Cardiomyopathy and Cardiovascular Conditions

• Cardiomyopathies and other cardiovascular conditions are the focus.

Cardiomyopathy Overview

• Cardiomyopathy refers to pathologies occurring within the cardiac myocytes, leading to abnormal structure and function.
• These changes result in an irreversible decline in cardiac function.
• Patients with long-term cardiomyopathy may become candidates for cardiac transplantation.
• Reduction in Ejection Fraction (EF) predicts mortality and morbidity.

Dilated Cardiomyopathy

• Dilated cardiomyopathy is characterized by abnormal cardiac morphology, specifically chamber dilation (enlargement) and contractile impairments, resulting in decreased EF and/or SV.
• The dilated heart undergoes significant remodeling, starting with ballooning of the Left Ventricle (LV) and extending to other chambers.
• It ultimately leads to heart failure.
• Significant remodeling of the heart occurs, leading to a larger and heavier heart.
• Cardiac myocytes become hypertrophied. There is a loss of myofibrils, reduced mitochondrial function, cardiac fibrosis, and thinned chamber walls.
• Systolic dysfunction is produced, along with reduced Stroke Volume (SV) and EF.
• It is the most common form of cardiomyopathies.
• Genetic mutations causing defects in cardiac myocytes, cellular cytoskeleton, sarcolemma, and nuclear membrane can cause dilated cardiomyopathy.
• Viral infections, including HIV, can lead to dilated cardiomyopathy.
• Various toxins such as ETOH, cocaine, and cancer drugs can cause it.
• Metabolic disorders such as Diabetes, Hypo and hyperthyroidism, and nutritional deficiencies can cause dilated cardiomyopathy.
• Myocarditis is a cause of dilated cardiomyopathy.
• Symptoms include fatigue, dyspnea on exertion, shortness of breath, cough, orthopnea, paroxysmal nocturnal dyspnea, and increasing edema, weight, or abdominal girth.
• Signs include Tachypnea (increased respiratory rate), Tachycardia (increased heart rate), and hypertension or hypotension.
• Other pertinent findings are similar to signs of heart failure like JVD, pulmonary edema, ascites, and peripheral edema.
• Hypoxia signs can be linked (cyanosis, clubbing).
• Nonpharmacologic management includes a sodium-restricted diet and fluid restriction.
• Pharmacologic management is similar to that of heart failure.
• Overstretching leads to the failure of the myocardial contractile unit, and the Frank-Starling mechanism becomes compromised.
• Other features Dilation & Contractile impairment, Systolic dysfunction, Reduced Ejection Fraction (<40% of normal).
• Gross Morphological Features include LV dilation; Often leads to dilation in other chambers, Heavy, baggy, Reduced wall thickness (poss.), Functional mitral valve regurgitation (poss.), Mural thrombi (poss.)
• Histological Features include: Interstitial fibrosis, Hypertrophied cells, Loss of myofibrils.
• Symptoms include LV dysfunction: Dyspnea, Fatigue, RV dysfunction: Peripheral edema.

Hypertrophic Cardiomyopathy (HCM)

