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Monthly Archives: October 2014

Coronary Calcium Scores

Coronary artery calcium scores are calculated based on imaging of the arteries, which visualize calcium deposits in the arteries.

Arterial calcification – Calcified plaque results when there is a build-up of fat and other substances under the inner layer of the artery. This material can calcify which signals the presence of atherosclerosis, a disease of the vessel wall, also called coronary artery disease (CAD).

The presence and extent of coronary arterial calcification (CAC) can predict the presence of coronary artery stenosis (narrowing), but in general it is a better marker of the extent of coronary atherosclerosis than the severity of stenosis.

Indications

Most of the clinical studies that examined the relationship between CAC and coronary artery stenosis have been performed in patients with chest pain who were referred for x-ray coronary angiography.

The 2010 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on screening for coronary artery disease indicated that measurement of coronary artery calcification is reasonable (level of evidence B) for cardiovascular risk assessment in asymptomatic adults at Framingham intermediate risk (10 to 20 percent 10-year risk). The guidelines noted that measurement of CAC “may be reasonable” for patients at low to intermediate risk (6 to 10 percent 10-year risk). It was not recommended for patients at low (<6 percent, 10-year risk) or high risk.

Scoring of CAD Lesions

The Agatston score is calculated in the following way

Each slice taken using an ultrafast CT is analyzed and weighted values are assigned to the highest density of calcification as measured by houndsfield units. A score of 1 is given for 130-199 HU, 2 is given for 200-299, 3 for 300-399 and 4 for 400 or greater (the whiter the lesion, the higher the HU). The weighted score is then multipied by the area of the calcification.

Example: coronary calcification in the LAD measuring 4 square millimeters with a peak density of 250 HU. The score would therefore be 8 (4mm^2 times 2 weighted score). The total score is the sum of all the slices.

Classification of CAD by calcium score:

Calcium Score Presence of CAD
0 No evidence of CAD
1-10 Minimal evidence of CAD
11-100 Mild evidence of CAD
101-400 Moderate evidence of CAD
Over 400 Extensive evidence of CAD

 

Predictive value of the Agatston Score

Positive Test:

Agatston Scores above 400 have increased occurrence of coronary procedure and events of myocardial infarction or cardiac death within 2-5 years after the Calcium Score Scan is performed. Examples of coronary procedures include:

  • bypass
  • stent placement
  • angioplasty

Negative Test:

This does not exclude the presence of atherosclerosis in one’s coronary arteries. It means there is simply minimal atherosclerosis. Predicts a very low likelihood of having a MI or cardiac death in the next 2-5 years.

In a study of 1764 patients with suspected CHD, as the Agatston CAC score varied from >20th percentile to >75th percentile for age, the sensitivity fell from 97 to 81 percent in men and from 98 to 76 percent in women but the specificity increased up to 77 percent. Patients with no CAC had a probability of stenosis of less than 1 percent.

Calcium vs Stenosis

  • Can you have a low calcium score and still have severe obstruction (i.e a 20% score leading to 90% obstruction)?

Yes, without contrast enhancement coronary artery calcification scoring through CT has a low sensitivity for detecting plaques without significant calcification and in one study, the cross-sectional plaque area found on histologic examination was approximately five times greater than the calcification area measured by electron beam computed tomography (EBCT)

Sensitivity and specificity of CAC score

Highly sensitive for the presence of ≥50 percent angiographic stenosis but only moderately specific, especially in individuals over 60 years of age. Both sensitivity and specificity vary with the degree of CAC.

USE OF CAC SCORE – Recommendations

  1. Use for CV risk assessment in intermediate risk patients as determined by their Framingham score when the result will reasonably alter management goals
    1. recommended against those who are classified in either the low or high score group
  2. Asymptomatic patients  with a high CAC score should undergo radionuclide stress testing
  3. CAC should not be used to monitor pharmacologic therapy or initiate preventative therapy

References:

Gerber, T.C., Kramer, C.M. (2014, October 10). Diagnostic and prognostic implications of coronary artery calcification detected by computed tomography. UpToDate. Retrieved from http://www.uptodate.com/contents/diagnostic-and-prognostic-implications-of-coronary-artery-calcification-detected-by-computed-tomography


http://circ.ahajournals.org/content/108/8/e50.full

Pulmonary Embolism

Definition and pathophysiology
Pulmonary embolism is a potentially life threatening emergency which refers to the obstruction of the pulmonary arteries (one of the vessels that leads out of the heart into the lungs) or one of its branches by thrombi most commonly. Thrombi are platelet groupings that pathologically grow within the vasculature anywhere in the body and can eventually break off lodging into smaller vessels elsewhere. In the coronary vessels of the heart, thrombi can lead to occlusion and cause heart attacks, but in the vasculature of the lung, thrombi can lodge leading to pulmonary embolism. There are a number of causes for thrombus formation, but the basic idea revolves around Virchow’s triad of vessel lining injury, blood not moving, or conditions where the blood clots inside of a vessel too easily.

