Myocardial Bridges (Tunneled Epicardial Coronary Artery)

The coronary arteries may dip into the myocardium for varying lengths and then reappear on the heart's surface (Figs. 212-1 to 212-9). The muscle overlying the intramyocardial segment of the epicardial coronary artery is termed a myocardial bridge (MB) and the artery coursing within the myocardium is called a tunneled artery (see Figs. 212-1 to 212-3). Tunneled coronary arteries have long been recognized anatomically, but suggested associations between myocardial ischemia and myocardial bridges have heightened their clinical relevance.
Tunneled coronary arteries have been presumed congenital in origin. At least three factors have been postulated to account for differences between the high frequency of tunneled major coronary arteries observed at necropsy (5-86 percent and the lower frequency of tunneled coronary arteries observed angiographically (0.5-12 percent) Fig. 212-11 or associated with symptoms of myocardial ischemia (18 percent):

(1) Length, thickness,and location of the tunneled coronary segment (MB), the presence of left ventriclar hypertrophy, hypertrophic cardiomyopathy, and aortic stenosis. The length of the coronary arterial narrowing markedly influences coronary hemodynamics, explaining why relatively long bridges are present in symptomatc patients. Ultrasound studies show that the thicker bridges are most frequent in symptomatic patients.

(2) Degree of systolic compression.The location and orientation of the muscle bundles over the imbedded coronary artery also affect systolic compression. Some are superficial and others are deeper surrounding the mid or even the proximal LAD. Progressive increases in left ventricular wall tension with the preceding mentioned diseases may play a part in producing symptoms.

Increased intracoronary Doppler flow velocities. As shown in Table 1 below, resting average peak-flow velocity (APV) and average diastolic peak flow velocity (ADPV) were higher within the bridged segment than in the corresponding proximal and distal segments. The flow velocity increase within the MB was bridged segment as compared to the proximal and distal segments. Mean diastolic/systolic flow velocity ratio (DSVR) at rest ranged from 2.4 to 2.9. Thus, intracoronary Doppler flow measurements reveal a significant increase in APV, ADPV, and MPV within the MB at rest, with only minor changes in systolic flow. These flow velocity abnormalities are very consistent across the different studies.
During rapid atrial pacing (Table 2 below), all flow velocitieswithin the MB were increased. The flow acceleration was largest for MPV and again smallest for ASPV within the bridge segment. There was a significant increment in DSVR within the MB during tachycardia, but no change proximally or distally. Thus, atrial pacing induced a further acceleration in flow velocities within the bridged segment, whereas the flow velocities proximal and distal to the bridge remained unchanged. A significant increase in DSVR appears to be the most prominent flow alteration within the MB during stress.

Finally, qualitative analysis of the Doppler flow profile shows a highly characteristic pattern in approximately 90% of the patients with an abrupt early diastolic flow acceleration, which has been termed the "finger tip" phenomenon, a rapid mid-diastolic deceleration and mid-to-late diastolic plateau (Fig. 212-12). A retrograde flow phenomenon during systole was detected in the majority of patients at the proximal entry site of the bridged segments. Atrial pacing led to further accentuation of the velocity profile, with shortening of the diastolic plateau as well as accentuation of the retrograde flow phenomenon.

Schwarz et al. (13) quantitatively analyzed consecutive stop-frame images from a complete heart cycle in 14 patients and correlated their results with Doppler flow measurements obtained in the same patients at an identical site. There was rapid lumen reduction during systole with the smallest diameter during late systole, the characteristic milking effect. Early diastolic diameter gain was clearly delayed with a persistent mid-diastolic diameter reduction always >30%. The abrupt early diastolic flow acceleration was due to this persistent diastolic diameter reduction. This was followed by rapid diastolic lumen gain, which reduced the flow velocity, and finally stabilization of the lumen diameter leading to a plateau during late diastole. As shown by this study, the speed of early diastolic diameter gain and systolic compression strongly depends on heart rate, contractile state, and peripheral resistance and may vary substantially.

CFR

The CFR, defined as the ratio of mean flow velocity achieved at peak hyperemia to mean resting flow velocity, was obtained after intracoronary injection of papaverine. A normal CFR ratio should be above 3.0. Thus, CFR distal to the bridge was abnormally reduced in all these studies, ranging from 2.0 and 2.6 (Table 2). Impaired CFR can be explained, besides systolic vessel compression, by the delayed early and mid-diastolic relaxation with increased diastolic blood flow velocities. The increase in CFR obtained after angioplasty of the bridge segment is described in the following text.

Additional mechanisms of myocardial ischemia

Several additional factors have been shown to influence both the degree of systolic compression and the speed of early diastolic gain and subsequent diastolic relaxation in patients with symptomatic MB (see effects of Length and degree of systolic compression above and heart rate below).

