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(Circulation. 1997;96:2905-2913.)
© 1997 American Heart Association, Inc.

Articles

Disturbed Intracoronary Hemodynamics in Myocardial Bridging

Early Normalization by Intracoronary Stent Placement

Heinrich G. Klues, MD; Ernst R. Schwarz, MD; Jürgen vom Dahl, MD; Thorsten Reffelmann, MD; Helmut Reul, PhD; K. Potthast, PhD; C. Schmitz, PhD; Jürgen Minartz, MD; Winfried Krebs, PhD; ; iPeter Hanrath, MD

From the Medical Clinic I, University Hospital, Rheinisch Westfälische Technische Hochschule, Aachen, and Helmholtz Institute for Biomedical Engineering (H.R., K.P., C.S.) Aachen, Germany.

Correspondence to Heinrich G. Klues, MD, Medical Clinic I, University Hospital, RWTH Aachen, Pauwelsstr 30, 52057 Aachen, Germany.

	Abstract

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Background The purpose of this study was to evaluate the hemodynamic mechanisms leading to myocardial ischemia in patients with myocardial bridging. Myocardial bridging is known to induce angina and even severe myocardial ischemia.

Methods and Results In 12 symptomatic patients with myocardial bridges, quantitative coronary angiography was performed to obtain systolic/diastolic vessel diameters within the bridged segments. Coronary flow velocities, flow reserve, and pressures were determined with a 0.014-in Doppler and a 0.014-in pressure microtransducer. In 3 symptomatic patients, coronary stents were implanted and hemodynamic measurements were repeated immediately and after 7 weeks. An in vitro validation of the pressure measurements was performed. Angiography revealed a systolic diameter reduction of 80.6±9.2% and a persistent diastolic reduction of 35.3±11% within the bridged segment. Diastolic flow velocities (cm/s) were increased (31.5±14.3 within versus 17.3±5.7 proximal and 15.2±6.3 distal, P<.001). Coronary flow reserve distal to the bridge was 2.5±0.5. There was an increased peak systolic pressure within the bridged segment (171±48 versus 113±10 mm Hg proximal, P<.001). Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, the intracoronary peak systolic pressure, and clinical symptoms. Coronary flow reserve improved to 3.8±0.3.

Conclusions Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.

Key Words: bridging • angiography • ultrasonics • pressure • stents

	Introduction

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Structural and anatomic abnormalities of the coronary vasculature other than atherosclerosis are infrequent causes of myocardial ischemia. Phasic external vessel compression due to myocardial bridging, however, may induce ischemia and anginal symptoms.^1-11 Although frequently identified by coronary angiography, it is still unknown how the intramural course of an otherwise normal coronary artery may lead to myocardial ischemia.^12-14 Controversy exists concerning the clinical and prognostic relevance and the adequate therapy for symptomatic patients with this anomaly.¹⁵

Recent quantitative angiographic and intravascular ultrasound studies in patients with myocardial bridging demonstrated that vessel compression is not limited to systole, causing the angiographic "milking" effect, but rather persists into diastole and thereby affects the predominant phase of coronary perfusion.^16-20 Although ischemia and hemodynamic alterations due to myocardial bridges are, in part, acutely eliminated by ß-receptor blockade, as demonstrated earlier in another patient subset, not all patients achieve persistent symptomatic relief.¹⁹ Alternative treatments other than surgical myotomy have not been systematically evaluated, mainly because of the incomplete understanding of the underlying hemodynamic mechanisms.

To evaluate the functional consequences of the phasic diameter changes, we combined measurements of coronary angiography, intracoronary Doppler flow, and pressure in patients with symptomatic myocardial bridging. In three selected symptomatic patients, intracoronary stents were implanted to prevent functional coronary obstruction. The acute hemodynamic and angiographic effects of this treatment were studied. In addition, an in vitro study was added to evaluate the accuracy of the 0.014-in intracoronary microtransducer in tortuous coronary segments and to reconstruct the hemodynamic phenomena in myocardial bridges.

