Monthly Archives: August 2014

By Minh Nugyen OMS III Western University of Health Sciences-Pomona, CA

Mitral Valve Prolapse and When to Have Surgery

What is mitral valve prolapse?

The mitral valve consists of two flaps that open and allow blood flow from the left atrium to the left ventricle. It prevents backward flow into the left atrium when it closes. In mitral valve prolapse, one or both flaps of the valve collapse backward into the left atrium and unable to close completely. In some cases, this lets a small amount of blood lead backward through the valve, and may cause a murmur.


Is mitral valve prolapsed dangerous?

            No, in most cases, mitral valve prolapse does not affect one’s health. However, in some cases where mitral valve prolapse becomes worse and causes significant valve leakage, or regurgitation, treatment is required.

When is surgery indicated for mitral valve prolapse?

According to the ACC/AHA, repair of mitral valve is recommended over replacement in most patients with moderate-to-severe or severe chronic mitral regurgitation:


  • New York Heart Association (NYHA) functional Class II-IV symptoms without severe LV dysfunction (EF ≥0.30 and/or end-systolic dimension ≤55 mm) (Class I).
  • Chronic severe MR due to a primary abnormality of the mitral valve apparatus and NYHA functional Class III-IV symptoms and  mild-to-moderate LV dysfunction (EF < 0.30 and/or end-systolic dimension >55 mm) in whom MV repair is highly likely (Class IIa).


  • Asymptomatic patients with chronic, severe MR and mild-to-moderate LV dysfunction (EF 0.65 and/or end-systolic dimension ≥45 mm) (Class I).
  • Mitral valve repair is reasonable in experienced centers for asymptomatic patients with chronic severe MR with preserved LV function (EF >0.65 and end-systolic dimension < 45 mm) in whom the likelihood of successful repair without residual MR is greater than 90% (Class IIa).
  • Surgery is reasonable for asymptomatic patients with chronic severe MR, preserved LV function, new onset atrial fibrillation, or pulmonary artery hypertension (pulmonary artery systolic pressure >50 mm Hg at rest or >60 mm Hg with exercise) (Class IIa).


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Image: Classic delta wave in WPW


Pictured: The bundle of Kent is an abnormal extra or accessory conduction pathway between the atria and ventricles. This pathway may communicate between the left atrium and the left ventricle, in which case it is termed a “type A pre-excitation”, or between the right atrium and the right ventricle, in which case it is termed a “type B pre-excitation”.


Wolff–Parkinson–White syndrome (WPW) is a disorder of the conduction system of the heart that is commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles (the bundle of Kent). Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.

Signs and symptoms

People with WPW are usually asymptomatic. However, the individual may experience

  • Palpitations
  • Dizziness
  • Shortness of breath
  • Syncope (fainting or near fainting) during episodes of supraventricular tachycardia. The telltale “delta wave” may sometimes—but not always—be seen on an electrocardiogram.


Transmission of a cardiac action potential through the conduction system of the normal human heart

Electrical activity in the normal human heart is initiated when a cardiac action potential arises in the sinoatrial (SA) node, in the right atrium.  From there, the electrical stimulus is transmitted via internodal pathways to the atrioventricular (AV) node. After a brief delay at the AV node, the stimulus is conducted through the bundle of His to the left and right bundle branches and then to the Purkinje fibers and the endocardium at the apex of the heart.

The AV node serves an important function as a “gatekeeper”, limiting the electrical activity that reaches the ventricles. In situations where the atria generate excessively rapid electrical activity (such as atrial fibrillation or atrial flutter), the AV node limits the number of signals conducted to the ventricles. For example, if the atria are electrically activated at 300 beats per minute, half those electrical impulses may be blocked by the AV node, so that the ventricles are stimulated at only 150 beats per minute—resulting in a pulse of 150 beats per minute. Another important property of the AV node is that it slows down individual electrical impulses. This is manifested on the electrocardiogram as the PR interval (the time from electrical activation of the atria to electrical activation of the ventricles), which is usually shortened to less than 120 milliseconds in duration.

Individuals with WPW have an accessory pathway that communicates between the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Kent (see below). This accessory pathway does not share the rate-slowing properties of the AV node, and may conduct electrical activity at a significantly higher rate than the AV node. For instance, in the example above, if an individual had an atrial rate of 300 beats per minute, the accessory bundle may conduct all the electrical impulses from the atria to the ventricles, causing the ventricles to contract at 300 beats per minute. Extremely rapid heart rates such as this may result in hemodynamic instability or cardiogenic shock. In some cases, the combination of an accessory pathway and cardiac dysrhythmias can trigger ventricular fibrillation, a leading cause of sudden cardiac death.


