As expected, with cardiac damage and dysfunction, there can be an elevation of these markers in patients with cardiac amyloidosis. These markers have been incorporated into the various staging/scoring systems used by physicians to determine severity of the disease and prognosis. Biopsies
Extracardiac biopsies of tissues of the kidney, liver, peripheral nerve, or abdominal fat can be used to confirm the presence of amyloid deposits. Amyloid deposits in biopsy samples are confirmed through the use of Congo red dye, which produces a green birefringence when viewed under polarized light. Sirius red staining or electron microscopy examination can also be done. The determination of the type of amyloid can be done by immunohisto-labeling techniques as well as immunofluorescence staining.For light-chain amyloidosis patients, bone marrow biopsies could be conducted to determine the baseline percentage of plasma cells and to rule out multiple myeloma. Catheterization
Right heart catheterization is the test used to test for elevated diastolic ventricular pressures. This test is more invasive and would be performed after inconclusive endomyocardial biopsy samples. Cardiac magnetic resonance imaging
Cardiac magnetic resonance (CMR) is capable of measuring the thickness of different areas of the heart. This can be used for quantification of the deposits in the heart. CMR also shows the characterization of myocardial tissue through patterns of gadolinium enhancements. However, none of the CMR technique is able to differentiate ATTR-CM and AL-CM definitely.For AL-CM, 68% of them have symmetrical and concentric left ventricular hypertrophy.
Camptodactyly is a medical condition that causes one or more fingers or toes to be permanently bent. It involves fixed flexion deformity of the proximal interphalangeal joints. Camptodactyly can be caused by a genetic disorder. In that case, it is an autosomal dominant trait that is known for its incomplete genetic expressivity. This means that when a person has the genes for it, the condition may appear in both hands, one, or neither. A linkage scan proposed that the chromosomal locus of camptodactyly was 3q11.2-q13.12. Causes
The specific cause of camptodactyly remains unknown, but there are a few deficiencies that lead to the condition. A deficient lumbrical muscle controlling the flexion of the fingers, and abnormalities of the flexor and extensor tendons.A number of congenital syndromes may also cause camptodactyly:

Jacobsen syndrome
Beals syndrome
Blau syndrome
Freeman–Sheldon syndrome
Cerebrohepatorenal syndrome
Weaver syndrome
Christian syndrome 1
Gordon syndrome
Jacobs arthropathy-camptodactyly syndrome
Lenz microphthalmia syndrome
Marshall–Smith–Weaver syndrome
Oculo-dento-digital syndrome
Tel Hashomer camptodactyly syndrome
Toriello–Carey syndrome
Trisomy 13
Stuve–Wiedemann syndrome
Loeys–Dietz syndrome
Fetal alcohol syndrome
Fryns syndrome
Marfan syndrome
Carnio-carpo-tarsal dysthropy

Genetics
The pattern of inheritance is determined by the phenotypic expression of a gene—which is called expressivity. Camptodactyly can be passed on through generations in various levels of phenotypic expression, which include both or only one hand. This means that the genetic expressivity is incomplete. It can be inherited from either parent. In most of its cases, camptodactyly occurs sporadically, but it has been found in several studies that it is inherited as an autosomal dominant condition. Treatment
If a contracture is less than 30 degrees, it may not interfere with normal functioning. The common treatment is splinting and occupational therapy.