The vignettes that follow were selected to illustrate the role of echocardiography in common clinical cases. Included in the discussion of each case are the salient guidelines from the ACC/AHA/ASE 2003 Task Force.9
Case 1: Congestive Heart Failure
A 75-year-old white man presents with a history of a myocardial infarction but no recent chest pain, easy fatigability, progressive dyspnea on exertion, dependent edema, nocturia, and a 20-pound weight gain.
Physical examination reveals distended jugular veins, bilateral rales, S3 and S4 gallops, abdominal swelling, and 3+ pretibial edema. ECG results are as follows: sinus rhythm; rate = 88 bpm; QRS = 130 ms; and poor precordial R wave progression.
Acc/Aha/Ase Guidelines: Patients with Dyspnea, Edema, or Cardiomyopathy
- Class I
- In patients with clinical diagnosis of heart failure
- In patients with edema and suspected heart disease
- In patients with dyspnea and signs of heart failure
- In patients with suspected cardiomyopathy
- In patients exposed to cardiotoxic agents
Heart failure is a common clinical syndrome and one of the most common indications for echocardiography. Approximately five million people in the United States have clinical heart failure, with more than 500,000 new cases of heart failure diagnosed annually.10 The presence of heart failure continues to increase with the overall aging of our population. Heart failure is the leading hospital discharge diagnosis for patients over the age of 65 years. Patients with clinical heart failure can have impaired LV systolic function and/or LV diastolic dysfunction.
Echocardiography is useful in differentiating between the various etiologies of heart failure such as coronary artery disease, hypertension, valvular heart disease, and primary cardiomyopathies. Echocardiography is also useful in ruling out the nonmyocardial disorders that can present as heart failure such as pericardial disease and hypovolemic shock.
Doppler allows for the quantification of the severity of valvular abnormalities, an estimate of pulmonary pressures, and an assessment of LV diastolic function.
Most adult patients who present with heart failure have an ischemic cardiomyopathy, hypertensive heart disease, or valvular abnormalities. Less common are primary disorders of the myocardium, which have been classified by the World Health Organization into five broad categories: dilated, hypertrophic, restrictive, arrhythmic right ventricular (RV), and unclassified, each of which has distinguishing echocardiographic features (Table 1–12).11
Table 1–12. World Health Organization/International Society and Federation of Cardiology: Classification of Cardiomyopathies ||Download (.pdf)
Table 1–12. World Health Organization/International Society and Federation of Cardiology: Classification of Cardiomyopathies
|Cardiomyopathy||LV Chamber Size||LV Wall Thickness||LV Systolic Function||LV Diastolic Function|
|Dilated||Dilated (RV may be dilated)||Normal or thinned||Reduced (regional or global)||Abnormal|
|Hypertrophic||Normal||Increased (concentric or asymmetric)||Normal||Abnormal (LVOT obstruction)|
|Arrhythmogenic right ventricular dysplasia||RV dilated||Normal||RV reduced (LV may be reduced)||Abnormal|
Patients with a dilated cardiomyopathy will often have spherical LV chamber dilatation. The LV wall motion is most typically globally reduced; however, regional wall motion abnormalities are not uncommon. Echocardiography can provide accurate measurements of LV dimensions, volumes, pressures, and LV systolic and diastolic function (Figs. 1–31, 1–32, 1–33).
Dilated cardiomyopathy. Parasternal long axis M-mode images of a dilated left ventricle (normal LVId < 6.0 cm) with a severely reduced left ventricular systolic function and fractional shortening of 6.85% (normal >27%). EF, ejection fraction; FS, fractional shortening; LVIDd, left ventricular internal dimension in end-diastole; LVIDs, left ventricular internal dimension in end-systole.
Dilated cardiomyopathy. Parasternal long axis image of a dilated LV chamber with an end-diastolic dimension of 6.5 cm (normal <6.0 cm). LA, left atrium; LV, left ventricle; LVIDd, left ventricular internal dimension in end-diastole.
Dilated cardiomyopathy. Parasternal long axis image of a dilated LV chamber with an end-systolic dimension of 5.8 cm (normal < 4.0 cm). LA, left atrium; LV, left ventricle, LVIDs, left ventricular internal dimension in end-systole.
As previously described, dobutamine stress echocardiography can give important additional information regarding the etiology of the dilated cardiomyopathy. An inducible wall motion abnormality would suggest coronary artery disease. Another indicator of ischemia would be an akinetic or hypokinetic "hibernating" wall that contracts more normally when stimulated.
Cardiac Resynchronization Therapy
Tissue Doppler imaging is used in cardiac resynchronization therapy, which is the use of multiple lead/biventricular pacing to help optimize LV systolic function and improve morbidity and mortality in patients with severe LV systolic impairment.12-14
A 62-year-old African American man presents with a long history of poorly controlled hypertension, increasing exercise intolerance, and chronic renal insufficiency.
Physical examination reveals a sitting blood pressure of 176/94 mm Hg, clear lungs, prominent point of maximal intensity (PMI), and an S4 gallop. ECG results are as follows: normal sinus rhythm; left axis deviation; and LVH with repolarization changes.
ACC/AHA/ASE Guidelines: Patients with Hypertension
- Class I
- To assess resting LV function and LVH
- Class IIa
- Identification of LV diastolic filing abnormalities
- Class III
- Reevaluation to assess LV mass or function to guide antihypertensive therapy
Approximately one-third of the adult US population, 40% of African Americans, and more than two-thirds of people over the age of 65 have hypertension.10 Although hypertension is a significant factor in the development of atherosclerotic vascular disease, it is the principal contributing factor to developing LVH.
The Framingham Heart Study demonstrated the prognostic value of electrocardiographically determined LVH.15 Subsequently, the Framingham Heart Study investigators and others have demonstrated the superiority of echocardiographically determined LV mass and hypertrophy predicting coronary heart disease, strokes, and increased mortality (Figs. 1–34 and 1–35).16,17
Hypertensive heart disease. Parasternal long axis M-mode image illustrating markedly increased left ventricular wall thickness of approximately 2.0 cm (normal <1.1 cm), with a normal left ventricular chamber size and normal left ventricular fractional shortening. IVSd, interventricular septal wall thickness; LVIDd, left ventricular internal dimension in end-diastole; LVIDs, left ventricular internal dimension in end-systole; LVPWd, left ventricular posterior wall thickness.
