Hein Wellens

Hein Wellens
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Hein J Wellens MD, Emeritus Professor of Cardiology, University of Maastricht, The Netherlands
Hein J Wellens MD, Emeritus Professor of Cardiology, University of Maastricht, The Netherlands

, M.D., (born 13 November 1935, The Hague) is a Dutch cardiologist who is considered one of the founding fathers of the cardiology subspecialty known as clinical cardiac electrophysiology. Clinical cardiac electrophysiology enables patients with cardiac arrhythmmias to be subjected to catheter electrode mapping and stimulation studies. Paul Puech, first in Mexico and later in France; Benjamin Scherlag and Onkar Narula in the USA; and Dirk Durrer and Philippe Coumel in Europe were the field’s pioneers in the 1950s and 1960s. The field’s second wave of innovators used these techniques to unravel the mechanisms of tachycardia in humans and set the bases for their treatment. Among them, Hein Wellens in Europe and Kenneth Rosen, John Gallagher, and Mark Josephson in the USA had the greatest impact as researchers and teachers. Josephson is the author of the first and most successful textbook of clinical cardiac electrophysiology, now in its fourth edition.

Wellens, known among European cardiologists as “the giant of Maastricht”, has for many years been associated with the University of Limburg School of Medicine in Maastricht, Netherlands. At his department of cardiology, many future clinical cardiac electrophysiologists trained from 1976 until his retirement in 2002.


As a pupil and collaborator of the late Professor Dirk Durrer in Amsterdam, Dr. Wellens was involved in the early developments in programmed electrical stimulation of the heart in patients with the Wolff-Parkinson-White syndrome. In these patients, cardiac arrhythmias it was shown for the very first time that were first shown to be possibly initiated and terminated by critically timed premature beats. In 1971, he reported on the use of programmed electrical stimulation of the heart in patients with atrial flutter, AV nodal tachycardia, and accessory atrioventricular connections. In 1972, he showed that the arrhythmia of patients with ventricular tachycardia could also reproducibly be initiated and terminated by timed premature stimuli. These investigations were the basis for the new surgical and pacing approaches to the treatment of cardiac arrhythmias that became known as “cardiac electrophysiology”.[3] to be Wellens also demonstrated that the reproducible initiation and termination of arrhythmias by programmed electrical stimulation of the heart allowed the study of the effect of antiarrhythmic drugs on the mechanism of the arrhythmia. In 1977, he moved to the new University of Limburg in Maastricht, Netherlands, to develop academic cardiology there. Starting from scratch, he created an internationally known center for the study and treatment of cardiac arrhythmias.[3]

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Electrokinetic Potentials in a Left Ventricle/Aorta Simulator

Electrokinetic Potentials in a Left Ventricle/Aorta Simulator
ARK Research, Farmingdale, N.Y. 11735

Electrochemical Studies of Biological Systems
Chapter 11, pp 180–193
Chapter DOI: 10.1021/bk-1977-0038.ch011
ACS Symposium Series, Vol. 38
ISBN13: 9780841203617eISBN: 9780841203242
Publication Date (Print): June 01, 1977

Peer Reviewed Book Chapter


Several left ventricle/aorta mechanical simulators were fabricated to evaluate the possibility of generating EKG like electrical signals by electrokinetic methodology. The simulators produced pulsed turbulent flows, simulating mammalian heart pumping conditions. EKG like signals were generated by the motion of the electrolyte through the simulators.

Reflections on the lowly PVC

Published in Heart Rhythm
The official Journal of the Heart Rhythm Society
April 2015 Volume 12, Issue 4, Pages 714–715

by David J. Callans, MD, FHRS
Andrew E. Epstein, MD, FHRS
Cardiovascular Division, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
Published Online: December 26, 2014

Using a healthy degree of editorial license, we wanted to set the scene for the excellent study by El Kadri et al1 in this issue of HeartRhythm by reflecting on how much we have learned about premature ventricular complexes (PVCs) in the span of 5 decades or so. PVCs were first considered a harbinger of risk in patients with structural heart disease. This was largely informed by the initial observations in the critical care unit caring for patients early after myocardial infarction. The association between PVCs and increased risk of sudden death in ambulatory patients was demonstrated in an analysis from the Tecumseh Study. Patients with PVCs had a 6-fold increase in sudden death over a follow-up period of 6 years.2 Reports by Bigger et al3 for the Multicenter Post Infarction Research Group clearly demonstrated that in patients convalescing from acute infarction, a high burden of PVCs (>3 per hour) as well as reduced ejection fraction was associated with an increased risk of total mortality and death caused by arrhythmia. The PVC hypothesis—that frequent PVCs served as the trigger that launched life-threatening ventricular arrhythmias and that successful antiarrhythmic drug treatment would reduce risk—was tested in the Cardiac Arrhythmia Suppression Trial (CAST) and soundly refuted.4 Furthermore, the Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) study, among other findings, further dissociated PVC burden and specifically successful treatment of PVCs with antiarrhythmic drugs from subsequent risk of sustained ventricular arrhythmias.5 These disappointing results turned focus away from PVC burden as a risk factor for poor outcome in patients with structural heart disease.

