Topic: Palpitations vs QT prolongation - can you tell the difference?
johnnyb
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Many of the macrolide antibiotics can cause a prolongation of the QT interval, which can potentially cause a serious heart rhythm problem, or even death.
I am now taking mepron and zithromax, a macrolide, and I have been noticing palpitations (some of a quivering nature).
Question is - How would you ever tell the difference? Does everyone get prolonged QT from macrolides, or just some?
If it IS present, would it be present 100% of the time, so if I went for an EKG to see if I had it, we would know for sure, regardless of when it was done?
I am a little fuzzy on all this stuff. Looking for someone knowledgeable.
Thanks,
- JB
Posts: 1197 | From New Jersey | Registered: Jul 2005
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Keebler
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very good question - and an important one.
I did a lot of research on this some time ago as I am no stranger to fainting (syncope). Startles (and seizures from startles) have been horrible for me for over a decade . . . . severe startle reactions with immediate nausea since childhood, though I may have simply had low magnesium or other factors.
One doctor has suggested I get the cardiac impedance test, but that's not an option right now. So, I study how to make things better.
I have heard of many lyme patients with similar stuff and once the lyme/TBI was treated the startle stuff became history. It could be, too, that some of those may have the long QT stuff, too, but that would be hard to know.
Pardon me if I post a lot of stuff. I need to look at this again anyway, so it gives me a chance to sort a bit . . . and share what might be good for everyone to know - even if it's not for us - it could be helpful for others. AND . . . I always try to end with some solutions.
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A faint feeling would be one indicator (though, perhaps, not necessary). Family history of any sudden deaths or fainting might help regard genetic predisposition.
If sudden sounds or motions trigger severe, sickening startles, that might be one important piece of information for QT. However, that is also very common with lyme and has cleared for many after abx tx and adrenal support.
Even an alarm clock has been fatal to some with QT - the sudden startle from deep sleep was too much for their hearts. Only after delving into family genetics or a victim's history have a few cases been solved.
I have to wonder if the deep bass and harsh powerful rhythms of certain rap or hip-hop would also be hard on those with QT tendancies.
Arnold Peckerman, MD and Paul Cheney, MD have both written about this (QT, not the bass rhythm stuff). You might google and PubMed search their name with cardiac impedance or just "QT" -
And genetic tests can be done. PBS had a documentary on this about 4-6 months ago as part of a series on the heart.
[ Caution: if you ask your family about relatives (back a few generations) who may have been easily startled or died suddenly, be aware you may be thought of a hypochrondriac. I asked one member of my family this and it just blew up in my face.
I also wonder if this is why some people feel the need for a glass of wine, etc. to calm down so as to not startle. Don't know if that would be good, but it may be the only way some can self-medicate. Just wondering if alcohol use could mask a genetic tendency in a family. ]
A special test can be done, but not every cardiologist does it. This goes beyond the tilt table test for NMH and beyond the EKG. It's a test called something like "cardiac impedance" - described in Peckerman and Cheney's writings.
CFS and Diastolic Cardiomyopathy - Paul Cheney, M.D., Ph.D.
(Note, he does not take the infection connection to CFS. Still, good info. although it's alway important to treat infections.)
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From my file: I cannot copy the link or the text, but you might copy and search part of this title by Peckerman, et.al. " Abnormal Impendance Cardiography Predicts Symptom Severity in Chroninc Fatigue Syndrome"
Note that while both Peckerman and Cheney write in reference to CFS, that still can be good information (and safety tips) for those with chronic infections that cause chronic fatigue.
One treatment for long QT is a pacemaker. Magnesium, too, may be of value in helping to regulate cardiac rhythm (many abstracts on PubMed about magnesium and the heart).
QT can have a genetic cause, and many meds can also affect this in those with or without that genetic involvement.
Somewhere I read that the herbal supplement, Gotu Kola (which is not a cola and not stimulating) helped reduce startle. I'll see if I can find that. Reducing startle may not be the same thing as helping QT, but it might in some cases.
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[ 25. January 2008, 09:11 PM: Message edited by: Keebler ]
Posts: 48021 | From Tree House | Registered: Jul 2007
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If you look on your EKG printout, there should be a number that says "QTc." This is the measure of your QT Interval, and you should be able to find on a Google search what the appropriate range is for your age and gender.
