Did a web search. I'm sure there is a lot more out there but I did find this:
PROGNOSIS: POTENTIAL FOR RECOVERY
While peripartum cardiomyopathy shares many features of other forms of non-ischemic dilated cardiomyopathy, an important distinction is that women with this disorder have a much higher rate of spontaneous recovery of left ventricular function. As many as 50% of women presenting with this disorder will normalize their ejection fraction during subsequent follow-up, (12) most within the first six months. This higher rate of spontaneous recovery compared to other forms of IDCM likely reflects differences in timing, not in pathogenesis. Patients presenting with idiopathic dilated cardiomyopathy may do so months to years after the initial myocardial injury, long after the time for spontaneous recovery has past. In contrast, for women presenting with peripartum cardiomyopathy, the timing of the initiating event is clear. As women present in the acute phase of the illness, there is a greater chance of spontaneous recovery once the hemodynamic or "inflammatory" stress of pregnancy resolves.
Prognosis is directly correlated to recovery of left ventricular function. For those women whose LVEF normalizes during follow-up their prognosis is excellent as without the stimulus of a subsequent pregnancy the chance of development of heart failure or future LV dysfunction is minimal. For those women whose left ventricular function does not recover, prognosis remains guarded and mortality rates as high as 10-50% in some series have been reported (13,14).
Few clinical clues exist which help predict which women will recover their LV function. Our experience suggests that LV size is an important predictor, as women presenting without significant LV dilatation appeared to have a greater chance of spontaneous recovery during follow-up. In contrast, women with marked LV dilatation at presentation appeared to have a greater likelihood of developing into a chronic cardiomyopathy. Initial NYHA class or hemodynamics do not seem to predict the likelihood of subsequent recovery. Women who remain severely functionally limited or inotrope dependent despite therapy should be evaluated for possible cardiac transplantation, however, we attempt to delay transplantation if possible for the first six months postpartum in the hopes that some recovery of LV function will allow transplant to be deferred.
The medical management of peripartum cardiomyopathy is similar to other forms of heart failure due to systolic dysfunction with the exception that in women presenting during pregnancy, potential effects to the fetus must be considered (15,16). Therapy with angiotensin converting enzyme inhibitor are the core of therapy of women postpartum, but are contraindicated during pregnancy itself due to potential teratogenic effects ACE inhibitor use during pregnancy, particularly in the second and third trimester, has been associated with increased fetal loss and a fetopathy characterized by fetal hypotension, oligohydramnios-anuria and renal tubular dysplasia. Angiotensin receptor antagonist (ARB's) while a reasonable alternative to ACE inhibitor therapies postpartum, should be similarly avoided during pregnancy due to potential adverse effects.
For women presenting during pregnancy with symptoms of congestion due to cardiomyopathy, a loop diuretic can be utilized generally at the lowest effective dose. A small daily dose of digoxin can be added. In terms of afterload reduction, hydralazine and nitrates can be used as an alternative. Despite the growing evidence of the effectiveness of beta receptor antagonist (beta blockers) as heart failure therapy, less is known about their effectiveness for PPCM and their use must be individualized. In terms of safety, there is a long history of the use of beta blocker therapy in treating pregnant women with hypertension without any known adverse effects to the developing fetus, and for patients on these agents prior to diagnosis, they can be safely continued.
For patients presenting postpartum, ACE inhibitor therapy should be initiated. In those patients not tolerating ACE inhibitors due to cough, ARB's are an acceptable alternative. Symptoms of congestion should be treated with a loop diuretic and digoxin. For patients who remain symptomatic despite ACE inhibitor and diuretic therapy, beta blocker therapy can be initiated. These should be used with caution in the occasional acute patient who presents with significant systolic dysfunction without ventricular enlargement. These patients with normal LV chamber size have a markedly reduced stroke volume, and occasionally the reductions in heart rate associated with beta blocker therapy are poorly tolerated.
Like other forms of heart failure, this syndrome can lead to thrombotic and embolic complications. Patients with evidence of a systemic embolus, or with severe left ventricular dysfunction and documented mural thrombus, anticoagulation should be considered. Warfarin therapy is contraindicated during pregnancy and for women requiring anticoagulation, heparin must be utilized. Postpartum, in patients with either a clinical embolic event or with ultrasound evident of thrombus formation, Warfarin therapy should be utilized for a period of six months. The need for chronic anticoagulation should then be reassessed depending on the state of LV recovery.
As in other forms of non-ischemic dilated cardiomyopathy, ventricular arrhythmias can be an important clinical issue. Patients presenting with sudden death or ventricular tachycardia with hemodynamic compromise, strong consideration of an ICD is warranted due to the potential for a fatal recurrence. For patients presenting with symptomatic ventricular tachyarrhythmia which are hemodynamically well tolerated, management can be tempered somewhat by the potential transient nature of the myopathy and amiodarone therapy at 200 to 400 mg po qd is an alternative. If left ventricular function recovers, the risk of serious arrhythmic event is markedly diminished and amiodarone therapy can be discontinued. For patients with asymptomatic non-sustained ventricular tachyarrhythmia we would not initiate amiodarone therapy, but would focus on correction of metabolic abnormalities and consider the addition of a beta receptor antagonist if not already being utilized.
ACTIVITY AND FOLLOW-UP
Although patients are encouraged to remain as active as their functional status allows, aerobic activities and heavy lifting are discouraged for at least the first six months postpartum while assessing the degree of left ventricular recovery. Given the metabolic demands of lactation, breast feeding is strongly discouraged in more symptomatically limited patients. As pharmacologic therapy to the patient can be passed on to the child in breast milk, we also discourage breast feeding in more functional patients, though this could be considered with careful monitoring of the child.
In terms of the reassessment of LV function, the echocardiogram should be repeated at 6 months post delivery; for those patients with persistent cardiomyopathy beta blockers should be added at this point if not already on therapy.