• Hypertrophic cardiomyopathy is the single most common cause of death in apparently healthy young people.
• Characterized by a thickened LV wall with a non-dilated LV chamber.
• The resulting cardiac hypertrophy is out of proportion to the hemodynamic load.
• Identified cause defects in sarcomeric proteins stemming from 9 gene defects.
• It is a genetic disease with autosomal (not sex-linked) dominance.
• The myocytes perceive normal blood pressures, falsely perceiving them as insufficient.
• The LV free wall hypertrophies to increase contractility.
• The septal wall can also hypertrophy, disrupting normal LV outflow tract.
• The heart ultimately decompensates (decrease functional capacity) and fails due to high metabolic demand.
• Most cases are asymptomatic.
• The first clinical manifestation is often sudden death.
• Subtypes: Obstructive HCM and Nonobstructive HCM
• Obstructive HCM: The septal wall thickens, and the LV free wall of the ventricles stiffens, obstructing blood flow into the aorta.
• This mechanism causes sudden death.
• Nonobstructive HCM: The walls of the LV stiffen, reducing LVEDV and SV, but blood flow is not blocked.
• Signs and symptoms include chest pain (especially with physical exertion), shortness of breath (especially with physical exertion), fatigue, arrhythmias (abnormal heart rhythms), dizziness, lightheadedness, fainting (syncope), and swelling in the ankles, feet, legs, abdomen, and veins in the neck.
• It is a chronic disease that can worsen over time.
• It leads to reduced physical function and quality of life.
• Long-term complications include atrial fibrillation, dysrhythmias, heart failure, and a history of MIs.
• Treatment includes alcohol septal ablation, implantable cardioverter defibrillator (ICD)(Pacemaker), and heart transplants.
• In septal ablation, a small portion of the thickened heart muscle is destroyed by injecting alcohol through a long, thin tube (catheter) into the artery supplying blood to that area. This procedure generally requires a three- to five-day stay in the hospital after the procedure.

Restrictive/Infiltrative Cardiomyopathy

• Characterized by restricted diastolic filling/loss of compliance, i.e., diastolic dysfunction.
• Characterized by idiopathic fibrosis-rigid heart walls/reduced compliance.
• Systolic function is normal.
• EDVs are diminished/chambers cannot expand.
• ESVs and EFs are normal, but SV is compromised.
• Ventricular filling pressures are very high.
• Symptoms include dyspnea with exertion, abdominal swelling, ankle edema, and fatigue.
• Is reasonably rare.
• Causes include: Scleroderma, Amyloidosis, Sarcoidosis (fibrotic scarring to myocardial infiltrates), Diabetes, Hemochromatosis (excessive deposition of iron), Chemotherapeutic agents leading to cardio oncology, and Radiation exposure (mediastinal, can lead to cardio oncology).

Other Cardiovascular Disorders

• Peripheral arterial disease (PAD) is a narrowing of peripheral arteries, resulting in a decreased supply of blood.
• It is the result of the same atherosclerotic process for CAD but is commonly found in the lower extremities.
• Symptoms appear when blood flow to the distal tissues is blocked.
• Physical therapists should assess for signs of PAD in the extremity, including: pain (intermittent claudication or other atypical symptoms), pallor, pulses decreased or absent, with an extremity cool to touch, paresthesia (tingling, loss of sensation), paresis (such as muscle atrophy), and trophic changes (dry, shiny skin, hair loss, thick toenails, and wounds).
• Aortic Aneurysm (AA)
• Aortic aneurysm is a permanent pathologic dilation of the aortic wall that is at least 50% greater than the expected normal diameter (>3 cm in adults).
• Described in terms of location, size, morphological appearance, and origin.
• Abdominal aortic aneurysms (AAAs) are at significant risk for rupture (usually fatal).
• Physical therapy implications for AAAs: During the initial assessment, identify risk factors for aneurysm, especially age (>60 years) and immediate family history.
• Assess vital signs at rest and with activity. High blood pressure during activity may produce excessive stress on the already weakened area.
• Tachycardia, low blood pressure, and patient complaints of sudden abdominal pain could be a sign of rupture.
• Venous disease includes venous insufficiency, venous stasis ulcers, and venous thromboembolism (VTE).
• Venous insufficiency: Results from inadequate muscle action, incompetent venous valves, or venous obstruction.
• Venous stasis ulcers: Chronic venous insufficiency leads to skin changes, swelling, and wounds.
• Venous thromboembolism (VTE): Includes both deep venous thrombosis (DVT) and pulmonary embolism (PE).
• DVT is the development of a clot in a deep vein of the lower extremity or pelvis (or less often, in the arm).
• Interventions for venous insufficiency and venous ulcers: Exercise, Extremity elevation, Avoiding long periods of sitting or standing, Compression, Aggressive wound management, Education to prevent further progression.