Monthly Archives: February 2015

Aortic Stenosis

-referred to the narrowing of the aortic valve opening
-3 main causes: congenital abnl resulting in unicuspid or bicuspid valve, age-related calcification, and rheumatic fever
– Worldwide, rheumatic heart disease is most common
-US, age related calcification and congenital biscuspid valve are most common

Signs and symptoms
-transient loss of consciousness, difficulty breathing, syncope, dizziness, and angina with exertion due to reduced blood flow from the heart.

Physical Exam
-systolic crescendo-decrescendo murmur heard in the intercostals space between ribs 2 and 3 that radiates to the carotid arteries.

-aortic stenosis can develop into abnormal heart rhythms including A-fib, V-tach, bradycardia leading to sudden cardiac death.
-Patients also at risk for developing endocarditis
-Other risks include formation of blood clots in major blood vessels of the brain and body

Diagnostic tests
-EKG – evaluates rate and rhythm of the heart
-Echocardiogram – to evaluate structural integrity of the heart’s valves and to check blood flow.
-CT or MRI of the aorta may be necessary if ECHO is inconclusive
Cardiac cath – may be warranted to measure flow of blood through the valve


-asymptomatic patients – may be advised to avoid strenuous sports and exercise
-medications can be utilized to manage symptoms of aortic stenosis but do not prevent the progress of valvular disease. However, medical therapy is useful in managing coexisting conditions that correlate with aortic stenosis:
-BBs, CCBs, and/or nitrates may be useful in treat coexisting hypertension
-Digoxin and diuretics may be useful in treating coexisting congestive heart failure

-prophylactic antibiotics currently not recommended for prevention of infective endocarditis in patients who undergo dental procedures.
-survival of patients with aortic stenosis dramatically decreases once patients develop symptoms of angina, syncope, or heart failure.

-According to the American College of Cardiology and American Heart Association, it is recommended to have the valve replaced in patients who are asymptomatic but have a reduced ejection fraction of <50%, measured on echocardiogram. Other factors considered for valve replacement include likelihood of aortic stenosis progression which factors in age, calcification, and coronary artery disease. The severity of stenosis based on specific valve dimensions and an abnormal stress test can also play a role in the deciding whether to have the aortic valve replaced.
-Aortic valve replacement is recommended for patients who develop symptoms and is considered most effective in improving survival. Aortic valve replacement can be replaced surgically or trans-catheter implantation. Tran-catheter implantation repairs the aortic valve without removing the old, damaged valve.


Dr. Ben- Zur is an elctrophysiologist and board certified cardiologist in the Burbank area who can help diagnose and treat valvular diseases like aortic stenosis. Here at the Cardiovascular institute we also perform replacements, pacemaker implantation, stress tests, electrocardiograms and various other procedures in our state of the art facilities.

Basics of Aortic Dissection

Aortic Dissection is classically described as a sudden tearing, stabbing, or sharp pain in the chest or mid-back.

Aortic Dissection Videos:

  1. Nucleus Medical Media: Aortic Aneurysm and Aortic Dissection (Start at 2:30)
    2. <iframe width=”560″ height=”315″ src=”” frameborder=”0″ allowfullscreen></iframe>
  2. Khan Academy Medicine: What is Aortic Dissection?
    2. <iframe width=”560″ height=”315″ src=”” frameborder=”0″ allowfullscreen></iframe>



Previous entry 1:

Aortic Dissection

Published December 20, 2014 | By admin

Aortic Dissection

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: (most commonly used)

Type A: Involves ascending aorta up to 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.

Risk Factors:

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.

Diagnostic Tests:

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.

Previous Entry 2:

Aortic Dissection

Published August 14, 2014 | By admin

What is an aortic dissection?

The aorta is the biggest artery in the body.  It originates from the left ventricle and supplies virtually every part of the body with oxygenated blood.  A dissection is a tear of the innermost layer of tissue of the vessel.  This causes blood to flow into the middle layer of tissue and damages it causing it to become weak.  Aortic dissection is often a surgical emergency that requires careful management.

