Classification of Atrial Fibrillation
** Definitions taken from UpToDate.
Management of atrial fibrillation (AF) is guided by 2 major principles: symptom control and prevention of thromboembolism.
These are typically managed through rhythm control or rate control. Rhythm- and rate-control strategies are associated with similar rates of mortality and serious morbidity, such as embolic risk, which is best addressed using anticoagulation based on the CHADS2 or CHA2DS2-Vas criteria.
For asymptomatic or mildly symptomatic AF patients who are 65 years or older, it is suggested to use a rate-control as opposed to a rhythm-control strategy using medical therapy. This recommendation places a high priority on concerns about side effects of antiarrhythmic drug therapy or radiofrequency catheter ablation. Patients for whom a rhythm-control strategy may be reasonable include those who continue with clinically significant symptoms on a rate-control strategy.
For most patients with AF younger than age 65, particularly those who are symptomatic, rhythm controlmay be a better option. For younger, asymptomatic patients who are concerned about the potential side effects of antiarrhythmic drug therapy, and who are not inclined to undergo radiofrequency catheter ablation, a rate-control strategy is reasonable.
RATE CONTROL: Can be achieved with beta blockers, calcium channel blockers (verapamil, diltiazem), or digoxin. Intravenous (IV) amiodarone may be needed for patients with poor left ventricular function. The drug selected and the route of administration (oral versus intravenous) are dictated by the clinical presentation. Overall, beta blockers or verapamil or diltiazem are the preferred therapeutic choices in the absence of heart failure. Digoxin is used mainly in heart failure as it is less likely to control the ventricular rate during exercise (when vagal tone is low and sympathetic tone is high), has little ability to terminate the arrhythmia, and often does not slow the heart rate in patients with recurrent atrial fibrillation (AF). IV amiodarone may help control rate when the other drugs are ineffective or cannot be given.
RHYTHM CONTROL: For those patients in whom a rhythm control strategy is chosen, catheter ablation or antiarrhythmic drugs are the two principle therapeutic options.
For most patients with symptomatic paroxysmal atrial fibrillation (AF) who have chosen a rhythm rather than a rate control strategy antiarrhythmic drug (AAD) therapy rather than catheter ablation as first-line therapy is often attempted first. Patients who may reasonably prefer catheter ablation include younger individuals or those who are concerned about the potential complications of AAD.
Recommendations for Catheter ablation:
In an acute management setting for new onset Atrial Fibrillation, calcium channel blockers such as diltiazem 10mg every 10 minutes is a good first option. If that does not break the arrhythmia, digoxin may be added. The third line is oftentimes Amiodarone. Amiodarone can be effective as both an antiarrhythmic as well as for rate control.
The decision to pursue acute cardioversion is largely dictated by the severity of the patient’s symptoms. In patients with mild to moderate symptoms, concurrent with the initiation of the appropriate anticoagulation treatment, the initial therapy includes slowing the ventricular rate without an immediate strategy to restore sinus rhythm. Slowing the ventricular rate often results in significant improvement or even resolution of symptoms. Attempts to get the rate below 110 beats per minute should be the initial goal for rate.
Four circumstances for which urgent or emergent cardioversion may be needed. They include:
In a patient with any of these indications for urgent cardioversion, the need for restoration of normal sinus rhythm (NSR) takes precedence over the need for protection from thromboembolic risk. Intravenous anticoagulation with heparin should be started, but it should not cause a delay in emergent cardioversion. However, these four circumstances differ with regard to the urgency of cardioversion and in most cases rate control is possible as a temporizing measure.
Many patients begun on antiarrhythmic drug therapy should be hospitalized for continuous electrocardiographic monitoring due to a 10 to 15 percent incidence of adverse cardiac events during the initiation of therapy .
