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<ArticleSet>
<Article>
<Journal>
				<PublisherName>Iranian Heart Association</PublisherName>
				<JournalTitle>Iranian Heart Journal</JournalTitle>
				<Issn></Issn>
				<Volume>7</Volume>
				<Issue>2</Issue>
				<PubDate PubStatus="epublish">
					<Year>2006</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>WHAT IS THE MECHANISM OF GROUP BEATING?</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>42</FirstPage>
			<LastPage>43</LastPage>
			<ELocationID EIdType="pii">84024</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>M.</FirstName>
					<LastName>SHOJAEIFARD</LastName>
<Affiliation></Affiliation>

</Author>
<Author>
					<FirstName>ARASH.</FirstName>
					<LastName>ARIA</LastName>
<Affiliation>DEPARTMENT OF PACEMAKER AND ELECTROPHYSIOLOGY, RAJAIE CARDIOVASCULAR MEDICAL AND RESEARCH CENTER, MELLAT PARK, VALI-ASR AVENUE, TEHRAN 1996911151, IRAN</Affiliation>

</Author>
<Author>
					<FirstName>M.</FirstName>
					<LastName>HAGHJOU</LastName>
<Affiliation></Affiliation>

</Author>
<Author>
					<FirstName>M.</FirstName>
					<LastName>SADR AMELI</LastName>
<Affiliation></Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2019</Year>
					<Month>03</Month>
					<Day>07</Day>
				</PubDate>
			</History>
		<Abstract>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 cm&lt;sup&gt;2&lt;/sup&gt;.&lt;br /&gt;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.&lt;br /&gt;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 (4&lt;sup&gt;th&lt;/sup&gt; 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.&lt;br /&gt;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.</Abstract>
<ArchiveCopySource DocType="pdf">https://journal.iha.org.ir/article_84024_27290b81e2340fc4fe3690469860d728.pdf</ArchiveCopySource>
</Article>
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