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S. Rizzo et al.

den death. Cardiovasc Pathol. 1994;3:269–71. https://

doi.org/10.1016/1054- 8807(94)90013- 2.

60. Thiene G, Ho SY.Aortic root pathology and sudden death in youth: review of anatomical varieties. Appl Pathol. 1986;4:237–45.

61. Basso C, Corrado D, Thiene G. Congenital coronary artery anomalies as an important cause of sudden death in the young. Cardiol Rev. 2001;9(6):312–7.

62. Basso C, Corrado D, Thiene G. Coronary artery anomalies and sudden death. Card Electrophysiol Rev. 2002;6(1–2):107–11.

63. Basso C, Maron BJ, Corrado D, Thiene G. Clinical prole of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. J Am Coll Cardiol. 2000;35(6):1493–501.

64. Frescura C, Basso C, Thiene G, Corrado D, Pennelli T, Angelini A, etal. Anomalous origin of coronary arteries and risk of sudden death: a study based on an autopsy population of congenital heart disease. Hum Pathol. 1998;29:689–95. https://doi.org/10.1016/

S0046- 8177(98)90277- 5.

65. Burke AP, Farb A, Virmani R, Goodin J, Smialek JE.Sports-related and non-sports-related sudden cardiac death in young adults. Am Heart J. 1991;121(2 Pt 1):568–75.

66. Angelini P, Cheong BY, Lenge De Rosen VV, Lopez A, Uribe C, Masso AH, et al. High-risk cardiovascular conditions in sports-related sudden death: prevalence in 5,169 schoolchildren screened via cardiac magnetic resonance. Tex Heart Inst J. 2018;45(4):205–13.

67. Cheitlin MD, MacGregor J.Congenital anomalies of coronary arteries: role in the pathogenesis of sudden cardiac death. Herz. 2009;34(4):268–79.

68. Taylor AJ, Rogan KM, Virmani R. Sudden cardiac death associated with isolated congenital coronary artery anomalies. J Am Coll Cardiol. 1992;20(3):640–7.

69. Corrado D, Thiene G, Cocco P, Frescura C. Nonatherosclerotic coronary artery disease and sudden death in the young. Br Heart J. 1992;68(6):601–7.

70. Cheitlin MD, De Castro CM, McAllister HA.Sudden death as a complication of anomalous left coronary origin from the anterior sinus of Valsalva, A not-so-minor congenital anomaly. Circulation. 1974;50(4):780–7.

71. Thiene G, Basso C, Favretto D, Rizzo S.Sudden death in athletes: autoptic ndings. In: Delise P, Zeppilli P, editors. Sport-related sudden cardiac death. Cham: Springer; 2022. p.85–7.

72. Elias MD, Meza J, McCrindle BW, Brothers JA, Paridon S, Cohen MS. Effects of exercise restriction on patients with anomalous aortic origin of a coronary artery. World J Pediatr Congenit Heart Surg. 2017;8(1):18–24.

73. Basso C, Burke M, Fornes P, Gallagher PJ, de Gouveia RH, Sheppard M, etal. Guidelines for autopsy investigation of sudden cardiac death. Virchows Arch. 2008;452(1):11–8.

74. Basso C, Aguilera B, Banner J, Cohle S, d’Amati G, de Gouveia RH, etal. Guidelines for autopsy investigation of sudden cardiac death: 2017 update from the Association for European Cardiovascular Pathology. Virchows Arch. 2017;471(6):691–705.

Normal Coronary Flow Physiology

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CarloTrani, CristinaAurigemma, andFilippoCrea

Introduction

The heart is the unique organ responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood ow is quite complex and, after over 100years of dedicated research, is understood to depend on multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal inuences [1]. Each of

C. Trani (*) · F. Crea Dipartimento di Scienze Cardiovascolari, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy

Università Cattolica del Sacro Cuore, Rome, Italy e-mail: carlo.trani@unicatt.it; lippo.crea@unicatt.it

C. Aurigemma Dipartimento di Scienze Cardiovascolari, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy e-mail: cristina.aurigemma@policlinicogemelli.it

these determinants can have a profound inuence on myocardial perfusion, largely through effects on end- effector ion channels and collectively modulate coronary vascular resistance and act to ensure an adequate refueling of oxygen and substrates. Owing to the limited anaerobic capacity of the heart, coronary vascular resistance is continuously regulated to deliver sufcient quantities of oxygen to meet any change in the demand of surrounding myocardial tissue (Fig.3.1).