You may have heard in the past that if you’re on a long transcontinental flight you should get up and walk around, stretching your legs. The reason is to help prevent the formation of these thrombi, by sitting in one place for too long you’re keeping your blood in stasis, fulfilling one part of Virchow’s triad, giving the system the opportunity to form intra-vessel clots.

Thrombi love forming in the deep vessels of the lower extremities, if for whatever reason they break off and lodge into the small vessels of the lung, the clot will impede flow of blood to the lungs, preventing oxygenation of the blood and thus oxygen delivery to the rest of the vital organs. It’s important to keep in mind that not all pulmonary embolisms are deadly. Some small ones can pass and be completely gobbled up by our immune system. The large ones however, can potentially cut off circulation and result in hemodynamic instability very, very quickly and so, prevention is key.

Risk factors
-Recent surgical procedure, especially orthopedic surgery
-Cancer (hypercoagulable)
-Acquired Thrombophilia (Lupus Anticoagulant, Nephrotic Syndrome, Oral Contraceptive usage)
-Inherited Thrombophilia (ie Factor V Leiden Mutation)
-Pregnancy

Symptoms/signs
-Sudden onset of difficulty breathing
-Unilateral thigh or calf swelling
-Chest pain during inhalation
-Coughing up of blood
-Increased Respiratory Rate
-Increased Heart Rate
-Lungs are clear to auscultation
-Hypotensive
-Increased Jugular Venous Distention

Cardiac manifestations/Consequences

When a clot lodges in the pulmonary arterial circuit, pulmonary vascular resistance increases which can lead to right ventricular (RV) dysfunction. Increase in right pulmonary artery pressure brings about increased right ventricular wall tension, which ultimately leads to impaired right ventricular dilatation, ischemia, and impairment. It can also lead to left ventricular (LV) filling impairment and thus reduced cardiac output and systemic hypoperfusion.
Its important to clinically evaluate such patients in order to attain early diagnosis. The most common complaint is dyspnea (82%) and the most common physical exam finding is tachypnea (62%) (Goldhaber, Visani and De Rosa, 1999). Other indicators of RV dysfunction on exam include right sided S3, accentuated P2, systemic arterial hypotension, tricuspid regurgitation murmur, elevated JVP and parasternal lift.
An electrocardiogram may also be useful in determining the severity of the PE. An anterior ischemic pattern of negative T waves in leads V1-V4 is a common finding in a massive PE, and has been shown to correlate with the severity of the PE. Other patterns include S1Q3T3, a new or incomplete right bundle branch block, a pulmonary P wave (Stein, Dalen, McIntyre 1975). Moreover, an EKG scoring system has been shown to correlate with severity of pulmonary hypertension and defect on V/Q scanning due to PE.
While echocardiogram are not shown to be useful in assessing the severity of acute
PE, it is useful in identifying severe RV dysfunction, including RV/LV end diastolic diameter >1 in the apical 4 chamber view, RV end diastolic diameter >30mm and the paradoxical RV septal motion. Another common echocardiogram finding with RV dysfunction associated with PE is the McConnel sign, which is where this is akinesia of the RV free wall but normal motion at the apex.
Troponin levels have been shown to be elevated in 30 to 40% of patients with PE, which may be due to the development of microinfarctions from abrupt increase in PA pressure and the elevation of a RB wall tension (Sohne, ten Wolde, Buller 2004). Troponins have been shown to be a risk factor for poor outcomes in acute PE and elevation of troponin T are correlated to serious complications including hypotension/shock, CPR and intubation.
RV dysfunction due to PE predicts increased PE related mortality if normatensive and hypotensive subjects are grouped together (Nijkeuter et al.). However, the ability of RV dysfunction to predict PE in purely normatensive patients is still inconclusive (Sanchez et al.).

Diagnosis
General Tests Performed for Diagnosis
-Arterial Blood Gas
-Chest X-Ray
-Electrocardiogram

Specific Tests Performed for Diagnosis:
-Spiral CT Scan
-Ventilation Perfusion Scan
-Pulmonary Angiogram
-Duplex Ultrasound
-D-Dimer (only diagnostic in low risk patients)

Treatment

Resuscitation (stabilize)
-Respiratory
Give oxygen
Consider intubation and mechanical ventilation if there is severe hypoxemia (low oxygen in the blood)
-Hemodynamics (get hypotension under control)
Give intravenous (IV) fluid, usually normal saline (no more than 500-1000 mL in one period)
If no improvement, give medication (norepinephrine, dopamine, epinephrine, dobutamine with norepinephrine)
-Anticoagulation
Heparin, if appropriate

After resuscitation (treatment after stabilized)
-Anticoagulation (if not already started)
-Inferior vena cava filter (mesh that allows blood to pass through but stops clots from traveling into the heart and lungs)
Used in people who have failed anticoagulant therapy or developed complications from it
Also used for those who have a high bleeding risk
-Thrombolytic therapy for severe cases
-Embolectomy (removal of emboli surgically or using catheters)
Appropriate in severe cases who have failed thrombolytics or cannot use thrombolytics

References:

Daniel KR, Courtney DM, Kline JA. Assessment of Cardiac Stress From Massive Pulmonary Embolism With 12-Lead ECG. Chest 2001;120;474 – 481.

