Fenómeno de Milking como causa de cardiopatía isquémica

Presentación de un caso y revisión de la bibliografía

Velayos C., Córdoba LA., Moreno F., *Escaned J., Prado LM., Martín, JC:, Blesa LA

Unidad de Cuidados Intensivos y Coronarios y *Servicio de Cardiología Intervencionista

Hospital Clínico San Carlos

Caso Clínico:

Se trata de una mujer de 37 años de edad con antecedentes personales de:

1.- Hipertensión arterial (HTA) de 10 años de evolución tratada con Amlodipino y Enalapril. En el último mes le había sido retirado el tratamiento antihipertensivo para estudio de función suprarrenal.

2.- Hipopotasemia desde hace 6 años tratada con suplementos de potasio

3.- Cefaleas hemicraneales frecuentes, que coinciden con la menstruación.

Acude a urgencias con un cuadro de dos horas de evolución de dolor centrotorácico que describe como quemante, que se irradia a miembro superior izquierdo y que comenzó estando en reposo después de una fuerte discusión.

La exploración física era normal, a excepción de una tensión arterial de 210/120 mmHg.

Tanto la analítica urgente como la radiografía de torax eran normales. El ECG que se le realizó a su llegada a urgencias muestra corriente de lesión subepicárdica en cara anteroseptal. Es ingresada en la unidad coronaria con el diagnóstico de infarto de miocardio transmural en cara anterior.

Se decide realización de cateterismo cardiaco. En el ventriculograma se observó disquinesia apical y en la coronariografía un milking largo y severo de la descendente anterior sin otros hallazgos.

Se inició tratamiento con betabloqueantes, nitroglicerina intravenosa y ácido acetilsalicílico a bajas dósis con buena evolución clínica. Hizo pico de CPK de 1640 a las 10 horas del inicio del cuadro con fracción MB elevada. Cinco días después de su ingreso en la UCI se trasladó a la planta de cardiología continuar estudio y tratamiento.

En la planta de cardiología presentó buena evolución siendo dada de alta siete días más tarde. Al alta la paciente se encuentra asintomática y en el ECG se observa signos de necrosis anterior.

 ECG al ingreso:

Curva de CPK:

Ventriculograma:

Milking. Revisión bibliográfica

Definición

Las arterias coronarias principales tienen un trayecto epicárdico. En algunos pacientes, pequeños segmentos de estas arterias se introducen en el espesor del miocardio teniendo trayectos de longitud variable intramiocárdicos. (1) (2)

Decimos que existe un puente miocárdico cuando un segmento de arteria coronaria principal discurre dentro del espesor de la pared muscular.

Parece ser una anomalía congénita debido a un fallo en la exteriorización de la primitiva red arterial intratrabecular cuya causa es desconocida.

En cada sístole se producirá una estenosis de la luz vascular, llegando incluso a colapsar la arteria afectada (fenómeno de ordeñamiento o milking).

Incidencia y Epidemiología

Según series angiográficas la incidencia del milking es de 0’6 a 4%. Sin embargo, la incidencia de puentes miocárdicos en estudios autópsicos dirigidos se eleva hasta un 55%-85%. (2) (4). De estos datos se deduce que no todos los puentes miocárdicos producen un fenómeno de milking angiográficamente significativo.

La DA en su tercio proximal o medio es la arteria más afectada, con una longitud de 4-35 mm (25 mm como media). El grado de estenosis sistólica también es variable (40-90%, media de 70%) (2)

Se ha establecido su asociación con la existencia de hipertrofia ventricular izquierda. (2)

 Patogenia

Los puentes miocárdicos se consideran una variante anatómica de la normalidad. El milking suele tratarse de un hallazgo angiográfico sin implicaciones patológicas, ya que la perfusión miocárdica se produce en diástole, que resulta poco afectada en estos pacientes.(1)

Sin embargo existen en la literatura muchas comunicaciones sobre distintos grados de insuficiencia coronaria en relación con puentes miocárdicos con fenómeno de Milking en la coronariografía. (3)

Hay comunicaciones de casos con gravedad variable, desde angina estable de esfuerzo hasta infarto agudo de miocardio (5) y muerte súbita (6). Frecuentemente es complicado establecer la relación causa-efecto entre el puente miocárdico y la cardiopatía isquémica, ya que suelen estar implicados, además, otros fenómenos como la trombosis local o el vasoespasmo.

