ECG of ventricular hypertrophy?

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.
ST amplitude is elevated. usually two leads are taken, i.e. V1 and V5, and the sum is greater than 35 mm.

edit: sorry, i didn't mean ST. deflection of largest amplitude in V1, V5
 
Last edited:
ST amplitude is elevated. usually two leads are taken, i.e. V1 and V5, and the sum is greater than 35 mm.

So, if the S's amplitude in V1 + the R's amplitude in V5 > 35 mm, should I order a TTE to confirm, or perform ethanol septal ablation and prescribe verapamil immediately?
 
So, if the S's amplitude in V1 + the R's amplitude in V5 > 35 mm, should I order a TTE to confirm, or perform ethanol septal ablation and prescribe verapamil immediately?

:laugh:

Usually I give my patients the option to combine the oral route with direct catheter administration. I've found it increases patient compliance.

-The Trifling Jester
 
:laugh:

Usually I give my patients the option to combine the oral route with direct catheter administration. I've found it increases patient compliance.

-The Trifling Jester

So, give them the option of verapamil, ESA, or both? That seems reasonable.
 
So, give them the option of verapamil, ESA, or both? That seems reasonable.

DP, are you serious? I seriously can't tell. I know you aren't a med student/doctor, so I just need reassurance you are joking. 🙂
 
I'm a PRE-medical student, so, yeah, I don't know a lot.

No that's ok, it's just some of the stuff you say is off the wall. Ethanol ablation is not done often, or really at all, in the US that I'm aware of for ventricular hypertrophy. You control systemic hypertension mainly, to reduce its progression. And verapamil is fine if the patient is hypertensive, but it isn't favored over any other drug class.

Ventricular hypertrophy is usually something that is found incidentally on ECG or echocardiogram. It is not a medical emergency, merely a finding. Usually the patient has systemic hypertension that has necessitated the ventricle becoming larger to pump against higher pressures. There is no specific treatment other than Ace-inhibitors and B-blockers, which have shown some efficacy in reducing progression to dilated cardiomyopathy. They are usually given because the patient is hypertensive, but I suppose you could make a case for small doses if the patient is normotensive if you find ventricular hypertrophy incidentally.

Make sense?
 
Last edited:
No that's ok, it's just some of the stuff you say is off the wall. Ethanol ablation is not done often, or really at all, in the US that I'm aware of for ventricular hypertrophy. You control systemic hypertension mainly, to reduce its progression. And verapamil is fine if the patient is hypertensive, but it isn't favored over any other drug class.

Ventricular hypertrophy is usually something that is found incidentally on ECG or echocardiogram. It is not a medical emergency, merely a finding. Usually the patient has systemic hypertension that has necessitated the ventricle becoming larger to pump against higher pressures. There is no specific treatment other than Ace-inhibitors and B-blockers, which have shown some efficacy in reducing progression to dilated cardiomyopathy. They are usually given because the patient is hypertensive, but I suppose you could make a case for small doses if the patient is normotensive if you find ventricular hypertrophy incidentally.

Make sense?

Yes, I know ventricular hypertrophy itself isn't an emergency, but it's a big sign of disease processes that could become emergent at a drop of a hat, like PAH. If I saw an V1 S wave and a V5 R wave whose amplitudes were > 35mm, I'd order a TTE to confirm and go from there.

Wouldn't verapamil + valsartan be better combo? Verapamil to ease the heart's workload, and valsartan to block angiotensin II --ACEIs don't completely eradicate angiotensin II, as some is produced outside of the renin-angiotensin system--.

Now it makes a lot more sense.
 
No a calcium channel blocker wouldnt be better than any other class of medication for LVH. There is a study out there I'm sure, but I can tell you its actually one of the last meds I'll reach for. For garden variety hypertension, even with LVH, thiazides, ACE-I, ARB's, BBlockers are my first line choices. I go to a CCB after that.

LVH is not a sign of PAH. RVH or Tricuspid regurg is.

Your discussion about ARB's vs. ACE-I's may hold some water, but I'd have to research it more. This is a moving target, and drug companies are constantly pushing ARB's because they cost more, so I wouldnt be surprised if some study has shown ARB's to be superior in some way.
 
So, if the S's amplitude in V1 + the R's amplitude in V5 > 35 mm, should I order a TTE to confirm, or perform ethanol septal ablation and prescribe verapamil immediately?

