SPC365

Left bundle branch block – Is it possible to predict left ventricle dysfunction?

Session: Posters (Sessão 1 - Écran 4) - Insuficiência Cardíaca 1 - Vários 1
Speaker: Joao Santos Fonseca

Congress: CPC 2022
Topic: D. Heart Failure
Theme: 10. Chronic Heart Failure
Subtheme: 10.3 Chronic Heart Failure – Diagnostic Methods
Session Type: Pósters Electrónicos
FP Number: ---
Authors: Joao Santos Fonseca; Pedro Silvério António; Sara Couto Pereira; Joana Brito; Beatriz Valente Silva; Pedro Alves da Silva; Ana Beatriz Garcia; Ana Margarida Martins; Catarina Simões de Oliveira; Ana Abrantes; Miguel Azaredo Raposo; Joana Rigueira; Rui Plácido; Cláudio David; Fausto j. Pinto; Ana g. Almeida

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction: </strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Left bundle branch block (LBBB) might be a cause of left ventricle dysfunction (LVD) even in patients without cardiomyopathy or ischemic heart disease. Predict which patients (pts) with LBBB and normal left ventricle ejection fraction (LVEF) will develop LVD remains challenging.</span></span></span></p>

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<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Objective: </strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Our aim was to identify echocardiographic and electrocardiographic (ECG) predictors of LVD in pts with LBBB.&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods: </strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Retrospective, single-centre study</span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong> </strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">of 839 consecutive pts with documentation of </span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><em>LBBB</em></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#ff0000"><em> </em></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><em>and LV disynchrony</em></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"> from our echocardiographic and ECG database from January 2010 to December 2020. Other inclusion criteria were (1)initially preserved LVEF (&ge;50%), (2)absence of documented clinically relevant coronary arterial disease/cardiomyopathy and (3)echocardiographic reassessment of LVEF after a follow up period (FUP) of &ge;6 months. Baseline echocardiographic, ECG and clinical data were recorded. Statistical analysis was performed using Kaplan-Meier curves for survival, Chi-square and Mann-Whitney tests to look for predictors of LVD.&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results: </strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">After screening, 59 pts were included with a mean age of 70&plusmn;12 years, 35.6% males, 83.1% hypertensive, 27.1% diabetic, 39% with dyslipidemia and atrial fibrillation in 25.4%. Most of the pts were at sinus rhythm (74.6%), with mean average QRS 151&plusmn;13.5 msec and 59.3% with typical LBBB pattern. At baseline, the mean LVEF was 59&plusmn;6%, enddiastolic (TD) and endsystolic (TS) diameter was 52&plusmn;6mm and 34&plusmn;7mm, respectively; mean TD and TS volume was 106&plusmn;30 mL and 44&plusmn;16 mL, respectively. The global longitudinal strain (GLS) was globally reduced (mean -14.3&plusmn;-3.2%; normal cut-off value &ge;-18%). During FUP (mean 51&plusmn;25 months), LVEF decreased to &lt;45% in 23.7% pts and a reduction &ge;10% from baseline was seen in 35.6% pts. A higher TS (p=0.013) was associated with LVD with LVEF&lt;45%. Higher TD (p=0.048) and TS (p=0.002) also associated with LVD with LVEF&lt;50%. GLS and QRS duration didn&rsquo;t associate with LVD during FUP. Pts who developed LVD had higher risk of HF hospitalizations (Log rank 11.4, p&lt;0,001; </span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>figure 1</strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">) and death (9 vs 2pts in LVEF&lt;45%, p=0.013).</span></span></span></p>

<p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusion: </strong></span></span></span><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Our study supports that LBBB might be a cause for LVD even without documented structural heart disease. TD and TS associated LVD in our sample. Although prospective trials with a higher number of pts are warranted, we hypothesized that these group of pts might benefit of early cardioprotective treatment and closer FUP.</span></span></span></p>