Tachyarrhythmia-induced cardiomyopathy

P.T. Trindade, R. Lerch
Center and Division of Cardiology, University Hospital Geneva, Geneva, Switzerland
Correspondence: Professor René Lerch, Cardiology Center, Geneva University Hospital, 24 rue Micheli-du-Crest, 1211 Geneva 14, Switzerland.
Tel: +41 22 372 7193, fax: +41 22 372 7229, e-mail: rene.lerch@hcuge.ch

Introduction
Atrial fibrillation and heart failure are frequent cardiovascular disorders and are often connected. In the SOLVD treatment study,[1] 10% of patients with reduced left ventricular ejection fraction (<35%) and symptoms of heart failure also demonstrated atrial fibrillation. Even in patients with asymptomatic systolic left ventricular dysfunction the incidence of atrial fibrillation is as high as 4%.[1] Traditionally, the occurrence of atrial fibrillation in left ventricular dysfunction is considered to be the consequence of increased atrial loading, which in animal models favors profibrillatory changes of atrial conduction and refractoriness.[2] The following case report highlights the concept of tachycardia-induced heart failure, which suggests that in some patients rapid atrial fibrillation may be the cause, or at least a contributory factor, rather than the consequence of depressed left ventricular ejection fraction.

Case history
A 37-year-old housewife presented to her general practitioner complaining of dyspnea on exertion, dry cough, and palpitations persisting for 2 to 3 weeks. Her past medical history was relevant for episodes of palpitations, which had been linked to supraventricular ectopic beats. Antibiotic treatment had been started 1 week prior to her office visit but without any effect. Apart from oral contraception no other cardiovascular risk factors could be identified. An electrocardiogram showed atrial fibrillation with a fast ventricular rate of up to 190 bpm (Figure 1) and the patient was admitted to our hospital.


Figure 1. Twelve-lead surface electrocardiogram showing atrial fibrillation with a rapid ventricular rate of up to 190 bpm.

On examination she was apyretic, blood pressure was at 120/70 mm Hg, heart rate at around 160 bpm, and respiratory rate at 18/min. Heart sounds were normal, with no murmurs nor pericardial friction rub. There was bilateral basal pulmonary hypoventilation, with no pulmonary rales. Full blood count was within the normal range, and blood chemistry showed elevated D-dimers at 1680 mg/L. Echo Doppler examination of the leg veins and a pulmonary ventilation-perfusion scan ruled out pulmonary embolism. An echocardiogram showed a mildly dilated left atrium, moderate mitral regurgitation (Figure 2A) and severely depressed left ventricular systolic function, with an estimated ejection fraction of 20%. Thyroid function tests were normal. The patient was anticoagulated, put on an ACE inhibitor, and rate control was initially attempted with digoxin but with only a mild effect. Diuretics were given during the first days of hospitalization, which rapidly improved the symptoms of heart failure.

Figure 2. The transthoracic echocardiogram in the parasternal long-axis view depicts moderate mitral regurgitation (panel A) during atrial fibrillation, which disappears after cardioversion to sinus rhythm (panel B).

No specific causes for the decreased left ventricular function could be found either by history, physical examination, or ancillary tests. A cardiac angiogram showed normal coronary arteries. To reduce the heart rate, a b-blocker was started on the third hospital day but the ventricular response remained fast with an average heart rate of 110 bpm, varying between 82 bpm and 182 bpm during Holter monitoring. The decision was made to proceed with early cardioversion after exclusion of atrial thrombi by transesophageal echocardiography (TEE). This examination revealed mild spontaneous contrast in the left atrium, normal flow velocity, and no thrombus in the left atrial appendage (Figure 3). These findings allowed electrical cardioversion, which reverted the heart to normal sinus rhythm.







Figure 3. The left atrial appendage is examined during a TEE examination in which no thrombi could be detected.