The two complications of greatest concern are bradycardia and proarrhythmia. Other adverse cardiac events can include significant QT prolongation, heart failure, rapid ventricular rate, conduction abnormalities, hypotension, and stroke. The risk is greatest in the first 24 hours and in patients with a prior myocardial infarction.
Outpatient initiation of antiarrhythmic drug therapy with the following agents may be considered:
Patients with an implantable cardioverter-defibrillator (ICD) represent another group in which outpatient initiation of therapy can be tried, since the ICD provides protection against the risks associated with bradyarrhythmias and tachyarrhythmias.
UPTODATE: ATRIAL FIBRILLATION MANAGEMENT.
Definition: Classically an intimal tear in the aorta resulting in hematoma formation. Accumulating blood in false lumen of arterial wall leads to propagation of a dissection. Alternatively may begin as an intrawall hematoma without intimal tear.
Stanford: (mot commonly used)
Type A: Involves ascending aorta up to the or including the aortic notch
Type B: Involves the descending aorta
Non Type A/Non-type B: isolated involvement of the aortic notch
Type 1: Ascending Aorta
Type 2: Aortic notch
Type 3: Descending Aorta
Type A is most commonly occurs in patients greater than 60 years of age. Type B dissection patients are typically older. Patients with Marfan’s average 36 years of age.
Hypertension (70%), old age, atherosclerosis, collagen abnormalities (marfan’s, ehlers-danlos), drug use, inflammatory vasculitis (takayasu, giant cell arteritis), chest trauma, turner syndrome, bicuspid aorta.
Maintain a high index of suspicion in a male patient 60-80 years old with a history of hypertension. Patients will oftentimes describe the pain as abrupt onset, sharp and severe, Most often type A affects the patient in the chest/sternal area and type B occurs in the back or abdomen. A positive family history of dissection should also raise suspicion. Physical exam findings include hypotension in Type A, hypertension in Type B, pulse deficit, aortic regurgitation, signs of CHF, limb ischemia or MI.
MRI, TEE and CT with IV contrast all have around a 95% sensitivity. MRI however is not indicated for unstable patients and patients with certain pacemakers and devices. It is often used for long-term management and follow-up.
CT with IV contrast may be done as a CT scanner is usually readily available.
A transesophageal echocardiogram may be done bedside in an unstable patient. It takes around 15-20 minutes to perform. If there is a high index of suspicion and the 1st test is negative a 2nd test must be performed.
Contrast angiography may be used specifically as a diagnostic tool especially when visceral perfusion defects are suspected. It may also provide an entry point into endovascular treatment of dissection.
** Of note, 60% of intimal tears occur in the proximal ascending aorta. The rest occur at the origin of the left subclavian artery and the ligamentum arteriosum, the descending aorta, in the aortic notch and in the abdomen.
Aortic Dissection is an acute occurrence. The first priority is to maintain hemodynamic stability. There should be a low threshold for ICU admission. Arterial blood pressures should be monitored in less stable patients.
For uncomplicated Type B dissections, medical management is considered first line treatment. Patients should be started on Beta-Blockers such as Labetalol, Propranolol, Metoprolol or Esmolol. If the patient is unable to handle Beta-Blockers or has severe asthma, calcium channel blockers with negative inotropic and chronotropic effect such as Verapamil or Diltiazem may be used. Surgical intervention is indicated for Type B only if the patient has continued aortic expansion, impending aortic rupture, occlusion of a major arterial vessel, persistent or recurrent chest pain, or a pre-aortic or mediastinal hematoma. Surgical intervention is typically associated with worse outcomes than medical therapy.
On the other hand, the first line treatment for a Type A dissection is surgical intervention. Those patients who are inappropriate candidates for surgery have a mortality rate of 50%. Surgical correction aims to resect the ascending aorta with a conduit graft.
