Ask the Clinical Instructor

Part III.
In our third and final article in this series, we will touch on valve interventions that can be done in the cath lab.
In Part I (April 2008) and Part II, (May 2008), we showed different ways that the aortic valve and mitral valve can be analyzed. When gradients are found, this can often be seen with signs and symptoms. As mentioned previously, stenosis and regurgitation could be present as well. The patient can present with a variety of symptoms depending upon the severity of their valve problem.

Aortic Valve Final Analysis
When a gradient is seen, it also has to be evaluated to determine the severity, as the patient will have symptoms if the gradient affects forward flow and cardiac output. Most of the time, this severity is determined by echo. However, sometimes it is determined by usage of the Gorlin Formula. DON’T PANIC! This can be something that is easily done once the formula is available to you (it will also be required for the registered cardiovascular invasive specialist [RCIS] exam). You just plug in the number.

The Gorlin Formula for aortic valves is:

CO (in mls) / (Systolic Ejection Period [SEP] x HR) _________________________________ 44.3 x √of mean valve gradient

An Explanation of the Gorlin Formula for Aortic Valves
• CO = Cardiac output. In this formula, we must use it in the milliliter format (i.e., 6,200)
• Systolic ejection period = The period during the cardiac cycle when the valve is open. As we remember from our ‘rules,’ the aortic valve is open in systole. This will be reported in fractions of a section.
• HR = Heart rate. Including this element gives us, in the top part of the equation, the flow across the valve in 1 minute.
• 44.3 = This is a constant (sometimes seen as ‘K’) for this particular formula
• Square root of mean valve gradient = This will be the square root of the gradient identified in our interrogation of the valve.

With the following data, the hemodynamic status of the valve can be obtained:

CO = 5.2 L/min
SEP = 0.22 seconds
HR = 72
MVG = 42

Note: Depending upon your recording system, the SEP and HR are already calculated. You will have to notice whether you have a small number (like 0.22) or whether you have a larger number (like 15.84). Just remember that this is the amount of time that the valve is open for 1 minute. If your valve was only open for 0.22 seconds a minute, you wouldn’t last very long.
This gives you the amount of area that the valve is open. Now that you know the value, knowing what is normal is important. Much like “normal” hemodynamic pressures, you can get different standards of ‘normal’ from text to text. Braunwald, Grossman and Kern all reference ‘normal’ readings within these standards:

Mitral Valve Final Analysis
Guess what? The process is exactly the same, except with a few small changes.

The Gorlin Formula for mitral valves is:

CO (in mls)/ (Diastolic Filling Period [dfp] x HR) _____________________________ 37.7 x √ of mean valve gradient

An Explanation of the Gorlin Formula for Mitral Valves
• CO = Cardiac output. In this formula, we must use it in the milliliter format (i.e., 6,200).
• Diastolic Filling Period = The period during the cardiac cycle when the valve is open. As we remember from our ‘rules,’ the mitral valve is open in diastole. This will be reported in fractions of a section.
• HR = Heart rate. Including this element gives us, in the top part of the equation, the flow across the valve in 1 minute.
• 37.7 = This is a constant (sometimes seen as ‘K’) for this particular formula.
• Square root of mean valve gradient = This will be the square root of the gradient that the computer identified in our interrogation of the valve.

With the following data, the hemodynamic status of the valve can be obtained:

CO = 5.2 L/min
DFP = 0.18 seconds
HR = 72
MVG = 15

Note: Depending upon your recording system, the SEP and HR are already calculated. You will have to notice whether you have a small number (like 0.22) or whether you have a larger number (like 15.84). Just remember that this is the amount of time that the valve is open for 1 minute. If your valve was only open for 0.22 seconds a minute, you wouldn’t last very long.
Again, you must also know what normal values are for these valve areas.

Treatments for bad valves are fairly standard. The choices are generally limited to:
1. Do nothing if signs and symptoms are not life-threatening or do not greatly impact quality of life
2. Aortic valve replacement or repair
3. Valvuloplasty (commissurotomy: a cutting of two things that are joined)
4. Percutaneous valve replacement.

Due to limitations of space, we will only discuss valvuloplasty.

Aortic Valve Intervention
There are times when surgery is not an option for the patient, either due to their current medical condition, or because of desires/beliefs they hold that require them to avoid surgery. Aortic valvuloplasty can provide a temporary relief in the patient’s condition, and is quite useful for those who need immediate help, but are not quite yet stable enough for surgery.
“Balloon aortic valvotomy has only a modest hemodynamic effect in patients with calcific aortic stenosis and does not favorably impact long-term outcome… In selected cases, balloon valvotomy might be reasonable as a bridge to surgery in unstable patients or as a palliative procedure when the surgery risk is very high.”¹
In aortic valvuloplasty, a special balloon specifically intended for dilation of aortic and pulmonary valves is used. “Pre” valve gradient readings are obtained, and the balloon is inserted percutaneously and inflated. This “cracks” the stenosed valve open.
Theoretically, this then creates a larger valve opening, allowing more forward flow of blood. Ultimately, it is used as an attempt to reduce signs and symptoms rather than eliminate the actual problem.

This special, very large balloon does not expand and deflate quickly. Due to the obstruction of the outflow tract, there can be patient fainting due to the temporary stoppage of forward flow. Also, the existing flow from the contracting ventricle can also push the balloon out of the valve, creating the difficult challenge of getting the balloon centered on the valve. One trick is to insert a transvenous pacer and pace the heart at 200+/minute for the duration of the balloon inflation. Because of the reduction in forward flow with the tachycardia, the balloon can be easier manipulated to maintain its position over the aortic valve.
After balloon inflation, “post” valve gradient readings will be measured to ensure that positive changes are being made.

Mitral Valve Intervention

Unlike aortic valvuloplasty, mitral valve balloon valvuloplasty “is the procedure of choice for treatment of (symptomatic patients with moderate to severe) MS so that surgical intervention now is reserved for patients who require intervention and are not candidates for percutaneous procedure.”¹
In this procedure, the same process occurs as in aortic valvuloplasty: “pre” assessment of gradients, the ballooning process and “post” assessment of gradients. With the mitral valve, the procedure to access the valve includes the use of transeptal technique, passing of a specific balloon for use in these cases. The Inoue Balloon from Toray (Houston, TX) is advanced through the transeptal catheter to the mitral valve. It has an hourglass shape, allowing it to be appropriately centered.

As technologies advance that allow valves to be assessed in non-invasive ways, the use of these procedures will become fewer and fewer in the lab. However, there will always be patients that require these invasive assessments and interventions for numerous reasons. It is up to the cath lab professional to ensure they know how to complete these procedures. Blindly relying on the computers to complete them can lead to problems. Being able to corroborate, or dispute, those results will become more and more difficult the less that they are performed. Practicing whenever possible will lead to proficiency.

To view images related to this article, please visit: https://www.rcisreview.com/AskTheInstructorJune2008.htm

If you have any questions about this article, or you or your lab have a question about a particular topic, please send an email to tginapp@rcisreview.com. Next month, a question will be answered about correlating the 12-lead ECG to your preparation for a ST-elevation myocardial infarction case.

Reference

1. Libby P, Bonow RO, Mann DL, Zipes DP. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th Edition. Philadelphia: Elsevier Science; 2007, 1-2183.