Myocardial bridges (MBs) are recognized angiographically by the characteristic narrowing of the coronary lumen occurring predominantly during systole.1–4 The incidence of angiographically-proven MB is between 0.5–12%.2,3 Although MBs are mostly confined to the left anterior descending coronary artery (LAD),1,4 several cases of right coronary artery (RCA) myocardial bridge have been reported in the literature.5–8 Most of the MBs seen in pathological examinations are invisible on angiography because only the deep type of bridges may be apparent with this imaging modality.9 Although known as a benign and asymptomatic condition in a majority of the patients, MBs may cause angina, myocardial ischemia, life-threatening cardiac arrhytmias and even sudden cardiac death.10–12 We present here the case of a 65-year-old female with a well-functioning mechanichal mitral valve prosthesis, severe pulmonary hypertension and right ventricle wall motion abnormality in whom diagnostic angiography revealed MB confined to the right ventricular branch of the right coronary artery. Case Report In June 2005, a 65-year-old female was admitted to the coronary care unit with the complaints of chest pain on exertion and paroxysmal nocturnal dyspnea. Her past medical history revealed mechanichal mitral valve replacement in 1996 (St. Jude Medical mechanical prosthesis, no. 27) due to severe mitral insufficiency. On physical examination, her arterial blood pressure was 100/80 mmHg; her heart and respiration rates were 86 beats per minute (irregular) and 28 per minute, respectively. During palpation of the chest, we observed right ventricular lift in the left lower sternal area. Cardiac auscultation showed 2–3/6 grade holosystolic murmur in the left lower sternal area, 1–2/6 grade holosytolic murmur, a closing click of the mechanichal mitral valve in the apical region, and loud pulmonic valve closure combined with 2/6 grade systolic murmur. On the resting ECG, right ventricular hypertrophy, significant right axis deviation and atrial fibrillation were present. Bedside transthoracic echocardiography revealed severe pulmonary hypertension (60 mmHg) and a well-functioning mechanichal mitral valve with mild mitral regurgitation. We also detected mild-to-moderate hypokinesia in the free wall of the right ventricle, accompained by right ventricular hypertrophy. In order to determine the origin of her chest pain associated with a right ventricular wall motion abnormality, we performed diagnostic coronary angiography. During angiography, the right coronary artery dye injection clearly showed severe MB confined to the right ventricular branch of the right coronary artery (Figures 1 and 2). However, the left coronary system was angiographically normal. She was then disharged with the medical treatment including calcium channel blocker (a daily dose of 120 mg diltiazem) and a daily dose of 5 mg warfarin with Class II functional capacity. The patient has been asymptomatic on calcium channel blocker at 6-month follow up. Discussion The coronary arteries may deep into the myocardium and then reappear on the surface of the heart.1,4 MB is defined as the intramural course of a major epicardial coronary artery and is usually confined to the left ventricle and LAD.1,4 Although the most frequent location of MB is on the LAD, a few cases of right ventricular MB have been published in the medical literature up to now.5–8 Hence, the data about right ventricular MBs are limited only to several case reports. The usual location of MBs in the RCA is reported to be in the posterior descending coronary artery, and coronary luminal constriction is usually related to hypertrophic left ventricular myocardium.5 However, our patient did not have MB in the posterior descending coronary artery and also did not have hypertrophic cardiomyopathy involving the left and/or right ventricle. Systolic collapse of the right ventricular branches of the RCA has been reported in only two cases.6,7 The patients presented in these reports also had chronic obstructive lung disease and pulmonary hypertension.6,7 To the best of our knowledge, systolic obliteration of the right ventricular branches is not expected unless there is right ventricular systolic hypertension together with anatomical abnormality. Woldow et al8 reported a patient with chronic obstructive lung disease and dilated cardiomyopathy who had systolic constriction of the RCA beyond the crux. In that report, the patient had no chest pain. However, our patient had chest pain, probably due to systolic compression in the right ventricular branch of the RCA associated with severe pulmonary hypertension. Also, in our patient, the location of the MB was in the right ventricular branch of the RCA, and the patient did not have chronic obstructive lung disease as in the above-mentioned case. On the other hand, it is unusual to find isolated RCA bridging without an associated similar pathology in the LAD. The present case had no MBs except from the right ventricular branch of the RCA. However, since our patient did not undergo cardiac surgery, no direct visual inspection of the right coronary artery could be made, and as a result, we were not able to visually confirm the presence of MB in the right ventricular branch of the RCA. To our knowledge, the current case is the third report of significant, angiographically-proven systolic constriction of the RCA in a patient with chest pain and significant pulmonary hypertension. Although MBs are most frequently seen in the LAD, all cardiologists should not forget that MBs in the RCA, which might cause myocardial ischemia, can be found in patients with pulmonary hypertension during coronary angiography. This case report is presented to inform cardiologists of the existence of this unusual clinical and angiographic entity.
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