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BRAUNWALD'S HEART DISEASE > STEMI > Flashcards

STEMI Flashcards

1
Q

The pathologic diagnosis of myocardial infarction (MI) requires evidence of myocardial cell death caused by ischemia. Characteristic findings include

A

coagulation necrosis and contraction band necrosis, often with patchy areas of myocytolysis at the periphery of the infarct

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2
Q

acute coronary syndrome (ACS) encompasses the diagnoses of

A

unstable angina, non–ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI)

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3
Q

According to estimates from the American Heart Association (AHA), the short-term mortality rate of patients with STEMI ranges from 5% to 6% during the initial hospitalization and from 7% to 18% at 1 year.

A

5% to 6% during the initial

7% to 18% at 1 year.

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4
Q

The highest risk of ischemic complications following MI occurs within ——-, after which the risk becomes fairly linear.

A

180 days

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5
Q

Criteria for Previous Myocardial Infarction

A

Any of the following criteria meets the diagnosis for prior MI:

  • Pathologic Q waves with or without symptoms in the absence of nonischemic causes.
  • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract in the absence of a nonischemic cause.
  • Pathologic findings of previous MI.
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6
Q

Criteria for Acute Myocardial Infarction

Detection of a rise and/or fall in cardiac biomarker values (preferably cTn), with at least one value above the 99th percentile URL and with at least one of the following

A
  • Symptoms of ischemia
  • New or presumed new significant ST-segment–T wave (ST-T) changes or new LBBB
  • Development of pathologic Q waves on the ECG
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of an intracoronary thrombus by angiography or autopsy
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7
Q

PCI-related MI is arbitrarily defined by elevation of cTn values ——- ) in patients with normal baseline —–% if the baseline values are elevated and are stable or falling

A

(to >5 × 99th percentile URL

a rise in cTn values >20%

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8
Q

Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischemia and with a rise and/or fall in cardiac biomarker values and at least one value higher than the 99th percentile URL.

A

AT LEAST ONE

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9
Q

CABG related MI is arbitrarily defined by elevation of cardiac biomarker values ———) in patients with normal baseline cTn values (≤99th percentile URL). In addition, either

A

(to >10 × 99th percentile URL

(1) new pathologic Q waves or new LBBB
(2) angiographically documented new graft or new native coronary artery occlusion
(3) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality is required.

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10
Q

types of MI

A

TYPE i Spontaneous Myocardial Infarction
TYPE 2: Myocardial Infarction Secondary to Ischemic Imbalance
TYPE 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable
TYPE 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention
TYPE 4b: Myocardial Infarction Related to Stent Thrombosis
TYPE 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting

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11
Q

Type 1: Spontaneous Myocardial Infarction

A

Spontaneous 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. The patient may have underlying severe CAD but on occasion nonobstructive or no CAD.

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12
Q

Myocardial Infarction Secondary to Ischemic Imbalance

A

In cases of myocardial injury with necrosis in which 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, tachy/bradyarrhythmias, anemia, respiratory failure, hypotension, hypertension ± left ventricular hypertrophy).

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13
Q

Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable

A

Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic changes on the ECG or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarkers could rise, or in rare cases, when cardiac biomarkers were not collected.

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14
Q

Type 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention

A

MI associated with PCI is arbitrarily defined by elevation of cTn values to

> 5 × the 99th percentile URL in patients with normal baseline values (≤99th percentile URL) or a rise in cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (1) symptoms suggestive of myocardial ischemia, (2) new ischemic changes on the ECG or new LBBB, (3) angiographic loss of patency of a major coronary artery or a side branch or persistent slow flow or no flow or embolization, or (4) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality is required.

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15
Q

Type 4b: Myocardial Infarction Related to Stent Thrombosis

A

I associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial ischemia and with a rise and/or fall in cardiac biomarkers values with at least one value above the 99th percentile URL.

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16
Q

Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting

A

MI associated with CABG is arbitrarily defined by elevation of cardiac biomarker values to >10 × the 99th percentile URL in patients with normal baseline cTn values (< 99th percentile URL). In addition, either (1) new pathologic Q waves or new LBBB (2) angiographically documented new graft or new native coronary artery occlusion, or (3) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality is required.

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17
Q

Almost all acute coronary syndromes result from coronary athero sclerosis, generally with superimposed coronary thrombosis caused by rupture or erosion of an atherosclerotic lesion 2

A

T

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18
Q

STEMI - > cause transmural myocardial ischemia

A

Q wave infarction was frequently considered to be virtually synonymous with “transmural infarction,”

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19
Q

non–Q wave infarctions were often referred to as

A

“subendocardial infarctions.”

