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Newsletter

December 2005

Volume 1, No 1


 Atrial Fibrillation
A Cardiac Arrthymia
 

         Definition of Cardiac Arrhythmia:  An arrthymia is any disorder of heart rate or rhythm.

                    Alternative Names of Cardiac Arrthymia are:  Dysrhythmia, Abnormal heart
          rhythm.


          Definition of Atrial Fibrillation/Flutter:  A disorder of heart rhythm (arrthymia) usually
                    with rapid heart rate in which the upper heart chambers (atria) are stimulated
                    to contract in a very disorganized and abnormal manner.
                   
                    Alternative Name of Atrial Fibrillation (Atrial Fib.) is: auricular fibrillation.
   

          From the University of Maryland Medical Center Health Library:
          http://www.umm.edu/ency/article/000184.htm


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  Causes of Arrhythmias
       
        "Each arrhythmia may have its own specific cause.  Common causes include:

  •      Congenital Defects

  •      Myocardial Ischemia or Infarction

  •      Organic Heart Disease

  •      Drug Toxicity

  •      Degeneration or Obstruction of Conductive Tissue

  •      Connective Tissue Disorders

  •      Electrolyte Imbalances

  •      Hypertrophy of Heart Muscle

  •      Acid-Base Imbalances

  •      Emotional Stress"

    Atrial Fibrillation/Flutter is one of the Atrial Arrhythmias. 

                                                                         Source:

    Atlas of Pathophysiology, Second Edition.  Lippincott Williams and Wilkins, 2005.


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    "Arrhythmias are caused by a disruption of the normal electrical conduction system of the heart. Normally, the 4 chambers of the heart (2 atria and 2 ventricles) contract in a very specific, coordinated manner.

    The signal for the heart to contract in a synchronized manner is an electrical impulse that begins in the "sinoatrial node" (also called the SA node), which is the body's natural pacemaker.

    The signal leaves the sinoatrial node and travels through the two atria, stimulating them to contract. Then, the signal passes through another node (the AV node), and finally travels through the ventricles and stimulates them to contract in synchrony.

    Problems can occur anywhere along the conduction system, causing various arrhythmias. There can be a problem in the heart muscle itself, causing it to respond differently to the signal, or causing the ventricles to contract independently of the normal conduction system.

    Arrhythmias include "tachycardias" (the heartbeat is too fast), "bradycardias" (the heartbeat is too slow), and "true" arrhythmias (a disturbed rhythm).

    Arrhythmias can be life-threatening, if they cause a severe decrease in the pumping function of the heart. When the pumping function is severely decreased for more than a few seconds, blood circulation is essentially stopped, and organ damage (such as brain damage) may occur within a few minutes.

    Life-threatening arrhythmias include ventricular fibrillation; ventricular tachycardia that is rapid and sustained, or pulseless; and sustained episodes of other arrhythmias.

    Other arrhythmias include     atrial fibrillation/flutter, multifocal atrial tachycardia, paroxysmal supraventricular tachycardia, Wolff-Parkinson-White syndrome, sinus tachycardia, sinus bradycardia, bradycardia associated with heart block, sick sinus syndrome, and ectopic heartbeat.

    People who have a history of     coronary artery disease, heart valve disorders, or other cardiac conditions and people with imbalances of blood chemistries are at higher risk for arrhythmias and complications from arrhythmias.

    Arrhythmias can also be caused by some substances or drugs. These include antiarrhythmics, beta blockers, psychotropics, sympathomimetics,     caffeine, amphetamines, and cocaine."
     

       From the University of Maryland Medical Center Health Library:
              http://www.umm.edu/ency/article/000184.htm


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    AHA Recommendation for Stroke Prevention

    Treating atrial fibrillation is an important way to help prevent stroke. That's why the
     American Heart Association recommends aggressive treatment of this heart arrhythmia.