A follow-up echocardiogram performed 5 days after cardioversion showed a moderate to severe decrease of left ventricular systolic function (estimated ejection fraction 35%), normal-sized cavities, and a regression of the mitral regurgitation (Figure 2B). The patient left the hospital on a b-blocker, an ACE inhibitor, digoxin, and anticoagulation.
The patient was seen again 8 months later while she was asymptomatic and remained in sinus rhythm. A new echocardiogram showed a normal-sized left ventricle and a normal left ventricular ejection fraction of 55%. In light of the fact that no other cause had been identified to explain the episode of severely decreased systolic function and the fact that the left ventricular function recovered after conversion to sinus rhythm, a diagnosis of tachyarrhythmia-induced cardiomyopathy was made.

Discussion
Tachycardia may reduce left ventricular ejection fraction by at least two mechanisms which, at the subcellular level, may be related. The first mechanism is the negative force-frequency relationship observed in heart muscle strips from severely failing explanted hearts.[3] Accordingly, in contrast with normal hearts, the force of contraction, and consequently the ejection fraction at a given load, decreases with increasing heart rate. A proposed hypothesis for this “acute” deterioration of contractile force during tachycardia includes impaired calcium reuptake by the sarcoplasmic reticulum during tachycardia-related shortening of diastole.[3] The second mechanism is progressive structural “remodeling” of the myocardium in response to long-lasting tachycardia, leading to persistent deterioration of myocyte function. Indeed, the hearts of pigs,[4] dogs,[5] and rabbits[6] develop during rapid pacing for 2 to 4 weeks, morphological and functional alterations of the left ventricular myocardium, which are similar to those observed in dilated cardiomyopathy. Among the observed changes in the myocyte phenotype is altered expression of cytoskeletal proteins,[7] creatine kinase, and atrial natriuretic peptide.[8] The reduced left ventricular function persists after cessation of rapid pacing, but may recover over a period of several weeks.
Although the concept of tachycardia-induced depression of left ventricular function has initially been documented under in vitro conditions, observations in patients indicate that the phenomenon is clinically relevant. In patients with atrial fibrillation and medically insufficient heart rate control, improvement of left ventricular ejection fraction has been observed after direct current countershock (DC) cardioversion[9] or ablation of the atrioventricular node and pacing.[10] In our patient, ejection fraction improved only slightly immediately after cardioversion but recovered completely during the 8-month follow-up.
The case reemphasizes the importance of adequate heart rate control in patients presenting with depressed left ventricular function and atrial fibrillation. Classical treatment of decompensated heart failure by diuretics and ACE inhibitors alone may reduce heart rate to some extent by reducing sympathetic stimulation. Digoxin is often the preferred initial choice for additional heart rate control in patients with severe depression of left ventricular function. Diltiazem, which has proven at least as effective, entails the disadvantage of negative inotropy, and starting doses of b-blocker regimens of heart failure are often insufficient for this purpose, as was the case in this patient. Therefore, rapid cardioversion is often desirable.
In patients with atrial fibrillation lasting for more than 48 h, therapeutic anticoagulation for 3 to 4 weeks followed by medical or DC cardioversion is standard practice. Because of inappropriate medical heart rate control in our patient, TEE-guided cardioversion was selected. Using this approach, medical or electrical cardioversion is performed even after only a few hours of anticoagulation, provided cardiac intracavitary thrombus and intense spontaneous contrast are excluded at TEE. In the ACUTE study,[11] 1222 patients with atrial fibrillation and no indication for immediate cardioversion were randomized to cardioversion after either 4 weeks of anticoagulation or early exclusion of thrombus by TEE. The incidence of thromboembolic events within the 8 weeks of observation was not significantly different between groups, averaging 0.81% in the TEE group and 0.50% in the control group. Thus, TEE-guided cardioversion offers an alternative to the conventional approach and may be particularly useful in patients with severe depression of left ventricular function and insufficient medical heart rate control.

