Lown-Ganong-Levine

LGL Syndrome, or Lown-Ganong-Levine Syndrome was first described by Lown, Ganong, and Levine in 1952. They noted an association of the occurrence of tachycardia (paroxysmal) with presence of a short PR interval in the setting of a normal QRS duration.

Specific criteria for Lown-Ganong-Levine includes a PR interval less than or equal to 0.12 second (120 ms), a normal QRS complex duration of less than 120 ms, and occurrence of a clinical tachycardia. (19)

Researchers have many hypotheses about what causes LGL Syndrome, however, no accessory pathway has been definitively identified as a known cause of this syndrome. Many researchers believe that LGL is a varient of other tachycardias and not it's own seperate entity.

LGL remains a clinical diagnosis, termed before the advent of electro-physiology studies. Many mechanism and accessory pathways have been described which can meet the criteria of LGL (short PR, normal QRS, tachycardia).

Approximately 1 in 200 people in the world (and USA) meet criteria for LGL.

Symptoms are much the same as most tachyarrythmias. They include lightheadedness, palpitations, shortness of breath, chest discomfort, nausea, and occasionally, hemodynamic compromise.

This arrhythmia has not been extensively studied, however, it seems as though the mortality rate is very small, though, as with any arrhythmia, people with coronary artery disease have more adverse outcomes than the general population with LGL.

Some evidence does show a predilection to LGL within families, pointing towards a genetic cause. However, no known genes have been isoloated as a cause for LGL Syndrome.