Hypertensive heart disease. Parasternal long axis image illustrating marked concentric left ventricular hypertrophy, approximately 2.0 cm (normal <1.1 cm), with a normal left ventricular chamber size, normal left ventricular fractional shortening, and left atrial dilatation. IVSd, interventricular septal wall thickness; LA, left atrium; LVPWd, left ventricular posterior wall thickness; RV, right ventricle.
Heart Failure with Preserved LV Systolic Function
Hypertension is also the principal etiology for preserved systolic function heart failure (ie, diastolic heart failure). In the Framingham Heart Study, 75% of patients with heart failure had a history of hypertension, and mild hypertension doubled the lifetime risk of developing heart failure.18
In the Mayo Clinic's report from Olmsted County, approximately 40% of the heart failure patients had diastolic heart failure with preserved LV systolic function.19 In the Framingham Heart Study, 51% of patients with heart failure and preserved LV systolic function had an annual mortality rate of 8.7%, which was approximately four times that of the age-matched controls.20
The four elements of diastolic heart failure are:
- Symptoms suggestive of heart failure
- Normal LV systolic function, LVEF ≥45%
- Abnormal myocardial relaxation
- Increased filling pressures
The optimal management of diastolic heart failure with preserved systolic function is the subject of several ongoing clinical trials.
A 29-year-old man with no known heart disease presents with the sudden onset of rapid palpitations and near syncope.
Physical examination is normal with the exception of a rapid irregularly irregular pulse. ECG results are as follows: atrial fibrillation with a ventricular response rate averaging 170 bpm.
Acc/Aha/Ase Guidelines: Patients with Palpitations and Arrhythmias
- Class I
- Patients with suspected structural heart disease
- Evaluation of patients prior to radiofrequency ablation
- Class III
- Palpitations without arrhythmia or other cardiac signs or symptoms
- Isolated premature ventricular beats without suspicion of heart disease
Arrhythmias can occur in the presence or absence of structural heart disease. Echocardiography can identify common cardiac abnormalities associated with arrhythmias, thereby providing the clinician with important prognostic and therapeutic useful information.
Ventricular Arrhythmias/Sudden Death
For patients who present with ventricular arrhythmias, in the absence of a history of sudden death, the best predictor of a future sudden death event is the severity of the LV systolic dysfunction. In addition to providing quantitative information regarding LV systolic and diastolic function, echocardiography also provides information regarding RV size and function.
Arrhythmogenic RV dysplasia (ARVD) is due to progressive myocardial atrophy with fibrofatty infiltration of the right ventricle. ARVD can be inherited as an autosomal dominant trait and has been reported as a cause of sudden death in the young.21 The resting ECG shows RV conduction delay and characteristic epsilon waves–terminal notching of the QRS in leads V1 to V3. The morphology of the ventricular tachycardia is left bundle branch block because it originates in the right ventricle. Echocardiographic changes can appear late and generally include RV outflow and inflow dilatation and RV global or regional hypokinesis. Dilatation of the RV outflow tract >30 mm in the parasternal long axis view has been reported to be the most sensitive and specific sign of ARVD.22 LV dilatation and hypokinesis occur in approximately 50% of patients with ARVD.
Echocardiography plays a central role in the workup and treatment of patients with supraventricular arrhythmias, in particular, atrial fibrillation.23 The prevalence of atrial fibrillation in the United States now exceeds two million, and atrial fibrillation results in more than 500,000 hospital admissions annually.10 This increased prevalence and incidence reflects the aging of our population. Approximately 1% of people over the age of 60 years, 5% over the age of 70 years, and 10% over the age of 80 years have atrial fibrillation.24 Ten percent of patients with heart failure have atrial fibrillation.
Echocardiographically demonstrated moderate to severe LV systolic dysfunction has been shown to predict a greater than two-fold increase in the rate of stroke.25 Of note, atrial fibrillation occurs in 10% to 30% of patients in the absence of underlying disease and is called lone atrial fibrillation.26
Atrial fibrillation is responsible for up to 20% of all strokes. Patients with atrial fibrillation have an annual stroke rate of 5% and a two-fold increase in the risk of recurrent stroke.27-29 In addition, patients in atrial fibrillation have an increase in heart failure and total mortality compared with people in sinus rhythm.
In recognition of the long-term deleterious effects of atrial fibrillation, clinicians are becoming more aggressive in their attempts to restore sinus rhythm before left atrial remodeling and scarring become irreversible.
Traditionally, echocardiographic measures of left atrial size and LV systolic function have been used to predict a patient's stroke risk and the outcome of cardioversion (Fig. 1–36).29,30 Echocardiography is also being used more frequently to determine the timing of cardioversion.
Parasternal long axis image demonstrating left atrial enlargement of 6.5 cm (normal <4.0 cm) with normal LV chamber size and LV wall thickness. Ao, aorta; LV, left ventricle; RV, right ventricle.
In the absence of 3 to 4 weeks of anticoagulation, the incidence of a cardioembolic complication following cardioversion is up to 5%, depending on the severity of the underlying heart disease. The left atrial appendage is the source of most of the embolic events. Although not visible by transthoracic echocardiography, the left atrial appendage is visible in most patients by transesophageal echocardiography (Fig. 1–37). Using transesophageal echocardiography to screen patients for stasis or visible thrombi in the left atrial appendage, the incidence of acute neurologic events following cardioversion has been demonstrated to be <0.1%, which is comparable to the incidence in patients on long-term anticoagulation.31
Left atrial thrombus. Transesophageal echocardiographic image of a dilated left atrium and large left atrial thrombus. LA, left atrium; LAA, left atrial appendage.
Echocardiographic-derived measures of left atrial size and volume are also being used in decision making regarding radiofrequency ablation. Increasingly, transesophageal echocardiography, intracardiac ultrasound, and three-dimensional echocardiography are being used in new catheter-based interventions, including radiofrequency ablation of sinus node dysfunction, atrial fibrillation, and left-sided accessory atrioventricular pathways.32-35
Case 4: Mitral Regurgitation
A 72-year-old man presents with increasing dyspnea on exertion and exercise intolerance.
Physical examination reveals distended neck veins, basilar rales, an enlarged displaced PMI, and a grade 4/6 holosystolic murmur at the cardiac apex radiating to the anterior axillary line. ECG results are as follows: atrial fibrillation; normal QRS; and nonspecific ST-T wave changes.