Unless your interval is prolonged to begin with, as I understand it, you should be okay on the drugs. I talked to a cardiologist who studies Long QT, and though my QT interval was only moderately prolonged, he recommended I stay away from any of the risky drugs including Biaxin, etc.
Being on a beta blocker can reduce the risk of torsades de pointe (sp?), which is the life-threatening condition caused by Long QT. So that's always an option.
But it's true: anything startling can cause a person with Long QT to drop dead. It's very scary to contemplate. Any strong emotion, a loud noise, etc.
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Keebler
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I can't begin to understand all this, however, it does illuminate how certain classifications - or combinations - of drugs may affect someone with long QT.
For example, when aforementioned CYP3A4 inhibitors are coadministered with terfenadine, cisapride or astemizole (all CYP3A4 substrates), torsades de pointes (a life-threatening ventricular arrhythmia associated with QT prolongation) may occur.
. . . However, predicting drug-drug interactions involving CYP3A4 inactivation is difficult, since the clinical outcomes depend on a number of factors that are associated with drugs and patients.
Clin Pharmacokinet. 2005;44(3):279-304.
Mechanism-based inhibition of cytochrome P450 3A4 by therapeutic drugs.
Zhou S, Yung Chan S, Cher Goh B, Chan E, Duan W, Huang M, McLeod HL.
Department of Pharmacy, Faculty of Science, National University of Singapore, Singapore.
Consistent with its highest abundance in humans, cytochrome P450 (CYP) 3A is responsible for the metabolism of about 60% of currently known drugs. However, this unusual low substrate specificity also makes CYP3A4 susceptible to reversible or irreversible inhibition by a variety of drugs.
Mechanism-based inhibition of CYP3A4 is characterised by nicotinamide adenine dinucleotide phosphate hydrogen (NADPH)-, time- and concentration-dependent enzyme inactivation, occurring when some drugs are converted by CYP isoenzymes to reactive metabolites capable of irreversibly binding covalently to CYP3A4.
Approaches using in vitro, in silico and in vivo models can be used to study CYP3A4 inactivation by drugs.
Human liver microsomes are always used to estimate inactivation kinetic parameters including the concentration required for half-maximal inactivation (K(I)) and the maximal rate of inactivation at saturation (k(inact)).
Clinically important mechanism-based CYP3A4 inhibitors include antibacterials (e.g. clarithromycin, erythromycin and isoniazid), anticancer agents (e.g. tamoxifen and irinotecan), anti-HIV agents (e.g. ritonavir and delavirdine),
antihypertensives (e.g. dihydralazine, verapamil and diltiazem), sex steroids and their receptor modulators (e.g. gestodene and raloxifene), and several herbal constituents (e.g. bergamottin and glabridin).
Drugs inactivating CYP3A4 often possess several common moieties such as a tertiary amine function, furan ring, and acetylene function.
It appears that the chemical properties of a drug critical to CYP3A4 inactivation include formation of reactive metabolites by CYP isoenzymes, preponderance of CYP inducers and P-glycoprotein (P-gp) substrate, and occurrence of clinically significant pharmacokinetic interactions with coadministered drugs.
Compared with reversible inhibition of CYP3A4, mechanism-based inhibition of CYP3A4 more frequently cause pharmacokinetic-pharmacodynamic drug-drug interactions, as the inactivated CYP3A4 has to be replaced by newly synthesised CYP3A4 protein.
The resultant drug interactions may lead to adverse drug effects, including some fatal events.
For example, when aforementioned CYP3A4 inhibitors are coadministered with terfenadine, cisapride or astemizole (all CYP3A4 substrates), torsades de pointes (a life-threatening ventricular arrhythmia associated with QT prolongation) may occur.
However, predicting drug-drug interactions involving CYP3A4 inactivation is difficult, since the clinical outcomes depend on a number of factors that are associated with drugs and patients.
The apparent pharmacokinetic effect of a mechanism-based inhibitor of CYP3A4 would be a function of its K(I), k(inact) and partition ratio and the zero-order synthesis rate of new or replacement enzyme.
The inactivators for CYP3A4 can be inducers and P-gp substrates/inhibitors, confounding in vitro-in vivo extrapolation.
