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      •   صفحهٔ اصلی
      • نشریات انگلیسی
      • Iranian Heart Journal
      • Volume 7, Issue 2
      • مشاهده مورد
      •   صفحهٔ اصلی
      • نشریات انگلیسی
      • Iranian Heart Journal
      • Volume 7, Issue 2
      • مشاهده مورد
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      WHAT IS THE MECHANISM OF GROUP BEATING?

      (ندگان)پدیدآور
      SHOJAEIFARD, M.ARIA, ARASH.HAGHJOU, M.SADR AMELI, M.
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      نمایش کامل رکورد
      چکیده
      An eighty-year-old male was referred to our center because of dizziness and palpitation for the previous two weeks. He had no history of syncope and the drug history was unremarkable. Figure 1 shows the resting ECG, interpreted as complete heart block by the referring physician. A transthoracic echocardiography was done and showed a left ventricular ejection fraction of 35% and a severely calcified mitral valve with an estimated mitral valve orifice area of 1.4 cm2.Group beating was observed on the ECG, and a closer look at the ECG suggested the diagnosis of sino-atrial node Wenckebach (SANW) exit block. Premature atrial beat trigeminy could have also explained the group beating of the P-waves. However, the similarity of the P-wave morphologies and the confirmation of the diagnosis of sick sinus syndrome by electrophysiology study made this diagnosis unlikely and suggested the SANW as the cause of P-wave group beating.Apparently there seems to be a conduction defect at the atrio-ventricular nodal (AVN) level. The PR interval of the first conducted P-wave is longer (first black arrow) than the subsequent PR interval, which is then followed by a non-conducted P-wave. Nevertheless, a close look at the ECG reveals the real underlying mechanism of apparent AV block. Due to SANW, the PP intervals gradually shorten and the third P-wave is blocked as it encounters the physiologic refractory period of the AVN. After the third P-wave, there is a pause due to SA exit block (4th P-wave, blocked at the SAN level) followed by a conducted P-wave with a long PR interval. This phenomenon could be best explained by phase-four (bradycardia-dependent) conduction blocks.Electrocardiographic changes in this patient could also be explained by the effect of cyclelength duration on infra-Hissian conduction. Thus, PR interval prolongation can be due to His-Purkinje refractoriness in the longer cycle length. The shorter PR interval in the next beat may be due to a decrease in the HV interval in the shorter cycle length. In this scenario, the last P-wave would be blocked in the AV node.

      شماره نشریه
      2
      تاریخ نشر
      2006-03-01
      1384-12-10
      ناشر
      Iranian Heart Association
      سازمان پدید آورنده
      DEPARTMENT OF PACEMAKER AND ELECTROPHYSIOLOGY, RAJAIE CARDIOVASCULAR MEDICAL AND RESEARCH CENTER, MELLAT PARK, VALI-ASR AVENUE, TEHRAN 1996911151, IRAN

      URI
      http://journal.iha.org.ir/article_84024.html
      https://iranjournals.nlai.ir/handle/123456789/42308

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