One beat from a rhythm strip in V2 demonstrating characteristic findings in Wolff–Parkinson–White syndrome. Note the characteristic delta wave (above the blue bar), the short PR interval (red bar) of 80 ms, and the long QRS complex (blue bar plus green bar) at 120 ms.

WPW is commonly diagnosed on the basis of the electrocardiogram in an asymptomatic individual. In this case it is manifested as a delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval. The short PR interval and slurring of the QRS complex is actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node.

When an individual is in normal sinus rhythm, the ECG characteristics of WPW are a short PR interval (less than 120 milliseconds in duration), widened QRS complex (greater than 120 milliseconds in duration) with slurred upstroke of the QRS complex, and secondary repolarization changes (reflected in ST segment-T wave changes).

In case of type A pre-excitation (left atrioventricular connections), a positive R wave will be seen in V1 (“positive delta”) on the precordial leads of the electrocardiogram, while in type B pre-excitation (right atrioventricular connections), a predominantly negative delta wave will be seen in lead V1 (“negative delta”)


The definitive treatment of WPW is a destruction of the abnormal electrical pathway by radiofrequency catheter ablation. This procedure is performed by cardiac electrophysiologists. Radiofrequency catheter ablation is not performed in all individuals with WPW because there are inherent risks involved in the procedure. When performed by an experienced electrophysiologist, radiofrequency ablation has a high success rate. Findings from 1994 indicate success rates of as high as 95% in people treated with radiofrequency catheter ablation for WPW.

However, people with WPW who are experiencing tachydysrhythmias may require synchronized electrical cardioversion if they are demonstrating severe signs or symptoms (for example, low blood pressure or lethargy with altered mental status). If they are relatively stable, pharmacologic treatment may be used.

People with atrial fibrillation and rapid ventricular response are often treated with amiodarone or procainamide to stabilize their heart rate. Procainamide, amiodarone, and cardioversion are now accepted treatments for conversion of tachycardia found with WPW.








AV node reentry tachycardia: The basics and more advanced:


What is supraventricular tachycardia (SVT)? — Supraventricular tachycardia, also called “SVT,” is a heartbeat that is faster than normal. It usually starts and stops suddenly, without warning. SVT is also called “paroxysmal supraventricular tachycardia” or PSVT. (Paroxysmal means a sudden attack.)

 SVT happens because of a problem with the heart’s electrical system. It starts in the upper chambers of the heart, called the “atria” (figure 1). The fast heartbeat can last from a few minutes to hours, but usually lasts for 10 to 15 minutes. It often happens when you are at rest. But in some people, exercise triggers it.

 The 3 main types of SVT are called:

 ●Atrioventricular nodal reentry tachycardia (AVNRT)

●Atrioventricular reentry tachycardia (AVRT)

●Atrial tachycardia

What are the symptoms of SVT? — You might not have symptoms. But you might feel that your heart is beating too fast, beating hard, or seems to skip a beat. These kinds of heartbeat changes are called “palpitations.”


You might also feel:



●Very tired


 If you also have coronary heart disease, you might also:

 ●Have trouble breathing

●Feel a tightness in your chest

Should I see a doctor or nurse? — If you have trouble breathing or have chest pain, call Dr. Uri Ben-Zur at 818-483-3832 or dial 911. Dr. Ben-Zur is the best cardiologist in Los Angeles and can assist you on any issue that you may have with your heart. If you are concerned that you may be at risk, schedule an appointment today so we can keep your heart strong and healthy. 

 If you do not have these problems, but you often feel your heart beating fast or irregularly, talk to your doctor or nurse.

 Is there a test for supraventricular tachycardia? — Yes. Your doctor or nurse will do a test called an electrocardiogram, also known as an “ECG” or “EKG.” This test measures the electrical activity in your heart.

 Other possible tests include:

 ●Holter monitor – This is a small, portable machine you wear that records all the heart’s electrical activity over 1 or 2 days.

●Event or loop monitor – These are similar to Holter monitors but smaller, because they don’t record all the time. Instead, you start the monitor when you feel symptoms. Your doctor will likely have you wear one of these monitors every day for about a month.

How is supraventricular tachycardia treated? — The treatment depends on the cause of the tachycardia. When your heartbeat is very fast, your doctor might suggest ways to slow it down. He or she might have you cough, or bear down as if you’re having a bowel movement. He or she might also suggest that you put an ice pack on your face. Doing these things can affect the nerve that helps control your heartbeat.

Other treatments can include:

 ●Medicines to control the speed or rhythm of your heartbeat

●A treatment called “cardioversion” that involves applying a mild electrical current to the heart to fix its rhythm

●Treatments called “ablation.” Ablation treatments use heat (called “radiofrequency ablation”) or cold (called “cryoablation”) to destroy the small part of the heart that is sending the abnormal electrical signals.