Iles S, Le Heron CJ, Davies G, et al. ECG Score Predicts Those With the Greatest Percentage of Perfusion Defects Due to Acute Pulmonary Thromboembolic Disease. Chest 2004; 125;1651 – 1656.

Lualdi J, Goldhaber S. Right Ventricular Dysfunction After Acute Pulmonary Embolism: Pathophysiologic Factors, Detection, and Therapeutic Implications. American Heart Journal 1995;130;1276-1282

Nijkeuter M, Söhne M, Tick LW, et al. The natural course of hemodynamically stable pulmonary embolism: Clinical outcome and risk factors in a large prospective cohort study. Chest 2007; 131:517.

Ouellette, D. (2014, September 2). Pulmonary Embolism . Retrieved October 27, 2014, from http://emedicine.medscape.com/article/300901-overview

Sanchez O, Trinquart L, Colombet I, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review. Eur Heart J 2008; 29:1569.

Sohne M, ten Wolde M, Buller H. Biomarkers in Pulmonary Embolism. Current Opinion in Cardiology 2004;19;558-562.

Stein PD, Dalen JE, McIntyre KM, et al. The Electrocardiogram in Acute Pulmonary Embolism. Prog Cardiovasc Dis 1975;17;247-257.

Tapson, V.F. (2014, March 25). Treatment of acute pulmonary embolism. UpToDate. Retrieved from http://www.uptodate.com/contents/treatment-of-acute-pulmonary-embolism

Coronary Sinus Catheter Placement Procedure

 

Video on Bi-Ventricular Defibrillator lead placement

https://www.youtube.com/watch?v=1kHKakGI3WI

There are three phases to placement:

  1. Screening exam
  1. Introducer placement and catheter preparation
  2. Engaging the CS ostium with the catheter tip
  3. Advancing the catheter beyond the CS ostium
  4. Verifying that balloon is in the correct position
  5. Testing for satisfactory occlusion of the coronary sinus by inflation

Imaging is used to ensure catheter placement and reduce complications

  • transesophageal echocardiography
  • fluoroscopy

1) Screening exam

Look out for heart conditions that can cause complications:

  • atheromatous aortic disease – possibly pass guidewires into aorta or use retrograde aortic flow
  • previously undiagnosed thrombi, masses, valvular disease, etc. might require surgical exposure or standard sternotomy
  • persistent left superior vena cava – prevents retrograde cardioplegia depending on the caliber of the vessel; confirm with bubble contrast study or occlusive venography

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  • aortic insufficiency – may cause difficulty for antegrade cardioplegia

Investigate diameter, taper, and angle of coronary sinus

  • “deep” 4-chamber view (non-standard view)

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    • assess size of proximal CS and CS ostium to prevent occlusion by balloon placed in tapered area; if proximal CS dilated → use 2-chamber view to check dilation more distally
    • visualize side branches joining CS near ostium to prevent obstruction
    • check proximity of IVC and tricuspid valve to prevent cannulation of wrong structure
  • 2-chamber view

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    • assess CS taper and diameter to prevent balloon overinflation, occlusion, and CS injury
  • modified bivaval view (non-standard; classic working view for catheter placement)

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    • assess angle between axes of proximal CS and superior vena cava (angle typically 90⁰, guides catheter; catheters too small may dislodge, and too large may enter side branches)

2) Introducer placement and catheter preparation

  • give heparin before insertion (5000 units recommended)
  • use ultrasound for screening or real-time guidance to ensure proper right internal jugular placement
  • use shallow angle of entry (45⁰ or less) to avoid small-radius curve in catheter at insertion point
  • consider securing introducer at 2 anchor sites
  • check stopcocks of all catheter ports; locking tab for stylet should be engaged to prevent folding of the tip within CS
  • thoroughly flush pressure channel of CS catheter to get rid of bubbles (prevents poor signaling which can lead to balloon overinflation)
  • prime the cardioplegia channel with radiopaque contrast (fill the hub and channel)
  • adjust curvature of the distal catheter based on angle in modified bicaval view

3) Engaging the coronary sinus ostium with the catheter tip

It’s vital to understand the relationship between the coronary sinus, tricuspid valve, and IVC:

The IVC is right (C), CS is in a mid position (D), and tricuspid is left (E)

 

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[Deep 4-chamber view of a catheter

directed toward the tricuspid valve. The catheter

[white arrow] is again directed toward the tricuspid valve,

and appears to need to be turned “counterclockwise”

from “4 o’clock” toward the CS ostium near 1 o’clock. A

catheter directed toward the tricuspid valve does need to

be torqued counterclockwise to direct it toward the CS

ostium. The needed action is the same as what is

suggested by a direct reading of the TEE display.]