Acc/Aha/Ase Guidelines: Patients with Native Valvular Regurgitation
- Class I
- Assess LV and RV size and function and/or hemodynamics
- Reevaluate patients with mild or moderate regurgitation and changing symptoms
- Periodic reevaluation of asymptomatic patients with severe regurgitation
- Periodic reevaluation of asymptomatic patients with mild or moderate regurgitation and LV dilatation
- Assessment of medical therapy
- During pregnancy
- Patients with a history of anorectic drug use who are symptomatic or have cardiac murmurs
- Class III
- Routine reevaluation of asymptomatic patients with mild mitral or aortic regurgitation with normal LV size and function
Valvular regurgitation is a common echocardiographic finding. In the absence of other cardiac abnormalities, trace or mild mitral, tricuspid, or pulmonic regurgitation can be a normal finding, whereas aortic regurgitation is never considered normal. Mild or moderate mitral or aortic regurgitation can also be missed when auscultation is performed by an inexperienced or distracted observer.
Mitral regurgitation can be congenital or acquired, which can be acute or chronic. Common etiologies of chronic mitral regurgitation include degenerative disorders including mitral valve prolapse and mitral annular calcification; structural due to ischemia or LV dilatation; infectious endocarditis; and inflammation due to rheumatic or connective tissue disorders.
Two-dimensional echocardiography provides important structural information regarding the possible etiology of the mitral regurgitation including leaflet prolapse, flail leaflets, ruptured chordae tendineae, vegetations, and LV chamber size and function. Doppler indices provide a direct assessment of the hemodynamic significance of valvular regurgitant and stenotic abnormalities.
Figure 1–38 demonstrates moderately severe (3+) mitral regurgitation, as evident by the left atrial enlargement, mitral regurgitant jet, LV dilatation, and global LV hypokinesis.
Mitral regurgitation. Apical four-chamber color flow Doppler image of severe mitral regurgitation with prominent PISA. LA, left atrium; LV, left ventricle; PISA, proximal isovelocity surface area; RA, right atrium; RV, right ventricle.
Natural history studies have demonstrated that the onset of symptoms occurs late in the course of patients with chronic mitral insufficiency.36 Current echocardiographic indications for mitral valve surgery on asymptomatic patients include LV chamber dilatation and/or LV systolic dysfunction and Doppler evidence of pulmonary hypertension.37 Newer Doppler indices include an assessment of the regurgitant jet's length, area, and width; the width of the vena contracta; the effective regurgitant orifice area (EROA); regurgitant volume using the proximal isovelocity surface area; right-sided pressures; and pulmonary venous flow reversal (Table 1–13).38-41
Table 1–13. Echo Doppler Assessment of the Severity of Mitral Regurgitation ||Download (.pdf)
Table 1–13. Echo Doppler Assessment of the Severity of Mitral Regurgitation
|Severity||LA/LV Size||MR Jet Area||MR Jet Volume (ML/Beat)||MR Jet Fraction (%)||EROA (cm2)||Pisa Radius (mm)|
|Mild (1+)||Normal||Small <20% LA||<30||<30||<0.20||<4|
|Moderate (2+)||Mildly increased||Moderate||30-44||30-39||0.20-0.29||4-7|
|Severe (4+)||Dilated||Large >40% LA||>60||>50||>40||>10|
Proximal Isovelocity Surface Area
The proximal isovelocity surface area (PISA) method is based on the principle that flow will converge at the site of an orifice at symmetrical velocities, equal to the flow rate through the orifice. By measuring the distance from the first aliased color flow velocity at the regurgitant orifice, the blue-red interface, calculations can be made of the EROA and the regurgitant volume (see Fig. 1–38).
Mitral valve prolapse was once considered a common congenital abnormality. It is now believed to be primarily a degenerative abnormality related either to a systemic connective tissue disorder or aging, occurring in approximately 2% of the general population.42-44
Traditionally, the diagnosis of mitral valve prolapse has depended on the auscultatory findings of a mid-systolic click followed by a mid-systolic mitral regurgitant murmur.
Echocardiographic criteria for mitral valve prolapse include thickened mitral leaflets (>5 mm), redundant with pan- or mid-systolic posterior motion (prolapse) of the anterior and/or the posterior leaflets 2 mm or more beyond the plane of the mitral annulus in the parasternal long axis view (Figs. 1–39, 1–40, 1–41).
Mitral valve prolapse. Parasternal long axis M-mode image demonstrating pansystolic posterior ballooning of the posterior mitral valve leaflet.
Mitral valve prolapse. Parasternal long axis image demonstrating systolic ballooning of the posterior mitral valve leaflet approximately 7 mm beyond the plane of the mitral annulus into the left atrium. LA, left atrium; LV, left ventricle.
Mitral regurgitation. Apical four-chamber color flow image demonstrating severe eccentric mitral regurgitation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Transesophageal echocardiography has become an important part of the preoperative evaluation of patients with mitral regurgitation to help determine the feasibility of the clinically superior repair of the mitral valve rather than replacing it with a mechanical prosthesis or bioprosthesis.45
ACC/AHA/ASE Guidelines: Patients with Mitral Valve Prolapse
- Class I
- Diagnosis in patients with physical signs of mitral valve prolapse
- Class III
- Routine repetition in patients with mitral valve prolapse with no or mild regurgitation and no change in clinical signs or symptoms
Case 5: Cerebrovascular Accident/Syncope
An 83-year-old white woman presents with sudden onset of dysphasia and left-sided hemiparesis.
Physical examination reveals a blood pressure of 160/90 mm Hg, clear lungs, regular rhythm, S4 gallop, no edema, and right-sided upper and lower extremity weakness. ECG results are as follows: atrial fibrillation; LVH; and old inferior wall myocardial infarction.
Acc/Aha/Ase Guidelines: Patients with Neurologic Events
- Class I
- Abrupt occlusion of any major peripheral or visceral artery
Every year, approximately 800,000 Americans suffer an acute cerebrovascular accident.8 Stroke is the third leading cause of death in the United States, behind heart disease and cancer. It is currently estimated that approximately 20% of strokes are due to cardiac emboli, with higher rates in younger patients who do not have coexistent vascular disease.