Conclusion
Although tachycardia may be considered to some extent a compensatory response of the failing heart to maintain cardiac output, inappropriate high heart rate, which is present in most cases of untreated atrial fibrillation, may be causally involved in the mechanisms underlying left ventricular dysfunction. Although a cause-effect relationship is not proven in the present case, the dramatic improvement of left ventricular function after restoration of sinus rhythm and the absence of an alternative explanation for reversible myocardial impairment suggest that tachycardia may have been a major contributory factor to heart failure. However, longer follow-up will be required to exclude subclinical myocardial disease. Furthermore, the history of this patient illustrates the interest of TEE-guided cardioversion in patients with heart failure and insufficient medical heart rate control.

REFERENCES
 

1: Am J Cardiol 1992 Oct 1;70(9):894-900 Related Articles, Books, LinkOut

Clinical characteristics of patients in studies of left ventricular dysfunction (SOLVD).

Johnstone D, Limacher M, Rousseau M, Liang CS, Ekelund L, Herman M, Stewart D, Guillotte M, Bjerken G, Gaasch W, et al.

Division of Epidemiology and Clinical Applications Clinical Trials Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.

The Studies of Left Ventricular Dysfunction (SOLVD) trials were designed to evaluate the effects of enalapril on long-term mortality in patients with severe left ventricular (LV) dysfunction. Patients with LV ejection fractions less than or equal to 0.35 and symptoms of congestive heart failure (CHF) were enrolled in the treatment trial, whereas those with no history of overt CHF and taking no treatment directed for LV dysfunction were enrolled in the prevention trial. The baseline clinical characteristics of SOLVD patients were compared to characterize differences between patients in these 2 separate but concurrent trials. From over 70,000 patients screened with LV dysfunction, 4,228 patients were enrolled in the prevention trial and 2,569 patients in the treatment trial. Ischemic heart disease was the primary cause of LV dysfunction in both prevention (83%) and treatment (71%) trial patients. Prior myocardial infarction was present in 80% of the prevention and 66% of the treatment trial patients (p less than 0.001). In the prevention trial, infarction was recent (less than or equal to 6 months) in 27% patients and remote (greater than 6 months) in 57% patients. Treatment trial patients had proportionately more women (20 vs 13%; p less than 0.001) and non-Caucasians (20 vs 14%; p less than 0.001), as well as the coexisting risk factors of hypertension (42 vs 37%; p less than 0.001) and diabetes (26 vs 15%; p less than 0.001) than did prevention trial patients. Clinical characteristics of patients in both trials were influenced by the gender and race of enrolled patients. Similarly, coronary artery bypass surgery was performed less often in women and non-Caucasians.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication Types:
  • Clinical Trial
  • Multicenter Study
  • Randomized Controlled Trial


PMID: 1529944 [PubMed - indexed for MEDLINE]

 
2: Cardiovasc Res 1989 Oct;23(10):882-6 Related Articles, Books, LinkOut

The effect of atrial dilatation on the genesis of atrial arrhythmias.

Solti F, Vecsey T, Kekesi V, Juhasz-Nagy A.

Cardiovascular Surgical Clinic, Budapest, Hungary.

The effect of atrial stretching on the genesis of atrial arrhythmias was studied in 26 dogs. Left atrial dilatation was produced by inflation of a balloon catheter. Electrophysiological studies were performed by programmed electrical stimulation of the atrium and ventricle. The irritability of the atrium markedly increased when it was distended and atrial arrhythmias (sustained or non-sustained atrial tachyarrhythmias) could regularly be induced by administration of an early extrastimulus or--more rarely--by atrial burst pacing. In 10 cases spontaneous atrial tachycardia appeared during atrial balloon dilatation. The atrial effective refractory period shortened and the atrial conduction time lengthened on atrial stretching, while other electrical variables (cycle length, sinus node recovery time, atrioventricular conduction time, intraventricular conduction, ventricular refractory period, QT interval) remained unchanged. Atrial balloon dilatation was not accompanied by marked haemodynamic changes, and the left ventricular pressure curve, the contractility of the left ventricle and the central venous pressure did not change significantly on atrial stretching. The experimental data suggest that the atrial dilatation plays an important part in the pathogenesis of atrial arrhythmias.

