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TACHYCARDIA INDUCED CARDIOMYOPATHY
Dr.Rohit Manoj Kumar
Dilated cardiomyopathy (DCM): Characterized by dilation and impaired contraction of one or both ventricles
DCM - caused by a variety of specific diseases
≥ 50% of patients with DCM: - an etiologic basis will not be
identified - Idiopathic DCM
One series- 1278 patients with congestive heart failure Idiopathic — 51 percent Idiopathic myocarditis — 9 percent Occult coronary disease — 8 percent Other identifiable causes — 32 percent
Felker, et al. The spectrum of dilated cardiomyopathy. The Johns Hopkins experience with 1,278 patients. Medicine (Baltimore) 1999; 78:270
Clinical presentation Most patients present between age : 20-60 years
- Can occur in children and elderly
Symptoms of CHF Incidental detection of asymptomatic cardiomegaly Symptoms related to coexisting arrhythmia,
conduction disturbance Thromboembolic complications Sudden death
Reversible causes of cardiomyopathy
- Peripartum cardiomyopathy- Tachycardia-mediated cardiomyopathy- Takotsubo cardiomyopathy- Alcoholic cardiomyopathy- Cocaine - Medications- Ischemia- Endocrine dysfunction- SLE, Sarcoidosis- Nutritional deficiencies- Electrolyte abnormalities- Obstructive sleep apnea
Tachycardia induced cardiomyopathy
Introduction Defn: Impairment in left ventricular
function secondary to chronic tachycardia, which is partially or completely reversible once the tachyarrhythmia is controlled
Shown to occur both in experimental models and in patients with incessant tachyarrhythmia.
Fenelon et al proposed the following criteria:
Dilatation of the heart or heart failure
Chronic or very frequent cardiac arrhythmias, including incessant SVTs, AF or AFL and incessant VT
If chronic tachycardia continued more than 10-15% of the day, with an atrial rate of more than 150% of that predicted for age, cardiomyopathy occurs
Types Pure type:
chronic tachycardia causes LV dysfunction in a normal heart and completely recovers after termination
Impure Type: occurs in patients with structural heart diseases,
and cardiac dysfunction may only recover incompletely after termination of the tachycardia
Fenelon et al
Data from several studies and from case reports have shown that rate control by means of cardioversion, negative chronotropic agents, and surgical or catheter-based atrio-ventricular node ablation, resulted in significant improvement of systolic function
Diagnosis is usually made following observation of marked improvement in systolic function after normalization of heart rate
Clinicians should be aware that patients with unexplained systolic dysfunction may have tachycardia-induced cardiomyo-pathy, and that controlling the arrhythmia may result in improvement of systolic function
Exact incidence unclear, an association between tachycardia and cardiomyopathy has been recognized for some time*
*Kasper EK, J Am Coll Cardiol. 1994;23(3):586
Associations SVT: EAT, AF, Afl, AVNRT, AVRT, PJRT
VT: RVOT VT, Fascicular VT
Frequent ectopics: Ventricular, atrial
Pathophysiology Whipple et al. first described
experimental tachycardia-induced cardiomyopathy in 1962
They provided the first experimental model for the condition, demonstrating that rapid and protracted, atrial pacing led to low output heart failure
Proposed mechanisms Myocardial energy depletion
Impaired energy utilization
Ischemia
Abnormal calcium handling
Clinical features AGE:
can occur at any age reported in infants, children, adolescents, and adults
Follows any type of chronic or frequently recurring paroxysmal tachyarrhythmias
Atrial fibrillation, atrial flutter, ectopic atrial tachycardia, atrioventricular tachycardia, and ventricular tachycardia have all been reported to cause
Unclear why some patients with chronic tachyarrhythmia develop ventricular dysfunction whereas others tolerate high rates and maintain normal systolic function
Presumed risk factors include:
Type, rate and duration of tachyarrhythmia
Patient’s age
Underlying heart disease
Drugs
Coexisting medical conditions
Presentation: Variable
Palpitations due to tachycardia per se
Symptoms of heart failure like fatigue, exercise intolerance, dyspnea, pedal edema etc
Relation between AF and HF
Triggers
Atrial Fibrillation
Substrate
Diagnosis
No specific tests or markers available
A high index of suspicion derived from history and clinical features remains the only available tool
Diagnosis should be considered in any patient with left ventricular systolic dysfunction and chronic or frequently recurring cardiac arrhythmia
Evidence of previously normal systolic function, is particularly suggestive of this disorder
Ventricular rate that causes tachycardia-induced cardiomyopathy has not been determined, although any prolonged heart rate greater than 100 beats per minute may be important.