(3) Heart rate. With slow rates,most coronary blood flow is in diastole.But at higher rates the diastolic period is shortened. In table 3 it is shown that most of the flow disturbances occur in dastole in symptomatic patients. Changes in systemic arterial pressure and coronary perfusion can also singnificantly affect the severity of systolic and consequently of early and mid-to-late diasltolic compression in patients with MB. For example, sublingual or intracoronary nitroglycerine and sodium nitroprusside increase the coronary narrowing in patients with MB, whereas noradrenaline, phenylephrine,and ergonovine decrease it.

Longer tunneled segments of coronary arteries, more severe systolic diameter narrowing of the tunneled segment, and tachycardia may contribute to the production of myocardial ischemia with myocardial bridging (see Figs. 212-7 and 212-8 and myocardiobridge-table 1 and table 2). The length of coronary tunneling may not always be an important factor in causing myocardial ischemia, since three patients with left main intramyocardial tunneling of greater than 40 mm have been described without evidence of myocardial ischemia (Fig. 212-9).

Clinical symptoms and objective signs of myocardial ischemia.

Myocardial bridges can be an incidental finding at the time of coronary angiography. Conversly, a wide variety of clinical syndromes including unstable angina, acute myocardial infarction (AMI), life-threatening cardiac arrhythmias, and sudden cardiac death have been associated with MB .

Typically, these patients are predominantly males, 5 to 10 years younger than patients with symptomatic coronary disease, and they have fairly severe anginal symptoms. Typical angina is present in 55% to 70% of the cases, and atypical angina is often reported in association with rest angina.

The mean time interval between onset of symptoms and coronary angiography is >18 months, and there were an average of 2.5 previous hospital admissions for angina or suspected AMI. Some patients had documented prior anterior or septal non-Q wave AMI. Except for 12 patients (18%) of Ge et al. who had significant stenoses in the proximal segment of the bridged artery, all these selected patients had isolated MB with >50% systolic lumen diameter reduction, without angiographic evidence of significant coronary atherosclerosis or left ventricular hypertrophy.

Symptom-limited exercise electrocardiograms were performed in 73% to 100% of patients. As a rule, patients not undergoing stress testing before cardiac catheterization had unstable symptoms. Significant ischemic ST-segment depression >0.1 mV in the anterior leads was identified in 28% to 67% of patients in whom the test was done. Myocardial scintigraphy was obtained in 38% to 100% of patients. Stress-induced perfusion defects of the anterior wall or septum were documented in 33% to 63% of the patients in whom the myocardial scan was performed.

Therefore, compared to patients with significant singlevessel coronary disease, these selected patients with isolated symptomatic myocardial bridging and >50% systolic lumen diameter narrowing of the LAD probably exhibit a comparable severity of anginal symptoms and of noninvasive signs of myocardial ischemia. This probably also includes a similar incidence of prior or recent unstable angina and AMI (acute myocardial infarction). Finally, the long-term outcome of these patients may also be as favorable as that of patients with single-vessel coronary disease or even better, because, in contrast to atherosclerosis, little late progression is to be expected.

Invasive diagnostic methods.

Quantitative coronary angiography, usually in the plane showing the most severe narrowing, objectively measures the lumen diameter reduction within the bridge segment as compared to the proximal and distal segments and determines the percent MLD (mean lumen diameter) narrowing both during systole and during mid-to-late diastole. As a rule, a significant milking effect shows an approximate 70% MLD reduction during systole and an approximate 35% MLD reduction during mid-to-late diastole ( Myocardiobridge -Table 1a). The severity of the systolic and mid-to-late diastolic MLD narrowing can be confirmed by IVUS, which has the advantage of assessing lumen area instead of only diameter in an invariably nonspherical vessel lumen. Ge et al.have described a highly specific "half moon" phenomenon surrounding the MB in all 62 patients in whom the IVUS catheter could be passed through the bridge segment (Figure 212-10). This ultrasound phenomenon is only found in the bridge segment and not in the proximal or distal segment or in other coronary arteries. In some cases where the specific "half moon" phenomenon was demonstrated but the typical angiographic milking effect was not obvious presumably because of only slight myocardial bridging, the milking effect could be provoked by intracoronary administration of nitroglycerin.

