Ischemic Heart Disease-Assessment Exam 2 Flashcards
1
Q
What are the two most important risk factors for the development of atherosclerosis involving the coronary arteries?
A
Male gender
Increasing age
2
Q
____% of our surgical pts are at increased risk for IHD
A
30
3
Q
What are the common manifestations for IHD?
A
Angina pectoris
Acute MI
Sudden Death
4
Q
What is the full list of risk factors for IHD?
A
Male gender
Increasing age
Hypercholesterolemia
Hypertension
Smoking
Diabetes
Obesity
Sedentary lifestyle
Genetic factors/family history
5
Q
Things that cause sudden cardiac death
A
CAD
Overdose
Cardiomyopathy
6
Q
What is angina pectoris?
A
Imbalance between coronary blood flow (supply) and myocardial oxygen consumption (demand)
Can precipitate ischemia, which frequently manifests as chest pain
7
Q
Release of what 2 cardiac nociceptors occurs in angina?
A
Adenosine
Bradykinin
8
Q
Stable angina typical develops in the setting of _______ or significant (what percent?) ________ of a segment of coronary artery
A
Partial occlusion
Chronic narrowing (>70%)
9
Q
With adenosine and bradykinin, the afferent neurons converge with the upper __________ and _________ in the spinal cord
A
5 thoracic sympathetic ganglia
Somatic nerve fibers
10
Q
After the afferent neurons converge, they produce what type of stimulation? What does this result in?
A
Thalamic and cortical stimulation
Chest pain of angina pectoris
11
Q
What does bradykinin and adenosine slow?
What do they decrease?
A
AV conduction
Cardiac contractility
12
Q
What is the most common cause of impaired coronary blood flow resulting in angina pectoris?
A
Atherosclerosis
13
Q
Angina pectoris may also occur in the absence of coronary obstruction, as a result of what 3 things?
A
myocardial hypertrophy
severe aortic stenosis
aortic regurgitation
14
Q
What are causes of decreased coronary blood flow?
A
Reduction in lumen size
clot/plaque in vessel
decrease in BP (anesthesia can cause this)
15
Q
With angina pectoris, we don’t really worry about the chest pain, but we worry about:
A
The decrease in cardiac contractility and decreased AV conduction
16
Q
What are the symptoms of angina?
A
Retrosternal chest pain, pressure, heaviness (from C8 to T4)
Radiates to neck, left shoulder, left arm, or jaw
- Occasionally to back or down both arms
Shortness of breath, dyspnea
Lasts several minutes
17
Q
What two pt populations have a weird presentation of chest pain?
A
Women
Diabetics
18
Q
Other causes of chest pain?
How do differentiate?
A
- GERD: give GI cocktail
- Musculoskeletal: if you touch it and it hurts, it’s MS
- Pericarditis: WBC elevated, ST elevation in all leads
-PE: gold standard is CT angio, ABGs - AAA dissection: tearing pain in back and chest (if aortic root is involved, more chest than back pain)
19
Q
How does a saddle PE present?
A
o2 levels low
syncope
confused
air hungry
may be combative
demarcation line on chest b/c one side of body is oxygenated and the other is not
20
Q
Chronic stable vs unstable angina?
A
Chronic:
- Chest pain that does NOT change in frequency or severity in 2-month period
Unstable:
- Chest pain increasing in frequency and/or severity without increase in cardiac biomarkers (troponin, cp-k)
- If elevated cardiac biomarkers but no EKG changes, then probably NSTEMI
- typically lasts >10 minutes
21
Q
Chest pain differential chart:
What are the most dangerous ones we would treat first?
A
Aortic dissection, PE, MI
22
Q
Pneumothorax causes:
A
Trauma
Spontaneous
23
Q
Diagnostic tools for chest pain:
Which one is the gold standard?
A
12 lead EKG
Exercise stress test
Nuclear stress imaging
Echo
Coronary angiography (gold standard)
24
Q
When is an echo useful?
A
Pts with a LBBB or an abnormal EKG in whom the diagnosis of AMI is uncertain
25
You will see what type of abnormality on an echo in pts with an AMI?
Regional wall motion
26
How fast does a troponin jump in an MI? How long is it elevated for?
3-4 hours
up to 2 weeks
27
What type of EKG change is a characteristic of subendocardial ischemia?
