Talk:Heart arrhythmia

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Causes[edit]

What causes arrhythmia? Are there too many things to put down? I'm sure most people come to this page, like me, because they are experiencing arrhythmia and are wondering what to do. Shouldn't there be sections here directed at the concerned layman explaining what symptoms warrant a visit to the doctor, what causes it, what triggers it, and so on. Kimholder 03:51, 28 March 2007 (UTC)


I was wondering what the relationship between antipsychotic medications with Sudden Cardiac Death warnings and Death from Cardiac dysrythmia is. Do these medications include dysrythmia in the warning? any idea whould be helpful. —Preceding unsigned comment added by 174.29.164.153 (talk) 20:11, 19 September 2010 (UTC)

Do primates experience arrhythmia in the same way that humans do? Has there been any research into arrhythmia experienced by chimpanzees, baboons, or gorillas? — Preceding unsigned comment added by 75.164.247.233 (talk) 20:34, 19 October 2015 (UTC)

ICD9[edit]

Is the ICD9 code correct? 427.9 is, I think, too specific. Even the icd9.chrisendres.com site linked to calls all of 427.x 'Cardiac dysrhythmias'. --user:Somej

SADS[edit]

Removed:

SADS, or sudden arrythmia death syndrome, is a rare condition blamed for some otherwise unexplained deaths. It is related to long QT syndrome, QT being the time taken by the heart to recover after each beat. Patients with long QT can be given beta-blocker drugs to slow the heartbeat, and are advised to refrain from competitive sports.

-> Plan to add a new page on long QT syndrome.

Over-complication[edit]

I cut the following cryptic bullet-point outline from the Diagnosis section. Some of them are now addressed (with explanation) in "Origin of impulse", but, as with most Powerpoint-style presentations detached from their lecture, I couldn't reconstruct the train of thought behind the rest of the bullets. I hope someone can add some of this content back in a way that will make sense to readers who aren't cardiologists. Hob 20:29, 2004 Sep 2 (UTC)

  • Mode of initiation
    • Automaticity
      • Enhanced or abnormal
      • Spontaneous onset of tachycardia
      • No premature beats leading to the arrhythmia
      • Gradual increase in the rate of the arrhythmia over the first 5-10 beats ("warm up")
      • EKG appearance of the first tachycardia's beat is identical to the rest
    • Reentry
      • Initiation is with a premature beat followed by a slight pause
      • This is followed by the arrhythmia (corresponding to premature beat, unidirectional block, slow conduction)
      • "Warm up" is unusual
      • EKG appearance of the first tachycardia beat need not be identical to the rest
    • Mode of termination in response to overdrive pacing (pacing the heart at a rate faster than the tachycardia rate). Sometimes the application of electrical pacing from outside the heart itself is useful diagnostically. This is most commonly done by placing an electrode into the cardiac chambers and delivering electrical current across the endocardium
      • Automaticity
        • Often shows "overdrive suppression"
        • The arrhythmia seems to be terminated by pacing only to return after several seconds with a gradual resumption of the pre-pacing rate
        • This is related to increased activity of the Na+ - K+ pump with Na+ loading. This causes the cell to have a more negative resting membrane potential and takes longer to reach threshold.
      • Reentry
        • Often terminates in response to overdrive pacing
          • Without subsequent arrhythmia resumption

          Tachycardia stops because paced impulses have entered circuit in both limbs causing bi-directional block

(Also, I really can't figure out what this paragraph was trying to say:)

The precise role of triggered activity as a mechanism on human arrhythmias has not been studied in adequate detail to characterize modes of initiation or response to pacing. Other means exist to differentiate more clearly among arrhythmias at the time of invasive electrophysiologic study.


Arrythmia[edit]

Cardiac dysrhythmia is technically more correct, as arrhythmia would imply that there is "no rhythm,"

In Greek "Rhythmia" means evidently "Rythm", (the Greek one being the original). So "Arrhythmia" indeed (not implied at all) means "no rhythm" as it is stated in the article.

But why this is not correct???. "No rhythm" doesn't mean "No pulse" or “No bit”. "Arrhythmia" means simply "pulse without rhythm".

Yet, I can still support the article’s suggestion, saying (as a Greek) that the word "Dysrtythmia" (Bad-rhythm) is also correct and identical in meaning (literature-wise - not aware if also medically). I guess that “Bad-rhythm” and “No-rhythm” is logically the same thing. I also guess that we could say “Mal-rhythm”..

