Update on Myocardial Bridging

Möhlenkamp, Stefan; Hort, W; Ge, Junbo; Erbel, Raimund

doi:10.1161/01.cir.0000038420.14867.7a

Cited by 529 publications

(605 citation statements)

References 70 publications

(90 reference statements)

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“…The systolic compression can also be seen with IVUS [3][4][5]. Our case illustrates that additional IVUS can help in choosing the appropriate treatment strategy.…”

mentioning

confidence: 62%

A cataclasm due to spasm

2012

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We describe a 59-year-old patient presenting with ST-elevation acute coronary syndrome. Coronary angiography with intravascular ultrasound (IVUS) showed an important nonsignificant atherosclerotic lesion in the proximal left anterior descending artery (LAD) and presence of bridging in the mid-LAD. Our hypothesis was that focal spasm at this site was the cause of transmural ischaemia; therefore, treatment was given by performing a percutaneous coronary intervention (PCI) of the lesion. The patient remained symptom-free which confirmed our conclusion. The myocardial bridging had no clinical implications at this moment.Keywords Coronary spasm . Myocardial bridging . Intravascular ultrasound A 59-year-old negroid male presented to the emergency department with chest pain. His previous medical history consisted of heterozygous alpha thalassaemia type 2, reflux disease and lumbar hernia. A coronary angiogram 6 years ago had shown only slight vessel wall abnormalities. Cardiac risk factors were hypertension, a positive family history for coronary artery disease and nicotine abuse in the past. There was no history of cocaine abuse. During the last 5 months he had been complaining of sudden chest pain occurring at rest, which radiated to the left arm and only lasted for roughly 10 min. He had never had any exerciseinduced symptoms. The pain also reacted swiftly to sublingual nitrate. An exercise test performed in the week before his admission showed no abnormalities. His current medication was acetylsalicylic acid, amlodipine, losartan, bisoprolol, proton pump inhibitor and ranitidine. Blood pressure was 129/79 mmHg with a pulse of 53 beats/min. Further physical examination revealed no abnormalities. The symptom-free electrocardiogram showed sinus rhythm and diffuse repolarisation abnormalities with T-wave inversion in leads II, III and V4 to V6. During chest discomfort, there was ST elevation in leads I, aVL, and V2 to V6 with reciprocal depression in leads III and aVF (Fig. 1). Laboratory tests showed no abnormalities and the cardiac enzymes remained normal. He was treated for an acute coronary syndrome with clopidogrel, fraxiparine and intravenous nitroglycerin. Coronary angiography showed 50 % stenosis of the proximal LAD (Fig. 2), myocardial bridging of the mid LAD, 90 % stenosis of the first and second diagonal branch and 70 % stenosis of margo obtuse and posterolateral branches. The culprit lesion appeared to be the proximal LAD as this could explain the electrographic changes. Due to the fact that this stenosis did not seem to be significant on visual assessment, an FFR measurement was performed. This showed a value of 0.96; therefore, the lesion was not considered to be haemodynamically important and PCI was not performed. Although the angiogram showed no evidence of coronary spasm the clinical evidence started to point in this direction. After discontinuing bisoprolol and under treatment with maximum doses of oral nitrate and calcium antagonist he had recurring short and sudden episodes of chest pain. ...

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“…The systolic compression can also be seen with IVUS [3][4][5]. Our case illustrates that additional IVUS can help in choosing the appropriate treatment strategy.…”

mentioning

confidence: 62%

A cataclasm due to spasm

2012

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“…Overall, the frequency of myocardial bridges in adults varies substantially, with higher prevalence (15% to 80%) reported in histopathology studies than in angiographic studies (0.5% to 2.5%) (1,3,4). The length of bridges varies from 4 mm to 40 mm, and the depth from 1 mm to 10 mm (1,3). Although bridges are usually clinically silent, some, such as the longer and deeper ones, manifest with myocardial ischemia, rhythm conduction disturbances, acute coronary syndromes or even sudden cardiac death (3).…”

Section: Epidemiology Clinical Manifestation and Diagnosis Of Myocarmentioning

confidence: 98%

Myocardial bridges are free from atherosclerosis: Overview of the underlying mechanisms

Chatzizisis

Giannoglou

2009

Canadian Journal of Cardiology

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“…This difference has been attributed to insensitivity of angiography to MB. (1,2) MB is generally considered a benign condition that most commonly affects the mid portion of the left anterior descending (LAD) coronary artery. It is characterized by systolic compression of intramyocardial course of coronary artery, which remains clinically silent in the vast majority of patients.…”

Section: Introductionmentioning

confidence: 99%

“…However, numerous clinical cases of this anomaly have reported the association of MB with myocardial infarction. (1,3) We describe the case of a 13 year old patient with MB and a post traumatic myocardial infarction. We discuss the physiopathology of this event, the real role of MB in myocardial infarction after chest trauma.…”

Section: Introductionmentioning

confidence: 99%