What else may accompany this?
ST segment depression
transient T wave inversion
28
Pts with chronically inverted _____ waves resulting from previous MI may show a return of the _____ waves to normal upright position during MI.
What is this called
T waves (for both blanks)
Pseudonormalization of the T wave
29
What is an exercise stress test useful for?
Detecting signs of myocardial ischemia and establishing their relationship to chest pain and determining the relationship to exercise capacity
30
Exercise testing if often combined with what imaging studies?
Nuclear
Echo
MRI
31
Why is exercise testing not always feasible?
Inability of the pt to exercise, d/t peripheral vascular or MS disease, deconditioning, dyspnea on exertion, prior stroke, or the presence of chest pain at rest or with minimal activity
32
The _____ the degree of ST segment depression, the _____ the likelihood of significant CAD
Greater (for both)
33
At least ___ mm of horizontal or downscoping ST segment depression during or within ___ minutes after exercise indicates CAD
1 mm
4 min
34
What is the overall sensitivity of the exercise test?
around 75%
35
What test has a greater sensitivity than exercise testing for detection of IHD?
Nuclear stress imaging
36
During a nuclear stress test, what will cause tracer activity to be LESS present?
A significant coronary obstructive lesion causing a reduction in blood flow
37
What are the tracers in a nuclear stress test made of?
Thallium
Technetium
38
What is the most important indicator of the significance of the coronary artery disease?
The size of the perfusion abnormality
39
What can you administer to produce rapid heart rate to create cardiac stress during nuclear testing?
Atropine
Dobutamine
Institution of artificial cardiac pacing
40
Cardiac stress can be produced by administration of what?
Coronary vasodilator such as adenosine or dipyridamole
41
What is an echo used for?
Wall motion abnormalities
Valvular function
42
_____ provides the best information about the condition of the coronary arteries
Stress echocardiography
43
Who is a stress echocardiography indicated in?
- patients with known or possible angina pectoris who have survived sudden cardiac death
- those who continue to have angina pectoris despite maximal medical therapy
- those who are being considered for coronary revascularization
- those who develop a recurrence of symptoms after coronary revascularization
- those with chest pain of uncertain cause
- those with a cardiomyopathy of unknown cause
44
What is a coronary spasm?
What does this result in?
a sudden, temporary narrowing or tightening of a small part of an artery
a temporary situation where the heart does not get enough blood
45
What is variant angina?
How is this diagnosed?
angina that results from coronary vasospasm rather than occlusive coronary artery disease
diagnosed by ST-segment elevation during an episode of angina pectoris.
46
What is a vulnerable plaque?
What are the characteristics of this?
those most likely to rupture and form an occlusive thrombus
a thin fibrous cap and a large lipid core containing a large number of macrophages
47
T/F
The presence of vulnerable plaque predicts a greater risk of MI regardless of the degree of coronary artery stenosis.
True
48
AMI most often results from rupture of a plaque that had produced less than ___% stenosis of a coronary artery
50
49
Prevention of IHD
- Smoking cessation
- Ideal body weight
- Low fat, low cholesterol diet (statins if not)
- Regular aerobic exercise
- HTN treatment
- GLP-1 agonists
50
Losing ____ % of body weight decreased CAD risk by _____ %
10
50
51
When is drug treatment recommended based on LDL?
What is the goal?
LDL exceeds 160 mg/dl
Goal is >50% reduction or <70 mg/dl
52
HTN increases risk of coronary events, such as what?
direct vascular injury
left ventricular hypertrophy
increased myocardial oxygen demand
53
Drug therapy for IHD includes:
- ASA
- Platelet glycoprotein IIb/IIIa receptor antagonists
- Thienopyridines (P2Y12 inhibitors)
- Nitrates
- Beta blockers
- Calcium channel blockers
- ACE inhibitors
- statins
54
MOA of ASA?
What is the dose?
Inhibits COX-1… thromboxane A2
- Irreversible, platelet life span
75-325 mg/day
55
What is the alternative for AMI pts who are allergic to aspirin?
P2Y12 inhibitors
56
What is TXA2?
Thromboxane A2 (TXA2) is a type of thromboxane that is produced by activated platelets during hemostasis and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.
57
What is the platelet lifespan?
7-14 days
58
What are examples of Platelet glycoprotein IIb/IIIa receptor antagonists?