Intracardiac Echocardiography (ICE)
ICE is a type of cardiac ultrasound. It uses mechanical waves with frequencies greater than 20,000 Hz and the laws of sound reflection and refraction while crossing borders between materials of different densities. Additionally, it uses a miniature transducer to create images. The transducer is at the edge of the catheter and uses a series of crystals or a single crystal where the beam is moved by mechanical means around a circle. The images are displayed in either M or B modes with Doppler effect.
Two-dimensional echo is the modality typically used for ICE. It is used in electrophysiology laboratories for procedures such as ablations, trans-septal punctures, evaluation for intracardiac thrombus, ASD/PFO closure, and other electrophysiological procedures. ICE allows for improved anatomic visualization for areas such as the pulmonary veins and the A-V junction. ICE also enables continued radiofrequency monitoring during ablation, hemodynamic performance of the myocardium and pericardial space monitoring.
INSERTION AND STRUCTURE RECOGNITION
The typical ICE catheter is inserted via the inferior vena cava and positioned along the right atrium to the level of the mid-septum. Most often the right atrium is the area of the heart visualized most often during EP procedures. Thus, it is called the “Home View” or the “basic point of orientation”. Figure (A) shows the tricuspid valve and the right ventricle. Counterclockwise rotation of the catheter in the RA will show the terminal crest. Clockwise rotation from the inferior RA will show the Eustachian ridge with the tricuspid-caval isthmus (B).
Turning the catheter clockwise along its axis reveals the aortic valve, the right ventricular outflow tract and occasionally the pulmonary artery (figure C). Additional long axis views can be seen of both the aorta and the pulmonary trunks. When the catheter is rotated from the low right atrium, a short axis view of the coronary sinus is seen (figure D). Moving the catheter left-to-right at this same point provides a long axis view of the same structures (figure E). If the catheter is moved counterclockwise, views of the left atrium, mitral valve and left ventricle can be seen (figure F). If the depth setting of the catheter is increased with the transducer directed towards the left atrial posterior wall and placed at the level of the atrial septum, then the left and right pulmonary veins and the left atrial appendage can be visualized. The long and short axis views of the left ventricle are seen in figures G and H. See figure 1 below.
The following images (Figures 2-10) provide additional information and diagrams of anatomical landmarks seen during an ICE.
Comparison of Rotational and Phased-Array ICE
(A) Rotational or cross-sectional view of the right atrium (RA), left atrium (LA), and interatrial septum using a rotational intracardiac echocardiography (ICE) catheter. Note that the shaft of the ICE catheter (circular structure) can be seen in the RA, with the tip apposed to the interatrial septum for optimal imaging of the fossa ovalis. (B) Two-dimensional view of the interatrial septum using a phased-array ICE catheter. The catheter terminates within the body of the RA. (C) Schematic drawing of a phased-array ICE catheter in the RA in the optimal position to image the interatrial septum. Note that the ultrasound array is facing the septum but is not in apposition to it. Figure 1C provided by St. Jude Medical.
Below: The top and bottom rows demonstrate typical intra-cardiac echocardiography images obtained with the transducer in various locations within the left enclosed region. The centre row uses computed tomography images to illustrate how the intra-cardiac echocardiography images were used to integrate electrograms with anatomy. and to demarcate myocardium enclosed by encircling lesions (highlighted in blue) from myocardium which is not enclosed:
(A) whole-heart, left-lateral vantage; (B) left atrial, viewed from a posterior extra-cardiac vantage; (C) left atrial, with the left antrum viewed from an intra-cardiac vantage; (D) the two endocardial halves of (C) resulting from a cleavage plane along the red line shown in (C). On all computed tomography images, the dotted lines show the encircling lesion, and solid lines the venoatrial junctions. Numbered locations on the computed tomography images correspond to those on the intra-cardiac echocardiography images. The enclosed region was conceptualized as having four ‘walls’: 1, posterior; 2, inferior; 3, anterior; and 4, superior. The confluence of superior and inferior veins was defined as the intervenous ridge (5→6).