Aortic dissection can be acute or chronic

Acute dissection – Symptoms or dissection occurring within the last 14 days

Chronic dissection – Symptoms or dissection occurring after the 14th day

It is also important to differentiate between complicated vs. uncomplicated aortic dissection

Complicated aortic dissection – patient has developed a rupture, malperfusion syndromes refractory pain or rapid aortic expansion.

Un-complicated – do not exhibit the above features

How do we classify aortic dissections?

We classify aortic dissections based mainly on where the tear is and if/where it propagates.  There are two widely used protocol for classifications; The DeBakey classifications and The Stanford classifications.

The DeBakey Classifications

  • Type I – propagate from the ascending aorta, extend to the aortic arch, and commonly, beyond the arch distally.
  • Type II – confined to the ascending portion of the aorta.
  • Type III – limited to the descending aorta.

The Stanford

  • Stanford type A – involve the ascending aorta
  • Stanford type B – Do not involve the ascending aorta


Below is a third way to classify dissections but only applies to dissections of the descending aorta.

  • Type 1 – no identifiable intimomedial tears in the descending thoracic aorta.
  • Type 2 – one or more intimomedial tears in the descending thoracic aorta and there is no tear at or distal to the level of the celiac artery.
  • Type 3 – intimomedial tears involving the abdominal aorta (with or without concomitant tears in the descending thoracic aorta).
  • Type 4 – intimomedial tears distal to the aortic bifurcation (with or without concomitant tears in the descending thoracic and abdominal aorta).

Uri M. Ben-Zur, M.D., F.A.C.C. completed a residency in internal medicine and fellowships in interventional cardiology, clinical cardiology, and clinical electrophysiology.  He currently practices at the The Paulette Tashnek-Wagner Cardiovascular Institute of Greater Los Angeles located in Tarzana, CA.

Aortic Dissection. Digital image. Wikipedia. N.p., n.d. Web. <>.

Interview Questions and Answers for Residency


By Edward Lin, Matthew Gill, and Michael Sheflo


  1. Why do you want to go into this specialty?


  1. What are you looking for in a residency program?


  1. What have you learned about yourself during medical school?


  1. Do you have any teaching experience?


  1. How do you make clinical decisions?


  1. How did you deal with a difficult time in your life?


  1. What do you do to cope with stress and disappointment?


  1. What kinds of patients are most difficult for you to relate to and how do you overcome this?


  1. What are your strengths?


  1. What are your weaknesses?


  1. How do you establish rapport with patients?


  1. How do you establish relationships with colleagues and hospital staff?


  1. What motivates you in medicine?


  1. What is something that you have learned outside of medicine that has been beneficial to know within medicine?


  1. What are your interests in research?


  1. How do you compare to the rest of your medical school class?


  1. What are your long-term goals?


  1. How do you deal with disagreement?


  1. What are you most proud of?


  1. Who is your role model?


  1. What other specialties did you consider applying to?


  1. We have many strong applicants, why should we choose you?


Hypertension defined as systolic blood pressure > 140 mmHg or diastolic blood pressure > 90 mmHg.

Hypertension is diagnosed after two or more consecutive elevated blood pressure readings at two or more office visits after an initial screening.

Systolic Diastolic
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

*Essential (primary or idiopathic HTN) comprises of 85-95% of all HTN cases

​-Although the mechanism is unclear, Factors such as dietary sodium, obesity, stress, and sedentary lifestyle are responsible for hypertension in genetically predisposed individual. 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, Cushing syndrome, congenital adrenal hyperplasia, hyperthyroidism and coarctation of aorta. Use of sympathomimetics, excessive alcohol, corticosteroids, or cocaine worsen blood pressure control.

*Hypertensive urgency

-defined as systolic blood pressure > 180 or diastolic blood pressure > 120 without signs of end organ damage

-blood pressure should be slowly lowered over a period of minutes to hours with an antihypertensive agent. The initial goal in hypertensive emergencies is to reduce the blood pressure by no more than 25% within minutes to 2 hours, and then toward a level of 160/100 mmHg within a total of 2 to 6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and possibly infarction.​

*Hypertensive emergency

-defined as systolic blood pressure >  180 or diastolic blood pressure > 110 with signs of end organ damage.