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Fig. 3.1 Determinants of coronary blood ow

Physiology ofMyocardial BloodFlow

The coronary circulation is divided into three compartments, the large epicardial conduit vessels (proximal compartments with vessels range from 5.0 to 0.5mm), the prearterioles (intermediate compartments with vessels range from ≈500 to 100 μm) and the arterioles (distal compartments with vessels diameters <100 μm) (Fig.

3.2). The conduit vessels exert little resistance to

ow, indeed resistance to ow progressively rises in prearterioles and arterioles. The vasomotor actions of the prearterioles are independent of diffusible myocardial metabolites, but are more responsive to changes in ow (in proximal prearterioles, 500–150μm) and in pressure (in distal prearterioles, 150–100μm). Instead, the tone of arterioles depends on substances produced by the surrounding cardiac myocytes, representing the place of metabolic regulation of coronary ow [2]. Flow across the myocardium largely depends on the pressure gradient between the aortic root and the right atrium (the “coronary driving pressure”). Under normal conditions, the driving pressure is fully maintained along the epicardial conduit vessels with little if any pressure loss in the distal epicardial arteries. However, intra-coronary pressures decline along the microvasculature (with most of the pressure dissipating in the 300–100 μm diameter vessels) until reaching a pressure of 20–30mmHg, still adequate to main-

C. Trani et al.

Fig. 3.2 The main anatomic features of the coronary circulation

tain a gradient across the capillaries. Extravascular resistive forces, that are directly related to the left ventricular systolic pressure, the contractile state of the myocardium, and the heart rate, represent additional determinants of the resistance to ow. The interaction between intra-coronary driving pressure and microvascular resistance is coordinated by auto-regulatory mechanisms in order to maintain adequate ow across the capillaries. The ow is mathematically described in the vascular system as a correlate to Ohm’s Law

3 Normal Coronary Flow Physiology

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(Flow = ΔPressure/Resistance). Therefore, through this regulatory mechanism, dened “coronary autoregulation”, decreases in driving pressure are compensated by decreases in resistance and conversely, increases in driving pressure by increases in resistance, so that ow remains constant for a given cardiac workload. This regulatory mechanism operates within the range of physiologic arterial pressures (60 and 200mmHg) but fails during hypotension when ows become strongly dependent on the driving pressure [3].

The specics of metabolism-perfusion matching are unique in the coronary circulation because of the continuous pumping and high workload of the heart. Based on a constantly functioning contractile machine, the heart demonstrates the highest per gram oxygen consumption of any organ (~50–100μLO2/min/g) and, as such, extracts ~70–80% of delivered oxygen even under resting conditions (coronary venous PO2 ~ 18–20 mmHg), unlike skeletal muscle which utilizes only ~30–40% of delivered oxygen at rest (venous PO2~ 40 mmHg) [4]. This high extraction percentage results in a system that is almost completely dependent on the delivery of blood to the tissue as enhancements to extraction are rather limited. Therefore, coronary vascular tone must be constantly modulated to ensure adequate myocardial perfusion. This point is evident in examination of coronary responses to a variety of physiologic perturbations including alterations in metabolism, perfusion pressure, arterial oxygen content, and/or a transient coronary artery occlusion. These wellestablished phenomena clearly illustrate the tight coupling between coronary blood ow and myocardial oxygen consumption (MVO2) in response to exercise. Indeed, in non-diseased coronary vessels, whenever cardiac activity and oxygen consumption increase there is an increase in coronary blood ow that is nearly proportionate to the increase in oxygen consumption (functional hyperemia) [5]. Coronary blood ow analogously increases in response to the repayment of “oxygen- debt” occurring following the interruption of myocardial oxygen, such as a transient coronary artery occlusion (reactive hyperemia) [6]. Work-related ow increases are

initiated by a metabolically mediated decrease in microvascular resistance, involving adenosine and causing vascular smooth muscle relaxation [7]. The resulting ow is augmented by endothelium- dependent factors; higher ow velocities exert greater shear stress upon the endothelium with stimulation of the endothelial nitric oxide synthase (eNOS) and release of the smooth muscle- relaxing nitric oxide (NO). In this scenario, endothelial cells closely interact with vascular smooth muscle cells in order to adjust the vessel diameter to changes in ow velocities (“ow- mediated dilation”), both at the level of the microvessels and the epicardial conduit vessels.