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20
Q

Other morphologic c acteristics associated with rupture-prone plaque include expansive remodeling that minimizes luminal obstruction (mild stenosis by angiography), neovascularization (angiogenesis), plaque hemorrhage, adventitial inflammation, and a “spotty” pattern of calcification. 24

A

t

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21
Q

The most characteristic change in QRS that develops in most patients with STEMI is the

A

evolution of Q wave

n a minority of patients with ST elevation, no Q waves develop but other abnormalities in the QRS complex occur frequently, such as diminution in R wave height and notching or splintering of the QRS

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22
Q

Gross alterations in the myocardium are difficult to identify until at least 6 to 12 hours has elapsed following the onset of necrosis

A

Gross alteration occur ij 6-12 hours

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23
Q

but a variety of histochemical stains can identify zones of necrosis after only

A

2 to 3 hours

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24
Q

triphenyltetrazolium chloride (TTC), which turns noninfarcted myocardium a brick-red color

A

while the infarcted area remains unstained

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25
Q

the earliest ultrastructural changes in cardiac muscle after ligation of a coronary artery, noted within

A

20 minutes,

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26
Q

the earliest ultrastructural changes in cardiac muscle: . These early changes are reversible.

A

reduction in the size and number of glycogen granules; intracellular edema; and swel ing and distortion of the transverse tubular system, sarcoplasmic reticulum, and mitochondria

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27
Q

Changes after 60 minutes of occlusion include

Myocyte swells
mitochondria disruption
nuclear chromatin
relaxation of myofibril

A

myocyte swelling, swelling and internal disruption of mitochondria, development of amorphous (flocculent) aggregation and margination of nuclear chromatin, and relaxation of myofibril

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28
Q

results from severe, persistent ischemia and is usually present in the central region of infarcts; it causes arrest of muscle cells

A

Coagulation necrosis

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29
Q

Leads V1-V2

A

Septal

LAD

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30
Q

Leads V1-V2 to V4-V6

A

Apical anteroseptal

LAD

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31
Q

V1-V6 occasioanlly aVL and I

A

Extensive anterior

Lad

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32
Q

I and aVL, V5-V6

A

Lateral

LCX

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33
Q

2,3,aVF

A

Inferior

RCA LCX

STE III >II means RCA

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34
Q

2 3 avf
I aVL
V5-B6

A

Inferateral

RCA LCX

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35
Q

Necrosis with contraction bands is caused by increased influx of calcium ions (Ca 2+ ) into dying cells, which results in the arrest of cells in the contracted state in the periphery of large infarcts and, to a greater extent, in nontransmural than in transmural infarcts

A

Calcium

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36
Q

During a later phase (days 3 to 7), less inflammatory monocytes predominate and produce the angiogenic mediator vascular endothelial growth factor (VEGF)

A

days 3 to 7

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37
Q

When reperfusion of myocardium undergoing the evolutionary changes from ischemia to infarction occurs sufficiently early (i.e., within 15 to 20 minutes), it can prevent necrosis from developing

A

15-20mimutes

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38
Q

but isolated infarction of the right ventricle is seen in just 3% to 5% of autopsy-proven cases of MI

A

T

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39
Q

Acute management of RV infarction complicated by cardiogenic shock includes judicious volume replacement, early revascularization, maintenance of atrioventricular synchrony, and in refractory cases, mechanical circulatory support (see Chapter 59).

A

T

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40
Q

The classic presentation of an RV infarct is

A

hypotension, clear lung fields, and elevated jugular venous pressures

41
Q

two most common myocardial or microvascular mimickers of MI are acute myocarditis (see Chapter 79) and acute stress (takotsubo) cardiomyopathy.

A

T

42
Q

An increase in the size of the infarcted segment, known as infarct expansion, is defined as “acute dilation and thinning of the area of infarction not explained by additional myocardial necrosis.”

A

T

43
Q

Bezold-Jarisch reflex

A

nvolves a variety of cardiovascular and neurological processes which cause hypopnea (excessively shallow breathing or an abnormally low respiratory rate) and bradycardia (abnormally low resting heart rate).

44
Q

Body temperature often begins to rise within 4 to 8 hours after onset of infarction, and rectal temperature may reach 38.3°C to 38.9°C (101°F to 102°F). The fever usually resolves by the fourth or fifth day after MI.