PMID: 2620315 [PubMed - indexed for MEDLINE]
 
3: Circulation 1995 Sep 1;92(5):1169-78 Related Articles, Books, LinkOut
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Alterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy.

Pieske B, Kretschmann B, Meyer M, Holubarsch C, Weirich J, Posival H, Minami K, Just H, Hasenfuss G.

Medizinische Klinik III, Universitat Freiburg, Germany.

BACKGROUND: The present study was performed to test the hypothesis that the altered force-frequency relation in human failing dilated cardiomyopathy may be attributed to alterations in intracellular calcium handling. METHODS AND RESULTS: The force-frequency relation was investigated in isometrically contracting ventricular muscle strip preparations from 5 nonfailing human hearts and 7 hearts with end-stage failing dilated cardiomyopathy. Intracellular calcium cycling was measured simultaneously by use of the bioluminescent photoprotein aequorin. Stimulation frequency was increased stepwise from 15 to 180 beats per minute (37 degrees C). In nonfailing myocardium, twitch tension and aequorin light emission rose with increasing rates of stimulation. Maximum average twitch tension was reached at 150 min-1 and was increased to 212 +/- 34% (P < .05) of the value at 15 min-1. Aequorin light emission was lowest at 15 min-1 and was maximally increased at 180 min-1 to 218 +/- 39% (P < .01). In the failing myocardium, average isometric tension was maximum at 60 min-1 (106 +/- 7% of the basal value at 15 min-1, P = NS) and then decreased continuously to 62 +/- 9% of the basal value at 180 min-1 (P < .002). In the failing myocardium, aequorin light emission was highest at 15 min-1. At 180 min-1, it was decreased to 71 +/- 7% of the basal value (P < .01). Including both failing and nonfailing myocardium, there was a close correlation between the frequencies at which aequorin light emission and isometric tension were maximum (r = .92; n = 19; P < .001). Action potential duration decreased similarly with increasing stimulation frequencies in nonfailing and end-stage failing myocardium. Sarcoplasmic reticulum 45Ca2+ uptake, measured in homogenates from the same hearts, was significantly reduced in failing myocardium (3.60 +/- 0.51 versus 1.94 +/- 0.18 (nmol/L).min-1.mg protein-1, P < .005). CONCLUSIONS: These data indicate that the altered force-frequency relation of the failing human myocardium results from disturbed excitation-contraction coupling with decreased calcium cycling at higher rates of stimulation.

PMID: 7648662 [PubMed - indexed for MEDLINE]
 
4: Aust N Z J Med 1999 Jun;29(3):395-402 Related Articles, Books, LinkOut

Large animal models of heart failure.

Power JM, Tonkin AM.

Department of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Vic. jmp@austin.unimelb.edu.au

Congestive heart failure (HF) is a major focus of medical research. Its incidence has greatly increased in recent decades because of an aging population base and the increasingly successful treatment of other forms of chronic cardiac disease. Relevant large animal models of HF should reflect the complex interactions of cardiac dysfunction, neurohumoral dynamics and peripheral vascular abnormalities found in human HF. A number of large animal models have been developed, especially in dogs, sheep and swine, using naturally occurring HF, or single or combinations of interventions, as instruments to trigger the development of HF. Naturally occurring HF models are not commonly used because of ethical or perceived ethical grounds, however, King Charles Cavalier Spaniel and Yucatan Mini Pig models have been described. Tachycardia induced HF is the most commonly used HF model. Ventricular pacing at 220-240 bpm results in profound low output, biventricular, oedematous failure in two to three weeks. Lower pacing rates result in a more stable, sustainable, lesser degree of failure. Positive features of this model include 'acceptance', aetiological relevance to patient tachycardia induced HF, neurohumoral and functional profile similar to most human HF, relatively low cost simple preparation, ability to manipulate the degree of failure with pacing rate, reversibility, reliability and a large amount of published multi species data. Limitations to the use of the model are the rapid onset, the fact that reversibility is only relevant to the tachycardia induced patient HF, the absence of hypertrophy in failure, the diminished plasma atrial natriuretic peptide (ANP) levels, absence of ANP of ventricular origin, and the interference between rapid pacing and therapeutic interventions. Myocardial damage models of HF include those models induced by ischaemia, eg due to coronary occlusion (ligation or aneroid) or intracoronary microembolism, transmyocardial DC shock, toxic cardiomyopathy from adriamycin, doxorubicin or catecholamines. Overload models of HF may be induced by high pressure from aortic constriction, aortic regurgitation, renal artery constriction, pulmonary stenosis or aortocaval shunts, or by induction of mitral regurgitation from chordae or leaflet damage. No single, all-encompassing, large animal model of HF exists to date. Selection of the type of model to be used should be based primarily on the hypotheses to be tested and secondarily on the available resources and facilities.