Lo que si parece ser cierto es que, además de la compresión sistólica y las altas presiones que se detectan en la zona del milking, también se produce un cierto grado de reducción del diámetro diastólico del vaso, un incremento en la velocidad del flujo sanguíneo y flujo retrógrado,(7) todo lo cual podría explicar como el puente miocárdico puede producir isquemia, especialmente en determinadas situaciones de compromiso diastólico, como la taquicardia o la miocardiopatía hipertrófica.

El caso presentado parece responder a esta última situación: un compromiso diastólico en relación con la taquicardia por la descarga adrenérgica de la situación de estrés emocional que sufrió la paciente.
Diagnóstico

El milking se diagnostica por su imagen característica en la coronariografía. Se trata de un segmento que se estenosa o colapsa en sístole y que recupera el calibre en diástole. Esta diferencia de calibre suele descartar una placa ateromatosa, que causa una estenosis fija o un espasmo coronario, confirmando el diagnóstico de puente miocárdico.

Este fenómeno de milking se puede acentuar con la perfusión intracoronaria de nitroglicerina (8) o con la administración de inotropos positivos como la dobutamina (2), resultando así más evidente el diagnóstico.

La realización de una ecografía intravascular puede resultar de utilidad para diagnosticar una placa ateromatosa subyacente (9), ya sea en la zona del puente intramiocárdico o, más frecuentemente, en la zona proximal a este. Así como para caracterizar y estudiar más a fondo los límites y el resto de características de este tipo de lesiones. (10)

Coronariografía. Imagen en diástole

Imagen en sístole. MILKING en la DA

 

Tratamiento
Médico:

El tratamiento clásico son los beta bloqueantes. Su efecto inotropo y cronotropo negativo produce un alargamiento de la diástole y una disminución de la compresión arterial.

El fármaco con el que más experiencia se tiene es el propranolol, aunque también se ha demostrado la eficacia del uso del esmolol. (11)

Se debe tener en cuenta la posibilidad de asociación con vasoespasmo y valorar el tratamiento con antagonistas del calcio (3) y añadir siempre AAS.

En cuanto a la NTG, se sabe que su utilización intracoronaria acentúa la estenosis sistólica y hace más evidente el fenómeno de milking, (8) por lo que podría empeorar la isquemia. Quizá debería quedar reservada para las situaciones en las que el dolor precordial es prolongado y existe elevación del ST en el electrocardiograma.

 Percutaneo:

Hay bastantes casos descritos de colocación de stent en la zona del milking con buenos resultados angiográficos y control de los síntomas.(12)

Estaría indicado en pacientes en los que ha fracasado el tratamiento médico máximo y se quiere evitar la opción quirúrgica.

Parece ser que un stent intracoronario en la zona del milkig puede revertir las alteraciones hemodinámicas locales que causan la isquemia así como normalizar la reserva coronaria. (7)

En un estudio reciente (13), once pacientes portadores de un puente miocárdico sintomático fueron tratados con un stent y se volvieron a estudiar a las siete semanas y a los seis meses.

A las siete semanas en 5 pacientes (36%) la coronariografía demostró reestenosis que precisó revascularización percutanea en dos pacientes y by pass aortocoronario en otros dos. A los seis meses y a los dos años los nueve pacientes portadores de stent permanecían libres de síntomas.

Con estos datos se puede concluir que el stent parece una opción útil, si aceptamos una alta tasa de reestenosis y que no está demostrada cual es su indicación frente a la cirugía.

 Quirúrgico:

El tratamiento quirúrgico del puente miocárdico consiste en la liberación de la arteria mediante miotomía suprarterial.

Parece reservado a los casos en los que el paciente presenta un puente miocárdico sintomático con angina refractaria al tratamiento médico, en los que se prefiera evitar la colocación de un stent intravascular.

Existen varios casos descritos (14) (15), incluída una serie de nueve pacientes (16), con buenos resultados quirúrgicos, así como en el seguimiento clínico y angiográfico posterior.

