

Under these conditions any of the following criteria meet the diagnosis of MI:

  • Detection of a rise and/or fall in cardiac biomarkers (preferably cardiac troponins/cTn), with at least one value above the 99th percentile with at least one of the following:
    • Symptoms of Ischemia
    • New or presumed new significant ST-segment and/or T wave changes or new LBBB
    • Development of pathologic Q waves on the ECG
    • Imaging evidence of a new loss of viable myocardium or new wall motion abnormality
    • identification of an intracoronary thrombus by angiography or autopsy
  • Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB (Type 3)
  • PCI-related MI (type 4a)
  • Stent thrombosis associated with MI (type 4b)
  • CABG-related MI (type 5)
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26
Q

Criteria for Previous Myocardial Infarction

A

Any of the following:

  • Pathologic Q waves with or without symptoms in the absence of non-ischemic causes
  • Imaging evidence of a region of loss of viable myocardium that is thinnd and fails to contract in the absence of a non-ischemic
  • Pathologic finding of previous MI
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27
Q

Universal Classification of Types ofMyocardial Infarction

A
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28
Q

Type of MI

Related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries that leads to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis

A

TYPE 1

(Spontaneous MI)

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29
Q

Type of MI

A condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand (e.g., coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachyarrhythmias/bradyarrhythmias, anemia, respiratory failure, hypotension, and hypertension with/without LV hypertrophy

A

Type 2

MI secondary to Ischemic Imbalance

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30
Q

Type of MI

Cardia death with symptoms suggestive of ischemia and presumed new ischemic changes (or new LBBB), but death occuring before blood samples could be ontained

A

Type 3

MI resulting in Death when biomarkers are Unavailbale

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31
Q

Type of MI

Defined by elevation of cardiac troponin values >5x the 99th percentile of the upper reference limit in those with normal baseline values or a rise in cTn values >20% if baseline values are elevated and are stable or falling: and one of the following

  • Symptoms suggestive of MI
  • new Ischemic changes on the ECG or new LBBB
  • Angiographic loss of patency of a major coronary artery or a side branch or persistent slow flow or no flow or embolizaion
    • Imaging demonstration of a new loss of viable myocardium or new regional wall motion abnormality
A

Type 4a

MI related to PCI

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32
Q

Type of MI

Associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial schemia and with a rise and/or fall in cardiac biomarkers with at least one value >99th percentile of the upper reference limit

A

Type 4b

MI related to stent thrombosis

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33
Q

Type of MI

Defined as elevation of cardiac biomarker values >10x the 99th percentile of upper refernce limit in patients with normal bseline values; AND either;

  • New pathologic Q waves or new LBBB or
  • new graft or new native coronary artery occlusion on angiogram or
  • Imaing evidence of new loss of viable myocardium or new regional wall motion abnormality
A

Type 5

MI related to CABG

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34
Q

Myocardial infarction with Non-Obstructive Coronary Arteries (MINOCA)

A
  • AMI occuring in the absence of obstrucibe (>50%) CAD
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35
Q

Etiologies of MINOCA

A
  1. Secondary to coronary artery disease (MI type 1)
  2. Imbalance between oxygen supply and demand (MI type 2)
  3. Coronary endothelial dysfunction (MI type 2)
  4. Secondary to myocardial disorders without involvement of coronaries
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36
Q

Etiopathogenesis of NSTE-ACS

A
  • Most commonly caused by imbalance between oxygen supply and demand
  • usually due to a partially occluding thrombus forming on a disrupted coronary plaque or on eroded coronary artery endothelium
37
Q

Four Basic Pathophysiologic processes for NSTE-ACS

A
  • Most common cause:
    • Plaque rupture or erosion with superimposed non-occlusive thrombus
  • Dynamic obstruction (e.g., coronary spasm as in Prinzmetal’s variant angina)
  • Severe mechanical obstruction (e.g., stent thrombosis)
  • Increased myocardial O2 demand (e.g., tachycardia) and/or decreased supply (e.g., anemia)
38
Q

Angina or equivalent ischemis discomfort with at least one of the following:

  • occurs at rest (or with minimal exertion), usually lasting >10 minutes
  • Severe and of new onset (i.e., within the prior 4-6 weeks) of at least CCS III severity
  • Occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previous episodes)
A

Unstable Angina

39
Q

Clinical features of UA plus evidence of myocardial necrosis (elevated cardiac biomarkers)

A

NON-ST-segment Elevation Myocardial Infarction (NSTEMI)

40
Q

Ischemic pain that occurs at rest but not usually with exertion, associated with transient ST-segment elevation

Due to transient, focal spasm of an epicardial coronary artery

A

Prinzmetal Variant Angina

41
Q

Symptoms of NSTE-ACS

A
  • Symptoms that Increase likelihood of AMI
    • Typical pain with radiation to shoulders
    • Typical pain associated with exertion, diaphoresis, nausea, or vomiting
  • Symptoms that Decrease likelihood of AMI
    • Inframammary location of pain
    • Pain reproducible with palpation
    • Pain described as sharp, positional, or pleuritic
42
Q

usual PE findings of NSTE-ACS

A
  • Pale coll skin
  • tachycardia
  • S3 or S4
  • basilar rales
  • hypotension
43
Q

12 lead Electrocardiogram of NSTE-ACS

A
  • Should be performed and interpreted within 10 minutes of patient’s arrival
  • Changes may include:
    • ST-segment depression
    • new T-wave inversion
    • Transient ST-segment elevation
  • May also be initially normal,which is why serial ECGs should be done to detect ischemic changes if patient remains symptomatic with a high suspicion for ACS
44
Q

Cardiac biomarkers for NSTE-ACS

A
  • Elevated levels distinuis patients with NSTEMI from UA
  • Serial cardiac troponin I or T levels should be obtained to identify a rising and/or falling pattern of values:
    • First level taken at prescription
    • Second level taken at 3-6 hours after symptom onset
    • Additional level taken beyond 6 hours in those with nomal levels ons erial examination when ECG and/or presentation confer an intermediate or high index of suspicion for ACS
  • Cut off of tropinin value for myocardial necrosis: 99th percentile of the upper reference level
45
Q

Cardiac troponins vs CK-MB

A
46
Q

Imaging for NSTE-ACS

A
47
Q

RISK STRATIFICATION: TIMI SCORE for NSTE-ACS

A
48
Q

Non pharmacologic management of NSTE-ACS

A
  • Bed rest with continuous ECG monitoring
  • Supplemental oxygen if O2 saturation <94%
  • Stool softeners as needed
49
Q

Anti-Ischemic Therapy for NSTE-ACS

A
50
Q

Standard Medications for NSTE-ACS

A
  • ACE inhibitors
    • Reduce mortality in those with recent MI (especially if EF <40%)
  • ARBs
    • Recommended in HF or MI with LVEF <40% who are ACE-I intolerant
  • Aldosterone Blockers
    • Recommended in post-MI patients without significant renal dysfunction (whoa re already on ACEi and BB)
  • Statins
    • High intensity statin therapy should be initiated or continues
    • Early administration of statins (e.g., atorvastatin 80 mg/day) has been shown to reduce adverse outcomes
51
Q

Antiplatelet Therapy for NSTE-ACS

A
  • Aspirin
    • Established first-line therapy for NSTE-ACS
    • Platelet cyclooxygenase inhibitor which blocks the synthesis and release of thromboxane A2 (platelet activator), causing decreased platelet aggregation and thrombus formation
    • 165-325 mg LD chewed (non enteric), then 80-162 mg OD maintenance dose indefinitely
    • Contraindications: active bleeding or aspirin intolerance
  • P2Y12- inhibitors
    • in the absence of high bleeding risk, patients with NSTE-ACS should also receive a P2Y12 inhibitor for up to 1 months (at least 12 months if patient is to undergo PCI with stenting)
52
Q

P2Y12-Inhibitors

A
53
Q

Anticoagulation Therapy for NSTE-ACS

A
  • Unfractionated Heparin (UFH)
  • Enoxaparin
  • Fondaparinux
  • Bivalirudin
54
Q

