Epidemiology

Both the incidence and prevalence of HF are growing in the United states. More than 6 million persons are diagnosed with HF in the United States with more than 670,000 new cases and nearly 300,000 deaths per year. The lifetime risk of developing HF is 20% for Americans 40 years of age or older. The annual incidence of HF increases from 1 per 1000 people younger than 45 years of age to more than 10 per 1000 people older than 65 years of age. In the Medicare-eligible population, HF prevalence is over 100 per 1000 (10%).

Heart failure is significantly increasing, primary because of advances in medical technology in preserving and maintaining life after cardiovascular events. 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 diagnosis. These figures are also true worldwide. A study from the Mayo Clinic reported a 40% increase in the incidence of HF in the past 20 years. Because it is a chronic outcome of several cardiovascular diseases over time, HF is primarily a condition of older adults. A typical dental practice serving 2000 patients would expect to treat approximately 15 to 20 individuals with HF.

Pathophysiology and Complications

Heart failure is not an actual diagnosis but rather represents a symptom complex that is characterized by signs and symptoms of intravascular and interstitial volume overload and/or manifestations of inadequate tissue perfusion ( Fig. 6.1 ). The ACC/AHA 2013 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult defines HF as a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

Effects of right- and left-sided heart failure. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Patients with untreated or poorly managed HF are at high risk during dental treatment for complications such as cardiac arrest, cerebrovascular accident, and MI. The dentist must be able to detect these patients based on history and clinical findings, refer them for medical diagnosis and management, and work closely with the physician to develop a dental management plan that will be effective and safe for the patient.

A decline in mortality rates from HF will likely occur because of evidence-based approaches to treat it with angiotensin-converting enzyme inhibitors, beta-blockers, coronary revascularization, ICDs, and cardiac resynchronization therapeutic strategies.

Because many cases of HF go undiagnosed and patients may not be aware that they have HF, the dentist must be particularly aware of the signs and symptoms of HF ( Boxes 6.2 and 6.3 ). HF may occur as a result of (1) impaired myocardial contractility (systolic dysfunction, commonly characterized as reduced left ventricular ejection fraction [LVEF] ); (2) increased ventricular stiffness or impaired myocardial relaxation (diastolic dysfunction, which is commonly 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 ( Fig. 6.2 ).

Interactions in the intact circulation of preload, contractility, and afterload in producing stroke volume. Stroke volume combined with heart rate determines cardiac output, which, when combined with peripheral vascular resistance, determines arterial pressure for tissue perfusion. The characteristics of the arterial system also contribute to afterload, an increase in which reduces stroke volume. The interaction of these components with carotid and aortic arch baroreceptors provides a feedback mechanism to higher medullary and vasomotor cardiac center and to higher levels in the central nervous system to effect a modulating influence on heart rate, peripheral vascular resistance, venous return, and contractility.

(From Starling MR: Physiology of myocardial contraction. In Colucci WS, Braunwald E, editors: Atlas of heart failure: cardiac function and dysfunction, ed 3, Philadelphia, Current Medicine, 2002, pp 19-35.)

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

Box 6.1 lists the potential causes of HF with the most common causes identified. Because HF may not be diagnosed in a dental patient, the dentist should be alerted to that possibility if the patient presents with a history of any of these underlying conditions.

The most common underlying causes of HF in the United States are coronary heart disease (secondary to atherosclerosis), hypertension, cardiomyopathy, and valvular heart disease, with coronary heart disease accounting for 60% to 75% of cases. 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. Although hypertension is often 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; however, with the rates of rheumatic heart disease and congenital heart disease declining in the United States, there has been a subsequent decline in HF resulting from valvular disease. Type 2 diabetes mellitus may also be a risk for developing HF.

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 an inadequate volume of blood being supplied 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 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 a large MI, or, more commonly, from a chronic process. By the time most patients are seen for medical treatment, failure of both sides of the heart usually has occurred. The cardinal manifestations of HF are dyspnea and fatigue.

Heart failure can result from an acute injury to the heart such as from MI or more commonly from a chronic process such as from hypertension or cardiomyopathy. Failure of the heart most often begins with LVHF brought on by an increased workload or disease of the heart muscle. The determination of left ventricular failure is often based upon 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 at rest vary between 55% and 70% ( Fig. 6.3 ). Although arbitrary, an LVEF of 45% to 50% is often used as a threshold 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, thus the term congestive HF. Acute pulmonary edema is often the result of left ventricular failure. Left-sided HF leads to pulmonary hypertension, which increases the work of the right ventricle pumping against increased pressure and often leads to right-sided HF.

The progression of heart failure with depression of ejection fraction. Heart failure begins with a decline in the heart’s pumping capacity (ejection fraction, 60%) at which time several compensatory mechanisms are activated. For a time, these compensatory mechanisms can keep the heart functioning, but over time because of increasing myocardial damage and secondary damage from other end organs, the heart’s function (and ejection fraction) deteriorate. An ejection fraction of 20% is considered to be severe heart failure.

The most common cause of right-sided HF is preceding failure of the left ventricle. The outcomes of right ventricular failure are systemic venous congestion and peripheral edema (see Figs. 6.1 and 6.2 ). Failure of the right side of the heart alone is uncommon. The most common cause of pure right-sided HF 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 increases the force and volume of the subsequent systolic contraction. This leads 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 .

