| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 1999;68:1547-1551
© 1999 The Society of Thoracic Surgeons
a Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, Washington Hospital Center, Washington, DC, USA
Address reprint requests to Dr Mintz, Cardiovascular Research Foundation, 110 Irving St, NW, Suite 4B-1, Washington, DC 20010;
e-mail: gsm1{at}mhg.edu
Presented at Evolving Techniques and Technologies in Minimally Invasive Cardiac Surgery, San Antonio, TX, Jan 22–23, 1999.
Abstract
Despite the fact that the coronary angiogram is the gold-standard in assessing a coronary artery stenosis for the purposes of clinical decision making, it has many limitations. Alternative methods are available. This article discusses three of these: intravascular ultrasound, coronary flow reserve, and fractional flow reserve.
The importance of the severity of a coronary artery stenosis was shown in the Coronary Artery Surgery Study (CASS). In this study, the risk of myocardial infarction (MI) over a period of 3 years was 2% for patients with a coronary artery stenosis of less than 50%, 7% for a stenosis of 50%–70%, 8% for a stenosis of 70%–90%, and 15% for a stenosis of greater than 90% [1]. Conversely, other studies have shown that 80% of all MIs occur in lesions with a diameter stenosis less than 50% [2, 3]. There are two potential explanations for this discrepancy. First, patients with coronary artery disease have a large number of angiographically "insignificant" lesions, but only a few "significant" stenoses. Thus, while the more significant stenosis is more likely to lead to an MI, the shear number of "insignificant" lesions makes it more likely that a culprit lesion will have started out as "insignificant." Second, recent intravascular ultrasound (IVUS) and physiologic lesion assessment studies question the ability of angiography to define the critical stenosis.
In this article we review currently available invasive modalities for the assessment of coronary artery disease. These modalities are illustrated in Figure 1.
|
Early studies correlating angiographic and histopathologic anatomy concluded that angiography usually underestimates severity of a lesion, especially with a 51% to 75% histolopathologic cross-sectional area narrowing [4, 5] and in patients with multivessel disease [6]. When compared to computerized quantitative coronary angiographic (QCA) measurements, visual angiographic interpretation overestimates lesion severity prior to percutaneous transluminal coronary angioplasty (PTCA) and underestimates lesion severity after the procedure. At follow-up, there is underestimation of lesion severity 50%–70% stenosis and an overestimation of lesion severity for more mild stenoses [7, 8].
One major factor contributing to this discrepancy is the assumption that the segment of the artery adjacent to the lesion is normal; in fact, it is typically involved in the atherosclerotic disease process. An important explanation for the discrepancy between pathologic and angiographic findings is the presence of compensatory dilation of the arterial wall in direct response to the accumulation of atherosclerotic plaque. An absolute reduction in lumen dimensions typically does not occur until the lesion occupies approximately an estimated 40%–50% of the area within the internal elastic membrane (40%–50% cross-sectional narrowing). As a result, most of the atherosclerotic burden is contained within angiographically normal reference segments.
Quantitative coronary angiographic
Visual interpretation of coronary artery remains the gold standard for clinical diagnosis and treatment. However, the need for an objective, accurate, unbiased, and reproducible assessment of stenosis severity and vessel size led to development of QCA—an inexpensive, fast, and reproducible technique that can be used during the procedure (on-line), after the procedure, or at a core laboratory. Quantitative coronary angiographic measurements are reproducible [9–11]; as a result, these techniques have been used in most major interventional trials. However, there are a number of QCA systems with different performance characteristics. In one study, most QCA systems overestimated smaller luminal diameters and underestimated larger lumens [12]. Some of these errors have been resolved by recalibration of the QCA software. Nevertheless, these systems are still confounded by a number of potential sources of error: overlapping side branches, emergence of a side branch immediately before or after a stenosis, foreshortening of the stenotic segment, post-stenotic dilatation, and marked irregularities of the segment adjacent to the lesion [13, 14].
Intravascular ultrasound
Intravascular ultrasound provides transmural tomographic images of coronary arteries in vivo. The normal coronary arterial wall, the major components of the atherosclerotic plaque, and the serial changes that occur with the atherosclerotic disease process can be studied in humans in a manner otherwise not possible. Previous studies comparing coronary angiography and IVUS have consistently shown disparities between the presence, location, distribution, composition, and severity of coronary artery atherosclerosis [15–20]. Intravascular ultrasound studies have confirmed the pathologic observations that atherosclerosis is invariably present in angiographic, apparently normal, reference segments [18]. Intravascular ultrasound detects target lesion calcification twice as often as does angiography (73% versus 38%), and can determine not only its location (superficial versus deep), but also its distribution [21]. Calcium is a sensitive marker for coronary atherosclerosis and a determinant of the success of some interventional devices.
In certain groups of patients (ie, those with intermediate lesions) QCA correlates poorly with IVUS. Alfonso found a moderate correlation between both techniques at sites which were angiographically normal, but contained plaque on IVUS [16]. De Scheerder compared IVUS and QCA for measurement of luminal diameters in normal and moderately diseased coronary arteries; the correlation was excellent (r = 0.92, p < 0.0001) in angiographically normal coronary arteries, but only moderate for mild stenoses (r = 0.467, p < 0.001) [19].