	Methods

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Patient Selection
The study population consisted of 12 otherwise healthy male patients (mean age, 44±6 years). All of them underwent diagnostic coronary angiography for suspected coronary artery disease. None of these patients were part of previous investigations.¹⁹ Myocardial bridges of the midportion of the left anterior descending coronary artery were documented in all subjects. There were no angiographic signs of coronary atherosclerosis or other cardiac malformations. Bicycle ergometry demonstrated significant anterior ST-segment depression of >0.2 mV or terminal T-wave inversion during or after exercise in 8 patients (67%). The remaining 4 patients had reproducible angina pectoris during stress testing. The study protocol was approved by the local ethics committee, and written informed consent was obtained from all patients before inclusion into the study.

Coronary Angiography and Quantitative Diameter Measurements
All cardiovascular medications, including ß-receptor blockers, were withheld 24 hours before the procedure. Cardiac catheterization was performed routinely by the Judkins technique with 7F or 8F catheters. Quantitative measurements of the coronary arteries were obtained from monoplane, digitized images on a workstation (AWOS 4.01, Siemens) as described previously.¹⁹ Percent stenosis, reference diameter of the adjacent segments, and minimal diameter of the bridged segments were calculated.

Intracoronary Flow Velocity Measurements
Intracoronary Doppler flow profiles were obtained with a 0.014-in flexible Doppler guidewire (FloWire, Cardiometrics Inc).^19,21-23 Flow velocities were measured proximally, distally, and within the bridged segment as previously described.¹⁹ All Doppler signals were analyzed on-line by fast Fourier transformation. The measurements are based on the average of two complete cardiac cycles. Coronary flow reserve was determined after intracoronary injection of 12 mg papaverine, with the transducer located distal to the myocardial bridge.²⁴

Intracoronary Pressure Measurements
Intracoronary pressures were obtained with a fiberoptic pressure microtransducer incorporated into the distal segment of a 0.014-in guidewire (Radi Medical Systems). This system has been validated.^25-27 In addition, an in vitro validation was performed by use of a complex pulsatile model simulating left ventricular and coronary hemodynamics to study measurement precision of the pressure guidewire in extremely tortuous coronary segments and to reconstruct the conditions of myocardial bridges (see "Appendix: In Vitro Validation").^28,29 The pressure signal was calibrated immediately before insertion. The accuracy of the measurements was tested by superimposing the prestenotic coronary pressures from the guiding catheter and the sensor tip. Measurements were obtained proximal and distal to and from multiple positions within the bridged segments during repeated pullback maneuvers. To avoid artificial measurements due to direct external compression of the laterally mounted transducer, the guidewire was rotated by 45° after each pullback. The location of the pressure transducer was repeatedly validated by simultaneous contrast injections and documented on angiographic images.

Stent Implantation and Intravascular Ultrasound
Standard techniques were applied for stent delivery in three selected patients. An extra support guidewire was chosen to facilitate stent advancement through the usually tortuous proximal segments of the myocardial bridges. A balloon-expandable stent with a tubelike design and a length of 15 mm was used (Multi-Link, Guidant Ltd). This stent was chosen because of its high flexibility in combination with the ability to withstand external compression forces. Inflation pressures of 12 atm were used during primary implantation. High-pressure inflations (>14 atm) with a minimally compliant balloon were performed when suboptimal stent expansion was identified during intravascular ultrasound examination with a 3.5F, 20-MHz monorail mechanical ultrasound catheter (Boston Scientific) connected to a Sonos 100 ultrasound console (Hewlett Packard). Optimal stent expansion was judged on-line on the basis of criteria described previously.³⁰ All patients received 250 mg ticlopidine twice daily starting the day before implantation for a period of 2 months, in combination with 100 mg/d aspirin. The patients were reevaluated after 7 weeks with coronary angiography. This relatively short control interval was chosen to detect early intima proliferation or mechanical stent recoil.

Statistical Analysis
Values are given as mean±SD. Doppler flow and pressure values proximal to, within, and distal to the myocardial bridges were compared by ANOVA for repeated measurements. A value of P<.05 was considered significant.

