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J Appl Physiol 98: 1076-1082, 2005. First published October 29, 2004; doi:10.1152/japplphysiol.00724.2004
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TRANSLATIONAL PHYSIOLOGY

Determinants of coronary blood flow in humans: quantification by intracoronary Doppler and ultrasound

Heinrich Wieneke, Clemens von Birgelen, Michael Haude, Holger Eggebrecht, Stefan Möhlenkamp, Axel Schmermund, Dirk Böse, Christoph Altmann, Thomas Bartel, and Raimund Erbel

Department of Cardiology, University Essen, Essen, Germany

Submitted 12 July 2004 ; accepted in final form 21 October 2004

ABSTRACT

The direct determinants of coronary flow are lumen area and blood flow velocity; however, the precise mechanisms that control these factors are not fully understood. The aim of the present study was to assess by which mechanisms lumen area and coronary flow velocity interact with hemodynamic and morphometric factors, thereby influencing coronary flow. Intracoronary Doppler and ultrasound measurements were performed in 28 patients without coronary lumen irregularities. Flow velocity and lumen cross-sectional area were measured in the proximal segments of all three coronary arteries. Global lumen cross-sectional area and global flow were obtained by adding up the values of all three coronary arteries. Left ventricular mass was assessed by echocardiography. Stress-mass-heart rate and pressure-rate products reflecting myocardial oxygen demand were calculated. Global coronary flow increased during adenosine-induced hyperemia from 197 ± 72 to 637 ± 204 ml/min (P < 0.001). Global coronary flow closely correlated with the stress-mass-heart rate product (r = 0.62; P < 0.001). Looking at the two constituents of flow separately, global coronary cross-sectional area was closely related to left ventricular muscle mass (r = 0.61; P < 0.001), whereas mean coronary flow velocity at rest showed a strong linear relation with the pressure-rate product (r = 0.64; P < 0.001). There was no interaction between cross-sectional area and blood flow velocity in any of the coronary vessels. Coronary lumen size and flow velocity, the two determinants of coronary flow, are principally determined by different physiological factors. Long-term flow adaptation is achieved by an increase in coronary lumen size, whereas short-term myocardial oxygen requirements are met by changes in resting flow velocity.

ultrasonics; microcirculation; coronary flow; left ventricular muscle mass

THE TWO CONSTITUENTS OF CORONARY flow are lumen area and blood flow velocity. Both closely interact with each other and are not independent factors (16, 18). Experimental data suggest that blood flow velocity determines lumen area by wall shear stress and thereby governs vessel enlargement and narrowing (21). On the other side, atherosclerotic vessel narrowing itself significantly affects coronary blood flow velocity when a critical value of vessel obstruction is exceeded (2). Besides this bilateral interdependency, both coronary cross-sectional area and coronary blood flow velocity are determined by accessory factors. Thus patients with aortic stenosis exhibit an increase in coronary cross-sectional area with growing muscle mass and a decline with regression of hypertrophy (37). In contrast, increased blood flow velocity has been reported in a variety of disorders, such as hypertrophic cardiomyopathy (25), aortic stenosis (27), and atrial fibrillation (20).

The mechanisms by which the body regulates the factors determining coronary flow are not yet fully understood (7, 40). One reason for this incomplete understanding of coronary perfusion might be that often parameters are assessed separately under distinct conditions, precluding a comprehensive view of the entire system. Another reason might be that often relative parameters such as coronary flow velocity reserve are assessed, which only represent surrogates of global coronary perfusion. They are used because their acquisition is technically easier than the determination of global or regional coronary flow in absolute terms (22).

In the present study, we directly measured total coronary blood flow, based on intracoronary Doppler and intravascular ultrasound (IVUS) assessment in humans. Aims of our study were to 1) assess a potential interaction between flow velocity and cross-sectional area, 2) relate the hemodynamic data to echocardiography-derived morphometric data of the heart, and 3) relate coronary perfusion values to composited parameters such as stress-mass-heart rate product, which recently have been shown to reflect myocardial oxygen demand (1).