 

Identifying the coronary sinus in the modified bicaval view:

There are three “identification” landmarks that will identify the coronary sinus reliably: the Eustachian ridge, the insertion point of the tricuspid valve leaflets and tracking back from the coronary sinus in short axis.

As the catheter is approaching the ostium, a characteristic increase in amplitude of the atrial component of the electrogram as compared to the ventricular signal is noted. When such a

typical signal is obtained, the catheter is carefully advanced into the CS under fluoroscopic guidance in the LAO 30-45 view. The sheath is advanced over the EP catheter and the EP

Actual Maneuvering of the Catheter:

If the catheter tip is in the right ventricle, a small degree of counterclockwise torque is applied prior to withdrawal of the catheter to the point where the waveform changes

to a venous pattern. If IVC entry is suspected, a slight clockwise torque is applied prior to withdrawal of the catheter to the point where it appears (or to a depth of 20 cm). Either correction will usually cause the catheter to appear in the TEE image, often with the tip very near the CS ostium. (If a pulsatile waveform is seen, the catheter tip is in the RV. A venous waveform suggests IVC cannulation, but is also seen when the catheter is in the RA appendage)

cs6

Difficulties in engaging the CS:

 

cs7

 

  • Advancement beyond the coronary sinus ostium
    1. after engagement, the catheter should only be advanced centimeters at a time.
    2. fluoroscopy should be engaged at this point in order to visualize advancement and impediments
      1. these will appear as either bowing of the cath or by stopping completely
    3. catheters will advance through one of two possible routes
      1. left-superior- this is where you want to be
      2. towards the cardiac apex
    4. halting advancement
      1. Deeper placement (approx. 6-10 cm from tip to ostium) reduces the likelihood of catheter dislodgment, but obstacles may prevent deeper placement in some patients.
      2. can be achieved with pullback and turning the catheter
      3. but ultimately the “correct” depth is based on operator judgement
    5. troubleshooting
      1. pullback with turning usually helps
      2. adjustment of the distal curve which i think is based on a tool
      3. careful injection of contrast to help figure out the tributaries making sure not to cause the vessel to burst
  • Verification of Placement
    1. Done by non-occlusive fluoroscopic imaging , which is injection of contrast into a deflated balloon.
    2. Determination of fluoroscopic placement
      1. How to tell between the RVOT and the Coronary sinus: Containment of contrast within a tube like structure vs seeing dilution of the contrast with blood
  1. Final Positioning of the Cath
    1. Dependant on
      1. location of the catheter tip relative to the true location of the CS ostium.
      2. taper of the coronary sinus, you may want to adjust so that the tip of the catheter is just beyond an area of significant taper.

6) Verification of occlusion

  • estimate balloon volume to avoid CS injury from over-inflation

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  • monitoring balloon inflation – continuous fluoroscopic monitoring is done while the balloon is inflated with diluted contrast

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  • stop inflation if:
    • expanding diameter matches venography diameter
    • ventricularization pattern begins to appear
    • predicted volume reached
    • maximum recommended volume (1 mL) reached
  • inject small amount of contrast (small leak is okay if ventricularization trace present ← desired endpoint)
  • stop movement of balloon toward ostium (normal during inflation) if:
    • balloon contacts sides of CS
    • bowing of proximal catheter
  • confirm catheter depth using 2.5 cm distance between catheter tip to proximal side of balloon as reference
  • occlusive venography: after satisfactory occlusion, inject radiopaque contrast with balloon inflated
    • contrast from middle cardiac vein confirms retrograde cardioplegia will be widely distributed, persistent left SVC (vertical vessel slightly left of pulmonary artery) is absent, CS catheter depth

cs10

    • after the balloon is deflated, check the fluoroscopic field for injury, i.e. extravasation
    • tighten the locking ring at the base of the sheath to secure the catheter
    • tape the hub to the patient’s head

 

Sources:

http://market360online.com/sqlimages/1246/119090.pdf

http://cdn.intechopen.com/pdfs-wm/27006.pdf

https://crbard.com/uploadedFiles/CorpSite/Healthcare_Professionals/lt04z0094a.pdf

http://www.eplabdigest.com/article/971

https://www.youtube.com/watch?v=nxJXzYEA-WM

 

In conjunction with our ongoing efforts to encourage a healthier lifestyle and help everyone realize the importance of good eating habits, we came up with an exciting project to get everyone motivated and involved.

The Cardiovascular Institute’s First Recipe Book!!

We will be collecting recipes to put together a healthy Vegetarian Cookbook. The book will be complied using all unique vegetarian or vegan recipes from employees as well as patients and Facebook followers.