I see what you are doing here...you're confusing left ventricular hypertrophy (LVH) with Hypertrophic Cardiomyopathy. These are distinct clinical entities and their management is different. Septal ablation is not part of the treatment of LVH, and neither is verapamil part of the management of hypertension (HTN).

Septal ablation is an alternative therapy used in Hypertrophic cadiomyopathy (HCM) because the ventricular septum is asymmetrically thickened and narrows the aortic valve outflow tract. The gold standard treatment is septal myomyectomy (cutting a chunk out of the septum). Below is a link for more info, it's from 2002 but it's written by the world's expert of HCM Barry Maron.

http://jama.ama-assn.org/cgi/reprint/287/10/1308

Lastly, there are numerous criteria to identify LVH. The most sensitive is the Stanford criteria, however, this comes with the added liability of numerous false positives. The best approach would be to combine 2-3 different criteria to identify LVH.

DarkProtonics said:
Yes, I know ventricular hypertrophy itself isn't an emergency, but it's a big sign of disease processes that could become emergent at a drop of a hat, like PAH. If I saw an V1 S wave and a V5 R wave whose amplitudes were > 35mm, I'd order a TTE to confirm and go from there.
:laugh:...and where would you go?

No...LVH does not become "emergent at the drop of a hat." It is one of many signs of a chronic disease (hypertension) with a chronic course. One reason it is important to identify LVH is because it can complicate the EKG interpretation of treadmill stress tests...not because the person will die of sudden cardiac death. A TTE would be overkill if you were simply going to verify LVH...treating the blood pressure with a thiazide diuretic would be the standard approach. ACEI or ARBs would be reserved for second-drug treatment of hypertension or in special patient populations (diabetics, chronic kidney disease, post MI).
 
Last edited:
I see what you are doing here...you're confusing left ventricular hypertrophy (LVH) with Hypertrophic Cardiomyopathy. These are distinct clinical entities and their management is different. Septal ablation is not part of the treatment of LVH, and neither is verapamil part of the management of hypertension (HTN).

Septal ablation is an alternative therapy used in Hypertrophic cadiomyopathy (HCM) because the ventricular septum is asymmetrically thickened and narrows the aortic valve outflow tract. The gold standard treatment is septal myomyectomy (cutting a chunk out of the septum). Below is a link for more info, it's from 2002 but it's written by the world's expert of HCM Barry Maron.

http://jama.ama-assn.org/cgi/reprint/287/10/1308

Lastly, there are numerous criteria to identify LVH. The most sensitive is the Stanford criteria, however, this comes with the added liability of numerous false positives. The best approach would be to combine 2-3 different criteria to identify LVH.

:laugh:...and where would you go?

No...LVH does not become "emergent at the drop of a hat." It is one of many signs of a chronic disease (hypertension) with a chronic course. One reason it is important to identify LVH is because it can complicate the EKG interpretation of treadmill stress tests...not because the person will die of sudden cardiac death. A TTE would be overkill if you were simply going to verify LVH...treating the blood pressure with a thiazide diuretic would be the standard approach. ACEI or ARBs would be reserved for second-drug treatment of hypertension or in special patient populations (diabetics, chronic kidney disease, post MI).

I see, but you parsed my sentence wrong, I didn't say LVH would become emergent, I said that disease which causes it may.
 
I see, but you parsed my sentence wrong, I didn't say LVH would become emergent, I said that disease which causes it may.

Then in those instances, you treat the underlying dz. Ablations are exceedingly rare in practice. If you get into medicine, you'll hear the saying "if you hear hoofs, think horses, not zebras" often. The most common cause by of ventricular hypertrophy is Hypertension, and I can't think of an instance where hypertensive emergencies would result in ablation.
 
Then in those instances, you treat the underlying dz. Ablations are exceedingly rare in practice. If you get into medicine, you'll hear the saying "if you hear hoofs, think horses, not zebras" often. The most common cause by of ventricular hypertrophy is Hypertension, and I can't think of an instance where hypertensive emergencies would result in ablation.

I'd put my patients on an ARB/verapamil if they hypertensive w/ VH, like everyone else.
 
Ok, I'll be open minded here and entertain your arguement...(and the outside chance you've read something recently I'm not aware of).

What exactly is the basis for your preference for Verapamil in HTN?

Verapamil acts primarily as an anti-chronotropic (rate) and anti-inotropic (contractility) drug. Neither of these is the primary physiologic component underlying essential HTN. This is further evidenced by the fact that beta-blockers aren't particularly effective in treatment of chronic HTN.


