Poor clinical education (or lack thereof) for DID and other dissociative disorders has been described in literature: "most clinicians have been taught (or assume) that DID is a rare disorder with a florid, dramatic presentation." Symptoms in patients are often not easily visible, which complicates diagnosis. DID has a high correlation with, and has been described as a form of, complex post-traumatic stress disorder. There is a significant overlap of symptoms between borderline personality disorder and DID, although symptoms are understood to originate from different underlying causes. Historical prevalence
Rates of diagnosed DID were increasing in the late 20th century, reaching a peak of diagnoses at approximately 40,000 cases by the end of the 20th century, up from less than 200 diagnoses before 1970. Initially DID along with the rest of the dissociative disorders were considered the rarest of psychological conditions, diagnosed in less than 100 by 1944, with only one further case reported in the next two decades. In the late 1970s and 80s, the number of diagnoses rose sharply. An estimate from the 1980s placed the incidence at 0.01%. Accompanying this rise was an increase in the number of alters, rising from only the primary and one alter personality in most cases, to an average of 13 in the mid-1980s (the increase in both number of cases and number of alters within each case are both factors in professional skepticism regarding the diagnosis).
Contractility in the heart
People experiencing some forms of heart failure have a significant decrease in the contractile ability of muscle cells in the heart (cardiomyocytes). This impaired contractility occurs through a number of mechanisms. Some of the main problems associated with decreased contractility in those with heart failure are issues arising from imbalances in the concentration of calcium. Calcium permits myosin and actin to interact which allows initiation of contraction within the cardiomyocytes. In those with heart failure there may be a decreased amount of calcium within the cardiomyocytes reducing the available calcium to initiate contraction. When contractility is decreased the amount of blood being pumped out of the heart into circulation is decreased as well. This reduction in cardiac output can cause many systemic implications such as fatigue, syncope and other issues associated with decreased blood flow to peripheral tissues. Mechanism of action
cAMP causes increased activation of protein kinase A (PKA). PKA is an enzyme that phosphorylates many elements of the contractile machinery within the heart cell. In the short term this leads to an increased force of contraction. Phosphodiesterases are enzymes responsible for the breakdown of cAMP. Therefore, when phosphodiesterases lower the level of cAMP in the cell they also lower the active fraction of PKA within the cell and reduce the force of contraction. Milrinone is a phosphodiesterase-3 inhibitor. This drug inhibits the action of phosphodiesterase-3 and thus prevents degradation of cAMP. With increased cAMP levels there is an increase in the activation of PKA.