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Temporal changes of noninvasive electrocardiographic risk factors for sudden cardiac death in post-myocardial infarction patients with preserved ejection fraction: Insights from the PRESERVE-EF study.

ABSTRACT: BACKGROUND:Several noninvasive risk factors (NIRFs) have been proposed for sudden cardiac death risk stratification in post-myocardial infarction (post-MI) patients with preserved ejection fraction (EF). However, it remains unclear if these factors change over time. METHODS:We evaluated seven electrocardiographic NIRFs as they were described in the PRESERVE-EF trial in 80 post-MI patients with EF ? 40%, at least 40 days after revascularization and 1 year later. RESULTS:Mean patient age was 56 ± 10 years, and 88% were men. Mean EF was 50 ± 5%. The prevalence of (a) positive late potentials (27.5% vs. 28.8%, p = .860), (b) >30 premature ventricular complexes/hour (8.8% vs. 11.3%, p = .598), (c) nonsustained ventricular tachycardia (8.8% vs. 5%, p = .349), (d) standard deviation of normal RR intervals <75 ms (3.8% vs. 3.8%, p = 1.000), (e) QTc derived from 24-hr electrocardiography >440 ms (men) or >450 ms (women) (17.5% vs. 17.5%, p = 1.000), (f) deceleration capacity ?4.5 ms and heart rate turbulence onset ?0% and slope ?2.5 ms (2.5% vs. 3.8%. p = 1.000), and (g) ambulatory T-wave alternans ?65 ?V in two Holter channels (6.3% vs. 6.3%, p = 1.000) were similar between the two measurements. However, five patients (6.3%) without any NIRFs during the first assessment had at least one positive NIRF at the second assessment and six patients (7.5%) with at least one NIRF at baseline had no positive NIRFs at 1 year. CONCLUSIONS:While the prevalence of the examined electrocardiographic NIRFs between the two examinations was similar on a population basis, some patients without NIRFs at baseline developed NIRFs at 1 year and vice versa, highlighting the need for risk factor reassessment during follow-up.

SUBMITTER: Xenogiannis I

PROVIDER: S-EPMC7358883 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Temporal changes of noninvasive electrocardiographic risk factors for sudden cardiac death in post-myocardial infarction patients with preserved ejection fraction: Insights from the PRESERVE-EF study.

Xenogiannis Iosif I Gatzoulis Konstantinos A KA Flevari Panagiota P Ikonomidis Ignatios I Iliodromitis Efstathios E Trachanas Konstantinos K Vlachos Konstantinos K Arsenos Petros P Tsiachris Dimitrios D Tousoulis Dimitrios D Brilakis Emmanouil S ES Alexopoulos Dimitrios D

Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc 20191012 1

<h4>Background</h4>Several noninvasive risk factors (NIRFs) have been proposed for sudden cardiac death risk stratification in post-myocardial infarction (post-MI) patients with preserved ejection fraction (EF). However, it remains unclear if these factors change over time.<h4>Methods</h4>We evaluated seven electrocardiographic NIRFs as they were described in the PRESERVE-EF trial in 80 post-MI patients with EF ≥ 40%, at least 40 days after revascularization and 1 year later.<h4>Results</h4>Mean ...[more]

PMID: 31605453

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Project description:BACKGROUND:The role of coronary microvascular disease and its impact on functional and energetic reserve in heart failure with preserved ejection fraction (HFpEF) remains unclear. We hypothesized that in response to submaximal pharmacologic stress (dobutamine), patients with HFpEF have impairment in left ventricular (LV) myocardial mechanical (external work [EW]), energetic (myocardial O2 consumption [MVO2]), and myocardial blood flow (MBF) reserve. We further assessed whether coupling of MBF to EW is impaired in HFpEF and associated with compensatory increases or pathological decreases in myocardial O2 extraction. Lastly, we assessed whether coupling of MVO2 to EW (mechanical efficiency) was impaired in HFpEF. METHODS AND RESULTS:In prospectively enrolled patients with HFpEF (n=19) and age/sex-matched healthy controls (n=19), we performed 11C-acetate positron emission tomography assessing MVO2 and MBF at rest and during dobutamine infusion. EW was calculated as stroke volume (echo)×end-systolic pressure×heart rate. At rest, compared with controls, patients with HFpEF had higher LV EW, MVO2, and MBF. With dobutamine, LV EW, MVO2, and MBF increased in both HFpEF and controls; however, the magnitude of increases was significantly smaller in HFpEF. In both groups, MBF increased in relation to EW, but in HFpEF, the slope of the relationship was significantly smaller than in controls. Myocardial O2 extraction was increased in HFpEF. Mechanical efficiency was similar in HFpEF and controls. In a post hoc analysis, HFpEF patients with LV hypertrophy (n=10) had significant reductions in LV mechanical efficiency relative to controls. CONCLUSIONS:In HFpEF during submaximal dobutamine stress, there is myocardial mechanical-, energetic- and flow-reserve dysfunction with impaired coupling of blood flow to demand and slight increases in myocardial O2 extraction. These findings provide evidence that coronary microvascular dysfunction is present in HFpEF, limits O2 supply relative to demand, and is associated with reserve dysfunction.