Echocardiography has become an integral part of the workup of every patient admitted to a hospital with a cerebrovascular accident or transient ischemic attack. In addition to information relevant to an arrhythmia workup, LV function and valvular lesions, echocardiography provides valuable information to rule out a possible cardiac source of emboli (Table 1–14).
Table 1–14. Potential Cardiac Sources of Emboli Causing Neurovascular Events ||Download (.pdf)
Table 1–14. Potential Cardiac Sources of Emboli Causing Neurovascular Events
|Atrial septal defects||Rheumatic||Dilated with reduced left ventricular ejection fraction|
|Atrial septal aneurysm||Mitral annular calcification||Aneurysm|
|Patent foramen ovale||Prosthetic bacterial endocarditis||Mural thrombus|
Transesophageal echocardiography provides superior spatial resolution for identifying vegetations as well as other potential cardiovascular sources of emboli including papillary fibroelastomas and aortic atheroma.
The role of echocardiography in the workup, risk stratification, and management of atrial fibrillation in the prevention of cardiac embolic events was discussed earlier in Case 3.
Prior to the era of reperfusion and the widespread use of antiplatelet and antithrombin agents, LV mural thrombi occurred in up to 50% of patients with large anterior wall myocardial infarctions. Contributing factors include the hypercoagulable postinfarction state, localized endocardial inflammation, and regional akinesis or dyskinesis. An estimated 10% of mural thrombi result in thromboembolic events (Fig. 1–42).46 Figure 1–42 demonstrates a dilated left ventricle with apical akinesis/dyskinesis and an apical LV filling defect consistent with a mural thrombus.
Left ventricular mural thrombus. Apical four-chamber image demonstrating a large, 2 cm × 2 cm left ventricular apical filling defect consistent with a mural thrombus. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Atrial Septal Defect/Patent Foramen Ovale
Atrial septal defects occur in approximately 5% to 10% of children with congenital heart disease. Secundum atrial septal defects are the most common. They are located in the central portion of the atrial septum and encompass the region of the foramen ovale. The degree of the left-to-right shunt is dependent on the size of the atrial septal defect. Large defects result in diastolic volume overload of the right ventricle and increased pulmonary blood flow.
In the apical four-chamber view, two-dimensional echocardiography can identify right atrial and RV dilatation and atrial septal wall echo dropout, which is a nonspecific finding. Diastolic flattening of the intraventricular septum can be seen in the parasternal short axis view. Doppler recordings can demonstrate elevated right-side pressure.
A patent foramen ovale has been reported to occur in approximately 30% of the general population.47
In addition to routine transthoracic echocardiography, patients who present with a cerebrovascular accident frequently undergo contrast studies to rule out paradoxical shunts due to an intracardiac shunt.
Transesophageal echocardiography with intravenous injection of agitated saline with or without simple physiologic maneuvers such as coughing or Valsalva enhances the detection of shunts due to either an atrial septal defect (Figs. 1–43 and 1–44) or a patent foramen ovale (Figs. 1–45 and 1–46).
Atrial septal defect. Transesophageal echocardiogram demonstrating a right atrial enlargement and a 1-cm secundum-type atrial septal defect. ASD, atrial septal defect; LA, left atrium; RA, right atrium.
Atrial septal defect. Transesophageal echocardiogram with saline contrast opacifying the right atrium and demonstrating a right to left (R → L) interatrial shunt of contrast bubbles into the left atrium. LA, left atrium; RA, right atrium; RVOT, right ventricular outflow tract.
Patent foramen ovale. Transesophageal color flow image demonstrating a left to right (L → R) interatrial shunt from the left atrium across the patent foramen ovale to the right atrium. LA, left atrium; RA, right atrium.
Patent foramen ovale. Apical four-chamber intravenous contrast image demonstrating right to left interatrial shunt with bubbles appearing in the left atrium and the left ventricle. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
The presence of an atrial septal defect or a patent foramen ovale in the presence of an atrial septal aneurysm has been associated with an increased incidence of acute neurologic deficits.48 Intracardiac echocardiographic imaging and three-dimensional echocardiography are new technologies that are being used to facilitate the implantation of percutaneous vascular closure devices.48-50
An association between patent foramen ovale and migraine headaches remains controversial.51,52 A recently concluded prospective, randomized clinical trial showed no utility for the percutaneous closure of patent foramen ovale in treating migraines.53
Atrial myxomas are the most common tumors of the heart. Myxomas appear as pedunculated masses most commonly located in the left atrium attached to the atrial septum in the area of the foramen ovale, and less commonly located in the right atrium, right or left ventricles, pulmonary veins, or vena cava. In addition to presenting as an acute thromboembolic event, a large, mobile, atrial myxoma can cause syncope by obstructing diastolic mitral inflow (Figs. 1–47, 1–48, 1–49).
Myxoma. Parasternal long image view demonstrating a large, 3 cm × 4 cm left atrial myxoma. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Myxoma. Parasternal long axis image demonstrating prolapse of a large left atrial myxoma across the mitral valve orifice into the left ventricle. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Myxoma. Parasternal long M-mode image demonstrating an echo-dense mass filling the mitral valve orifice from mid to late diastole. MV, mitral valve.
Syncope is a common clinical problem for patients of all ages but occurs most frequently in the elderly, who have an approximate 6% annual rate.54 Cardiac causes for syncope are most common in the elderly. However, in the absence of a preexisting cardiac history or symptoms or abnormalities evident on physical examination or ECG, the incidence of unsuspected echocardiographic abnormalities is low. Current AHA/ACC guidelines recommend echocardiography as part of the workup of all patients with unexplained syncope.55
Acc/Aha/Ase Guidelines: Patients with Syncope
- Class I
- In patients with suspected heart disease
- In patients with periexertional syncope
- Class IIa
- In patients in high-risk occupations
- Class III
- In patients with classic neurogenic syncope
A 26-year-old active woman presents with no cardiopulmonary complaints.
Physical examination reveals normal vital signs. Cardiac auscultation reveals normal S1 and physiologically split S2 and a grade 1/6 short systolic murmur at the left sternal border without appreciable clicks or gallops. ECG results are normal.