Unfractionated Heparin

A
  • Dose
    • 60 U/kg IV bolus (maximum 4000 U), then 12 U/kg infusion (1000 U/hour) for 48 hours or until PCI is performed (most trials continued therapy for 2-5 days)
  • Description
    • Mainstay of therapy
    • Prevents coagulation by blocking thrombin (factor IIa) and factor Xa
    • Daily monitoring of aPTT is needed to target 50-70 secs or 1.5-2.5 times control
55
Q

Enoxaparin

A
  • Dose
    • 30 mg IV loading dose, then 1 mg/kg SC q12 for the duration of hospitalization or until PCI is performed
    • For >=75 years olf: no IV bolus needed
    • Renal adjustment needed (1 mg/kg SC OD for CrCl <30)
  • Desription
    • ​Superior to UFH in reducing recurrent cardiac events, especially in patients managed conservatively
    • Greater anti-factor Xa activity (relative to factor IIa) inhibits thrombin generation more effectively
    • No monitoring needed (unlike UFH)
56
Q

Fondaparinux

A
  • DOSE
    • 2.5 mg SC OD for duration of hospitalization or until PCI is performed
  • DESCRIPTION
    • ​Indirect factor Xa inhibitor
    • Equivalent in efficacy to enoxaparin, but with lower risk of major bleeding
    • Should not be used as sole anticoagulant to support PCI, due to increased risk of catheter thrombosis
57
Q

Bivalirudin

A
  • DOSE
    • 0.75 mg/kg IV bolus, then infusion of 1.75 mg/kg/hr
  • DESCRIPTION
    • Direct thrombin inhibitor
58
Q

Conservative versus Early Invasisve Strategy

A
59
Q
  • Syndrome of severe ischemic pain that usually occurs a rest and it associated with transient ST-segment elevation
  • Caused by focal spasm of an epicardial coronary artery (most common the RCA)
A

Prinzmetal’s variant Angina

60
Q

Diagnostic hallmark of Prinzmetal’s Variant Angina

A
  • Coronary arteriograpy demonstrates transient coronary spasm
61
Q

Main therapeutic agent for Prinzmetal’s variant angina

A
  • Nitrates
  • CCB

!!!!Aspirin may increase severity of ischemic episodes

62
Q

Etiopathogenesis of ST-Segment Elevation Myocardial Infarction (STEMI)

A
  • acute plaque rupture is central to the pathogenesis of STEMI
  • STEMI occurs when coronary blood flow decreases abruptly after a thrombotic (usually total) occlusion of a coronary artery previously affected by atherosclerosis
63
Q

Temporal Stages of STEMI

A
  • Acute: <7 days
  • Healing: 7-28 days
  • Healed: >=29 days
64
Q

KIllip Scoring for Prognostication for STEMI

A
65
Q

12-lead EG for STEMI

A
  • Must be interpreted within 10 minutes of patient arrival
  • Total occlusion of an epicardial coronary produces ST-segment elevation, and most ultimately evelove into Q-waves
  • Diagnosis of STEMI requires:
    • typcal ST segment elevation in at least 2 contigous leads or new-onset LBBB
66
Q

Cardiac biomarkers and Other Blood tests for STEMI

A
  • troponin T and Troponin I: increases after STEMI many times higher than upper reference limit
  • CK(non specific): rises within 4-8 hours and returns to normal by 48-72 hours
  • Other blood tests similar to NSTE-ACS
67
Q

Cardiac Imaging for STEMI

A
  • Echocardiography: abnormalities of wall motion are almost universally present
  • Radionuclide techniques such as MPI with thallium or setamibi
  • Cardiac MRI
68
Q

TIMI Risk Score for STEMI

A
69
Q

Goals of Management for STEMI

A
  • Control of Chest pain
  • Identify candidates for urgent reperfusion (PCI or thrombolysis)
  • Hospital phase management and risk stratisfication
70
Q

Initial management in the emergency room for STEMI

A
71
Q

Control of Chest Pain

A
72
Q

Supportive care for STEMI

A
73
Q

Secondary Prevention and Long term Management for STEMI

A
74
Q

Reperfusion therapy for STEMI

A
  • Reperfusion terapy (fibrinolysis or percutaneous coronary intervention) should be administered to all eligible patients with STEMI with symptom onset within the last 12 hours
  • Reperfusion is reasonable if symptom onset is between 12-24 hours + evidence of ongoing ischemia (primary PCI preferred in these patients)
75
Q

