|
|||||||
|
|
|
|||||
|
|
|||||||
|
|||||||
|
|
|
|||||
|
|
|||||||
The Nurse Practitioner ; Beattie, Sally; Stapleton, Ann; 08-01-1997
In the era of managed care, primary health care providers are mandated to keep pace with current practices and management strategies in clinical situations that might formerly have been addressed by a "specialist." Therefore, providers must be prepared to discuss myriad treatment modalities with their patients. Cardiology represents one of the most rapidly changing specialties as cardiovascular-related diseases remain the most frequent cause of morbidity and death in the United States.
The assessment of myocardial viability in the setting of coronary artery disease (CAD) is one of the most challenging areas in modern cardiology. It is now known that left ventricular (LV) dysfunction secondary to CAD is not always an irreversible process. LV function may improve substantially, even normalize, after treatment for acute myocardial infarction (MI) (such as thrombolysis), and after revascularization procedures in patients with chronic CAD. Therefore, differentiating viable from nonviable myocardium is highly relevant, especially for patients with impaired LV function who are being considered for coronary revascularization. These are the patients who will benefit the most from interventions, as LV function represents one of the most important determinants of long-term prognosis[1,2].
Myocardial stunning and myocardial hibernation are two processes that help explain the mechanisms of reversible LV dysfunction. Myocardial stunning implies a process of myocardial injury in which blood flow is restored to previously ischemic myocardium. It represents a "blood flow-contraction mismatch" in that blood flow has been restored (e.g., after infusion of a thrombolytic agent), but contractile dysfunction is present. It may persist for several days to several weeks before function spontaneously returns to normal[1]. Initially, myocardial stunning was believed to occur only in the setting of acute myocardial infarction, but there is growing evidence that it may result from less severe episodes of myocardial ischemia, including unstable angina and exercise-induced ischemia in patients with chronic CAD. Myocardial hibernation, on the other hand, implies an adaptive, protective process to maintain myocardial viability in the presence of chronically reduced coronary blood flow. It is a form of "blood flow-contraction match" in which there is down regulation of the contractile elements in order to reduce energy in the face of reduced oxygen availability secondary to a severely stenosed coronary artery [1]. How long a segment of myocardium can remain viable in the presence of chronically reduced blood flow is unknown. Clinically, these processes may coexist, as the boundaries between them are often indistinct. Stunning and hibernation have in common the fact that in both cases LV dysfunction is reversible. The major difference is that blood flow is normal, or near normal, in stunned myocardium, whereas it is reduced in hibernating myocardium[3].
Stress Echocardiography and Stress Myocardial Nuclear Perfusion Imaging
The clinical approach of utilizing data from a standard exercise stress test (EST) for the detection and guidance regarding optimal management of CAD, myocardial ischemia, and viability has been augmented by advances in cardiac imaging techniques in combination with provoked physiologic stress. The two most commonly performed of these modalities are stress echocardiography and stress myocardial nuclear perfusion imaging (MNPI). These techniques provide physiologic data "which are produced by methods that can demonstrate some abnormal effect of compromised myocardial perfusion"[4]. The use of positron emission tomography (PET) for the identification of myocardial viability will not be discussed, because it is available in only a small number of large centers due to its prohibitively high cost. Likewise, the use of magnetic resonance imaging and computed tomography is just beginning to be investigated for use in this area; therefore, neither procedure will be discussed.
In the setting of a relatively low likelihood, EST alone may be helpful in excluding CAD. And, in the setting of a normal resting electrocardiogram (ECG) in patients not taking digoxin, the EST is almost as accurate as the aforementioned procedures for identifying significant CAD and for evaluating prognosis[4]. However, stress imaging provides increased sensitivity for diagnosing CAD (averaging 80% to 85% compared to 65% to 70% for EST) as well as information about LV function. Likewise, the specificity of the EST is clearly poor in the presence of ST-t abnormalities on a resting ECG and may be uninterpretable in the presence of left bundle branch block, intraventricular conduction delay, paced rhythm, left ventricular hypertrophy, and Wolff-Parkinson- White syndrome[5]. Also, the conventional EST does not accurately localize the site of ischemia as might be important in clinical situations such as identifying the "culprit" lesion in a patient with multi-vessel CAD being considered for a catheter-based intervention. This is an important concept because it means that these procedures are often recommended and performed after a coronary angiogram to quantify the physiologic significance of a stenotic coronary artery. EST also does not characterize the extent of ischemia, nor as mentioned, provide direct information related to LV function. Stress myocardial imaging techniques provide data pertinent to all these issues and are therefore recommended for diagnosis when the EST does not suffice or for coronary disease localization, prognosis, or viability assessment. Imaging may actually reduce costs in such cases[5].