In the majority of organs, the compressive tissue force is constant and therefore its contribution to the pressure gradient is only minimal yet consistent. Instead, the pattern of ow in the coronary vascular system is more complex due to the periodicity of contractions in the heart and tremendous compressive forces of the myocardium. Coronary vascular ow is described as phasic ow in that the compressive forces of systole counteract the driving force for ow in the coronary circulation and, therefore, the majority of anterograde blood ow to the left ventricle occurs during diastole (Fig.3.3) [8]. The physiologic interaction between myocardial contraction and the phasic nature of coronary ow is further

Fig. 3.3 Phasic trace of coronary blood ow

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Fig. 3.4 Schematic cross-section of the myocardial wall at end-diastole and end-systole. (Figure modied from Bell JR, Fox AC.Pathogenesis of subendocardial ischemia. Am J Med Sci. 1974; 268:3–13)

C. Trani et al.

complicated by the disparity in compressive forces across the wall of the left ventricle, as described in the early 1950s by Rushmer [9]. The greatest degree of vascular compression is found in endocardial layers, with little if any compressive force at the level of the epicardium (Fig.3.4). This disparity leads to a reduced blood ow in endocardial tissue during systole as the compressive forces are of sufcient magnitude to exceed the driving force of arterial pressure. Thus, the endocardium only receives ow during diastole and is therefore extremely dependent on an adequate diastolic lling period to maintain sufcient coronary ow. By contrast, the lack of compressive forces at the epicardial layer allows for perfusion throughout the entire cardiac cycle. Therefore, there is a linear decrease in dependence on diastolic time fraction for the maintenance of coronary ow in the endocardial to epicardial direction [10]. Given the higher compressive forces and oxygen requirements of the left ventricular endocardium, there is a gradient for coronary ow across the wall of the heart. Typically, epicardial to endocardial ow ratio ranges from ~1.1–1.5 and is only partially compensated by the higher density and the lower resistance of the endocardial microcirculation. As such, the left ventricle receives ~80% of its blood supply during diastole whereas the much thinner right ventricle, which is subject to much lower myocardial tissue pressures, is primarily perfused during systole.

Coronary Flow Assessments

Maximum hyperemic ows reect the total vasodilator capacity of the coronary circulation. Blood ow during pharmacologically stimulated vasodilation strongly depends on the driving pressure, therefore the ratio of mean arterial blood pressure over myocardial blood ow, dened as minimal coronary vascular resistance (CVR), represents an index of the coronary vasodilator capacity that is however normalized to the perfusion pressure. The coronary (or more appropriately, myocardial) ow reserve (CFR) is also been accepted as another measure of the vasodilator capacity. It reects the ratio of hyperemic over rest myocardial blood ow, which limits its accuracy because it not only reects the maximally achieved hyperemic blood ow, but depends also on myocardial blood ow at rest. In patients with hypertension, for example, ows at rest are elevated due to the higher myocardial work so that even when hyperemic blood ows are in the range of normal, the actual ow reserve may be diminished. Therefore, resting blood ow is adjusted to cardiac work by normalizing ows to the rate pressure product. The CFR is reported as the ratio of hyperemic to “normalized” resting blood ows [3] and it is considered an index of microvascular function with a cutoff >2.0. The index of microcirculatory resistance (IMR) is an invasive quantitative assessment of the minimum microcirculatory resistance in a target coronary artery territory. The IMR is dened as the ratio

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Fig. 3.5 Coronary ow assessments: coronary ow reserve (CFR) and index of microcirculatory resistance (IMR)

between the distal intracoronary pressure (Pd) and the inverse of the hyperemic mean transit time (Tmn). Because IMR incorporates only hyperemic parameters, it eliminates the variability of hemodynamics and resting vascular tone and estimates the minimum achievable microvascular resistance. Importantly, IMR is based on indirect measurements of coronary ow using Tmn, in contrast to CFR, based on direct measurements of coronary ow velocity [11]. IMR is used as a marker of microvascular dysfunction with a cutoff ≥25 (Fig.3.5).

rate and systolic blood pressure together with local norepinephrine release from adrenergic nerve terminals in the coronary circulation. The increase in myocardial work, as reected by the increase in the rate pressure product, is under normal conditions associated with a proportionate increase in myocardial blood ow [13]. A metabolically induced work-related increase in ow is augmented by endothelium-related vasodilator forces. Indeed, vasoconstrictor effects on the vascular smooth muscle mediated by adrenergic stimulation are balanced by largely endothelium- related vasodilator forces affecting

