Vasodilator Stress Agents

Sunday, November 22, 2015

Vasodilator Stress Agents

	Mechanism of action	T 1/2	Administration	Side effects	Contraindications
Adenosine	A2A receptorà direct coronary vasodilationà 3.5- 4 x increased blood flow àstenotic epicardial coronaries will have attenuated hyperemic response. True ischemia may be induced by coronary steal phenomenon.	Secs	140 mcg/kg/min over a 6 min period Minimum time to tracer injection: 2 mins Continue infusion for 2 mins after tracer injection	Nonspecific chest pain: not an indicator of CAD ST depression >1mm: indicative of significant CAD A1 receptor: AV block àdoes not require termination of infusion A2b receptor: Hypotension A2b and A3 receptors: Bronchospasm Resolve in few seconds (due to extremely short half-life of adenosine)	Asthma with ongoing wheezing 2/3 AV block without a pacemaker SBP <90 mmHg Use of dipyridamole in last 48 hours; aminophylline in 24 hours or caffeine in last 12 hours (pentoxifylline OK) ACS
Regadenoson	A2A receptorà direct coronary vasodilation (lower affinity than adenosine)	2-4 mins	0.4mg/10 ml given as rapid injection followed by saline flush Tracer injection 10-20 secs after	SOB, flushing, headache Most resolve within 15 mins, headaches resolve in 30 mins (Use aminophylline 50-250 mcg infused slowly) Hypotensionѱ	Asthma with ongoing wheezing 2/3 AV block without a pacemaker SBP <90 mmHg Use of dipyridamole in last 48 hours; aminophylline in 24 hours or caffeine in last 12 hours (pentoxifylline OK) ACS
Dipyridamole	Prevents reuptake and deamination of adenosineà indirect coronary vasodilator Dipyridamole induced hyperemia lasts more than 15mins	30-45 mins (liver)	0.56mg/kg IV over 4 mins (142mcg/kg/min) Tracer injection after 3-5 mins	Flushing, chest pain, headaches, dizziness. Resolve in 15-25 mins (Use aminophylline 125-250 mcg infused slowly- should also be used in the presence of ischemic changes after dipyridamole)	Same as adenosine. CAN be used in patients taking oral dipyridamole.
Dobutamine	Direct B1 and B2 stimulation Increase in heart rate, blood pressure and myocardial contractility. Increases regional myocardial blood flow (similar to exercise, less than adenosine). Does not increase venous return (no increase in wall stress)	2 mins	5mcg/kg/min increased at 3 minute intervals to 40mcg/kg/min. Tracer injection at peak dose and continue infusion for 2 mins after	Palpitations, chest pain, headache, flushing, dyspnea (Use esmolol 0.5mg/kg over 1 min)	ACS Hemodynamically significant LVOT obstruction Severe AS Prior h/o VT Aortic dissection/large aortic aneurysm Uncontrolled hypertension B blockers

Ѱ Risk of hypotension higher in patients with autonomic dysfunction, hypovolemia, left main coronary artery stenosis, stenotic valvular heart disease, pericarditis, pericardial effusions, stenotic carotid artery disease with cerebrovascular insufficiency

Other Myocardial Tracers

Rb-82	Ultra short half life	Myocardial perfusion PET scanning
O-15 Water	Free diffusible, uptake directly proportional to blood flow	Best tracer for myocardial blood flow detection PET Scanning
N-13 ammonia		Myocardial perfusion PET Scanning
C-11 acetate	Oxidative substrate	Can be used for both perfusion and metabolism PET Scanning
C-11 palmitate	Fatty acid substrate	Metabolism PET Scanning
FDG	Glucose metabolism	Metabolism PET Scanning
BMIPP (I-123)	Fatty acid	Myocardial ischemic memory imaging (normal myocardium metabolizes fatty acids, during ischemia switches to glucose; if ischemia occurred dark spots on BMIPP imaging, used for detection of ischemia that occurred hours prior. Also, provides viability assessment)
MIBG	Similar to norepinephrine	Sympathetic neuronal imaging for heart failure