A

Develops 24-48 hours

Resolves in 4-5

45
Q

Killip

A

Class I patients are free of rales and a third heart sound (S 3 ). Class I patients have rales, but only to a mild to moderate degree (<50% of lung fields), and may or may not have an S 3 . Class III patients have rales in more than half of each lung field and frequently have pulmonary edema. Class IV patients have cardiogenic shock.

46
Q

An S 3 may result not only from LV failure but also from increased inflow into the left ventricle, as occurs when mitral regurgitation or a ventricular septal defect complicates STEMI.

A

T

47
Q

MURMUR secondary to dysfunction of the mitral valve apparatus (papillary muscle dysfunction, LV dilation).

A

mitral regurgitation

48
Q

Although friction rubs can be heard within 24 hours or as late as 2 weeks after onset of infarction, they occur most frequently on the second or third day

A

24-2 weeks

49
Q

The increased motion of the noninfarcted region subsides within 2 weeks of infarction, during which some degree of recovery often occurs in the infarct region as well, particularly if reperfusion of the infarcted area occurs and myocardial stunning diminishes.

A

subsides within 2 weeks of infarction

50
Q

Increasing stiffness in the infarcted zone of myocardium improves LV function because it prevents paradoxical systolic wall motion (dyskinesia).

A

paradoxical systolic wall motion (dyskinesia).

51
Q

The earliest abnormality is —/-////(see later), which occurs with infarcts involving only a small portion of the left ventricle

A

v tricular stiffness in diastole

52
Q

When the abnormally contracting segment exceeds ??? of the myocardium, the EF may decline, and LV end-diastolic pressure and volume may increase

A

15%

53
Q

Clinical heart failure accompanies areas of abnormal contraction exceeding ———% and loss of more than ——% has of the LV myocardium usually leads to cardiogenic shock, often fatal.

A

25

40

54
Q

acute dilation and thinning of the area of infarction not explained by additional myocardial necrosis

A

Infarct Expansion

55
Q

patients with MI, particularly when complicated by LV failure or cardiogenic shock, the affinity of hemoglobin for oxygen falls (i.e., P50 increases). The increase in P50 results from increased levels of erythrocyte 2,3-diphosphoglycerate, which is an important compensatory mechanism that mediates an estimated 18% increase in release of oxygen from oxyhemoglobin in patients with cardiogenic shock.

A

P50

56
Q

Natriuretic peptides are released early after STEMI, with a peak at approximately 16 hours

A

16 hours

57
Q

serum triiodothyronine (T 3 ) levels can decrease transiently, a fall that is most marked on approximately the third day after the infarct.

A

T

58
Q

Nausea and vomiting may occur, presumably because of activation of the vagal reflex or stimulation of LV receptors as part of the

A

BezoldJarisch reflex

59
Q

elevations in cTnI may persist for 7 to 10 days after MI; elevations in cTnT may persist for up to 10 to 14 days

A

Trop I 7-10 days

Trop T 10-14 days

60
Q

CK-MB seen in

A

small intestine, tongue, diaphragm, ute us, and prostate

61
Q

TRITON-TIMI 38 trial [Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction 38]. Circulation 2012;125:577.)

A

TRITON-TIMI 38 trial

62
Q

Elevation of the white blood cell count usually develops within 2 hours after the onset of chest pain, reaches a peak 2 to 4 days after infarction, and returns to normal in 1 week

A

T

63
Q

ELECTROC ArdioGr APhic MANiFestAtioNs oF Acute MYoc ArdiAl ischeMiA (iN THE ABseNce oF leF T BuNdle Br ANch BlocK)

A

New ST elevation at the J point in two contiguous leads with the following cut points:

≥ 0.1 mV in all leads (except V 2 -V 3 )

  • In leads V 2 -V 3 the following cut points apply:
  • ≥ 0.2 mV in men ≥40 years
  • ≥ 0.25 mV in men <40 years
  • ≥ 0.15 mV in women
64
Q

ST Depression and T Wave Changes

A

New horizontal or downsloping ST depression ≥ 0.05 mV in two contiguous leads

• T-wave inversion ≥ 0.1 mV in two contiguous leads with a prominent R wave or R/S ratio >1

65
Q

ELECTROC ArdioGr APhic MANiFestAtioNs oF ischeMiA iN THE sett NG oF leF T BuNdle Br ANch BlocK