Vasodilator Stress Pharmacological stress with vascular smooth muscle relaxing agents (e.g. dipyridamole, adenosine, adenosinetriphosphate, and more recently, adenosine receptor subtype A2A agonists like regadenoson) reduce maximally the vascular resistance through relaxation of the vascular smooth muscle cell at the level of the microcirculation, thereby uncoupling coronary ow (supply) from myocardial work (demand). Flows during vasodilatorinduced hyperemia then depend largely on the coronary driving pressure and, thus, on the arterial blood pressure, and the residual coronary

both the microvasculature and the epicardial conduit vessels. The endothelium-dependent modulation of ow during sympathetic stimulation corresponds to the endothelium-related ow augmentation during pharmacologically stimulated hyperemia. For example, in healthy subjects without coronary risk factors, the change in vascular resistance in response to cold pressor testing is signicantly correlated with the adenosine- or dipyridamole-induced decline in CVR, suggesting proportionate contributions of endothelium-related mechanisms to both types of ow responses [3].

resistance [12].

Positive Inotropic Stimulation Pharmacologic

Sympathetic Stress Sympathetic stimulation,

such as cold pressor testing, more specically targets endothelium-related determinants of the coronary circulatory function. It increases heart

inotropic stimulation is an alternate to physical stress. Intravenous administration of dobutamine, a synthetic sympathomimetic amine with a dominant positive inotropic effect via stimulation of

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C. Trani et al.

β- and α-adrenoreceptors, produces signicant increases in MVO2 and consequently commensurate increases in myocardial blood ow. The dobutamine-induced changes in MVO2 are closely correlated to changes in myocardial work and, further, myocardial blood ow [14].

Coronary Artery Anomalies: Eect onCoronary Flow

The pathophysiology of anomalous coronary arteries originating from the opposite sinus of Valsalva (ACAOS) is not well understood. Anatomic high-risk features of slit-like ostium and proximal narrowing are not only relevant due to the reduced cross-sectional area (CSA), compared with a round vessel shape, but also due to higher resistance. Decreasing CSA increases the resistance, as a function of the height/width ratio. Furthermore, the intramural length directly increases resistance to ow (Fig.3.6). Therefore, the increased resistance along the anomalous segment, due to the progressive deformation, results in compensatory coronary vasodilatation for the preservation of adequate perfusion at the expense of decreased CFR [15]. A two-tier concept for the pathomechanisms of ischemia in ACAOS based on the combination of a xed

(anatomic high-risk features of slit-like ostium and proximal narrowing) and a dynamic (acute take-off angle, intramural course with the elliptic vessel shape) component is recently proposed [15]. In previous studies, none of the anatomic features correlated with ischemia, indicating a complex interaction between the different components [16]. In addition, the hemodynamic relevance depends directly on the supplied viable myocardial mass downstream of the stenosis, providing an explication for the diverging prognosis of right and left ACAOS.Moreover, ischemia is unlikely to occur every time, suggesting the presence of additional factors such as volume status and type of physical activity [17].

Fixed Component Slit-like ostium and proximal narrowing are present at rest and behave in a similar manner to classic coronary lesions. The reduction of the CSA creates ow restrictions, which can be evaluated by coronary angiography or intravascular imaging and/or the pressure gradient over the stenotic segment. Fractional ow reserve (FFR) with hyperemia induced by pharmacological vasodilatation (i.e. adenosine) was used to assess the hemodynamic relevance of ACAOS in multiple studies, but only a poor correlation with symptoms and/or anatomic features could be documented [18]. Indeed, these studies

Fig. 3.6 The impact of deformed vascular shape, such as lateral compression, on coronary ow. Decreasing crosssectional area is associate to increasing resistance as a function of the height/width ratio in a vessel with a xed circumference is calculated (a theoretical model with the limitation that deformation will rarely result in a perfect

elliptic shape). (Figure modied from Bigler MR, Ashraf

A, Seiler C, Praz F, Ueki Y, Windecker S, Kadner A, Räber L, Gräni C. Hemodynamic Relevance of Anomalous Coronary Arteries Originating From the Opposite Sinus of Valsalva-In Search of the Evidence. Front Cardiovasc Med. 2021 Jan 21;7:591326)

3 Normal Coronary Flow Physiology

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assessed the xed component alone but the dynamic component cannot be sufciently reproduced using pharmacological stress with vasodilators.