Publication Types:
  • Review
  • Review, Tutorial


PMID: 10868511 [PubMed - indexed for MEDLINE]

 
5: Cardiovasc Res 1999 Oct;44(1):146-55 Related Articles, Books, LinkOut

Comment in:

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Abnormal Ca2+ release from cardiac sarcoplasmic reticulum in tachycardia-induced heart failure.

Yamamoto T, Yano M, Kohno M, Hisaoka T, Ono K, Tanigawa T, Saiki Y, Hisamatsu Y, Ohkusa T, Matsuzaki M.

Second Department of Internal Medicine, Yamaguchi University School of Medicine, Japan.

OBJECTIVE: In heart failure, little information is available as to the Ca2+ release function of sarcoplasmic reticulum (SR), which plays a major role in cardiac contractile function. Here, we assessed the rapid kinetics of drug-induced Ca2+ release from cardiac SR in combination with a measurement of ryanodine binding in heart failure. METHODS: The SR vesicles were isolated from dog left ventricular (LV) muscles (normal (N), n = 10; pacing induced heart failure (HF), n = 10). The time course of SR Ca2+ release was continuously monitored by a stopped-flow apparatus using arsenazoIII as a Ca2+ indicator, and Ca2+ uptake and [3H]ryanodine binding assays were done using a filtration method. RESULTS: The amount of Ca2+ uptake was reduced in HF to 55% of N (P < 0.05). Even the more marked and earlier appeared decrease was seen in the rate constant and the initial rate of polylysine (PL; a specific release trigger)-induced Ca2+ release (P < 0.05). However, the PL concentration dependency of the initial rate shifted towards lower concentrations of PL in HF than in N ([PL] at half maximum stimulation = 0.13 vs. 0.35 microM). The [3H]ryanodine binding assay revealed a lower Bmax (pmol/mg) in HF than in N (0.91 +/- 0.19 vs. 2.64 +/- 0.59, P < 0.05), but no difference in Kd (nM) (0.95 +/- 0.29 vs. 0.90 +/- 0.11, P = n.s.). The [PL] dependency on the enhancement of [3H]ryanodine binding again showed a shift towards lower [PL] in HF than in N. CONCLUSIONS: In pacing-induced heart failure, the Ca2+ releasing function of SR is disturbed, which may result in an intra-cellular Ca2+ transient that was slowed down.

PMID: 10615398 [PubMed - indexed for MEDLINE]

 
6: Basic Res Cardiol 1998 Feb;93(1):50-5 Related Articles, Books, LinkOut
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Myosin heavy chain synthesis during the progression of chronic tachycardia induced heart failure in rabbits.

Eble DM, Walker JD, Samarel AM, Spinale FG.