El inconveniente principal de esta opción terapéutica viene derivado de las complicaciones de la cirugía con circulación extracorporea y la dificultad técnica que la disección de la arteria y su liberación posterior conlleva, que no está exenta de complicaciones, como por ejemplo la aparición de un aneurisma ventricular.(17)

No existen estudios que comparen el tratamiento percutaneo frente al quirúrgico en esta patología, por lo que, cuando el tratamiento médico fracasa no existe una evidencia sobre el método terapeútico de elección.
Pronóstico

La mayoría de los estudios de seguimiento demuestran un pronóstico a largo plazo bueno (2).

El grado de estenosis sistólica es determinante en el pronóstico, estableciendo en el 75% el límite a partir del cual se puede esperar que el Milking pueda ser sintomático. (18), sin embargo para otros autores el pronóstico es independiente del grado de estenosis y bueno en la mayoría de los casos (4).

 

Bibliografía:

  1. Frank RE. Myocardial Bridging. J Insur Med 1999 31 (1); 31-4. Abstract: Human myocardial bridging is a normal anatomic variation in which a coronary artery is bridged by a short segment of myocardium. It can cause variable degrees of systolic obstruction. The majority of patients are asymptomatic. A wide variety of syndromes can occur, including myocardial infarction and sudden death. All patients with myocardial bridges have systolic artery compression, but it is postulated that ischemia develops only in those who have a concomitant decrease in diastolic coronary artery blood flow. Surgical removal of the myocardial bridge can be curative, and various other treatments can alleviate symptoms. The overall prognosis is good.
  2. Harikrishnan S, Sunder KR, Tharakan J, Titus T, Bhat A, Sivasankaran S, Bimal F. Clinical and angiographic profile and follow-up of myocardial bridges: a study of 21 cases. Indian Heart J. 1999 Sep-Oct; 51; 503-7. Abstract: Myocardial bridging describes an angiographic entity, which is any degree of systolic narrowing of a coronary artery observed in at least one angiographic projection. Among the cineangiograms of 3200 patients reviewed, there were 21 cases (19 males) of myocardial bridges--incidence of 0.6 percent. Of these, seven had hypertrophic cardiomyopathy, six had atherosclerotic coronary artery disease and remaining eight had no evidence of either. All 21 patients had myocardial bridges in proximal or mid left anterior descending coronary artery. In addition, one case of hypertrophic cardiomyopathy had whole posterior descending coronary artery under a myocardial bridge. Another case of hypertrophic cardiomyopathy had a short normal segment of 5 mm inside a long myocardial bridge of 35 mm (tandem myocardial bridges). The length of the bridges varied from 10 to 35 mm (mean 24.5 +/- 4.5 mm) and diameter stenosis during systole varied from 40-90 percent (mean 70 +/- 8%). Two patients had large saccular coronary aneurysms proximal to the muscle bridge. Four of the eight patients who had neither hypertrophic cardiomyopathy nor coronary artery disease presented with acute anterior wall myocardial infarction and three of them had regional wall motion abnormality of left descending territory. Of the six patients who had coronary artery disease, one had 60 percent left descending artery lesion and two had recanalized segments proximal to the bridge. Five of the above six patients had significant stenosis of other coronary vessels. Four patients were lost to follow-up (mean period 3.4 +/- 2 years). In the coronary artery disease group, one patient underwent coronary artery bypass graft surgery for 3-vessel disease including graft to left descending artery and one developed inferior wall myocardial infarction. The patients in the hypertrophic cardiomyopathy group and "no hypertrophic cardiomyopathy-no coronary artery disease" group were free of events at last follow-up. Long-term prognosis of isolated myocardial bridges appears to be excellent. Degree of systolic narrowing or length of myocardial bridge does not correlate with event rates on follow-up.