	Results

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Quantitative Angiographic Measurements
Quantitative angiographic measurements are provided in Table 1. At the level of the myocardial bridge, the average maximal systolic diameter reduction was 80.7±9.2% (range, 72% to 100%). In addition, there was a persistent diastolic diameter reduction of 35.3±10.9% (range, 22% to 58%). The mean length of the myocardial bridge was 27±5 mm (range, 19 to 38 mm).

View this table: [in this window] [in a new window]   Table 1. Quantitative Coronary Angiography, Intracoronary Doppler Flow Velocity, and Pressure Measurements in 12 Patients With Myocardial Bridging of the Left Anterior Descending Coronary Artery

Intracoronary Doppler Flow Velocity Measurements and Flow Reserve
The average peak flow velocity and diastolic peak flow velocity were significantly higher within the myocardial bridge than in the proximal and distal segments. The mean average peak flow velocity was 27.0±13.6 cm/s within, 13.5±4.9 cm/s proximal to, and 12.2±4.9 cm/s distal to the myocardial bridges (P<.001 within versus proximal and distal); average diastolic peak flow velocity was 31.5±14.3 cm/s within, 17.3±5.7 cm/s proximal to, and 15.2±6.3 cm/s distal to the bridged segment (P<.001 within versus proximal and distal). The mean coronary flow reserve obtained distal to the myocardial bridge was 2.5±0.5 (Table 1). None of the patients had a ratio of >3.0, which is considered normal in our laboratory. Qualitative analysis of Doppler flow profiles within the myocardial bridges revealed a characteristic pattern with an abrupt early diastolic flow acceleration, a rapid mid-diastolic deceleration, and a mid-to-late-diastolic plateau. Retrograde flow phenomena during systole were detected proximal to the site of maximal lumen reduction within the bridged segments in all patients (Fig 1).

View larger version (102K): [in this window] [in a new window]   Figure 1. Typical intracoronary Doppler flow velocity profile obtained within a myocardial bridge of left anterior descending coronary artery. Abrupt diastolic flow velocity acceleration is followed by mid-diastolic plateau and retrograde systolic flow. APV indicates average peak flow velocity; ADPV, average diastolic peak flow velocity; MPV, maximal peak flow velocity; ASPV, average systolic peak flow velocity; S, systole; and D, diastole. All values are cm/s.

Intracoronary Pressure Measurements
Intracoronary pressures proximal to the bridged segments were identical to simultaneous pressure recordings from the tip of the guiding catheter (Table 1). There were significantly higher peak systolic pressures within the bridged segments (171.3±48 mm Hg; range, 125 to 280 mm Hg) compared with segments proximal (113.1±10.3 mm Hg; range, 100 to 130 mm Hg, P<.001) and distal (112.9±9.8 mm Hg; range, 100 to 130 mm Hg, P<.001, Fig 2) to the bridge. Pressures distal to the myocardial bridge were identical to pressures obtained proximal to the bridged segment. The mean peak-to-peak pressure difference between the proximal and the maximal systolic pressures within the bridged segment was 58.6±43.7 mm Hg (range, 20 to 160 mm Hg). During diastole, there was an inverse pressure relation, with lower pressures within the bridged segment (70.6±10.9 versus 79.5±9.8 mm Hg proximal and 78.8±9.3 mm Hg distal, P<.05 for both comparisons, Fig 2). The maximal diastolic pressure gradient was 9.3±11.1 mm Hg; range, 2 to 35 mm Hg. This pressure phenomenon could be reproduced in all patients by repeated pullback maneuvers and occurred in a small central portion of the myocardial bridge, usually between a proximal and distal segment of predominant compression, producing a central "high-pressure chamber" (see "Appendix: In Vitro Validation").

View larger version (33K): [in this window] [in a new window]   Figure 2. Typical pressure tracings simultaneously recorded at tip of guiding catheter (aortic pressure) and from intracoronary pressure sensor placed within myocardial bridge. There is high overshooting systolic pressure within bridged segment and diastolic pressure gradient.

