Cardiac arrhythmias: The quest for a cure
A historical perspective
Hein J.J. Wellens, MD, FACC*
Cardiovascular Research Institute, Maastricht, the Netherlands
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Figure 1 A programmed ventricular stimulation study done during the early 1970s. The selected extra and intracardiac electrograms in the four panels show the reproducible initiation of a ventricular tachycardia by single ventricular premature beats during right ventricular pacing with a basic cycle length of 700 ms. As shown, ventricular premature beats given in the interval range 500 to 410 ms result in the initiation of the ventricular tachycardia. Premature beats given later than 500 ms or earlier then 410 ms do not create the conditions required for initiation and maintenance of a reentrant ventricular tachycardia.
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Figure 2 Same patient as Figure 1. A critically timed premature beat invades the re-entry circuit and causes refractoriness of the tissue in front of the circulating impulse resulting in termination of the ventricular tachycardia.
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Figure 3 Drawing explaining why antiarrhythmic drug studies during programmed stimulation of the heart result in more dependable information in supraventricular re-entrant tachycardia (SVT) than in ventricular tachycardia (VT) occurring in a scar after myocardial infarction. In the tachycardia on the left, a fixed tachycardia circuit is present consisting of atrial tissue, the atrioventricular node-His bundle and bundle branches, ventricular tissue, and an accessory atrioventricular connection. This allows the selection of a drug that blocks conduction in the "weakest" part of the circuit. In contrast, in the scar after myocardial infarction, VT usually has several possible reentry circuits that, because of differences in size and electrophysiologic properties, are affected differently by antiarrhythmic drugs.
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Figure 4 Risk stratification after myocardial infarction (MI). BNP = brain natriuretic peptide; CRP = C-reactive protein; ECG = electrocardiogram; EPS = electrophysiologic study; LV = left ventricle; LVEF = left ventricular ejection fraction; MIBG = meta-iodobenzylguanidine; NYHA = New York Heart Association.
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Figure 5 Examples of right and left ventricular activation in left bundle branch block. In panel A, septal breakthrough of the activation front coming from the right ventricle occurs in the superior part of the intraventricular septum. This results in desynchronized contraction of both ventricles with the right ventricle contracting in an apicobasal direction and the left ventricle in a basoapical direction. In panel B, septal breakthrough takes place in the inferior portion of the intraventricular septum. Right and left ventricular contraction is desynchronized but occurs in both in apicobasal direction.
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Figure 6 A cross-section of the right ventricle (RV) and left ventricle (LV) in the horizontal plane. As shown during left bundle branch block, the site of septal breakthrough may affect desynchronized contraction of the two papillary muscles (PMs) resulting in mitral incompetence. As shown in panel A, desynchronization of the PMs is most marked in posteroseptal breakthrough. More synchronized activation of the PMs occurs in case of anteroseptal breakthrough (panel B).
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