--62.38.24.151 Dimitri GIANNAKOPOULOS / dimitri999@lycos.com / 00:20, 21 November 2005 (UTC)

Good points, but "arrhythmia" is more commonly used. Andrew73 02:35, 21 November 2005 (UTC)
Dysrhythmia is the more accurate term, and the term taught at my medical school. Visium 10:22, 24 August 2009 (UTC)

Defibrillation[edit]

I found this in the main article, so I transferred it to discussion:

" "In defibrillation, the recipient has lost consciousness so there is no need for sedation."

As someone who has recently had 17 defibrillations from an implanted unit, I can state, unequivocally, that it hurts like hell and the shock comes before there is any loss of consciousness. " Snodawg 22:32, 3 February 2006 (UTC) (P.S. I did not type this originally, merely transferred it)


I have sinus arrythmia and tried searching for it on here to see what we have and nothing on this page talks about it though it is one of the most common forms of arrhythmia for athletes and adolesence. I think it should be added. Anomalycp 18:01, 26 April 2006 (UTC) I stand corrected from the opening paragraph, perhaps we need to change it to a subheading in the "common arrhythmias" section. --User:Strolch1983 German wikipedia / 15:02, 27 March 2006 (UTC)

German wiki[edit]

Hallo, if you are ever interested in writting an article for the reentry mechanism in english, you can link it, if you want, with the German wikipedia article "Kreisende Erregung". best greetings. --Strolch1983

Computer model of reentry and fibrillation[edit]

I produced a PC based model that dynamically illustrated the mechanisms of reentry and fibrillation and other cardiac behaviour. I did this for my masters thesis in Biomed Engineering.

It allowed the student to set up the preconditions for the arrythmia and then watch it develop. I called it XCITE.

This was fifteen years ago. I don't know if it was ever picked up by educators. It was good.

Too fast/too slow/skip a few: my heart.[edit]

I have been searching the web for information, yet finding anything in "laymans" terms is almost impossible! The Dr. told me that my "middle" chamber of my heart is not beating correctly with the top and bottom. His recomendation is an imediate pace maker! I can feel it skipping 1-3 beats some times and it feels like some one is inside my chest punching outward. then it will race and at other times will slow down, i get extremely tired, and at times get suddenly dizzy and will lose my eyesight aprox. 3-6 seconds. then the dizzyness is gone and my eyesight comes back. during and EEG and EKG and echo, the techs. told me they had never seen some one with so many skipped beats.

MY QUESTION; what are some possible reasons for this to happen? and why is there no photo of the heart showing each chamber and the flow of function.

Further work to be done on this article...[edit]

Just reverted a change from last week that chopped about the first third of the article off... I'd be the first to admit there is a lot of work waiting to be done here, but axing the Definition, Manifestations and Mechanisms section probably didn't help its cause.

This article could use lotsof, some, any REFERENCES. The mechanism section needs copyediting... a lot of other arrhtymia articles (such as the VT and SVT) link to this bit. The treatment section needs expanding and linking. The chapter headings could be brought into line with the Manual of Style for Medical Articles And the whole thing needs to be looked at carefully by a non-doctor to de-jargon it.

I don't think it needs many more external links - Google gets you more university and medical school sites than you can poke a stick at! I'll keep chipping away at it from time to time... Happy editing.TamePhysician (talk) 05:32, 29 March 2008 (UTC)

News and Current Events[edit]

Would it be appropriate to add a section about SADS in the media? Various police agencies have blamed the death of prisoners/arestees on "Sudden Adult Death Syndrome"

Loimprevisto (talk) 14:12, 3 September 2008 (UTC)

I am starting on a Zio Patch heart monitor. It's similar to a Holter Monitor, but you use it for up to two weeks of dat a collection. The Zio Patch was a 2010 winner of the Medical Design Excellence Awards (MDEA) [1] and here is more about the Zio Patch [2] This is my first time using a wiki talk page, apologies if I didn't format correctly.

