ischemic heart disease ch 4
Risk Assessment: Assessment of risk for the dental management of patients with ischemic heart disease involves three determinants
1.Severity of the disease 2.Stability and cardiopulmonary reserve of the patient ( ability to tolerate dental care) 3.Type and magnitude of the dental procedure
Coronary heart disease is the leading cause of death in the United States after age
65, and it is responsible for 735,000 new or recurrent heart attacks annually, of which 40% are fatal ØDespite this decline, cardiovascular diseases continue to pose the most serious threat to health in America, accounting for about 31% of all deaths ØThe average dental practice with 2000 patients is expected to include at least 100 patients with ischemic heart disease Ø
ischemic heart disease
Atherosclerosis is the thickening of the intimal layer of the arterial wall caused by the accumulation of lipid plaques ØThe process results in a narrowed arterial lumen with diminished blood flow and oxygen supply ØAtherosclerosis is the most common underlying cause of not only coronary artery disease but also cerebrovascular disease and peripheral arterial disease
mangament may include
Management may include ØGeneral lifestyle measures, such as an exercise program ØWeight control ØRestriction of salt, cholesterol, and saturated fatty acids ØCessation of smoking ØControl of exacerbating conditions, such as anemia, hypertension, and hyperthyroidism
angina pectoris
Medical management of a patient with chronic stable angina consists of a varied array of interventions ØIdentification and treatment of associated diseases that can precipitate or worsen angina ØReduction in risk factors for cardiovascular disease ØBehavioral modifications and lifestyle interventions ØPharmacologic management ØRevascularization by percutaneous catheter-based techniques or by coronary artery bypass surgery
myocardial infarction
Patients who have experienced an acute myocardial infarction (MI) should be hospitalized or should receive emergency treatment as soon as possible ØThe basic management goal is to minimize the size of the infarction and prevent death from lethal arrhythmias ØEarly administration of oxygen, nitrates, and aspirin is recommended to decrease platelet aggregation and limit thrombus formation
patients who have significant angina are encouraged to
Patients who have significant angina are encouraged to ØAvoid long hours of work ØTake rest periods during the working day ØObtain adequate rest at night ØUse mild sedatives ØTake frequent vacations ØIn some cases, change occupations or retire
Angina pectoris usually is described as a sensation of
aching, heavy, squeezing pressure or tightness in the mid-chest region ØThe area of discomfort is reported to be approximately the size of a fist and may radiate into the left or right arm, the neck, or the lower jaw ØThe pain is of brief duration, lasting 5 to 15 minutes if the provoking stimulus is stopped or for a shorter time if nitroglycerin is used
Numerous studies have reported an association between periodontal disease and
cardiovascular disease ØIt is hypothesized that the chronic inflammatory burden of periodontal disease may lead to impaired functioning of the vascular endothelium Causation has not been proved ØAdditional interventional studies will be required to further elucidate this relationship
Atherosclerosis is a inflammatory disorder of the
cellular lining of the arteries, with inflammation playing a fundamental role at all stages of the disease The formation of atheromatous plaques involves several steps
Most atheromatous plaques are not associated with clinical signs and symptoms and may never produce
clinical manifestations ØFor lesions that do produce symptoms, flow-limiting intact plaques typically precipitate symptoms such as chest pain (angina) when oxygen need exceeds demand, as during exercise ØPlaque rupture produces an acute or unstable clinical picture with signs and symptoms such as angina at rest, myocardial infarction, or sudden death
Atherosclerosis usually is a focal disease that
commonly occurs in certain areas or regions of arteries while sparing others ØThose affected include the brain, heart, aorta, and peripheral arteries ØThe lumen of the affected artery may be circumferentially narrowed evenly or eccentrically
Chest pain is the most important symptom of
coronary atherosclerotic heart disease ØThe pain may be brief, as in angina pectoris resulting from temporary ischemia of the myocardium, or it may be prolonged, as in unstable angina or acute myocardial infarction Ischemic pain results from an imbalance between the oxygen supply and the oxygen demand of the muscle ØThe exact mechanism or agents involved in producing the cardiac pain are not known
Cigarette smoking is the single most important modifiable risk factor for
coronary heart disease ØPersons who smoke more than 20 cigarettes daily have a two- to four-fold increase in coronary heart disease ØIn the Framingham Study, participants who discontinued smoking lowered their risk of MI within 2 years ØPipe and cigar smoking apparently convey little risk for development of heart disease