Time to ECG

A
  • AHA/ACC 2013
    • FMC to ECG : <=10 minutes
  • ESC 2017
    • FMC to ECG: <= 10 minutes
76
Q

Time to thrombolysis

A
  • AHA/ACC 2013
    • Door to needle time : <= 30 minutes
  • ESC 2017
    • Time from STEMI diagnosis to start of fibrinolysis: <=10 minutes
77
Q

Time to PCI

A
  • AHA/ACC 2013
    • door to balloon time <= 90 minutes
  • ESC 2017
    • Time from STEMI diagnosis tp wore crossing <= 60 minutes
78
Q

Primary PCI is preferred in the following

A
  • Time to treatment delays are short: symptoms <12 hours and PCI can be performed <120 minutes from STEMI diagnosis
  • Contraindication to fibrinolysis, irrespective of time delay from FMC
  • High risk from STEMI (cardiogenic shock, Killip >III)
  • Late presentation of patient (symptom onset >3 hours)
  • Diagnosis of STEMI is in doubt
79
Q

Fibrinolysis is preferred in the following

A
  • Symptoms <12 hours and primary PCI cannot be performed within 120 mins from STEMI diagnosis
  • Prolonged transport to PCI-capable center with FMC to device time>120 mins (if initially received in non PCI capable center)
  • PCI is not available
80
Q

Primary PCI

A
  • Emergent PCI with balloon,s tent, or other device, performed on the infarct-related artery without previous fibrinolytic treatment
  • For symptoms <=12 hours: PCI is recommended (over fibrinolysis) when it can bbe performed in a timely fasgion
  • For symptoms >12 hours: PCI is recommended in the presence of ongoing ischemia, hemodynamic instability, or life threatening arrhythmias
81
Q

Pharmocoinvasive Strategy

A
  • Fibrolysis combined with rescue PCI (in case of failed fibrinolysis) or routine early PCI strategy (in case of successful fibrinolysis)
82
Q

Rescue PCI

A
  • Emergent PCI performed immediately for failed fibrinolysis (persistent chest pain and <50% ST-segment resolution at 60-90 mins after)
83
Q

Routine Early PCI Strategy after fibrinolysis

A

Angiography with PCI of infarct-related artery, performed between 2-24 hours after successful fibrinolysis

84
Q

Adjunctive Pharmacotherapyduring Primary PCI

A
85
Q

Fibrinolysis

A
  • Largest benefit: when offered < 2hours after symptom onset
  • Reperfusion strategy when PCI cannot be done in a timely manner
  • MEchanismof thrombolytics: Promote conversion of plasminogen to plasmin, which then lyses fibrin thrombi
86
Q

Drugs for Fibrinolysis

A
87
Q

Absolute Contraindications for Fibrinolysis

A
  • Any prior intracranial hemorrhage
  • Structral cerebral vascular lesion
  • Malignant intracranial neoplasm
  • Ischemic Stroke within 3 months (exept acute ischemic stroke within 4.5 hours)
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis
  • Closed-head or facial trauma within 3 months
  • Intracranial or infaspinal surgery within 2 months
  • Severe uncontrolled hypertension (unresponsive to emergency therapy)
  • For streptokinase, previous treatmeent within the last 6 months
88
Q

Relative Contraindications

A
  • History of chronic, severe, poorly controlled HPN
  • Significant hypertension at initial evaluation (SBP >180 mmHg or DBP >110 mmHg)
  • History of previous ischemic stroke > 3months
  • Dementia
  • Intracranial pathology not covered in Absolute Contraindications
  • Traumatic or prolonged (> 10 minutes) cardiopulmonary resucitation
  • Major surgery <3 weeks
  • Recent (within 2 to 4 weeks) internal bleeding
  • Noncompressibe vascular punctures
  • Pregnancy
  • Active peptic ulcer
  • Oral anticoagulant therapy
89
Q

Usual Complication of STEMI

A

Internal Medicine (IM platinum) (14 decks)

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