    Drugs are also used to help reduce stroke risk in people with AF.  Anticoagulant
     and antiplatelet medications thin the blood and make it less prone to clotting. 
     Warfarin is the anticoagulant now used for this purpose, and aspirin is the
    antiplatelet drug most often used. Long-term use of warfarin in patients with AF
    and other stroke risk factors can reduce stroke by 68 percent.

    • Physicians differ on the choice of drugs to prevent embolic stroke — stroke caused
       by a blood clot. It's clear that warfarin is more effective against this type of stroke
      than aspirin. However, warfarin has more side effects than aspirin.
      Examples include potential bleeding problems or ulcer.
       
    • Patients at high risk for stroke should probably be treated with warfarin rather
       than aspirin unless there are clear reasons not to do so. 
       
    • Aspirin is the standard treatment for patients at low risk for stroke and under 75 years of age.

      http://www.americanheart.org/presenter.jhtml?identifier=4451

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    Diagnostic Test Results
     

  •      "Electrocardiography detects arrhythmias as well as ischemia and infarction by
                    showing prolonged or shortened intervals elevated or depressed T waves,
                    premature contractions, or absence of waves.

  •      Blood tests reveal electrolyte abnormalities, such as hyperkalemia (high  
         potassium)
                    or hypokalemia and hypermagnesemia or hypomagnesemia, as well as drug
                    toxicities.

  •       Arterial blood gas analysis reveals acid-base abnormalities, such as acidemia or
                    alkalemia.

  •      Holter monitoring, event monitoring, and loop recording show the presence of an
                    arrhythmia.

  •      Exercise testing detects exercise-induced arrhythmias.

  •      Electrophysiologic testing identifies the mechanism of an arrhythmia and the
                   location of accessory pathways; it also assesses the effectiveness of
                   antiarrhythmic drugs, radiofrequency ablation, and implantable
                   cardioverter-defibrillators (ICDs)."

                
                                                                            Source:                                  

    Atlas of Pathophysiology, Second Edition.  Lippincott Williams and Wilkins, 2005.
     

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Causes of Atrial Fibrillation
 

          "In atrial fibrillation and flutter, the atria are stimulated to contract very quickly and    
         differently from the normal activity originating from the sinoatrial node. This results in
         ineffective and uncoordinated contraction of the atria in atrial fibrillation, and in a
         peculiarly organized contraction pattern in atrial flutter.

         The condition can be caused by impulses which are transmitted to the ventricles in an  
          irregular fashion or by some impulses failing to be transmitted. This makes the
          ventricles
          beat irregularly, which leads to an irregular (and usually fast) pulse in atrial fibrillation.

         In atrial flutter, however, the ventricles may beat rapidly, but regularly. If the atrial
         fibrillation/flutter is part of a condition called sick sinus syndrome, the ventricles may
         beat  more slowly than normal. Thus, during atrial fibrillation the ventricles, by beating
         too fast or too slow, may fail to pump enough blood to meet the needs of the body.

         Underlying causes of atrial fibrillation and flutter include dysfunction of the sinus node
         (the "natural pacemaker" of the heart) and a number of heart and lung disorders,
         including coronary artery disease, rheumatic heart disease, mitral valve disorders,
         pericarditis, and others.

         Hyperthyroidism, hypertension, and other diseases can cause arrhythmias, as can
         recent heavy alcohol use (binge drinking). Some cases of atrial fibrillation or flutter
         occur in the setting of a heart attack or soon after surgery on the heart.

         Atrial fibrillation can affect both men and women. The prevalence of atrial fibrillation
         increases with age and varies from 1 case out of 200 persons for people younger
         than 60 years, to almost 9 cases out of 100 persons for people over 80 years."

       

        Treatment of Atrial Fibrillation

         "In certain cases, atrial fibrillation may require emergency treatment to convert the
         arrhythmia to normal (sinus) rhythm, either with electrical cardioversion or with the
         administration of intravenous drugs, such as dofetilide or ibutilide.

         Long-term treatment varies depending on the cause of the atrial fibrillation or flutter.
         Medication may include beta-blockers, calcium channel blockers, digitalis or other
         medications (such as anti-arrhythmic drugs) which slow the heartbeat or slow
         conduction of the impulse from the atria to the ventricles.