aAo, ascending aorta; MPA, main pulmonary artery; LAAd, distal portion of appendage complex;15 LAAp, proximal portion of appendage complex;15 LAAo, ostium of LAAp, defined as the region of transition between smooth (LAAp) and trabeculated (LAAd) endocardial contours; CS,coronary sinus; Cx, circumflex coronary artery; LV, left ventricle; RV, right ventricle; LA, body of left atrium; LPV, left pulmonary venous antrum; LAD, left anterior descending coronary artery; SCV, superior caval vein; LS, left superior pulmonary vein; LS’, branch of left superior pulmonary vein; LI, left inferior pulmonary vein; RS, right superior pulmonary vein; RI, right inferior pulmonary vein; dAo, descending aorta; LPA, left pulmonary artery; eso, oesophagus; P, pericardial recess; MA, mitral annulus; T, intra-cardiac echocardiography transducer; Tr, muscular trabeculum in appendage, tissue bridging left atrial body and contiguous left superior vein roof
Typical intra-cardiac echocardiography and computed tomography images of the right enclosed region
(A) is whole-heart, superior vantage; (B) and (C) are left atrium, extra-cardiac, posterior and right lateral vantages, respectively; (D) is left atrium, with the right antrum viewed from an intra-cardiac vantage; (E) shows the two endocardial halves resulting from the cleavage of (D) along the red line. The white circle shown in computed tomography images (A), (C), (D), and (E) as well as some intra-cardiac echocardiography images demarcates the right atrial septal ‘origin’ of the inter-atrial bundle, which is echocardiographically distinct as the region along the right septum where the anterior wall of the superior caval vein joins the atrial body.2 The enclosed region was conceptualized as having four ‘walls’: 1, posterior; 2, inferior; 3, anterior; and 4, superior. The intervenous ridge (5→6) was single in the two-vein anatomy demonstrated here, but multiple when there are supernumerary veins. The intra-cardiac echocardiography image on the top left was obtained with the intra-cardiac echocardiography transducer in the right atrium (fossa ovalis), to demonstrate the relationship between the right antrum (RPV), Waterston’s groove (w), fossa ovalis (fo), and encircling lesion. Abbreviations are as in Figure 3; in addition: RA, body of right atrium; LM, left main coronary artery; RS’, branch of right superior pulmonary vein; RPA, right pulmonary artery.
Typical electrograms obtained during mapping within enclosed regions, with data from left and right antra. The top figures show electrograms recorded from a single site (superior wall, just in enclosed region) just prior to encircling lesion deployment, immediately after the encircling lesion which did not result in isolation of the enclosed region, and again after a single secondary lesion at a distant site which resulted in isolation of the enclosed region. Surface lead V1 is also shown. Prior to ablation, overlap of non-enclosed myocardium (timing demarcated by black square) and enclosed myocardium (timing demarcated by white square) electrograms was apparent, preventing their separate assessment. After the encircling lesion, non-enclosed myocardium and enclosed myocardium electrograms have separated, attributable to delay in the latter. In this example, the amplitude of the non-enclosed myocardium electrogram was reduced after the encircling lesion, likely due to its proximity to this lesion. After the secondary lesion, only the non-enclosed myocardium electrogram remains. The bottom figure shows electrograms obtained after encircling lesions (dashed lines) which did not produce isolation of enclosed myocardium (highlighted in blue). The letters on the computed tomography images are anatomical locations from where the correspondingly lettered electrograms were recorded. At each site, activation times (in milliseconds) of both non-enclosed myocardium (first number) and enclosed myocardium (second number) electrograms were measured. In addition to electrograms recorded within the enclosed region, in each figure the electrograms from a single site outside but contiguous to the enclosed region is shown; for the right antrum example, this site was on the contiguous wall of the superior caval vein. In each case, complete isolation of the enclosed myocardium was achieved by a single secondary lesion delivered at site 5.