Acc/Aha/Ase Guidelines: Patients with a Heart Murmur
- Class I
- Patients with a heart murmur and cardiorespiratory symptoms
- Asymptomatic patients with suspected structural heart disease
- Class III
- Asymptomatic adults with innocent or functional heart murmurs
Echocardiography plays a central role, along with a careful history, cardiac auscultation, and ECG, in the assessment of patients who present with heart murmurs.
Not all murmurs reflect significant underlying cardiac abnormalities. Murmurs with the characteristics of this case are "innocent" functional flow murmurs often heard in children, adolescents, and young lean adults. Trace or mild mitral, tricuspid, and/or pulmonic regurgitation are common and can be considered normal in the otherwise normal heart. Soft systolic ejection murmurs due to aortic leaflet thickening/sclerosis are a degenerative process common in the elderly and, in the absence of an increase in the LV outflow velocity, are of no clinical significance.
Calcific aortic stenosis due to congenital bicuspid aortic valves or rheumatic heart disease generally presents in a patient's sixth decade, whereas degenerative aortic stenosis occurs one or two decades later. Unlike the patient who presents with an innocent flow murmur or aortic leaflet sclerosis, the characteristics of a hemodynamically significant aortic stenosis include diminished carotid pulses with a palpable thrill and audible transmitted cardiac murmurs; a prominent PMI; a precordial thrill; and a long late-peaking systolic murmur at the left sternal border with a diminished, absent, or paradoxically split S2.
The severity of the aortic stenosis can be assessed echocardiographically by visual inspection of M-mode and two-dimensional recordings (Figs. 1–50, 1–51, 1–52, 1–53, 1–54). In the parasternal echocardiographic view, normal aortic leaflets will appear thin (ie, less thick than the walls of the aorta). Normal aortic leaflets are freely mobile. During ventricular systole, the leaflets will separate a minimum of 2 cm, opening the full width of the aortic root. Newer three-dimensional imaging technologies provide improved spatial, structural, and functional information (Fig. 1–55).
Aortic stenosis. Parasternal long axis M-mode image demonstrating thickened aortic valve leaflets with diminished systolic opening.
Aortic stenosis. Parasternal short axis image demonstrating heavily calcified aortic valve leaflets and mild concentric left ventricular hypertrophy. LA, left atrium; LV, left ventricle.
Aortic stenosis. Parasternal short axis image showing heavily calcified aortic valve leaflets. LA, left atrium; RA, right atrium; RVOT, right ventricular outflow tract.
Aortic stenosis. Apical five-chamber image of heavily calcified aortic valve leaflets. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
Aortic stenosis. Apical five-chamber Doppler display demonstrating high-velocity turbulent flow. The transvalvular gradients were calculated using the Bernoulli equation, and the aortic valve area was calculated using the continuity equation. AV, aortic valve; AVA, aortic valve area; PG, pressure gradient; V, velocity; VTI, velocity time integral.
Aortic stenosis. Three-dimensional illustration of calcific aortic stenosis.
The severity of the aortic stenosis can be more accurately assessed by Doppler-derived peak and mean transvalvular gradients using the modified Bernoulli equation and by calculation of the aortic valve area using the continuity equation (Table 1–15).
Table 1–15. Echo Doppler Assessment of the Severity of Aortic Stenosis ||Download (.pdf)
Table 1–15. Echo Doppler Assessment of the Severity of Aortic Stenosis
|Severity||LV Wall Thickness||Aortic Valve Area (cm2)||Mean Pressure Gradienta (mm Hg)||Peak Pressure Gradienta (mm Hg)||Peak Aortic Velocity (m/s)|
The Bernoulli equation is used to calculate pressures in the cardiac chambers, across valves, and across intracardiac and vascular shunts. The Bernoulli equation is based on the principle that the total energy in a closed system is constant. Therefore, the energy flowing into the system must be equal to the energy flowing out of the system.
Flow is dependent on pressure differences between two locations. In the presence of a narrowing, the velocity distal to the narrowing must be increased to maintain the energy in the -system. Because velocity and pressure are inversely proportional, the pressure distal to the narrowing must be decreased relative to the pressure proximal to the narrowing.
The pressure difference proximal and distal to the narrowing is measured by the Bernoulli equation: ΔP = 4V2.
The continuity equation is also dependent on the principle of conservation of mass (ie, in a closed system, what flows in must flow out). To maintain flow within a system, the flow velocities at a stenotic orifice must be greater than the flow velocities proximal and distal to the stenosis. Because the flow rate is the product of the area and mean flow velocity, valve areas can be calculated from flow and velocity measurements.
The continuity equation uses these measurements to calculate valve areas, regurgitant volumes and regurgitant fractions, regurgitant orifice areas (EROA), and intracardiac shunt areas.
The continuity equation is as follows: CSA1 × V1 = CSA2 × V2. CSA1 is the cross-sectional area proximal to the stenosis; V1 is the velocity proximal to the stenosis; CSA2 is the cross-sectional area of the stenotic area, and V2 is the velocity at the stenosis. Because blood flow in the heart is pulsatile, the velocity time integral is substituted for mean velocity for calculation of valve areas.
Confounding factors in the echocardiographic assessment of the severity of aortic stenosis include the presence of coexistent subvalvular LV outflow tract obstruction due to hypertrophic cardiomyopathy, moderate or severe aortic valve regurgitation, and significantly reduced LV systolic function.
Low-Flow/Low-Gradient Aortic Stenosis
Doppler imaging during dobutamine administration can help differentiate patients with severe aortic stenosis from patients who have only mild or moderate aortic stenosis with severe LV dysfunction.
Dobutamine should cause an increase in LV contractility with a resultant increase in stroke volume. In patients with mild to moderate aortic stenosis and LV dysfunction, dobutamine infusion will increase the stroke volume, with a resultant increase in the calculated aortic valve area (>0.2 cm2) with no change in the outflow gradient. In patients with severe aortic stenosis and a relatively fixed valve area, dobutamine infusion will result in an increase in the calculated LV outflow gradient.
Lack of contractile or inotropic reserve is defined as failure of dobutamine to increase the patient's stroke volume by >20%. These patients generally have a poor prognosis whether treated medically or surgically.56
ACC/AHA/ASE Guidelines: Native Valvular Stenosis
- Class I
- Initial diagnosis with an assessment of chamber dimensions and hemodynamic severity
- Reevaluation in patients with worsening symptoms
- Reevaluation during pregnancy
- Class III
- Routine reevaluation of stable asymptomatic adults with mild aortic stenosis
- Routine reevaluation of stable asymptomatic adults with mild to moderate mitral stenosis
Chronic Aortic Regurgitation
Aortic valve regurgitation can be the result of an abnormality of the aortic valve, including congenital, degenerative, or infectious abnormalities, or the result of diseases affecting the aortic root, such as acute aortic dissection, Marfan syndrome, syphilis, or trauma.
