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Myocardial bridging has been observed to provoke symptoms in association with strenuous physical activity and hypertrophic cardiomyopathy; more recently, bridging has been thought to cause coronary vasospasm. Autopsy findings tend to reveal higher incidences of bridging than do angiography series, but both show an almost uniform predilection for left coronary artery distribution—especially in regard to bridging that manifests itself clinically. Herein, we report an unusual case of myocardial bridging with right coronary artery distribution and important clinical implications for physicians' management of similar cases in the future.
The phenomenon of coronary artery bridging has been recognized for several centuries and was described on cineangiography as early as 1960.1 The pathologic impact of bridging on coronary physiology has been the subject of considerable debate. Myocardial bridging has been observed to provoke symptoms in association with strenuous physical activity and hypertrophic cardiomyopathy; more recently, bridging has been thought to cause coronary vasospasm.2
Autopsy findings tend to reveal higher incidences of bridging than do angiography series, but both show an almost uniform predilection for left coronary artery distribution.3 The angiographic evidence of myocardial bridging depends upon a variety of factors, including but not limited to the thickness and the length of the myocardial bridge, the presence of loose connective or adipose tissue around the bridged segment, the state of myocardial contractility, the nature of the tissue interposed between the coronary artery and the myocardium, and the observer's experience.2 Hence, many examples of bridging, including involvement of the left circumflex artery and the right coronary artery, may go unrecognized.
Herein, we report an unusual case of myocardial bridging with right coronary artery distribution and important clinical consequence.
In February 2006, an 81-year-old woman presented emergently at an outlying community hospital with chest pain of 4 hours' duration, in association with jaw tightness and dyspnea during showering. She had a history of aortic regurgitation and hyperlipidemia. Recently, she had taken pseudoephedrine for bronchitis. Her initial electrocardiographic evaluation in the emergency department showed ST-segment elevation in the inferolateral leads with reciprocal anterior ST-segment depressions (Fig. 1). A presumed diagnosis of inferolateral myocardial infarction was made, and the patient experienced minimal relief of symptoms with the administration of aspirin, sublingual nitroglycerin, and a thrombolytic agent.
She was transferred to our tertiary care facility for further evaluation and treatment. During transit, the patient experienced another brief episode of chest pain with jaw tightness, which showed similar dynamic electrical changes on telemetry. Upon her assessment by our cardiology service, the following agents were added to her previous regimen: an angiotensin-converting enzyme inhibitor, a β-blocker, a hydroxymethylglutaryl-CoA reductase inhibitor (statin), and a glycoprotein IIb/IIIa receptor inhibitor. Despite this, symptoms recurred during early observation in the coronary care unit, and urgent left heart catheterization was performed. Those cineangiographic findings are shown in Figures 2 and and33.
The angiograms showed normal-caliber left main, left anterior descending, and left circumflex vessels, without focal obstructive lesions. In the right coronary anatomy, the angiograms revealed substantial myocardial bridging in the 2nd posterolateral branch and some degree of bridging in the 1st posterolateral branch. Systolic obliteration and diastolic filling were seen; no transluminal intervention was performed. The systolic obliteration persisted despite intracoronary nitroglycerin administration. During catheterization, the left ventricular ejection fraction was 0.55 without any wall-motion abnormality, and the left ventricular end-diastolic pressure was 18 mmHg. Upon completion of angiography, the patient was returned to the telemetry unit without complication. We made an empirical diagnosis of symptomatic myocardial bridging with superimposed coronary vasospasm. In addition to continued β-blocker therapy, we prescribed a non-dihydropyridine calcium channel blocker to reduce heart rate and myocardial contractility. The angiotensin-converting enzyme inhibitor was discontinued.