Effects of Stent Implantation
Stent implantation was performed in three patients with severe angina despite extensive medical therapy, including ß-adrenergic receptor blocking agents and calcium channel antagonists. All were candidates for surgical myotomy. Intracoronary hemodynamics and angiographic appearance of the myocardial bridges in this subset of patients were representative of the entire study population (Table 2). Coronary flow reserve was 2.4±0.5 before intervention. All three patients required two 15-mm Multi-Link stents to cover the entire length of the bridged coronary segment. Intravascular ultrasound was used to define the proximal and distal boundaries of the myocardial bridges on the basis of typical ultrasonic images with eccentric phasic vessel compression within the bridged segments (Fig 3). None of the patients demonstrated left anterior descending coronary artery atherosclerosis. High-pressure inflations (>14 atm) after stent placement were necessary in two patients because of incomplete stent expansion. Repeated hemodynamic measurements 15 minutes after the final balloon inflation demonstrated completely normalized intracoronary blood flow velocity profiles and intracoronary pressures (Figs 4 and 5). Stent placement totally abolished both systolic and diastolic diameter reductions (Fig 3, Table 2). Coronary blood flow reserve was normalized after stent implantation (Table 2). Coronary angiography after 7 weeks revealed an identical lumen enlargement without any systolic or diastolic diameter reduction and a further increase in coronary flow reserve (Table 2). Intravascular ultrasound revealed no signs of neointimal proliferation within or proximal or distal to the stented segments or evidence of mechanical stent recoil at this 7-week follow-up. All patients reported a remarkable clinical improvement, with increased physical capacity.

View this table: [in this window] [in a new window]   Table 2. Invasive Measurements in Three Patients With Myocardial Bridging Before and After Stent Implantation

View larger version (137K): [in this window] [in a new window]   Figure 3. Angiographic and ultrasound stop-frame images of left coronary artery of 38-year-old male patient with severely symptomatic myocardial bridge of left anterior descending coronary artery (patient 1; Table 2). Left: Left anterior oblique 90° projections. A, End-systolic; B, end-diastolic; and C, after stent implantation. Right: Intravascular ultrasound images of same patient obtained at most severe site of vessel compression (arrows). D, Systolic; E, end-diastolic; and F, after stent implantation.

View larger version (109K): [in this window] [in a new window]   Figure 4. Doppler flow velocity tracings within bridged segment of 52-year-old male patient with severely symptomatic myocardial bridging of left anterior descending coronary artery (patient 3; Table 2) before and directly after stent implantation. APV indicates average peak flow velocity; DSVR, diastolic-systolic flow velocity ratio; MPV, maximal peak flow velocity; ACC, acceleration; BAPV, basic average peak flow velocity; PAPV, peak average peak flow velocity (cm/s); and Ratio, coronary flow reserve.

View larger version (44K): [in this window] [in a new window]   Figure 5. Composite of intracoronary pressure tracings from three patients with severely symptomatic myocardial bridges before and after stent implantation. A, Patient 1; Table 2. B, Patient 2; Table 2. C, Patient 3; Table 2.

	Discussion

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
It has been difficult to determine the functional significance of myocardial bridging despite the presence of recurrent and often severe anginal symptoms in many patients. The present study used quantitative coronary angiography in combination with intracoronary Doppler flow and pressure measurements to extend the knowledge of local hemodynamic parameters in patients with severe myocardial bridging. On the basis of recent studies, the pathophysiology of myocardial bridges is characterized by two major mechanisms: (1) phasic systolic vessel compression with a persistent mid-to-late-diastolic diameter reduction and (2) increased intracoronary Doppler flow velocities with abnormal qualitative flow profiles.^19,20,31 In addition, it was possible to demonstrate an overshoot in the peak systolic pressure within the bridged segment. All of these factors contribute to a reduced coronary flow reserve.

