A reclined position and forced bed rest were the most beneficial.Other treatments evident from the previous studies were improving physique and posture, appropriate levels of exercise where possible, wearing loose clothing about the waist, and avoiding postural changes such as stooping, or lying on the left or right side, or the back in some cases, which relieved some of the palpitations and chest pains, and standing up slowly can prevent the faintness associated with postural or orthostatic hypotension in some cases. Pharmacological intervention came in the form of digitalis, a group of glycoside drugs derived from the foxglove (Digitalis purpurea), which is now known to act as a sodium-potassium ATPase inhibitor, increasing stroke volume and decreasing heart rate; at the time it was used for the latter effect in patients with palpitations. History
Da Costas syndrome is named for the surgeon Jacob Mendes Da Costa, who first observed it in soldiers during the American Civil War. At the time it was proposed, Da Costas syndrome was seen as a very desirable physiological explanation for "soldiers heart". Use of the term "Da Costas syndrome" peaked in the early 20th century. Towards the mid-century, the condition was generally re-characterized as a form of neurosis. It was initially classified as "F45.3" (under somatoform disorder of the heart and cardiovascular system) in ICD-10, and is now classified under "somatoform autonomic dysfunction". Da Costas syndrome involves a set of symptoms which include left-sided chest pains, palpitations, breathlessness, and fatigue in response to exertion.
As with all antipsychotics thioridazine has been linked to cases of tardive dyskinesia (an often permanent neurological disorder characterised by slow, repetitive, purposeless and involuntary movements, most often of the facial muscles, that is usually brought on by years of continued treatment with antipsychotics, especially the first-generation (or typical) antipsychotics such as thioridazine) and neuroleptic malignant syndrome (a potentially fatal complication of antipsychotic treatment). Blood dyscrasias such as agranulocytosis, leukopenia and neutropenia are possible with thioridazine treatment. Thioridazine is also associated with abnormal retinal pigmentation after many years of use. Thioridazine has been correlated to rare instances of clinically apparent acute cholestatic liver injury. Pharmacology
Thioridazine has the following binding profile:
Note: The Binding affinities given are towards cloned human receptors unless otherwise specified
Acronyms used
HB – Human brain receptor
RC – Cloned rat receptor
ND – No data

Metabolism
Thioridazine is a racemic compound with two enantiomers, both of which are metabolized, according to Eap et al., by CYP2D6 into (S)- and (R)-thioridazine-2-sulfoxide, better known as mesoridazine, and into (S)- and (R)-thioridazine-5-sulfoxide. Mesoridazine is in turn metabolized into sulforidazine. Thioridazine is an inhibitor of CYP1A2 and CYP3A4. History
The manufacturer Novartis/Sandoz/Wander of the brands of thioridazine, Mellaril in the US and Canada and Melleril in Europe, discontinued the drug worldwide in June 2005. Antibiotic activity
Thioridazine is known to kill extensively drug-resistant tuberculosis and to make methicillin-resistant Staphylococcus aureus sensitive to β-lactam antibiotics. A possible mechanism of action for the drugs antibiotic activity is via the inhibition of bacterial secretion pumps.