If you can all take a couple of minutes to email a recipe along with a picture (if available) of your healthiest and of course appetizing dish that would be very much appreciated. The dish can be anything from an appetizer to a main dish to a dessert. All recipes accepted! It can be a family recipe or one you received from a friend or read in a cookbook. THANK YOU IN ADVANCE!!!!

PLEASE EMAIL: OurCookbook2014@gmail.com by November 9th.

Subject Title the email with the name of the dish and your name.

In your email please include the following:

1. Name of your dish
2. The Recipe…(Ingredients and preparation method)
3. A Picture of your dish ( if available- as it would make the book much more colorful)
4. Your full name ( and if you prefer to leave the dish “ anonymous” let us know)

What is Atrial Fibrillation?

 

Your heart is separated into four chambers, a left and right atria and a left and right ventricle. Blood is efficiently pumped through the body as a result of synchronized contraction where the atria will first contract to push blood down into the ventricles and then the ventricles will pump to push blood up and out into either the body or lungs .

 

What allows for this synchrony is ‘electrical coupling’ so that when one heart cell within a chamber fires, it can tell its neighbor to also fire. Your brain isn’t in direct control of this firing, and despite your best attempts, you aren’t consciously making your heart beat nor can you make your heart beat faster or slower.

 

There are groups of specialized cells at specific points within the heart called ‘pacemaker’ cells which do this job for you. This group of specialized cells will fire at regular intervals on their own causing a cascade of firing or depolarization in adjacent heart muscle cells in a very orderly manner. This is very similar to a row of dominos that we might have set up as children where one domino falling causes the ones next to it to also fall. One pacemaker cell firing causes the ones downstream to also fire. It’s all very coordinated and very efficient.

 

Problems arise when points within the heart or even the tubes coming off the heart ‘rebel’ and decide to stop listening to the pacemaker cells and fire on their own. Atrial fibrillation is a result of progressive scarring, or fibrosis, of the atria believed to arise from either the chamber getting too large (called dilatation), genetics, or inflammation. It is hypothesized that scarring is a major factor in the development of these ‘rebellious’ heart cells. Without the control of its pacemaker, the rebel cells of the atria contract whenever they please at a VERY fast rate (150-300 beats a minute).

 

In this situation, there are essentially two bosses in the heart, the pacemaker cells and these rebellious cells. Both are trying to get everyone downstream to listen to them, some do and others don’t. It’s all very chaotic and messy. This loss of beautiful synchrony leads to ineffective pumping of the atria which then results in inefficient filling of the ventricles and finally poor blood distribution to the lungs and body.

 

Your doctor may give your atrial fibrillation a classification. This is meant to help communicate your condition to other doctors as well as help to drive treatment decisions. The classifications can be based on ECG pattern, epicardial or endocavitary recordings, mapping of atrial electrical activity or clinical features.

 

 

Atrial Fibrillation Category Defining Characteristics
First detected only one diagnosed episode
Paroxysmal recurrent episodes that stop on their own in less than 7 days
Persistent recurrent episodes that last more than 7 days
Permanent an ongoing long-term episode
Lone absence of clinical or ECG findings of other cardiovascular disease(including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years
Nonvalvular no rheumatic heart disease, prosthetic heart valve or mitral valve repair
Secondary where a pre-existing cardiac condition like a heart attack, heart surgery, pulmonary embolism or pneumonia is the cause of the AF

 

 

Symptoms of Atrial Fibrillation

AFib may be noticeable to some people while others are not aware of the the fibrillating. Symptoms range from mild to difficulty in breathing, shortness of breath, and palpitations. Additional symptoms include fatigue, weakness, dizziness, confusion,  lightheadedness, and chest pain and /or discomfort.

 

How is it diagnosed?

History and physical exam

To discover signs, symptoms, and risk factors

Electrocardiogram (ECG)

To look at electrical activity of the heart and see the atrial fibrillation

Echocardiogram

To look inside of the heart and see how it is working

Additional testing – exercise testing, Holter monitoring, thyroid testing, complete blood count (CBC), serum creatinine, analysis for proteinuria, test for diabetes mellitus

To look for the atrial fibrillation, causes, risk factors, and baseline

 

**Risk factors:

 

Heart

*Hypertensive heart disease (high blood pressure)

*Coronary heart disease

Heart failure

Heart valve disease (stenosis, regurgitation, prolapse)

Recent heart surgery (coronary artery bypass graft or CABG, cardiac valve surgery)

Rheumatic heart disease

Heart attack

Hypertrophic cardiomyopathy

Congenital heart disease (atrial septal defects, Ebstein’s anomaly, patent ductus arteriosus, etc.)