Intracoronary Doppler flow velocity measurements reveal another highly, characteristic diagnostic pattern in patients with MB. In approximately 90% of cases, the flow velocity curve within the bridge segment is characterized by an early diastolic "finger tip" phenomenon, followed by a rapid mid-diastolic deceleration and a mid-to-late diastolic plateau (Figure 212-11). The typical "finger tip" phenomenon is produced by an abrupt early diastolic flow acceleration as a result of delayed vessel relaxation within the bridge segment. As a result of the systolic compression, there is also a markedly reduced to absent antegrade systolic flow and quite often a typical local systolic retrograde flow phenomenon directly proximal to the more severe site of the MB. Rapid atrial pacing accentuates these characteristic early diastolic and retrograde systolic flow phenomena, while it also shortens the mid-to-late diastolic plateau (Figure 212-11). Typically, intracoronary Doppler flow velocities at rest, especially APV (average peak flow velocity), ADPV, and MPV (maximal peak flow velocity) should be higher in the bridge segment than in the proximal and distal segments and they should be accentuated by rapid atrial pacing (Myocardiobridge -Table 1b and Table 2). Finally, a <3.0 CFR(coronary flow reserve) distal to the MB obtained after intracoronary administration of papaverine reflects a hemodynamically significant mid-to-late diastolic coronary, flow reduction as a result of the increased resistance produced by the MB (Myocardiobridge -Table 1b).

Medical treatment

Medical treatment of symptomatic, clinically recognized myocardial bridges includes optimal doses of beta and calcium-channel blockers (control of tachycardia and antispasmodic effects) and antiplatelet agents with the objective of relieving symptoms and signs of myocardial ischemia and /or protecting against the risk of future coronary events. Negative inotropic blockers and chronotropic agents, especially beta-adrenergic receptor blockers, can reduce external vessel compression by lowering systemic and intramural pressures and can improve coronary prefusion by prolonging the period of diastole. Calcium channel blockers are especially useful if there is a contraindication to beta-blocker therapy or as primary therapy when coronary vasospasm is suspected. Nitrates have been used effectively in some patients, possibly because of their capability to reduce preload and to relieve vasospasm. Limitation of strenous physical activity is usually advised to avoid the deletrious effect of tachycardia.

Percutaeous Coronary Intervention (PCI)

Stables et al. first demonstrated, in 1995, that intracoronary stent implantation could achieve internal stabilization of the coronary artery lumen against external compression in a patient with a muscular bridge. In 1997, Klues et al. reported hemodynamic, angiographic, and IVUS data immediately and seven weeks after successful coronary stent implantation in three symptomatic patients. Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, and clinical symptoms. The CFR improved from 2.4 ± 0.5 to 3.8 ± 0.3. Coronary angiography after seven weeks revealed an identical lumen enlargement without any systolic or diastolic diameter reduction and a further increase in CFR. Intravascular ultrasound revealed no signs of neointimal proliferation within or proximal or distal to the stented segments. All patients reported remarkable clinical improvement, with increased physical activity. Favorable short-term clinical and angiographic results after coronary stenting were also reported by others.

Haager et al. recently described successful coronary stenting in 11 patients who subsequently underwent repeat coronary angiography at seven weeks and six months as well as clinical follow-up at two years. Immediately after stent deployment, quantitative coronary coronary angiography (QCA) showed absence of systolic compression, and all flow abnormalities including abrupt early diastolic flow acceleration, rapid mid-diastolic deceleration and mid-to-late plateau, and retrograde flow during systole were normalized. At seven weeks, QCA showed in-stent restenosis in 5 of 11 patients (46%). Four underwent repeat target lesion revascularization; two received coronary angioplasty and two underwent coronary bypass surgery with an internal mammary artery graft to the LAD. At two years, all remained free of angina and cardiac events. As stated by the investigators, the incidence of in-stent restenosis in these patients was not different from that of lesions of 25-mm length and relatively small-vessel calibers in coronary patients (Table 1a).
Long-term studies are necessary to evaluate the stability of stent geometry, in-stent restenosis, and clinical outcome in these patients.

Surgical treatment.

Before the current era of coronary stenting, surgical myotomy was regarded as perhaps the treatment of choice for patients with persistent symptoms despite intensive medical therapy. Indeed, cleavage of the overlying muscle fibers eliminates the phasic compression of the coronary vessel. Thus, supra-arterial myotomy for myocardial bridging and milking effect of the LAD was reported by several surgical centers. However, this approach is more invasive than that of a catheter-based intervention and probably also carries a higher risk of postprocedural complications. In addition, the unpredictable intramural course of the coronary artery may require deep incision of the ventricular wall, potentially leading to subsequent ventricular wall aneurysm. Alternatively, internal mammary artery anastomosis to the LAD may be the treatment of choice in patients with unsuccessful coronary stenting or in-stent restenosis. Likewise, patients with significant coronary disease in other vessels who require coronary bypass surgery might be suitable candidates for internal mammary artery grafting.

Conclusions.