The purpose of the remaining discussion is to familiarize primary health care providers with current information regarding the procedures of stress echocardiography and MNPI since primary care providers are now taking on more responsibility for the management of patients with ischemic CAD.
In any setting of stress testing for the detection of ischemia, it is essential that an adequate level of exercise or stress be achieved to obtain accurate and reliable results. Ideally, all patients should undergo a physical exercise stress test with or without myocardial imaging, but only if an adequate stress stimulus can be applied; otherwise the sensitivity of the test is lost. However, primary care providers now more than ever are managing patients with multiple comorbidities that render them unable, or unwilling, to walk on a treadmill or climb onto and sit upon a bicycle ergometer. These comorbidities include peripheral vascular disease, pulmonary disease, musculoskeletal abnormalities, obesity, and general poor physical conditioning. Although cardiac imaging techniques are frequently performed concomitantly with exercise, this discussion is limited to cardiac imaging techniques in the setting of pharmacologically provoked stress. This mode of "stressing" the myocardium has demonstrated diagnostic capabilities equal to those of dynamic exercise and therefore provides an acceptable alternative method for assessing the presence of myocardial ischemia/viability and CAD[4,6].
Both procedures may be done on an outpatient basis, but must be performed in an area equipped to handle cardiovascular emergencies. The procedures require written consent, and are conducted by specialists in each of the respective areas of echocardiography and nuclear cardiology.
Myocardial Response to Physiologic Stress
The normal response of the myocardium to stress is an increase in LV contractility. In the presence of a coronary artery stenosis, stress- induced ischemia results in an alteration of contractility, or wall motion, in the myocardial region or segment supplied by the stenosed vessel [9,10]. These alterations are described as hypokinesis, dyskinesis, akinesis, or aneurysm of the segment involved (Figure 1)[7]. These alterations may be present in the resting state with resultant exacerbations under stress or there may be no change observed.
Stress echocardiography allows real-time visualization of wall motion during physiologic stress. Ischemia is manifested as a wall motion abnormality in one or more segments. Each segment is correlated with the distribution of one or more stenotic coronary arteries[11]. MNPI, on the other hand, provides direct evaluation of coronary blood flow to specific myocardial regions during physiologic logic stress. Adequately perfused myocardium will pick up a circulating isotope and be visualized with subsequent imaging. The presence of a stenotic coronary artery will result in a decreased amount of radioisotope in the myocardium. Thus, ischemic areas will be identified. Both techniques also provide calculation of the left and/or right ventricular ejection fraction.
Dobutamine Stress Echocardiography (DSE)
The inotropic agent dobutamine hydrochloride is most commonly used in conjunction with two-dimensional echocardiography to provoke physiologic stress. As a synthetic catecholamine, dobutamine produces an increase in myocardial contractility by stimulating beta-1 adrenergic receptors in the myocardium. "Echoes" are obtained from predetermined segments of the LV that are correlated with a specific coronary artery or arteries. A DSE is considered positive for myocardial ischemia if a new wall motion abnormality develops. Segments abnormal at rest that do not improve their contractility during the infusion represent irreversible scar tissue. Conversely, improvement of a severely preexisting hypokinetic or dyskinetic segment suggests the presence of viable myocardium (either stunned or hibernating). Depending on the degree of improvement, the expectation for these patients is that they will likely benefit from a revascularization procedure, either via a catheter-based intervention or bypass surgery[9,10].
