In 1756, Alexander Russell, after examining a Turkish patient, gave one of the most detailed clinical descriptions of the disease. Physicians in the Indian subcontinent would describe it as kala-azar (pronounced kālā āzār, the Urdu, Hindi, and Hindustani phrase for "black fever", kālā meaning black and āzār meaning fever or disease). In the Americas, evidence of the cutaneous form of the disease in Ecuador and Peru appears in pre-Inca pottery depicting skin lesions and deformed faces dating back to the first century CE. Some 15th- and 16th-century texts from the Inca period and from Spanish colonials mention "valley sickness", "Andean sickness", or "white leprosy", which are likely to be the cutaneous form.It remains unclear who first discovered the organism. David Douglas Cunningham, Surgeon Major of the British Indian army, may have seen it in 1885 without being able to relate it to the disease. Peter Borovsky, a Russian military surgeon working in Tashkent, conducted research into the etiology of "oriental sore", locally known as sart sore, and in 1898 published the first accurate description of the causative agent, correctly described the parasites relation to host tissues and correctly referred it to the protozoa. However, because his results were published in Russian in a journal with low circulation, his results were not internationally acknowledged during his lifetime.
Hydralazine with nitrates may replace ACE-I in breastfeeding mothers or before delivery; however, evidence suggests that this course of treatment may not be as effective as ACE-I but beneficial when necessary.If EF is less than 35%, anticoagulation is indicated, as there is a greater risk of developing left ventricular thrombi (blood clots). Sometimes implantation of a left ventricular assist device (LVAD) or even heart transplant also becomes necessary.It is important that the patient receives regular follow-up care including frequent echocardiograms to monitor improvement or the lack thereof, particularly after changes of medical treatment regimes. Patients who do not respond to initial treatment, defined as left ventricular EF remaining below 20% at two months or below 40% at three months with conventional treatment may merit further investigation, including cardiac magnetic resonance imaging (MRI), cardiac catheterization, and endomyocardial biopsy for special staining and for viral polymerase chain reaction (PCR) analysis. Antiviral therapy, immunoabsorption, intravenous gamma globulin, or other immunomodulation therapy may then be considered accordingly, but following a controlled research-type protocol.Since no one knows for sure exactly when to discontinue treatment, even when recovery occurs quickly, it is still recommended that both ACE-I and B-B be continued for at least one year after diagnosis.PPCM patients have an increased risk for sudden death and it is seen that they benefit from implantable cardioverter defibrillator (ICD) and cardiac resynchronization therapy to prevent sudden cardiac death.