METHODS

Study population.   The study was performed in 28 patients who underwent diagnostic coronary angiography for suspected coronary artery disease and showed angiographically normal coronary arteries (i.e., coronary arteries with an angiographically smooth silhouette). Patients with valvular heart disease, hypertrophic obstructive cardiomyopathy, dilative cardiomyopathy, endocarditis, or myocarditis were not considered for evaluation. In addition, patients with a proximal branching marginal or diagonal branch were not considered for inclusion, because no distinct segment 11 or 6 (according to the American Heart Association classification) could be defined. Intracoronary Doppler and IVUS examinations were performed in segment 6 of the left anterior descending artery (LAD), segment 11 of the left circumflex artery (LCX), and segment 1 of the right coronary artery (RCA). The study was approved by an institutional review board, and all patients gave written, informed consent.

Doppler measurements.   Intracoronary Doppler measurements were performed with a 0.014-in. Doppler wire (FloWire, Cardiometrics), as validated and described by Doucette et al. (11) in detail. ECG, coronary ostial pressure, instantaneous spectral peak velocity, and time average spectral peak flow velocity were recorded online. Heart rate (obtained from the ECG) and blood pressure (obtained from the guiding catheter) were recorded simultaneously with the Doppler flow velocity measurement. For offline analysis, angiography and Doppler measurements were recorded on compact disk and videotape, respectively. The positions of the Doppler wire and IVUS catheter were documented in a picture-in-picture mode via the Echomap-System (Siemens, Erlangen, Germany) and saved in DICOM3 format (6).

Coronary flow velocity measurements were performed after routine coronary angiography. A 6-Fr or 8-Fr guiding catheter without side holes was inserted into the left or right coronary artery ostium without damping of the aortic pressure signal. All patients received 5,000 international units (IU) heparin and 0.2 mg intracoronary nitroglycerine before angiography and additional 3,000 IU heparin at the beginning of the intracoronary Doppler examination. The Doppler wire was advanced into the target segment of the vessel; baseline parameters were recorded when a stable and high-quality baseline signal without significant artifacts could be obtained. Then an intracoronary bolus of adenosine was injected (18 µg into the left coronary artery and 12 µg into the right), and further measurements were obtained under peak hyperemic conditions. Coronary flow velocity reserve was calculated as the ratio of hyperemic average peak velocity and baseline average peak velocity (3). All measurements were performed twice, and mean values were calculated from two consecutive measurements. Spatially averaged flow velocity was calculated as V = (average peak velocity)/2 (11, 26), and coronary flow for a certain vessel (Qvessel) was calculated as Qvessel = V x A, where V is average peak velocity and A is lumen area. Because coronary flow occurs during diastole and systole and lumen area of the coronary vessel changes during the heart cycle, flow for each coronary vessel was obtained by using lumen area measurements for systolic and diastolic IVUS frames. A weighted average flow was obtained by using the following equation:

where DSVR is diastolic-to-systolic flow velocity integral ratio, defined as the ratio of diastolic to systolic flow velocity integral provided by the Doppler system; dCSA is diastolic cross-sectional area; and sCSA is systolic cross-sectional area.

Intravascular ultrasound protocol.   Intravascular ultrasound was performed after intracoronary Doppler under baseline conditions. An intracoronary bolus of 200 µg nitroglycerin was administered before image acquisition. Intravascular ultrasound studies were performed with two commercially available systems during continuous recording of the ECG. The first IVUS system was a mechanical sector scanner (Ultra Cross, Boston Scientific, San Jose, CA) incorporating a 30-MHz single-element beveled transducer rotating at 1,800 rpm. The second system was a solid state electronic device (Avanar, Endosonics, Rancho Cordova, CA). With both systems, the transducer was first withdrawn through the entire vessel at a speed of 0.5 mm/s; the pullback was started as distal as possible, and the entire artery was imaged to the aorto-ostial junction. Consecutively, exact positioning of the IVUS probe at the site of intracoronary Doppler measurement was achieved by using the Echomap picture-in-picture imaging system (6). Intravascular ultrasound measurements were performed using systolic and diastolic frames. On the basis of the ECG, diastolic frames were identified at the beginning of the QRS complex and systolic frames at the end of the T wave (Fig. 1) (14). Measurements were done in the proximal coronary segments of all three coronary arteries (in segment 6 of the LAD, in segment 11 of the LCX, and in segment 1 of the RCA). Calibration equations were used for adjusting for different IVUS systems (34; P. Schoenhagen, personal communication, revised equations, 09/2004).



