1.
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What is dynamic
cardiomyoplasty?
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| Dynamic cardiomyoplasty is a therapy for end-stage heart failure that has
been applied in more than 600 patients world-wide since its clinical introduction in 1985.
In cardiomyoplasty, the patient's own latissimus dorsi muscle is mobilized as a pedicle
graft, wrapped around the heart, and then stimulated in synchrony with cardiac systole.
The key principle behind muscle-powered cardiac assistance is that with chronic electrical
stimulation, skeletal muscle can be converted from fatiguing muscle to fatigue-resistant
muscle. |
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2.
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Who are the candidates for
this procedure?
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| In general, candidates for dynamic cardiomyoplasty include class III
NYHA heart failure patients who are deteriorating despite maximal medical therapy, but
still have some cardiac reserve. The objective criteria of this would be V max O2
of at least 10 ml/kg/min. Presently, patients with either heart failure caused by dilated
cardiomyopathy or ischemic heart disease have been included. Hypertrophic cardiomyopathy
is considered a contraindication. The patients must also have an intact latissimus dorsi
muscle and adequate function of muscular, neurologic pulmonary, hepatic, and renal
systems. |
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3.
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What are the major risk
factors of cardiomyoplasty?
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In a multicenter risk analysis from 31 centers worldwide, it was found
that patients with severely limited exercise ability (peak VO2 < 10 ml/kg/min.) have a
higher risk for procedure-related death. Both LVEF < 20% and a peak VO2 < 15
ml/kg/min., represent a significant risk for procedure-related death. Other reported risk
factors for early or late death include: high pulmonary vascular resistance, pulmonary
hypertension, a forced vital capacity of <55%, or severe biventricular heart failure,
preoperative dependence or intravenous intropic medications, and intractable NYHA Class IV
heart failure. Less clearly, some centers consider older age, very large heart, (end
diastolic dimension >80 mm), concomitant surgery, atrial fibrillation, low right
ventricular ejection fraction or right ventricular dysfunction, severe mitral
regurgitations, and severe ventricular arrhythmias as significant risk factors of poor
outcome. Experienced centers have shown a lower incidence of procedure-related death for
both low risk and high risk patients. However, experience has shown, a consultation
between new centers with more experienced centers can reduce or nearly eliminate the
learning curve for new centers.
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4.
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What are the clinical
results?
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| Overall, approximately 80 to 85% of surviving patients have shown NYHA
Class improvement (1.4 classes on average). This improvement has been consistent at all
follow-up points beginning at three months following surgery and present in every
multicenter report published. Quality of life, as measured in a Phase II FDA sponsored
study, reveals scores of quality of life that moved close to the normal range in all four
categories of the survey (daily activities, social activities, quality of interaction, and
mental health). Despite the consistent subjective improvement of cardiomyoplasty patients,
statistical objective improvement of ventricular function was lacking until completion of
the Phase II multicenter FDA study. In this study, significant improvement at one year was
found in left ventricular ejection fraction, left ventricular stroke work, and left
ventricular stroke index. Presently, Class III heart failure patients, cardiomyopathy can
be done with a mortality, for most patients, < 10%. |
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5.
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What is the mechanism of
action of cardiomyoplasty?
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Cardiomyoplasty was a procedure envisioned, and when first
performed, to benefit the patient by actively augmenting systolic function. It is now
believed, based on clinical and animal studies, that cardiomyoplasty results in clinical
improvement primarily by two mechanisms:
- A chronic girdling effect of the stimulated muscle wrap, which results in stabilization
of the remodeling process of heart failure and, at times, a reversal of this process
resulting in decrease LV dilatation, there by decreasing myocardial wall stress and
myocardial oxygen demand.
- Active systolic dynamic assistance has been shown in some patients, as well as in canine
heart failure models, to decrease myocardial stress and improve myocardial energetics.
It is probable that both mechanisms contribute heavily to the clinical improvement
seen. |
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