Interest in PVCs was reawakened by initial case reports6 followed by an initial clinical series of patients without preexisting heart disease who had frequent PVCs and potentially reversible left ventricular (LV) dysfunction. Yarlagadda et al7 studied 27 patients with “repetitive monomorphic ventricular ectopy” who were referred for catheter ablation. Their study demonstrated several important findings: (1) successful ablation (achieved in 7/8 patients with LV dysfunction) resulted in dramatic improvement in LV function; (2) LV dysfunction was observed with as few as 5500 PVCs per day; and (3) there was no difference in PVC burden between patients with and those without LV dysfunction.
Important studies attempting to more completely characterize this syndrome followed. The causality and response to treatment were validated by comparison with untreated controls.8 Originally, PVC-related myopathy was considered tachycardia-related cardiomyopathy. Subsequent studies have not arrived at an accurate mechanism, although dyssynchrony and even bradycardia-dependent hypotheses have been offered. Considerable effort was expended trying to determine the “dose” of PVCs required to cause cardiomyopathy. Work by the Michigan group was important in establishing a typical “threshold” dose of 20% in patients without preexisting heart disease.9 Nonetheless, as presaged by the original Cornell experience, there is considerable variability in susceptibility to PVC-related myopathy. In fact, referral bias aside, it seems as though most patients without structural heart disease who have frequent PVCs will not develop cardiomyopathy, although serial monitoring is still recommended.10 The key characteristics of those who develop myopathy include frequent PVCs and lack of symptoms related to PVCs (implying some effect of duration). Although not fully characterized in the literature, it was clear that PVCs that caused myopathy were idiopathic in mechanism and in location, that is, they arose from typical sites, particularly the right ventricular outflow tract and the sinuses of Valsalva, associated with sites of origin with normal bipolar voltage.

Closer to the present, focus again turned to the effect of frequent PVCs in patients with established heart disease. Sarrazin et al11 studied a group of 30 patients with remote myocardial infarction and LV dysfunction, 15 with a high burden of PVC (>5%) and 15 without. All 15 patients with frequent PVCs had successful ablation procedures, resulting in a reduction of PVC burden and improvement in LV function (0.38 ± 0.11 to 0.51 ± 0.09); no improvement was observed in the control group. Although the authors state that PVCs were ablated from areas of voltage map defined scar in 13 of 15 patients, many of these PVCs arose from sites associated with idiopathic mechanisms (aortic cusps, which are not associated with infarction; papillary muscles, which often are spared). Mountantonakis et al12 evaluated the effects of catheter ablation on 69 patients with cardiomyopathy and frequent outflow tract PVCs (mean 29 ± 13%). Twenty of these patients had a history of cardiomyopathy that preexisted the development of PVCs. In these 20 patients, successful ablation resulted in significant improvement in LV function, but less dramatic than that observed in patients with “pure” PVC-related myopathy. After these studies, the message was still fairly clear: even patients with structural heart disease who have “idiopathic looking” PVCs may benefit from ablation.

El Kadri et al1 add an important new dimension to this discussion. They studied a series of 30 consecutive patients with frequent PVCs (>5%) and unrelated nonischemic cardiomyopathy, as evidenced by the presence of scar on delayed gadolinium enhancement imaging (26 patients) or documented LV dysfunction before the diagnosis of frequent PVCs (4 patients). Magnetic resonance imaging demonstrated intramural scar in 50% of patients, endocardial or transmural scar in 37%, and multifocal scar distribution in 2%. Compared to previous studies, this population was more likely to have pleomorphic PVCs (18 patients, this finding negatively affected success) and multiple PVC morphologies. Ablation was successful in 18 patients; in these patients a secure site of origin could be established. Imaging data were available for 16 of these patients. Magnetic resonance imaging and voltage map–defined scar was present at the site of origin in 12 patients. The most frequent cause of ablation failure was an intramural site of origin. In 10 of 18 patients with successful procedures, the ejection fraction normalized (pre/post ejection fraction: 39% ± 7%/55% ± 3%). The authors conclude that in patients with frequent PVCs and preexisting nonischemic cardiomyopathy, LV function can be improved by successful ablation and that the arrhythmogenic substrate in this clinical setting often involves scar tissue.

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Blood Clots, the Olympics & the New York Yankees


Blood clots are common among athletes.

Olympic athletes suffer from exercise induced asthma.

Tall athletes seem to develop more blood clots.

Marathon runners have lactic acid and develop premature ventricular beats.

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