PET Perfusion Tracers

	Rb-82	N13 ammonia
T 1/2	75 secs	10 mins
Dose/Injection Rate	20mCi Bolus <30secs BGO/LSO/GSO scanners	10-20mCi Bolus <30secs
Extraction Mechanism	Na/K ATPase pump Extraction decreases with increasing blood flow Can be decreased by hypoxia, acidosis and ischemia	Na/K transporter Passive diffusion
Type of stress used	Pharm stress (short t1/2 of Rb, patient needs to remain still in camera)	Pharm stress
Imaging delay after injection	EF>50%: 70-90secs EF <50%: 90-130 secs	1.5-3mins
Imaging duration	3-6 mins	10-15 mins
Reconstructed pixel size	4 mm	2-3 mm
Organ receiving maximum dose	Kidney	Urinary bladder

Radiotracers: Thallium and Technetium

	Thallium 201	Technetium 99m (Sestamibi/ Cardiolite, Tetrofosmin/Myoview)
	Potassium analog; monovalent cation	Lipid soluble, cationic
Preparation	Cyclotron	Generator (eluted from Mo 99m)
Half life	73.1 hours	6 hours (therefore larger doses can be given resulting in higher counts, less scatter and less tissue attenuation)
Decay	Electron capture to Hg-201/ X rays	Isomeric transition/ Gamma ray emission
Energy release	68-80 keV	140 keV
First pass extraction	High (85%)	Lower (55%)
Pharmacodynamics	Active membrane transport in to the myocyte through Na/K pumps Rapid clearance from intravascular space	Diffuses in to cells- no active uptake Uptake depends on blood flow Enters mitochondria due to transmembrane energy potentials (mitochondria ànegatively charged membrane)
Myocardial extraction coefficient	Highest: 85% (peak concentration 10 mins after injection)	65% (S) 54% (T)
Redistribution	Mono-exponential  (depends on initial tracer concentration in the myocyte and myocardial blood flow) washout that starts 10-15 mins after injection	Negligible washout therefore no redistribution
Clearance	Kidneys	Hepatobiliary system (tetrofosmin clears liver earlier than sestamibi)
Dose administered	2.5-4 mCi	10-20 mCi: sestamibi 5-33 mCi: tetrofosmin
Whole body radiation dose	0.68 rad	0.5 rad
Whole body effective dose	6.3mSv/mCi of Tl-201 injected	0.3mSv/mCi of Tc 99m injected
Collimator	GAP/ LEAP	High Resolution (LEHR)
Imaging protocol	Exercise/Pharm Stress àTh-201 injection à 10-15minsàImaging (stress) à 2-4 hoursà Imaging (rest/redistribution)	1 day protocol: Patient at restà  Tc injection à 45 mins àImaging à -Exercise Stress à Tc injection (2-3 times higher dose) à15-20 mins àImaging -Pharm stress à Tc injection (2-3 times higher dose) à45mins à Imaging 2 day protocol*: Stress imaging on day 1; rest imaging on day 2 (if needed)
Time to imaging Rest/ resdistribution: Pharmacologic stress: Exercise:	2.5- 4 hours after stress 10-15 mins 10-15 mins	45-60 mins (S)/ 30-45 mins (T) 60 mins (S)/ 45 mins (T) 15-20 (S)/ 10-15 mins (T)
Limitations	Low energy emission, therefore: -More image attenuation (especially obese patients) -Longer imaging times	Short shelf life: must be ordered everyday/ twice a day
Clinical uses	CAD diagnosis Viability assessment	CAD diagnosis: sharper images LV function
Minimum number of counts	100 counts/ pixel	200 counts/pixel
Minimum number of projections	32	60-64

*2-day protocol used in BMI >30; female patients where significant breast attenuation in expected

Wednesday, October 7, 2015

Stable Ischemic Heart Disease Guidelines: Summary

Stable Ischemic Heart Disease Guidelines: Summary

Revascularization to improve mortality:

- Left Main >50% (CABG Class I, PCI Class IIa)- CASS, VA Co-op Study, MASS II

- 3 vessel disease or pLAD and one other (CABG, Class I)- CASS, VA Co-op Study, MASS II

- 2 major coronary arteries with significant ischemia (CABG, Class IIa)

- LVSD 35-50% EF when viable myocardium present (Class IIa)

- SCD in presumed ischemia related VT (CABG/PCI, Class I)

Revascularization options:

- CABG vs BMS: 

o No difference at 5 years, single or multi-vessel disease

o Procedural stroke CABG>PCI

o Angina relief CABG>PCI

o Repeat revascularization PCI>CABG

- CABG vs DES

o MACE and mortality: PCI>CABG at 3 years in higher syntax scores >22 (<22, no difference)

Special groups

- Left main (selected patients- ostium or trunk)

o Mortality, MI and stroke at 1 and 2 years, PCI=CABG (syntax >33, higher mortality)

o TVR at 1, 2 and 3 years, PCI>CABG

- PLAD

o (PCI =CABG) >medical therapy

- LV systolic dysfunction

o LVEF <35%, CABG = GDMT at 5 years- STICH

- Diabetes

o Survival: CABG >PCI – BARI, FREEDOM

o Revascularization: PCI>CABG - SYNTAX

Medical therapy of angina:

- Beta blockers

o For patients with PAD/ Prinzmetal’s angina: labetalol/carvedilol (alpha adrenergic blocking) or nebivolol (direct vasodilator)

- CCBs: verapamil or diltiazem

- Long acting nitrates

- Ranolazine: contraindicated in significant hepatic impairment. 500mg BID max dose with diltiazem and verapamil. Increases plasma concentration of simvastatin 2 fold.

Monday, October 5, 2015

Pulmonary Vein Flow

	S1	S2	D	S/D	Ar
Atrial Fibrillation	Absent	Blunted	Increased	Decreased	Absent
Abnormal Relaxation			DT increases	Increases	Increases
Pseudonormal		Blunted	Increased velocity	Decreases	>35cm/s
Restrictive		Blunted	Increased	Decreases	Increased
Severe MR		Blunted (left) or reversed (right)	Increased
Mitral stenosis		Decreased	Decreased		Decreased

Wednesday, September 23, 2015

General Cardiology Guidelines

Link to guidelines for cardiology boards

https://drive.google.com/open?id=0B0hWtBiN0PaHUEhERkpiOVZUbE0

Echo Guidelines

Here is a link with all the guidelines you need to know for the boards (I have highlighted the important stuff!)
https://drive.google.com/open?id=0B0hWtBiN0PaHSEEzeEpvUGRtSVk

Wednesday, September 9, 2015

Predictors of Adverse Outcomes

Endocarditis	Aortic valve >10mm vegetation (Increased risk of embolization) TV- generally good prognosis
Cardiac amyloidosis	DT < 150 ms Other less validated markers of worse prognosis: LV wall thickness > 15 mm, RV enlargement

Peripartum Cardiomyopathy	LVEF < 30 % LVEDD ≥60mm Elevated troponin ??Abnormal dobutamine stress predicts recurrence
Cardiomyopathy	RV dysfunction Sphericity index < 0.76  Diffuse hypokinesis (RWMA more favorable prognosis) Chemotherapy induced CM (worse prognosis compared with idiopathic)

Pericardiectomy	Post radiation (worst prognosis) **idiopathic- best prognosis
LV thrombus (risk for embolization)	Large pendulous thrombus (>0.8cm2 ) Mobile thrombus
Post MV repair (Risk of SAM)	Co-aptation to septal distance (C-sept) < 2.6 cm Posterior mitral valve leaflet height > 1.5 cm Anterior leaflet/Posterior leaflet height ratio (AL/PL) < 1  Aortic Mitral angle < 130

Thursday, September 3, 2015

Changes seen in rejection post transplant

Impairment of diastolic function:

-          Decrease DT >20%

-          Decrease in IVRT >20%

-          Increase in E velocity

New onset MR

>10% decrease in ejection fraction

Increased wall thickness >4mm (IVS + post wall)

Increased myocardial echogenicity

New/increasing pericardial effusion

Good to know

Angle independent	Speckle tracking
Age independent	Ar-A for LA pressure
Load independent	Dp/dt
Congenital diseases more common in women	PDA ASD Ebstein’s
If ASD >15mm on color	Qp: Qs:: 2:1
AV valves seen at same level	Primary ASD Corrected tGA
Bernoulli’s equation is based on	Law of Conservation of Energy
Continuity equation is based on	Law of Conservation of Mass
Flow across an ASD is determined by	Difference in compliance and capacity of the two ventricles
Holodiastolic flow reversal in the descending aorta seen in	Severe AI Aorto-pulmonary window
LV apex motion	Counterclockwise
LV base motion	Clockwise
Size of vegetations detected	TTE 5mm TEE 1mm
Rupture of coronary sinus aneurysms                          Right             Left             Non	RV LA RA

Named Findings

Saw tooth pattern on Doppler	Co-arctation of aorta
Broken ring	Anomalous drainage to SVC
Popcorn thrombus	RA thrombus (multilobulated)
LVOT goose neck deformity	AV canal defects
Pear shaped aorta Erlenmeyer deformity	Marfan’s
Charcoal heart	Melanoma metastases
Keshan disease	Se deficiency
Seagull sign	Restricted anterior leaflet in functional MR
Tear drop heart	Apical view in congenital absence of pericardium (elongated atria, widened ventricles)
Gerbode defect	Communication between RA and LV

Thursday, September 3, 2015

Best TTE views

MV prolapse	PLAX
SAM	PLAX
Abnormal insertion of anterior mitral leaflet	PLAX
Sinus venosus ASD	Subcostal 4C
Inlet VSD	Apical 4C
RUPV	Apical 4C
PDA flow	High left PSAX
Aortic valve gradient/flow	A5C/ Apical long (3C)
Pulmonary valve flow	Basal PSAX (TEE: Aov SAX, transgastric 70 degrees)
Superior Vena Cava	Suprasternal notch
LAA	Apical 2 chamber (on TTE)
Left persistent superior vena cava	Left supraclavicular view
MV cross sectional area (annulus diameter)	Apical long (3C)
Suspected paravalvular MR	PLAX
Aortic root abscess	PSAX
MV Leaflet Tips	LV dimensions (PLAX) Mitral inflow for diastology assessment (A4C) PHT for MS (A4C)
Mitral annulus	A wave duration (for Ar-A calculation) CW for volume/flow rate measurement through the MV AV optimization
LVOT diameter	Within 1cm of AV annulus
PVF	Place sample volume 1cm in to PV
Atrial volumes	A4C

Cannot Use (Limitations of echocardiographic parameters)

Mitral E/DT/A	More than mild MS More than mild MR Hypertrophic cardiomyopathy
Propogation Velocity (Vp)	LVH (falsely fast) Small LV cavity May be normal in restrictive cardiomyopathy Normal EF
E/A	Normal EF Mitral stenosis Prosthetic valves
e'	MAC Prosthesis/surgical rings Mitral stenosis Constrictive pericarditis Regional wall motion abnormalities
Hepatic Vein Flow	TS Transplant patient High degree AV block Pericardial compression syndromes
Dp/dt	Severe MR
Mahan’s Equation (for pulmonary hypertension)	HR must be 60-100bpm
2 chamber view (TTE)	VC measurements in MR (parallel to line of co-aptation, shows wide VC even in mild MR)

