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.
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
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:
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
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
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
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.
-Recent surgical procedure, especially orthopedic surgery
-Acquired Thrombophilia (Lupus Anticoagulant, Nephrotic Syndrome, Oral Contraceptive usage)
-Inherited Thrombophilia (ie Factor V Leiden Mutation)
-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
-Increased Jugular Venous Distention
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.).
General Tests Performed for Diagnosis
-Arterial Blood Gas
Specific Tests Performed for Diagnosis:
-Spiral CT Scan
-Ventilation Perfusion Scan
-D-Dimer (only diagnostic in low risk patients)
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)
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
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
There are three phases to placement:
Imaging is used to ensure catheter placement and reduce complications
1) Screening exam
Look out for heart conditions that can cause complications:
Investigate diameter, taper, and angle of coronary sinus
2) Introducer placement and catheter preparation
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)
[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)
Difficulties in engaging the CS:
6) Verification of occlusion
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
To look at electrical activity of the heart and see the atrial fibrillation
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
*Hypertensive heart disease (high blood pressure)
*Coronary heart disease
Heart valve disease (stenosis, regurgitation, prolapse)
Recent heart surgery (coronary artery bypass graft or CABG, cardiac valve surgery)
Rheumatic heart disease
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)
Long-term binge drinking of alcohol
Chronic obstructive pulmonary disease (COPD)
Obesity (BMI > 30 kg/m2)
Chronic kidney disease
Family history (1st degree relative with Afib)
Genetics (if present, usually > 1 gene involved)
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:
→ 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.
Surgical vs. Nonsurgical Treatment
Informational Video on Atrial Fibrillation: http://www.youtube.com/watch?v=HyQjpQf_eME
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
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.
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.
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.
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.
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.
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.
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.
What is Cardiac Resynchronization Therapy CRT, and how does it work?
WPW (Wolff-Parkinson-White Syndrome) Animation Video