HEART FAILURE

HEART FAILURE

DEFINITION

EPIDEMIOLOGY

Clinical syndrome with a recognizable pattern of signs and symptoms. It occurs because of an inherited or acquired abnormality of cardiac structure and/or function, resulting in heart cannot pump enough blood to meet the body's needs.

HF is a burgeoning problem worldwide, with more than 20 million people affected. The overall prevalence of HF in the adult population in developed countries is 2%. HF prevalence follows an exponential pattern, rising with age, and affects 6–10% of people over age 65.

ETIOLOGY

Preserved Ejection Fraction (>40–50%)

Depressed Ejection Fraction (<40%)

Pulmonary Heart Disease

High-Output States

Coronary artery disease

Hypertension

Nonischemic dilated cardiomyopathy

Chronic volume overload​​​​​

Pathologic hypertrophy: It includes primary (hypertrophic cardiomyopathies) and secondary (hypertension).

Restrictive cardiomyopathy: It includes primary infiltrative disorders (amyloidosis, sarcoidosis) and storage diseases (hemochromatosis).

Is the predominant cause in men and women and is responsible for 60–75% of cases of HF.

Contributes to the development of HF in 75% of patients, including most patients with CAD.

Caused by (1) Prior viral infection or toxin exposure (2) Genetic defects (3) Dilated cardiomyopathy associated with muscular dystrophies

As regurgitant valve disease and intracardiac shunt (from left to right)

Caused by cor pulmonale and pulmonary vascular disorders

Are seldom responsible for the development of HF in a normal heart; however, in the presence of underlying structural heart disease. The most remarkable causes are: (1) Metabolic disorders (2) Thyrotoxicosis (3) Nutritional disorders (beriberi) (4) Chronic anemia

PATHOPHYSIOLOGY

Also called diastolic heart failure, here the filling of the left ventricle is affected, resulting in an increase in the end-diastolic pressure of the left ventricle. Diastolic dysfunction is usually the result of compromised left ventricular relaxation, increased ventricular stiffness, valve disease, or constrictive pericarditis.

Heart failure with reduced ejection fraction (HEFF):

Where global systolic dysfunction of the left ventricle predominates. Predominant systolic dysfunction is common in heart failure secondary to myocardial infarction, myocarditis, and dilated cardiomyopathy. Systolic dysfunction can mainly affect the left ventricle

Heart failure with preserved ejection fraction (HFpEF):

The cardinal symptoms of HF are fatigue and shortness of breath. In the early stages of HF, dyspnea is observed only during exertion; however, as the disease progresses, dyspnea occurs with less strenuous activity, and it ultimately may occur even at rest.

CLINICAL MANIFESTATIONS

The most important mechanism is pulmonary congestion with accumulation of interstitial or intra-alveolar fluid, which activates juxtacapillary J receptors, which in turn stimulate the rapid, shallow breathing characteristic of cardiac dyspnea.

DIAGNOSIS

Electrocardiogram (ECG): A routine 12-lead ECG is recommended. The major importance is to assess cardiac rhythm and determine the presence of LV hypertrophy or a prior MI (presence or absence of Q waves)

Routine laboratory testing: Patients should have a complete blood count, a panel of electrolytes, blood urea nitrogen, serum creatinine, hepatic enzymes, and a urinalysis.

Chest X-ray: provides useful information about cardiac size and shape, as well as the state of the pulmonary vasculature, and may identify noncardiac causes.

Biomarkers: Circulating levels of natriuretic peptides are useful adjunctive tools in the diagnosis of patients with HF. Both B-type natriuretic peptide (BNP) and N-terminal pro-BNP, which are released from the failing heart, are relatively sensitive markers for the presence of HF with depressed EF

Exercise testing: Treadmill or bicycle exercise testing is not routinely advocated for patients with HF, but either is useful for assessing the need for cardiac transplantation in patients with advanced HF.

Assessment of LV function:The most useful test is the two-dimensional (2-D) echocardiogram/Doppler, which can provide a semiquantitative assessment of LV size and function as well as the presence or absence of valvular and/or regional wall motion abnormalities (indicative of a prior MI). Magnetic resonance imaging (MRI) is now the gold standard for assessing LV mass and volumes.

TREATMENT

ACE INHIBITORS: They have shown a reduction in mortality and morbidity in patients with HF + reduced EF and are indicated unless the patient cannot tolerate them. They are also indicated in left ventricular systolic dysfunction to avoid progression to HF, hospitalization and death

BETA BLOCKERS: They reduce mortality and morbidity in HF patients with reduced LVEF. Beta-blockers should be started in clinically stable patients, at low doses and then titrated up to the maximum tolerated dose.

MINERALOCORTICOIDS: Spironolactone and Eplerenone are recommended in all symptomatic patients (despite treatment with ACE inhibitors and beta-blockers) with reduced LVEF less than 35%, to reduce mortality and hospitalizations

DIURETICS: recommended to reduce congestive signs and symptoms, but have not been shown to have an effect on morbidity and mortality.

IVABRADINE: reduces heart rate through inhibition of If channels in the sinus node. Ivabradine has shown a reduction in mortality and hospitalization for HF in patients with LVEF reduced to <35%, in patients with HR> 70 bpm who have been hospitalized in the last 12 months

ANGIOTENSIN II RECEPTOR ANTAGONISTS: they are recommended only as an alternative in patients who do not tolerate ACE inhibitors.