The clinical significance of CYP3A inhibition for drug safety and efficacy warrants closer understanding of the mechanisms for each inhibitor. Furthermore, such inactivation may be exploited for therapeutic gain in certain circumstances.
[QTc-prolonging drugs and the risk of sudden death] [Article in Lithuanian]
Reingardiene D, Vilcinskaite J.
Department of Intensive Therapy, Kaunas University of Medicine, Kaunas, Lithuania.
Various drugs can be associated with QT prolongation. A prolonged QT interval leads to an increased risk for the development of ventricular tachyarrhythmias, particularly polymorphic ventricular tachycardia (torsades de pointes).
Polymorphic arrhythmia may rapidly develop into ventricular fibrillation and cause sudden death. Torsades de pointes is classically associated with early depolarization.
This review article discusses the mechanisms of QTc prolongation and triggering factors for proarrhythmia, drugs that prolong QT interval
(class III antiarrhythmic agents, antimicrobial agents - fluoroquinolone and macrolide antibiotics, antipsychotic and antidepressant drugs, agents used in general anesthesia, antimycotics, and several other drugs),
nonpharmacological and pharmacological risk factors for arrhythmias (due to pharmacokinetic-pharmacodynamic interactions), the treatment and recommendations to prevent arrhythmia related to QT prolongation.
Drugs that cause Torsades de pointes and increase the risk of sudden cardiac death. Wolbrette DL.
Milton S. Hershey Medical Center, Division of Cardiology, 500 University Drive/H047, Hershey, PA 17033, USA.
Torsades de pointes (TdP) is a potentially life-threatening arrhythmia associated with not only antiarrhythmic drugs, but noncardiac drugs of many different classes.
All these drugs prolong the QT interval by their blocking of the potassium channel I(Kr), and many are metabolized by the cytochrome P450 isoenzyme CYP3A4.
Polypharmacy with other drugs utilizing the same enzyme, or inhibiting CYP3A4, can lead to TdP. A consistent finding of all the QT-prolonging drugs is predominance of TdP in women. Other risk factors for QT prolongation and TdP include hypokalemia, congestive heart failure, and structural heart disease.
Knowledge of potential drug interactions and other risk factors for TdP can help in reducing the number of adverse events associated with the use of QT-prolonging drugs.
Intravenous magnesium sulfate enhances the ability of intravenous ibutilide to successfully convert atrial fibrillation or flutter.
Tercius AJ, Kluger J, Coleman CI, White CM.
University of Connecticut Schools of Medicine, Farmington, CT, USA.
BACKGROUND: A previous randomized trial found that adjunctive use of intravenous magnesium (a total of 4 grams) can attenuate the corrected QT interval (QTc) prolongation associated with ibutilide, but its impact on ibutilide efficacy has not been elucidated.
METHODS: This was a cohort evaluation of 229 consecutive patients who received ibutilide in the presence or absence of intravenous magnesium.
Multivariate logistic regression analysis was used to determine the impact of magnesium on ibutilide efficacy as well as the impact of magnesium dosing intensity on ibutilide efficacy.
RESULTS: The overall chemical conversion rate with ibutilide in the presence or absence of magnesium was 59.8%.
The concurrent administration of magnesium (n = 141) was associated with a 78% increased odds of successful chemical conversion (adjusted odds ratio, AOR; 1.78 [95% confidence intervals,CI 1.02-3.09]) compared to those who did not receive magnesium (n = 88).
Magnesium dosing intensity appeared to be an important determinant of ibutilide efficacy, with the 4 grams dose associated with a threefold increase in the odds of successful chemical conversion (AOR; 2.98 [95% CI 1.46-6.11).
The 1 to 3 grams subgroup was associated with only a trend toward an improvement. There was only one case of Torsade de Pointes (TdP) which occurred in the no adjunctive magnesium group.
CONCLUSIONS: Concurrent use of magnesium enhanced the ability of ibutilide to successfully convert atrial fibrillation (AF) or flutter (AFl). The 4 grams magnesium dose appeared to provide the greatest benefit.
Keebler
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The Mysterious Human Heart - PBS SERIES - watch on your computer - DSL, or high speed best. Windows for PCs or Quicktime for Macs.
The Mysterious Human Heart .Electrical Impulses Within the Heart ... ... If the QT interval is abnormally long or short, it may be due to long QT syndrome or short QT syndrome, hereditary diseases that may result in potentially ...