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  		Fig. 1. Typical investigation of segment 6 of the left anterior descending artery (LAD). Doppler and intravascular ultrasound (IVUS) measurements are done in the same position. The same position could be assured by integrating the IVUS and Doppler recordings into the angiographic images via the Echomap System (Siemens, Erlangen, Germany).

 
For the Endosonic Avanar catheter, the following equation was used:


For the Boston Scientific Ultra Cross catheter, the following equation was used:

Global cross-sectional area was obtained by summing values of LAD, LCX, and RCA.

Echocardiography imaging protocol.   Echocardiography was performed within 7 days after catheterization. Images were taken with patients in the left lateral position with simultaneous ECG recording. The echocardiographic examination was performed by an experienced examiner according to the Guidelines of the American Society of Echocardiography (33). Ejection fraction was uniformly determined in the apical two-chamber view by calculating (LVEDV – LVESV)/LVEDV x 100, where LVEDV is left ventricular end-diastolic volume and LVESV is left ventricular end-systolic volume. Parameters for assessing myocardial muscle mass were acquired by M-mode in the parasternal short axis, and values were calculated by using the method described by Devereux and Reichek as left ventricular mass = 1.04 x [(LVEDD + IVSEDD + PWEDD)3 – LVEDD3] –13.6, where LVEDD is left ventricular end-diastolic diameter, IVSEDD is interventricular septum end-diastolic diameter, and PWEDD is posterior wall end-diastolic diameter (9).

Left ventricular peak-systolic stress was calculated using the following formula: (0.334 x SBP x LVDd)/LVPWT x (1 + LVPWT/LVDd), where SBP is systolic blood pressure, LVDd is left ventricular diameter at end-diastole, and LVPWT is left ventricular posterior wall thickness. Body surface area was calculated as body weight (kg)0.425 x body height (cm)0.725 x 0.007184.

Statistics.   Body mass index was calculated as body weight (kg)/[body height (m)]2. Linear regression analyses were performed by standard methods. Continuous variables were compared by use of the two-tailed (unpaired) Student's t-test. If more than two groups were compared, one-way analysis of variance was used for comparison of intergroup differences. Data analysis was performed with the SPSS computer software package (SPSS, Chicago, IL, version 11). A value of P < 0.05 was considered significant.

RESULTS

Study population.   Clinical characteristics and echocardiographic data of the study population are presented in Table 1.


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  		Table 1. Clinical and echocardiographic details of study population

 
Differences between coronary arteries.   A total of 16 men and 12 women were examined. In the LAD, resting flow was significantly higher than in the LCX. In all three vessels, a significant increase in coronary flow velocity occurred after application of adenosine. Hyperemic flow was significantly higher in the LAD and RCA than in the LCX (Fig. 2), whereas there was no difference in resting flow velocity (LAD 14.6 ± 5.4 cm/s; LCX 14.2 ± 4.4 cm/s; RCA 13.1 ± 5.2 cm/s) or hyperemic flow velocity (LAD 48.8 ± 14.3 cm/s; LCX 43.9 ± 11.5 cm/s; RCA 42.4 ± 12.4 cm/s). Diastolic and systolic cross-sectional areas of the LAD and the RCA were significant larger than cross-sectional areas of the LCX (diastolic: LAD 17.5 ± 4.9 mm2 vs. LCX 12.9 ± 4.2 mm2, P < 0.001; RCA 17.4 ± 3.7 mm2 vs. LCX 12.9 ± 4.2 mm2, P < 0.001; systolic: LAD 17.2 ± 4.7 mm2 vs. LCX 12.6 ± 4.2 mm2, P < 0.001; RCA 16.9 ± 3.7 mm2 vs. LCX 12.6 ± 4.2 mm2, P < 0.001), whereas there was no significant difference between LAD and RCA. Average coronary flow velocity reserve was similar in the three main coronary vessels (LAD 3.5 ± 0.9; LCX 3.2 ± 0.7; RCA 3.5 ± 0.9). Mean area stenosis was in the LAD 12.6 ± 10.3%, in the LCX 7.4 ± 8.3%, and in the RCA 7.7 ± 9.5% with no difference between the vessels.



