Monthly Archives: February 2016

Mitral Valve Prolapse

-condition where the two flaps of the mitral valve prolapsed do not close smoothly or evenly. When the heart contracts, one or both flaps collapse back into left atrium leading to regurgitation and a potential murmur.
-most common cause of MVP is myxomatous change. Excess connective tissue that thickens the spongiosa and separates collagen bundles in the fibrosa. This is due excess glycosaminoglycans called dermatan sulfate.

Risk factors
-Increased risk in rheumatic fever, Ehler-Danlos syndrome, Marfan syndrome, polycystic kidney disease, and chest wall deformities such as pectus excavatum.
-Rheumatic fever damages the heart valves via repeated inflammation with fibrinous resolution.

Signs and symptoms
-most patients are asymptomatic
-symptomatic patients related to autonomic dysfunction, progression to mitral regurgitation, and associated complications
-symptoms related to progression to mitral regurgitation include fatigue, dyspnea, exercise intolerance, PND, orthopnea, CHF
-symptoms related to autonomic dysftn include atypical chest pain, orthostasis, syncope, and neuropsychiatric symptoms.
-symptoms related to associated complications include stroke, endocarditis, or arrythmia

Physical exam
-mid-systolic click followed by a late systolic murmur heard at the apex.
-Murmur is accentuated by standing and valsalva . This leads to decreased venous return to the heart, thereby decreasing diastolic filling and causing more laxity to the chordate tendinae. This allows mitral valve to prolapsed earlier in systole, leading to earlier systolic click and longer murmur
– Murmur is decreased with squatting.

-asymptomatic patients often require no treatment
-patients with palpitations and chest pain may benefit from beta-blockers
-patients with a hx of stroke or a-fib may require blood thinners such as aspirin or warfarin
-if associated with severe mitral regurgitation, surgical mitral valve repair or replacement may be necessary. Repair preferred to replacement. Current American Heart Association guidelines promote repair of mitral valve in patients before symptoms of heart failure develop​e



Restenosis à with only angioplasty (without stenting) restenosis occurs in 30% of cases. Bare-metal stents reduce the chance of restenosis by 20% and use of drug-eluting stents reduce risk to < 10%.

MI à can occur during the procedure (rare). Blood clots formed within the stent can block arteries causing ischemic damage. Importance of anti-coagulation.

Stroke à can occur if plaque breaks loose when the catheters are being threaded through the aorta. Blood clots can form in catheters and travel to the brain if they break loose.


Bleeding à at catheter site.

Kidney damage à from the contrast used during the procedure.

Carotid à risk of atheroembolization, to reduce the risk use cerebral protective devices. It captures the emboli during catheter manipulation, angioplasty, and stenting. During balloon inflation à bradycardia and hypotension can occur. Dissection with a carotid approach vs. femoral. Stent fractures are another possible complication 2-4 years later.  Study showed a 15% rate of fracture or deformation at 2 years and 50% rate at 4 years. Open cell stents led to deformation more frequently than closed cell stents, and the stent fractures were significantly associated with heavy calcification.


Dr. Ben-Zur a cardiologist performs Atrial Ablations. Treats atrial fibrillations in Tarzana. Treats arryhthmias in pacemakers.

US guided axillary vein insertion:

US guided axillary vein insertion:

Pacemaker Access and Lead Placement:

A-fib Catheter Ablation:

ICD Implantation Basics:

Cath Lab/Fluoro/Stent Video:

Angio Basics:

LVAD animation:

A-fib Ablation:

Imagine, a 44 y/o moderately active male presents with shortness of breath on exertion, chest discomfort, weakness, racing heart and passing out. The provider orders an ECG and the following pattern is seen:


Patient is in what is known as atrial fibrillation, or afib.

Atrial fibrillation is caused by the rapid, disorganized electrical signals that cause the atria to fibrillate, or, contract fast and irregularly. Rather than a signal coming from that of the SA node, the signal comes from the left atrium at sites of the pulmonary veins. This is a problem because the ventricles do not contract as fast as the atria do and this causes decreased blood flow into the ventricles and causes decreased cardiac output systemically. Patients with afib, due to the rapid rate at which the atrium contracts, tend to have blood pool in their atria. This is a dire problem because the patient becomes susceptible to clots which in turn can lead to a stroke.

There are several types of afib:

Paroxysmal:  faulty signal types start and stop on their own. Typically last less than one week but usually resolve more so in 24-48 hours.

Persistent: Abnormal rhythm lasts more than a week but eventually stops on its own or with treatment.

Permanent: has failed rate and rhythm control through antiarrythmics and cardioversion and normal rhythm cannot be restored. If paroxysmal or persistent become more frequent, permanent afib may occur.

There are many factors that contribute to afib, such as high blood pressure, coronary heart disease, pericarditis, heart failure, congenital heart disease, structural heart disease such as mitral valve prolapsed, congenital heart disease, sick sinus syndrome and an increased age over 75, although many cases are now being linked to an age under that of 75. Hormone imbalances such as thyroid (hyper and hypothyroid can exacerbate the likelihood as well as binge drinking alcohol consistently. Sleep apnea, high dose steroids for asthma or any other inflammatory condition can induce the chances of atrial fibrillation.

Controlling afib is of utmost importance to the provider. Anticoagulation therapy with that of warfarin, dabigatran or aspirin is essential for the prevention of clots. Calcium channel blockers such as verpamil and diltiazem; or beta blockers such as metoprolol, propanolol, esmolol and atenolol are considered first line rate control medications and also are beneficial in the acute onset of afib if it has been persistent greater than 48 hours. Digoxin can be used in the treatment of afib in patients with heart failure and decreased left ventricle function. Treating the underlying disorder such as hyper or hypothyroid as well as lifestyle changes can maximize the benefit of alleviating afib.

Patients with afib that is less than 48 hours will benefit from that of cardioversion. Those with afib lasting longer than 48 hours require thrombolytic therapy before cardioversion due to the potential from dislodging a thrombus and causing an embolus.

For those patients who fail cardioversion and rate/rhythm control with at least one of the aforementioned medications, ablation is considered to be an optimal choice for the patient. In order to ensure that a patient can qualify for an ablation procedure, a transesophageal echocardiogram, or TEE, is performed. This echocardiogram looks at both the left atrium and left atrial appendage to ensure that there is not a clot in either location. Patients are continued on thrombolytic therapy for approximately three weeks to ensure an adequate PT/INR level of 2.0-3.0 prior to procedure. Once they are able to have the procedure, a catheter is directed into the right atrium through the right femoral artery and through the inferior vena cava where it then enters into the right atrium. From there, a puncture through the atrial septum from the right to the left is then made where the provider then isolates the pulmonary veins and then ablates them. Some patients see relief right away, some patients, who have been in afib for quite some time see gradual changes.  There are patients, who, if were in permanent afib greater than six months, tend to not see any return to sinus rhythm following an ablation procedure.


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