Quantitative Coronary Angiography
Recent angiographic and intracoronary ultrasound studies have demonstrated that systolic vessel compression is followed by a delay in diastolic lumen gain, which is even more pronounced in late diastole, especially during tachycardia when diastole is shortened.^19,20,31 In the present study, the percent systolic diameter reduction was >70% in all patients and thus more severe (according to the classification of Noble et al¹⁶) than in the majority of previous studies. All patients showed significant tortuosity at the entry and exit sites of the bridged segment, most evident during systole.¹⁵

Intracoronary Doppler Flow Velocity
Intracoronary flow velocities were significantly higher within the bridged segments than in proximal and distal sites.¹⁹ Typical flow profiles were identified along the myocardial bridges, characterized by an early overshoot in diastolic flow acceleration, a rapid mid-diastolic deceleration, and a mid-to-late-diastolic plateau. All patients demonstrated a local systolic retrograde flow phenomenon directly proximal to the most severe site of the myocardial bridge. A similar phenomenon of local flow inversion was already proposed on the basis of qualitative angiographic observations.¹⁵ During early diastole, a rapid reduction in peripheral coronary resistance induces an immediate increase in volumetric flow, leading to an increase in diastolic flow velocities in normal coronary arteries. In the presence of a persistent diastolic diameter reduction, the sudden increase in volumetric flow induces the abrupt early diastolic peak flow velocity, probably combined with a passive squeezing by vessel relaxation. The ensuing lumen gain reduces these maximal flow velocities, with a subsequent plateau during late diastole.

Intracoronary Pressure Measurements
Pressure measurements with a 0.014-in intracoronary pressure guidewire identified a characteristic local systolic/diastolic pressure phenomenon within the myocardial bridges characterized by a systolic pressure in excess of the proximal aortic driving pressure. To understand the underlying hemodynamic mechanisms leading to this unique pressure phenomenon, a complex in vitro study simulating left ventricular and coronary hemodynamics was performed (see "Appendix: In Vitro Validation"). Several approaches to reconstruct the local characteristics of myocardial bridges finally revealed that the overshoot in systolic pressure could be produced within a central "high-pressure chamber" induced by predominant proximal and distal vessel compression. The drawing in Fig 8 ("Appendix") illustrates the possible mechanisms as they may occur in myocardial bridges.

View larger version (80K): [in this window] [in a new window]   Figure 8. A, Angiographic stop-frame image of left anterior descending coronary artery at end systole with long and severe myocardial bridge demonstrating typical inhomogeneous transmural course of coronary artery producing "compression chamber" (magnification) with prominent proximal and distal vessel compression. B, Semi-schematic drawing illustrates possible underlying pathophysiological mechanisms with stronger proximal and distal compression due to deeper transmural course of coronary artery with less affected central segment. C, Intracoronary pressure tracings were obtained proximal to, within, and distal to bridged segment from same patient as shown in A.

From autopsy reports and surgical findings, it is well known that the intramural course of the coronary artery is heterogeneous.¹⁵ This is consistent with the angiographic appearance of myocardial bridges in the majority of patients, in which short portions with severe systolic compression may coexist with moderate or minor vessel obstruction. This anatomic heterogeneity can result in heterogeneous compression forces on the artery and result in the creation of a high-pressure chamber. Careful pullback maneuvers of the pressure transducer and comparison with simultaneous angiography identified such a central portion of the myocardial bridge as the origin of this pressure phenomenon. This observation is in contrast to a previous description of a segment proximal to the myocardial bridge in a single case using a 3F intracoronary pressure transducer.³² Inhomogeneous vessel compression creating a central high-pressure chamber, however, can occur only when high intramural pressures, above the aortic and left ventricular pressure, are manifest along the muscle bridge. High intramural pressures, mainly subendocardial, have indeed been described in different models, with systolic pressures 30 to 60 mm Hg above intraventricular pressures.^33-35 High intramural pressures and external compression forces along the myocardial bridge should be most prominent where the vessel course is deeply intramural.

The occurrence of systolic retrograde flow proximal to the most severe obstruction site, as demonstrated by intravascular Doppler, can be explained as a direct consequence of high local systolic pressure. Rapid loss of the external compression force during diastole leads to a steep drop in local pressures and induces an inverse diastolic pressure gradient within this portion of the myocardial bridge. This pressure gradient further promotes the rapid early diastolic blood flow velocity in addition to the above-described mechanisms of persistent diameter reduction, caused by a delay in muscular relaxation and drop in peripheral resistance.