In a series of 73 patients studied pre-intervention, IVUS minimum lumen cross-sectional area correlated strongly with coronary flow reserve measured by Doppler FloWire (EndoSonics Corp, Rancho Cordova, CA) velocimetry (r = 0.831, p < 0.0001) [22]. In addition, a pre-intervention minimum lumen area greater than or equal to 4.0 mm2 had a diagnostic accuracy of 92% in predicting a coronary flow reserve greater than or equal to 2.0.
We followed 300 patients (357 de novo intermediate native artery lesions) in whom intervention was deferred based on IVUS findings [23]. Long-term follow-up showed a low event rate. Intravascular ultrasound assessment of lumen compromise (especially, the minimum lumen area) was the only anatomic predictor of events. While the event rate decreased with increasing lumen area, there seemed to be a significant difference between lesions with minimum lumen areas above and below 4.0 mm2. In 248 patients with a minimum lumen area greater than or equal to 4.0 mm2, the event rate was especially low: 4.4% overall and 2.8% target lesion revascularization.
Intravascular ultrasound and transplant vasculopathy
Allograft vasculopathy is the leading cause of morbidity and mortality after the first year of transplantation [24]. By the fifth year, 50% of recipients will have angiographic evidence of coronary disease. However, angiography underestimation its severity. On the other hand, an IVUS intimal thickness greater than or equal to 0.3 mm was associated with reduced survival, increased events, and higher rejection rates; conversely, an intimal thickness of less than or equal to 0.3 mm was associated with an excellent 4-year survival [25, 26].
Intravascular ultrasound and left main coronary artery disease
There is significant interobserver variability in the angiographic assessment of LMCA disease. Interpretations of a single lesion have varied from 0% to 80% stenosis, and interobserver disagreement has been as high as 20% [27, 28]. The arteriograms from the Coronary Artery Surgery Study (CASS) were independently read by two observers; measurements of the left main coronary artery were the least reproducible of any arterial segment [29]. When one angiographer reported a stenosis of greater than 50%, a second one reported no lesion 19% of the time. A second, three-way analysis from CASS showed only a 41% to 59% agreement on stenosis severity [30].
We followed 122 patients after angiographic and IVUS evaluation of indeterminate left main coronary artery disease and no catheter or surgical intervention. During the 1-year follow-up, 4 patients died, none had a myocardial infarction, 3 underwent stenting of the left main coronary artery, and 11 underwent bypass surgery. Using multivariate logistic regression analysis, diabetes mellitus, an untreated vessel (with a DS greater than 50%), and IVUS lumen dimensions were the independent predictors of cardiac events [31].
Coronary flow reserve and flow-derived measurements
Invasive physiologic assessment is an alternative method for quantifying stenosis severity [32–35]. Coronary flow reserve (CFR) is the ratio of hyperemic to baseline blood flow velocity distal to a lesion. In the presence of a hemodynamically significant stenosis, the distal microvasculature dilates to preserve resting blood flow, blunting any additional hyperemic response to vasodilators. Multiple studies have examined the relation between QCA, thallium scintigraphy, positron emission myocardial tomography, and clinical follow-up versus CFR. A CFR of less than 2.0 was associated with abnormal scans, whereas patients with a CFR greater than 2.0 had a favorable prognosis. Kern reported 100 lesions in 88 patients in whom intervention was deferred based on normal coronary flow dynamics [36]. At 9 months, 2 patients died (2.3%), 4 had angioplasty (4.7%), and 6 underwent bypass surgery (6.9%). However, other disease states may falsely lower the CFR: abnormal microcirculation (left ventricular hypertrophy, diabetes, connective tissue disease, prior myocardial infarction, syndrome X), changes in vasomotor tone, submaximal vasodilator dose, and general patient hemodynamic instability.
In order to overcome some of these limitations, other measurements have been proposed. The relative flow velocity reserve is calculated as the ratio between CFR in the target vessel and CFR in a nonstenotic reference vessel. This ratio has shown excellent correlation with myocardial fractional flow reserve (FFRmyo) and with percent area stenosis assessed by QCA [34].
Myocardial fractional flow reserve
Translesional pressure gradients have been used to assess coronary stenoses since the early days of PTCA. Only with the development of ultra-thin, sensor-tipped, pressure-monitoring guidewires have reliable translesional pressure measurements become a reality. However, it is not the gradient across the stenosis that is important, but the maximal coronary pressure attainable distal to the lesion; this actually determines myocardial perfusion [32]. Thus, FFRmyo is expressed as the ratio between the distal coronary artery pressure and the pressure at the tip of the guide catheter during maximal vasodilatation. The normal FFRmyo (1.0) is independent of vessel, patient, and hemodynamic variations. An FFRmyo less than 0.75 identifies a functionally important stenoses. Myocardial fractional flow reserve has high diagnostic accuracy when compared to noninvasive tests (greater than 90%) [35].
Pijls reported 24 patients with intermediate lesions, chest pain, and an FFRMYO greater than 0.75; at 14-month follow-up, none required revascularization [35]. Bech reported 100 patients with an intermediate coronary artery stenosis and FFRMYO greater than 0.75. At 13 months, 2 patients died of noncardiac causes and 8 patients had coronary events, 4 of which were lesion-related [37].
In the assessment of the severity of coronary artery stenosis, there are a variety of tools beyond coronary angiography, each with its own specific advantages and disadvantages. Each catheterization laboratory should be familiar and comfortable with at least one.
Acknowledgments
Supported in part by Cardiolovascular Research Foundation Washington, DC. Dr. Luis Gruberg is a recipient of a fellowship from the Physicians Fellowship for Medicine in Israel.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