         Medications may also include blood thinners, such as heparin or coumadin,
         to reduce the risk of a thromboembolic event such as a stroke.

         Some selected patients with atrial fibrillation, rapid heart rates, and intolerance to
         medication may require a catheter procedure on the atria called radiofrequency
         ablation.

         For most patients with atrial flutter, radiofrequency ablation is the current treatment of
         choice. Some patients with atrial fibrillation and rapid heart rates may need the
         radiofrequency ablation done not on the atria, but directly on the AV junction
         (i.e., the area that normally filters the impulses coming from the atria before they
         proceed to the ventricles).

         Ablation of the AV junction leads to complete heart block. These patients then
         require a permanent pacemaker.

        The disorder is usually controllable with treatment. The natural tendency
        of atrial fibrillation, however, is to become a chronic condition."

From the National Institutes of Health http://www.nlm.nih.gov/medlineplus/ency/article/000184.htm


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                            Parental Atrial Fibrillation Increases Risk in Offspring,
                                        Finds NHLBI'sFramingham Heart Study        

          "Having a parent with atrial fibrillation (AF) strongly increased an offspring’s risk of
          developing this heart rhythm disorder, according to a study of participants in the
          National Heart, Lung, and Blood Institute’s (NHLBI) Framingham Heart Study.

          The risk doubled for offspring with at least one parent with AF compared to offspring
          whose parents did not have the condition. The study of 2,243 adults, published in the
          June 16 issue of The Journal of the American Medical Association, is the first to find a
          genetic connection for AF in a community sample.

         “This important research finding will need to be confirmed but it opens up a new
          avenue
          of research on atrial fibrillation. Now scientists can start looking at genetic factors that
          might contribute to AF – searching for the genes involved in this increasingly
          common disorder,” said Barbara Alving, M.D., acting director of the NHLBI, one of the
          components of the National Institutes of Health.

          The study’s findings strongly support the notion that AF has genetic underpinnings.
          Most cases of AF occur in older people. The disorder affects about 1 in every 10
          persons aged 80 and over. In the new study, the risk of AF tripled when both parents
          and the and the offspring were under age 75. The risk also tripled when the analysis
          was limited to offspring who had no clinically apparent heart disease.

          “Disorders with a genetic component often occur at a younger age or in the absence
          of major diseases like heart disease that trigger the condition,” said the study’s lead
          investigator Caroline Fox, M.D. M.P.H., of the Framingham Heart Study.

          "Atrial fibrillation is the most common heart rhythm disorder in the U.S., affecting
          more than 2 million adults. The prevalence of the condition is rising and scientists
          predict that about 5.6 million Americans will have the disorder by 2050.
          Known causes of AF include abnormalities in the heart's structure and long-term
          uncontrolled high blood pressure.

          AF occurs when electrical signals in the heart's upper chambers (the atria) are fired in 
          a very fast, uncontrolled manner. Electrical signals then arrive in the heart's lower
          chambers (the ventricles) in an erratic pattern, creating an irregular heartbeat and
          affecting the heart’s ability to pump blood. Atrial fibrillation can produce symptoms
          including palpitations, an unexplained, rapid heartbeat, lightheadedness, or
          occasionally chest pain. It can also be asymptomatic. AF can lead to complications
          such as stroke and congestive heart failure. Treatment via drugs, surgery or devices, 
          is designed to slow the heart rate and/or restore normal rhythm, and to prevent
          stroke.  Blood-thinning medications (anticoagulants) are an important means of
          preventing stroke in AF patients.

          The Framingham Offspring study of AF involved 1165 women and 1078 men whose
          parents were members of the “original” Framingham Heart Study. The offspring were
          at least 30 years of age and free of atrial fibrillation at the first exam. Offspring and
          original study participants had routine clinic exams, including physical examinations,
          interviews, lab tests, and electrocardiograms.