Dynamic Component Anatomic features like acute take-off angle or lateral compression in the intramural segment have hemodynamic relevance during exercise. After the increase in heart rate, an increase of systolic blood pressure, myocardial contractility, systolic expansion, and higher wall stress of the proximal aorta can be observed because of increased dP/dt and stroke volume [19]. These modications increase lateral compression of the intramural segment and subsequent ow resistance, affecting CFR during conditions of increased myocardial oxygen demand. This phenomenon causes myocardial ischemia that cannot be triggered by vasodilatory drugs alone. Hence, assessment of the hemodynamic component of ACAOS should be performed preferably by physical exercise or dobutamine, which increases heart rate and stroke volume. Of note, in multiple studies, FFR dobutamine was usually lower than FFR adenosine, revealing the inconstant presence of the dynamic component [20]. Increasing age, thickening, and stiffness of the aortic wall decrease distensibility, and thus, the dynamic component loses its relevance. These ndings are in line with the autoptic studies that reported a decreased risk of sudden cardiac death beyond the age of 30 [16].

Stress Testing The ideal stress test for ACAOS in patients with suspected angina should be able to assess both dynamic and xed components. Stress tests based on vasodilators (i.e. adenosine or regadenoson) fail to assess the dynamic components (i.e. dynamic lateral compression of the intramural abnormal coronary artery) and therefore may provide false negative results. Dobutamine stress test is more adequate to test both xed and dynamic components. Unfortunately, dobutamine stress test typically achieves less than 85% of the maximal heart rate and does not result in a substantial increase in blood pressure. Therefore, a dobutamine stress test sensitized by saline infusion to prevent pre-

load decrease and by atropine administration to reach 100% of the maximal heart rate, has been proposed [16]. This enhanced dobutamine stress test should be considered in patients with suspected angina and ACAOS, in particular in athletes, to predict the risk of ischemia-induced sudden death during strenuous physical exercise.

References

1. Goodwill AG, Dick GM, Kiel AM, Tune JD. Regulation of coronary blood ow. Compr Physiol. 2017;7(2):321–82.

2. Kaski JC, Crea F, Gersh BJ, Camici PG.Reappraisal of ischemic heart disease. Circulation. 2018;138(14):1463–80.

3. Schelbert HR.Anatomy and physiology of coronary blood ow. J Nucl Cardiol. 2010;17:545.

4. Duncker DJ, Bache RJ. Regulation of coronary blood ow during exercise. Physiol Rev. 2008;88:1009–86.

5. Berwick ZC, Dick GM, Moberly SP, Kohr MC, Sturek M, Tune JD.Contribution of voltage-dependent K(+) channels to metabolic control of coronary blood ow. J Mol Cell Cardiol. 2012;52:912–9.

6. Berwick ZC, Payne GA, Lynch B, Dick GM, Sturek M, Tune JD. Contribution of adenosine A(2A) and A(2B) receptors to ischemic coronary dilation: role of K(V) and K(ATP) channels. Microcirculation. 2010;17:600–7.

7. Lupi A, Buffon A, Finocchiaro ML, Conti E, Maseri A, Crea F. Mechanisms of adenosine-induced epicardial coronary artery dilatation. Eur Heart J. 1997;18(4):614–7.

8. Feigl EO. Coronary physiology. Physiol Rev. 1983;63:1–205.

9. Rushmer RF, Thal N. The mechanics of ventricular contraction; a cineuorographic study. Circulation. 1951;4:219–28.

10. Bell JR, Fox AC. Pathogenesis of subendocardial ischemia. Am J Med Sci. 1974;268:3–13.

11. Kobayashi Y, Fearon WF.Invasive coronary microcirculation assessment. Circ J. 2014;78(5):1021–8.

12. Chan SY, Brunken RC, Czernin J, Porenta G, Kuhle W, Krivokapich J, Phelps ME, Schelbert HR.Comparison of maximal myocardial blood ow during adenosine infusion with that of intravenous dipyridamole in normal men. J Am Coll Cardiol. 1992;20:979–85.

13. Prior JO, Schindler TH, Facta AD, HernandezPampaloni M, Campisi R, Dahlbom M, Schelbert HR.Determinants of myocardial blood ow response to cold pressor testing and pharmacologic vasodilation in healthy humans. Eur J Nucl Med Mol Imaging. 2007;34:20–7.

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C. Trani et al.

14. Krivokapich J, Huang SC, Schelbert HR.Assessment of the effects of dobutamine on myocardial blood ow and oxidative metabolism in normal human subjects using nitrogen-13 ammonia and carbon-11 acetate. Am J Cardiol. 1993;71:1351–6.

