Tachycardia induced cardiomyopathy is a type of dilated cardiomyopathy caused by chronic or frequent tachycardia that leads to impaired left ventricular function. This impairment is partially or fully reversible by controlling the heart rate. The document discusses the criteria, types, pathophysiology, diagnosis, and treatment of tachycardia induced cardiomyopathy. Treatment focuses on heart rate control through medications, ablation, or devices, which can improve ejection fraction and heart failure symptoms over time.

1. TACHYCARDIA INDUCED
CARDIOMYOPATHY
Dr.Rohit Manoj Kumar

2.  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

3.  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

4. 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

5. 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

6. Tachycardia induced
cardiomyopathy

7. 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.

8. 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

9.  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

10. 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

11.  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

12.  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

13. Associations
 SVT: EAT, AF, Afl, AVNRT, AVRT, PJRT
 VT: RVOT VT, Fascicular VT
 Frequent ectopics: Ventricular, atrial

14. 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

15. Proposed mechanisms
 Myocardial energy depletion
 Impaired energy utilization
 Ischemia
 Abnormal calcium handling

16. 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

17.  Unclear why some patients with chronic
tachyarrhythmia develop ventricular
dysfunction whereas others tolerate high rates
and maintain normal systolic function

18.  Presumed risk factors include:
 Type, rate and duration of tachyarrhythmia
 Patient’s age
 Underlying heart disease
 Drugs
 Coexisting medical conditions

19.  Presentation:
 Variable
 Palpitations due to tachycardia per se
 Symptoms of heart failure like fatigue, exercise
intolerance, dyspnea, pedal edema etc

20. Relation between AF and HF

21. Triggers
Atrial Fibrillation
Substrate

23. Diagnosis

24.  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

25.  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.

26.  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

27.  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

28.  Right ventricular biopsy studies revealed
nonspecific findings of varying degrees of
cellular hypertrophy and interstitial fibrosis
consistent with a nonspecific cardiomyopathy

29. Treatment

30.  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

31.  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

32. AF THERAPY
ANTITHROMBOTIC RX
RHYTHM
CONTROL
RATE
CONTROL
OR ?
AND

33. The AFFIRM Investigators. N Engl J Med. 2002;347:1825-1833.
AFFIRM Trial: Rate vs Rhythm Control
Management 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%

34. AFFIRM: All-Cause Mortality
Rate N:
Rhythm N:
2027
2033
1925
1932
1825
1807
1328
1316
774
780
236
255
0
5
10
15
20
25
30
0 1 2 3 4 5
Mortality,%
Rate
Rhythm
p=0.078 unadjusted
Time (years)
p=0.068 adjusted
The AFFIRM Investigators. N Engl J Med. 2002;347:1825-1833.

35. 100 –
80 –
60 –
40 –
20 –
0 –
Time (years)
Percent
With AF
Recurrence
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 = 58.62
p < 0.0001

36. Risk of Death in Affirm:
Is Sinus Rhythm the Goal?
*HR <1.00: Decreased risk of death, HR >1.00: Increased risk of death
AFFIRM Investigators. Circulation. 2004;109:1509-13.
AFFIRM: Selected time-dependent covariates associated with survival
Sinus rhythm <0.0001 0.53 0.39–0.72
Warfarin <0.0001 0.50 0.37–0.69
Digoxin 0.0007 1.42 1.09–1.86
Antiarrhythmic 0.0005 1.49 1.11–2.01
Covariate P Hazard ratio* 99% CI

37. 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

39. Rate control plus
anticoagulation preferred
Rhythm control
preferred
• 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

40. 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.

41. 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
Dronedaron
e
Flecainide
Propafenon
e
Sotalol Dronedaron
e
Flecainide
Propafenon
e
Sotalol
Cathete
r
Ablation
Cathete
r
Ablation
Amiodarone
Amiodaron
e
Cathete
r
Ablation
Amiodarone
Dofetilide
AblCath
eteratio
n
Cathete
r
Ablation
Amiodaron
e
Dofetilide
Substantial
LVH
No Yes
Dofetilide
Dronedaro
ne
Sotalol
Amiodaron
e
Dofetilide
No (or
Minimal)
Heart
Disease
Hypertension
Coronary
Artery
Disease
Heart Failure

42. Prognosis

43.  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

44.  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

45.  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

46.  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

47. Conclusion

48.  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.