Recent techniques available in the cardiac catheterization laboratory, such as QCA, IVUS, and intracoronary Doppler, have shown that significant myocardial bridging of a coronary artery, especially the LAD, is characterized by the following morphological and hemodynamic alterations:
1) phasic systolic vessel compression;
2) persistent diastolic lumen diameter reduction;
3) increased blood flow velocities;
4) retrograde systolic flow; and
5) reduced CFR.
These alterations, particularly in association with aggravating factors such as increased heart rate, decreased systolic blood pressure, and coronary vasospasm, may explain the occurrence of symptoms and myocardial ischemia in patients with symptomatic MB. As a rule, these patients present with symptoms and signs of ischemia, as well as a prior history of unstable angina and non-Q-wave AMI in some patients. In this respect, they are not strikingly different from patients with significant single vessel coronary disease. The severity of coronary vessel narrowing during both systole and diastole can be established by QCA and IVUS and the degree of flow velocity acceleration by intracoronary Doppler. In addition, highly specific morphological and flow velocity patterns include the "half moon" phenomenon on IVUS and the "finger tip" phenomenon on intracoronary Doppler.High-frequency intraoperative echocardiography has been used to image the intramyocardial coronary artery before (Fig. 212-10)and after surgical release. Finally, the treatment options include medical therapy in the majority of patients and stent implantation, surgical myotomy, or internal mammary artery bypass grafting in patients with persistent symptoms despite medical therapy. The long term outcome of such interventions, however, is not well known and requires further study.

Bourassa, M.G.,MD and others, Symptomatic Myocardial Bridges: Overview of Ischemic Mechanisms and Current Diagnostic and Treatment Strategies, JACC,Vol.41,No.3,2003,pp.351-358.

FIGURE 212-1 (Left) Diagram showing tunneled left anterior descending coronary artery (LAD) (arrowheads). (Right) Opened left ventricle showing intramyocardial segment. (Below) Transverse section of LV wall showing tunneled coronary artery surrounded by myocardium.

FIGURE 212-2 Diagram showing segments of tunneled and nontunneled epicardial coronary artery with changes during ventricular systole and diastole. Ao, aorta; LV, left ventricle; RV, right ventricle.

FIGURE 212-3 Tunneled epicardial coronary arteries. Two examples of tunneled left anterior descending coronary arteries. Each artery is surrounded by myocardium.

FIGURE 212-4 Transverse section of ventricular myocardium showing the "arcade" of tunneled epicardial coronary arteries (arrows). A, anterior LV, left ventricle; RV, right ventricle; P, posterior.

FIGURE 212-5 Tunneled epicardial coronary artery. A. Coronary angiogram showing tunneled segment of epicardial coronary artery. B. Corresponding segment of tunneled Left circumflex coronary artery (arrow).

FIGURE 212-6 Tunneled left anterior epicardial coronary arteries trom two newborn intants. (Left) Tunneled left anterior descending. (Right) Tunneled marginal branch of right coronary artery.

FIGURE 212-7 Diagram showing some of the clinical and anatomic factors in a tunneled epicardial artery

FIGURE 212-8 Diagram showing morphologic variations in tunneling (length of tunneled segment, depth of tunneled segment

FIGURE 212-9 Diagram showing extremes of tunneled coronary arteries: left main (LM) tunneled through the ventricular septum, total Length of the left anterior descending (LAD) located within the myocardium, tunneled segment of LAD becoming intracavitary. AV, aortic valve; LAD, left anterior descending IC, Left circumflex; LM, Left main; LV, Left ventricular; PT, pulmonary trunk; PV, pulmonary valve; RVOFT, right ventricular outflow tract; RV, right ventricle; TV, tricuspid valve.

Waller,B.F.,Hurst's The Heart,10th edition, Myocardial Bridges ,chp.39,pg.1168.

Figure 212-10 Intravascular ultrasound imaging of the myocardial bridging in diastole (A) and in systole (B). A typical half-moon-shaped echolucent area surrounds the bridge during the entire cardiac cycle (arrows). Note the catheter artifact in diastole (A) at seven o'clock.
Boorassa,M.G. and others,Symptomatic Myocardial Bridges:An Overview.JACC,Vol. 41,No.3, Feb.5.2003, pp.351-359.

Figure 212-11 Coronary angiogram of a patient with myocardial bridging of the left anterior descending coronary artery in the right anterior oblique position. (A) An absence of constriction during diastole is shown. (B) This depicts the "milking effect" during systole (arrow).
Symptomatic Myocardial Bridges:An Overview.JACC,Vol. 41,No.3, Feb.5.2003, pp.351-359.