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  		Fig. 2. Comparison of baseline and hyperemic coronary flow between the major coronary vessels, LAD, left circumflex artery (LCX), and right coronary artery (RCA). Values are means ± SD.

 
Impact of gender and age.   Men had a significant higher body surface area than women (2.06 ± 0.14 vs. 1.76 ± 0.17 m2, P < 0.0001), whereas there was no difference in body mass index (27.3 ± 3.5 vs. 26.1 ± 3.4, P = 0.3). Global coronary flow at rest was 197.1 ± 71.9 ml/min and increased during hyperemia to 637.2 ± 204.4 ml/min. Both global resting and hyperemic flow were identical in men and women. Men had a significantly higher left ventricular muscle mass than women (242.2 ± 59.2 vs. 196.9 ± 51.5 g; P = 0.04). There were no significant differences in global cross-sectional area and in baseline and hyperemic peak velocity. When coronary flow was related to left ventricular muscle mass, baseline myocardial perfusion was 85.4 ± 33.7 ml/100 g in men and 99.6 ± 23.6 ml/100 g in women.

For analysis of potential impact of age on the coronary flow parameters, patients were categorized into those aged ≤50 yr (n = 13) and those aged >50 yr (n = 15). The older patients showed a higher global resting flow, but hyperemic global flow was equal. In addition, analysis of mean coronary flow velocity showed a higher baseline flow velocity in the group of older patients, whereas there were no differences in hyperemic flow velocity. Global coronary cross-sectional area was equal between young and older patients (Table 2). When coronary flow was related to left ventricular muscle mass, baseline myocardial perfusion was 77.1 ± 26.4 ml/100 g in patients 50 yr or younger and 101.6 ± 28.4 ml/100 g in patients older than 50 yr.


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  		Table 2. Hemodynamic and intravascular ultrasound parameters

 
Determinants of coronary flow.   There was a close correlation between global coronary flow and stress-mass-heart rate product (Fig. 3A). Global coronary flow was distinctly less (but significantly) related to both pressure-rate product (Fig. 3B) and muscle mass (Fig. 3C).



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  		Fig. 3. Univariate regression analysis between global coronary flow and stress-mass-heart rate product (STR-MASS-HR; A), pressure-rate product (B), and left ventricular muscle mass (C). Note that the closest relation exists between STR-MASS-HR and global coronary flow. Because global coronary flow is related to left ventricular muscle mass but not to total myocardial muscle, mass approximation of borderline values is not valid in C.

 
For further analysis, the two constituents of coronary flow, i.e., flow velocity and cross-sectional area, were separately evaluated. Coronary flow velocity was significantly related to the pressure-rate product (Fig. 4A), but there was no relation between coronary flow velocity and left ventricular muscle mass (Fig. 4B). Although global coronary cross-sectional area showed a strong relationship to muscle mass (Fig. 5A), no relation was found with the pressure-rate product (Fig. 5B).



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  		Fig. 4. Univariate regression between pressure-rate product (A), left ventricular muscle mass (B), and mean baseline average peak velocity (bAPV) as a parameter reflecting instantaneous oxygen demand.

 


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  		Fig. 5. Univariate regression between left ventricular muscle mass (A), pressure-rate product (PRP; B), and global coronary cross-sectional area. Because global cross-sectional area is related to left ventricular muscle mass but not to total myocardial muscle mass, approximation of borderline values is not valid in B.

 
All patients had an area-to-muscle mass ratio >10 mm2/100 g without a significant difference between men and women (21.3 ± 4.8 vs. 23.5 ± 3.7 mm2/100 g, P = 0.2). Mean average peak velocity, however, showed no relationship with the area-to-muscle-mass ratio (r = 0.13; P = 0.48). In no coronary vessel was there an interdependency between cross-sectional area and coronary flow velocity (LAD: r = 0.05, P = 0.77; LCX: r = 0.01, P = 0.94; RCA: r = 0.05; P = 0.78).