  3. Arnau Vives MA. Martinez Dolz LV, Almenar Bonet L, Lalaguna LA, Ten Morro F, Palencia Perez M. Myocardial bridging as a cause of acute ischemia. Description of a case and review of the literature. Rev Esp Cardiol 1999 Jun; 52: 441. Abstract:Myocardial bridges consist of muscle fiber bundles lining an epicardial coronary artery for a variable distance. They are a relatively common finding, with incidence changing on the basis of the study method used (angiographic/necropsy). Although myocardial bridges are usually associated with a benign prognosis, being in many cases asymptomatic and only found by chance, their presence has also been considered a cause of angina, malignant arrhythmia, myocardial infarction and sudden death. They are diagnosed in vivo by angiography when a systolic compression of a coronary artery which disappears during diastole is evidenced. We report the case of a patient with electrocardiographic signs of severe ischemia in the territory of the anterior descending artery, which was initially assessed as myocardial infarction and treated as such. Eventually, the ECG returned to normal, and no new Q waves of necrosis occurred. An angiohemodynamic study confirmed the existence of an isolated muscular bridge over the middle third of the anterior descending artery, with no other associated coronary lesions.
  4. Juilliere Y, Berder V, Suty-Selton C, Buffet P, Danchin N, Cherrier F. Isolated myocardial bridges with angiographic milking of the left anterior descending coronary artery: a long-term follow-up study. Am Heart J 1995 Apr;129:663-5. Abstract: Among 7467 consecutive coronary angiograms performed during an 8-year period, 61 patients had a myocardial bridge of the left anterior descending coronary artery. The overall prevalence of myocardial bridges was 0.82% (from 0.41% to 1.16% per year). Among these patients, 26 had coronary artery disease, 4 had valvular heart disease, and 3 had cardiomyopathy. We studied the long-term outcome (11 +/- 3 years) of the other 28 patients with isolated milking at baseline. Two groups were constituted according to the percentage of systolic reduction of the left anterior descending coronary artery lumen: group A, < 50%(15 patients) and group B, > or = 50% (13 patients). During follow-up, 1 group A patient (cancer) and 2 group B patients (1 cancer and 1 suicide) died. Moreover, 1 group B patient was lost to follow-up. None of the patients sustained a myocardial infarction during follow-up. In group A patients, 71% felt very well or well and 50% had clinical symptoms; 64% took antianginal medications. In group B patients, 50% felt well and 70% had clinical symptoms; 50% took antianginal drugs. The long-term prognosis of isolated myocardial bridges of the left anterior descending coronary artery is good and is independent of the severity of systolic narrowing of internal lumen diameter.
  5. Baldassarre S, Unger P, Renard M. Acute myocardial infarction and myocardial bridging: a case repor. Acta Cardiol 1996;51:461-5. Abstract: The present report describes a 55-year-old man who presented an anterior myocardial infarction in association with myocardial bridge of the left anterior descending artery (LAD). We discuss the pathophysiology of myocardial infarction occurring with myocardial bridge.
  6. Cutler D, Wallace JM. Myocardial bridging in a young patient with sudden death. Clin Cardiol 1997 Jun;20:581-3. Abstract: Systolic compression of a coronary artery is considered to be a benign phenomenon, although numerous case reports have suggested an association between bridging and sudden death or ischemia in certain patients without other abnormalities on cardiovascular evaluation. We present the case of a young patient with two episodes of spontaneous ventricular fibrillation and electrocardiographic evidence of ischemia, whose only primary abnormality on extensive workup was a long segment of left anterior descending systolic compression. This case adds to the growing body of anecdotal evidence that myocardial bridging may be associated with significant cardiac events.
  7. Heinrich G. Klues HG, Schwarz ER, vom Dahl J, Reffelmann T, Reul H, Potthast K, Schmitz C, Minartz J, Krebs W, Hanrath P. Disturbed intracoronary hemodynamics in myocardial bridging: early normalization by intracoronary stent placement. Circulation 1997 Nov 4;96:2905-13. Abstract: The purpose of this study was to evaluate the hemodynamic mechanisms leading to myocardial ischemia in patients with myocardial bridging. Myocardial bridging is known to induce angina and even severe myocardial ischemia. METHODS AND RESULTS: In 12 symptomatic patients with myocardial bridges, quantitative coronary angiography was performed to obtain systolic/diastolic vessel diameters within the bridged segments. Coronary flow velocities, flow reserve, and pressures were determined with a 0.014-in Doppler and a 0.014-in pressure microtransducer. In 3 symptomatic patients, coronary stents were implanted and hemodynamic measurements were repeated immediately and after 7 weeks. An in vitro validation of the pressure measurements was performed. Angiography revealed a systolic diameter reduction of 80.6+/-9.2% and a persistent diastolic reduction of 35.3+/-11% within the bridged segment. Diastolic flow velocities (cm/s) were increased (31.5+/-14.3 within versus 17.3+/-5.7 proximal and 15.2+/-6.3 distal, P<.001). Coronary flow reserve distal to the bridge was 2.5+/-0.5. There was an increased peak systolic pressure within the bridged segment (171+/-48 versus 113+/-10 mm Hg proximal, P<.001). Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, the intracoronary peak systolic pressure, and clinical symptoms. Coronary flow reserve improved to 3.8+/-0.3. CONCLUSIONS: Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.