A

ST-segment elevation ≥1 mm and concordant with the QRS complex 5pts

ST-segment depression ≥1 mm in lead V1, V2, or V3

3pts

ST-segment elevation ≥5 mm and discordant with the QRS complex

2pts

A score of ≥ 3 had a specificity of 98% for acute MI

66
Q

most recent universal definition of MI, however, retains the category of posterior MI. 1 Patients with an abnormal R wave in V 1 (0.04 second in duration and/or R/S ratio ≥1 in the absence of preexcitation or RV hypertrophy) and inferior or lateral Q waves have an increased incidence of isolated occlusion of a dominant left circumflex coronary artery without collateral circulation; such patients have a lower EF, increased end-systolic volume, and higher compl cation rate than RCA

A

T

67
Q

ST-segment elevations in aVR, reflecting the basal intraventricular septum, can be observed in up to 30% of STEMIs and identifies patients with a higher likelihood of left main coronary artery or multivessel disease and worse outcomes. 83

A

30% of STEMIs

68
Q

pattern of “pseudoinfarction” include

A

ventricular hypertrophy, conduction disturbances, preexcitation, primary myocardial disease, pneumothorax, pulmonary embolism, amyloid heart disease, hypertrophic cardiomyopathy, primary and metastatic tumors of the heart, traumatic heart disease, intracranial hemorrhage, hyperkalemia, pericarditis, early repolarization, forms of muscular dystrophy, and cardiac sarcoidosis.

69
Q

ST-segment elevation in the right precordial leads is a relatively sensitive and specific sign of RV infarction.

A

V 1 , V 3 R through V 6 R)

70
Q

Up to 12 hours can elapse before pulmonary edema accumulates after ventricular filling pressure has increased. The post-therapeutic phase lag represents a longer interval; up to 2 days is required for pulmonary edema to resolve and the radiographic signs of pulmonary congestion to clear after ventricular filling pressure have returned toward normal

A

T

71
Q

Most deaths associated with STEMI occur within the first hour of its onset and usually result from

A

ventricular fibrillation (VF)

72
Q

The CAPTIM (Comparison of Primary Angioplasty and Pre-hospital Fibrinolysis in Acute Myocardial Infarction) trial, for example, reported a trend toward a lower mortality rate in patients with STEMI who received prehospital fibrinolysis compared with patients who received primary PCI, especially if they were treated within 2 hours of the onset of symptoms

A

The CAPTIM (Comparison of Primary Angioplasty and Pre-hospital Fibrinolysis in Acute Myocardial Infarction)

73
Q

f the EMS has fibrinolytic capability and the patient qualifies for therapy, prehospital fibrinolysis may be considered and, if used, should be started within 30 minutes of arrival of the EMS on scene

A

30 min

74
Q

hospital door–to-needle time should be 30 minutes or less.

A

T

75
Q

he time from first medical contact (FMC) to deployment of the first PCI device (FMC-to-device time) should be 90 minutes or less

A

T

76
Q

interhospital transfer of the patient to a PCI-capable hospital for mechanical revascularization is also appropriate if use of a fibrinolytic is contraindicated or PCI can be initiated promptly (anticipated FMC-to-device time ≤120 minutes) or if fibrinolysis is unsuccessful

A

T

77
Q

for recurrent ischemia or routine invasive evaluation 3 to 24 hours after fibrinolysis

A

T

78
Q

Absolute Contraindications

A

Any previous intracranial hemorrhage Known structural cerebral vascular lesion (e g., arteriovenous

malformation) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months except acute ischemic stroke within 4.5

hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months Intracranial or intraspinal surgery within 2 months Severe uncontrolled hypertension (unresponsive to emergency therapy) For streptokinase, previous treatment within the previous 6 months

79
Q

Each 30-minute delay from symptom onset to PCI increases the relative risk (RR) for 1-year mortality by

A

8%

80
Q

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 infa ct related artery occlusion, with a negative predictive value (NPV) of approximately 50%.

A

T

81
Q

o trials, LATE (Late Assessment of Thrombolytic Efficacy) and EMERAS (Estudio Multicéntrico Estreptoquinasa Repúblicas de América del Sur), when viewed together, provide evidence that a reduction in mortality may still be observed in patients treated with thrombolytic agents between 6 and 12 hours after the onset of ischemic symptoms

A

6-12hours

82
Q

is the least fibrin-specific thrombolytic agent in clinical use

A

Streptokinase

83
Q

If the time from first medical contact to PCI is expected to be more than 120 minutes, fibrinolysis is recommended in the absence of

A

(1) significant contra ndications to fibrinolysis, (2) shock or acute severe heart failure, or (3) late presentation.