DISCUSSION

In the present study, global myocardial flow was directly assessed by intracoronary Doppler and IVUS. Using this approach in patients with nonobstructed coronary arteries, we were able to show that the two components of coronary flow, lumen diameter and flow velocity, are principally determined by different physiological factors. Although lumen area is closely related to left ventricular muscle mass, coronary flow velocity is mainly determined by the pressure-rate product, a surrogate of the instantaneous myocardial oxygen demand. These results suggest that long-term flow adaptation is achieved by an increase in lumen area of the coronary circulation, whereas short-term myocardial oxygen requirements are satisfied by changes in resting flow velocity.

Comparison with other methods.   So far, there is only a limited appreciation of myocardial perfusion in humans, given that perfusion studies in humans often provide only indirect measures. In addition, insights from invasive studies in animal models cannot simply be translated.

Importantly, in the present study, we now assessed global coronary flow in humans directly. The Doppler technology, applied in the present study, precisely reflects coronary flow velocity. Previously, it has been extensively validated by timed-venous coronary sinus collection and labeled microspheres (23, 39). In addition, IVUS allows the exact quantification of coronary lumen cross-sectional areas (8). Via these techniques, global coronary resting flow was found to be 197 ± 72 ml/min (range: 59–376 ml/min) in patients without significant coronary luminal narrowing.

Our directly assessed value of global coronary resting flow is higher than values (123 ± 24 ml/min) reported by Ganz et al. (13) using the coronary sinus thermodilution method. A reason for this discrepancy may be the fact that some cardiac veins drain into the coronary sinus very close to the orifice of coronary sinus (in the right atrium); blood of these veins is not measured by thermodilution, which may lead to an underestimation of global myocardial flow (4).

We found that total coronary resting flow is closely related to the total left ventricular mass. When total coronary resting flow was related to the left ventricular mass, mean flow was 91 ± 30 ml·100 g–1·min–1. Anderson et al. (2) measured regional perfusion invasively by the use of a Doppler technique and quantitative coronary angiography. Myocardial muscle mass was assessed by measuring the lengths of all distal coronary branches in the perfusion area of the corresponding perfusion area. By using these techniques, a mean value of 58 ± 15 ml·100 g–1·min–1 was obtained in patients without, with mild, and with moderate coronary artery disease. In the present study, we could only relate total coronary flow to left ventricular mass, but total coronary flow also includes supply to the right ventricle and both atria. When we take into account the fact that right ventricular muscle mass and atria account for about one-third of the whole myocardial muscle mass, the difference between the studies can be explained (17).

With positron emission tomography, perfusion values ranging from 72 to 117 ml·100 g–1·min–1 have been reported (12, 28, 36). Although there is a wide range with this imaging technique with respect to patients with different disorders, these data are rather similar to our invasively obtained flow values.

Physiological interactions.   We found in the present study a strong correlation between global coronary flow and the stress-mass-heart rate product, a parameter that incorporates both instantaneous hemodynamic parameters (blood pressure and heart rate) and a static parameter that reflects long-term adaptation (left ventricular muscle mass) (1). There were also significant relations between global coronary flow and both the pressure-rate product and left ventricular mass; however, these relations were less close.

Coronary flow is principally determined by two components: lumen area and coronary flow velocity. We separately assessed potential factors that may be related to one or both component(s). There was a close relation of global cross-sectional area and left ventricular muscle mass, but not with resting flow velocity. In fact, myocardial muscle mass increases generally in response to enhanced hemodynamic requirements (15). Our data suggest that adaptation of coronary flow to long-term demands is achieved by upregulation of vessel size; this is supported by studies that revealed increased coronary artery dimensions in both primary and secondary left ventricular hypertrophy (19, 25, 27). This adaptation might be a long-term process; however, the regression of coronary artery dimensions observed after successful valve replacement suggests that this is a dynamic process (37). Because, in the present study, patients with overt severe cardiac disease such as aortic stenosis or hypertrophic cardiomyopathy were excluded, our data suggest that this mechanism of long-term adaptation might also work under physiological conditions. Although patients with arterial hypertension participated, which might in part determine myocardial muscle mass, muscle mass is also influenced by physiological variables such as age, body surface area, and training status (31, 38).