Natural history studies have demonstrated the predictive value of echocardiographic indices of LV size and systolic function.57-59 Several newer Doppler and color flow imaging parameters have been correlated to angiographically assessed aortic regurgitation including (Figs. 1–56, 1–57, 1–58; Table 1–16):
Aortic regurgitation. Parasternal long axis color flow image of aortic valve regurgitation. LA, left atrium; LV, left ventricle.
Aortic regurgitation. Apical five-chamber color flow image of aortic valve regurgitation. LA, left atrium; LV, left ventricle; RV, right ventricle.
Aortic regurgitation. Apical five-chamber Doppler display of aortic valve regurgitation with a pressure half-time of 480 ms. P½t, pressure half-time.
Table 1–16. Echo Doppler Assessment of the Severity of Aortic Regurgitation ||Download (.pdf)
Table 1–16. Echo Doppler Assessment of the Severity of Aortic Regurgitation
|Severity||Jet Length||AR Jet Width (mm)||AR Jet Width ÷ LVOT Width (%)||AR Jet Fraction(%)||Pressure Half Time (ms)||EROA (cm2)|
|Mild (1+)||Minimal||< 4||<25||<30||>500||<0.10|
|Moderate (2+)||To leaflet tips||4-7||25-46||30-39||350-500||0.10-0.19|
|Severe (4+)||Papillary muscle||>10||>65||>50||<200||>30|
- Length of the aortic regurgitant jet
- Width of the aortic regurgitant jet at its origin
- Width of the aortic regurgitant jet relative to the width of the LV outflow tract
- Diastolic dysfunction including decreasing pressure half-times, a restrictive mitral inflow pattern due to increasing LV pressure, and EROA
Rheumatic mitral stenosis is rare in the United States; however, the increasing aging of the population has led to more degenerative valvular disease. When coupled with heavy mitral annular calcification, the patient can present with symptoms and hemodynamic features similar to mitral stenosis but is not as amendable to surgical repair (Figs. 1–59, 1–60, 1–61, 1–62).
Mitral stenosis. Apical four-chamber image of a stenotic mitral valve. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Mitral stenosis. Apical four-chamber Doppler display of severe mitral valve stenosis with a pressure half-time of 249 ms and a mitral valve area of 0.88 cm2. P½ t, pressure half-time; MVA, mitral valve area.
Mitral annular calcification. Parasternal long axis image of a mildly thickened anterior mitral valve leaflet and heavy posterior mitral annular calcification. LA, left atrium; LV, left ventricle; MAC, mitral annular calcification.
Mitral annular calcification. Parasternal long axis M-mode recording showing normal anterior mitral valve leaflet thickness, a decreased E → F slope, and mitral annular calcification.
Mitral valve area can be estimated by the mean transmitral pressure gradient or by the proximal isovelocity surface area method (Fig. 1–63; Table 1–17). However, the mean transmitral pressure gradient can underestimate the severity of mitral stenosis in the setting of a low cardiac output and overestimate the severity of the mitral stenosis in the setting of mitral regurgitation. Because the pressure half-time method is independent of cardiac output and mitral regurgitation, it is preferred in the setting of heart failure or significant mitral regurgitation.
Mitral stenosis. Apical four-chamber color flow image showing turbulent flow across the mitral valve orifice. LA, left atrium; PISA, proximal isovelocity surface area; RA, right atrium; RV, right ventricle.
Table 1–17. Echo Doppler Assessment of the Severity of Mitral Stenosis ||Download (.pdf)
Table 1–17. Echo Doppler Assessment of the Severity of Mitral Stenosis
|Severity||Left Atrial Size||Mitral Valve Area (cm2)||Mean Pressure Gradient (mm Hg)||Pressure Half- Time (ms)||Pulmonary Artery Pressure (mm Hg)|
The pressure half-time (PHT) is the time for a pressure gradient to decay to half its peak value. The PHT is proportional to the deceleration time, the time from the peak mitral inflow E wave velocity to return to the baseline. PHT equals 0.29 times the deceleration time. The mitral valve area (MVA) can be estimated using the following simple equation: MVA = 220 ÷ PHT.
Family history, symptoms, ECG abnormalities, and the classic auscultatory findings of a nonradiating systolic murmur that increases after ventricular premature contractions, standing, during Valsalva, or after amyl nitrite administration are the hallmarks of obstructive hypertrophic cardiomyopathy.
Echocardiography confirms the clinical diagnosis of hypertrophic cardiomyopathy by identifying the location and severity of the LVH, which can be concentric or localized to the septum as in asymmetric septal hypertrophy (ASH), the apex, or the lateral free wall. Patients with obstructive hypertrophic cardiomyopathy also have abnormal systolic anterior mitral leaflet motion (SAM) and premature, mid-systolic aortic valve closure (Fig. 1–64).
Hypertrophic cardiomyopathy. Parasternal long axis M-mode recording asymmetric left ventricular septal wall thickening, asymmetric septal hypertrophy, and systolic anterior motion of the anterior mitral valve leaflet. IVSd, interventricular septal wall dimension; LVPWd, left ventricular posterior wall dimension; SAM, systolic anterior motion.
Doppler provides quantitative information regarding a possible subvalvular LV outflow or intraventricular cavity gradients both at rest and with provocation, LV diastolic abnormalities, and common associated abnormalities such as mitral regurgitation.
Acc/Aha/Ase Guidelines: Patients with Cardiomyopathy
- Class I
- Suspected hypertrophic cardiomyopathy based on family history, abnormal physical examination, or ECG
A 65-year-old white man presents with the acute onset of severe substernal chest pain.
Physical examination reveals normal vital signs, mild bibasilar rales, a regular rhythm, grade 2/6 apical systolic murmur, and an S3 gallop. ECG results are as follows: normal sinus rhythm and T wave inversion in precordial leads V2 to V4.