MOA?
abciximab, eptifibatide, tirofiban
Inhibit platelet activation, adhesion, and aggregation
59
What are examples of P2Y12 inhibitors?
MOA?
Clopidogrel, prasugrel
Inhibits ADP receptor P2Y12 and platelet aggregation
60
P2Y12 inhibitors can be a prodrug. What is the % of people that are hypo/hyper responsive?
10-20
61
Between clopidogrel and prasugrel, which has a higher risk of bleeding?
Prasugrel
62
What type of drug can affect the enzyme that metabolizes clopidogrel to its active compound and thereby can reduce the effectiveness of it?
PPIs
63
What are two common blood tests to check platelet function?
P2Y12 panels
TEG
64
Nitrates decrease what 3 things about angina
frequency, duration, and severity
65
Antianginal effects of nitrates are greater when these drugs are used in combination with what other two drug classes?
Beta blockers
Calcium channel blockers
66
What do nitrates do?
- Dilate coronary arteries and collaterals
- Decrease peripheral vascular resistance
- Decreases preload
- Potential anti-thrombotic effects
67
T/F
People taking chronic nitrates respond to sublingual nitrates just as well
False!
Will have to have IV nitrates before they respond appropriately
68
What are nitrates contraindicated in?
aortic stenosis and hypertrophic cardiomyopathy
69
What is the only drug to prolong life in CAD pts?
Beta blockers
70
What are the 3 main purposes of beta blockers??
Anti-ischemic, anti-hypertensive, anti-dysrhythmic
71
If someone is on beta blockers, do we continue them or d/c them for surgery?
Continue them or at least give a dose
72
What is a consideration of beta blockers with anesthesia induction?
They have an exaggerated hypotensive response
73
What is the difference in blockade of B1 vs B2?
What are the different drugs?
Beta 1: atenolol, metoprolol, acebutolol, or bisoprolol
- Heart rate
- Diastolic time
- Myocardial contractility
- Myocardial oxygen demand
Beta 2: propranolol, nadolol
- Increased risk of bronchospasm in reactive airway disease
74
What are two other things that propranolol is used for?
anxiety
tremors
75
Which beta blocker do we give in the OR most often?
Labetolol
- We give this one because it affects both heart rate and blood pressure
76
Esmolol affects ____, but not _____
Heart rate
Contractility
77
Metoprolol affects ______, but not ____
Contractility
Heart rate
78
Calcium channel blockers are uniquely effective for what?
Decreasing frequency/severity of spasm
79
What are CCB used for?
Dilate coronary arteries
Decrease
- Vascular smooth muscle tone
- Contractility
- Oxygen consumption
- Systemic BP
80
Which works better in decreasing incidence of MI, CCB or BB?
BB
CCB do a good job of controlling symptoms but not at reducing mortality
81
Angiotensin pathway picture
82
Angiotensin II increases what 4 things?
- Myocardial hypertrophy
- Interstitial myocardial fibrosis
- Coronary vasoconstriction
- Inflammatory responses
83
ACE inhibitors are used to treat what 3 things?
Hypertension
Heart failure
Cardioprotective
84
Statins decrease what 4 things?
Lipid oxidation
Inflammation
Matrix metalloproteinase
Cell death
85
When is revascularization indicated?
Failure of medical therapy
> 50% L main coronary artery
> 70% epicardial coronary artery
Impaired EF <40%
86
When is CABG preferred over PCI?
- patients with significant left main coronary artery disease,
- those with three-vessel coronary artery disease
- patients with diabetes mellitus who have two- or three-vessel coronary artery disease.
87
What is angioplasty?
Putting balloon in plaque to push it back against the walls
88
What is transluminal intervention?
devices uses net and grinder to grind plaque off vessel and it catches pieces of plaque off vessel – potentially could replace CABG
– also seen in cerebral interventions
89
What 4 things happen in acute coronary syndrome?
- Focal disruption of atheromatous plaque
- Triggers coagulation cascade
- Thrombin generation
- Arterial occlusion by a thrombus
90
Define acute coronary syndrome
Acute or worsening imbalance of myocardial oxygen supply to demand
91
What are the 3 categories of ACS?
What are these based on?