Errors in Pressure Measurements due to Catheter Entrapment?
Catheter entrapment as a cause of artificial pressure measurements has been described in hypertrophic obstructive cardiomyopathy and might also occur in the present situation.³⁶ The pressure sensor that was used in this study has a diameter of 0.43 mm and is extremely thin, and true entrapment can be expected only at vessel diameters <0.45 mm. Two patients had minimal end-systolic vessel diameters (by quantitative coronary angiography) <0.45 mm, but because of the eccentricity of vessel compression in myocardial bridges, all other diameters were clearly larger. Direct compression of the laterally mounted transducer would therefore occur in only one orientation. For this reason, the pressure wire was rotated by 45° after each pullback maneuver to reduce the likelihood of catheter entrapment. Furthermore, during the in vitro study, no evidence of artificial pressure measurements was found. Earlier in vitro validations using the 0.018-in pressure guidewire had demonstrated that tortuous coronary segments might negatively influence measurement precision.²⁷ The present in vitro validation with the 0.014-in guidewire revealed a mean difference between the aortic and coronary pressure of <6 mm Hg even in extremely tortuous segments exceeding possible anatomic variations encountered in humans.

Treatment Strategies in Symptomatic Myocardial Bridging
On the basis of these pathophysiological observations, three therapeutic strategies carry the potential to affect one or more of the influencing variables. Negative inotropic agents, especially ß-adrenergic receptor blockers, are capable of reducing systemic and intramural pressures and thereby the external vessel compression. The accompanying negative chronotropic effect mainly prolongs diastole, also improving coronary perfusion.^19,37 A recent study indeed demonstrated that intravenous application of the short-acting ß-blocker esmolol significantly reduces diameter reduction and flow velocities and normalizes the systolic/diastolic flow ratio, thus alleviating anginal symptoms during atrial pacing.¹⁹

In patients with persistent symptoms despite extensive medical therapy, surgical myotomy was regarded as the treatment of choice. Although cleavage of the bridging muscle fibers eliminates the underlying cause of the myocardial bridge, this treatment strategy carries considerable risk.^38-41 The unpredictable intramural course of the coronary artery may require deep incision of the ventricular wall, potentially leading to subsequent left ventricular wall aneurysms.⁴²

Intracoronary stent implantation was performed in three patients with persistent and severe angina despite treatment with ß-blockers. This strategy was described before in a single patient without concomitant hemodynamic measurements and allows "internal" stabilization of the coronary artery lumen against external compression, thereby eliminating the abnormal flow and pressure phenomena.⁴³ Hemodynamic, angiographic, and intravascular ultrasound studies immediately after stent deployment and 7 weeks later demonstrated normalization of the flow velocity profile, lumen diameters, and intracoronary pressures. Coronary flow reserve immediately after implantation and during follow-up was completely normalized. Angiography and intravascular ultrasound revealed no evidence of neointimal proliferation or mechanical stent recoil. Stent implantation, therefore, may represent an effective alternative treatment strategy; however, larger long-term studies are necessary to evaluate the incidence and the degree of in-stent restenosis, the stability of the stent geometry, and clinical improvement.

Conclusions
The present study demonstrates a variety of local hemodynamic abnormalities in myocardial bridging. All of them are a consequence of phasic external vessel compression and high local systolic pressures within the bridged segment. Even though all of these phenomena occurred within the bridged segments and did not alter distal flow velocities and pressures (ie, in particular, no pressure gradient along the myocardial bridge), coronary flow reserve was abnormal. This may signify reduced ischemic threshold and help to explain anginal symptoms in these patients. Stent implantation into the bridged segments eliminated all hemodynamic abnormalities in the short term and normalized coronary flow reserve. Whether stent implantation in symptomatic patients is the treatment of choice remains to be proved.

View larger version (41K): [in this window] [in a new window]   Figure 6. Pulsatile coronary flow model. 1, Silicon model of left ventricle; 2, compression fluid; 3, piston of electrohydraulic drive unit; 4, micromanometer-tip transducer for measurement of aortic pressures; 5, pressure guidewire introduced into coronary artery via sidearm of aortic root; 6, external vessel compression simulating myocardial bridge with electrical motor and piston with adjustable piston strike; 7, 8, and 9, hydraulic elements for adjustment of compliance and resistance; 10, model of left atrium; 11, mitral valve (bioprosthesis); 12, aortic valve (artificial prosthesis).