P wave is falling below the QRS complex


Atrioventricular nodal reentrant tachycardia (AVNRT) is one of the common supraventricular tachycardias (SVTs). As with the majority of SVTs, the QRS complex in AVNRT is usually narrow (ie, ≤120 msec), reflecting normal ventricular activation through the His-Purkinje system. There are a number of synonyms for AVNRT, including:

●AV nodal reentry

●Reciprocal or reciprocating AV nodal reentrant tachycardia

●Junctional reciprocating tachycardia

Symptoms — the symptoms associated with arrhythmia episodes are nonspecific. The nature and severity of symptoms are often influenced by the rate of the tachycardia. Because of the paroxysmal nature of the arrhythmia, the onset and termination of the symptoms are usually sudden.

Patients most commonly complain of palpitations, an odd feeling in the chest, and, on occasion, lightheadedness. Those with significant heart disease may have additional symptoms such as dyspnea and chest pain. Some patients with AVNRT have a feeling of polyuria and experience a diuresis during or after AVNRT; the mechanism probably is related to an elevated mean right atrial pressure and plasma level of atrial natriuretic peptide, which are present during the arrhythmia .


V nodal reentry presents with the following symptoms and frequencies:

●Palpitations – 98 percent

●Dizziness – 78 percent

●Dyspnea – 47 percent

●Chest pain – 38 percent

●Fatigue – 19 percent

●Syncope – 16 percent

Dual AV nodal physiology — the simplest concept of AV nodal physiology that allows for reentry involves separate electrical pathways within or proximal to the AV node.

●One pathway conducts rapidly and has a relatively long refractory period. This is called the fast pathway (common).

●The second pathway conducts relatively slowly and has a shorter refractory period. This is called the slow pathway (uncommon).

See these Youtube videos for more information with visual references:

The origins of the fast and slow pathways are probably in perinodal atrial tissue. These pathways join and enter a final common pathway in the AV node. While atrial tissue above the AV node appears to be part of the reentrant circuit, the bundle of His below the node is probably not a necessary part of the circuit. This can be illustrated by the following observations:

●AVNRT is associated with 2:1 AV block in approximately 10 percent of patients [15]. With this form of block, the completion of two complete circuits is evidenced by two retrograde P waves while only one of the impulses traverses the His bundle on the way to the ventricles. Thus, the bundle of His is not a required component of the circuit. The AV block in this setting is probably a functional infranodal block within the bundle of His.


General features — The usual electrocardiographic features of AVNRT include the following:

●The rate is generally between 120 and 220 beats/minute.

●In the common form, retrograde atrial activation and anterograde ventricular activation occur almost simultaneously. The P wave, therefore, is usually buried within or fused with the QRS complex. A component of the P wave is often evident slightly after, or less commonly before, the QRS. When the P wave occurs shortly after the QRS complex, the fused waveform can produce a pseudo-R’ (a second R wave) in lead V1 and a pseudo-S wave in the inferior leads.

●If the initiation of the tachycardia is captured on a tracing, the tachycardia often begins with a premature atrial depolarization with sudden prolongation of the PR interval.

●In the uncommon form of AVNRT, retrograde atrial activation occurs long after ventricular activation, resulting in a P wave so late after the QRS complex that it appears to be occurring shortly before the next QRS complex. This pattern resembles that seen in atrial tachycardias. In such cases, an EP study may be required to define the arrhythmogenic mechanism.

Because of the relationships between the QRS complex and the following P wave, the common form of AVNRT is referred to as a “short RP tachycardia,” while the uncommon form is a “long RP tachycardia.”

P wave morphology — The axis of the P wave, when seen, is abnormal due to retrograde atrial activation. This is usually manifested on the electrocardiogram by inverted P waves in leads I, II, III and aVF. In atypical AVNRT, however, the P wave is generally upright or isoelectric in lead I.

ST segment depression — Significant ST segment depression during tachycardia has been observed in 25 to 50 percent of patients with AVNRT, although it is more commonly seen in those with an AV reentrant tachycardia associated with an accessory pathway. Although the presence of ST segment depression suggests myocardial ischemia, the majority of patients do not have underlying coronary artery disease; in these patients ST segment changes represent either repolarization changes or a retrograde atrial activation.

T wave inversions after termination — After acute termination of AVNRT and other paroxysmal SVTs, T wave inversions may be seen in the anterior or inferior leads. In a series of 63 patients with paroxysmal SVT, such abnormalities were present in about 40 percent of patients. They may be seen immediately upon AVNRT termination or may develop within the first six hours, and can persist for a variable duration (mean of 34 hours). The occurrence of negative T waves is not predicted by clinical parameters, tachycardia rate or duration, or the presence and extent of ST segment depression during the tachycardia. They are not the result of coronary artery disease, but are repolarization abnormalities, likely due to ionic current alterations resulting from the rapid rate.