The Mysterious Human Heart . Lesson Plans | PBS ... Long QT Syndrome -- Mayo Clinic www.mayoclinic.com/health/long-qt-syndrome/ This page provides an explanation of Long QT syndrom, which leaves . . .
VIDEO - you can watch the ENTIRE PROGRAM HERE. Every ten minutes, just hit the next part of the segment in the menu bar just above the video.
THE MYSTERIOUS HUMAN HEART - some video available on-line. (note for sound sensitive. Episode 2, has snare drums at the beginning. Turn down your volume. The irritating percussion lasts for a couple minutes.
This features a college freshman whose heart stopped. His friends saved his life with CPR. His friends happened to be volunteer EMTs. The entire hour details QT stuff.
Every time your heart beats, an electrical impulse generated by the sinoatrial node travels through it. The sinoatrial node is a small mass of specialized cells in the top of the right atrium that serves as the heart's natural pacemaker.
The electrical activity generated there contracts the cardiac muscle, pumping blood throughout the body.
An electrocardiogram (ECG or EKG) measures the electrical activity of the heartbeat. This activity is recorded and displayed on a monitor, allowing a doctor to measure the amount of time that it takes for an electrical impulse to travel from one part of the heart to another.
In an arrhythmia, the heart's electrical activity becomes uncoordinated, and an ECG may look like a disorganized jumble of spikes and valleys. A doctor can use the ECG to determine the type of arrhythmia a patient has -- and how to treat it.
The left and right atria make the first wave seen on an ECG, called a P wave. In a normal heartbeat, the P wave looks like a short hump on the ECG.
The next wave, the tall spike known as the QRS complex, indicates activity from the right and left ventricles. The final wave, or T wave, appears shorter and represents the ventricles' return to a resting state.
The amount of time that passes from the beginning of the QRS complex to the end of the T wave is referred to as the QT interval. If the QT interval is abnormally long or short, it may be due to long Q-T syndrome or short Q-T syndrome, hereditary diseases that may result in potentially fatal arrhythmias.
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[ 25. January 2008, 04:12 PM: Message edited by: Keebler ]
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Keebler
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Some DEFINITIONS - while Wikipedia is a public - uh . . . anyone can contribute . . . it's a good place to begin.
A palpitation is an abnormal awareness of the beating of the heart, whether it is too slow, too fast, irregular, or at its normal frequency.
The difference between an abnormal awareness and a normal awareness is that the latter is almost always caused by a concentration on the beating of one's heart and the former interrupts other thoughts.
Palpitations may be brought on by overexertion, adrenaline, alcohol, disease (such as hyperthyroidism) or drugs, or as a symptom of panic disorder. More colloquially, it can also refer to a shaking motion. It can also happen in mitral stenosis.
Nearly everyone experiences an occasional awareness of their heart beating, but when it occurs frequently, it can indicate a problem. Palpitations may be associated with heart problems, but also with anemias and thyroid malfunction.
Attacks can last for a few seconds or hours, and may occur very infrequently, or more than daily. Palpitations alongside other symptoms, including sweating, faintness, chest pain or dizziness, indicate irregular or poor heart function and should be looked into.
Ventricular fibrillation (V-fiB or VF) is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart.
As a result, the heart fails to adequately pump blood; hypoxia soon occurs, followed by unconsciousness within twenty to thirty seconds.[cita
Introduction
Ventricular fibrillation is a medical emergency. If the arrhythmia continues for more than a few seconds, blood circulation will cease -- as evidenced by lack of pulse, blood pressure, and respiration -- and eventually death will occur.
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly, rather than contracting in unison, and so the ventricles fail to pump blood into the arteries and into systemic circulation.
Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, mostly brought on by ischaemic heart disease.
Despite much work, the underlying nature of fibrillation is not completely understood. Most episodes of fibrillation occur in diseased hearts, but others occur in so-called normal hearts. Much work still has to be done to elucidate the mechanisms of ventricular fibrillation
The long QT syndrome (LQTS) is a heart condition associated with prolongation of repolarisation (recovery) following depolarisation (excitation) of the cardiac ventricles.
It is associated with syncope (fainting) and sudden death due to ventricular arrhythmias.
