Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease

Kyndaron Reinier, Celia Dervan, Tejwant Singh, Audrey Uy-Evanado, Shenghan Lai, Karen Gunson, Jonathan Jui, Sumeet S. Chugh

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Background: Following myocardial infarction, individual patients can have wide variations in the extent of left ventricular systolic dysfunction (LVSD) and increased left ventricular (LV) mass. Both affect the risk for sudden cardiac death, but only LV ejection fraction is used for risk prediction. Objective: The purpose of this study was to evaluate the independent as well as the additive contributions of increased LV mass and decreased LV ejection fraction to sudden cardiac death in the general population. Methods: In the ongoing Oregon Sudden Unexpected Death Study, we studied consecutive SCD cases (n = 191) and coronary artery disease controls (n = 203) from the Portland, Oregon, metropolitan area (population approximately 1,000,000; 20022008). Comparisons of echocardiographic LV mass obtained prior and unrelated to sudden cardiac death (SCD) were conducted, and a logistic regression model was used to evaluate the relationship between SCD, severe LVSD, LV mass, and other relevant clinical variables. Results: In a multivariate model, both severe LVSD and left ventricular hypertrophy (LVH) were associated with increased SCD risk (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.13.2 for severe LVSD; OR 1.8, 95% CI 1.12.9 for LVH). In patients with coexisting severe LVSD and LVH, risk of SCD was additive (OR 3.5, 95% CI 1.77.2). In the same model, increased age, atrial fibrillation/flutter, elevated creatinine, and diabetes independently increased risk, and use of angiotensin receptor blockers attenuated risk. Conclusion: Reduced LV ejection fraction and increased LV mass had independent and additive effects on risk of sudden death. Despite the significant overlap between the two conditions, these findings point toward the existence of independent mechanistic pathways for ventricular arrhythmias that occur due to LVSD and LVH.

Original languageEnglish (US)
Pages (from-to)1177-1182
Number of pages6
JournalHeart Rhythm
Volume8
Issue number8
DOIs
StatePublished - Aug 2011

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Sudden Cardiac Death
Left Ventricular Function
Left Ventricular Dysfunction
Coronary Artery Disease
Left Ventricular Hypertrophy
Odds Ratio
Stroke Volume
Confidence Intervals
Sudden Death
Logistic Models
Atrial Flutter
Angiotensin Receptor Antagonists
Atrial Fibrillation
Population
Cardiac Arrhythmias
Creatinine
Myocardial Infarction

Keywords

  • Arrhythmogenesis
  • Heart failure
  • Hypertrophy
  • Population
  • Sudden death

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease. / Reinier, Kyndaron; Dervan, Celia; Singh, Tejwant; Uy-Evanado, Audrey; Lai, Shenghan; Gunson, Karen; Jui, Jonathan; Chugh, Sumeet S.

In: Heart Rhythm, Vol. 8, No. 8, 08.2011, p. 1177-1182.

Research output: Contribution to journalArticle

Reinier, Kyndaron ; Dervan, Celia ; Singh, Tejwant ; Uy-Evanado, Audrey ; Lai, Shenghan ; Gunson, Karen ; Jui, Jonathan ; Chugh, Sumeet S. / Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease. In: Heart Rhythm. 2011 ; Vol. 8, No. 8. pp. 1177-1182.
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T1 - Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease

AU - Reinier, Kyndaron

AU - Dervan, Celia

AU - Singh, Tejwant

AU - Uy-Evanado, Audrey

AU - Lai, Shenghan

AU - Gunson, Karen

AU - Jui, Jonathan

AU - Chugh, Sumeet S.

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N2 - Background: Following myocardial infarction, individual patients can have wide variations in the extent of left ventricular systolic dysfunction (LVSD) and increased left ventricular (LV) mass. Both affect the risk for sudden cardiac death, but only LV ejection fraction is used for risk prediction. Objective: The purpose of this study was to evaluate the independent as well as the additive contributions of increased LV mass and decreased LV ejection fraction to sudden cardiac death in the general population. Methods: In the ongoing Oregon Sudden Unexpected Death Study, we studied consecutive SCD cases (n = 191) and coronary artery disease controls (n = 203) from the Portland, Oregon, metropolitan area (population approximately 1,000,000; 20022008). Comparisons of echocardiographic LV mass obtained prior and unrelated to sudden cardiac death (SCD) were conducted, and a logistic regression model was used to evaluate the relationship between SCD, severe LVSD, LV mass, and other relevant clinical variables. Results: In a multivariate model, both severe LVSD and left ventricular hypertrophy (LVH) were associated with increased SCD risk (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.13.2 for severe LVSD; OR 1.8, 95% CI 1.12.9 for LVH). In patients with coexisting severe LVSD and LVH, risk of SCD was additive (OR 3.5, 95% CI 1.77.2). In the same model, increased age, atrial fibrillation/flutter, elevated creatinine, and diabetes independently increased risk, and use of angiotensin receptor blockers attenuated risk. Conclusion: Reduced LV ejection fraction and increased LV mass had independent and additive effects on risk of sudden death. Despite the significant overlap between the two conditions, these findings point toward the existence of independent mechanistic pathways for ventricular arrhythmias that occur due to LVSD and LVH.

AB - Background: Following myocardial infarction, individual patients can have wide variations in the extent of left ventricular systolic dysfunction (LVSD) and increased left ventricular (LV) mass. Both affect the risk for sudden cardiac death, but only LV ejection fraction is used for risk prediction. Objective: The purpose of this study was to evaluate the independent as well as the additive contributions of increased LV mass and decreased LV ejection fraction to sudden cardiac death in the general population. Methods: In the ongoing Oregon Sudden Unexpected Death Study, we studied consecutive SCD cases (n = 191) and coronary artery disease controls (n = 203) from the Portland, Oregon, metropolitan area (population approximately 1,000,000; 20022008). Comparisons of echocardiographic LV mass obtained prior and unrelated to sudden cardiac death (SCD) were conducted, and a logistic regression model was used to evaluate the relationship between SCD, severe LVSD, LV mass, and other relevant clinical variables. Results: In a multivariate model, both severe LVSD and left ventricular hypertrophy (LVH) were associated with increased SCD risk (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.13.2 for severe LVSD; OR 1.8, 95% CI 1.12.9 for LVH). In patients with coexisting severe LVSD and LVH, risk of SCD was additive (OR 3.5, 95% CI 1.77.2). In the same model, increased age, atrial fibrillation/flutter, elevated creatinine, and diabetes independently increased risk, and use of angiotensin receptor blockers attenuated risk. Conclusion: Reduced LV ejection fraction and increased LV mass had independent and additive effects on risk of sudden death. Despite the significant overlap between the two conditions, these findings point toward the existence of independent mechanistic pathways for ventricular arrhythmias that occur due to LVSD and LVH.

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KW - Heart failure

KW - Hypertrophy

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