No single risk factor is responsible for the
development of coronary atherosclerosis, but many factors act synergistically ØModification of risk factors that can be controlled may reduce or modify the clinical effects of the disease
Symptoms and signs of congestive heart failure developing as a complication of coronary atherosclerotic heart disease and its sequelae include
dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema, hemoptysis, fatigue, weakness, and cyanosis ØFatigue and weakness may be manifest early in the course of heart disease, before the onset of congestive heart failure
Patients with diabetes mellitus have a greater incidence of coronary atherosclerotic
heart disease and more extensive lesions ØPatients with diabetes have two- to eight-fold higher rates of future cardiovascular events as compared with age-matched and ethnically matched nondiabetic patients ØAlthough hyperglycemia is associated with microvascular disease, insulin resistance itself promotes atherosclerosis even before it produces frank diabetes
Elevation in serum lipid levels is a major risk factor for atherosclerosis ØIncreased levels of
low-density lipoprotein (LDL) cholesterol pose the greatest risk for coronary atherosclerosis ØIncreased levels of high-density lipoprotein (HDL) cholesterol have been shown to reduce the risk Persons with elevated triglyceride or β-lipoprotein levels have an increased risk for the disease A diet rich in total calories, saturated fats, cholesterol, sugars, and salts also enhances the risk
Intra-arterial complications of coronary atherosclerosis consist of
luminal narrowing, intramural hemorrhage, thrombosis, embolism, and aneurysm ØIntramural hemorrhage, which results from weakening of intimal tissues, may lead to thrombosis ØThe localized blood also may serve as an irritant to precipitate a reflex reaction, resulting in spasm of the collateral vessels ØOnce formed, a thrombus may become encapsulated and may undergo fibrous organization and recanalization
Before the age of 75, the risk of coronary atherosclerosis is greater for
men than for women ØAfter menopause, a rapid reduction occurs in this gender difference ØThe fact that men are more prone to the clinical manifestations of coronary atherosclerosis is accentuated in nonwhite populations People with parents or siblings affected by coronary atherosclerotic heart disease are at risk for development of the disease at a younger age than that typical for those without such a history
Acute coronary syndrome describes a continuum of
myocardial ischemia that ranges from unstable angina at one end to non-ST segment myocardial infarction at the other ØDifferentiation requires diagnostic and laboratory testing Prinzmetal's variant angina occurs at rest and is caused by focal spasm of a coronary artery, usually with varied amounts of atherosclerosis
Palpitations of the heart may be present in patients with coronary atherosclerotic heart disease with
normal or abnormal rhythm ØSyncope, a transient loss of consciousness resulting from inadequate cerebral blood flow, also may occur in patients with coronary atherosclerotic heart disease Ø
Plaques may grow and proliferate
outwardly, or inwardly, into the lumen ØWith inward proliferation, the size of the lumen is progressively reduced (stenosis) ØBlood flow may be chronically decreased When the demand for oxygen exceeds supply, the outcome is ischemic pain ØIschemic symptoms may be produced when occlusion reaches 75% of the cross-sectional area of the artery
Symptomatic coronary atherosclerotic heart disease often is referred to as i
schemic heart disease ØIschemic symptoms are the result of oxygen deprivation secondary to reduced blood flow to a portion of the myocardium ØOther conditions, such as embolism, coronary ostial stenosis, coronary artery spasm, and congenital abnormalities, also may cause ischemic heart disease
Increased blood pressure appears to be one of the most
significant risk factors for coronary atherosclerotic heart disease ØIn general, systolic blood pressure (SBP) is more strongly related to the incidence of cardiovascular disease than is diastolic blood pressure, especially in the elderly ØSBP rises throughout life, and diastolic blood pressure (DBP) tends to level off or decrease after the age of 50
Angina is defined in
terms of its pattern or symptom stability ØStable angina is pain that is predictably reproducible, unchanging, and consistent over time •Pain typically is precipitated by physical effort, such as walking or climbing stairs, but also may occur with eating or stress •Pain is relieved by cessation of the precipitating activity, by rest, or with the use of nitroglycerin ØUnstable angina is defined as new-onset pain, pain that in increasing in frequency, pain that is increasing in intensity, pain that is precipitated by less effort than before, or pain that occurs at rest •This pain is not readily relieved by nitroglycerin
If the degree of ischemia that results from coronary atherosclerosis is significant and the oxygen deficit is prolonged, the area of myocardium supplied by that vessel may