15. Bigler MR, Ashraf A, Seiler C, Praz F, Ueki Y, Windecker S, Kadner A, Räber L, Gräni C. Hemodynamic relevance of anomalous coronary arteries originating from the opposite sinus of Valsalva-in search of the evidence. Front Cardiovasc Med. 2021;7:591326.

16. Angelini P, Flamm SD.Newer concepts for imaging anomalous aortic origin of the coronary arteries in adults. Catheter Cardiovasc Interv. 2007;69:942–54.

17. Grani C, Chappex N, Fracasso T, Vital C, Kellerhals C, Schmied C, Saguner AM, Trachsel LD, Eser P, Michaud K, Wilhelm M.Sports related sudden cardiac death in Switzerland classied by static and

dynamic components of exercise. Eur J Prev Cardiol. 2016;23:1228–36.

18. Driesen BW, Warmerdam EG, Sieswerda GT, Schoof PH, Meijboom FJ, Haas F, Stella PR, Kraaijeveld AO, Evens FCM, Doevendans PAFM, Krings GJ, van Dijk APJ, Voskuil M.Anomalous coronary artery originating from the opposite sinus of Valsalva (ACAOS), fractional ow reserve–and intravascular ultrasoundguided management in adult patients. Catheter Cardiovasc Interv. 2018;92:68–75.

19. Cheitlin MD, MacGregor J.Congenital anomalies of coronary arteries: role in the pathogenesis of sudden cardiac death. Herz. 2009;34:268–79.

20. Lee SE, Yu CW, Park K, Park KW, Suh JW, Cho YS, Youn TJ, Chae IH, Choi DJ, Jang HJ, Park JS, Na SH, Kim HS, Kim KB, Koo BK.Physiological and clinical relevance of anomalous right coronary artery originating from left sinus of Valsalva in adults. Heart. 2016;102(2):114–9.

Myocardial Bridge(s)

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AlbertoBarioli, FlaviaBelloni, andGiuseppeTarantini

Introduction

A myocardial bridge (MB) is dened as an anatomical variant in which a segment of a coronary artery (referred to as a tunneled artery) deepens into the myocardium for a variable distance, before returning to the epicardial surface. The presence of a band of myocardial bers (i.e. the “myocardial bridge”) overlying the coronary artery may result in compression of the artery during the systolic phase of the cardiac cycle. This anatomic variant, despite being traditionally considered a benign condition, has been associated with various clinical presentations, such as silent ischemia, exertional angina, acute coronary syndromes, Takotsubo cardiomyopathy, and sudden cardiac death [1–5].

Supplementary Information The online version contains supplementary material available at

https://doi.org/10.1007/978- 3- 031- 36966- 7_4.

A. Barioli Cardiology Unit, Cardio-Neuro-Vascular Department, Ca’ Foncello Hospital, Treviso, Italy e-mail: alberto.barioli@aulss2.veneto.it

F. Belloni Division of Cardiology, Santo Spirito Hospital, Rome, Italy e-mail: avia.belloni@aslroma1.it

G. Tarantini (*) Department of Cardiac, Thoracic, Vascular Science and Public Health, University of Padua, Padua, Italy

The prevalence of this congenital coronary anomaly is highly variable, and depends largely on the techniques used to detect its presence and on patient’s condition. In necropsy series, the reported rate of MB varies between 5 and 86% [1, 6], with a mean frequency of 25%. Recently, a meta-analysis of 15 autopsy studies reported an average prevalence of 42% [7]. These numbers are consistent with those observed in studies involving coronary-computed tomography (CCT) [8, 9]. Conversely, these rates are considerably higher than those found in angiographic studies, where the reported prevalence of MBs varies from 0.5% to 12% in basal conditions to 40% if provocative tests or intracoronary injection of nitroglycerin are used [10]. The observed rates of MBs increase to 23% when intravascular ultrasound (IVUS) is performed [11]. Prevalence of MBs has been reported to be higher in patients with hypertrophic cardiomyopathy and in cardiac transplant recipients [1, 12, 13].

The differences between the rates observed at necropsy or CCT and those detected at coronary angiography may lie in the different sensitivity of the investigative methods. As a matter of fact, if autopsy and CCT permit the direct visualization of the anatomy and course of the bridged segment, coronary angiography allows only the visualization of the “milking effect” (i.e. the dynamic narrowing of the coronary artery during systole). Intuitively, small intramyocardial courses with no hemodynamic signicance can-

https://doi.org/10.1007/978-3-031-36966-7_4

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