Tuesday, August 25, 2015

Number to Remember

E velocity	1m/s
A velocity	0.5-1m/s
S velocity (PVF)	0.6m/s
D velocity (PVF)	0.4m/s
Ar velocity (PVF)	≤0.35m/sec
IVRT	70-90msec
DT	150-240msec
Propogation velocity (Vp)	>50
E’ (Septal)	8cm/s
E’ (lateral)	10cm/s
EF (males)/ mean	52-72%/ 62
EF (females)/ mean	54-74%/ 64
LA volume index
Normal	16-34 cc/m2
Mild dilatation	35-41
Moderate dilatation	42-48
Severe dilatation	>48
LV mass index: linear method (males)	115 gm/m2
LV mass index: linear method (females)	95 gm/m2
Global longitudinal strain (averaged from three apical long axis views)	-20%
Sphericity Index	≥ 1.5

Valsalva in echocardiography

Definition of adequate Valsalva: Pressure of 40mmHg against a closed glottis

Uses:

Diastolic dysfunction	Phase II	Differentiate between normal and pseudonormal*
Interatrial communication (PFO/ASD)	Phase III (release of valsalva, increased RA pressure)
Hypertrophic cardiomyopathy	Phase II	Provoke gradients (exercise provokes higher gradients)

*With adequate Valsalva E velocity should decrease by 20cm/s

Decrease in E/A ratio by ≥50% is specific for increased filling pressures (pseudonormal pattern at rest)

Stress echocardiography

Monophasic response	Improvement in wall motion by one grade in two or more segments
Biphasic response	Improvement in wall motion abnormality at low dose dobutamine and subsequent worsening at higher doses
Suggestion of viability	Monophasic response
Suggestion of viability and ischemia	Biphasic response
Most predictive of functional recovery after revascularization	Biphasic response
Highest sensitivity for viability	Monophasic response
Highest specificity for viability	Biphasic response
False negatives	Single vessel disease -LCX lesion; inferolateral wall (use apical long axis) Suboptimal stress Concentric remodeling
False positives	Hypertensive response HCM Microvascular disease Tethering of stationary mitral valve (MAC/MVR): basal segments appear hypo/akinetic LBBB/pacing Post bypass: basal anteroseptum appears hypo/akinetic
False positive EKG stress test	Women Men on estrogen Digoxin therapy
EKG stress test- cannot report ischemia in	LBBB RBBB- if ST-T changes seen only in septal leads

Exercise/ Dobutamine stress echo in severe CAD (From Oh Manual)                      

	Exercise	Dobutamine
WM abnormalities	Multiple	Multiple
LV cavity	Dialtes	Usually does not dilate
LVEF	Decreases	May not decrease
ST segment depression	Common	Uncommon
Hypotension	Specific	Non specific

*LV end systolic volume may not decrease during bicycle stress echo (due to increased venous return)

Timing of echocardiographic measurements

LV dimensions	End diastole
Aortic dimensions	End diastole
LA dimensions	End systole
LVOT diameter/aortic annulus*	Mid systole
Pericardial effusion	Diastole
Mitral valve annulus	Mid diastole (one frame after maximum opening of valves)
Mitral valve anterior leaflet	Diastole