Table 1a. Quantitative Coronary Angiography in Patients With Symptomatic Myocardial Bridges

	Schwarz et al. (12) n=15	Schwarz et al. (13) n=42	Klues et al. (14) n=12	Haager et al. (16) n=11
Systolic MLD (mm)
Proximal	2.7± 0.5	3.1 ± 1.3	2.8±0.3	2.3±0.5
Distal	2.2 ± 0.4	2.5 ± 0.8	2.2±0.3	1.8±0.4
Within MB	0.7 ± 0.3	0.8 ± 0.6	0.5±0.2	0.6±0.3
% Diameter reduction
Mean (SD)	83 ± 9	71±16	81±9	74±12
Range	71-99	-	-	55-89
Mid-diastolic MLD (mm)
Proximal	2.6±0.5	3.0±1.0	2.9 ± 0.5	-
Distal	2.4 ± 0.4	2.5±0.8	2.2 ± 0.3	-
Within MB	1.7 ± 0.3	1.7±0.4	1.6±0.4	1.4±0.4
% Diameter reduction
Mean (SD)	41 ± 11	35 ± 13	35 ± 11	34 ± 10
Range	24-58	18-69	-	22-58
Length of MB (mm)
Systolic
Mean (SD)	27 ± 8	23 ± 8	28 ± 4	25 ± 2
Range	19-44	11-44	-	13-36
Diastolic
Mean (SD)	25 ± 5	22 ± 7	27 ± 5	-
Range	21-42	-	-	-

MB = myocardial bridge; MLD = mean lumen diameter, SD = standard deviation.

Myocardiobridge-Table 1b. lntracoronary Doppler Flow Velocity Measurements at Rest in Patients With Symptomatic Myocardial Bridges

	Schwarz et al. (12) n=15	Schwarz et al. (13) n=42	Klues et al. (14) n=12	Ge et al. (15) n=48	Haager et al. (16) n=11
APV (cm/s)
Proximal	21.2 ± 7.4	18.3 ± 5.3	13.5±4.9	-	-
Distal	14.3 ± 3.2	15.6 ± 3.7	12.2±4.9
Within MB	26.7 ± 9.6	30.6 ± 16.0	27.0 ± 13.6	19.0 + 7.9	35.0 4.0
ASPV (cm/s)
Proximal	12.3 ± 4.6	10.2 ± 4.3	6.1 ± 3.7
Distal	9.1±2.3	9.6 ± 3.0	6.5±3.3
Within MB	13.7±6.6	14.0 ± 5.2	14.7 ± 9.8
ADPV (cm/s)
Proximal	25.5 ± 13.3	22.4 ± 7.7	17.3 ± 5.7
Distal	16.5±3.6	18.6±4.6	15.2 ± 6.3
Within MB	33.1 ± 13.4	38.6 ± 19.0	31.5 ± 14.3
MPV (cm/s)
Proximal	31.5 ± 13.5	33.5 ± 9.6	28.6 ± 8.8
Distal	24.3 ± 11.6	29.3 ± 7.8	24.7 ± 14.4
Within MB	78.1 ± 21.1	70.5 ± 33.7	63.7 ± 26.2	43.2 ± 18.7
DSVR
Proximal	-	2.2 ± 0.6	-	-	-
Distal	-	2.0 ± 0.5
Within MB	2.4 ± 1.0	2.5±1.2		2.9±1.4
CFR
Proximal	2.7 ± 0.8	2.9 ± 0.9
Distal	2.0 ± 0.6	2.3±0.05	2.5±0.5	2.03±0.54	2.6±-0.5

ADPV = average diastolic peak flow velocity; APV = average peak flow velocity ASPV = average systolic peak flow velocity, CFR = coronary flow reserve; DSVR = diastolic/systolic flow velocity ratio; MB = myocardial bridge; MPV = maximal
Symptomatic Myocardial Bridges:An Overview.JACC,Vol. 41,No.3,Feb.5.2003, pp.351-359.

Myocardiobridge-Table 2. Intracoronary Doppler Flow Velocity Measurements During Atrail Pacing in Patients With Symptomatic MB's

	Schwarz et al. (12) n=15	Schwarz et al. (13) n=42
APV (cm/s)
Proximal	29.1 ± 12.2	20.3 ± 6.0
Distal	20 ± 4.2	17.0 ± 4.5
Within MB	63.3 ± 21.3	46.3 ± 20.0
ASPV (cm/s)
Proximal	10.9 ± 3.4	10.9 ± 3.9
Distal	9.1 ± 4.0	10.0 ± 4.2
Within MB	16.2 ± 7.0	15.8 ± 7.5
ADPV (cm/s)
Proximal	29.1 ± 12.2	27.1 ± 9.5
Distal	20.2 ± 4.2	22.7 ± 6.6
Within MB	63.3 ± 21.2	64.7 ± 25.0
MPV (cm/s)
Proximal	34.4 ± 8.0	39.8 ± 12.3
Distal	27.8 ± 8.4	33.8 ± 8.8
Within MB	104.80 ± 35.7	104.7± 36.7
DSVR
Proximal		2.3 ± 0.4
Distal		2.7 ± 1.0
Within MB	4.9 ± 2.9	4.4 ± 2.8

Symptomatic Myocardial Bridges:An Overview.JACC,Vol. 41,No.3,Feb.5.2003,pp.351-359.