Figure 6: Distant (top) and close (bottom) proximity between enclosed and appendage regions:
(A) Multidimensional computed tomography image, left lateral vantage. (B) Two-dimensional computed tomography image. The space separating the enclosed and appendage regions is demarcated by the arrows. (C) Intra-cardiac echocardiography image. The lines approximate the contiguous endocardial surfaces of enclosed and appendage regions. The asterisks demarcate the sites from which the electrogram shown in (D) was recorded. (D) Electrograms recorded from comparable enclosed region locations, recorded after encircling lesions which did not achieve electrical isolation. The black and white squares demarcate timing of non-enclosed myocardium and enclosed myocardium electrograms, respectively. Patients demonstrating close proximity between enclosed and appendage regions have larger non-enclosed myocardium electrogram amplitudes and slopes.
Radial ICE Guidance during AVNRT Ablation of the Slow AV Node Pathway. The left image depicts initial ablation catheter not in contact with the endocardial location of slow AVN pathway. The right image clearly depicts adequate electrode-endocardial contact which resulted in a successful ablation.
Figure 8 Completion of AV Nodal Ablation under Radial ICE Guidance. This figure depicts radial ICE catheter location in the RVOT near the level of aortic valve. The radial ICE allows catheter position nearer to the leftward extension of the His purkinje system in an attempt to complete AV node ablation.
Miscellaneous (Atrial Tachycardia, Difficult CS Anatomy)
Radial ICE can be used for detailed assessment of RA anatomy especially during mapping of difficult atrial tachycardias.
Figure 9 shows the level of RA detail radial ICE can provide to assist EP study catheter localization.
Figure 9 Radial ICE Assessment of RA Anatomy. Figure from Springer, Journal of Interventional Cardiac Electrophysiology
Radial ICE Assessment of RA Anatomy. Right atrial anatomy is nicely visualized with radial ICE and corresponding anatomic specimen. One can see how adjunctive imaging during difficult RA ablation may help visualize catheter position and endocardial contact. Figure taken from Springer, Journal of Interventional Cardiac Electrophysiology
Figure 10 depicts radial ICE imaging of both anatomic variants. A minimally fenestrated Thebesian valve can make CS access unfeasible as in this case. A prominent Eustachian ridge can mandate CS access using a subclavian or jugular venous approach as it often impedes catheter placement when using a femoral venous approach.
Figure 10 Radial ICE Imaging of CS Anatomic Variants.
The left image shows a Thebesian valve with no obvious fenestrations covering the CS os. The right image shows a prominent Eustachian ridge extending from the IVC and overlying the superior aspect of the CS os.
Images and captions adapted from Schwartzman D, Williams J. Electroanatomic properties of pulmonary vein antral regions enclosed by encircling ablation lesions. Europace. 2009 Apr;11(4):435-44.
Jongbloed M R M, Schalij M J, Zeppenfeld K, Oemrawsingh P V, van der Wall E E, Bax JJ. Clinical applications of intracardiac echocardiography in interventional procedures. Heart. Jul 2005; 91(7): 981-990.
Differentiating Between Right and Left Ventricular Outflow Tract Tachycardia
Right ventricular outflow tract (RVOT) tachycardia is associated with two conditions, idiopathic ventricular tachycardia and arrhythmogenic right ventricular dysplasia. RVOT make up around 90% of the common form of idiopathic ventricular tachycardia. The mechanism of idiopathic VT is c-AMP mediated activity and hence usually responds to adenosine. Arrhythmogenic right ventricular dysplasia is an inherited disorder which involves fibro-fatty deposition within the myocardium. This disorder causes paroxysmal ventricular tachycardia and sudden cardiac death. Triggers of RVOT include ….
RVOT will demonstrate the following characteristics in an electrocardiogram:
In RVOT, there can also be the presence of a septal or lateral wall involvement.