During this patient's brief hospital course, her symptoms were rapidly controlled and suppressed without hemodynamic consequence. Serial tests of cardiac enzymes, including troponin and creatine kinase, showed normal levels except for creatine kinase-MB, which was elevated. This elevation was attributed to periods of vasospasm, presumably due to the effect of pseudoephedrine on myocardial bridge segments. In addition, 2-dimensional echocardiography, performed on hospital day 2, revealed normal left ventricular function (ejection fraction of 0.55 with no wall-motion abnormality), moderate-to-severe aortic regurgitation, and mild aortic stenosis. After an uneventful course, the patient was discharged from the hospital on oral β-blocker and calcium channel blocker therapy. She continued to be asymptomatic at the 3-month follow-up visit with her primary care physician; however, she died at home 6 months after the hospitalization.
Myocardial bridging occurs when a segment of the coronary artery takes an intramural course. This phenomenon was first described by Reyman in 1737.4 The epicardial artery is compressed during each systole and relaxes in diastole. The incidence of myocardial bridging ranges widely, from 5% to 80% in autopsy studies, whereas angiography series have recorded incidences ranging from 0.5% to 12%.5 The inclusion of epicardial artery loops with myocardial bridging accounts for the much higher incidence in autopsy series.
Numerous manifestations of myocardial bridging have been described: angina, myocardial infarction, arrhythmias, and sudden cardiac death.3 Chest pain in myocardial bridging has its pathophysiologic origin in vasospasm, vessel thrombosis, and (rarely) shear stress due to atherosclerosis.6 Our patient's ST-elevation myocardial infarction could have arisen from myocardial bridging with severe spasm, thrombi cleared by thrombolytic treatment, or emboli. Myocardial bridging of the left anterior descending artery is not uncommon and continues to be a subject of investigation and reporting interest. Our review of the medical literature shows that right coronary artery distribution bridging is indeed a rare occurrence, at least in regard to focal clinical presentation.7–9 We believe that further investigation into coronary vasospasm may reveal a higher incidence of bridging as a proximate cause.
It should be noted that our patient's consumption of pseudoephedrine for bronchitis a few days before hospital admission may have contributed to her clinical presentation. Amphetamine-induced spasm of a bridged coronary artery has been described previously, in a single case report.10 By using a 6F catheter to compare our patient's 2 small posterolateral branch segments of right coronary artery by means of quantitative coronary analysis by computer, we determined that these vessels were approximately 1.5 mm in diameter. Thrombosis or prolonged spasm of such small branches can cause myocardial infarction. We also noted no apical ballooning or basal contractility of the left ventricle on catheterization and echocardiography.
There is no real consensus regarding the treatment of myocardial bridging. Reported treatment has included medical management with β-blockers11,12 and calcium channel blockers. Nitroglycerin may worsen symptoms by reducing intrinsic coronary wall tension and increasing reflex sympathetic stimulation of contractility, so its use is controversial.3 Our patient had received nitroglycerin before being transferred to our tertiary facility. Stenting, although performed in selected cases, may not be beneficial, because compression of the stented segments can lead to stent thrombosis, restenosis, and stent fractures.13 Resection of the myocardial bridge and coronary artery bypass grafting have been reported in the surgical literature.14
Recent intravascular ultrasonographic and enhanced computed tomographic techniques are yielding further physiologic and anatomic insights into clinically relevant myocardial bridging.15 These improved diagnostic methods will doubtless increase the reported incidence of bridged coronary segments. The direct correlation between myocardial bridging and ischemic symptoms has been clarified and is now established.16,17 Notably, there has been recent encouragement of selective repair of myocardial bridged segments in patients with hypertrophic cardiomyopathy,18 although no consensus has been achieved. It is our hope that future investigations will consolidate the diagnosis and management of symptomatic myocardial bridging, which would benefit a substantial portion of the population that has anginal symptoms.
Address for reprints: Trung H. Nguyen, MD, University of Kansas Medical Center, IM Medical Education, MS 2027, 3901 Rainbow Blvd., Kansas City, KS 66160. E-mail: ude.cmuk@2neyugnt