Figure 212-12 Intracoronary Doppler blood flow velocity profile showing the characteristic "finger-tip"-like flow velocity acceleration during early diastole (single arrow) followed by a plateau phase at mid-to-late diastole (arrows in A and B). During systole, there is almost no flow within the bridged segment, but a retrograde flow phenomenon occurs at the entry site of the myocardial bridge (arrows in A). During rapid atrial pacing, absolute diastolic flow velocities are increased, and the duration of the plateau phase is reduced owing to shortened diastole (C). Reproduced from Schwarz et al. (13), with permission.
Symptomatic Myocardial Bridges:An Overview.JACC,Vol. 41,No.3,Feb.5.2003,pp.351-359.

"Western Suburban Cardiology"

video of Myocardial Bridge

for broadband connection only

When coronary arteries travel below the epicardial surface, myocardial bridges may develop. During systole (heart muscle contraction), the segment of artery surrounded by the myocardium narrows as the muscle contracts. This gives an appearance of a focal narrowing or stenosis. In diastole, the artery appears normal without evidence of focal narrowing. Luckily, most coronary blood flow occurs during diastole when the heart is not actively contracting.

Most bridges are seen in the LAD distribution and are generally thought to be benign. They are present in more than 5% of otherwise normal angiograms in patients who do not have evidence of ischemia in the LAD distribution. If ischemia is proven, treatment can be provided with coronary revascularization. Infarction, while rare, can occur as demonstrated in the literature.

Clin Cardiol. 1997 Dec; 20(12): 1032-1036.
Myocardial Bridge as a Cause of Thrombus Formation and Myocardial Infarction in a Young Athlete
M. Agirbasli, M.D., G. S. Martin, M.D., J. B. Stout, M.D., H. S. Jennings, III, M.D., J. W. Lea, IV, M.D., J. H. Dixon, Jr., M.D.

This paper reports on a young male athlete who had an acute myocardial infarction after strenuous exercise. Coronary angiography demonstrated thrombus formation within a prominent myocardial bridge. Thrombus formation within a myocardial bridge may be a potential mechanism whereby this anatomic curiosity may cause a tragic clinical event.

Polish Heart Journal, June 1998, Vol XLVIII, Nr 6

JANUSZ RZEZ'NICZAK, DARIUSZ ANGERER, RYSZARD KALAWSKI, ROBERT PARUCKI, MAREK S?OMCZYN'SKI, JAROSLAW MAN'CZAK, TOMASZ SIMINIAK

[Intracoronary stent implantation for treatment of myocardial ischemia induced by myocardial bridge. A case report.]

Pracownia Badan' Serca i Naczyn, Oddzial Kardiochirurgii Szpitala im. J. Strusia w Poznaniu

Intracoronary stent implantation for treatment of myocardial ischemia induced by myocardial bridge. A case report.
A case of 69-year-old male, referred to coronary angiography due to episodes of unstable angina is presented. Angiography has shown a myocardial bridge over the left anterior descending coronary artery, causing systolic lumen reduction of 87%, and lack of atherosclerotic changes. Myocardial ischaemia produced by the myocardial bridge was confirmed by perfusion scintigraphy. Despite intensive pharmacotherapy severe symptoms were present. Coronary angioplasty followed by intracoronary stent implantation was performed. which led to decrease in systolic lumen reduction. In a 3 month follow-up the patient was free of anginal symptoms, no signs of restenosis were seen on angiography and no myocardial ischaemia was detected in perfusion scintigraphy.

Augmentation of Vessel Squeezing at Coronary-Myocardial Bridge by Nitroglycerin: Study by Quantitative Coronary Angiography and Intravascular Ultrasound

from American Heart Journal

Yoichiro Hongo, MD, Hiroshi Tada, MD, Kenichi Ito, MD, Yoshio Yasumura, MD, Kunio Miyatake, MD, Masakazu Yamagishi, MD, Cardiology Division of Medicine, National Cardiovascular Center, Osaka, Japan.