  8. Hongo Y, Tada H, Ito K, Yasumura Y, Miyatake K, Yamagishi M. Augmentation of vessel squeezing at coronary-myocardial bridge by nitroglycerin: study by quantitative coronary angiography and intravascular ultrasound. Am Heart J 1999 Aug;138:345-50. Abstract: 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 microgram 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.
  9. de Winter RJ, Kok WE, Piek JJ. Coronary atherosclerosis within a myocardial bridge, not a benign condition.Heart 1998 Jul;80: 91-3. Abstract: In patients with myocardial bridging, the area within the bridge usually remains free from atherosclerotic disease. The case of a 47 year old man is described who had the rare combination of myocardial bridging with an atherosclerotic plaque within the area of bridging, which was detected with intravascular ultrasound but not with coronary angiography. The clinical history of the patient demonstrates that this is not a benign condition. In symptomatic patients the bridged segment should be screened for the presence of plaque with intracoronary ultrasound.
  10. Ge J, Jeremias A, Rupp A, Abels M, Baumgart D, Liu F, Haude M, Gorge G, von Birgelen C, Sack S, Erbel R. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler. Eur Heart J 1999 Dec;20(23):1707-16. Abstract: Large discrepancies exist concerning the incidence of myocardial bridging. This has been reported to be 0.5%-2.5% following coronary angiography but 15%-85% following autopsy. The purpose of the study was to use intravascular ultrasound and intracoronary Doppler to study the morphology and flow characteristics of myocardial bridging in order to find feasible parameters of this syndrome. METHODS AND RESULTS: intravascular ultrasound was performed in 62/69 patients in whom typical angiographic 'milking effects' were present. In 48 patients, intracoronary Doppler was performed. A specific, echolucent 'half moon' phenomenon surrounding the myocardial bridge was found in all the
    patients. The thickness of the half moon area was 0.47 +/- 0.19 mm in diastole and 0.52 +/- 0.23 mm in systole. There was systolic compression of the myocardial bridge with a lumen reduction during systole of 36.4 +/- 8.8%. Using intracoronary Doppler, a characteristic early diastolic 'finger tip' phenomenon was observed in 42 (87%) of the patients. All patients showed no or reduced antegrade systolic flow. Coronary flow velocity reserve was 2.03 +/- 0. 54. After intracoronary nitroglycerin injection, retrograde systolic flow occurred in 37 (77%) of the 48 patients, with a velocity of -22. 2 +/- 13.2 cm. s(-1). Intravascular ultrasound revealed atherosclerotic involvement of the proximal segment in 61 (88%) of the 69 patients, with an area stenosis of 42 +/- 13%. No plaques were found in the bridge or distal segments in the 62 patients in whom it was possible to introduce the ultrasound catheter throughout the bridging segment. CONCLUSION: Myocardial bridging is characterized by the following morphological and functional signs: a specific, echolucent half moon phenomenon over the bridge segment, which exists throughout the cardiac cycle; systolic compression of the bridge segment of the coronary artery; accelerated flow velocity at early diastole (finger-tip phenomenon); no or reduced systolic antegrade flow; decreased diastolic/systolic velocity ratio; retrograde flow in the proximal segment, which is provoked and enhanced by nitroglycerin injection.