Edsregistry (talk) 22:09, 28 January 2014 (UTC)

References

Naming[edit]

There is only one arrhythmia it is asystole. The rest are dysrhythmias. The name of this page should be changed to reflect that.Doc James (talk · contribs · email) 16:13, 11 October 2009 (UTC)

As no one seems to mind I have moved the page from cardiac arrhythmia.Doc James (talk · contribs · email) 20:07, 14 December 2009 (UTC)
I've gone ahead and history merged the page. Cut and paste moves are a very bad idea because they break attribution; if you can't perform a page move yourself, ask for assistance from an administrator at Wikipedia:Requested moves. Graham87 03:29, 19 February 2010 (UTC)
Hey Graham will post you a note when I come across pages that need to be moved :-) thanks. Doc James (talk · contribs · email) 03:32, 19 February 2010 (UTC)

Types (aka section 3) needs two more subtypes[edit]

I noticed that 2 different mechanisms for causing dysrhythmias are missing - bypass tracts, where the impulse loops around the heart in abnormal ways, due to birth defects etc (see Wolff-Parkinson White Syndrome). The second is conduction blocks, see heart blocks for this. These should be added by someone who knows fully about it, I'm not confident enough to add the section (and have exams now :P) FruitywS (talk) 13:40, 23 April 2010 (UTC)

Analogy with problems[edit]

I pasted the following analogy of reentry to here, because some issues need fixing: Actually, even in the normal case, people would see other people standing up when they sit down after 3 seconds. A functional analogy could be to sit down and close the eyes for 3 seconds to avoid seeing other people standing up. But at this level it seems to be as complicated as what goes on in nerves, so an analogy seems of little help. 193.235.173.250 (talk) 12:51, 7 May 2010 (UTC)

By analogy, imagine a room full of people all given these instructions: "If you see anyone starting to stand up, then stand up for three seconds and sit back down." If people are quick enough to respond, the first person to stand will trigger a single wave which will then die out; but if there are stragglers on one side of the room, people who have already sat down will see them and start a second wave, and so on.

Does the above have a WP:MEDRS to cite? LeadSongDog come howl 13:51, 7 May 2010 (UTC)

Even with a reliable source I would be hesitant to add this analogy even though I agree it is rather nice.Doc James (talk · contribs · email) 14:55, 7 May 2010 (UTC)

Source[edit]

PMC 1502051 that editors here might find useful. LeadSongDog come howl! 17:06, 5 November 2010 (UTC)

sinus arrhythmia wrt alcohol abuse[edit]

As somebody who's just had to have an A-fib turned using electricity for the first time, with the problem most likely having been precipitated by my abuse of alcohol... From pure experience, I'm pretty much perfectly sure overuse of alcohol could be one of the things which causes sinus arrhythmia in adults, perhaps in conjunction with non-lifethreating, recurrent atrial fibrillation. Especially upon "sleeping it off". Earlier I've talked about my own experience by referring to "morning after hyperventilation", but now I think that's not it.

I haven't seen this one mentioned in either this article or the one about sinus arrhythmia, but after my most recent episode, it sounds like something that could/should be easily found in the literature as well. I can't write anything about the phenomenon, though, because I'm not in this field, so that I don't have access to the relevant research literature. Thus, I'd like to suggest somebody else around here could perhaps take a look at the addiction and cardiac research, to verify whether my intuition/anecdote pans out. After all, given the huge rate of alcohol abuse all over the world, and even my not having been able to find words for something that prolly forsaged a more serious arrhythmia, I'm pretty sure that this stuff should be on Wikipedia. I mean, if it proves to be a well-researched and easily citable result. Decoy (talk) 21:22, 24 August 2011 (UTC)

Define normal[edit]

Normal hearts are not perfectly rhythmic. Please add information about the details of the range of "normal" -- how many PACs, PVCs etc normal hearts have per 24 hrs, etc.-96.237.13.111 (talk) 14:12, 21 November 2011 (UTC)

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Sentence that contradicts itself[edit]

There is a sentence that contradicts itself: "SADS is used to describe sudden death due to cardiac arrest brought on by an arrhythmia in the absence of any structural heart disease on autopsy. The most common cause of sudden death in the US is coronary artery disease.[citation needed]" If there is an absence of any structural heart disease in autopsy, then why does it go on to say that the cause is coronary artery disease, which WOULD show as a structural heart problem on autopsy? Medical experts please enlighten and perhaps correct that sentence as it is very misleading. 58.167.196.2 (talk) 03:29, 29 November 2012 (UTC)

Gene therapy[edit]