undergo necrosis ØThe extent of involvement is reflected in the electrocardiogram (ECG) ØThe ST segment is not elevated in cases with only partial obstruction to blood flow and limited myocardial necrosis ØElevation of the ST segment is seen in cases with more profound ischemia and a larger area of necrosis
Patients with coronary atherosclerosis who experience prolonged pain as a result of myocardial ischemia usually have
unstable angina or are having an acute myocardial infarction ØThis pain usually is more severe and lasts longer than 15 minutes but has the same general character as that described for stable angina ØUse of vasodilators or cessation of activity does not relieve the pain caused by infarction
Chair: The clinician should ensure a comfortable chair position and avoid rapid position changes
ØA rapid change in chair position can cause hypotension and a change in hemodynamics that can potentially affect the heart and blood pressure, especially in patients who take nitrates and antihypertensive medications
Definitive treatment for patients with acute MI depends on the extent of ischemia as reflected on the electrocardiogram, which shows the presence or absence of ST segment elevation
ØAn MI without ST segment elevation (non-STEMI) is due to partial blockage of coronary blood flow ØAN MI with ST segment elevation is due to complete blockage of coronary blood flow and more profound ischemia involving a relatively large area of myocardium ØEarly fibrinolytic therapy improves outcomes in STEMI but not in non-STEMI
Angiotensin-converting enzyme (ACE) inhibitors are indicated for use in patients with coronary heart disease who also have diabetes, left ventricular dysfunction, or hypertension
ØAngiotensin receptor blockers (ARBs) are used in patients who are intolerant to ACE inhibitor drug use.
Recommendations: There are general management strategies for patients with stable angina or a past history of MI without ischemic symptoms and no other risk factors. These factors are based upon
ØAssessment of medical risk ØType of planned dental procedure ØStability and anxiety level of the patient
Currently, two types of stents are used
ØBare metal stents maintain mechanical patency; however, they do not prevent endothelial proliferation that results in restenosis ØDrug-eluting stents are coated with antiproliferative agents that are very effective in controlling restenosis ØDrug-eluting stents carry an increased risk for thrombosis after 1 year, so patients with such stents require long-term use of aspirin and/or clopidogrel With percutaneous intervention, a successful outcome is achieved in more than 95% of patients, with very few complications
Coronary atherosclerotic heart disease does not directly induce oral lesions or oral complications
ØCarotid calcifications can be detected on panoramic images in about one-third of patients who have atherosclerosis ØAn association between ischemic heart disease and periodontal disease, poor oral health and tooth loss has been documented ØDrugs used in the treatment of ischemic heart disease may produce oral changes such as dry mouth, taste aberrations, and stomatitis
Patients should avoid known precipitating factors that may bring on cardiac pain, such as
ØCold weather ØHot and humid weather ØBig meals ØEmotional upset ØCigarette smoking ØDrugs (e.g. amphetamines, caffeine, ephedrine, cyclamates, alcohol)
Blood tests are used in the evaluation of patients with symptoms of angina pectoris to screen for abnormalities that may contribute to or worsen coronary heart disease
ØComplete blood count to rule out anemia ØThyroid function tests to exclude hyperthyroidism ØRenal function tests to exclude renal insufficiency ØLipid screening for hypercholesterolemia ØGlucose screening for diabetes ØHomocysteine level determination ØC-reactive protein assay
Drug Interactions: Many patients who have ischemic heart disease take cholesterol-lowering medications, such as simvastatin (Lipitor)
ØConcurrent use of macrolide antibiotics has been shown to increase the plasma level of statin drugs and increases the risk of rhabdomyolysis (myalgia and muscle weakness) ØA dentist should not prescribe erythromycin or clarithromycin to patients taking HMG CoA reductase inhibitors or calcium channel blockers
The development of an arrhythmia in a patient who has had an acute MI constitutes an emergency that must be treated aggressively with antiarrhythmic drugs
ØDuring the first several weeks after an infarction, the conduction system of the heart may be unstable and patients are prone to serious arrhythmias and reinfarction ØA pacemaker may be used in patients who have severe myocardial damage and resultant heart failure
The management of acute MI has undergone significant change over the past several years =
ØEarly recanalization with thrombolytic therapy and/or percutaneous coronary intervention can result in significant reduction in morbidity and mortality associated with STEMI ØEarly use of thrombolytic drugs may decrease the extent of necrosis and myocardial damage and dramatically improve outcome and prognosis
