Changes in ventricular refractoriness after an extrastimulus: Effects of prematurity, cycle length and procainamide

Michael E. Cain; Thomas C. Martin; Francis E. Marchlinski; Mark E. Josephson

doi:10.1016/0002-9149(83)90519-2

Changes in ventricular refractoriness after an extrastimulus: Effects of prematurity, cycle length and procainamide

Michael E. Cain
, Thomas C. Martin
, Francis E. Marchlinski
, Mark E. Josephson

Medicine

University at Buffalo

Washington University St. Louis
University of Pennsylvania

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

This study was performed to determine the ability of extrastimuli to change ventricular refractoriness. We prospectively evaluated the effects of stimulus prematurity and paced cycle length (PCL) in 30 patients and the effect of procainamide in 8 patients on changes in the ventricular effective refractory period (ERP) after a right ventricular extrastimulus (S₂). An S₂ was introduced at preselected coupling intervals at a PCL (S₁-S₁) of 600 and 400 ms. At each S₁-S₂ interval, a second extrastimulus (S₃) was introduced in 5-ms decrements and the ERP of S₂ measured. The decrease in the ERP after an S₂ was directly related to prematurity and most of the shortening occurred over a narrow range of S₁-S₂ intervals. At a PCL of 600 ms, the ERP of S₂ at S₁-S₂ intervals ≤ 400 ms was significantly shorter than the ERP of S₁ (maximal shortening 23%). At a PCL of 400 ms, the ERP of S₂ at S₁-S₂ intervals ≤ 350 ms was significantly shorter than the ERP of S₁ (maximal shortening 25%). The ERP of S₂ at the shortest S₁-S₂ interval was greater with a PCL of 600 ms than with 400 ms (200 ± 31 versus 180 ± 26 ms, p < 0.001). However, the total shortening in ERP (ERPS₁ - ERPS₂ at shortest S₁-S₂ interval) was similar at both PCLs (55 ± 14 versus 59 ± 13 ms). Procainamide significantly prolonged the ERP of S₂ at each S₁- S₂ interval. Procainamide increased the ERP of S₂ at the shortest S₁-S₂ interval by 15 and 20%, whereas total shortening in the ERP decreased by 15 and 29% at PCLs of 600 and 400 ms, respectively. Thus, the ERP of S₂ is dependent on prematurity and PCL, whereas total shortening in ERP is similar at both PCLs. Procainamide prolongs the ERP of S₂ regardless of S₁-S₂ interval and decreases the total shortening in the ERP induced by S₂. These findings clarify the effect of double ventricular extrastimuli on ventricular ERP with a stimulation protocol often used in clinical electrophysiology laboratories.

Original language	English
Pages (from-to)	996-1001
Number of pages	6
Journal	American Journal of Cardiology
Volume	52
Issue number	8
DOIs	https://doi.org/10.1016/0002-9149(83)90519-2
State	Published - Nov 1 1983

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@article{dbe6b58e35c64543b10fc27a79db75c6,

title = "Changes in ventricular refractoriness after an extrastimulus: Effects of prematurity, cycle length and procainamide",

abstract = "This study was performed to determine the ability of extrastimuli to change ventricular refractoriness. We prospectively evaluated the effects of stimulus prematurity and paced cycle length (PCL) in 30 patients and the effect of procainamide in 8 patients on changes in the ventricular effective refractory period (ERP) after a right ventricular extrastimulus (S2). An S2 was introduced at preselected coupling intervals at a PCL (S1-S1) of 600 and 400 ms. At each S1-S2 interval, a second extrastimulus (S3) was introduced in 5-ms decrements and the ERP of S2 measured. The decrease in the ERP after an S2 was directly related to prematurity and most of the shortening occurred over a narrow range of S1-S2 intervals. At a PCL of 600 ms, the ERP of S2 at S1-S2 intervals ≤ 400 ms was significantly shorter than the ERP of S1 (maximal shortening 23\%). At a PCL of 400 ms, the ERP of S2 at S1-S2 intervals ≤ 350 ms was significantly shorter than the ERP of S1 (maximal shortening 25\%). The ERP of S2 at the shortest S1-S2 interval was greater with a PCL of 600 ms than with 400 ms (200 ± 31 versus 180 ± 26 ms, p < 0.001). However, the total shortening in ERP (ERPS1 - ERPS2 at shortest S1-S2 interval) was similar at both PCLs (55 ± 14 versus 59 ± 13 ms). Procainamide significantly prolonged the ERP of S2 at each S1- S2 interval. Procainamide increased the ERP of S2 at the shortest S1-S2 interval by 15 and 20\%, whereas total shortening in the ERP decreased by 15 and 29\% at PCLs of 600 and 400 ms, respectively. Thus, the ERP of S2 is dependent on prematurity and PCL, whereas total shortening in ERP is similar at both PCLs. Procainamide prolongs the ERP of S2 regardless of S1-S2 interval and decreases the total shortening in the ERP induced by S2. These findings clarify the effect of double ventricular extrastimuli on ventricular ERP with a stimulation protocol often used in clinical electrophysiology laboratories.",

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year = "1983",

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doi = "10.1016/0002-9149(83)90519-2",

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pages = "996--1001",

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T1 - Changes in ventricular refractoriness after an extrastimulus

T2 - Effects of prematurity, cycle length and procainamide

AU - Cain, Michael E.