Cardiovascular Institute, Loyola University Chicago, Maywood, IL 60153, USA. deble@luc.edu

Chronic tachycardia causes LV dilatation and dysfunction, with no hypertrophy. However, the contributing mechanisms responsible for the left ventricular (LV) remodeling in the absence of myocardial growth in this model of heart failure remain unclear. Therefore, the goal of the present study was to serially examine changes in LV function, steady state myosin heavy chain (MHC) mRNA levels, in vivo synthesis rates, and abundance with the progression of chronic tachycardia induced heart failure. Adult rabbits (3.5-4.5 kg) were studied after one, two, or three weeks of pacing ventricular tachycardia (VT; 400 bpm) and in controls (n = 6 for all groups). LV fractional shortening was reduced by 30% at week one and by over 50% at week three of chronic VT. End-diastolic dimension (EDD) increased at week two compared to controls (1.66 +/- 0.10 vs 1.35 +/- 0.11 cm, p < 0.05) and increased further at week three of VT (1.70 +/- 0.06 cm, p < 0.05). The progressive changes in LV geometry and function with chronic VT were not associated with concomitant time dependent changes in LV mass or MHC mRNA levels. In contrast, MHC fractional synthesis rates increased and reached statistical significance at week three of VT compared to controls (8.3 +/- 0.8 vs 5.5 +/- 0.5%/day, p < 0.05). Despite the stable or increased MHC protein synthesis rates, there was no change in MHC protein abundance at any point during the progression of VT induced heart failure, implicating enhanced MHC protein degradation. Thus, this study demonstrated that a contributory mechanism for the LV remodeling and lack of myocardial growth, which occurs with VT induced heart failure, is enhanced contractile protein degradative processes.

PMID: 9538937 [PubMed - indexed for MEDLINE]
 
7: Am J Physiol 1995 Jun;268(6 Pt 2):H2426-39 Related Articles, Books, LinkOut

Contractile and cytoskeletal content, structure, and mRNA levels with tachycardia-induced cardiomyopathy.

Eble DM, Spinale FG.

Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425, USA.

Chronic supraventricular tachycardia (SVT)-induced cardiomyopathy is associated with left ventricular (LV) dilatation, increased wall stress, neurohormonal activation, and no change in LV mass. To determine mechanisms for changes in LV geometry and function with SVT cardiomyopathy, LV and myocyte function, contractile protein content and mRNA levels, and cytoskeletal protein structure and mRNA levels were examined in 12 pigs with SVT cardiomyopathy (paced at 240 beats/min for 3 wk) and in 12 controls. With SVT cardiomyopathy, LV fractional shortening fell by 61%, and end-diastolic dimension increased by 42%, with no change in LV mass-to-body weight ratio (3.36 +/- 0.15 vs. 3.14 +/- 0.13 g/kg). Myocyte contractile function was reduced by 33%, myocyte length was increased by 28%, and cross-sectional area was decreased by 19% with SVT cardiomyopathy. Total protein, myosin heavy chain (MHC), and actin appeared unchanged with SVT cardiomyopathy at the LV or myocyte level. Moreover, there was no change in mRNA levels for MHC (0.57 +/- 0.05 vs. 0.59 +/- 0.09 mRNAOD/rRNAOD) or cardiac alpha-actin (0.58 +/- 0.08 vs. 0.58 +/- 0.04 mRNAOD/rRNAOD) with SVT cardiomyopathy. In contrast, mRNA levels for specific cytoskeletal proteins were significantly increased with SVT cardiomyopathy, and immunofluorescent localization of contractile and cytoskeletal proteins in isolated myocytes revealed alterations in cytoskeletal architecture. Thus changes in LV and myocyte geometry with SVT cardiomyopathy were associated with no change in contractile protein content or mRNA at the chamber or myocyte level. Furthermore, increased cytoskeletal protein abundance and mRNA and reorientation of cardiocyte cytoarchitecture may have contributed to the LV and myocyte remodeling with SVT cardiomyopathy.

PMID: 7611495 [PubMed - indexed for MEDLINE]
 
8: Circ Res 1994 Oct;75(4):615-23 Related Articles, Books, LinkOut

Endomyocardial gene expression during development of pacing tachycardia-induced heart failure in the dog.