Abstract and Introduction
Abstract
Background: Nitroglycerin is known to augment vessel wall squeezing at the site with coronary-myocardial bridging (CMB). This study was designed to define the mechanism of nitroglycerin-induced augmentation of CMB in clinical settings.
Methods: We analyzed nitroglycerin reactivity at the site with CMB in 39 patients. Maximal and minimal diameters of CMB during a cardiac cycle were measured by quantitative angiography before and after intracoronary administration of 250 µg nitroglycerin. In 15 patients, CMB sites were observed by intravascular ultrasound to determine the intimal thickness and the time-serial change in vessel area.
Results: Before nitroglycerin, CMB was demonstrated with angiography in 25 patients, and the remaining 14 patients showed CMB after nitroglycerin. The maximal diameter during diastole increased from 1.4 ± 0.4 mm to 1.9 ± 0.4 mm after nitroglycerin, whereas the minimal diameter during systole decreased from 1.0 ± 0.4 mm to 0.7 ± 0.4 mm (P < .01). Thus nitroglycerin augmented the percent vessel narrowing during systole from 24% ± 21% to 65% ± 16% (P < .01). Under these conditions, intravascular ultrasound showed the reduction of the cross-sectional area of the sites with CMB by -38% ± 16% (P < .01) during systole, and this phenomenon continued to early diastole (-30% ± 16%). The intimal thickness was 0.32 ± 0.10 mm, which suggests the absence of atherosclerotic disease at CMB sites.
Conclusions: These results indicate that nitroglycerin-induced augmentation of the percent narrowing of CMB can be derived from further systolic compression of the vessel lumen as well as diastolic expansion, probably because of the increase in vessel compliance after nitroglycerin. We suggest that the delayed dilation of coronary lumen during the early diastole may contribute to the occurrence of myocardial ischemia.

Augmentation of Vessel Squeezing at Coronary-Myocardial Bridge

from American Heart Journal

Results
Before nitroglycerin, systolic blood pressure and diastolic blood pressure were 132 ± 17 and 72 ± 7 mm Hg, respectively, and were 116 ± 5 mm Hg (P < .01) and 66 ± 9 mm Hg (P < .01) after nitroglycerin. Heart rate slightly increased from 68 ± 13 to 73 ± 15 beats/min (P < .01) after nitroglycerin.

Angiographic Presence of CMB
Of 39 patients examined, CMB was demonstrated in 25 patients before nitroglycerin ( Figures 1 and 2 ). The remaining 14 patients did not show the apparent systolic coronary narrowing before nitroglycerin ( Figure 3 ). The lumen diameter of CMB sites was 1.4 ± 0.4 mm in diastole and 1.0 ± 0.4 mm in systole (P < .05). The calculated percent CMB narrowing before nitroglycerin was 24% ± 21% ( Figure 4 ).

The administration of nitroglycerin augmented the angiographic appearance of CMB ( Figures 1, 2 and 3 ), and all the patients including 14 patients who did not show CMB before nitroglycerin exhibited CMB. Under these conditions, the lumen diameter of the CMB site was 1.9 ± 0.4 mm in diastole and 0.7 ± 0.4 mm in systole (P < .01). The calculated percent CMB narrowing was 65% ± 16% (P < .01, Figure 4 ).

Morphology of CMB Observed by Ultrasound
In 15 coronary sites in which CMB was observed by intravascular ultrasound, the maximal cross-sectional area was 6.2 ± 1.5 mm2 at end diastole. At end systole, the lumen was narrowed to 3.8 ± 1.3 mm2 or by -38% ± 16% (P < .01). It was interesting that the reduction of the cross-sectional area continued to the phase of isovolumic relaxation (-30% ± 16%) when the coronary blood flow velocity was maximally accelerated ( Figure 5 ).

The thickness of the vessel wall at the sites with CMB was 0.32 ± 0.10 mm, and this indicated the absence of atherosclerotic disease at the sites of the CMB.

Interobserver and Intraobserver Variabilities
For measurement of the lumen diameter by angiography, interobserver correlation coefficient and error were 0.96 and 5.3% ± 3.8%, and intraobserver correlation coefficient and error were 0.98 and 3.0% ± 3.3%. As for the lumen cross-sectional area by intravascular ultrasound, interobserver correlation coefficient and error were 0.96 and 5.6% ± 3.3%, and intraobserver correlation coefficient and error were 0.98 and 3.6% ± 3.2%.

Discussion
Previous Studies
CMB was reported to be present in 23% of the cases examined by pathology[15] and in 0.5% to 1.5% by angiography.[1,2] Although the functional significance of CMB in myocardial ischemia is still controversial, there exists the clinical evidence for the role of CMB in provoking angina or acute myocardial infarction.[3-7] Therefore demonstration of CMB is clinically important for the determination of the cause of myocardial ischemia, particularly in patients without organic coronary stenosis.