Acc/Aha/Ase Guidelines: Patients with Chest Pain
- Class I
- Patients with structural heart disease
- Patients with suspected myocardial ischemia during pain
- Patients with hemodynamic instability
- Patients with suspected aortic dissection
Chest pain is one of the leading complaints of patients who present to emergency departments. When the physical examination, ECG, and cardiac enzymes are nondiagnostic, echocardiography can provide valuable information that can be available immediately to help determine the etiology of the patient's chest pain (Table 1–18).
Table 1–18. Potential Cardiovascular Causes of Acute Chest Pain ||Download (.pdf)
Table 1–18. Potential Cardiovascular Causes of Acute Chest Pain
|Etiology||Echo Doppler Findings|
|Ischemic||Abnormal regional wall motion|
|Aortic stenosis||Calcified leaflets with a significant left ventricular outflow gradient|
|Aortic dissection||Dilated aortic root; possible dissection flap; aortic regurgitation|
|Left ventricular hypertrophy; hypertrophic cardiomyopathy||Hypertrophy with or without left ventricular outflow obstruction|
|Pulmonary embolism||Right-sided dilatation; elevated right-sided pressures|
Coronary heart disease remains the number one killer in the United States. Each year, approximately 800,000 Americans are hospitalized with acute coronary syndromes, ST-segment elevation and non–ST-segment elevation myocardial infarction, or unstable angina.
Acc/Aha/Ase Guidelines: Patients with Acute Coronary Syndromes
- Class I
- Diagnosis of acute coronary syndrome not evident by standard means
- Measurement of baseline LV function/infarct size
- Assessment of the extent of jeopardized myocardium
- Assessment of myocardial viability
- In patients with inferior wall infarction and suspected RV infarction
- When mechanical complications and/or mural thrombus are suspected
In the setting of an acute coronary syndrome, echocardiography can:
- Confirm the diagnosis
- Transient regional wall motion abnormalities associated with ECG changes and/or episodes of chest pain
- Contribute to the initial risk assessment
- Based principally on overall LV function
- Assess possible complications
- Acute mitral regurgitation
- LV remodeling
- Ventricular septal rupture
- LV free wall rupture
- Mural thrombi
- RV infarction
- Pericardial effusion
- Help assess the efficacy of the acute treatment
- Contribute to the predischarge risk assessment
- LV function
- Stress echocardiography
A regional wall motion abnormality evident on two-dimensional echocardiography is suggestive but not diagnostic of ischemic heart disease unless the wall motion abnormality is transiently associated with the patient's chest pain or ECG changes. On the other hand, normal regional and global wall motion in the setting of ongoing chest discomfort has an excellent negative predictive value for coronary artery disease.
For patients unable to exercise, pharmacologic dobutamine stress echocardiography can give important information regarding the presence of jeopardized myocardium either in the area of the acute infarct or in remote regions supplied by other coronary arteries.
Proximal aortic dissection is a life-threatening condition that needs to be considered in patients who present to the emergency department with chest pain and have nondiagnostic ECGs and negative cardiac enzymes. Classically, these patients will have a history of hypertension and the sudden onset of severe chest pain that radiates to their backs.
Two-dimensional transthoracic echocardiographic demonstration of aortic valve incompetence in the setting of dilatation of the aortic root and possibly an intimal flap is highly predictive of an acute proximal aortic dissection.60 Either a transesophageal echocardiogram or chest computed tomography with contrast would be warranted pending emergent surgical evaluation (Fig. 1–65).61,62
Aortic dissection. Transesophageal image demonstrating an intimal flap separating two aortic lumina. The true versus the false lumen cannot be determined by this single image.
Case 8: Acute Pericarditis
A 56-year-old college professor presents 6 weeks following an upper respiratory viral infection with shortness of breath and constant diffuse chest discomfort exacerbated by lying flat and deep inspiration.
Physical examination reveals a temperature of 100°F, clear lung fields, diminished heart sounds, and a three-component pericardial rub. ECG results are as follows: normal sinus rhythm, low QRS amplitude, and depressed PR segments in multiple leads.
Acc/Aha/Ase Guidelines: Patients with Pericardial Disease
- Class I
- Patients with suspected pericardial disease
- Follow-up of patients with known pericardial disease
- Postinfarction patients with pericardial friction rubs accompanied by symptoms such as persistent pain, hypotension, and nausea
- Class III
- Routine follow-up of small pericardial effusions in stable patients
- Routine follow-up in terminally ill patients
- Pericardial rubs following uncomplicated myocardial infarction or open heart surgery
Acute pericarditis is an inflammatory reaction to a variety of infectious and systemic abnormalities, the most common being viral, metabolic, oncologic, and systemic connective diseases and large transmural myocardial infarctions.
One of the earliest clinical uses for echocardiography was in diagnosing pericardial effusions.62 Echocardiography can establish or confirm the presence of the pericardial effusion and provide a semiquantitative assessment of its size (Figs. 1–66 and 1–67; Table 1–19).
Pericardial effusion. Parasternal long axis image of a moderate-sized pericardial effusion, approximately 1.5 cm. LA, left atrium; LV, left ventricle; RV, right ventricle.
Pericardial effusion. Subxiphoid/subcostal image of a large pericardial effusion, approximately 2.0 cm. LA, left atrium; LV, left ventricle; RV, right ventricle.
Table 1–19. Echocardiographic Assessment of Pericardial Effusion Volume ||Download (.pdf)
Table 1–19. Echocardiographic Assessment of Pericardial Effusion Volume
|Physiologic||Echo-free space only in systole||Posterior||Trace (<25 cc)|
|Small||<1 cm||Posterior||<100 cc|
|Medium||1-2 cm||Anterior and posterior||100-500 cc|
|Large||>2 cm||Circumferential||>500 cc|
The diagnosis of pericardial tamponade is based on classical physical findings and intracardiac pressure recordings. Increased intrapericardial pressure results in decreased right-sided filling, which may ultimately compromise left-sided filling and cardiac output. Echocardiography can provide confirmatory information regarding the size and hemodynamic effects of a pericardial effusion (Fig. 1–68). Echocardiographic signs of pericardial tamponade include:
Pericardial tamponade. Apical four-chamber view demonstrating a large circumferential pericardial effusion with right atrial collapse. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
- A large circumferential pericardial effusion. In some cases, smaller rapidly accumulating effusions following traumatic myocardial perforation and loculated effusions following open heart surgery may be hemodynamically significant.