  11. Schwarz ER, Klues HG, Dahl J, Klein I, Krebs W, Hanrath P. Functional, angiographic and intracoronary Doppler flow characteristics in symptomatic patients with myocardial bridging: effect of short-term intravenous beta-blocker medication. J Am Coll Cardiol 1996; 27: 1.637-1.645. Abstract:We sought to define the effects of short-term beta-adrenergic blocking medication on intracoronary flow characteristics, clinical symptoms and angiographic diameter changes in patients with severe myocardial bridging of the left anterior descending coronary artery. BACKGROUND: Controversy exists regarding the pathophysiology, clinical relevance and optimal therapy in symptomatic patients with myocardial bridges because antianginal drugs have not been systematically tested. METHODS: In 15 symptomatic patients with myocardial bridging of the left anterior descending coronary artery, maximal lumen diameter reductions were evaluated by quantitative coronary angiography. There were no angiographic signs of coronary artery disease. Coronary blood flow velocities (using a 0.014-in. [0.035 cm] Doppler guide wire) were measured at rest, during atrial pacing and during intravenous administration of a short-acting beta-blocker (esmolol, 50 to 500 micrograms/kg body weight per min) with continuous atrial pacing. RESULTS: The maximal angiographic systolic lumen diameter reduction within the myocardial bridges was 83 +/- 9% at rest, with a persistent diastolic diameter reduction of 41 +/- 11% (mean +/- SD). Short-term intravenous beta-blocker therapy decreased the diameter reduction during both systole (from 83 +/- 9% to 62 +/- 11%) and diastole (from 41 +/- 11% to 30 +/- 9%, both p < 0.001). The average diastolic peak flow velocity was higher within the myocardial bridges (33 +/- 13 cm/s) than the proximal (26 +/- 13 cm/s) and distal bridges (17 +/- 4 cm/s, both p < 0.001). During tachypacing, average diastolic peak flow velocity increased within the bridged segments to 63 +/- 21 cm/s versus 29 +/- 12 cm/s in the proximal and 20 +/- 4 cm/s in the distal bridges (both p < 0.001). Beta-receptor blockade produced a return to baseline values (average diastolic peak flow velocity within bridge 35 +/- 16 cm/s, p < 0.001). ST segment changes and symptoms were abolished with beta-blocker administration. CONCLUSIONS: In patients with myocardial bridges, administration of short-acting beta-blockers during atrial pacing alleviates anginal symptoms and signs of ischemia. This effect was mediated by a reduction of vascular compression and maximal flow velocities within the bridged coronary artery segment.
  12. Bayes A, Marti V, Auge JM. Coronary stenting for symptomatic myocardial bridging. Heart 1998 Jul; 80: 102-3. No abstract.
  13. Haager PK, Schwarz ER, vom Dahl J, Klues HG, Reffelmann T, Hanrath P. Long term angiographic and clinical follow up in patients with stent implantation for symptomatic myocardial bridging. Heart 2000 Oct; 84: 403-8. Abstract:To assess long term results of coronary stent implantation in patients with symptomatic myocardial bridging. METHODS: Intracoronary stent implantation was performed within the intramural course of the left anterior descending coronary artery in 11 patients with objective signs of myocardial ischaemia and absence of other cardiac disorders. All had myocardial bridging of the central portion of the left anterior descending coronary artery. Quantitative coronary angiography was performed before and after stent deployment, and again at seven weeks and six months. Clinical evaluation was done at two years. RESULTS: After stent deployment, quantitative coronary angiography showed absence of systolic compression along the left anterior descending coronary artery; the minimum luminal diameter (mean (SD)) increased from 0.6 (0.3) mm before stent implantation to 1.9 (0.3) mm after implantation (p < 0. 05). Intravascular ultrasound showed an increase in cross sectional area from 3.3 (1.3) mm(2) at baseline to 6.8 (0.9) mm(2) (p < 0.005) after stent deployment. Coronary flow reserve was normalised from 2. 6 (0.5) at baseline to 4.0 (0.5) (p < 0.005) after stent implantation. At seven weeks, quantitative coronary angiography showed mild to moderate or severe in-stent stenosis in five of the 11 patients; four of these underwent repeat target vessel revascularisation (percutaneous transluminal coronary angioplasty in two; coronary artery bypass grafting in two). At six months, all patients (n = 9) showed good angiographic results, including those who had target vessel revascularisation. On clinical evaluation at two years, all patients (including those with target vessel revascularisation) remained free of angina and cardiac events. CONCLUSIONS: Intracoronary stent implantation prevents external compression of bridged coronary artery segments, with increase in luminal diameter and alleviation of symptoms. The incidence of in-stent stenosis requiring target vessel revascularisation (36%) is comparable with that of lesions of 25 mm length in coronary artery disease. The symptom free and event free two year follow up data suggest that stent implantation is a useful way of treating symptomatic patients with myocardial bridges.
