Muskelbr�cken der Koronararterien: m�gliche isch�mierelevante Normvarianten

Abstract

Approximately 20-30% of patients with cardiac chest pain have a normal coronary angiogram. In about 5% of these patients, a myocardial bridge can be identified. The characteristic feature is systolic compression of an epicardial vessel, usually the left anterior descending artery (LAD), with the angiographic "milking effect". Using modern imaging techniques, such as intravascular ultrasound (IVUS), intracoronary Doppler ultrasound (ICD) and intracoronary pressure wires, the pathophysiological consequence of myocardial bridging could be established. While previously considered a clinically insignificant variant, ICD recordings demonstrated an increased flow velocity in the tunneled segment. Frame-by-frame IVUS analysis revealed a delayed relaxation after systolic compression, which may extend significantly into diastole. This explains both the impaired coronary flow reserve and ischemia. In IVUS, a circular or eccentric rhythmic compression of the vessel is visible, which may be partial or complete. Latest computed tomography technology can also be used to visualize myocardial bridging noninvasively. Provocation tests, such as application of nitroglycerin, orciprenaline, dobutamine or atrial stimulation, may augment systolic compression and explain symptoms and the beneficial effect of beta-blockers. In severe cases (i.e. limiting symptoms with ischemia despite medication), surgical myotomy may be performed after careful appraisal of the benefit-risk ratio. A high restenosis and complication rate associated with coronary stenting precludes a general recommendation of this interventional approach. Whether drug-eluting stents help to overcome this limitation remains to be shown. Long-term prognosis is good, although previous investigations have been performed in a limited number of cases only.

Oscillatory flow in a tube with time-dependent wall deformation and its application to Myocardial Bridges

“…Published data from patient studies and experiments in [14,16,17] show good qualitative and quantitative agreement to our simulations. A similar set of parameters was used to compare the peak flow velocities which in our simulations are u s1 = 24.2 cm/s proximal, u s2,s4 = 86 cm/s within, and u s5 = 26.5 cm/s distal the bridge.…”

“…We applied an exponential flow wave with amplitude q 0 = 400 cm 3 /s and attack time of τ = 0.14 s to the aorta, resulting in a total cardiac output (CO) of 5.25 l/min. The time dependent part of the deformation function along the z-axis f z (t) was assumed to be periodic (see measurements in [16]) and is approximated by f z (t) = 3 n=1 0.8 n sin(n ω (t+ t)+φ n ). Here t is the time shift with respect to the cardiac cycle and the phases φ n in radian were chosen to be φ 1 = 3.5, φ 2 = 1.5, and φ 3 = 3.9.…”

Angiographic and Clinical Characteristics according to Intracoronary Acetylcholine Dose in Patients with Myocardial Bridge

“…First, previous studies proposed that symptomatic MB itself is one of the causes and long MB was a major risk factor of readmission [8]. The length of coronary arterial narrowing influences coronary hemodynamics and a delayed diastolic phase in cases of longer MB may contribute to myocardial ischemia [9]. Second, as an alternative mechanism, CAS associated with MB has been suggested.…”

Myocardial bridging is a potential risk factor of very late stent thrombosis of drug eluting stent

“…MB’s prevalence has been reported to range between 5.4% and 85% in autopsy series and 0.5–29.4% on coronary angiography [20]. Although it is clinically silent in the majority of cases, approximately 20–30% of patients with cardiac chest pain have a normal coronary angiogram, and in about 5% of these patients an MB can be identified [21]. In other words, MB is common, but its pathophysiological response is always ignored.…”