In lateral wall involvement there will be a wider and notched QRS complex whereas the opposite will be true of a septal wall RVOT tachycardia. Additionally, a positive QRS complex in aVL indicates lateral wall involvement whereas a negative QRS in aVL indicates septal wall involvement.
The opposite can be said about lateral wall and septal wall involvement in regards to polarity in aVL when discussing LVOT tachycardias. That is, a positive deflection in aVL indicates septal wall involvement whereas a negative deflection in aVL indicates lateral wall involvement.
In contrast, the left ventricular outflow tract tachycardia can demonstrate the following characteristics:
Aortic stenosis is the obstruction of blood flow across the aortic valve. It can be caused by congenital abnormalities such as unicuspid or bicuspid valve, rheumatic fever and age-related calcific changes. When the valve becomes stenotic, resistance to systolic ejection develops. A pressure gradient develops between the left ventricle and the aorta. Left ventricular pressure increases and left ventricular hypertrophy occurs in response. In most patients, LV systolic function is preserved and cardiac output is maintained despite increased systolic pressure. Although cardiac output is normal during rest, it fails to increase during exercise and exercise-related symptoms may be seen.
Diastolic dysfunction occurs as a result of LV relaxation impairment, decreased LV compliance, increased afterload or LV hypertrophy. LV hypertrophy can reverse following relief of valvular obstruction. Atrial filling plays an important role in diastolic filling of the left ventricle. Development of atrial fibrillation in aortic stenosis can lead to heart failure due to the inability to maintain cardiac output.
Symptoms of aortic stenosis are dyspnea on exertion, syncope and anginal chest pain. A slow upstroke of the arterial pulse and low pulse volume, known as pulsus parvus etc tardus, is also noted. Systolic crescendo-decrescendo murmur is heard at the 2nd intercostal space.
Indications for surgery
Indications for intervention are expanded from previous to include patients with very severe AS (above) and low surgical risk (Class IIa); asymptomatic severe AS and decreased exercise tolerance or exercise-related decrease in blood pressure (Class IIa); and symptomatic patients with LFLG severe AS and normal LVEF if clinical, hemodynamic, and anatomic data support valve obstruction as the likely cause of symptoms (Class IIa).
Hypertension refers to systolic blood pressures greater than 140 mm Hg or diastolic blood pressures greater than 90 mm Hg. Hypertension is diagnosed by two or more elevated blood pressure readings on two or more office visits after an initial screening.
|Normal||< 120 mmHg||and < 80 mmHg|
|Prehypertension||120-139 mmHg||or 80-89 mmHg|
|Stage I Hypertension||140-159 mmHg||or 90-99 mmHg|
|Stage II Hypertension||greater than or equal to 160 mmHg||greater than or equal to 100 mmHg|
Hypertension can be primary or secondary. Primary hypertension constitutes 85-95% of cases.
Primary hypertension:The mechanism of primary hypertension is unclear and seems to be lifestyle related. Factors such as dietary sodium, obesity, stress and a sedentary lifestyle are responsible for hypertension in genetically predisposed individuals. In patients > 65, high sodium intake is more likely to precipitate hypertension.
Secondary hypertension: Causes include primary aldosteronism, renal parenchymal disease such as glomerulonephritis, polycystic renal disease, pheochromocytoma, Cushing syndrome, congenital adrenal hyperplasia, hyperthyroidism and coarctation of the aorta. Use of sympathomimetics, excessive alcohol, corticosteroids, or cocaine worsen blood pressure control.
Symptoms and signs
Hypertension is usually asymptomatic until complications develop in target organs. Uncomplicated hypertension usually causes dizziness, flushed facies, fatigue, headache or epistaxis. Severe, untreated hypertension can cause cardiovascular, neurological, renal and retinal symptoms. It is important to treat hypertension early, before it causes damage to the organs.