THERAPY — The general approach to the therapy of AVNRT includes two components, acute termination of the arrhythmia and prevention of recurrent episodes.

Acute termination — The recommended approach to acute termination of AVNRT depends upon the severity of the arrhythmia.

Hemodynamic collapse or severe symptoms — Severe hemodynamic decompensation is uncommon in AVNRT. Hemodynamic compromise may be manifested clinically by one or more of the following features:

●Hypotension and shock

●Angina pectoris

●Shortness of breath and/or heart failure

●Syncope or near-syncope

In such cases, immediate restoration of normal sinus rhythm is essential. Based upon their speed of onset and high therapeutic efficacy, treatment options in this setting include:


●DC Stable patient — There are few data regarding the optimal approach to the acute termination of AVNRT. Management recommendations are based upon an understanding of the properties and risks of the treatment options. In 2003, the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) published guidelines for the management of patients with supraventricular arrhythmias, which included recommendations on the acute treatment of AVNRT [36]. Our recommendations are in general agreement with those guidelines.

In patients who are hemodynamically stable, whether symptomatic or asymptomatic, we suggest the following approach to acute termination of the arrhythmia:

●Vagal maneuvers (eg, Valsalva maneuver or carotid sinus massage) — Vagal maneuvers increase parasympathetic tone, which produces a gradual slowing of conduction in the antegrade slow pathway. Slowing and eventual block in the antegrade slow pathway are the usual cause for arrhythmia termination with these interventions, although they can also produce abrupt block in the retrograde fast pathway. Vagal maneuvers are less effective in hemodynamically unstable patients, since this state is typically characterized by increased sympathetic tone and parasympathetic withdrawal.

●Adenosine — If vagal maneuvers cannot be performed or if they fail to terminate the arrhythmia, adenosine is usually the first pharmacologic agent administered. The advantages of adenosine over other agents include rapid onset and a short half-life. Adenosine terminates AVNRT in over 80 percent of cases. It is well tolerated in most patients, with the exception of those with severe bronchospastic asthma or severe coronary artery disease. Detailed discussions of the use of adenosine for the evaluation and termination of SVTs are presented separately.

●Nondihydropyridine calcium channel blockers — If adenosine is ineffective, intravenous verapamil and diltiazem can be used to terminate AVNRT. These drugs are generally well-tolerated, although potential adverse effects include hypotension (due to both negative inotropic and vasodilatory effects) and bradycardia.

●Beta blockers — Intravenous beta blockers (eg, metoprolol, esmolol), are alternatives to verapamil or diltiazem in patients who do not respond to or are intolerant of adenosine. Similar to the calcium channel blockers, beta blockers have the potential to cause hypotension and/or bradycardia, and therefore they should be used cautiously, particularly if calcium channel blockers have already been administered.

Because of their longer half-lives, verapamil, diltiazem, and beta blockers have the potential to suppress arrhythmia recurrence. Thus, these drugs should be used in patients who have early arrhythmia recurrence after termination with adenosine.

Pill-in-the-pocket — In selected patients with infrequent, well-tolerated, and long lasting episodes of AVNRT, a single dose of an antiarrhythmic agent that was previously evaluated under observation can be effective for acute termination of the arrhythmia. This strategy can both reduce the need for emergency department visits and avoid chronic medical therapy or invasive procedures. This approach has been evaluated with the nondihydropyridine calcium channel blockers, beta blockers, and the class IC antiarrhythmic drug flecainide. However, based upon the efficacy of alternative, lower-risk therapies, flecainide is rarely used in the management of AVNRT.

Chronic therapy — Not all AVNRT patients require long-term suppressive therapy. The decision to treat is based upon the following factors:

●The frequency of the arrhythmia

●The significance of the symptoms

●Patient tolerance of medications

●Patient preference

Patients with symptomatic and/or frequent episodes of AVNRT are generally treated with either catheter ablation or chronic suppressive pharmacologic therapy. There are few data to guide the selection of a specific therapy, and choices are influenced by patient preference. The 2003 ACC/AHA/ESC guidelines on the management of supraventricular arrhythmias included recommendations for the chronic therapy of AVNRT, and as with acute therapies, our recommendations are in general agreement with those guidelines.

No treatment — Patients with infrequent and well-tolerated episodes of AVNRT may choose no chronic therapy. Such patients can be taught to terminate the arrhythmia using safe vagotonic maneuvers, particularly the Valsalva maneuver and its variants.