-blood pressure can be gradually lowered over 24 to 48 hours. The initial goal in hypertensive urgency is to reduce the blood pressure by no more than 25% within the first 24 hours and toward a level of 160/100 mmHg

*Signs and symptoms

– HTN 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


*Management of atrial fibrillation (AF): symptom control and prevention of thromboembolism.

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.

-Beta blockers
-Calcium channel blockers (verapamil, diltiazem)
-Digoxin may be needed for patients with congestive heart failure. Less likely to control ventricular rate during exercise and does not slow the heart rate in patients with recurrent AF
– IV amiodarone may be needed for patients with poor left ventricular function.

-Catheter ablation as first-line therapy for rhythm control. Patients who may reasonably prefer catheter ablation include younger individuals or those who are concerned about the potential complications of antiarrythmia drugs (AAD).

Recommendations for Catheter ablation:
-For younger patients (age ≤70 years) with symptomatic paroxysmal AF and a LVEF >40% who choose to not receive AAD therapy.
-Patients with symptomatic paroxysmal AF and who have failed or become intolerant to one or more AAD.
-For patients with symptomatic persistent or longstanding persistent AF who have failed or become intolerant of one or more AAD or who choose not to start antiarrhythmic therapy.

*Acute management for new onset AF
-calcium channel blockers such as diltiazem 10mg every 10 minutes is a good first option.
-If that is unsuccessful in resolving the AF, digoxin may be added as second line treatment.
-Amiodarone may be added as third line treatment.  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, with concurrent initiation of the 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:

  1. Active ischemia
  2. Organ hypoperfusion.
  3. Severe manifestations of heart failure (HF) i.e. pulmonary edema
  4. Pre-excitation syndrome, which may lead to an extremely rapid ventricular rate due to the presence of an accessory pathway.

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. IV anticoagulation with heparin should be started, but it should not cause a delay in emergent cardioversion.

-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:
-Flecainide or propafenone in patients in sinus rhythm who have no underlying structural heart disease, normal baseline QT intervals, and no profound bradycardia or suspected sinus or atrioventricular (AV) node dysfunction.
-Amiodarone or dronedarone in selected patients who have no other risk factors for torsades de pointes (eg, hypokalemia, hypomagnesemia) or sinus node dysfunction or AV conduction disease. Dronedarone and amiodarone are the only two drugs that can be initiated in outpatients while in atrial fibrillation.
-Patients with an implantable cardioverter-defibrillator (ICD) represent another group in which outpatient initiation of therapy can be tried


Idiopathic Hypertrophic Subaortic Stenosis (IHSS) is an obstructive type of Hypertrophic Cardiomyopathy (HCM). HCM can be classified as obstructive or non-obstructive depending on whether the anatomy of the heart impedes the flow of blood from the left ventricle into the systemic circulation. IHSS is sometimes also called hypertrophic






IHSS – Idiopathic Hypertrophic Sub Aortic Stenosis

Published December 31, 2014 | By admin

What is it?

Idiopathic hypertrophic sub aortic stenosis (IHSS) is a genetic disease characterized by marked hypertrophy of the left ventricle in the absence of chronic pressure overload (HTN, or aortic stenosis), involving specifically the interventricular septum and the left ventricular outflow tract. Also called hypertrophic obstructive cardiomyopathy (HOCM). Umbrella term: hypertrophic cardiomyopathy (HCM).


  • Most common cause of sudden cardiac death in young athletes in the US.
  • Occurrence rate of 1 in 500.
  • Most common (Mendelian) genetic heart disease.
  • Presents after puberty (average age in mid-20s, but more and more in 40s and 50s).