Venous thromboembolic disease (deep vein thrombosis or DVT, pulmonary embolism or PE)

Endocarditis

 

Other Risks

Long-term binge drinking of alcohol

Hyperthyroidism

Chronic obstructive pulmonary disease (COPD)

Obesity (BMI > 30 kg/m2)

Diabetes

Chronic kidney disease

Family history (1st degree relative with Afib)

Genetics (if present, usually > 1 gene involved)

Male sex

Older age

Low birth weight

Inflammation and infection

 

* Most common in developed countries

** This list does not include every possible risk factor; please refer to your doctor for more information about your risk factors

 

Drug Treatment for New Onset Atrial Fibrillation:

  1. In patients who are asymptomatic or mildly symptomatic elderly patients with cardiovascular or hypertensive issues, the first goal is to establish rate control. For rate control, the first line of therapy is typically Beta Blockers and Calcium Channel Blockers.

→ Metoprolol (Beta Blocker) and Diltiazem (Calcium Channel Blocker) are commonly used

If the patient is unresponsive to the first line of therapy, Amiodarone is next suggested.

  1. Anticoagulation is another important aspect to medical therapy for atrial fibrillation, due to the risk of forming clots, which may lead to a stroke. The patient is typically started on both Heparin and Warfarin. The patient is subsequently monitored for a therapeutic level of anticoagulation using International Normalized Ratio (INR), which is between 2 and 3.    Other anticoagulation therapy that may be used in substitution of warfarin include the following: Dabigatran, Rivaraxaban, and Apaxiban.  Although more costly, these medications don’t require monitoring of INR levels.

 

Surgical vs. Nonsurgical  Treatment

 

  1. Electrical cardioversion
  • Electrical cardioversion is a procedure where the patient receives a shock outside the chest via paddles or patches; It is used to reset the heart’s normal rhythm. The procedure is similar to defibrillation but uses lower levels of electricity
  • Before doing electrical cardioversion, provider will have the patient undergo Transesophageal echocardiography (TEE)
    • This involves using a small ultrasound device that doctors will place down your mouth and looks in and around the heart
  1. Radiofrequency ablation (RFA)
  • Ablation is used when long term medical therapy or electrical cardioversion is not effective or contraindicated in the patient
  • Before ablation is performed, electrical mapping is used to identify where the origin of the atrial fibrillation is located. the map tells which areas are creating problematic electrical signal
  • A catheter or thin flexible tube is inserted into patients blood vessels and guided to the heart. the physician carefully destroys malfunctioning tissue via extra electrical currents in the pulmonary veins
  1. AV node ablation and pacemaker placement
  • If the trigger for AF occurs in the AV node, then the AV is ablated and pacemaker is implanted
  • A pacemaker is a small device implanted with chest with wires that placed in various parts of the heart; used to regulate heart beat
  • Implanted under the skin, near the collarbone
  • Sends steady, contracting rhythm in the heart
  • Pacemaker sense when heart is too fast or too slow
  1. Open Heart Maze Procedure
  • Maze procedure is where the heart surgeon creates small cuts in the upper part of your heart; the cuts are then stitched together and scar tissue forms; the scar tissue interferes with the transmission of electrical impulses that cause AFib.

 

 

Informational Video on Atrial Fibrillation:  http://www.youtube.com/watch?v=HyQjpQf_eME

 

 

References:

 

Cheng, A., & Kumar, K. (2014, October 21). Overview of atrial fibrillation. UpToDate. Retrieved from http://www.uptodate.com/contents/overview-of-atrial-fibrillation

Rosenthal, L. (2014, August 25). Atrial Fibrillation – Practice Essentials  Medscape Emedicine. Retrieved from http://emedicine.medscape.com/article/151066-overview on October 22, 2014.

 

Ganz, L. (2014, September 11). Epidemiology of and risk factors for atrial fibrillation. UpToDate. Retrieved from http://www.uptodate.com/contents/epidemiology-of-and-risk-factors-for-atrial-fibrillation


(2014, September 14). Understand your risk for arrhythmia. American Heart Association. Retrieved from http://www.heart.org/HEARTORG/Conditions/Arrhythmia/UnderstandYourRiskforArrhythmia/Understand-Your-Risk-for-Arrhythmia_UCM_002024_Article.jsp

Indications for use of Adenosine

 

  1. Adenosine: what is it?

Adenosine is a purine nucleoside.  It forms the building blocks of energy storage and transfer in cells (ATP/ADP) as well as signal transduction within the cells (via cAMP). More importantly, it plays a role in cardioversion of SVT and in regulating blood via organs via vasodilation.