  14. Katznelson Y, Petchenko P, Knobel B, Cohen AJ, Kishon Y, Schachner A. Myocardial brdging: surgical techique and operative results. Mil Med 1996 Apr; 161: 248-50 Abstract:We report a case of a 37-year-old symptomatic male with anterior myocardial ischemia. Coronary angiography demonstrated systolic obstruction of the midportion of the left anterior descending coronary artery due to myocardial bridging. The patient was treated with a supra-arterial myotomy. Two years postoperatively, the patient is without evidence of myocardial ischemia. Angiography, 2 years postoperatively, shows no evidence of systolic narrowing of the left anterior descending coronary artery.
  15. Hillman ND, Mavroudis C, Backer CL, Duffy CE. Supraarterial decompression myotomy for myocardial bridging in a child. Ann Thorac Surg 1999 Jul; 68: 244-6. Abstract: A 10-year-old boy presented with a history of exertional chest pain. An electrocardiogram demonstrated an inferior apical myocardial infarction. Cardiac catheterization revealed myocardial bridging of the left anterior descending coronary artery with evidence of intramyocardial obstruction during systole. The patient underwent successful treatment with supraarterial decompression myotomy and remains symptom free at 1 year.
  16. Iversen S, Hke U, Mayer E, Erbel R, Diefenbach C, Oelert H. Surgical treatment of myocardial bridging causing coronary artery obstruction. Scand J thorac Cardiovasc Surg 1992; 26: 107-11. Abstract: Nine patients with obstruction of coronary artery blood flow caused by myocardial bridging underwent surgery after failure of medical treatment. The diagnoses were made angiographically at rest or during beta-stimulation. Impaired blood flow was found only in the left anterior descending artery in seven patients and additionally in the diagonal branch in two. The operations, performed with cardiopulmonary bypass consisted of complete dissection of the overlying myocardium. All patients survived the operation. Major intraoperative complications were accidental opening of the right ventricle in two patients. Postoperative scintigraphic and angiographic studies demonstrated restoration of coronary flow and myocardial perfusion without residual myocardial bridges under beta-stimulation. Surgical relief of myocardial ischemia due to systolic compression of intramyocardial coronary arteries can be accomplished with low operative risk and with excellent functional results.
  17. de Zwaan C, Wellens HJJ. Left ventricular aneurysm subsequent to cleavage of myocardial bridging of a coronary artery. J Am Coll Cardiol. 1984; 3: 1345-1348. Abstract:In two patients, an aneurysm of the left anterior wall developed at the site of periarterial muscle resection of a myocardial bridge over the proximal portion of the left anterior descending coronary artery. One patient had a severe atherosclerotic stenosis proximal to the bridge. He also received a bypass graft to the left anterior descending coronary artery distal to the bridge. In the other patient without signs of atherosclerotic disease, only cleavage of the myocardial bridge was performed. Observations in these two cases suggest the need to reevaluate the risks of surgical treatment in symptomatic patients with myocardial bridging.
  18. Domínguez B, Valderrama V, Arrocha R, Lombana B. Myocardial bridging as a cause of coronary insufficiency. Rev Med Panama 1992; 17: 28-35. Abstract:The authors studied the clinical and angiographic findings in two patients who had a myocardial bridge (MB) in the right anterior descending coronary artery and did not have any arteriosclerotic lesions in the coronary arteries. The two patients were men, 57 and 58 years old. Both had a history of arterial hypertension (for 19 years and 6 months, respectively) and angina pectoris (for 7 years and 6 months, respectively). The resting EKG showed subepicardial ischemia in one and was normal in the other. The stress test was positive in both. Coronary artery angiography showed an MB in the right anterior descending coronary artery which caused a systolic constriction of 90% and 80%, 3 and 2 cm. long. Both patients had left ventricular hypertrophy. The authors conclude that MB is a frequent cause of coronary insufficiency and that the appearance of symptoms and their severity depends on the degree of systolic constriction, greater than 75%, and on the presence of left ventricular hypertrophy. The majority of patients are controlled with medical treatment and only a small number require surgical therapy.