Resting flow velocity, however, showed a close relation with the pressure-rate product, an indirect index of instantaneous myocardial oxygen consumption (5), but not with left ventricular muscle mass. Changes in resting flow velocity may be the mechanism by which the heart responses to short-term changes in myocardial oxygen requirement (e.g., as a result of an increase in heart rate or an elevation of blood pressure). This assumption is supported by previous experiments, which showed that changes in heart rate or blood pressure are accompanied by changes in resting coronary perfusion (30, 24).

Besides these external parameters that control coronary vessel area and coronary flow velocity, an interdependency of both parameters exists, at least in advanced atherosclerosis. Anderson et al. (2) found in their study an inverse relation between resting flow velocity and the ratio of lumen area to regional muscle mass (assessed by measuring coronary branch length). This suggests that an increase in resting flow velocity may compensate for a reduction of lumen area to maintain coronary perfusion. We could not reproduce this relation in the present study. The reason for this disagreement may be the fact that Anderson and colleagues also included patients with moderate coronary artery disease (50–70% stenosis), whereas our present study addressed only patients with angiographically normal coronary arteries (no or minimal plaque burden by IVUS). In the present study, all patients had an area-muscle-mass ratio >10 mm2/100 g; this value is suggested to be a minimum normal area-to-muscle mass ratio that requires no compensation (37). Our data in unobstructed coronary arteries show that resting flow is primarily determined by myocardial oxygen demand, whereas the data of Anderson et al. suggest that this mechanism may be superimposed, when atherosclerotic lumen encroachment starts to cause a critical reduction of the ratio between lumen area and the muscle mass subtended. In addition, this explains our previous observation that advanced stages of coronary heart disease, identified by electron beam tomography, are associated with an increased variability in resting coronary flow velocity, although no significant stenoses were observed (41).

Study limitations.   In the present study, we did not directly compare values of our global myocardial perfusion measurements to perfusion data obtained by other techniques. Although it may be interesting to compare different methods, no specific method can currently be regarded as the "gold standard" for the assessment of global coronary flow in humans, and no normal values have been established so far (29).

In the present study, we isolated different factors that influence absolute coronary flow. We are aware that a mutual dependency between these parameters exists. In fact, there is an association between blood pressure and left ventricular hypertrophy, although resting blood pressure and heart rate showed a quite poor correspondence with the severity of left ventricular hypertrophy, and there is a lack of association between short-term blood pressure elevations and left ventricular mass (32, 10). Nevertheless, the interaction of the assessed parameters does not disprove our hypothesis that short-term adaptation of coronary flow is achieved via flow velocity and long-term adaptation via vessel area.

In the present study, summarized coronary flow was related to left ventricular mass. We are aware that this parameter includes supply for the right ventricle, which contributes about one-third of total myocardial mass (17). Because no patients with echocardiography criteria of right ventricular hypertrophy were included in the study, we think this fact does not influence the conclusion of this study.

When interpreting the present results, one has to consider that the patients under investigation cannot be taken as truly normal. Because all patients presented with angina suspicious for obstructed coronary artery disease, microvascular disease must be assumed as a potential reason for their complaints.

GRANTS

This study was supported by a grant of the Deutsche Forschungsgemeinschaft (DFG) DFG E 155/2-1,SE.

ACKNOWLEDGMENTS

Present addresses: C. von Birgelen, Twente, Hospital Enschede, Department of Cardiology, Enschede, The Netherlands. C. Altmann, Klinikum Krefeld, Lutherplatz 4, 47805 Krefeld, Germany.

FOOTNOTES


Address for reprint requests and other correspondence: H. Wieneke, Dept. of Cardiology, Univ. Essen, Hufelandstr. 55, D-45122 Essen, Germany (E-mail: heinrich.wieneke{at}uni-essen.de)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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