with diuretic administration to reduce preload. Hypertension is common, and afterload reduction is accomplished with hydralazine or another vasodilator. Because of marked fetal efects, angiotensin-converting enzyme inhibitors are withheld until after delivery. With chronic heart failure, the incidence of associated thromboembolism is high, and thus prophylactic heparin is often recommended.
Lt ventricular assist devices are now employed more fre quently for acute and chronic heart failure treatment. A few reports describe their use during pregnancy (LaRue, 2011;
Sims, 2011). Extracorporeal membrane oxygenation (ECMO) was reported to be lifesaving in a woman with fulminating peri partum cardiomyopathy, and it may be used in women with pulmonary hypertension (Meng, 2017; Smith, 2009).
In the United States, those at greatest risk for endocarditis are those with congenital heart lesions, intravenous drug use, degenerative valve disease, and intracardiac devices (Karchmer, 2015). Subacute bacterial endocarditis usually stems from a low-virulence bacterial infection superimposed on an underlying structural lesion. These are usually native valve infections. Organisms that cause indolent endocarditis are most often viridans-group streptococci or Staphylococcus or Enterococcus species. Among intravenous drug abusers and those with catheter-related infections, Staphylococcus aureus predominates. With prosthetic valve infections, Staphylococcus epidermidis is a frequent cause. Streptococcus pneumoniae and Neisseria gonorrhoeae may occasionally cause acute, fulminating disease. Others have reported Neisseria sicca and N mucosa, group B streptococcus, and Escherichia coli endocarditis during pregnancy or peripartum (Cox, 1988; Deger, 1992; Kangavari, 2000; Kulas, 2006).
Infective endocarditis symptoms vary and often develop insidiously. Fever, often with chills, is seen in 80 to 90 percent of cases, a murmur is heard in up to 85 percent, and anorexia, fatigue, and other constitutional symptoms are common (Karchmer, 2015). Clinical clues are anemia, proteinuria, and manifestations of embolic lesions that include petechiae, focal neurological changes, chest or abdominal pain, and ischemia in an extremity. In some cases, heart failure develops. Symptoms may persist for several weeks before the diagnosis is found, and a high index of suspicion is necessary.
Diagnosis is made using the Duke criteria, which include positive blood cultures for typical organisms and evidence of endocardial involvement (Hoen, 2013; Pierce, 2012). Echocardiography may be diagnostic, but lesions <2 mm or those on the tricuspid valve may be missed. If uncertain, transesophageal echocardiog raphy is accurate and informative. Importantly, a negative echo cardiographic study does not exclude endocarditis.
Treatment is primarily medical, and ascertainment of the infecting organism and its sensitivities is imperative for antimi crobial selection. Guidelines for appropriate antibiotic treatment (Habib, 2015; Karchmer, 2015). Recalcitrant bacteremia and heart failure due to valvular dysfunction are but a few reasons that persistent valvular infection may require replacement.