Pharmacologic therapy — There are few data comparing the relative efficacy of various agents. Because they are effective and well tolerated, the medications that are most commonly used for the chronic suppression of AVNRT are the nondihydropyridine calcium channel blockers verapamil and diltiazem, and ß-blockers.

Among patients who do not respond to diltiazem, verapamil or ß-blockers and who do not want to pursue EP study and ablation, the following antiarrhythmic drugs may be considered:

●Flecainide (class IC)

●Propafenone (class IC)

●Sotalol (class III)

●Amiodarone (class III)

However, due to the potential for significant toxicities, including proarrhythmia, the use of class I and class III antiarrhythmic drugs for the management of AVNRT should be reserved for rare cases and should be administered in consultation with an electrophysiologist. In particular, because of the risk of toxicities with long-term use, amiodarone is usually avoided in young patients.

Catheter ablation — Catheter ablation offers the opportunity for definitive control of the arrhythmia and the avoidance of chronic medical therapy. However, ablation incurs the risks of procedural complications, including a 1 percent risk of heart block requiring a pacemaker. Due to its favorable efficacy and safety profile, this option is increasingly favored among patients with recurrent AVNRT.

The general approach to the catheter ablation of AVNRT is based upon the concept of dual AV nodal pathways. The most common AVNRT circuit (80 to 90 percent) involves antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. The most common ablation target is the posterior slow pathway (figure 8) since ablation here carries the lowest risk of AV block, preserves fast pathway function (and a normal PR interval post-ablation), and is facilitated by reliable anatomic and electrophysiologic landmarks. The anterior fast pathway can also be ablated, but this approach is now limited to a few special circumstances since fast pathway ablation results in a long PR interval during sinus rhythm and is associated with a higher risk of heart block.

In the hands of experienced operators, the posterior approach eliminates arrhythmia recurrence in over 95 percent of patients. Evidence of dual pathway physiology can persist in one-third to one-half of cases, but it is not necessary to eliminate all slow pathway conduction to achieve clinical success (ie, elimination of arrhythmia recurrence).

The anterior approach to ablation targets the fast pathway in the anterior third of Koch’s triangle, somewhat anterior and proximal to the His Bundle. Although the success rate rivals the posterior approach, the risk of creating complete AV block with ablations in this area is higher than in the posterior third of Koch’s triangle. The anterior approach is now limited to unusual circumstances, such as patients with a previously unsuccessful posterior pathway ablation or those with a markedly prolonged baseline PR interval and absent antegrade fast pathway conduction in whom posterior pathway ablation may result in complete heart block and the need for a permanent pacemaker.

The most significant potential complication of RFA for AVNRT is AV block. Complete AV block is less common (about 1 percent, range 0 to 3 percent) with the posterior than the anterior approach. Older age and baseline PR interval prolongation are predictors of an increased risk of post-ablation AV block.

AV block may not be immediately observed, but may progress following the procedure. However, this is extremely rare in patients who did not have transient AV block during the ablation. The use of cryothermal ablation of the slow pathway is an approach that may reduce the potential for AV block; the ability to test prospective ablation sites before permanent destruction can prevent this inadvertent complication.

Catheter ablation in patients with cardiac implantable electronic devices — On occasion, catheter ablation is performed in patients who have a permanent pacemaker or implantable cardioverter-defibrillator (ICD). While transient elevations in pacing thresholds and diminished electrograms may be observed, these changes are rarely persistent or prolonged.

Pharmacologic therapy versus ablation therapy — AVNRT is usually well-tolerated, and a variety of treatment options are safe and effective. Thus, in the absence of compelling data favoring one therapy over another, the choice of chronic treatment strategies is influenced by patient preference.

The relative efficacy and costs of catheter ablation and medical therapy were compared in a series of 79 patients with newly documented SVT who were treated with either ablation or pharmacologic therapy, based upon patient preference. After a follow-up period of 12 months, both medication and ablation decreased the frequency of arrhythmia-related symptoms, but ablation was more likely to result in complete abolition of symptoms (74 versus 33 percent). Although ablation was initially more costly, the potential long-term costs were estimated to be similar after 9 to 12 years because of the cumulative cost of pharmacologic therapy.

Generally speaking, catheter ablation and medical therapy are comparable in both cost and efficacy, with ablation particularly useful in patients with frequent symptomatic episodes. Most of these studies evaluated patients with drug-refractory AVNRT, a population in whom catheter ablation would be expected to perform well. However, catheter ablation may also be cost-effective as initial therapy for patients with paroxysmal AVNRT.

When working with a patient to select a treatment strategy, the following issues should be considered:

●Many patients with well-tolerated symptoms prefer a more conservative initial approach, with either no specific therapy or pharmacologic suppression.