Can this treatment be mentioned in the article ?: Gene Therapy for fixing heart rythm disorder

About the article title[edit]

I saw dear Doc James has redirected the article to current name (Cardiac Dysrhythmia) with this reasoning that arrhythmia means there is no rhythm at [1] but I think this is a personal reasoning and we should use terms that used in scientific literature. A simple googling can show that "arrhythmia" is using in medical literature for example by American heart association at here or you can see many book titles here or more important that MeSH has chosen "Arrhythmia" at here. Dysrhythmia is an old term that had been used in 1970s and 1980s. However dysrhythmia is used in cerebral context as "cerebral dysrhythmia" or "Thalamocortical dysrhythmia". I think we should change the title to "Arrhythmia" event without "cardiac" word. Baqeri (talk) 15:52, 9 January 2015 (UTC)

Among review articles from the last 5 years they are used about the same number of times 4514 for arrhythmia and 4067 for dysrhythmia
Additionally the World Health Organization uses the term "cardiac dysrhythmia" [2] We should really go with the international classification rather than the local American one. Doc James (talk · contribs · email) 16:01, 9 January 2015 (UTC)
Despite not having strong views on the article title, I must add:
  • The main term in WHO's ICD-9 is dysrhythmia, but in ICD-10 is arrhythmia
  • Part V in the latest edition of Braunwald's Heart Disease is titled "Arrhythmias, sudden death and syncope".
  • The common clinical term for relevant drugs is "antiarrhythmics". --NikosGouliaros (talk) 17:16, 9 January 2015 (UTC)
NikosGouliaros, thanks for mentioning ICD term changing. I tried but I couldn't reach ICD 10 or 11. It is a strong criterion for article titles in Wikipedia. see this, but about the equal number of articles in PubMed, I think PubMed uses an algorithm that consider "arrhythmia" and "dysrhythmia" as a same concept. For example check this article. This is the second article in search of "review" articles in "recent 5 years" for "dysrhythmia" but you cannot find even one word of "dysrhythmia" however in this article more than 20 times "arrhythmia" used. This is a key point in PubMed Search. Baqeri (talk) 19:30, 9 January 2015 (UTC)

Yes can move back to cardiac arrhythmia. The term arrhythmia is also applied to sleep such as Circadian arrhythmia Doc James (talk · contribs · email) 20:32, 11 January 2015 (UTC)

Have moved back per ICD 10. Doc James (talk · contribs · email) 19:20, 13 January 2015 (UTC)

Technical query - Talk page name[edit]

@Redrose64: Just wondering why the talk page continues to come up as Talk:Cardiac_dysrhythmia (?) even though the page name has returned to Arrhythmia. Cheers, 86.181.67.166 (talk) 12:17, 14 January 2015 (UTC)

Not sure why I'm being asked... it's because Doc James (talk · contribs) only moved the article, not the talk page as well. I've moved this talk page to match the article name; now that they're linked again, in future they should be moved as a pair. --Redrose64 (talk) 13:16, 14 January 2015 (UTC)
Unless, of course, 86.181.67.166 is somebody that I occasionally meet in real life... perhaps this coming Sunday? --Redrose64 (talk) 13:18, 14 January 2015 (UTC)
Yes apologies. Not sure why they were not. Doc James (talk · contribs · email) 00:40, 15 January 2015 (UTC)

"Cardiac arrhythmia" or "arrhythmia"[edit]

Thanks Doc James. It is true that the term "circadian arrhythmia" is used but it is not frequent and it is not registered in MeSH. However the term "arrhythmia" is used frequent for the meaning of "cardiac arrhythmia" for example in MedlinePlus. When We use "arrhythmia" We refer to "cardiac arrhythmia" for example see this Uptodate article or this. Baqeri (talk) 10:00, 17 January 2015 (UTC)

No strong feelings either way. We could have a RfC regarding the name. Doc James (talk · contribs · email) 23:53, 17 January 2015 (UTC)

Histamine[edit]