Other risk factors for the development of atherosclerosis include
ØElevated levels of C-reactive protein (inflammatory marker) ØFibrinogen (procoagulant) ØPlasminogen activator inhibitor (thrombolytic) ØHomocysteine
For an asymptomatic patient with no other risk factors, risk for an adverse event is minimal, especially one month after the MI
ØHowever, symptoms such as chest pain, shortness of breath, dizziness, or fatigue are present, or the MI was less than one month, then the patient falls in the major risk category, and elective dental care should be deferred and medical consultation obtained
The use of vasoconstrictors in local anesthetics poses potential problems for patients with ischemic heart disease because of the possibility of precipitating cardiac tachycardias, arrhythmias, and increases in blood pressure =
ØIf a vasoconstrictor is necessary, patients with intermediate clinical risk factors and those taking nonselective beta blockers can safely be given up to 0.036 mg epinephrine (2 cartridges containing 1:100,000 epinephrine) at one appointment
For patients with symptoms of unstable angina or those who have had an MI within the past 30 days, elective care should be postponed
ØIf treatment becomes necessary, it should be performed as conservatively as possible and directed primarily toward pain relief, infection control, or the control of bleeding Pain occurring at rest or during sleep is particularly ominous ØConsultation with the physician is advised
Most acute coronary artery syndromes are caused by physical disruption or fracture of the atheromatous plaque, most commonly of a plaque that did not cause extreme stenosis
ØIn plaque rupture, the fibrous cap tears, allowing blood to enter the lipid core, where contact with tissue factor and collagen induces platelet adhesion and formation and sudden expansion of the lesion ØBlood flow through the affected artery may become compromised or completely blocked
Morbidity and mortality increase linearly with blood pressures greater than 115/75 mm Hg
ØIn the Framingham Study, even prehypertension (defined as SBP of 130 to 139 and DBP of 85 to 89) was associated with a risk of cardiovascular disease double that for lower pressures
Sudden cardiac death accounts for 325,000 deaths annually in the U.S. and is often, but not always, due to cardiac arrhythmia
ØMost cardiac arrest survivors have structural heart disease; nearly 75% have coronary artery disease. ØPredominant symptoms and signs that most often precede sudden death include chest pain, cough, shortness of breath, fainting, dizziness, palpitations, and fatigue ØThe most common cause of sudden death is ventricular fibrillation
Clinical signs of coronary atherosclerotic heart disease are few, and the patient's clinical appearance may be entirely normal
ØMost clinical signs relate to other underlying cardiovascular disease or other conditions such as congestive failure ØConditions such as corneal arcus and xanthoma of the skin are related to hyperlipidemia and hypercholesterolemia ØBlood pressure may become elevated, and abnormalities in the rate and/or rhythm of the pulse may occur ØDiminished peripheral pulses in the lower extremities may be noted, along with bruits in the carotid arteries ØPanoramic radiographs of the jaws may occasionally demonstrate carotid calcifications in the areas of C3 and C4
Drug Considerations: NSAIDs (except for aspirin) should be avoided in patients with established hypertension and coronary artery disease, especially those whose cardiac history includes an MI
ØNSAIDs should be used with caution, if at all, in patients who have had a previous MI, and that if an NSAID is used, naproxen be the drug of choice, administered for less than 7 days
Drug therapy consists of
ØNitrates (nitroglycerin or long-acting nitrates) ØAntiplatelet agents ØStatins Øβ-adrenergic blockers ØCalcium channel blockers ØACE inhibitors
Nitrates are vasodilators, predominantly venodilators, and are a cornerstone of the pharmacologic management of angina
ØNitroglycerin may be used acutely for the relief of anginal pain and prophylactically to prevent angina ØNitroglycerin tablets are placed under the tongue to dissolve; the spray can be administered beneath the tongue or onto the oral mucosa ØNitrates are taken orally to prevent anginal symptoms and are supplied in tablet form, as an ointment for topical application, or as long-acting transdermal nitrate patches applied to the skin
Beta blockers, which are effective in the treatment of many patients with angina, compete with catecholamines for β-adrenergic receptor sites
ØNonselective beta blockers block the β1 and β2 receptors, whereas cardioselective beta blockers preferentially block the β1 receptors at normal therapeutic doses
Metabolic syndrome describes a cluster of pathologic findings consisting of
ØObesity ØInsulin resistance ØLow HDL cholesterol ØElevated triglycerides ØHypertension The prevalence of metabolic syndrome among adults in the United States is estimated to be about 34%, which increases with age Ø