View larger version (22K): [in this window] [in a new window]   Figure 7. Two representative pressure tracings obtained from pulsatile coronary flow model. Aortic pressure was obtained with micromanometer-tip transducer and coronary pressure with pressure guidewire at heart rate of 70 bpm with cardiac output of 5.5 L/min. Difference in degree of overshooting systolic pressure was induced by variations in external vessel compression through adjustable piston strike. *Artifacts induced by prosthetic aortic valve.

	Appendix 1

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
In Vitro Validation
The in vitro validation was performed to address two issues: measurement precision of the 0.014-in pressure guidewire in tortuous segments and simulation of the pressure phenomenon within myocardial bridges.

Experimental Model
The experiments were performed in an electrohydraulic, computer-controlled pulsatile flow model simulating the left side of the human circulatory system modified to duplicate the predominant diastolic flow pattern of a coronary artery (Fig 6). The model has been described elsewhere.^28,29 In brief, input and output impedances of the ventricle are simulated by means of tuned hydraulic elements for adjustment of compliance and resistance. Volume displacement of a silicone flexible sac shaped like the left ventricle is achieved by an electrohydraulic drive unit by means of a compression fluid (degassed water). The piston expands or contracts the flexible sac according to a selected volume-time function The ventricular output is controlled by a displacement transducer coupled to the driving piston. A silicon tube with a diameter of 3.0 mm served as a model of the coronary artery originating from the aortic root and reentering the system through the mitral valve. The pressure guidewire was introduced through a rotating hemostatic valve into a sidearm of the aorta and placed in the coronary artery. Pressure signals were simultaneously recorded in the aorta with piezoelectric catheter-tip transducers (Sensodyne, Braun-Melsungen) and in the coronary artery with the pressure guidewire. The frequency varied between 70 and 140 bpm. The cardiac output was held constant at 5.5 L/min. The mean aortic pressure was 110 mm Hg (systolic, 130 and diastolic, 90 mm Hg).

External compression of the silicon tube simulating the coronary artery was achieved by an electrical motor. The compression was initiated 100 ms after the start of ventricular contraction. The piston strike was adjusted to allow a 70% to 95% obstruction of the coronary tube during maximal compression, with a persistent diameter reduction of 30% during diastole.

Measurement Precision
The validation measurements are based on a total of 7200 samples obtained throughout a complete cardiac cycle in a variety of different curvatures. The angulations were produced by placing the silicon tube in preformed curves with arcs between 90° and 180° and curve diameters from 1 to 2 cm. The mean differences between the aortic reference pressure and the coronary pressures obtained from the pressure guidewire were 3.2±1.1 mm Hg (range, 1.8 to 6.8 mm Hg; n=2000 samples) for a single arc of 90° and curve diameters of 1 to 2 cm; 5.4±1.1 mm Hg (range, 2.8 to 8.7 mm Hg; n=1600 samples) for an arc of 180° and curve diameters of 1 to 2 cm; and 5.8±1.1 mm Hg (range, 3.2 to 11.8 mm Hg; n=3600 samples) for serial curves (2 to 4 arcs) of 90° to 180° with curve diameters between 1 to 2 cm.

Simulation of the Pressure Phenomenon
Several approaches to reconstructing the local characteristics of myocardial bridges were tested. It was only possible, however, to simulate the in vivo pressure curves by producing a proximal and distal segment of predominant obstruction, here induced by two sticks placed beneath the silicon tube (Fig 6). Simple compression of the tube induced no pressure differences at all. Two examples of the pressure phenomenon are given in Fig 7A and 7B. The degree of the overshoot in systolic pressure was dependent on the simulated heart rate and the degree of external vessel compression and ranged from 30 to >175 mm Hg. There was also a small early diastolic gradient of different degrees and durations as described during the in vivo studies. The possible in vivo mechanisms leading to this unique local pressure phenomenon in myocardial bridges are shown in Fig 8.

Received February 18, 1997; revision received July 25, 1997; accepted August 13, 1997.

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