Williams RE, Kass DA, Kawagoe Y, Pak P, Tunin RS, Shah R, Hwang A, Feldman AM.

Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Md.

Selective and specific changes in gene expression characterize the end-stage failing heart. However, the pattern and relation of these changes to evolving systolic and diastolic dysfunction during development of heart failure remains undefined. In the present study, we assessed steady-state levels of mRNAs encoding a group of cardiac proteins during the early development of left ventricular dysfunction in dogs with pacing-induced cardiomyopathy. Corresponding hemodynamic assessments were made in the conscious state in the same animals and at the same time points at baseline, after 1 week of ventricular pacing, and at the onset of clinical heart failure. Systolic dysfunction dominated after 1 week of pacing, whereas diastolic dysfunction was far more pronounced with the onset of heart failure. Atrial natriuretic factor mRNA was undetectable in 7 of 12 hearts at baseline but was expressed in all hearts at 1 week (P < .01 by chi 2 test), and it increased markedly with progression to failure (P = .05). Creatine kinase-B mRNA also rose markedly with heart failure (P < .01). Levels of mRNA encoding beta-myosin heavy chain, mitochondrial creatine kinase, phospholamban, and sarcoplasmic reticulum Ca(2+)-ATPase did not significantly change from baseline, despite development of heart failure. Additional analysis to determine if these mRNA changes were related to the severity of diastolic or systolic dysfunction revealed that phospholamban mRNA decreased in hearts with larger net increases in end-diastolic pressure (+19.2 +/- 1.9 mm Hg) compared with those hearts in which it did not change (+4.0 +/- 4.9, P < .02).(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 7923607 [PubMed - indexed for MEDLINE]
 
9: Am J Cardiol 1993 Sep 1;72(7):560-6 Related Articles, Books, LinkOut

Time course of hemodynamic changes and improvement of exercise tolerance after cardioversion of chronic atrial fibrillation unassociated with cardiac valve disease.

Van Gelder IC, Crijns HJ, Blanksma PK, Landsman ML, Posma JL, Van Den Berg MP, Meijler FL, Lie KI.

Department of Cardiology, Thoraxcenter, University Hospital Groningen, The Netherlands.

This study prospectively assessed the time course, magnitude and mechanism of the hemodynamic changes after restoration of sinus rhythm in patients with chronic atrial fibrillation (AF) unassociated with valvular disease. Severe cardiac dysfunction may occur after chronic supraventricular tachycardia in patients with and without underlying cardiac disease. Improvement may follow abolishment of the arrhythmia or adequate slowing of the ventricular rate. Eight patients were studied with a mean previous duration of AF of 10 +/- 9 months. Ejection fraction, exercise capacity and the atrial contribution to the left ventricular filling (only during sinus rhythm) were studied before cardioversion, after cardioversion and 1 week, 1 month and 6 months thereafter. A significant improvement in ejection fraction from 36 +/- 13 to 53 +/- 8% (p < 0.05) occurred at 1 month after cardioversion. Concomitantly, peak oxygen consumption had increased at 1 month, from 20.1 +/- 7 to 25.2 +/- 6 ml/min/kg (p < 0.05). Thereafter, no further improvement in hemodynamic parameters occurred. The atrial systole improved already at 1 week (from 3 +/- 5 to 16 +/- 11%, p < 0.05) and remained unchanged thereafter. Thus, restoration of sinus rhythm was associated with a delayed improvement in ejection fraction and maximal exercise capacity, preceded by an early restoration of atrial contractility and an acute slowing of the heart rate. The discrepancy in time course of restoration of atrial and ventricular function parameters suggests that an intrinsic left ventricular cardiomyopathy is present in patients with AF.

PMID: 8362771 [PubMed - indexed for MEDLINE]
 
10: Circulation 2000 Mar 14;101(10):1138-44 Related Articles, Books, LinkOut
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Clinical outcomes after ablation and pacing therapy for atrial fibrillation : a meta-analysis.

Wood MA, Brown-Mahoney C, Kay GN, Ellenbogen KA.