  • Genetic abnormality of muscle cell proteins:
    • Autosomal dominant with variable penetrance (i.e. everyone who has the genes does not necessarily get the disease).
    • Most genes are for sarcomere proteins (Beta myosin heavy chain and myosin-binding protein C are most common). Currently, 11 or more causative genes with over 1400 mutations in genes encoding the thick or thin myofilament proteins of the sarcomere have been reported.
    • Most mutations lead to a single amino acid change.
    • These mutations cause myofibral disarray. Muscle cells are normally lined up linearly but in IHSS the muscle fibers are in disarray (i.e. in all different directions).
  • These abnormalities do not allow the heart muscle to contract properly.
  • Because of this, the heart compensates for this lack of effective contraction by hypertrophying (i.e. the cells get bigger).
  • Thus, the walls of the heart get bigger, and distinctive of this disease is that the inter ventricular septum becomes asymmetrically enlarged. The papillary muscles and mitral valve are deformed by the thickened septum, and thickening of the mitral valve leaflet also commonly occurs.
  • This hypertrophy can result in two major problems:
    • Since the walls of the ventricle are bigger, the chambers have become smaller. This leads to decreased ability of the heart to fill during diastole and thus the heart cannot pump enough blood forward to the systemic circulation during systole. This is termed DIASTOLIC heart failure.
    • Intermittent outflow obstruction:
      • The thickened septum causes a narrowing of the left ventricle outflow tract. In 75% of cases there is no obstruction. Ejection of blood through a narrowed outlet leads to the Venturi effect. Venturi forces pull anterior mitral leaflet toward septum during systole causing obstruction. This is called systolic anterior movement of mitral valve (SAM).
      • It is intermittent because it is dependent on how hard the heart muscle is working. If someone with this disease is exercising really hard and the heart rate is really fast, the diastolic period (the time when the heart fills with blood) is shorter so there is even less time to fill the ventricle. Since there is less blood in the ventricle the outflow tract becomes narrower and you get more obstruction. On the other hand, when the heart rate is slower, there is more time for the ventricle to fill in diastole so the outflow tract is widened by the blood, and there is less obstruction.


1) History and physical

-Symptomatic vs. asymptomatic: Most patients have few or no symptoms

If a patient is symptomatic he/she may have dyspnea, syncope, angina, palpitations, dizziness, or sudden death

  • Dyspnea (most common symptom): Due to diastolic dysfunction. Blood backs up into the lungs because it cannot enter the chamber of the hypertrophied left ventricle. This causes fluid in the lungs and consequently dyspnea.
  • Palpitations: from arrhythmias that occur in IHSS such as premature atrial and ventricular beats, sinus pauses, atrial fibrillation, atrial flutter, supraventricular tachycardia, and ventricular tachycardia. The arrhythmias occur due to fibrosis and myofibrillar disarray of the heart muscle.
  • Angina: due to more oxygen demand from thickened wall, than supply of oxygen available. Exacerbated during exertion.
  • Orthopnea/paroxysmal nocturnal dyspnea: observed in severe IHSS. Due to a combination of impaired diastolic function and subendocardial ischemia.
  • Dizziness: due to outflow tract obstruction and thus less blood flow to brain
  • Syncope/sudden death: due to ventricular arrhythmias that are caused by fibrosis and myofibrillar disarray

2) Physical Exam:

  • A murmur is usually the first clinical manifestation of the disease.
  • You will hear a systolic crescendo-decrescendo ejection murmur along the lower left sternal border, or apex, that increases with a decrease in preload (valsalva or standing up) or after load (anti-hypertensive medications) or decreases with an increase in preload (squatting) or afterload (clenching fist).
  • Can also hear S4 murmur due to non-compliance of left ventricle during diastole.
  • May also have accompanying MR murmur from systolic anterior motion of the mitral valve and significant LV outflow gradients.
  • A double peaked carotid pulse that occurs due to a quick rise, then fall (due to outflow tract obstruction) of blood flow through left ventricular outflow tract, then secondary rise of blood flow through the outflow tract.

3) Routine tests:

  • Labs: usually normal, but may have elevated BNP.
  • CXR: The cardiac silhouette ranges from normal to markedly increased in size. Left atrial enlargement can be observed especially when significant mitral regurgitation is present.
  • ECG: You can see LVH, left atrial abnormality, and left axis deviation. You may also see WPW with certain mutations, deep and broad Q waves in inferior and precordial lateral leads (likely related to gross septal hypertrophy rather than MI), and T wave changes.

4) Special tests:

  • Echocardiogram will show an increased septum: LV wall thickness ratio (> 1.5:1)
  • Cardiac MRI: especially useful when echo is questionable.
  • Cardiac catheterization: most accurate test to determine precise gradients of pressure across outflow tract.