  1. Cardioversion of SVT
  • When administered intraveneously, adenosine can cause transient heart block in the AV node
  • This is mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K+ flux
  • adenosine is an endogenous nucleoside that slows the sinus heart rate (negative chronotropic effect) as well as impulse conduction through the AV node (negative dromotropic effect).
  • Adenosine is highly effective in terminating supraventricular tachycardias in which the AV node is part of a reentrant circuit 4.
  • In typical AV node reentrant tachycardia, adenosine may terminate the tachycardia either by causing block in the anterograde slow pathway or in the retrograde fast pathway.
  • Studies have adenosine is more potent in slowing anterograde than retrograde conduction through the AV node,
  • It can help terminate/cardiovert AV reentrant tracycardias (AVRT) and aV nodal reentrant trachycardias (AVNRT)
  • Fast rhythms of the heart that are confined to the atria (e.g., atrial fibrillation, atrial flutter) or ventricles (e.g., monomorphic ventricular tachycardia) and do not involve the AV node as part of the re-entrant circuit are not typically converted by adenosine. However, the ventricular response rate is temporarily slowed with adenosine in such cases.
  • Because of the effects of adenosine on AV node-dependent SVTs, adenosine is considered a class V antiarrhythmic agent. When adenosine is used to cardiovert an abnormal rhythm, it is normal for the heart to enter ventricular asystole for a few seconds. This can be disconcerting to a normally conscious patient, and is associated with angina-like sensations in the chest
  • Protocol to treat symptomatic SVT
    • Rapid IV 6mg, followed by 12mg and another dose of 12 mg if not effective
    • Vagal maneuvers should be tried first before pharmacological cardioversion
  1. Use of adenosine in Pulmonary vein isolated ablation
  • adenosine can be used to identify and eliminate dormant pulmonary vein conduction during radiofrequency ablation of paroxysmal atrial fibrillation, which in turn reduces recurrent atrial tachyarrythmias; this was shown in large, prospective, multicenter trial led by Dr. Laurent Macle, known as the ADVICE study (the Adenosine Following Pulmonary Vein Isolation to Target Dormant Conduction Elimination)
  • AF an recur in up to 50% of patient who underwent ablation, mainly due to reconnection of pulmonary veins
  • Adenosine can be used during the AF ablation to detect pulmonary vein at risk of later reconnection (dormant pulmonary vein conduction)
  • Adenosine has an indirect effect on atrial tissue, causing a shortening of the refractory period. When administered via a central lumen catheter, adenosine has been shown to initiate atrial fibrillation because of its effect on atrial tissue. In individuals with accessory pathways, the onset of atrial fibrillation can lead to a life-threatening ventricular fibrillation.
  1. use in Fractional flow reserve: FFR
  • Fractional flow reserve is defined as the pressure behind (distal to) a stenosis relative to the pressure before the stenosis. The result is an absolute number; an FFR of 0.80 means that a given stenosis causes a 20% drop in blood pressure. In other words, FFR expresses the maximal flow down a vessel in the presence of a stenosis compared to the maximal flow in the hypothetical absence of the stenosis.
  • FFR uses a small sensor on the tip of the wire (commonly a transducer) to measure pressure, temperature and flow to determine the exact severity of the lesion. This is done during maximal blood flow (hyperemia), which can be induced by injecting products such as adenosine or papaverine. A pullback of the pressure wire is performed, and pressures are recorded across the vessel.
  • Adenosine binds to the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K+ flux. It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilation of the “normal” segments of arteries, i.e. where the endothelium is not separated from the tunica media by atherosclerotic plaque. This feature allows physicians to use adenosine to test for blockages in the coronary arteries, by exaggerating the difference between the normal and abnormal segments.
  1. adenosine myocardial perfusion imaging (MPI)
  • Lexiscan / Adenosine Perfusion Imaging (L/AMPI) is a test that evaluates the blood flow to the heart at rest and under stress conditions. It is used instead of the treadmill for patients who cannot walk on the treadmill for any reason. An intravenous catheter is placed in the patient’s arm and a scanning tracer is injected. After adequate circulation, imaging of the heart at rest is done
  • The major vasodilators used for pharmacologic rMPI are adenosine, regadenoson and dipyridamole. These drugs produce coronary vasodilation resulting in hyperemia; the detection of differences in coronary hyperemia between stenosed and normal vascular territories is the basis for production of perfusion defects by MPI. Unless contraindicated, they are the first choice for rMPI pharmacologic stress and they can be combined with low-level exercise (algorithm 1) [1].
  • Contraindications:
  • Adenosine receptors are connected to Gi- and Go-coupled receptors, which, in turn, causes a decrease production in Cyclic adenosine monophosphate and therefore, causes bronchospasm. Non-selective adenosine antagonists such as caffeine or theophylline counteracts adenosine and its receptors. The relaxation effect of the airways dominate by the blocked action of adenosinergic neurons that are seen in patients that take methylxanthines to manage symptoms of an asthma attack.
  • Second- or third-degree heart block (without a pacemaker)
  • Sick sinus syndrome (without a pacemaker)
  • Long QT syndrome
  • Severe hypotension
  • Decompensated heart failure
  • Asthma, traditionally considered an absolute CI. This is being contended and it is now considered a relative CI (however, selective adenosine antagonists are being investigated for use in treatment of asthma)[14]
  • Poison/drug-induced tachycardia

3 Most Common Indications for a Pacemaker

To start off, it is important to understand some anatomy of the heart. The SA node is impulse generating tissue that begins the electrical pathway for contraction of the heart muscle. The SA node is the hearts natural pacemaker, meaning it is responsible for the normal rhythm of the heart. The AV node is a group of specialized muscle fibers located in the right atrium that receives a signal from the SA node. The AV node then regulates the impulses sent from the SA node and allows the atria and ventricles to contract in a coordinated fashion sending blood throughout the body.