AU - Martin, Thomas C.

AU - Marchlinski, Francis E.

AU - Josephson, Mark E.

PY - 1983/11/1

Y1 - 1983/11/1

N2 - This study was performed to determine the ability of extrastimuli to change ventricular refractoriness. We prospectively evaluated the effects of stimulus prematurity and paced cycle length (PCL) in 30 patients and the effect of procainamide in 8 patients on changes in the ventricular effective refractory period (ERP) after a right ventricular extrastimulus (S2). An S2 was introduced at preselected coupling intervals at a PCL (S1-S1) of 600 and 400 ms. At each S1-S2 interval, a second extrastimulus (S3) was introduced in 5-ms decrements and the ERP of S2 measured. The decrease in the ERP after an S2 was directly related to prematurity and most of the shortening occurred over a narrow range of S1-S2 intervals. At a PCL of 600 ms, the ERP of S2 at S1-S2 intervals ≤ 400 ms was significantly shorter than the ERP of S1 (maximal shortening 23%). At a PCL of 400 ms, the ERP of S2 at S1-S2 intervals ≤ 350 ms was significantly shorter than the ERP of S1 (maximal shortening 25%). The ERP of S2 at the shortest S1-S2 interval was greater with a PCL of 600 ms than with 400 ms (200 ± 31 versus 180 ± 26 ms, p < 0.001). However, the total shortening in ERP (ERPS1 - ERPS2 at shortest S1-S2 interval) was similar at both PCLs (55 ± 14 versus 59 ± 13 ms). Procainamide significantly prolonged the ERP of S2 at each S1- S2 interval. Procainamide increased the ERP of S2 at the shortest S1-S2 interval by 15 and 20%, whereas total shortening in the ERP decreased by 15 and 29% at PCLs of 600 and 400 ms, respectively. Thus, the ERP of S2 is dependent on prematurity and PCL, whereas total shortening in ERP is similar at both PCLs. Procainamide prolongs the ERP of S2 regardless of S1-S2 interval and decreases the total shortening in the ERP induced by S2. These findings clarify the effect of double ventricular extrastimuli on ventricular ERP with a stimulation protocol often used in clinical electrophysiology laboratories.

AB - This study was performed to determine the ability of extrastimuli to change ventricular refractoriness. We prospectively evaluated the effects of stimulus prematurity and paced cycle length (PCL) in 30 patients and the effect of procainamide in 8 patients on changes in the ventricular effective refractory period (ERP) after a right ventricular extrastimulus (S2). An S2 was introduced at preselected coupling intervals at a PCL (S1-S1) of 600 and 400 ms. At each S1-S2 interval, a second extrastimulus (S3) was introduced in 5-ms decrements and the ERP of S2 measured. The decrease in the ERP after an S2 was directly related to prematurity and most of the shortening occurred over a narrow range of S1-S2 intervals. At a PCL of 600 ms, the ERP of S2 at S1-S2 intervals ≤ 400 ms was significantly shorter than the ERP of S1 (maximal shortening 23%). At a PCL of 400 ms, the ERP of S2 at S1-S2 intervals ≤ 350 ms was significantly shorter than the ERP of S1 (maximal shortening 25%). The ERP of S2 at the shortest S1-S2 interval was greater with a PCL of 600 ms than with 400 ms (200 ± 31 versus 180 ± 26 ms, p < 0.001). However, the total shortening in ERP (ERPS1 - ERPS2 at shortest S1-S2 interval) was similar at both PCLs (55 ± 14 versus 59 ± 13 ms). Procainamide significantly prolonged the ERP of S2 at each S1- S2 interval. Procainamide increased the ERP of S2 at the shortest S1-S2 interval by 15 and 20%, whereas total shortening in the ERP decreased by 15 and 29% at PCLs of 600 and 400 ms, respectively. Thus, the ERP of S2 is dependent on prematurity and PCL, whereas total shortening in ERP is similar at both PCLs. Procainamide prolongs the ERP of S2 regardless of S1-S2 interval and decreases the total shortening in the ERP induced by S2. These findings clarify the effect of double ventricular extrastimuli on ventricular ERP with a stimulation protocol often used in clinical electrophysiology laboratories.

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U2 - 10.1016/0002-9149(83)90519-2

DO - 10.1016/0002-9149(83)90519-2

M3 - Article

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SP - 996

EP - 1001

JO - American Journal of Cardiology

JF - American Journal of Cardiology

IS - 8

ER -

Changes in ventricular refractoriness after an extrastimulus: Effects of prematurity, cycle length and procainamide

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