5) Confirmatory tests

  • Genetic testing.
  • Cardiac muscle biopsy: Will show myofibral disarray.


  • Asymptomatic patients
    • A significant number of patients will not have any symptoms and will have a normal life expectancy. However, these patients should still be counseled to avoid particularly strenuous activities and medications that decrease preload such as nitrates or diuretic blood pressure medications.

2) Medications

  • Medications are used to relieve symptoms: palpitations, dyspnea, angina, syncope
  • Beta blockers are considered first-line agents, as they can slow down the heart rate and allow for increased diastolic filling and decreased myocardial oxygen consumption. This reduces obstruction in outflow tract and ischemia respectively. Non-dihydropyridine calcium channel blockers such as verapamil and diltiazam can also be used.
  • Disopyramide: decreases contractility and SVT arrhythmias.
  • Amiodarone: the only agent proven to reduce the incidence and risk of cardiac sudden death. Very effective at converting atrial fibrillation and atrial flutter to sinus rhythm.

3) Surgical myomectomy

  • For patients who remain severely symptomatic despite medical therapy and/or with an outflow gradient of more than 50 mm Hg.
  • Involves removing a portion of the inter ventricular septum to widen the outflow tract.
  • Complications include possible death, arrhythmias, infection, incessant bleeding, septal perforation/defect, and stroke.

4) Alcohol septal ablation

  • Involves injection of alcohol into one or more septal branches of LAD.
  • The ablation is a “controlled heart attack” in which the part of the septum involved with the outflow tract is infarcted and subsequently contracts into a scar.
  • Less invasive but produces similar results to septal myomectomy.

5) Ventricular pacing

  • Pacemaker activates the inter ventricular septum before the ventricular free wall. This decreases the gradient across outflow tract.
  • Will also help treat arrhythmias.
  • Indications: 1) family history of sudden death 2) wall thickness > 30 mm. 3) unexplained syncope 4) history of ventricular arrhythmias

6) Cardiac transplant

  • For cases refractory to all treatments.

Natural history

  • The course of IHSS is extremely variable but in general the disease is progressive and there is usually a latency of 3 years between the discovery of a murmur and the manifestation of the first symptoms of the disease.
  • Occasionally symptoms actually diminish or disappear spontaneously with the passage of time.
  • About 1% per year suffer sudden cardiac death.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common cause of palpitations in patients with hearts exhibiting no structural abnormality. After consultation with a cardiologist and an electrophysiologist, an ablation may be needed to treat the condition.


Electroanatomical mapping utilizes several catheters with sensor tips connected to mapping and navigation software. During the ablation procedure, these catheters measure conduction in electrical pathways of the heart. One catheter is placed in the carotid sinus and another in the bundle of His near the AV node. Electrodes on the catheters are then used to induce the tachycardia. This system is able to map out a three-dimensional image of the associated anatomy and allow easy revisitation of relevant recording sites identified during the study for accurate ablation.


After the ablation, the catheters in the carotid sinus and bundle of His are used to try to induce the tachycardia once again, along with administration of isoproterenol. The ablation is successful if the original induced rhythm is not reproduced.


The most common type of AVNRT is slow-fast.  The fast pathway takes longer to repolarize, so the short pathway current can go up the fast pathway in a retrograde direction causing the reentry circuit that is causing the tachycardia. The slow pathway needs to be located and ablated in order to correct the slow-fast AVNRT.


The image below is an example of the three dimensional mapping. The anatomy focuses on the Triangle of Koch which is composed of the coronary sinus (CS), the tendon of Todaro, and the annulus of the tricuspid valve.  The slow pathway is most commonly located towards the posterior aspect of the triangle, between the tricuspid annulus and the coronary sinus. The red dots on the map are sites that have been ablated. Once sites have been ablated, the electrode data will confirm if the pathology is corrected by demonstrating a junctional rhythm.






The image below shows the electrophysiology data from the live electrocardiogram and intracardiac electrodes. The top three, white lines are electrocardiogram data. The next two, yellow lines yellow lines represent data from the electrodes located at the bundle of His. The next five, pink lines represent data from the coronary sinus electrode. The next two, red lines are data from the ventricular electrode.



This is a picture of the electrode placement for AVNRT ablation.





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