*Aortic annulus: Inner edge to inner edge

Aortic root/aorta: Leading edge to leading edge

Most common

Most common congenital heart abnormalitie	Bicuspid aortic valve
Second most common congenital heart abnormality	ASD
Most common location of pericardial cysts	Right cardiophrenic angle (behind RA)
Most common location of hiatal hernia on echo	Above atria
Most common location of post op effusion	Posterior and lateral
Most common location of pseudoaneurysmafter MI	Posterior>lateral>apical
Most common lesion associated with TGA	VSD
Most common type of ASD	Secundum
Most common type of VSD	Perimembranous
Most common type of cyanotic CHD	Tetrology of Fallot
Most likely cyanotic CHD to escape detection in childhood	Ebstein’s anomaly
Most common primary tumor of the heart	Myxoma
Most common primary pericardial malignancy	Mesothelioma
Most common primary malignant tumor of the heart	Angiosarcoma
Most common primary tumor associated with pericardial effusion	Angiosarcoma
Most common cause of echogenic pericardial effusion	Tuberculosis>Malignancy>Idiopathi
Most common cause of constrictive pericarditis	Idiopathic
Most common location of blunt aortic injury	Aortic isthmus just distal to the origin of the left subclavian artery> Supravalvular ascending aorta> Diaphragmatic aorta
Most common type of blunt aortic injury	Subadventitial (involving intima and media) with incomplete circumferential extension
Most common location of atherosclerosis	Descending aorta >Arch> Ascending aorta
Most common location of thoracic aorta aneurysms	Aortic root/ascending aorta: 60% Descending aorta: 40% Arch: 10% Thoracoabdominal aorta: 10%
Most common coronary artery affected by aortic dissection	Right coronary artery
Most common location of abscesses in infective endocarditis	Aortic root
Most common primary valve tumor	Papillary fibroelastoma
Most common location of papillary fibroelastoma	Aortic valve (aortic side) > Mitral
Most common cardiac manifestation of HIV	Pericardial effusion
Most common cause of primary MR (World)	Rheumatic
United States	Degenerative/Myxomatous
Most common cause of secondary MR	Ischemic
Most common cause of mitral stenosis	Rheumatic
Most common cause of AI (World)	Rheumatic
Most common cause of AS (World)	Rheumatic
Unites States	Bicuspid
Most common location of extra-adrenal cardiac mass in pheochromocytoma	AV groove
Most common complication after Ross procedure	AI
Most common complication after TOF repair	PI
Most common complication after AV canal defect repairs	MR
Most common complications of Mustard/Senning	RV failure Bradycardia
Most common location of mitral disease                                          Degenerative                                          Rheumatic	Base of leaflets Tips of leaflets
Most common location of MAC	Posterior annulus
Most common location of accessory pathway	Right lateral
Most common location of absent pericardium	Left (complete absence)
Most common complication of partial absence of pericardium	Herniation and strangulation of chambers
Most common chamber herniated	Left atrial appendage
Most common location of vegetations in endocarditis Mitral Aortic Bioprosthetic valve Metallic valve	Atrial side of valve Ventricular side of valve Leaflets Annulus
VSD	Septal Leaflet of TV >>RVOT/subpulmonic
Most common location of radiation induced calcification Monday, August 24, 2015 Doppler Flows: 2 The image on the right is suggestive of severe TR: early peaking dense jet. Remember: cannot use peak velocity to determine severity in regurgitant lesions Aortic regurgitation peak jet velocity must be >/= 4m/s Mitral stenosis velocities will usually be lower than 4m/s AS jet starts after the QRS; while MR jet starts with the QRS Note higher velocities seen in MR Doppler Flows: Pulmonary and Hepatic Vein Flows Restrictive cardiomyopathy: inspiratory exaggeration of diastolic reversal  Constrictive cardiomyopathy: expiratory exaggeration of diastolic reversal  Pulmonary hypertension: fixed diastolic reversal  TR: systolic reversal PVF: systolic flow reversal in severe MR Doppler Flows:1 Holodiastolic reversal  in the descending thoracic aorta is usually a sign of at least moderate aortic regurgitation and appears to be more specific if recorded from the thoraco-abdominal aorta Absence or brief diastolic reversal is specific for mild AI Tumors in Echocardiography Benign tumors:  Myxoma >> lipoma > papillary fibroelastoma Malignant tumors  Metastases > Angiosarcoma >> rhabdomyosarcoma > mesothelioma Pediatrics: most common benign tumor: rhabdomyoma > fibroma  Tumors that metastasize to the heart  RCC  Breast  Lung  Melanoma (charcoal heart)  Lymphoma  Carcinoid Common locations  Fibroma: anterior/ivs of LV  Myxoma: LA attachment to fossa ovalis (LA>RA>RV>LV; if attached to posterior wall of LA: consider malignancy)  Leiomyosarcoma: smooth muscle lining the pulmonary veins  Angiosarcoma: RA (M:F 3:1) Tumors associated with   AIDS: Kaposi's; Malignant lymphoma   Tuberous sclerosis: Rhabdomyoma  Mass seen extending from IVC to RA   Hypernephroma > Hepatoma > Uterine Leiomyoma	Anterior MAC Aortic-mitral continuity