Virginia Commonwealth University/Medical College of Virginia, Richmond, VA 23298-0053, USA.

BACKGROUND: Radiofrequency ablation of the atrioventricular node and permanent pacing are used for symptomatic relief in patients with medically refractory atrial fibrillation. In this study, meta-analysis was used to clarify clinical outcomes and survival after ablation and pacing therapy using data from the published literature. METHODS AND RESULTS: We used 21 studies with a total of 1181 patients in the meta-analysis. All patients had medically refractory atrial tachyarrhythmias, primarily atrial fibrillation (97%). Nineteen measures of clinical outcome, encompassing quality of life, ventricular function, exercise duration, and healthcare use, were derived from the studies. The meta-analysis demonstrated significant improvement after ablation and pacing therapy in all outcome measures except fractional shortening, which demonstrated a trend toward improvement (P=0.08). Ejection fraction did show significant improvement (P<0.001). The calculated 1-year total and sudden death mortality rates after ablation and pacing therapy were 6.3% and 2.0%, respectively. CONCLUSIONS: Ablation and pacing therapy improves a broad range of clinical outcomes for patients with medically refractory atrial fibrillation. The calculated 1-year mortality rates after this therapy are low and comparable with medical therapy.

Publication Types:
  • Meta-Analysis


PMID: 10715260 [PubMed - indexed for MEDLINE]

 
11: N Engl J Med 2001 May 10;344(19):1411-20 Related Articles, Books, LinkOut

Comment in:

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Use of transesophageal echocardiography to guide cardioversion in patients with atrial fibrillation.

Klein AL, Grimm RA, Murray RD, Apperson-Hansen C, Asinger RW, Black IW, Davidoff R, Erbel R, Halperin JL, Orsinelli DA, Porter TR, Stoddard MF; Assessment of Cardioversion Using Transesophageal Echocardiography Investigators.

Cleveland Clinic Foundation, Department of Cardiology, OH 44195, USA. kleina@ccf.org

BACKGROUND: The conventional treatment strategy for patients with atrial fibrillation who are to undergo electrical cardioversion is to prescribe warfarin for anticoagulation for three weeks before cardioversion. It has been proposed that if transesophageal echocardiography reveals no atrial thrombus, cardioversion may be performed safely after only a short period of anticoagulant therapy. METHODS: In a multicenter, randomized, prospective clinical trial, we enrolled 1222 patients with atrial fibrillation of more than two days' duration and assigned them to either treatment guided by the findings on transesophageal echocardiography or conventional treatment. The composite primary end point was cerebrovascular accident, transient ischemic attack, and peripheral embolism within eight weeks. Secondary end points were functional status, successful restoration and maintenance of sinus rhythm, hemorrhage, and death. RESULTS: There was no significant difference between the two treatment groups in the rate of embolic events (five embolic events among 619 patients in the transesophageal-echocardiography group [0.8 percent]) vs. three among 603 patients in the conventional-treatment group [0.5 percent], P=0.50). However, the rate of hemorrhagic events was significantly lower in the transesophageal-echocardiography group (18 events [2.9 percent] vs. 33 events [5.5 percent], P=0.03). Patients in the transesophageal-echocardiography group also had a shorter time to cardioversion (mean [+/-SD], 3.0+/-5.6 vs. 30.6+/-10.6 days, P<0.001) and a greater rate of successful restoration of sinus rhythm (440 patients [71.1 percent] vs. 393 patients [65.2 percent], P=0.03). At eight weeks, there were no significant differences between the two groups in the rates of death or maintenance of sinus rhythm or in functional status. CONCLUSIONS: The use of transesophageal echocardiography to guide the management of atrial fibrillation may be considered a clinically effective alternative strategy to conventional therapy for patients in whom elective cardioversion is planned.

Publication Types:

  • Clinical Trial
  • Multicenter Study
  • Randomized Controlled Trial


PMID: 11346805 [PubMed - indexed for MEDLINE]

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