Dilated Cardiomyopathy
| Overview |
|---|
- Dilated Cardiomyopathy is characterized by gross dilation of typically all four cardiac chambers and is the most common of all of the cardiomyopathies, accounting for nearly a third of all cases of Congestive heart failure.
| Morphology |
|---|
- Typically all four chambers of the heart are grossly dilated although in certain cases dilation may affect some chambers more than others. Dilation of the chamber walls is achieved by eccentric ventricular hypertrophy although in this context such hypertrophy is not adaptive and instead is a primary feature of the disease. In addition to the hypertrophy, histological signs of cardiomyocyte atrophy are observed along with intra-myocardial fibrosis.
| Etiologies |
|---|
- Overview
- Dilated Cardiomyopathy is likely a general morphological manifestation of myocardial injury in response to a variety of infectious, genetic, metabolic, or toxic insults. In the vast majority of cases the source of the insult is unknown and is thus the etiology is termed "Idiopathic". In a minority of cases, the myocardial insult can be identified allowing for the delineation of certain etiological subtypes of dilated cardiomyopathy.
- Etiological Subtypes
- Myocarditis-associated Dilated Cardiomyopathy: Possibly due to immune-mediated injury in response to myocarditis caused by Group B Coxsackie Viruses.
- Alcoholic Dilated Cardiomyopathy: Observed in alcoholics and may arise due to long-term alcohol-mediated myocardial damage.
- Peripartum Dilated Cardiomyopathy: Sometimes occurs during late pregnancy or after delivery in pregnant women.
- Hereditary Dilated Cardiomyopathy: Potentially accounts for 20-30% of cases and can result from diverse mutations of myocardial proteins involved in myocardial tension-generation.
| Pathophysiology |
|---|
- The myocardium undergoing dilated cardiomyopathy suffers from contractile dysfunction and is ultimately unable to produce sufficient cardiac output to meet the baseline physiological demands of the body. To meet this progressive decline in cardiac output a variety of compensatory mechanisms are engaged which maintain systemic arterial pressure. These include mechanisms of Systemic Arterial Pressure - Short-term Regulation and Long-term Regulation which boost cardiac output by increasing systemic vascular resistance, increasing venous return to the heart, and increasing total blood volume by enhancing renal salt and water retention.
- Although these mechanisms can maintain the disease under the clinical threshold for potentially years, they increase the functional demand on the progressively dilating myocardium by increasing both preload and afterload on the heart. In addition, progressive physical dilation of the heart often leads to dilation of valvular annuli which can result in mitral regurgitation and tricuspid regurgitation, further aggravating elevations in cardiac functional demand. The end result of this self-reinforcing decline in cardiac function is bi-ventricular heart failure.
| Clinical Consequences |
|---|
- Left Heart Failure Resulting in pulmonary edema and thus symptomology dyspnea and orthopnea
- Right Heart Failure Resulting in peripheral edema, ascites, chronic hepatic congestion
- Mural Thrombosis: Stasis of blood in the non-contractile heart can lead to mural thrombosis which can later result in arterial thromboembolism
- Atrial Fibrillation: May result due to electrophysiological derangements in dilated atria
- S3: A third heart sound is ausculatated in many patients