Aterosclerose coronariana casos inexplicados devem receber uma angiografia pode haver doena

oculta e miocrdio em hibernao.

Cardiomiopatia induzida por estresse: SCA com SST na ausncia de doena coronariana. Precipitada
por estresse psicolgico intenso, em mulheres na ps-menopausa. Recuperao em at 4 semanas.

Cardiomiopatia infecciosa:

Viral: por citotoxicidade direta ou por resposta autoimune contra os micitos infectados.

HIV

Doena de Chagas: miocardite aguda, dilatao cardaca e taquicardia.

Doena de Lyme: defeito de conduo. Autolimitada e leve. Cardiomegalia ou efuso pericrdica

reversveis.

Cardiomiopatia hipertrfica (progresso a cardiomiopatia dilatada)

Cardiomiopatia txica: exposio a lcool, cocana, quimioterpicos e radiao.

lcool: dilatao do VE com reduo da FE. Casos avanados biventricular.

Cocaina: abstinncia leva reverso da disfuno miocrdica.

Cirrose

Cardiomiopatia do periparto

Carencial: deficincia de tiamina, selnio e L-carnitina. Reposio pode melhorar a funo cardaca.

Tiamina: inicia com alto dbito secundrio a vasodilatao. A seguir: baixo dbito por depresso
miocrdica.

Acmulo de cobalto (cerveja, prtese metlica), arsnico. Outros: mercrio, antimnio, ouro, crmio.

Autoimunidade: autoanticorpos contra B-1 adrenoreceptor, alfa-miosina de cadeia pesada, betamiosina de cadeia pesada, miosina de cadeia leve e troponina.

DRC dialtica

Sarcoidose

Doena celaca: CMD associada a anemia ferropriva refratria. Melhora com dieta livre de gluten.

LES: pode haver doena valvular, pericrdica, coronariana ou miocardite. Pode haver taquicardia de
repouso e cardiomegalia.

Endocrinopatias: disfuno tireoidiana, feocromocitoma, sndrome de Cushing, alteraes do GH (IGF1). Cardiopatia reversvel.

Cardiomiopatia mediada por taquicardia: taquicardias supraventriculares crnicas (>130 bpm).Com o

tratamento da arritmia, reverso da cardiopatia em at 3 meses.

Clinical manifestations and diagnosis of myocarditis in adults

Chagas heart disease: Clinical manifestations and diagnosis

Familial disease AHAs are found in approximately 30 percent of DCM patients [34,35,38], and in 20 to 30
percent of their asymptomatic relatives [39]. The significance of AHAs in the healthy relatives of patients with
DCM was evaluated in a series of 169 probands and 592 of their first and second degree relatives [40]. The
following findings were noted:

AHAs were significantly more common in family members of DCM patients than in patients with
noninflammatory heart disease, patients with ischemic heart disease, or normal blood donors (32 versus
1, 1, and 2.5 percent, respectively).

Relatives of DCM patients who later developed DCM were more likely to have AHAs than were relatives
who did not progress (69 versus 37 percent).
Thus, AHAs were more common in family members of DCM patients than in control subjects, and the presence
of AHAs in asymptomatic family members was associated with an increased likelihood of developing disease.
However, fully defining the role of autoimmune factors in familial cardiomyopathy requires further study.
Genetic causes of dilated cardiomyopathy Among patients with idiopathic DCM, it is estimated that up to
50 percent have familial disease. No clinical or histologic criteria, other than family history and careful
examination of relatives (including those who are asymptomatic), have been derived to distinguish familial from
nonfamilial disease. The mode of inheritance is usually autosomal dominant, although autosomal recessive, Xlinked, and mitochondrial inheritance have also been described. These disorders, as well as recommendations
for screening and counseling family members, are discussed elsewhere. (See "Genetics of dilated
cardiomyopathy" and "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment".)
Antibodies to a variety of cardiac proteins are present in approximately 30 percent of patients with DCM. These
antibodies are also present in 20 to 30 percent of the first and second degree relatives of DCM patients,
compared to 1 to 2 percent of control subjects. Furthermore, among relatives of DCM patients, the presence of
such antibodies is associated with a greater likelihood of developing DCM. (See 'Autoimmunity' below.)
DCM in patients who do not have a known family history of disease may also have a genetic basis.
(See "Genetics of dilated cardiomyopathy", section on 'Sporadic dilated cardiomyopathy'.)
Inherited syndromes DCM can be a common and important component of a number of inherited disorders,
including a number of neuromuscular diseases (eg, muscular dystrophies and myotonic dystrophy), hereditary
hemochromatosis, and the hereditary sideroblastic anemias and thalassemias. (See "Inherited syndromes
associated with cardiac disease".)
Left ventricular noncompaction Left ventricular noncompaction (LVNC), also called isolated ventricular
noncompaction and left ventricular hypertrabeculation, is a rare unclassified cardiomyopathy with an altered
myocardial wall due to intrauterine arrest of compaction of the loose interwoven meshwork that makes up the
fetal myocardial primordium. LVNC has been identified in 0.05 percent of patients undergoing
echocardiography. Affected patients present with HF, thromboembolism, or ventricular arrhythmias. The

diagnosis is established by echocardiography, although the changes can also be seen on magnetic resonance
imaging. (See "Isolated left ventricular noncompaction".)