STEMI
NSTEMI
Unstable angina
12 lead EKG or cardiac specific biomarkers (troponin)
92
Decision tree picture for ACS
93
T/F
Some cardiac ischemia may not show up with cardiac biomarkers or EKG changes
True
94
What happens in a STEMI?
Coronary blood flow decreases abruptly
Acute thrombus formation
- Vulnerable plaques
Thrombogenesis
- Collagen, ADP, epinephrine, serotonin
- Thromboxane A2
- Glycoprotein IIb/IIIa receptors
- Fibrin deposit
95
What are the majority of STEMIS caused by?
In rare cases, what else can they be caused by?
Thrombotic occlusion of a coronary artery
coronary emboli, congenital abnormalities, coronary spasm, or inflammatory diseases
96
STEMI plaque pathway
(This card is stupid long, I'm sorry lol)
- A platelet monolayer forms at the site of ruptured plaque, and various chemical mediators such as collagen, ADP, epinephrine, and serotonin stimulate platelet aggregation.
- The potent vasoconstrictor thromboxane A2 is released, which further compromises coronary blood flow.
- Glycoprotein IIb/IIIa receptors on the platelets are activated, which enhances the ability of platelets to interact with adhesive proteins and other platelets and causes growth and stabilization of the thrombus.
- Further activation of coagulation leads to strengthening of the clot by fibrin deposition. This makes the clot more resistant to thrombolysis
- Plaques that rupture and lead to acute coronary occlusion are rarely of a size that causes significant coronary obstruction. - - By contrast, flow-restrictive plaques that produce chronic stable angina and stimulate development of collateral circulation are less likely to rupture.
97
STEMI diagnosis picture
98
What fraction of pts describe new-onset angina pectoris or a change in their anginal pattern during the 30 days preceding an AMI?
2/3
99
About a quarter of patients, especially the elderly and those with diabetes, have what type of pain at the time of AMI?
None or mild
100
How does a STEMI pt usually present on physical exam?
anxious, pale, and diaphoretic
- Sinus tachycardia is usually present.
- Hypotension caused by left or right ventricular dysfunction
- cardiac dysrhythmias may be present
101
What is the development of a Q wave on EKG more dependent on?
volume of the infarcted tissue
102
What two diagnostic test are powerful predictors of adverse cardiac events in patients with anginal pain?
Elevated troponins
EKG
103
The _____ the level of troponin, the _____ the MI is
Greater
Larger
104
Drug therapy for STEMIS include:
MONA
P2Y12 inhibitors (clopidogrel, prasugrel, or ticagrelor)
Platelet glycoprotein IIb/IIIa inhibitors
Unfractionated heparin
β blockers
RAAS
105
What is the primary goal in management of a STEMI?
reestablish blood flow in the obstructed coronary artery as soon as possible
106
Why is MONA necessary in STEMI treatment?
to reduce catecholamine release and the resultant increase in myocardial oxygen requirements.
107
What type of drugs should be avoided in a STEMI?
Glucocorticoids
NSAIDS
108
The time from ______ to ______ strongly influences the outcome of an acute STEMI.
Onset of symptoms
Reperfusion
109
Reperfusion therapy includes:
Tissue plasminogen activator (tPA), streptokinase, reteplase, or tenecteplase
110
When should thrombolytic therapy for STEMI be initiated?
Within 30-60 minutes of hospital arrival and within 12 hours of symptom onset
111
What things make someone high risk for thrombolytic therapy during STEMI?
Recent surgeries
Labs (abnormal)
Recent falls
HTN
Existing coagulopathy
112
Which is preferred, PCI or thrombolytic therapy?
Why?
PCI
In order to restore flow to an occluded coronary artery
113
Indications for PCI
Contraindication to thrombolytic therapy
Severe HF and/or pulmonary edema
Symptoms present for 2 - 3 hours
Mature clot
114
Indications for CABG
Coronary anatomy
Failed angioplasty
Evidence of infarction-related ventricular septal rupture or mitral regurgitation or stenosis
- May need CABG and valve replacement
115
Emergency CABG is reserved for what?