- Concave right atrial free wall with late diastolic or early systolic cavity collapse.
- Concave RV free wall with early diastolic collapse.
- Abnormal septal motion due to respiratory variation in LV filling.
- Distension of the inferior vena cava unchanged by deep inspiration or sniffing.
A Doppler sign of pericardial tamponade includes >25% respiratory variation in transmitral flow velocity.
The presence of pericardial tamponade requires emergent percutaneous or surgical pericardiocentesis. Echocardiographic-guided percutaneous pericardiocentesis has greatly reduced the procedural complications including myocardial and/or coronary laceration, pneumothorax, arrhythmias, and death.63,64
Case 9: Infective Endocarditis
A 27-year-old intravenous drug user presents with arthralgias, myalgias, fevers, sweats, and shaking chills.
Physical examination reveals an agitated patient with a resting tachycardia and temperature of 101°F. The patient's lung fields are clear. Cardiac auscultation reveals a grade 3/6 diastolic blowing murmur at the lower left sternal border. Abdominal examination reveals left upper quadrant fullness and tenderness. Peripheral signs include oral petechiae and digital splinter hemorrhages and Osler nodes. ECG results are as follows: sinus tachycardia and nonspecific ST-T wave changes.
Acc/Aha/Ase Guidelines: Patients with Native Valve Endocarditis
- Class I
- Diagnosis and assessment of hemodynamic severity
- Detection of associated abnormalities
- Reevaluation in patients with complex endocarditis including persistent fever or bacteremia or clinical deterioration
Infective endocarditis can involve any endocardial surface of the heart. Preexisting conditions such as congenital heart disease, rheumatic heart disease, mitral valve prolapse, and degenerative valve disease can be identified in approximately half of patients with infectious endocarditis. Predisposing vascular abnormalities include patent ductus arteriosus, coarctation of the aorta and atrioventricular shunts, as well as indwelling catheters or pacing wires.
The diagnostic criteria for infective endocarditis include classic clinical signs and symptoms coupled with two positive blood cultures and the following echocardiographic findings:
- An oscillating mobile mass or vegetation on a valve or chordae, in the path of a regurgitant jet or on an implanted device or wire
- A new regurgitant lesion
- An annular abscess
- Dehiscence of a prosthetic valve
The identification of a vegetation is the hallmark echocardiographic finding of infectious endocarditis (Figs. 1–69 and 1–70). Vegetations are generally characterized as mobile amorphous masses that begin as a composite of fibrous material and platelets and become secondarily infected following a bacteremia.65 The sensitivity of transthoracic echocardiography for visualizing vegetations in proven native valve infectious endocarditis is <75% and is only approximately 25% in prosthetic valve endocarditis.66,67 Therefore, infectious endocarditis cannot be ruled out by transthoracic echocardiography.
Infective endocarditis. Parasternal long axis image of a large, 1 cm × 1 cm, echo bright density attached to the anterior mitral valve leaflet. LA, left atrium; LV, left ventricle.
Infective endocarditis. Apical four-chamber image of a linear echo bright density attached to a pacing wire representing either a vegetation or thrombus. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
Transesophageal echocardiography is not recommended in patients with uncomplicated native valve endocarditis who have unambiguous transthoracic echocardiograms. However, because of its superior spatial resolution, transesophageal echocardiography is recommended in the following situations:
- When the transthoracic echocardiogram is technically limited or negative in the setting of a high clinical likelihood of endocarditis such as persistent unexplained fevers or positive blood cultures
- In the setting of preexisting native valve disease, for example, calcific aortic stenosis
- In patients with prosthetic valves
The identification of a vegetation does not independently establish the diagnosis of active infectious endocarditis because vegetations may persist after the treatment of the acute illness.68 The presence of a vegetation and its size and evolution have been correlated with clinical outcome; however, this remains controversial, and the mere detection of a vegetation is not an indication for surgery.69,70
Echocardiography can help in the assessment of the complications of infectious endocarditis, which include embolic events, native valve destruction and dysfunction, prosthetic valve dehiscence, abscess formation, conduction abnormalities, and acute decompensated heart failure.
Case 10: Routine Screening
An 18-year-old man experiences transient dizziness while participating in a summer preseason football camp. The athlete had no prior cardiopulmonary signs or symptoms. His symptoms were quickly relieved with rest and fluids.
Physical examination revealed a mildly diaphoretic agitated young adult. Supine pulse was 96 bpm and regular. Blood pressure was 90/60 mm Hg with orthostatic changes. Cardiac auscultation revealed an innocent short 2/6 systolic ejection murmur. ECG results were normal.
The majority of nontraumatic, nonheat or drug-related episodes of sudden death in young athletes are due to cardiovascular diseases. The most common cardiovascular disorders are hypertrophic cardiomyopathy, coronary anomalies, and myocarditis. However, the prevalence of significant underlying cardiovascular disease is ≤1/200 of approximately 12 million student athletes in the United States.71
Although recognizing the limits of current screening procedures, because the incidence of significant congenital and acquired abnormalities is low in the asymptomatic student athlete, current guidelines continue to recommend only a preparticipation history, physical examination, and ECG.72 Two-dimensional echocardiography is recommended in symptomatic student athletes in whom a cardiovascular disorder is suspected.
Older athletes with known coronary artery disease should have an LV function test and a maximal exercise stress test before competing in competitive or rigorous physical activity. Individuals with LVEFs ≥50%, normal age-adjusted exercise capacity, and no inducible ischemia can be considered to be at only mildly increased risk. Routine preparticipation screening is not recommended in asymptomatic adults.
The role of routine screening echocardiography in the asymptomatic young athlete or in the asymptomatic older individual who participates in strenuous physical exertion has not been established.
Acc/Aha/Ase Guidelines: Screening for Cardiovascular Disease
- Class I
- Patients with a family history or first-degree relatives with genetically transmitted cardiovascular disease such as idiopathic dilated cardiomyopathies, hypertrophic cardiomyopathy, or ARVD
- Patients with Marfan syndrome or connective tissue diseases
- Baseline and follow-up in patients receiving cardiotoxic agents
- Potential donors for cardiac transplantation
- Class III
- The general population
- Routine screening before competitive sports in patients with a normal cardiovascular history, physical examination, and ECG