Lastly, when you say "like everyone else," exactly who are you referring to? Physicians or patients?

Again, I think you are confusing Verapamil in the treatment of Hyperobstructive Cardiomyopathy (HCM) with ventricular hypertrophy secondary to chronic HTN. Verapamil is effective as an anti-inotropic agent in HCM because it decreases contractility, septal motion, and subsequent Left ventricular outflow tract obstruction.
 
Ok, I'll be open minded here and entertain your arguement...(and the outside chance you've read something recently I'm not aware of).

What exactly is the basis for your preference for Verapamil in HTN?

Verapamil acts primarily as an anti-chronotropic (rate) and anti-inotropic (contractility) drug. Neither of these is the primary physiologic component underlying essential HTN. This is further evidenced by the fact that beta-blockers aren't particularly effective in treatment of chronic HTN.


Lastly, when you say "like everyone else," exactly who are you referring to? Physicians or patients?

Again, I think you are confusing Verapamil in the treatment of Hyperobstructive Cardiomyopathy (HCM) with ventricular hypertrophy secondary to chronic HTN. Verapamil is effective as an anti-inotropic agent in HCM because it decreases contractility, septal motion, and subsequent Left ventricular outflow tract obstruction.

Verapamil's a vasodilator as well, correct? And it will prevent the heart from getting overworked, as it is trying to pump against a higher resistance, at a faster rate.

Physicians, not that I am one.
 
DarkProtonics said:
Verapamil's a vasodilator as well, correct? And it will prevent the heart from getting overworked, as it is trying to pump against a higher resistance, at a faster rate.

I will not elaborate on the pharmacology of calcium channel blockers because you can do this for yourself. Arguing with you over this is silly because you have read just enough to not know what you're talking about. I say this in the nicest possible way.

Homework assignment: read about the class effects of dihydropyridine and nondihydropyridine calcium channel blockers.
 
I will not elaborate on the pharmacology of calcium channel blockers because you can do this for yourself. Arguing with you over this is silly because you have read just enough to not know what you're talking about. I say this in the nicest possible way.

Homework assignment: read about the class effects of dihydropyridine and nondihydropyridine calcium channel blockers.

I will!
 
I'd put my patients on an ARB/verapamil if they hypertensive w/ VH, like everyone else.

DP, people are going to assume you are crazy if you start saying "what you would do" as a doctor without have gone to med school and learned the basics behind everything. Just an fyi.
 
DP, people are going to assume you are crazy if you start saying "what you would do" as a doctor without have gone to med school and learned the basics behind everything. Just an fyi.

Thanks for the info. I so badly want to shadow a physician, in order to see how these situations are *actually* handled, instead of relying on my *lame* comprehension of medicine.
 
Verapamil's a vasodilator as well, correct? And it will prevent the heart from getting overworked, as it is trying to pump against a higher resistance, at a faster rate.

Physicians, not that I am one.

Little buddy, if you prescribe verapamil in this instance, you might as well sign the death certificate. With this post in particular, you seem to have been smoking a little too much crack. Verapamil is a nondihydropyridine calcium channel blocker... so it has direct cardiac effects, like slowing the AV node. Some docs call this drug Verapakill. As above posters have said, you've probably confused HOCM and LVH. We dont really treat LVH, we treat the underlying disease process, which is usually HTN in concentric LVH.

As far as how to identify it on EKG, there are a number of methods. The one that I tend to use is the Sokolow Criteria: S in v1 + R in v5 or v6 > 35mm. The one that Ive seen most commonly used is the Cornell criteria... go look that up. You need an MD PhD to figure that one out.

Crack kills.
 
Little buddy, if you prescribe verapamil in this instance, you might as well sign the death certificate. With this post in particular, you seem to have been smoking a little too much crack. Verapamil is a nondihydropyridine calcium channel blocker... so it has direct cardiac effects, like slowing the AV node. Some docs call this drug Verapakill. As above posters have said, you've probably confused HOCM and LVH. We dont really treat LVH, we treat the underlying disease process, which is usually HTN in concentric LVH.

As far as how to identify it on EKG, there are a number of methods. The one that I tend to use is the Sokolow Criteria: S in v1 + R in v5 or v6 > 35mm. The one that Ive seen most commonly used is the Cornell criteria... go look that up. You need an MD PhD to figure that one out.

Crack kills.