The signs and symptoms of HF appear when the heart no longer functions properly as a pump. As the cardiac output falls, there is an increasing disproportion 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 (neurohumoral responses) occur in an attempt to compensate for the loss of function. 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.

The AHA/ACC classifies HF into four stages, reflecting the fact that HF is a progressive disease and whose outcome can be modified by early identification and treatment. Stage A and B denote patients with risk factors that predispose to the development HF, such as coronary artery disease, hypertension, and diabetes but who do not have any symptoms of HF ( Box 6.4 ).

The difference between stages A and B is that in stage A, patients do not demonstrate left ventricular hypertrophy (LVH) or dysfunction, but those in stage B do have LVH or dysfunction (structural heart disease). Stage C denotes patients with past or present symptoms of HF associated with underlying structural heart disease (the bulk of patients), and stage D designates 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 ( Box 6.5 ), which is discussed in the next section. Although the mortality rates from MI and stroke are declining, HF continues to be a major cause of morbidity and mortality. In the past 20 years, the number of HF hospitalizations increased more than 165%. 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. HF is a progressive disease, and symptoms worsen over time because of the ongoing deterioration of cardiac structure and function. HF also predisposes the patient to ischemic stroke, the risk for which is twice as high as normal. The prognosis is better if the underlying cause can be treated. One year after the diagnosis of HF, 20% of patients will succumb to the disease. In people diagnosed with HF, sudden death occurs six to nine times the rate of the general population.

Pathophysiology and Complications

Heart failure is not an actual diagnosis but rather represents a symptom complex that is characterized by signs and symptoms of intravascular and interstitial volume overload and/or manifestations of inadequate tissue perfusion ( Fig. 6.1 ). The ACC/AHA 2013 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult defines HF as a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

Effects of right- and left-sided heart failure. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Patients with untreated or poorly managed HF are at high risk during dental treatment for complications such as cardiac arrest, cerebrovascular accident, and MI. The dentist must be able to detect these patients based on history and clinical findings, refer them for medical diagnosis and management, and work closely with the physician to develop a dental management plan that will be effective and safe for the patient.

A decline in mortality rates from HF will likely occur because of evidence-based approaches to treat it with angiotensin-converting enzyme inhibitors, beta-blockers, coronary revascularization, ICDs, and cardiac resynchronization therapeutic strategies.

Because many cases of HF go undiagnosed and patients may not be aware that they have HF, the dentist must be particularly aware of the signs and symptoms of HF ( Boxes 6.2 and 6.3 ). HF may occur as a result of (1) impaired myocardial contractility (systolic dysfunction, commonly characterized as reduced left ventricular ejection fraction [LVEF] ); (2) increased ventricular stiffness or impaired myocardial relaxation (diastolic dysfunction, which is commonly 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 ( Fig. 6.2 ).

Interactions in the intact circulation of preload, contractility, and afterload in producing stroke volume. Stroke volume combined with heart rate determines cardiac output, which, when combined with peripheral vascular resistance, determines arterial pressure for tissue perfusion. The characteristics of the arterial system also contribute to afterload, an increase in which reduces stroke volume. The interaction of these components with carotid and aortic arch baroreceptors provides a feedback mechanism to higher medullary and vasomotor cardiac center and to higher levels in the central nervous system to effect a modulating influence on heart rate, peripheral vascular resistance, venous return, and contractility.

(From Starling MR: Physiology of myocardial contraction. In Colucci WS, Braunwald E, editors: Atlas of heart failure: cardiac function and dysfunction, ed 3, Philadelphia, Current Medicine, 2002, pp 19-35.)

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

Box 6.1 lists the potential causes of HF with the most common causes identified. Because HF may not be diagnosed in a dental patient, the dentist should be alerted to that possibility if the patient presents with a history of any of these underlying conditions.

The most common underlying causes of HF in the United States are coronary heart disease (secondary to atherosclerosis), hypertension, cardiomyopathy, and valvular heart disease, with coronary heart disease accounting for 60% to 75% of cases. 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. Although hypertension is often 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; however, with the rates of rheumatic heart disease and congenital heart disease declining in the United States, there has been a subsequent decline in HF resulting from valvular disease. Type 2 diabetes mellitus may also be a risk for developing HF.

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 an inadequate volume of blood being supplied 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 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 a large MI, or, more commonly, from a chronic process. By the time most patients are seen for medical treatment, failure of both sides of the heart usually has occurred. The cardinal manifestations of HF are dyspnea and fatigue.

Heart failure can result from an acute injury to the heart such as from MI or more commonly from a chronic process such as from hypertension or cardiomyopathy. Failure of the heart most often begins with LVHF brought on by an increased workload or disease of the heart muscle. The determination of left ventricular failure is often based upon 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 at rest vary between 55% and 70% ( Fig. 6.3 ). Although arbitrary, an LVEF of 45% to 50% is often used as a threshold 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, thus the term congestive HF. Acute pulmonary edema is often the result of left ventricular failure. Left-sided HF leads to pulmonary hypertension, which increases the work of the right ventricle pumping against increased pressure and often leads to right-sided HF.

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