Have moved this content here "Histamine modifies the heart rhythm and is responsible for many cardiac arrhythmias. The major arrhythmogenic actions of histamine are an H1-receptor-mediated slowing of atrioventricular conduction and H2-receptor-mediated changes in sinus rate and ventricular automaticity. Central nervous system H1-histamine receptors may mediate cardiac arrhythmias that occur after intracerebral hemorrhage or similar intracranial insults. Histamine, via the H2-receptor, attenuates the tachycardia produced by stimulation of cardiac sympathetic nerves or exogenous norepinephrine. H2-receptor blockade in this setting might therefore be expected to exacerbate ventricular arrhythmias secondary to loss of the histamine-mediated attenuation of sympathetic activity. The weight of clinical and experimental data justifies a trial of H1 and H2 receptor blockers when conventional antiarrhythmic therapy fails in the treatment of life-threatening cardiac arrhythmias in a clinical setting suggestive of histamine release.[1]"

We should use something newer than 1986. Doc James (talk · contribs · email) 21:16, 10 January 2015 (UTC)

The cited source is a review article, by a third-party, containing and referring published secondary sources and, accurately reflecting current medical knowledge. The fact that is was published in 1986 does not mean that the information ceases to be valid. If you can show that the information I extracted from the source has been superseded, became obsolete, or negated in any way, then prove it but, please do not simply delete the whole contribution. There is always the "Clarification needed" in superscript that could be added to invite further clarifications. The source meets the high-quality reliable sources guidelines. It is a review published in a reputable medical journal, reliably referring academic and professional books and work written by experts in the relevant field. The information that I posted in the article is not content that could be considered as coming from a primary source either. You are welcome to reword my contribution if you think you can improve it but, to simply delete it would deprive Wikipedia of important information. Thank you. 98.217.155.45 (talk) 10:49, 11 January 2015 (UTC)
If it accurately reflects current knowledge than you should be able to find something from the last 10 years. See WP:MEDDATE. Antihistamines appear to increase the risk of dysrhythmias [3]. Doc James (talk · contribs · email) 20:27, 11 January 2015 (UTC)
There are lots of primary source articles published within the last 10 years about studies involving histamine or it's inhibition, and cardiac effects including dysrhythmias. Just look at the usual databases (Pubmed, etc.). My source, albeit being older, is the best topic-specific review with second sources I found so far, with not much time to look for more. Regarding WP:MEDDATE, it says "These instructions... may need to be relaxed in areas where... few reviews are being published". While trying to accommodate your recentism, and agreeing with you on "Antihistamines appear to increase the risk of dysrhythmias" in some cases (yet, I've known several anecdotal cases where the opposite has been true and, H1-inhibitors treated PAC and supra-ventricular arrhythmias successfully, with better side effects profile than beta-blockers), I limited my contribution to our consensus on a lightweight claim. Your disruptive editing is approaching edit warring, further action may need to be taken against your disruptions. 98.217.155.45 (talk) 06:23, 12 January 2015 (UTC)
We have 348 reviews from the last 5 years for "cardiac arrhythmia" [4] Hardly a an area with "few reviews" Doc James (talk · contribs · email) 06:44, 12 January 2015 (UTC)
We are talking here about the few reviews specifically on histamine and dysrhythmias, not just any review on "cardiac arrhythmia". 98.217.155.45 (talk) 07:03, 12 January 2015 (UTC)
If no one since than has commented on it is likely wrong. Doc James (talk · contribs · email) 07:07, 12 January 2015 (UTC)
Not necessarily. That is nonsense. It can very well prove that the sourced review is just fine.98.217.155.45 (talk) 07:40, 12 January 2015 (UTC)
  • Comment from an uninvolved editor (via WT:MED): I think the biomedical claims here, including the one that "Histamine... is responsible for many cardiac arrhythmias", would require recent reliable medical sources. If these can't be produced (I haven't spotted any obvious recent reviews - tho this non-MEDRS editorial is at least pertinent) then I feel that due weight in the article is a real editorial concern. As regards antihistamines, I think PMID 20210720 (2010) might also be relevant here. 86.181.67.166 (talk) 14:40, 12 January 2015 (UTC)
Adding: As regards allergic reactions, this recent potential MEDRS wouldn't seem to provide the necessary support for the claim that histamine is responsible for *many* cardiac arrhythmias. 86.181.67.166 (talk) 14:54, 12 January 2015 (UTC)
  • The IP made a claim with an article which is MEDRS compliant other than being out or WP:MEDDATE. Doc James seems to have presented a source published later which gives information contrary to the older source. I think it is reasonable to ask that there be a response to information in the newer source, because it often happens in medicine that new information replaces older information. I say this because I anticipate that finding a newer source should not be difficult. Blue Rasberry (talk) 14:55, 12 January 2015 (UTC)
...though sometimes not altogether straightforward either. 86.181.67.166 (talk) 15:09, 12 January 2015 (UTC), a separate logged-out "IP")
Possibly helpful: ACC/AHA/ESC Guidelines for the Management of Patients with Supraventricular Arrhythmias European Society of Cardiology 2003, see end of p.14 and there-cited ref 101. LeadSongDog come howl! 22:51, 12 January 2015 (UTC)