- angiography reveals coronary anatomy that inhibits PCI
- Failed angioplasty
- evidence of infarction-related ventricular septal rupture or mitral regurgitation
116
Causes of NSTEMI/unstable angina
- Reduction of myocardial oxygen supply
- Rupture or erosion of a coronary plaque
- Nonocclusive thrombosis
- Dynamic obstruction due to vasoconstriction
- Prinzmetal-variant angina, cold (temperature), cocaine use
- Worsening coronary luminal narrowing due to progressive atherosclerosis, in-stent restenosis, or narrowing of CABGs
- Inflammation
- Vasculitis
- Myocardial ischemia due to increased oxygen demand
- Sepsis, fever, tachycardia, anemia
117
Presentation of unstable angina/nstemi
Angina at rest, lasting >10 minutes
- May last longer if chronic
Chronic angina pectoris … more frequent and more easily provoked
New-onset angina… severe, prolonged, or disabling
- May require fentanyl
118
Treatment of UA/nstemi
- Bed rest, oxygen, analgesia, and β-blocker therapy
- Sublingual or IV nitroglycerin
- Calcium channel blockers
- Aspirin, clopidogrel, prasugrel, or ticagrelor and heparin therapy (unfractionated heparin or LMWH)
Thrombolytic therapy not indicated
119
Management of UA/NSTEMI consists of an acute phase and long term phase. What is the difference?
Acute: directed at decreasing myocardial oxygen demand and stabilizing culprit lesion(s)
Long term: directed at prevention of disease progression and future plaque erosion and rupture.
120
What is the specific factor Xa inhibitor that can also be used as an anticoagulant?
Fondaparinux
121
What are other things that are associated with increased mortality with UA/nstemi?
- Older age (>65)
- (+) cardiac biomarkers
- rales
- hypotension
- tachycardia
- decreased LV function (EF <40%)
122
What are the two principal issues related to PCI with stent placement?
Thrombosis
Increased risk of bleeding
123
What are the 3 types of PCI?
Balloon angioplasty: 2-3 weeks
Bare-metal stent placement: 12 weeks
Drug-eluting stent: a full 1 year or longer
** Times are how long it takes the vessel to rendothelialize
124
Why are you prone to thrombosis after angioplasty?
Angioplasty causes vessel injury, especially destruction to the endothelium
125
What is the most significant independent predictor of stent thrombosis?
P2Y12 inhibitor discontinuation
126
What is considered dual anti platelet therapy?
aspirin with a P2Y12 inhibitor
127
How many days prior to surgery do you d/c clopidogrel?
How many for prasugrel?
5 days
7 days
128
We can give plts to counteract bleeding on someone on anti platelets. However, platelet transfusions can be administered as soon as ___ hours after discontinuation of clopidogrel, but they will be most effective _____ hours after the last dose of clopidogrel.
4
24
129
How long does someone need to be on DAPT after all 3 PCI procedures?
Balloon angioplasty without stenting: minimum 2 weeks
Bare-metal stent: minimum 6 weeks
Drug-eluting stent: minimum 1 year
130
How long after each PCI procedure should pts wait for elective surgery?
131
______ is not encouraged in patients who are receiving dual antiplatelet therapy.
Why?
Neuraxial blockade
Risk of developing spinal hematoma
132
You usually can't do a case for _____ months after coronary intervention
6-12 months
133
Pre op assessment should include:
- Determine presence of risk factors
- Evaluate METs
- Co-existing non-cardiac disease
- Physical exam
- Specialized testing
134
Limited exercise tolerance in the absence of significant lung disease is good evidence of what?
Decreased cardiac reserve
135
Silent myocardial ischemia usually occurs at a heart rate and blood pressure substantially _____ than that present during exercise-induced ischemia.
Lower
136
A cardiac bruit may indicate what?
Cerebrovascular disease
137
Orthostatic hypotension may reflect attenuated autonomic nervous system activity because of:
Treatment with antihypertensive drugs
138
Jugular venous distention and peripheral edema are signs of what?
RV dysfunction
139
Auscultation of the chest may reveal evidence of left ventricular dysfunction such as:
an S3 gallop or rales
140
Specialized pre op cardiac testing may include:
exercise ECG
stress echocardiography
nuclear stress imaging
cardiac catheterization
141
Effective beta blockade is suggested by what?
Resting heart rate of 50-60 bpm
142
What can be used to treat excessive bradycardia caused by β-blockers during the perioperative period?
Atropine or glycopyrrolate
143
What is the specific pharmacologic antagonist for excessive β-blocker activity?
