Ever since Brugada found the unique pattern of ECG on right pre- cardial leads and its association with premature electrical death ,cardiac electro-physiology got a new impetus. Hundreds of articles(May be thousands !) on Brugada are available . Many criterias were proposed. Brugada and his colleagues should be credited for bringing in such an interest in the field of inherited ventricular arrhythmias.
On the down side , as we have a habit of prematurely formulating criterias , it brings an artificial academic barrier Funnily , in medical science deviating from a criteria (However hastily it was proposed ) is a considered big offense Further . the hype surrounding any new scientific entity makes it difficult for others to overwrite it .
Brugada recognized a ECG pattern with a genetic predisposition for VT and VF . Now , we know there are many etiologies with a similar pattern of ECG . What Brugada did was , he exposed the tip of Iceberg called inherited ventricular arrhythmia . But the essential criteria – Absence of structural heart disease , to diagnose Brugada was always questionable.
(Please realize , presence or absence of structural heart disease depends , more on how advanced our imaging modalities are . If you can map a virtual histology of RV epicardium one may detect some microscopic abnormality in every case of Brugada. In human biological system , God usually bonds structure and function too closely and hence functional abnormality rarely occur in isolation )
Brugada is not a new disease , it is a recognition of a pattern of ECG related to sudden deaths . Subsequently , we realized any dispersion in repolarisation in RV epicardial surface , the risk of sudden death is increased. From the days of Brugada we have come a long way.
What is new in Brugada syndrome ?
(Not exactly new . . . it is known for many years )
Brugada is no more an exclusive functional disorder of sodium channels of RV epicardium .It can have structural defect (known & unknown ) .It may have infective , degenerative etiology as well .
How does these structural changes appear ?
Chronic sodium channel malfunction can result in cell membrane defects which can augment Idio-osmole inside the cell and result in apoptosis etc .
Which comes first , electrical or structural abnormality ?
It is an another chicken- egg tale waiting to be decoded within the RV epicardial cells
Can wall motion defect occur in Brugada ?
Early observations done in out hospital (MMC Chennai ) has found anterior RV free wall motion defects. Tissue Doppler studies are being undertaken.
The following paper wonderfully documents the structural and histo-pathological changes in RV epicardium . This implies , our belief about this unique electrical disorder is bound to take a beating and we expect a major perception makeover regarding Brugada in the years to come .
Probably the most important paper on Brugada syndrome was published in circulation in 2005