Arbitrary break: moved content[edit]

I'm moving [5] the following paragraph from the main page due to concerns about weighting (as well as the need for recent sourcing), and the way some of it is framed under "==Differential diagnosis=="[?]

Histamine modifies the heart rhythm and is responsible for many cardiac arrhythmias. The major arrhythmogenic actions of histamine are an H1-receptor-mediated slowing of atrioventricular conduction and H2-receptor-mediated changes in sinus rate and ventricular automaticity.[2] Also, some antihistamines appear to increase the risk of dysrhythmias.[3]

  1. ^ Andrew A. Wolff and Roberto Levi (January 1986). "Histamine and Cardiac Arrhythmias" (PDF). Circulation Research. 58 (1).
  2. ^ Andrew A. Wolff and Roberto Levi (January 1986). "Histamine and Cardiac Arrhythmias" (PDF). Circulation Research. 58 (1).
  3. ^ http://circ.ahajournals.org/content/122/14/1426.long

86.181.67.166 (talk) 09:14, 13 January 2015 (UTC)

The last source is under doi:10.1161/CIRCULATIONAHA.109.894725 (2010). Just because a drug inhibits the effect on mast cells doesn't mean that its pro-arrhythmic effects are also mediated by histamine receptor blockade. Au contraire, it seems that the main worry is with regards to potassium, sodium or calcium currents and especially IKr.
When I search PubMed with both "Histamine" and "Arrhythmias, Cardiac" as [MAJR], I get no secondary sources apart from the 1986 review and a paper from 1999 (PMID 10597866). I would strongly argue that this is an area of research that has simply not established enough to discuss in the context of a general encyclopedia article. JFW | T@lk 17:23, 13 January 2015 (UTC)
Agree. 86.181.67.166 (talk) 12:04, 14 January 2015 (UTC)

CANet - Cardiac Arrhythmia Network of Canada[edit]

I would like to share information about CANet (ideally with an article of its own), but I have a COI as I am an employee of the organization. It is one of 13 currently-funded Networks of Centres of Excellence - which are research-based networks that require multi-disciplinary (e.g. academic, industry, government) cooperation and multi-centre cooperation to fulfill their mandates. [1] This article announced CANet's funding, and discusses some of the network's goals: http://london.ctvnews.ca/26-3m-for-canadian-arrhythmia-network-at-western-1.2148623. NKC717 (talk) 19:14, 12 November 2015 (UTC)

We have an article on antiarrhythmic drugs[edit]

For this. It does not fit here IMO. The table we currently have at antiarrhythmic drugs is better than this one. This one tries to put to much info into a table. This content is better dealt with as prose and within the articles about the medications in question. Doc James (talk · contribs · email) 18:55, 11 March 2017 (UTC)

Massive table[edit]

Extended content

***Below is a table summarizing the drugs utilized in the treatment of cardiac arrhythmias. The table is currently undergoing development as a research project at the University of California, Los Angeles (UCLA). Expected date of completion is March 26, 2017 at 11:59 PM PST.

