Congestive Heart Failure
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
A cardiomyopathy is a primary myocardial disorder. It is different than structural cardiac disorders, including congenital heart disorders, coronary artery disease, or valvular disorders. There are three main types of cardiomyopathies which include dilated, hypertrophic, and restrictive cardiomyopathies. Dilated cardiomyopathy is myocardial dysfunction that results in HF, with ventricular dilation and systolic dysfunction. Hypertrophic cardiomyopathy is a congenital or acquired disorder, with extreme ventricular hypertrophy and diastolic dysfunction, lacking increased afterload – it may be caused by coarctation of the aorta, systemic hypertension, or valvular aortic stenosis. Restrictive cardiomyopathy involves noncompliant ventricular walls, which resist diastolic filling. When one ventricle is affected it is usually the LV. However, both ventricles can be affected. An ischemic cardiomyopathy can occur with severe CAD, with or without infarction. It is not a primary myocardial disorder. Cardiomyopathies are signified by signs and symptoms of HF, based on systolic, diastolic, or combined dysfunction. Diabetic cardiomyopathy is cardiac dysfunction with structural, functional, and metabolic alterations even though coronary artery disease may be absent.
Cardiomyopathies in Pregnancy
Afshan B. Hameed, Diana S. Wolfe in Cardio-Obstetrics, 2020
The cardiomyopathies are a diverse group of disorders characterized by structural abnormalities of the heart muscle, many of which have a genetic component. Abnormalities may be anatomic (dilatation, thickened, or stiff musculature), histologic (manifested by fiber disarray, fibrofatty dysplasia, or fibrosis) or functional (systolic or diastolic dysfunction). Nonischemic cardiomyopathies have several phenotypes that include dilated, hypertrophic, restrictive, arrhythmogenic right ventricular, and unclassified. Each of these types may have familial and non-familial forms [1–3]. Several classificatory schemes exist, but the most recently endorsed is the MOGE(S) system which incorporates morphofunctional phenotype (M), organ involved (O), genetic inheritance (G), etiologic annotation (E), and functional status [1–4]. Examples of major nonischemic cardiomyopathies are shown in Box 12.1.
Clinical studies on Shengmai San
Kam-Ming Ko in Shengmai San, 2002
Since there is no curative treatment for dilated cardiomyopathy, symptomatic treatment is mainly used at the present time. While the majority of cases of dilated cardiomyopathy were not diagnosed until the initial strike of heart failure, the treatment regimen is generally similar to that of treating heart failure, with the aims being to 1) relieve symptoms and thereby improve the quality of living; and 2) to protect the myocardium in order to prolong the survival time. For mild cases of heart failure, the treatment is mainly focused on protecting the myocardium, while the amelioration of symptoms and protection of the myocardium are more critically needed in severe cases of heart failure. If all these treatments remain ineffective, cardiac transplantation would be required.
AL type cardiac amyloidosis: a devastating fatal disease
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Adeel Nasrullah, Anam Javed, Thejus T Jayakrishnan, Aaron Brumbaugh, Ariel Sandhu, Brent Hardman
Clinical presentation of AL type cardiac amyloidosis is varied based on the involved site. Fatigue and weakness are the most common presenting symptoms. Restrictive cardiomyopathy presents with signs and symptoms of diastolic heart failure and decreased exercise tolerance. With progression of the disease, atrial dilation occurs, which predisposes patients to atrial fibrillation and further sequelae of clot formation and systemic embolization. Cardiac conduction may be disrupted by amyloid deposition, often causing a variety of heart blocks. Soft tissue involvement has been seen as periorbital ecchymosis and macroglossia in 12.5% and 27.2%, respectively [7]. Renal AL amyloid can cause myeloma kidney and nephrotic syndrome. With underlying kidney disease, the patient may develop progressive renal failure requiring renal replacement therapy, as seen in the present case. Similar deposits in the liver and peripheral nerves can present as hepatomegaly, transaminitis, and peripheral neuropathy, respectively.
Precision medicine in cardiac electrophysiology: where we are and where we need to go
Published in Expert Review of Precision Medicine and Drug Development, 2020
Ashish Correa, Syed Waqas Haider, Wilbert S. Aronow
The management of genetic cardiomyopathies begins with accurate diagnosis. Beyond bloodwork and imaging, genotyping plays a major role. Major cardiovascular societies recommend genetic counseling and testing in patients with evidence of familial DCM [82,109]. Other societies recommend genetic testing in any patient with a non-ischemic DCM with other risk factors such as conduction disease, LV dysfunction at an age <40 years or SCD in a first-degree relative <50 years of age [95]. For HCM, genetic testing is recommended in equivocal/atypical cases and in index patients to risk-stratify first-degree relatives [95,110]. The diagnosis of ARVC is made by the International Task Force (ITF) criteria, of which genetic testing is a component [86]. Genetic counseling and testing are recommended in all patients with clinically diagnosed and suspected ARVC [95].
Cardiotoxicity of cancer chemotherapy in clinical practice
Published in Hospital Practice, 2019
Diwakar Jain, Wilbert Aronow
In the cells, the damaged and unwanted proteins are degraded and removed by the proteasomal enzymes [66–69]. The proteins marked for degradation are first tagged with ubiquitin (named for its abundance in the cells). Ubiquitylation is essential for the recognition of proteins marked for degradation by the proteasomes. The ubiquitin-proteasome system is essential for proteostasis or the maintenance of an optimal protein level in the cells through a balance between synthesis and degradation. This system also permits the development of anticancer therapies. Bortizimib (Valcade™) and Carfilzomib (Kyprolis™) are proteasome inhibitors. Bortizimib has a boron atom in its structure, which binds and inactivates 26S proteasome. It prevents the proteasome from degrading the pro-apoptotic proteins, which actives apoptosis in the neoplastic cells that are dependent upon the suppression of proapoptotic pathways. This is used to treat multiple myeloma and mantle cell lymphoma. Cardiomyopathy has been observed in 2–4% of patients treated with this agent. Cardiac function should be monitored in the patients undergoing treatment with this agent.
Related Knowledge Centers
- Arrhythmia
- Cardiac Arrest
- Dilated Cardiomyopathy
- Edema
- Fatigue
- Shortness of Breath
- Syncope
- Hypertrophic Cardiomyopathy
- Cardiac Muscle
- Heart Failure
- Shortness of Breath