Incidence and Prevalence

The prevalence of HF is significantly increasing, primarily as a result of advances in medical technology in preserving and maintaining life after cardiovascular events. Approximately 6 million people in the United States have HF, with more than 550,000 new patients diagnosed each year.⁷ The annual incidence of new cases of HF increases with age, from less than 1 per 1000 patient-years among those younger than 45 years of age, to 10 per 1000 patient-years for those older than 65 years, to 30 per 1000 patient-years (3%) for those older than 85. Prevalence figures follow a similar pattern of progression, increasing from 0.1% before the age of 50 to 55 years to almost 10% after age 80 years.^6–8

HF is the most common Medicare diagnosis-related group (i.e., hospital discharge diagnosis), and more Medicare dollars are spent for the diagnosis and treatment of HF than for any other clinical entity.⁹ Similar data for these epidemiologic categories are reported worldwide. A study from the Mayo Clinic noted a 40% increase in the incidence of heart failure over the 20-year period ending in 2005.¹⁰ Because it is the chronic outcome of several cardiovascular diseases over time, HF is primarily a condition of the elderly, as noted. A typical dental practice serving 2000 patients would expect to treat approximately 14 persons with HF.

The HF syndrome is characterized by signs and symptoms of intravascular and interstitial volume overload and/or manifestations of inadequate tissue perfusion (Figure 6-1). Because HF often goes undiagnosed, patients may not know that they have the condition, so the dentist must be particularly aware of its signs and symptoms. HF may occur as a result of (1) impaired myocardial contractility (systolic dysfunction, commonly characterized as reduced left ventricular ejection fraction [LVEF]¹¹); (2) increased ventricular stiffness or impaired myocardial relaxation (diastolic dysfunction, which commonly is associated with a relatively normal LVEF); (3) a variety of other cardiac abnormalities, including obstructive or regurgitant valvular disease, intracardiac shunting, or disorders of heart rate or rhythm; or (4) states in which the heart is unable to compensate for increased peripheral blood flow or metabolic requirements^11,12 (Figure 6-2).

FIGURE 6-1 Effects of right- and left-sided heart failure.

FIGURE 6-2 How stroke volume is produced by the intact circulations of preload, contractility, and afterload. Cardiac output is established by combining stroke volume with heart rate. When this is merged with peripheral vascular resistance, the arterial pressure for tissue perfusion is established. The arterial system’s characteristics contribute to afterload. An increase in afterload lessens stroke volume. When carotid and aortic arch baroreceptors interact with these components, a feedback mechanism is provided to the higher medullary and vasomotor cardiac centers as well as to higher levels in the central nervous system. This results in a modulation influence on heart rate, peripheral vascular resistance, venous return and contractility.

Conditions that cause myocardial necrosis damage and/or produce chronic pressure or volume overload on the heart can induce myocardial dysfunction and HF.^11,12

Box 6-1 lists the potential causes of HF, with the most common causes identified. The most common underlying cause of HF in the United States is coronary heart disease, or coronary artery disease (secondary to atherosclerosis), accounting for 60% to 75% of cases, with cardiomyopathy, hypertension, and valvular heart disease also well-recognized contributory conditions.^11,12 The second most common cause of HF, accounting for about one fourth of all cases, is dilated cardiomyopathy (DCM). DCM is a syndrome characterized by cardiac enlargement with impaired systolic function of one or both ventricles, often accompanied by signs and symptoms of HF. About half of all cases of DCM have no identifiable cause and are therefore considered idiopathic. Known causes of cardiomyopathy include alcohol abuse, hereditary cardiomyopathies, and viral infections.^11,12 Although hypertension often is not a primary cause of HF, it is a major contributor to HF, with more than 75% of HF patients having a long-standing history of hypertension. Valvular heart disease used to be a more significant cause of HF; today, however, with declining rates of rheumatic heart disease and congenital heart disease in the United States, the frequency of HF resulting from valvular disease has decreased as well.^11,12 Type 2 diabetes mellitus also may be a risk factor for development of HF.^12,13

Although the mortality rates for MI and stroke are declining, HF continues to be a major contributor to morbidity and mortality. In the past 20 years, the number of HF hospitalizations increased more than 165%.¹⁴ In the United States, approximately 56,000 deaths each year are primarily caused by HF, and it is listed as a contributing cause in 262,000 deaths. The prognosis for patients with HF is poor. Of patients who survive an acute onset of HF, only 35% of men and 50% of women are alive after 5 years.^7,15