          AF in both offspring and original “parental” participants was confirmed by an
          electrocardiogram. Parental cases occurred from 1949-2002 and offspring AF cases
          occurred from 1983-2002.

          When the Framingham researchers analyzed the data, they found that 30 percent of
          participants had at least one parent with AF. Seventy offspring (23 women) developed
          AF during the study at a mean age of 62 years. When stated in terms of 1000 persons
          per year, the results indicate that the number of offspring developing AF would be
          4.5 if a parent had AF and 3 if parents did not have AF.

          Fox cautioned that the Framingham findings should not alarm people who have a
          parent with AF. “AF with or without a family history is a common condition in the
          elderly. Our findings indicate to the scientific community that we need more research
          on the genetic mechanisms of AF and how they interact with environmental
          influences," she said.

          Fox added that Framingham scientists hope to conduct further research
          into the genetic basis of AF.

          Study limitations, noted Fox, include the small number of offspring cases
          of AF and a predominantly Caucasian group of participants.

          To interview Dr. Fox about this study, please call the NHLBI Communications Office at
          301-496-4236 or e-mail NHLBInews@nhlbi.nih.gov."

                                           From The US Department of Health and Human Services
                                                         NIH NEWS (National Institutes of Health )
 

           http://www.nhlbi.nih.gov/new/press/04-06-15.htm


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Omega-3 Fatty Acid Prevents Heart Rate Variability Reductions Associated
With Particulate Matter

Isabelle Romieu, Martha Maria Téllez-Rojo, Mariana Lazo, Abigail Manzano-Patiño, Marlene Cortez-Lugo, Pierre Julien, Marie Claire Bélanger, Mauricio Hernandez-Avila and Fernando Holguin

Instituto Nacional de Salud Pública, Cuernavaca, Mexico; Division of Pulmonary Allergy and Critical Care, Emory University School of Medicine, Atlanta, Georgia; and Laval University, Lipid Research Center, Quebec City, Canada

Correspondence and requests for reprints should be addressed to Fernando Holguin, M.D.,
1600 Clifton Road, NE, MS E-17, Atlanta GA 30333. E-mail: fch5@cdc.gov

Context: Environmental exposure to particulate matter of 2.5 µm or less (PM2.5) has been associated with changes in heart rate variability (HRV).

Objective: To evaluate the effect of supplementation with omega-3 polyunsaturated
fatty acids on the reduction of HRV associated with PM2.5 exposure.

Design: Randomized double-blind trial.

Setting: Mexico City, Mexico.

Participants: 50 nursing home residents older than 60 yr.

Intervention: Randomization to either 2 g/d of fish oil versus 2 g/d of soy oil as the control, with 6 mo follow-up (1-mo presupplementation and 5-mo supplementation) or repeated
HRV measurements. PM2.5 was monitored indoors and outdoors.

Main Outcome Measure: The association between HRV and 1 SD change in PM2.5 (8 µg/m3).

Results: In the group receiving fish oil, the reduction in HRV–high-frequency log10-transformed associated with a 1-SD change in PM2.5 was –54% (95% confidence interval,
 –72, –24) in the presupplementation phase, and only –7% (95% confidence interval,
 –20,+7) in the supplementation phase (p < 0.01 for the effect of supplementation),
 with changes in other HRV parameters also being significantly less pronounced
 during supplementation. Small decreases in PM2.5-associated reductions in HRV
parameters also occurred in the group receiving soy oil, but these were not significant.
 Fish oil supplementation was significantly better in preventing the reduction in
percentage of successive normal RR intervals differing by more than 50 ms (p = 0.03)
and the root square of the mean of the sum of the squares of differences
 between adjacent intervals (p = 0.05) than soy oil supplementation.

Interpretation: Supplementation with 2 g/d of fish oil prevented HRV decline
related to PM2.5 exposure in the study population.



From:  American Journal of Respiratory and Critical Care Medicine Volume 172. pp. 1534-1540, (2005)
© 2005 American Thoracic Society
 

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