Saturday, 6 December 2014

Myocardial bridge

A myocardial bridge occurs when one of the coronary arteries tunnels through the myocardium rather than resting on top of it. This is generally confined when myocardial tissue covers part of the mid left anterior descending artery (LAD), resulting in a tunneled arterial segment, which can be regarded as a congenital variant. It usually has a benign prognosis, but in some cases myocardial ischemia, infarction and sudden cardiac death have been reported. Typically, the arteries rest on top of the heart muscle and feed blood down into smaller vessels that populate throughout the myocardium. But if the muscle grows around one of the larger arteries, then a myocardial bridge is formed.

Myocardial bridging is most commonly observed of the LAD (figure).
The depth of the vessel under the myocardium is more important that the length of the myocardial bridging. There is debate, whether some of these myocardial bridges are hemodynamically significant. image from:

As the heart squeezes to pump blood, the muscle exerts pressure across the bridge and constricts the artery. This defect is present from birth. It can lead to uncomfortable, powerful heartbeats and angina. The incidence of the condition in the general population is estimated at 5% based on autopsy findings, but significance when found in association with other cardiac conditions is unknown. Myocardial bridging occurs frequently in patients with hypertrophic cardiomyopathy, with a prevalence as high as 30%.

The condition is diagnosed on a scaled based on what percentage of obstruction occurs. If there is less than 50% blockage, then the condition is probably benign. A result of at least 70% usually causes some pain. Small amounts of myocardial bridging often are undetectable, as the blood usually flows through the coronary while the heart is relaxing in diastole. The degree of coronary obstruction by the myocardial bridge depends on such factors as location superficial' or ‘deep', thickness, length of the muscle bridge, and degree of cardiac contractility.

Clinical significance

Because myocardial bridging is a common finding at autopsy of normal subjects, it had been thought to be a benign anatomic variation. Although this malformation is present at birth, symptoms usually do not develop before the third decade; the reason for this is not clear. Bridging of the coronary arteries was observed after administration of drugs, such as nitroglycerin or a b-agonist, in up to 40% of patients with angina pectoris and normal coronary arteries. The diagnosis of clinically important myocardial bridging should be considered in patients who have angina and do not have the traditional risk factors and the evidence of ischemia. However, objective signs of ischemia cannot always be demonstrated in patients with myocardial bridging, most likely because of a large variability.


This condition can cause complications such as vasospasm, angina pectoris, arrhythmia, Ventricular tachycardia. Additionally many patients express discomfort in specific positions, (i.e. lying on the left side for a prolonged period of time).

Infarction Due to Myocardial Bridging

Karam Souibri, M.D., and Gilles Grollier, M.D.
N Engl J Med 2005; 353:1147September 15, 2005DOI: 10.1056/NEJMicm1050647
A 45-year-old man with dyslipidemia had a sudden onset of retrosternal chest pain and presented to the emergency department. Findings on the physical examination were unremarkable. His electrocardiogram showed ST-segment elevation in the anterior leads (Panel A). Coronary angiography was immediately performed. The left anterior descending (LAD) coronary artery and two large diagonal branches appeared to be normal during diastole (Panel B) but were severely compressed during systole (Panel C), suggesting compression by myocardial bridging. A rate of flow classified as grade 2 (according to the criteria of the Thrombolysis in Myocardial Infarction [TIMI] trial) was observed in these three arteries. The other coronary arteries were normal. Direct stenting of the intramyocardial segment of the LAD artery and the second large diagonal branch restored TIMI grade 3 flow and relieved the chest pain, with normalization of the electrocardiogram. The creatine kinase and troponin levels were elevated.


Therapeutic approaches that have been attempted for myocardial bridging include b-blockers, calcium channel blockers, stents, minimally invasive coronary artery bypass grafting (CABG), and surgical myotomy. Nitrates generally should be avoided because they increase the angiographic degree of systolic narrowing and can lead to worsening of the symptoms. B-blockers decrease the tachycardia and increase diastolic time, with a decrease in contractility and compression of the coronary arteries. Thus, these agents should be beneficial, although they have not been studied in randomized controlled trials.


Monday, 28 April 2014

AP Xray view of a bi-ventricular pacemaker, showing the electrodes in the right atrium, right ventricle, and left ventricle.

For more FREE ECG resources to use in classes and presentations, check out the ECG Guru at  

Tuesday, 22 April 2014

I’ve just developed an Glossary of ECG-Related Medical Terms to assist those new in the field and/or for laypersons without medical background — who may encounter written material regarding ECG interpretation. While intentionally not all-inclusive  my hope is that this illustrated PDF will be helpful to the above groups of people. The LINK for Download is at:
Feedback is welcome!   THANK YOU for your consideration  Ken Grauer, MD 

Saturday, 19 April 2014

Tuesday, 15 April 2014

Submit ECG case studies

Do you have any interesting ECG case studies you’d like to see featured on ECG & Cardiology blog?

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Please include: Patient information including age, gender, chief complaint, medical history, medications, vital signs, and physical exam. ECGs with excellent data quality (rhythm strip and 12-lead ECG preferred) Information about the patient’s clinical conditions, including treatment, response to treatment, and discharge diagnosis if available.

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Sunday, 6 April 2014

For a practical review on ECG Diagnosis of Chamber Enlargement - Please Check Out this PDF excerpted from my ECG-2014-Expanded Pocket Brain book:
Hope this is useful. Questions are welcome - Ken Grauer, MD