Capacity to tolerate care: Patients with stable angina pose an intermediate cardiac risk and can receive routine dental care when attention to is provided to minimize risk
ØPatients who have unstable angina should be considered to be at major cardiac risk and are not candidates for elective dental care
For patients at all levels of cardiac risk, the use of gingival retraction cord impregnated with epinephrine should be avoided because of the rapid absorption of a high concentration of epinephrine and the potential for adverse cardiovascular effects
ØPlain cord saturated with tetrahydrozoline HCl or oxymetazoline HCl provides gingival effects equivalent to those of epinephrine without adverse cardiovascular effects
Antiplatelet therapy with aspirin is another cornerstone of treatment in patients with angina
ØRegular use of aspirin in patients with stable angina is associated with a significant reduction in fatal events, and in patients with unstable angina, aspirin decreases the chances of fatal and nonfatal myocardial infarction ØAspirin in daily doses of 75 to 325 mg is recommended for all patients with acute and chronic ischemic heart disease ØClopidogrel has been shown to have effects equivalent to those of aspirin
Other diagnostic modalities that are specific for coronary heart disease include
ØResting ECG ØChest x-ray studies ØExercise stress testing ØAmbulatory (Holter) electrocardiography ØStress thallium-201 perfusion scintigraphy ØExercise echocardiography ØAmbulatory ventricular function monitoring ØCardiac catheterization and angiography
General pharmacologic measures for patients with acute MI include the use of
ØSedatives and anxiolytic medications ØNitrates ØBeta blockers ØCalcium channel blockers ØACE inhibitors ØLipid-lowering agents ØOxygen (if needed) ØBedrest ØAntiplatelet drugs (e.g., aspirin) and anticoagulants (e.g., heparin) may be used as well
Along with physical examination and diagnostic testing, serum enzyme determinations are necessary to establish the diagnosis of acute myocardial infarction and to determine the extent of infarction
ØSerum markers of acute myocardial infarction most commonly used in clinical practice include troponin I, troponin T, and creatine kinase isoenzyme (CK-MB), and myoglobin ØThese enzymes are released only when cell death (infarction) or injury to the myocyte occurs
The general management strategies for patients include
ØShort appointments in the morning ØComfortable chair position ØReduced stress environment ØPretreatment vital signs ØAvailability of nitroglycerin, oral sedation, and nitrous oxide-oxygen sedation ØProfound local anesthesia ØLimited amount of vasoconstrictor ØAvoidance of epinephrine-impregnated retraction cord ØEffective postoperative pain control Ø
Identification: Any patient whose condition remains undiagnosed but has cardinal clinical/radiographic signs or symptoms of ischemic heart disease should be referred to a physician for diagnosis and treatment
ØThe dentist must be able to distinguish a patient who has stable vs. unstable angina vs. MI ØLaboratory testing and diagnostic imaging is helpful in identifying those who have varying severity of ischemic heart disease
Calcium channel blockers are effective in the treatment of chronic stable angina when given alone or in combination with beta blockers and nitrates
ØThese drugs decrease intracellular calcium, resulting in vasodilatation of coronary, peripheral, and pulmonary vasculature, along with decreased myocardial contractility and heart rate
The cause of coronary atherosclerosis is related to a variety of risk factors
ØThese include male gender, older age, a family history of cardiovascular disease, hyperlipidemia, hypertension, cigarette smoking, physical inactivity, obesity, insulin resistance and diabetes mellitus, mental stress, and depression ØAdditionally, markers of inflammation, such as C-reactive protein, homocysteine, fibrinogen, and lipoprotein(a), have been found to be associated with atherosclerosis
The statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA) in the liver, thereby leading to enhanced expression of the LDL receptors that capture blood cholesterol
ØThey are used to lower LDL cholesterol and increase HDL cholesterol, and have been shown to decrease the risk for a major coronary event and the risk of death ØStatins also are anti-inflammatory
Troponins are proteins that are derived from the breakdown of myocardial sarcomeres
ØTroponin assays are the most sensitive and specific in differentiating cardiac muscle damage from trauma to skeletal muscle or other organs; and are virtually absent in the plasma of normal persons and are found only after cardiac injury. ØTroponins are first detectable 2 to 4 hours after the onset of an acute myocardial infarction
Causes of death in patients who have had an acute myocardial infarction include
ØVentricular fibrillation ØCardiac standstill ØCongestive heart failure ØEmbolism ØRupture of the heart wall or septum
Complications of myocardial infarction include
ØWeakened heart muscle resulting in acute congestive heart failure ØPostinfarction angina ØInfarct extension ØCardiogenic shock ØPericarditis ØArrhythmias