84
Q

REACT (Rapid Early Action for Coronary Treatment) study, patients with suspected failed reperfusion at 90 minutes by electrocardiographic criteria were randomly assigned to one of three treatment arms: rescue PCI, conservative care, or repeated fibrinolytic therapy. The composite of death, reinfarction, stroke, or severe HF at 6 months was significantly lower in patients randomly assigned to rescue PCI than in the two other treatment groups. 1

A

REACT

85
Q

n the setting of absolute contraindications to fibrinolysis (see Table 59.3) and lack of access to PCI facilities, antithrombotic therapy should be initiated because of the small but finite chance (approximately 10%) of restoring TIMI grade 3 flow in the infarct vessel and decreasing the chance of thrombotic compl cations of STEM

A

10%

86
Q

Nevertheless, a meta-analysis of trials in the fibrinolytic era suggested that for every 1000 patients treated with heparin versus aspirin alone, five fewer deaths (P = 0.03) and three fewer recurrent infarctions (P = 0.04) occur, but at the expense of three more major bleeding episodes (P = 0.001).

A

T

87
Q

Major h rhagic even s occur more frequently in patients with low body weight, advanced age, female sex, marked prolongation of the activated partial thromboplastin time (APTT) (>90 to 100 seconds), and performance of invasive procedures. 72

A

T

88
Q

PCI in the HORIZONS-AMI (Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction) trial, bivalirudin (open label), versus heparin plus glycoprotein (GP) IIb/IIIa inhibitors, reduced the 30-day rate of major bleeding or major adverse CV events, including death, reinfarction, target vessel revascularization for ischemia, and stroke (RR, 0.76; 95% CI 0.63 to 0.92; P = 0.005), driven by a significant 40% reduction in major bleeding

A

HORIZONS-AMI

89
Q

OASIS-6 (Organization for the Assessment of Strategies for Ischemic Syndromes)

A

Fondaparinux and heparin

90
Q

Accordingly, patients managed with pharmacologic reperfusion therapy should receive anticoagulant therapy for a minimum of 48 hours and preferably for the duration of hospitalization after STEMI, up to 8 days

A

48-8 days

91
Q

CLARITY-TIMI 28 provided insight into the mechanism of the benefit of clopidogrel in STEMI

A

clopidogrel did not increase the rate of complete opening of occluded infarct arteries when fibrinolysis was administered, but was effective in preventing reocclusion of an initially reperfused infarct artery.

92
Q

PLATO (Platelet Inhibition and Patient Outcomes) trial, compared with clopidogrel, treatment with the reversible P2Y 12 inhibitor ticagrelor in patients with STEMI undergoing primary PC (n = 7544) tende

A

Ticqgrelor versus clopidogrel

93
Q

PCICLARITY (PCI Clopidogrel as Adjunctive Reperfusion Therapy) study,

A

Pretreatment with clopidogrel reduces death

94
Q

Prehospital administration of ticagrelor did not improve the primary endpoint of coronary reperfusion, but did reduce the secondary endpoint of stent thrombosis without any additional bleeding, compared to in-hospital administration in patients with STEMI undergoing primary PCI

A

ATLANTIC trial ( tion of Ticagrelor in the Cath Lab or in the Ambulance for New ST Elevation Myocardial Infarction to Open the Coronary Artery).

95
Q

COMMIT

A

5 fewer events for each of these endpoints per 1000 patients treated; yet there were 11 more episodes of cardiogenic shock in the metoprolol group per 1000 patients treated

96
Q

CAPRICORN (Carvedilol Post Infarction Survival Control in Left Ventricular Dysfunction) trial randomly assigned 1959 patients with MI and systolic dysfunction (EF <40%) to carvedilol or placebo

A

True

97
Q

VALIANT (Valsartan in Acute Myocardial Infarction) trial

A

compared the effects of the ARB valsartan, valsartan and captopril, and captopril alone on mortality in patients with acute MI complicated by LV systolic dysfunction and/or HF within 10 days of MI. 26

98
Q

EPHESUS (Eplerenone Post-AMI Heart Failure Efficacy and Survival)

A

T

99
Q

Beta-Adrenergic Agonists. When LV failure is severe, as manifested by marked a reduction in the cardiac index (< 2.2 liters/min/m 2 ), and PCWP is at optimal (18 to 24 mm Hg) or excessive (>24 mm Hg) levels despite therapy with diuretics, beta-adrenergic agonists are indicated. 114

A

T

BRAUNWALD'S HEART DISEASE (6 decks)

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