●If pharmacologic therapy fails or if the side effects of chronic medications are poorly tolerated, patients often prefer EP study and ablation.

●For patients who prefer definitive therapy, even for rare, well-tolerated episodes, catheter ablation is a reasonable option.

●For patients with episodes of AVNRT that are poorly tolerated (eg, associated with near-syncope or syncope, angina, or severe dyspnea), we suggest catheter ablation as initial therapy. In such cases, the risks associated with recurrent arrhythmic events (eg, syncope with associated trauma) outweigh the procedural risks. In addition, the potential for definitive therapy makes ablation preferable to medical therapy in this setting.


References: Up-To-Date:


Definition  Once cardiac catheterization identifies blockage, interventional procedures can be performed. These procedures are an extent of the cardiac catheterization transitioning from probing to treatment.

Balloon Angioplasty: The technical name for balloon angioplasty is percutaneous transluminal coronary angioplasty (PTCA) or percutaneous coronary intervention (PCI). As the name suggest this procedure adds a small balloon at the tip of the catheter and inserted at the narrowed or blocked portion of the coronary artery. Once the balloon is in place it is inflated which compresses the plaque or any type of blockage material is pushed against the arterial wall. The overall width of the artery is widened and the blood flow is improved.


Before Angioplasty


After Angioplasty



Balloon angioplasty with stenting 

In most cases, balloon angioplasty is performed in combination with the stenting procedure. A stent is a small, metal mesh tube that provides a structural support inside the artery.
heart_stents 453gg34 Stent on a Balloon
A stent is fitted with a balloon catheter and inserted to the narrow artery. The balloon is inflated and stent is also expanded as well. The balloon is deflated and removed and the stent is left in the artery holding the diameter wide permanently.


The angiography shows the restoration of blood circulation beyond the stent placement.



Cardiac Catheterization and Coronary Interventional Procedures (ClevelandClinic)

General principles of the use of intracoronary stents (UptoDate)


Original recipe makes 4 servings
  • 20 mins
  • COOK30 mins
  • READY IN50 mins


  1. Bring 1 1/4 cup of no salt vegetable broth and water to a boil in a saucepan, stir in couscous, and mix in salt and black pepper. Reduce heat to low and simmer until liquid is absorbed, about 8 minutes.
  2. Heat 3 tablespoons olive oil in a skillet over medium-high heat; stir in pine nuts and cook, stirring frequently, until pine nuts smell toasted and are golden brown, about 1 minute. Remove from heat.
  3. Heat remaining 2 tablespoons olive oil in a saucepan; cook and stir garlic and shallot in the hot oil until softened, about 2 minutes. Stir black olives and sun-dried tomatoes into garlic mixture and cook until heated through, 2 to 3 minutes, stirring often. Slowly pour in 1 cup of no salt vegetable broth and bring mixture to a boil. Reduce heat to low and simmer until sauce has reduced, 8 to 10 minutes.
  4. Transfer couscous to a large serving bowl, mix with sauce, and serve topped with parsley and pine nuts.

“Your cholesterol is high,” said your physician, but what exactly does that mean?
There are different kinds of cholesterol.
HDL cholesterol (high-density liproprotein), commonly known as “the good cholesterol” plays a protective role in cardiovascular diseases. HDL removes fats and cholesterol from within the cells and artery walls, and transport them to the liver for excretion or reutilization, therefore preventing plaques, or thrombus, in the arteries.

LDL cholesterol (low-density lipoprotein), due to their low density, can easily build up in the walls of the blood vessels, causing blockages that can lead to heart attacks. This is the reason why LDL cholesterol is commonly known as “the bad cholesterol.”

Triglycerides are another factor that physicians look at when reviewing your cardiovascular risk. Simply put, triglycerides are fat in the blood that is used as fuel for the body. Extra triglycerides are stored in different places, commonly the hips and the belly, for later use. High triglycerides lead to a greater chance of heart disease and pancreatitis (inflammation of the pancreas).

Now, where does salmon come into play?
Salmon is a very rich source of omega-3 fatty acids. Omega-3 fatty acids can lower triglyceride levels by approximately 50 percent. Consequently, since triglyceride concentration is a determinant of LDL cholesterol, lowering triglycerides will also decrease the LDL cholesterol, reducing the risk of plaque or blockage formation in the blood vessels.

Another common source of omega-3 fatty acids is fish oils. Besides lowering triglycerides and LDL, fish oil supplements also modestly raises HDL-cholesterol, “the good cholesterol.” Additionally, in adults older than age 45, fish oils can also lower systolic blood pressure by 3-5 mmHg and diastolic blood pressure by 2-3 mmHg. Generally speaking, the effects of fish oil occur within weeks of habitual consumption.