Important to recognize that resting heart rates are poor indicators of overall heart rates in patients with AF
As heart rate response to exercise may vary
Patients with well-controlled resting heart rates may have a rapid ventricular response with minimal activity and develop tachycardia-induced cardiomyopathy
Assessment of exercise heart rates and 24-hour Holter monitoring useful in diagnosing tachycardiomyopathy in patients with AF and ventricular systolic dysfunction
Imaging : ECHO, C MRI
Right ventricular biopsy studies revealed nonspecific findings of varying degrees of cellular hypertrophy and interstitial fibrosis consistent with a nonspecific cardiomyopathy
Treatment
Initial treatment in lines of heart failure: ACEI, B blockers, Diuretics
Heart rate normalization, either by rate or rhythm control, is the cornerstone of therapy
Results in increase in ejection fraction, reduction in end-systolic and end-diastolic volumes and improvement of both symptoms and exercise tolerance
The best means to achieve heart rate control vary
depending on the type of arrhythmia
Include antiarrhythmic drug therapy, external DC
cardioversion, radiofrequency catheter ablation,
pacemaker therapy or insertion of an implantable
cardioverter defibrillator
AF THERAPY
ANTITHROMBOTIC RX
RHYTHMCONTROL
RATECONTROL
OR ?
AND
The AFFIRM Investigators. N Engl J Med. 2002;347:1825-1833.
AFFIRM Trial: Rate vs Rhythm ControlManagement Strategy Trial Design
5-year, randomized, rate control vs. AARx Primary endpoint: overall mortality
Patient population 4060 patients with AF and risk factors for
stroke Minimal symptoms Mean Age = 69 yo Hx of hypertension: 70.8% CAD: 38.2% Enlarged LA: 64.7% Depressed EF: 26.0%
AFFIRM: All-Cause Mortality
Rate N:Rhythm N:
20272033
19251932
18251807
13281316
774780
236255
0
5
10
15
20
25
30
0 1 2 3 4 5
Mor
talit
y, %
RateRhythm
p=0.078 unadjusted
Time (years)
p=0.068 adjusted
The AFFIRM Investigators. N Engl J Med. 2002;347:1825-1833.
100 –
80 –
60 –
40 –
20 –
0 –
Time (years)
PercentWith AFRecurrence
Rate Control
Raitt, et al. Am H J 2006
0 1 2 3 4 5 6
N, Events (%) Rate control: Rhythm control:
563, 3 (0)729, 2 (0)
167, 383 (69)344, 356 (50)
98, 440 (80)250, 422 (60)
42, 472 (87)143, 470 (69)
10, 481 (92)73, 494 (75)
2, 484 (95)18, 503 (79)
Recurrence of AF in Affirm
Rhythm Control
Log rank statistic = 58.62p < 0.0001
Risk of Death in Affirm: Is Sinus Rhythm the Goal?
*HR <1.00: Decreased risk of death, HR >1.00: Increased risk of deathAFFIRM Investigators. Circulation. 2004;109:1509-13.