Isoproterenol
144
The _____ period is a time when inadvertent withdrawal of β-blocker therapy may occur and result in rebound hypertension and tachycardia.
post op
145
T/F
Glycopyrrolate significantly reduces the incidence of atropine-related tachycardia and other arrhythmias
True
146
What do we commonly give with glyco because it balances HR effects?
Neostigmine
Neostigmine slows HR, glyco increases HR
147
What do alpha2 agonists do?
Decrease sympathetic outflow, blood pressure, and heart rate
148
What can you give for refractory hypotension?
Vasopressin
149
What is the goal peri op glucose?
< 180
150
Why do we want tachycardia in kids?
They have a fixed ventricular volume, so if they drop the HR too much, it will drastically drop BP
(LV has limited compliance)
151
Periop myocardial injury algorithm chart
152
Increased probability of peri-op cardiac complications
Cardiac death
cardiac arrest or VF
complete heart block
AMI
pulmonary edema
153
Revised cardiac risk index chart
154
Components of RCRI chart:
155
Functional capacity chart:
156
What is a MET?
What does 1 MET equal?
>4 METS is good or bad?
Metabolic equivalent of task
1 MET = 3.5 ml/kg/min
Good!
157
What is functional capacity an assessment of?
What is it used for?
Cardiopulmonary fitness
Estimates pt risk for major post-op morbidity or mortality
158
Differentiate between the urgencies of emergent, urgent, and time-sensitive surgery
Emergency: life or limb would be threatened in 6 hrs or less
Urgent: life or limb would be threatened in 6-24 hours
Time sensitive: delays exceeding 1-6 weeks would adversely affect outcomes
159
If surgery is emergent, we should focus on surveillance, which includes what?
erial cardiac enzymes, hemodynamic monitoring, serial ECGs
160
Pre op cardiac risk assessment chart:
161
ACC/AHA algorithm recommends that a patient with a functional capacity ________ METs should proceed directly to surgery
4 or more
162
Active cardiac conditions we have to worry about:
Unstable coronary syndrome
- Acute MI < 7 days or recent MI >7 days but < 1 month
- 60 days post MI is ideal
Unstable or severe angina
Decompensated heart failure
Severe valvular heart disease
- severe aortic stenosis or mitral stenosis
Significant dysthymia
- High-grade atrioventricular block, Mobitz type II atrioventricular block, third-degree heart block, and symptomatic supraventricular and ventricular tachydysrhythmias
Age
163
Goals of anesthesia for IHD pts
- Prevent myocardial ischemia by optimizing myocardial oxygen supply and reducing myocardial oxygen demand
- Monitor for ischemia
- Treat ischemia if it develops
164
In the OR, we need to prevent what in IHD pts?
Persistent tachycardia
Systolic HTN
SNS stimulation
Arterial hypoxemia
Hypotension
165
What is the induction DOC for IHD pts?
Why?
Etomidate
Does not affect cardiac status
166
Periop myocardial injury is closely associated with ______ in vascular surgery pts
Heart rate
167
What things decrease oxygen delivery?
- Decreased coronary blood flow
- tachycardia
- hypotension
- hypocapnia (coronary artery vasoconstriction)
- decreased oxygen content
- anemia
- arterial hypoxemia
- shift of oxyhemoglobin dissociation curve to the left
168
What causes increased oxygen requirements?
- SNS stimulation
- tachycardia
- HTN
- increased myocardial contractility
- increased afterload
- increased preload
169
What drugs can blunt increased HR caused by intubation?
Why?
aryngotracheal lidocaine
IV lidocaine
esmolol
fentanyl
remifentanil
dexmedetomidine
Histamine release caused by atracurium
170
Why are volatile anesthetics beneficial in pts that have IHD?
because they decrease myocardial oxygen requirements and may precondition the myocardium to tolerate ischemic events
171
Nitrous showed an increase in what 3 things?
pulmonary vascular resistance, diastolic dysfunction, and myocardial ischemia
172
What is the DOC for bradycardia and hypotension?
What else can you give for the hypotension?
Ephedrine
Fluid bolus, neo
173
Lead/area of myocardium involved chart:
174
What two leads do we commonly look at for ischemia?
Lead II and V5
175
What other factors can induce angina?
Physical exertion
Emotional tension
Cold weather