Primary care providers can prepare their patients for a DSE by explaining the following: Patients should not eat/drink 3 to 6 hours before the test (medications may be taken with sips of water). Baseline echocardiographic, hemodynamic parameters, and 12-lead ECG will be obtained before infusing the dobutamine hydrochloride. An intravenous (I.V.) line will be inserted, and the patient will be positioned in the left lateral decubitus position in order to bring the heart closer to the chest wall. Throughout the infusion, heart rate and rhythm and blood pressure will be continuously monitored. Patients need to be told they may experience symptoms associated with exercise such as an increased heart rate and increase in respirations. Table 3 fists endpoints for discontinuing the exam based on specific protocols from several centers[10-13]. Adverse reactions do occur, but several investigators have demonstrated that severe adverse effects are uncommon and rarely cause early termination of the DSE[14-17]. The onset of angina during DSE has reportedly been successfully treated with administration of sublingual nitroglycerine and beta blockers. Life-threatening arrhythmias, myocardial infarction, syncope, or death have not been reported in the aforementioned reviews. Continuous echocardiographic monitoring and the short half-life of dobutamine contribute to the safety of this exam.
After the dobutamine infusion is discontinued, the heart rate and blood pressure are recorded until the heart rate falls below 100 beats a minute and the blood pressure normalizes. On the basis of the DSE results, patients may undergo further workup or treatment.
Myocardial Nuclear Perfusion Imaging (MNPI)
Diagnosing CAD and myocardial viability via MNPI is achieved by the use of radioisotopes which are injected into a peripheral I.V. line. The isotopes are "traced" by a specialized gamma camera as they flow through the coronary arteries (perfusion) and are "picked up" by myocardial cells. Regional myocardial uptake of the isotope, or tracer, is dependent on tracer delivery (i.e., perfusion), sarcolemmal integrity, and intact metabolic function (viability). Images are captured during both a resting and stress-induced phase, and comparisons of the tracer uptake activity are made. Relative decreases or the absence in uptake activity correlate with diminished blood flow or myocardial ischemia/necrosis, or both[18]. Although the most accurate, state-of-the-art imaging techniques involve the use of a position camera, or PET scanner, this system is not widely available due to its prohibitively high cost. Consequently, this discussion refers only to those procedures that utilize the more commonly employed "SPECT" system.
Coronary vasodilating agents are used to elicit an ischemic response for nonexercise MNPI procedures. The most commonly given are dipyridamole or adenosine. When administered, noncritically stenosed and normal coronary arteries will dilate maximally and "steal" blood flow from critically stenotic arteries. These arteries are already maximally dilated secondary to autoregulation in response to local myocardial metabolic requirements. Thus, the radioisotope will not be "picked" up in regions supplied by the stenotic artery or arteries. Regardless of how the stress is induced, the imaging portion of the exam is most commonly accomplished by a dual-isotope protocol that maximizes images related to perfusion, viability, and ventricular function. The most frequently used radioisotopes are Thallium-201 (thallium) and Technetium- 99m Sestamibi (sestamibi), although others are currently undergoing investigation[1,18].
Patient preparation includes reviewing the following information: no food or drink containing caffeine or cigarettes 4 hours before injection of the vasodilating agent as these substances antagonize the vasodilation action. In addition, patients should not take the following medications 24 to 48 hours before the exam for the same reason: dipyridamole, pentoxifylline, and aminophylline. A valid concern may be related to the administration of a "radioactive" material. Patients should be reassured that there is not scientific evidence of adverse effects of such low-level radiation as is delivered with these procedures[4].
After I.V. access is established, thallium is injected and resting images of its distribution are obtained. Occasionally, the nuclear physician may elect to inject the thallium as much as 24 hours prior to obtaining the images to allow as much time as possible for the isotope to be distributed or "picked-up" by even marginally viable cells[1]. The dilating agent is then injected. Patients need to be told they may experience flushing, headache, dyspnea, and dizziness, as well as chest tightness. If they occur, these symptoms will last only a few minutes. Sestamibi is injected about 4 minutes later. Images are again obtained to assess myocardial perfusion during stress. Unlike those associated with DSE, there are no endpoints for discontinuing a MNPI procedure. Aminophylline is given shortly after the sestamibi to reverse the vasodilating effects of the dipyridamole. If adenosine is used, this reversal is unnecessary due to its extremely short half- life (about 6 seconds)[5]. After the test is completed, patients may resume their regular diet.
