Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.

Etiology

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.

Pathophysiology

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.

Clinical Manifestations

The signs and symptoms of DCM may develop acutely after an infection or slowly over time. Symptoms include:

• Reduced exercise capacity
• Fatigue
• Dyspnea at rest
• Paroxysmal nocturnal dyspnea
• Orthopnea

As the disease progresses, the patient may experience:

• Dry cough
• Palpitations
• Abdominal bloating
• Anorexia
• Abnormal S3 and S4 heart sounds
• Dysrhythmias
• Heart murmurs
• Pulmonary crackles
• Edema
• Weak peripheral pulses
• Pallor
• Hepatomegaly
• Jugular venous distention (JVD)

Diagnostic Studies

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:

• Diuretics such as furosemide and nitrates like nitroglycerin decrease preload.
• ACE inhibitors reduce afterload.
• Neurohormonal stimulation can be controlled by beta-blockers such as metoprolol and aldosterone antagonists such as spironolactone.
• Antidysrhythmics treat dysrhythmias, and anticoagulation therapy may reduce the risk of systemic embolization from clots forming in the heart chambers.

Non-drug therapy includes the following:

• Ventricular Assist Device (VAD): A VAD allows the heart to rest and recover from acute heart failure or serves as a bridge to a heart transplant.
• Cardiac Resynchronization Therapy (CRT): CRT improves the coordination of the heart's contractions by electrically stimulating both the left and right ventricles.
• Implantable Cardioverter-Defibrillator (ICD): An ICD prevents sudden cardiac death in patients with DCM who are at high risk for life-threatening arrhythmias. The device monitors the heart rhythm and delivers electric shocks when it detects dangerous arrhythmias, such as ventricular tachycardia or ventricular fibrillation.
• A heart transplant may be considered for patients with terminal or end-stage DCM. A permanent, implantable VAD, known as destination therapy, is an option for a patient with advanced disease who is not a candidate for a heart transplant.