Skip Navigation

European Heart Journal 1992 13(Supplement D):70-81; doi:10.1093/eurheartj/13.suppl_D.70
Copyright © 1992 by the European Society of Cardiology.
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Vester, E. G.
Right arrow Articles by Strauer, B. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vester, E. G.
Right arrow Articles by Strauer, B. E.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1992 The European Society of Cardiology

Electrophysiological and therapeutic implications of cardiac arrhythmias in hypertension

E. G. Vester, S. Kuhls, J. Ochiulet-Vester, M. Vogt and B. E. Strauer

Medizinische Klinik und Poliklinik B, Abteilung für Kardiologie, Pneumologie und Angiologie, Heinrich-Heine-Universität Düsseldorf Germany

Address for correspondence: Ernst Günter Voter, MD, Medizinische Klinik und Poliklinik B, Abteilung für Kardiologie, Pneumologie und Angiologie, Heinrich-Heine-Universitat Dueseldorf, Mooremtraβe 5, 4000 Dussddorf 1, Germany

Hypertension, especially if associated with left ventricular hypertrophy (LVH), is a risk factor in complex ventricular arrhythmia (VA) and sudden cardiac death (SCD). To determine the effectiveness of the clinical use of programmed ventricular stimulation (PVS) we studied 40 symptomatic hypertensive patients after excluding coronary heart disease (CHD), as characterized by dizziness and palpitation, syncope, aborted SCD and/or documented complex VA. PVS revealed a normal result, i.e. a maximum of six ventricular echobeats, in 70% (group A) and a pathological result, i.e. ventricular tachycardia (VT) or fibrillation (VF) in 30% (group B). Both groups differed significantly with respect to LV (left ventricular) muscle mass: 158±45 (A) vs. 222±112 (B)g. m–2, LVEF (left ventricular ejection fraction): 71±17% (A) vs. 47±18% (B) and LV end-systolic volume index: 34±25 (A) vs. 63±27 (B) ml. m–2. Coronary reserve was comparably reduced in both groups: 2·6±1·0 (A) vs. 2·3±0·6 (B). In 3/8 (37%) patients with aborted SCD and VT/VF the clinical VA (2/2 VT and 1/6 VF) could be induced, whereas in the remaining five patients nsVT or no complex VA was induced. The therapeutic regimen included no drugs in 30%, β-blockers in 50%, serial drug testing in 12% and implantation of an automatic cardioverter defibrillator (AICD) in 8% of patients.

Ventricular late potentials (LPs), detected by the signal averaging electrocardiogram, represent zones of delayed myocardial activation, which may become an origin of ventricular tachycardias. Three criteria constitute a positive LP: (1) QRS duration>114 ms, (2) root mean square voltage of the last 40 ms<20 µV and (3) duration of low amplitude signal below 40 µV>38 ms. To look for the prognostic value of LP in hypertension we investigated 43 hypertensive patients without evidence of CHD. All three criteria were positive in 4/43 patients (9%), three of them demonstrating inducible monomorphic VT during PVS. 17/30 patients (56%) with LVH had at least one positive criterion, whereas only one out of 13 patients without left ventricular hypertrophy (8%) had one positive criterion. Symptomatic patients presenting with syncope, aborted SCD or documented VT/VF differed significantly from patients without symptoms or complex arrhythmias in regard to all three criteria.

Conclusion: In hypertensive heart disease clinical arrhythmias as well as the result of electrophysiological testing are closely related to left ventricular performance and hypertrophy. PVS is appropriate to detect reentrant VT, whereas for induction of primary VF, trigger mechanisms other than PVS are necessary. Nevertheless, PVS is an aid to deciding whether to use conservative drug or invasive AICD therapy in high risk patients. Late potentials have a significantly higher prevalence in hypertensive patients with LVH compared to those without LVH. LP analysis aids identification of patients prone to VT and may therefore be used to screen symptomatic hypertensive patients.

Key Words: Hypertension • ventricular arrhythmias • sudden cardiac death • programmed ventricular stimulation • late potential analysis


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.