Arrhythmias in individuals with LQTS are often associated with exercise or excitement. LQTS is associated with the rare, ventricular arrhythmia torsade de pointes, which can deteriorate into ventricular fibrillation and ultimately death.
Individuals with LQTS have a prolongation of the QT interval on the ECG. The Q wave on the ECG corresponds to ventricular depolarization while the T wave corresponds to ventricular repolarization.
The QT interval is measured from the Q point to the end of the T wave. While many individuals with LQTS have persistent prolongation of the QT interval, some individuals do not always show the QT prolongation; in these individuals, the QT interval may prolong with the administration of certain medications.
Short QT syndrome is a genetic disease of the electrical system of the heart.
It consists of a constellation of signs and symptoms, consisting of a short QT interval interval on EKG (≤ 300 ms) that doesn't significantly change with heart rate, tall and peaked T waves, and a structurally normal heart.
Short QT syndrome appears to be inherited in an autosomal dominant pattern, and a few affected families have been identified.
Impedance cardiography is a hemorheology technique of using sensors to detect the properties of the blood flow in the Thorax.
Impedance cardiography (ICG), also referred to as thoracic electrical bioimpedance (TEB) and electrical impedance plethysmography (EIP), has been researched since the 1940's.
With ICG, the placement of four dual disposable sensors on the neck and chest are used to transmit and detect electrical and impedance changes in the thorax, which are used to measure and calculate hemodynamic parameters.
. . .
Invasive Hemodynamic Monitoring - discussed
Noninvasive Hemodynamic Monitoring - discussed
. . .
ICG Parameters
The electrical and impedance signals are processed to determine fiducial points, which are then utilized to measure and calculate hemodynamic parameters, such as cardiac output, stroke volume, systemic vascular resistance, thoracic fluid content, acceleration index, and systolic time ratio.
NICE CHART EXPLAINING TERMS - and - full article at link.
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[ 25. January 2008, 03:40 PM: Message edited by: Keebler ]
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Keebler
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As mentioned by LymeCFIDSMCS, a beta-blocker can be of help for some with QT stuff.
Even a tiny amount of propranol (sp?) just wipes me out. But, if that works for someone, I say "great" as it's easier and cheaper.
However, in addition to magnesium, I have used Hawthorn (root or berry?) extract and found that to have a beta-blocker action. It is verified in research, too. Not just any product, though. I've found only one that really works for me.
If you want more on that, I'll look up my notes.
Stephen Sinatra, MD has a book out on the heart. I've not read it and note that his site seems more like a flashy storefront. Still, you may be able to look inside the book at Amazon.
Surely some other authors have some nice educational guides. Maybe your LLMD can recommend resources for learning.
I learned a lot from the PBS programs detailed above. I used to teach CPR for the Red Cross - before lyme, that is. So I see this as valuable to everyone.
I'd like to see them do a series on adrenal function, too.
For anyone easily startled - there are more gentle alarm clocks out now. I have one that uses a CD and it turns on to music I am familiar with at a decent volume. Some have gentle lights that glow from soft to bright . . . some "Zen" chimes types, etc.
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I do think the EKG is an excellent idea. I don't know if you need a "challenge" with that but even a baseline can tell a lot.
I remember telling a cardiologist how certain music - or noise - seemed to really affect my heart beat. They all just looked at me like I'd landed in a Martian outfit. They had no way to test for what I was telling them. They'd never even considered - or heard - of such a thing.
So, I asked for an informal startle test during EKG recording - I asked a nurse to startle me. I had my eyes closed, resting, and she sneaked up and screamed in my ear.
Not a good idea. With my jump, the electrodes ripped off and the test was invalid. My ear rang like a siren and I was in "adrenal shock" for long time after that. I thought she would just drop a pen or something. Oy, Vey !
Take care. Good luck. Have some fun.
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[ 25. January 2008, 04:45 PM: Message edited by: Keebler ]
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Keebler
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I have major heart palpatations on any Macrolides. I ended up in the hospital twice. Once for 3 days. My LLMD and my cardiologist both said to never take a Macrolide antibiotic again. I was on a Beta Blocker at the time.
Kathy
-------------------- You never know how strong you are until being strong is the only choice you have. Posts: 807 | From South Dakota | Registered: Jul 2005
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