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.