Drugs Used for Treatment of Heart Failure
Vaughan Williams Classification Drug Name and Approval Date Indications for Drug Use Animal Model Mechanism of Action (MOA) Biomarker Advantage of the Drug Drawback of the Drug
Target Protein Channel Model Type Species Advantage Drawback
Class I Drugs Class Ia (E) Induces a fast open-channel block on the batrachotoxin (BTX)-activated sodium channels in electrophysiologically dysfunctional cardiomyocytes (i.e. in the presence of ventricular tachycardia) Procainamide Hydrochloride (Procanbid extended-release tablets) Approved January 1996 Warner-Lambert Treatment for ventricular arrhythmias (e.g. ventricular tachycardia) Internal defibrillating leads implanted through a left thoracotomy in dogs and via a subxiphoid approach in pigs. The voltage dependent block of the sodium channels can occur either from the inside of the cell via a hydrophilic pathway, or from the extracellular side via a hydrophobic pathway. The blocking is weaker from the extracellular side due to procainamide's polar structure 0.5% of the time initiates leukopenia and/or agranulocytosis, which are serious hematologic disorders
Class Ib (E) Exhibits its effects on the delayed rectifier current (hERG/IKr Potassium channels), inhibits Na+ current, moderate inhibitor for CYP3A and P-gp (cyclosporine), stimulates myogenesis, reduces a pro-oxidant inflammation/oxidative condition, and activates the calcium signaling pathway Ranolazine (Ranexa); Initial U.S. Approval in 2006 for oral use Chronic Angina Rabbit, Rat, & Mouse Prolongs action potential duration, with corresponding QT interval prolongation on electrocardiography
Class Ic (B) Propafenone (Rythmol) Approved January 1998 Knoll Pharmaceutical Treatment for paroxysmal atrial fibrillation Pre-treated with propafenone and untreated guinea pigs with induced atrial fibrillation; left, right atria and papillary muscles were dissected
Class II Drugs Class II (E) Inhibits adrenergic ß1 receptors of the pacemaker cells (sinoatrial and atrioventricular nodes) Metoprolol Succinate (Toprol-XL) Approved January 1995 AstraZeneca For the treatment of hypertension, angina pectoris and heart failure Dogs of mixed breed were fasted for 12 hours and then anaesthetized with sodium pentobarbital via IV. The catheter was inserted into femoral artery and vein through which frequent flushes of saline were applied. Additionally, metoprolol was injected via an IV into human patients to test its effects on atrial tachycardia and fibrillation, ventricular ectopic beats and tachycardia, and congestive heart failure Decreases the plasma free fatty acid (FFA) concentration, which is induced by noradrenaline, decrease the slope of phase 4 (decreased Na+ uptake, thus it takes longer to reach threshold) and prolong repolarization of phase 3 (K+ release is slowed down) of the nodal action potential.
Class III Drugs Class III with effects consistent with all of the I-IV classes (E) Inhibits the voltage-dependent K+ channels (Li 2016) Amiodarone HCl (Marketed as Cordarone and Pacerone); Initial FDA Approval in 1985 as an oral tablet and in 1995 as an injection for intravenous use (Herendael 2010). International Medication System, Ltd., Zydus Pharmaceuticals USA Inc., Teva, Mylan, etc. (Currently on the market as a tablet for oral uptake and as an injection) Reccurent ventricular fibrillation and recurrent hemodynamically unstable ventricular tachycardia, congestive heart failure, and atrial fibrillation (due to its effect on blocking the AV node, thus slowing the ventricular response rate) (Waldo 1998); Also, it is well known to treat high grade ventricular ectopic activity (VEA), Wolff-Parkinson-White syndrome, and sick sinus syndrome (Gould 1983, 275-279). Clinical need to suppress atrial fibrillation and an attempt to maintain the sinus rythm lead to patient trials of amiodarone administration (Waldo 1998). Amiodarone's transition from an antianginal agent (1962-1985) to the treatment of ventricular and supraventricular tachycardias originated due to its observed antiarrhythmic properties in Europe and South America in the early 1970s (Herendael 2010). Experimentally Induced Arrhythmias In the animal models below, amiodarone was administered intravenously; Ventricular arrhythmias: chloroform-induced VFib in mice, VFib induced in rats via an I.V. injection of CaCL2, VTach evoked in rats and dogs by aconitine hydrochloride, experimental arrhythmias in dogs and rabbits, VFib in isolated perfused heart of rats, experimental VTach in guinea pigs, and VFib after coronary artery ligation in dogs and rats. Supraventricular arrhythmias: acetylcholine-induced AFib in dogs, aconite-induced AFib in cats, and electrically induced AFib in dogs (Williams 1986, 7-10); Mongrel dogs were anaesthetized with sodium pentobarbital