On the other hand, the most common side effect of fish oil is gastrointestinal disturbances such as nausea, which occurs in about 4% of individuals taking less than 3g/day or in 20% of individuals taking more than 4g/day. Another common side effect is “fishy taste” or “fishy burping.” One can minimize this effect by freezing the fish oil, switching to a different formulation or consumption with meals.

Fish oils are easily found over the counter in many drug stores. Lovaza or Vascepa are brand-name highly concentrated fish oils that require a physician’s prescription, mostly for adults with high or very high triglycerides. Talk to your physician about your options, as well as your medical conditions, so that your physician can recommend the best kind of therapy for you.

What is it?

It is an invasive imaging procedure that allows the doctor to look at the heart structures that include, coronary arteries, cardiac valves, aorta, and heart muscles to determine a treatment plan.


cardiac_catheterization Cardiac-Catheterization-Nurse1


How does the procedure work? 

A catheter is a long narrow tube that is inserted through a plastic introducer sheath and introduced inside the blood vessel at the arm or leg. The doctor observes the course of the catheter’s movement through a special X-ray machine towards the coronary arteries (blood vessels surrounding the heart).

How is the procedure visualized? 


Contrast material appears dark inside the coronary vessels.

Once the catheter reaches the heart the procedure goes through what is called coronary angiography. This works by injecting contrast material through the heart’s chambers, valves, and major vessels.


Narrowing of a coronary vessel

Angiography allows to detect any narrowing or blockage in the coronary artery.

In more specialized hospitals and research centers, there is a more sophisticated methods of catheterization to visualize the walls of the vessels which is called intra-vascular ultrasound (IVUS). At the tip of the catheter a sound-probe is installed and inside the blood vessels sound waves map out the detailed images of the interior walls of the arteries. This can provide a first person point of view in the arteries and the extent of the vascular disease.


IVUS allows the doctor to visualize the narrowing or blockage of arteries.


Cardiac Catheteriation and coronary interventional procedures. (Cleveland Clinic)


Vitamins are organic substances that cannot be made by humans that must be ingested in the diet in small quantities, they  facilitate normal metabolism. Of the vitamins required by the body, vitamins A,D,K, and E are called the “fat soluble vitamins” because they absorbed by the intestines in the presence of fat.

Vitamin K:

Vitamin K is found in green vegetables like broccoli and spinach, and gut micro-flora also synthesize a form of vitamin K that humans absorb. The absorption of vitamin K requires pancreatic digestive enzymes and bile salts, therefore pancreatic disease or liver disease can cause a deficiency. Bowl disease such as Crohn’s  may affect absorption and create deficiencies. Secondary deficiencies may occur through long term antibiotic use or prolonged fasting or starvation. Newborns tend to have low vitamin K levels due to low vitamin K in breast milk and the time it takes for the intestines to be colonized with vitamin K producing flora. Because of this, infants are given vitamin K injections shortly after birth to protect them from potential bleeding issues.

Vitamin K is an essential component of several enzymes that are involved in creating clotting factors and is utilized in the liver. A deficiency in vitamin K, or liver disease, can create bleeding issues. Vitamin K is also involved in enzymes that mineralize bone and studies of its significance are ongoing. Symptoms of vitamin K deficiency include: easy bruising, mucosal bleeding, splinter hemorrhages under the nails, and blood in the urine or stool. The normal daily recommended intake of vitamin K is 120 micrograms in men, and 90 micrograms in women.

Several anticoagulants, such as Coumadin, inactivate the Vitamin K dependent enzymes and by that mechanism prevent clotting from occurring. The administration of vitamin K can be used to reverse the effects of Coumadin.

A Growing Trend

In the past decades it has become increasingly popular to hear the terms, “vegetarian” or “vegan”. An entire naming system exists to describe the foods people do and do not choose to eat. There exists a wide variety of reasons ranging from personal preference, to ethical considerations, to health for why people chose not to meat or meat products. With the increasing popularity of fad diets, it can be hard to know what is good or bad for your health.

A 2008 survey found that a whopping 10% of American adults follow a “vegetarian-inclined diet”, 3.2% are vegetarian, and 0.5% of Americans (1 million people!) follow a vegan diet. With so many other Americans doing it, we might ask why? What are the benefits, the risks, and the best approach to use in order to improve overall health while reducing cardiovascular risk factors?


Following a vegetarian or vegan diet translates to eating less or no animal or meat products. Vegetarians adhere with varying levels of strictness to a no-meat policy; however some may still drink milk, or eat butter, ice cream, fish or poultry. Vegans typically follow a more strict diet that excludes animal meat and animal products. Meat products are replaced with healthy alternatives and the diet is typically based on eating leafy green vegetables and other natural, plant based foods that are low in fat and high in vitamins, minerals, and antioxidants. Avoidance of tobacco and alcohol combined with exercise and a vegetarian diet results in a lower risk of obesity, coronary heart disease, high blood pressure and diabetes type 2.