AFFIRM: Selected time-dependent covariates associated with survival
Sinus rhythm<0.0001
0.53
0.39–0.72Warfarin
<0.0001
0.50
0.37–0.69Digoxin
0.0007
1.42
1.09–1.86Antiarrhythmic 0.0005
1.49
1.11–2.01
CovariateP
Hazard ratio* 99% CI
RACE II Hypothesis: Lenient rate control is not inferior to
strict rate control
Randomly assigned 614 patients with permanent AF to: lenient rate-control strategy (resting heart rate
<110 beats per minute) strict rate-control strategy (resting heart rate
<80 beats per minute and heart rate during moderate exercise <110 beats per minute).
Primary outcome was a composite of death from cardiovascular causes, hospitalization for heart failure, and stroke, systemic embolism, bleeding, and life-threatening arrhythmic events.
No Differerence between Lenient and Strict Rate Control Van Gelder, et.al, for the RACE II Investigators NEJM April 15, 2010, No. 15, Vol 362: 1363-1373
Rate control plusanticoagulation preferred
Rhythm controlpreferred
• No AF symptoms• Long AF Hx• More SHD• Toxicity Risk• Greater risk of
proarrhythmia• Greater AF symptoms• AF compromising LV function• Symptoms despite rate control• Younger age• No or lesser SHD• Rx option of class IC AAD
In anticoagulation candidates, continue anticoagulation indefinitely
APPROACHES TO AF THERAPY
Problems with Meds
Proarrhythmia:
VT with Flecainide, Propafenone in LVH, CAD, Decreased EF
Torsades in Dronedarone, Sotalol, Dofetilide
Organ Toxicity: Amiodarone, procainamide, quinidine Organ Toxicity: Lupus, agranulocytosis,
thrombocytopenia, optic neuritis, pulmonary fibrosis, hepatitis, etc.
ACCF/AHA/HRS 2011 Guidelines Update Treatment of Atrial Fibrillation
*Knight BP. HRS Practical Rate and Rhythm Management of Atrial Fibrillation. Updated January 2010. Available at: http://www.hrsonline.org/ClinicalGuidance/upload/2010_rate-rhythm_guide1.pdf
“In some patients, especially young individuals with very symptomatic AF, ablation may be preferred over years of drug therapy.”*
Maintenance of Sinus Rhythm
DronedaroneFlecainidePropafenoneSotalol Dronedaro
neFlecainidePropafenoneSotalol
CatheterAblation
CatheterAblation
Amiodarone
Amiodarone
CatheterAblation
AmiodaroneDofetilide
AblCatheteration
CatheterAblation
AmiodaroneDofetilide
Substantial LVH
No Yes
DofetilideDronedaroneSotalol
AmiodaroneDofetilide
No (or Minimal)Heart Disease
Hypertension
Coronary Artery Disease
Heart Failure
Prognosis
Recovery of ventricular function after termination of or control of the tachyarrhythmia is extremely variable
Recovery may be complete, partial, or totally absent
The greatest improvement in left ventricular function generally occurs after 1 month of termination or control of arrhytmia
Followed by a slower improvement that reaches its maximum after 6-8months
The gradual time course of recovery of left ventricular function resembles recovery in hibernating myocardium after revascularization and may take up to 1 year
Recovery of function is greater in patients with more profoundly depressed left ventricular function at initial evaluation
Recurrent tachycardia can lead to an abrupt decline in LVEF
Close ongoing monitoring with clinic visits, ambulatory (Holter) monitoring, and echocardiography is essential
Moniter every three to six months for up to one to two years following the initial clinical improvement
In some patients whose LVEF has normalized, the LV chamber may remain somewhat enlarged
If tachycardia-mediated cardiomyopathy recurs, these patients are at substantial risk for sudden death and ICD implantation should be contemplated
Conclusion
Tachycardiomyopathy is a rare but potentially curable form of dilated cardiomyopathy
It should be considered in all patients whose systolic dysfunction is diagnosed subsequent to or concomitant with atrial fibrillation or chronic tachyarrhythmia.