The inclusion of regular physical conditioning as part of a cardiac rehabilitation program can significantly improve quality of life and reduce the risk of hospital admission for worsening symptoms, but no evidence shows a reduction in mortality rates as a result of exercise. Despite cardiac rehabilitation being a recommended treatment for patients with heart failure with reduced ejection fraction (HFrEF), it is still underused. The reasons why this happens are complex, heterogeneous, and encompass healthcare system-, referring physician-, program-, and patient-level barriers. According to Alexandre et al., the main reasons for HFrEF patients not being enrolled in cardiac rehabilitation were no medical referral (31%), concomitant medical problems (28%), patient refusal (11%), and geographical distance to the hospital (9%). Furthermore, whether this evidence can be extended to people with HFpEF or to those whose exercise regimen takes place entirely at home is unclear.Home visits and regular monitoring at heart-failure clinics reduce the need for hospitalization and improve life expectancy. Medication
Quadruple medical therapy using a combination of angiotensin-receptor neprilysin inhibitors (ARNI), beta blockers, mineralocorticoid receptor antagonists (MRA), and sodium glucose cotransporter-2 inhibitors (SGLT2 inhibitors) is now the standard of care as of 2021. First line medications
First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme (ACE) inhibitors (ACE-I), or angiotensin receptor blockers (ARBs) if the person develops a long-term cough as a side effect of the ACE-I.
50% of affected individuals develop dental abnormalities such as delayed eruption, dental root exposure, or resorption of the dental roots on the affected side. 35% have difficulty or inability to normally open the mouth or other jaw symptoms, including temporomandibular joint disorder and spasm of the muscles of mastication on the affected side. 25% experience atrophy of one side of the upper lip and tongue. Causes
The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma. Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Further, the National Organization for Rare Disorders has stated there is currently no evidence that Parry–Romberg syndrome is genetic or that it can be passed on to children. Various other theories about the cause and pathogenesis have been suggested, including alterations in the peripheral sympathetic nervous system (perhaps as a result of trauma or infection involving the cervical plexus or the sympathetic trunk), as the literature reported it following sympathectomy, disorders in migration of cranial neural crest cells, or chronic cell-mediated inflammatory process of the blood vessels. It is likely that the disease results from different mechanisms in different people, with all of these factors potentially being involved.