Focusing on Your Health

If you are considering or already following a vegetable-based diet you have made a wonderful choice for improving your health. Just remember it is important to pay attention to the vitamins and minerals that you consume in your food, especially the amount of Vitamin B12. For some people zinc, calcium, and Vitamin D may also need to be monitored. The first step to a healthy diet is eating a variety of fresh vegetables. Vitamin B12, or cyanocobalmin, is primarily obtained through animal products, so those who consume some animal products are at less risk of deficiency. If you don’t consume animal products, supplements or fortified foods can be purchased to boost your B12 intake. Those deficient in Vitamin B12 may suffer from anemia or feel more tired than usual. They may also experience neurologic problems; the elderly are also at an increased risk of B12 deficiency due to an aging gastrointestinal system. Zinc is important in wound healing and helps your body to build immunity. Zinc can be found in grains, legumes, and nuts. Calcium and Vitamin D are important in bone formation. Calcium can be supplemented as well as being found in foods like broccoli, kale, turnip and lime-processed tortillas. Vitamin D is produced naturally from sun exposure and is also found in fortified foods and supplements.

With some consideration, great benefits can be obtained from following a plant-based diet. If you have questions or concerns about the process, or if you don’t know where to start, just ask. We are here to help! 2014. 

Keywords: vegan, vegetarian, diet, health, vitamins, vitamin B12, vitamin D, zinc, calcium, deficiency.


Most people are familiar with the morning rush from that first cup of coffee, or the quick pick-me-up from an afternoon soda. Developers of highly caffeinated energy drinks have made fortunes from campaigns directed at youths with catchy names and sugary beverages. Caffeine is one of the most widely used substances in the world; up to 90% of adults consume caffeine daily. With such rampant use, we may ask, is it safe? And at what level?

Caffeine is commonly found in coffee, tea, soda, energy drinks, as a supplement, in chocolate, and in some coffee flavored ice creams. Based on data collected from observational studies, it appears that consumption of up to 400 milligrams of caffeine in a day appears to be “safe”. What does that mean to the consumer? An 8 ounce cup of coffee may contain 102-200 mg of caffeine depending on the type of coffee and how it is produced. A 20 oz Mountain Dew soft drink has 118 mg. A 12 oz Pepsi has 36-38 mg, and Coke of the same size weighs in between 35-47 mg. An 8 oz Rockstar energy drink and an 8.3 oz Redbull tie at 80 mg of caffeine per serving. There is one gram of caffeine in a single Hershey’s milk chocolate kiss, and dark chocolate contains significantly more caffeine than milk chocolate.

Though widely used and found in many every day products, caffeine is a drug with numerous effects on the brain, cardiovascular, endocrine, and gastrointestinal systems. The drug works on adenosine receptors found throughout the body, acting as a key to unlock a stimulatory response. Caffeine is known for causing insomnia, headache, palpitations, dizziness, racing heart rates, tremor and diarrhea. It can also cause dangerous arrhythmias (abnormal heart rhythms), elevated blood pressure and electrolyte imbalances. At high levels, caffeine can be very dangerous or even lethal. Studies have shown that the response to caffeine varies among people based on their genetics; this explains why some people are able to drink many cups of coffee and fall fast asleep while others will have one cup early in the day and feel jittery late into the afternoon.

If a substance is so dangerous, why do people continue to use it? In studies caffeine has been shown to increase alertness and ability to concentrate at night. At moderate doses it can improve vigilance and reaction time. It can improve functioning in the sleep deprived by improving decision-making and ability to operate machinery. It is also mildly addictive and sometimes it feels as though it is “needed”.

Not good, but not all bad either. Who should reconsider?

Ultimately, you have the power to make choices about your health, but those choices will follow you into the future. The most important thing you can do for your health is to be empowered and informed so you can make wise decisions. Healthy individuals with normal blood pressures and low cardiac risk profiles may not suffer any adverse effects from using caffeine. If you have an arrhythmia, palpitations, or high blood pressure talk to your doctor about using caffeinated products. There are many safe and decaffeinated options available with the same flavor palate. If you are feeling tired or sleep deprived, consider your sleep hygiene. One 15 minute nap in the afternoon may revitalize you naturally without the added calories, sugar and cost of a caffeinated beverage. If you are still feeling tired, talk to your doctor, we are here to help.

Benefits and risks of caffeine and caffeinated beverages. 2014.

Keywords: health, caffeine, trends, culture, cardiovascular, heart, health

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