and atropinized. Adrenoceptor stimulation was achived by IV administration of adrenaline and measurement of increased blood pressure via a catheter inserted into the femoral artery, Increase in heart rate was measured after an IV administration of isoprenaline Slows conduction rate and prolongs the refractory period of the SA and AV nodes (Williams 1986, 12); prolongs the refractory periods of the ventricles, bundles of His, and the Purkinje fibres without exhibiting any effects on the conduction rate (Williams 1986, 16); Prolongs the myocardial cell action potential duration and refractory period and is a non-competitive ß-adrenergic inhibitor Pulmonary toxicity (hypersensitivity pneumonitis or interstitial/alveolar pneumonitis)
Class III with actions similar to all of the Vaughan-Williams classes (E) Dronedarone (Multaq) Approved July 2009 Sanofi-aventis For the treatment of paroxysmal or persistent atrial fibrillation or atrial flutter Anesthetized pigs with ventricular fibrillation and related arrhythmias induced via acute coronary artery occlusion and Mongrel dogs anesthetized with chloralose that had implanted electrodes in the right atrium and ventricle for electrical stimulation and proximal ECG measurements Illustrates antiadrenergic effects, and prolongs atrioventricular nodal conduction, atrial and ventricular refractory periods, and the duration of paced QRS interval (Castro 2002)
Class III (E) Sotalol (Betapace AF Tablet) Approved February 2000 Berlex Laboratories For treatment of the irregular heartbeats in patients with atrial fibrillation or atrial flutter
Class III: Blocks rapid component of cardiac delayed rectifier potassium current, IK (B) Cardiac Myocytes Ibutilide Fumarate (Corvert IV Injection) Approved December 1995 Pharmacia & Upjohn Treatment for irregular contractions of the heart and Atrial Fibrillation Chronic canine model of atrial flutter. Rabbit model with proarrhythmia Increases action potential duration No sedation necessary, alternative to electrical cardioversion. Increased AERP and prevention of induced atrial flutter in this model Can cause Torsades de Pointes
Class IV Drugs Class IV (B) Voltage-dependent L-type calcium channel subunits 1C,1D,1F, 1S and subunits beta-1-4 Verapamil; IVAX; Generic equivalent of Knoll's Isoptin SR and Searle's Calan SR, Approved December 1997 Supraventricular tachycardia, angina, hypertension Developed tension in guinea-pig papillary muscles, calcium current (Ica) and tension in cat ventricular muscle strands, Ica in guinea-pig and cat ventricular myocytes, single Ca2+ channel currents carried by Ba2+ in cell-attached membrane patches of guinea-pig ventricular myocytes. Chloralosed artificially respired mongrel dogs. Prolonged PQ interval Inhibits the transmembrane influx of ionic calcium into arterial smooth muscle as well as in conductile and contractile myocardial cells without altering serum calcium concentrations
Class IV (B) Bind and inhibit opening of L-type calcium channels Diltiazem HCl, Extended-Release Capsules; Biovail Laboratories; Approved January 2000 Angina pectoris, arrhythmia, hypertension Mybpc3 KI cardiomyopathy and WT mouse model Interferes with the slow inward (depolarizing) current in excitable tissue and causes excitation-contraction uncoupling in various myocardial tissues without changes in the configuration of the action potential
First in Class (B) Nesiritide (Natrecor); Scios; Approved August 2001 For the treatment of patients with acutely decompensated congestive heart failure
I(f) Current Inhibitor (B) Na+-K+ inward current of the cardiac sinoatrial node (SAN) myocytes (Pacemaker current). Target channel Ivabradine (Corlanor) Approved April 2015 Amgen S16257 For the treatment of chronic heart failure Human cloned K+ channels (hKv1.5) stably expressed in a mouse L cell line Resting and exercising (exercise-induced tachycardia) conscious dog (Experimentally Induced Models) Hyperpolarization-activated cyclic nucleotide-gated channel antagonist. Within the SA node, selectively blocks HCN channel How did they find out Iv blocks HCN channel that carries I(f) current (initiates the spontaneous diastolic depolarization phase, modulating heart rate) thus lowering heart rate Does not affect resting epicardial coronary artery diameter and only attenuated its increase during exercise Blurred vision, headaches, palpitations, vertigo, shortness of breath, bradycardia
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Article name: Heart versus cardiac[edit]

This article has been at "heart arrhythmia" for about a year. Probably should have a move discussion before changing it again. Mayo uses the term[6].

Often just called "arrhythmia" but as there are other types good to have a qualifier. Doc James (talk · contribs · email) 23:55, 14 May 2018 (UTC)