Tomographic images are produced by the gamma camera during both the resting and stress-induced portions of the study. Stress sestamibi and resting thallium images are compared. The nuclear specialist looks for the relative distribution of tracer uptake or activity in each LV region. If a defect or decrease in tracer uptake appears in a particular region during stress but is normal during rest, this is referred to as a "reversible" defect. The myocardium is deemed viable in that region and the patient is likely to benefit from revascularization. If a defect appears during both rest and stress, it is referred to as a "fixed" defect, representing myocardial scar, or nonviable tissue[18]. Revascularization of this area would not be beneficial. In addition, interpretation of results by a nuclear cardiologist includes information about regional and global LV wall motion and ejection fraction.
Which Procedure Is "Best?"
The verdict on which is the preferred cardiac imaging procedure for assessing myocardial viability and CAD has not been rendered. The criteria for choosing an imaging study over conventional EST has been well established; however, the decision between the imaging techniques is not as clear cut. A thorough discussion on this aspect of cardiac imaging is beyond the scope of this article, but readers are directed to some excellent reviews[4-6,12]. Several factors must be taken into account, such as cost effectiveness, availability of technology, safety, and operator experience.
Cost effectiveness is a function of the other factors just mentioned. It does not necessarily mean the technique that costs less; rather it rests on the accuracy of the data obtained and how the clinical decision may be enhanced.
The Mayo Clinic Cardiovascular Working Group on Stress Tests[5] determined that MNPI is a superior method for the detection of severe CAD and predicting prognosis, whereas DSE can provide more ancillary information such as regional wall motion, LV and right ventricular volumes, wall thickness, and valvular status.
In terms of dollars, the DSE is "cheaper" to perform, but may not be the optimal method in a given situation. Certain body conditions, such as obesity and chest deformities, preclude the use of echocardiography secondary to technical difficulties in establishing a good "window" (area in which to point the transducer) through which to send and receive the "echoes"[18]. On the other hand, if a patient is unable to discontinue taking aminophylline, a MNPI using thallium would not be indicated. Botvinick[12] determined the single most important factor to be the clinical information sought. He summarizes his discussion with the statement that "the overall choice of imaging modality must be based on the clinical needs, the clinical question to be answered, and the ability of the method to address it ... not on method availability."
Both methods have the advantage of being performed as outpatient procedures. The safety factor of infusing radioisotopes has been dismissed as negligible during MNPI, as has, for the most part, the administration of an inotropic agent during DSE; both methods offer an 80% to 85% sensitivity in detecting CAD and are able to localize the site of ischemia[5].
In locations that offer more than one modality, primary care providers must consider the clinical information needed and seek expert consultation. As the research and use of both methods by experienced operators is refined, will become clearer which procedure is "best."
REFERENCES
[1.] Hendel RC, Chaudhy FA, Bonow RO: Myocardial viability. Curr Probl Cardiology 1996;21(3):151-21.
[2.] Edmond M, Mock M, Davis K, et al: Long-term survival of medically treated patients in the Coronary Artery Surgery Study (CASS) registry. Circulation 1994;90(6):2645-57.
[3.] Bolli R: Myocardial `stunning' in man. Circulation 1992;86(6):1671- 91.
[4.] Botvinick EH: Stress imaging: current clinical options for the diagnosis, localization, and evaluation of coronary artery disease. Contemp Issues Cardiology 1995;79(4):105-61.
[5.] Mayo Clinic Cardiovascular Working Group on Stress Testing: Cardiovascular Stress Testing. Mayo Clin Proc 1996;71(1):43-52.
[6.] Nageuh SF, Zoghbi WA. Stress echocardiography for the assessment of myocardial ischemia and viability. Curr Probl Cardiology 1996;21(7):497- 20.
[7.] Beattie S, Billiard SJ, Meinhardt SL: The use of cardiac catheterization data to design nursing care plans. Crit Care Nurse 1989;10(6):43-53.
[8.] Dorland's Illustrated Medical Dictionary, 28th ed. Philadelphia: W.B. Saunders Company, 1994.
[9.] Thompson EJ, Detwiler DS, Nelson CM: Dobutamine stress echocardiography: A new, noninvasive method for detecting ischemic heart disease. Heart and Lung 1996;25(2):87-97.