Pathophysiology and Complications

Heart failure is caused by the inability of the heart to function efficiently as a pump, which results in either an inadequate emptying of the ventricles during systole or an incomplete filling of the ventricles during diastole. This in turn results in a decrease in cardiac output, with consequent delivery of an inadequate volume of blood to the tissues, or in a backup of blood, causing systemic congestion. HF may involve one or both ventricles. Most of the acquired disorders that lead to HF result in initial failure of the left ventricle. Left ventricular heart failure (LVHF) often is followed by failure of the right ventricle. In adults, left ventricular involvement is almost always present even if the clinical manifestations are primarily those of right ventricular dysfunction (fluid retention without dyspnea or rales). HF may result from an acute insult to cardiac function, such as with a large MI, or, more commonly, from a chronic process.^2,16 By the time most patients are seen for medical treatment, the pathoanatomic changes of HF usually are present on both sides of the heart. The cardinal manifestations of HF are dyspnea and fatigue.^11,12

HF can result from an acute injury to the heart such as with MI or, more commonly, from a chronic process such as that associated with hypertension or cardiomyopathy. Failure of the heart most often begins with LVHF brought on by an increased workload or disease of the heart muscle.^11,12 The determination of left ventricular failure often is based on a finding of an abnormal ejection fraction, which is the percentage of blood ejected from the left ventricle during systole. Normal values for ejection fraction determined with the patient at rest range between 55% and 70%.^11,12 Although arbitrary, an LVEF of 45% to 50% often is used as a threshold value to diagnose left ventricular failure. The outstanding symptom of left ventricular failure is dyspnea, which results from the accumulation or congestion of blood in the pulmonary vessels—hence the designation congestive. Acute pulmonary edema often is the result of left ventricular failure. Left-sided heart failure leads to pulmonary hypertension, which increases the work of the right ventricle pumping against increased pressure, often culminating in right-sided heart failure.^11,12

The most common cause of right-sided heart failure is preceding failure of the left ventricle.¹⁶ The outcomes of right ventricular failure are systemic venous congestion and peripheral edema (see Figures 6-1 and 6-2). Failure of the right side of the heart alone is uncommon. The most common cause of pure right-sided heart failure is emphysema.

Ventricular failure leads to dilation and hypertrophy of the ventricle as it attempts to compensate for its inability to keep up with the workload. Venous pressure and myocardial tone increase along with the increase in blood volume. The net effect is diastolic dilation, which serves to increase the force and volume of the subsequent systolic contraction. These changes lead to dyspnea, orthopnea, and pulmonary edema. When right-sided ventricular enlargement occurs as a result of a lung disorder (e.g., emphysema) that produces pulmonary hypertension, the condition is called cor pulmonale.^11,12

Signs and symptoms of HF appear when the heart no longer functions properly as a pump. As the cardiac output falls, an increasing disproportion is observed between the required hemodynamic load and the capacity of the heart to handle the load. With decreasing cardiac output, stimulation of the renin-angiotensin system and the sympathetic nervous system (i.e., neurohumoral responses) occurs in an attempt to compensate for the loss of function.^11,12,16 The effects of these responses include increased heart rate and myocardial contractility, increased peripheral resistance, sodium and water retention, redistribution of blood flow to the heart and brain, and an increased efficiency of oxygen utilization by the tissues. If these responses result in improved cardiac output with an elimination of symptoms, the condition is termed compensated HF. Symptomatic HF is termed decompensated HF.^11,12,14

The American Heart Association/American College of Cardiology (AHA/ACC) classification of HF consists of four stages, reflecting the fact that HF is a progressive disease for which the outcome can be modified by early identification and treatment.¹ Stages A and B denote the status of patients with risk factors that predispose to the development of HF, such as coronary artery disease, hypertension, and diabetes, but who do not have any symptoms of HF^8,17,18 (see Box 6-5).

The difference between stage A and stage B is that in stage A, patients do not demonstrate left ventricular hypertrophy (LVH) or dysfunction, whereas in stage B, LVH and/or dysfunction (structural heart disease) is present. Stage C is the disease designation for patients with past or present symptoms of HF associated with underlying structural heart disease (the bulk of patients), and stage D, for patients with refractory HF who might be eligible for specialized, advanced treatment or for end-of-life care. This classification system complements the New York Heart Association (NYHA) classification system, which is discussed in the next section (“Signs and Symptoms”).¹

HF is a progressive disease, and symptoms will worsen over time owing to the ongoing deterioration of cardiac structure and function. The prognosis is better if the underlying cause can be treated. At 1 year after the diagnosis of HF, 20% of patients will succumb to the disease. In people diagnosed with HF, sudden death occurs at a rate six to nine times that for the general population.^11,12

Signs and Symptoms

The symptoms and signs of HF (Boxes 6-2 and 6-3) reflect respective ventricular dysfunction. Left ventricular failure produces pulmonary vascular congestion with resulting pulmonary edema and dyspnea. Dyspnea is the most common symptom of HF and usually is present only with exertion or physical activity. Dyspnea experienced by the patient at rest is an indication of severe HF.^11,12