Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.
Various factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin, doxorubicin (in a dose-dependent manner), cyclophosphamide, and trastuzumab, have cardiotoxic effects that can result in DCM. Endocrine disorders such as thyrotoxicosis and myxedema can disrupt normal heart function, leading to the dilation and weakening of the heart chambers. When no specific causative factor can be identified, the condition is termed idiopathic dilated cardiomyopathy. Familial DCM, which accounts for a substantial proportion of cases, often has a definitive genetic etiology.
DCM is characterized by diffuse inflammation and rapid degeneration of heart fibers, resulting in ventricular dilation, impaired systolic function, atrial enlargement, and blood stasis in the left ventricle. Hemodynamically, the dilated ventricles lead to increased wall stress and decreased cardiac output, activating compensatory mechanisms such as the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS). The activation of RAAS increases angiotensin II levels, causing vasoconstriction and aldosterone release, which contribute to fluid retention and increased afterload. These compensatory responses initially help maintain cardiac output but eventually worsen heart failure by promoting further myocardial remodeling, sodium and water retention, and increased afterload.
The signs and symptoms of DCM may develop acutely after an infection or slowly over time. Symptoms include:
As the disease progresses, the patient may experience:
A chest X-ray may show cardiomegaly with signs of pulmonary venous hypertension and pleural effusion. An ECG may reveal tachycardia or bradycardia and dysrhythmias with conduction abnormalities. Laboratory studies may show increased B-type natriuretic peptide (BNP) levels if heart failure occurs.
Interprofessional Care
Interventions focus on controlling heart failure by enhancing heart contractility and decreasing preload and afterload. Several drugs manage heart failure:
Non-drug therapy includes the following:
Dilated cardiomyopathy, or DCM, is a progressive disorder of the myocardium marked by the dilation of the ventricular chambers and impaired contractile function.
While many cases of DCM are idiopathic, the condition can also result from myocardial insults such as hypertension, coxsackievirus B infections, chemotherapeutic agents like doxorubicin, and endocrine disorders such as thyrotoxicosis.
DCM is characterized by diffuse myocardial damage, which can include inflammation, fibrosis, and loss of myocardial cells.
These changes lead to ventricular dilation, impaired systolic function, atrial enlargement, and blood stasis in the left ventricle, which in turn causes cardiomegaly and contractile dysfunction.
Next, clinical manifestations of DCM include reduced exercise capacity, fatigue, palpitations, dyspnea at rest, abnormal S3 and S4 heart sounds, arrhythmias, heart murmurs, pulmonary crackles, and edema.
Lastly, DCM can be diagnosed by chest X-ray, which reveals cardiomegaly. An ECG may show arrhythmias and elevated B-type natriuretic peptide levels can indicate cardiac failure.
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