Nitroglycerin is known to augment CMB and to increase the sensitivity to detect CMB by angiography.[12,13] According to the preliminary data by Erbel et al, [13] nitroglycerin augmented the systolic narrowing of the CMB by 29%, yielding the increase in the sensitivity for detection of the CMB. We also found that the intracoronary injection of nitroglycerin resulted in increases in percent narrowing of the CMB from 24% to 65%.

Advantage of the Study
In this study, we quantitatively evaluated the changes in coronary diameter at the sites of the CMB before and after nitroglycerin. We found a marked increase in percent narrowing of the CMB after nitroglycerin. The angiographic augmentation of the percent narrowing in systole at the sites of CMB was derived from not only increase in diastolic diameter but also decrease in systolic diameter. The increase in vessel wall compliance after nitroglycerin may contribute to the further compression of the vessel during systole and to an increase in the angiographic severity of systolic narrowing. Other factors such as change in myocardial contractility by nitroglycerin on the magnitude of systolic compression also should be considered.[16,17] However, we did not use any cardiotonic drugs during the angiographic procedure, although there remained the possibility of nitroglycerin-induced increase in cardiac contractility.[17]

By intravascular ultrasound, vessel narrowing at the cites with the CMB continued to the early diastole. Ge et al[18] have reported that there was a persistent diastolic narrowing of 41% that was caused by a delayed diastolic relaxation within the bridged segment. Krawczyk et al[19] and May et al[20] suggested that the delayed opening of the coronary vessel after systolic compression by CMB could contribute to the genesis of myocardial ischemia through the insufficient inflow time and decreased coronary perfusion pressure distal to the CMB. Under these conditions, measurement of coronary flow velocity by Doppler flow wire at CMB sites[18,19] before and after nitroglycerin might be helpful to gain an insight into to the physiologic significance of nitroglycerin-induced augmentation of CMB.

It is also interesting to point out that the vessel wall of the CMB was free from atherosclerotic disease. Continuous changes in vessel diameter may increase local shear stress,[22] contributing to preventing the occurrence of disease in the CMB segments, although the exact mechanism of this phenomenon is still unclear.

Clinical Implications and Limitations
In 14 of 39 patients, coronary angiography could not demonstrate CMB without the administration of nitroglycerin. This suggests the role of nitroglycerin in the improvement of sensitivity of the angiographic detection of the CMB. In fact, the previous study indicated that the CMB could be demonstrated by angiography in <10% of the patients examined, although pathologic examination demonstrated the presence of CMB in >20% cases studied. This may be important for the selection of the treatment because medical therapy such as a ß-blocking agents may be the first choice.[21,23] One might speculate that the evaluation of the CMB should be done after the appropriate dose of nitroglycerin.

By the observation with ultrasound, systolic narrowing of the CMB remained until the early diastole. This may be related to the fact that tachycardia that mainly shortens the diastolic period is primarily important in typical myocardial ischemia associated with CMB.[19,20] From this point of view, the ß-blocking agent is the most favorable drug to eliminate the occurrence of myocardial ischemia, although another mechanism such as reduction of myocardial contractility by ß-blockers may also be important to reduce the CMB. It is also interesting to consider whether the severity of CMB after nitroglycerin is related to the occurrence of myocardial ischemia. Further study with myocardial perfusion testing may demonstrate the significance of nitroglycerin-induced augmentation of CMB in determining the severity of myocardial ischemia in the clinical setting.

There remains a limitation to this study. The accuracy of quantitation of CMB by the single-plane dimension from angiography is limited. Actually, the mean degree of the reduction in systolic lumen diameter determined by quantitative angiography was less severe than that reported in previous studies.[2] Also, there was a difference between the cross-sectional area variation derived from intravascular ultrasound and angiography during cardiac cycles. This may be explained by the fact that the analysis of ultrasound measurements did not include the cases in whom the ultrasound transducer could not be passed through the CMB because the lumen diameter was too small.

Conclusions
The present data indicate that intracoronary nitroglycerin can improve sensitivity for the angiographic detection of CMB, where the presence of atherosclerotic disease is infrequent. This effect of nitroglycerin appears to be derived from further systolic compression of the vessel lumen as well as diastolic relaxation probably caused by the increase in vessel wall compliance. We suggest that the delayed dilation of coronary lumen during early diastole may contribute to the occurrence of myocardial ischemia.

High-Resolution Imaging of Myocardial Bridging

Panel A shows by arrow the results of coronary angiography demonstrating a myocardial bridge, which decreases the diameter of the left anterior descending coronary artery during systole. Optical coherence tomography showed no evidence of atherosclerosis. Instead it did show vessel patency during diastole (Panel B) and collapse during systole (Panel C).

The above images are from the New England Journal of Medicine 358;4, page 392, January 24, 2008 by Dirk Bose,M.D. and Sebastian Philipp, M.D.