Cardiomyoplasty

Introduction

Cardiac failure is a serious condition with various underlying pathophysiological mechanisms and having impact on multiple body functions. Cardiomyoplasty is a procedure for treating systolic type of congestive heart failure.

Procedure:

The left latissimusdorsi muscle is most commonly used for cardiomyoplasty. In this procedure, the latissimusdorsi muscle is wrapped around the left ventricle to contract during cardiac systole. Approximately 2 weeks after the surgery, electrical stimulation of the muscle with implanted electrodes is initiated. Fast fatigable type II skeletal muscle fiberscan be transformed into fatigue resistant type I fibers with 6–8 weeks of chronic electrical stimulation. The addition of sequential electrical stimuli leads to summation of skeletal muscle twitches which increases the duration and force of contraction. The skeletal muscle can be paced synchronously to every cardiac beat in variable modes such as 1:1 to 1:2 or to may be turned off during sleep. An epimyocardial sensing lead is placed over either the left or the right ventricle and connected to the cardio-myostimulator placed in a subcutaneous pocket. A period of 8 weeks is required to ‘train’ the muscle. A vascular delay period of 2 weeks is also required for recovery of distal muscle blood supply from a single vascular pedicle.

Cardiomyoplasty may improve peak oxygen consumption during exercise and also total exercise time.

Only clinically stable patients can undergo cardiomyolasty as patients with deranged general condition are unlikely to tolerate this prolonged preliminary period. The acute and chronic electrical stimulation and surgical manipulation with ischemia to distal muscle can damage the latissimusdorsi muscle. This can lead to muscle atrophy which may jeopardize a successful outcome after dynamic cardiomyoplasty.

Increase in the levels of enzyme creatinine kinase in the immediate post-operative period is suggestive of skeletal muscle flap ischemia. The skeletal muscle flap ischemia can lead to partial or total suppression of the muscle flap contraction due to electrical stimulation. The proper functioning of the latissimusdorsi muscle is important in the success of dynamic cardiomyoplasty.

Proposed mechanisms of action of cardiomyoplasty:

Experimental studies have postulated that dynamic cardiomyoplasty works as an active as well as a passive support of the damaged myocardium. The effects of this surgery include:

1. Assistance to cardiac systole

2. Reduction of left ventricular stress

3. Prevention of progressive ventricular dilation

4. Partial replacement of the damaged heart muscle

5. Reduction of myocardial oxygen consumption

6. Increase in blood flow to ischemic muscles

7. Improvement in the pressure–volume curves

8. Reversal of the remodeling process in heart failure

Some additional beneficial effects of cardiomyoplasty may include increased neuro-hormonal activity, modulation of baroreflex, effects on pathological factors such as endothelial dysfunction, hypertrophy, apoptosis, mitral or tricuspid regurgitation, atrial and ventricular arrhythmias, and oxidative stress. But these effects are yet to be proven.

Inclusion criteria:

Candidates for cardiomyoplasty should fulfill following criteria:

1. The most essential criteria is chronic systolic congestive heart failure due to ischemic or idiopathic dilated cardiomyopathy

2. Recurrent need of hospitalization

3. Left ventricular ejection fraction <30%

4. Cardiac index <2.5 l/min per m2 at rest

5. Stable condition on medical therapy enough to withstand a waiting time of 2–3 months before skeletal muscle flap can adaptor survive the operation

6. Patients with left ventricular tumor or aneurysms.

Cardiomyoplasty may improve peak oxygen consumption during exercise and also total exercise time. An increase in cardiac output and a reduction in pulmonary pressures has been documented in treadmill exercise test in patients with dilated cardiomyopathy.

Patients are not suitable for cardiomyoplasty if there is:

1. Requirement of intravenous inotropic drug support

2. Hemodynamic instability

3. Unstable clinical condition

4. Severe valvular dysfunction

5. Uncontrolled arrhythmia

6. History of resuscitation or ventricular tachycardia episodes

7. Major enlargement of left ventricle

8. Poor lung function with forced vital capacity <55% of predicted value

9. Drug or alcohol abuse

10. Atrial fibrillation

11. Older age

12. Syncope history

13. Severe pulmonary hypertension

14. Thrombus in left ventricle

15. Myocarditis

16. Coexistent severe systemic illness

17. Severe morbid obesity

18. Non-compliance with treatment

19. Coexisting disease with high surgical risk

The overall survival rates for cardiomyoplasty at 1 and 2 years range from 72 to 78% and from 57 to 60%, respectively. The 5 year survival rate is approximately 40%. The causes of mortality are mainly progressive heart failure and sudden death.