JNC 8 Hypertension treatment guidelines
The Joint National Committee (JNC 8) hypertension guidelines were published in the Journal of the American Medical Association in 2013. Compared with previous guidelines, the new guidelines emphasize higher blood pressure goals for systolic blood pressure and diastolic blood pressure and less use of several antihypertensive medications.
Goal blood pressures according to JNC 8:
|Patients 60 years or older who do not have diabetes or chronic kidney disease||<150/90 mmHg|
|Patients 18-59 years without major comorbidities||<140/90 mmHg|
|Patients 18-59 years with diabetes or chronic kidney disease||<140/90 mmHg|
Diabetes Mellitus Type 2
Criteria for diagnosis of Pre-Diabetes:
Fasting glucose 100-125mg/dL
2-hour plasma glucose >140-199mg/dL
Criteria for diagnosis of Diabetes Mellitus Type 2:
HbA1C >= 6.5%
Hyperglycemia crisis plus random plasma glucose >= 200mg/dL
Fasting plasma glucose >= 126 mg/dL on 2 occasions or 2-hour plasma glucose >= 200mg/dL during oral glucose tolerance test with a 75 gram glucose load.
Diabetic foot exam at every visit
Lifestyle interventions should be discussed
Every 3 months:
Nephropathy: urine microalbumin-to-creatinine ratio
Retinopathy:diabetic eye exam
Low-dose aspirin for all adults with CVD
ACE-I/ARB 1st line for increased blood pressure
Statin therapy for elevated LDL
Update the patient’s Hepatitis B vaccine
Lifestyle modifications including weight loss
Sulfonylureas: Consider in patients who cannot tolerate Metformin. Lowers A1C by 1-2%. However, their effectiveness decreases over time
Thiazolidenediones: lower blood glucose concentrations by increasing insulin sensitivity. Lowers A1C by 0.5 – 1.4%.
Dipeptidyl peptidase-4 inhibitors: More commonly used as a second to third line agent.
Alpha Glucosidase inhibitors: Have an additive hypoglycemic effect and are therefore used as an adjunct agent. Only decrease A1C by 0.5-0.8%. Taken pre-prandially to decrease post-prandial hyperglycemia.
Meglitinides: Useful in patients with a sulfa allergy or renal impairment. They are short-acting glucose lowering drugs.
Initiate insulin therapy for for patients
Diagram adapted from: Wallia A, Molitch M. Insulin therapy for type 2 diabetes mellitus. JAMA. 2014;311(22):2315-2325
Diagram adapted from: Wallia A, Molitch M. Insulin therapy for type 2 diabetes mellitus. JAMA. 2014;311(22):2315-2325
American College of Clinical Endocrinologists. Comprehensive Diabetes Management Algorithm 2013.
Rao S, Krishnasamy S. Diabetes Mellitus, Type 2. 5-The 5-Minute Clinical Consult Standard 2015, 23rd Edition. Accessed 11/26/2014.
Wallia A, Molitch M. Insulin therapy for type 2 diabetes mellitus. JAMA. 2014;311(22):2315-2325
Aortic Valve Anatomy
RCA: Right coronary artery
LCA: Left coronary artery
RCC: right coronary cusp
LCC: left coronary cusp
NCC: non-coronary cusp
RA: right atrium
LA: left atrium
The diagram above shows normal aortic valve anatomy on the far left (A). As demonstrated by the diagram, the right coronary artery comes off the right coronary cusp and the left coronary artery comes off the left coronary cusp. Note the non-coronary cusp is the posterior aspect of the valve.
Figures B-D show variations in bicuspid valve anatomy. A bicuspid valve can either be a true 2 valve anatomy or it is a fusion of two of the valves as seen in the figures above. The most common valves to fuse are the left and right coronary cusps (B). Then the right coronary cusp with the non-coronary cusp (C). The least common fusion pattern is the left coronary cusp with the non-coronary cusp (D).
Image taken from: http://www.intechopen.com/books/aortic-valve/bicuspid-aortic-valve