I see now. Verapamil would reduce the cardiac output, and we don't want that. Well, thanks for showing me that an ARB would be a superior choice to verapamil in treating LVH due to HTN.

What's verapamil used for? Arrhythymias?
 
Yes. A dysrhythmia like a flutter will bombard the av node with way more action potentials then are healthy. Luckily av node cells are slow response cells and have a slower conduction velocity then sa node cells due to their action potentials being produced by an influx of Ca instead of Na. Normally, this slows action potentials down slightly to allow the atria to contract first and then the ventricles slightly after. So when the atrial HR is up at 250 the ventricular HR won't be at 250 but will still be unnecessarily elevated. This would be an AV block, maybe there'd be a 2:1 block so for every 2 atrial APs only 1 gets to the ventricles. So with an atrial HR of 250 you'd have a ventricular HR of 125. By blocking Ca channels it's even harder for an action potential to be generated and refractory period is longer as it's harder for Ca to leave. This lowers ventricular HR. Instead of a 2:1 block maybe you'd get a 3:1 or 4:1 block.

left ventricular hypertrophy isn't always a sign of disease. athletes who need stronger contractions for increased cardiac output during exercise may have some degree of concentric hypertrophy.

my resting HR is 48, do I have some disease? nope. i have no problems with snycope or dizziness. Just because something is different doesn't always mean it's a sign of dz that requires meds. i'm not trying to tell you you're wrong, just trying to make a point. it's something to think about.
 
Last edited:
I see now. Verapamil would reduce the cardiac output, and we don't want that. Well, thanks for showing me that an ARB would be a superior choice to verapamil in treating LVH due to HTN.

What's verapamil used for? Arrhythymias?
You're still perseverating on "treating LVH." We (and by we, I mean physicians) don't "treat" LVH per se. Just as we don't "treat" chronic white matter ischemic changes due to HTN found incidentally on head CT. We treat hypertension, in order to try to avoid further consequences, and an ARB would be as good a choice as any antihypertensive (but not necessarily THE BEST! by any means - not too many people use the expensive ARBs as first line agents).
 
Yes, be sure not to confuse regular/garden variety left ventricular hypertrophy with hypertrophic cardiomyopathy (which is a distinct clinical entity that is due to an inherited geneetic defect, and goes by several different names in the research literature - IHSS, idiopathic hypertrophic subaortic stenosis, is the old term in papers from the 1960's and 1970's, etc., then HOCM, hypertrophic obstructive cardiomyopathy, or just HCM, hypertrophic cardiomyopathy, is what they call it in the newer research papers - that terminology used to confuse the hell out of me!).

There is nothing wrong with ARB's, but as posted above by others, they haven't been shown to be superior to ACE-I for garden variety hypertension that most people have. And they are CERTAINLY expensive which is an important consideration - your patient won't take a med he/she can't afford. Also, not good to give an expensive drug if a cheaper one will work equally well and has a similar side effect profile. ARB's are definitely beneficial in certain patient groups, however.

Yes, verapamil is useful for some arrhythmias, and is also one of the treatments for hypertrophic obstructive cardiomyopathy (either that or a beta blocker). Actually some arrhythmia docs use verapamil as the preferred agent to slow down atrial fibrillation...one attending doc who is an arrythmia expert at my med center likes it a lot better than diltiazem, which is commonly used. Basically, he says that it's more potent than the diltiazem in slowing down the a. fib. and that the reason everyone uses diltiazem more is that the marketing is better for diltiazem. One thing you have to watch out for with verapamil is that it tends to cause a lot of constipation, which can limit your ability to use it, particularly in outpatients.
 
I see now. Verapamil would reduce the cardiac output, and we don't want that. Well, thanks for showing me that an ARB would be a superior choice to verapamil in treating LVH due to HTN.

What's verapamil used for? Arrhythymias?


You could use verapakill for HTN, angina, or arrhythmia. For the first two, it almost never is (unless im much mistaken). The only time Ive ever used it was as a second line agent for SVT, when 30mg of adenosine didnt work.
 
You could use verapakill for HTN, angina, or arrhythmia. For the first two, it almost never is (unless im much mistaken). The only time Ive ever used it was as a second line agent for SVT, when 30mg of adenosine didnt work.

Oh, btw, thanks for showing me the difference b/w LVH and HTOCM.
 
I'm guessing it causes constipation because it inhibits Ca influx into smooth muscle cells in the intestines thus making for weaker contractions. Sound good?
 
Top Bottom