[10.] Pellika PA, Roger VL, Oh JK, et al: Stress echocardiography. Part II. Dobutamine stress echocardiography: Techniques, implementation, clinical applications, and correlations. Mayo Clin Proc 1995;70(1):16- 27.
[11.] Segar DS, Brown SE, Sawada SG, et al: Dobutamine stress echocardiography: correlation with coronary lesion severity as determined by quantitative angiography. JACC 1992; 19(6):1197-202.
[12.] Stanford W: Cost-effective testing for CAD: Is there a right way to go? Cont Int Med 1996;8(8):6-11.
[13.] Bach DS, Armstrong WF: Dobutamine stress echocardiography. Am J Cardiol 1992;9(20):90-96.
[14.] Mertes H, Sawada SG, Ryan T, et al: Symptoms, adverse effects, and complications associated with dobutamine stress echocardiography; experience in 1,118 patients. Circulation 1993;88(1):15-19.
[15.] Marcovitz PA, Armstrong WF: Accuracy of dobutamine stress echocardiography in detecting coronary artery disease. Am J Cardiol 1992;69(16): 1269- 73.
[16.] Mazeika PK, Nadasdin A, Oakley CM: Dobutamine stress echocardio- graphy for detection and assessment of coronary artery disease. JACC 1992; 19(6):1203-11.
[17.] Martin TW, Seaworth JF, Johns JP, et al: Comparison of adenosine, dipyridamole, and dobutamine in stress echocardiography. Ann Intern Med 1992; 116(3):190-96.
[18.] AHA/ACC Task Force: Guidelines for the clinical use of cardiac radionuclide imaging. Circulation 1995;91(5):1278-1303.
Left ventricular (LV) dysfunction secondary to CAD is not always in irreversible process. LV function may improve substantially, even normalize, after treatment for acute myocardial infraction (MI) (such as thrombolysis), and after revascularization procedures in patients with chronic CAD. Therefore, differentiating viable from nonviable myocardium is highly relevant, especially for patients with impaired LV function who are being considered for coronary revascularization. Myocardial stunning and myocardial hibernation are two processes that help explain the mechanisms of reversible LV dysfunction. Stunning and hibernation have in common the fact that in both cases LV dysfunction is reversible. The major difference is that blood flow is normal, or near normal, in stunned myocardium, whereas it is reduced in hibernating myocardium.
The clinical approach of utilizing data from a standard exercise stress test (EST) for the detection and guidance regarding optimal management of CAD, myocardial ischemia, and viability has been augmented by advances in cardiac imaging techniques in combination with provoked physiologic stress. The two most commonly performed of these modalities are stress echocardiography and stress myocardial nuclear perfusion imaging (MNPI). The purpose of the remaining discussion is to familiarize primary health care providers with current information regarding the procedures of stress echocardiography and MNPI since primary care providers are now taking on more responsibility for the management of patients with ischemic CAD. Both procedures may be done on an outpatient basis, but must be performed in an area equipped to handle cardiovascular emergencies.
The verdict on which is the preferred cardiac imaging procedure for assessing myocardial viability and CAD has not been rendered. The criteria for choosing an imaging study over conventional EST has been well established; however, the decision between the imaging techniques is not as clear cut. The safety factor of infusing radioisotopes has been dismissed as negligible during MNPI, as has, for the most part, the administration of an inotropic agent during DSE; both methods offer and 80% to 85% sensitivity in detecting CAD and are able to localize the site of ischemia. Both methods have the advantages of being performed as outpatient procedures.
ABOUT THE AUTHORS:
SALLY BEATTIE, MS, RN, CS, is an Advanced Practice Nurse, Cardiology, at Harry S. Truman VA Hospital, Columbia, Mo.
ANN STAPLETON, MS, RN, CS, NP, is a Nurse Practitioner, Geriatrics, at Harry S. Truman VA Hospital, Columbia, Mo.
COPYRIGHT 1997 Springhouse Corp. All rights reserved. Copying prohibited without written permission of Springhouse Corp.
HOME
--------------------------------------------------------------------------------
Copyright © 1998 Infonautics Corporation. All rights reserved. - Terms and Conditions