PM1

Three conditions indicated for pacemakers:

1) Symptomatic bradycardia.
By definition, bradycardia is slow heart rate, specifically a resting heart rate less than 60 beats per minute.

pm2

It is important to note that some people may be bradycardic and not have any symptoms. This can be a normal variant, especially in athletes and young persons. However, if you start to experience dizziness, weakness, fatigue, confusion, shortness of breath or chest pains, you should report these symptoms to your doctor for possible evaluation.

2) Third Degree Heart Block
Permanent Pacemaker implantation is indicated for third-degree heart block. Third- degree heart block is also referred to as complete heart block. It is a disorder of the cardiac conduction system, specifically in the AV node. Or more simply put, electrical impulses are not making their way through the heart tissue to cause proper muscle response.

pm3

3) Second degree heart block
Second degree heart block comes in two types, Type I and Type II. Both are described as a disruption in the impulse traveling from the AV node to the ventricles, but not as severe as third degree.

pm4

Second degree type II heart block in an asymptomatic patient is an indication for pacemaker implantation because of the possibility of progressing to a complete heart block.
Indications for permanent pacing in second-degree AV block are as follows: Second degree AV block associated with bradycardia, heart failure, neuromuscular diseases or asystole; Type 2 second degree AV block with wide QRS complexes; Asymptomatic Type 1 second degree AV block with the block at the level of the ventricles.

Reference:
http://emedicine.medscape.com/article/161919-treatment#a1156

5 Ways to Prevent a Heart Attack

You are never too young or too old to keep your heart healthy. Start at an early age to prevent heart disease. Making smart decisions now can prevent you from having a heart attack.

1. Eat a healthy diet
The food you eat plays a significant role in your health. A heart healthy diet comprised of mostly vegetables and fruit. Fruits and vegetables are packed with antioxidants, which fight free radicals in your body to protect your heart and to prevent cancer. Limiting fat, especially saturated and trans fat, is critical because they increase your cholesterol and contribute to coronary artery disease. Sources of saturated and trans fat include red meat, dairy products, deep-fried food, bakery products, packaged snack foods, and margarines so they should be avoided at all cost.

2. Maintain a healthy weight
Being obese or overweight puts more strain on your heart. It increases your risk of heart disease, high blood pressure, diabetes, and high cholesterol. Calculate your BMI to determine whether or not your weight is in a healthy range. A BMI between 18.5-2.9 is considered healthy, 25-29.9 is overweight, and >30 is obese. Another way to assess your weight is measuring your waist size. Males with a waist circumference > 40” and females with a waist circumference >35” are at higher risk of developing heart disease. By keeping a healthy weight, your heart will not have to work as hard.

3. Exercise Regularly for at Least 30 minutes every day
Combining regular exercise with a healthy diet will help control your weight. Being physically active at a young age helps you stay active throughout your life. As you get older, your metabolism slows down so it becomes easier to gain weight. It is important to get at least 30-60 minutes of moderate to vigorous exercise every day. Get as much physical activity as you can with everyday activities by gardening, taking the stairs, or walking the dog.

4. Don’t Smoke
One of the most significant risk factors for developing heart disease is smoking or using tobacco of any kind. Tobacco contains chemicals that directly damage your heart and blood vessels. They eventually cause a narrowing of the arteries in your heart and can ultimately lead to a heart attack. Furthermore, carbon monoxide replaces the oxygen in your blood, thus bringing less oxygen to your heart and the rest of your body. When you quit smoking, you can decrease your risk of heart disease close to that of a non-smoker.

5. Prevent or Control Diabetes
Diabetes itself is a risk factor for developing heart disease. Diabetics are twice as likely as non-diabetics to develop heart disease or a stroke and it tends to occur at an earlier age. The American Diabetes Association recommends screening with a fasting blood sugar at age 45 and re-testing every three years. If you have a family history of diabetes or are overweight, you may want to get screened at an earlier age. If you have diabetes, it is critical to monitor your blood sugar levels. Heart attacks in diabetics tend to be more serious and have a higher mortality rate. Controlling your blood sugar prevents the narrowing or blockage of your arteries and thus decreases your risk of a heart attack.

References:
1. http://www.heart.org/HEARTORG/GettingHealthy/Preventing-Heart-Disease—At-Any-Age_UCM_442925_Article.jsp
2. http://diabetes.niddk.nih.gov/dm/pubs/stroke/
3. http://www.mayoclinic.org/diseases-conditions/heart-disease/in-depth/heart-disease-prevention/art-20046502
4. http://www.cdc.gov/healthyweight/assessing/index.html


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