Project description:AimsThe prevalence of heart failure (HF) after acute myocardial infarction (AMI) is common. Contemporary data are lacking on the prognostic utility of the measurement of biomarker for patients with AMI complicated by HF according to preserved (HFpEF) and reduced ejection fraction (HFrEF). We aim to assess the association between D-dimer levels and all-cause mortality in patients with AMI complicated by different HF subtypes during hospitalization in the context of other risk factors.Methods and resultsWe enrolled 4495 patients with AMI with complete clinical and laboratory variable assessments in this cohort. D-dimer levels were measured on admission immediately at baseline. We used Cox proportional hazards analysis to assess this association accounting for 18 relevant clinical variables. During the index hospitalization, 589 patients with AMI developed HFpEF, 513 patients with AMI developed HFrEF, and 3393 patients with AMI did not develop HF. The patients were divided into HFpEF, HFrEF, and non-HF groups accordingly. The median length of follow-up was 1 year (range: 1 to 24 months). During the whole follow-up, 58 (15.5%), 107 (27.9%), and 96 (4.2%) of the patients experienced death event in HFpEF, HFrEF, and non-HF groups, respectively. In each group, the patients were divided into high or low D-dimer levels according to D-dimer concentration (145 ng/mL). In the fully adjusted model, the risk of all-cause mortality of those patients with high D-dimer levels was 2.09 [95% confidence intervals (CI): 1.08 to 4.02, P = 0.02] times as high as the risk of patients with low D-dimer levels in HFpEF group. When analysing D-dimer as a continuous variable, this associations still existed. But there was no significant association between D-dimer concentration and all-cause mortality in HFrEF [hazard ratio (HR): 1.25, CI: 0.76 to 2.04, P = 0.37] or non-HF (HR: 1.56, CI: 0.98 to 2.47, P = 0.06), respectively, after fully adjustment for other key clinical variables.ConclusionsHigh D-dimer levels on admission were found to be strongly associated with the subsequent cumulative incidence of all-cause mortality in patients with AMI complicated by HFpEF.

Project description:BackgroundHeart failure (HF) with preserved ejection fraction (HFpEF) constitutes half of all HF but lacks effective therapy. Understanding of its myocardial biology remains limited because of a paucity of heart tissue molecular analysis.MethodsWe performed RNA sequencing on right ventricular septal endomyocardial biopsies prospectively obtained from patients meeting consensus criteria for HFpEF (n=41) contrasted with right ventricular septal tissue from patients with HF with reduced ejection fraction (HFrEF, n=30) and donor controls (n=24). Principal component analysis and hierarchical clustering tested for transcriptomic distinctiveness between groups, effect of comorbidities, and differential gene expression with pathway enrichment contrasted HF groups and donor controls. Within HFpEF, non-negative matrix factorization and weighted gene coexpression analysis identified molecular subgroups, and the resulting clusters were correlated with hemodynamic and clinical data.ResultsPatients with HFpEF were more often women (59%), African American (68%), obese (median body mass index 41), and hypertensive (98%), with clinical HF characterized by 65% New York Heart Association Class III or IV, nearly all on a loop diuretic, and 70% with a HF hospitalization in the previous year. Principal component analysis separated HFpEF from HFrEF and donor controls with minimal overlap, and this persisted after adjusting for primary comorbidities: body mass index, sex, age, diabetes, and renal function. Hierarchical clustering confirmed group separation. Nearly half the significantly altered genes in HFpEF versus donor controls (1882 up, 2593 down) changed in the same direction in HFrEF; however, 5745 genes were uniquely altered between HF groups. Compared with controls, uniquely upregulated genes in HFpEF were enriched in mitochondrial adenosine triphosphate synthesis/electron transport, pathways downregulated in HFrEF. HFpEF-specific downregulated genes engaged endoplasmic reticulum stress, autophagy, and angiogenesis. Body mass index differences largely accounted for HFpEF upregulated genes, whereas neither this nor broader comorbidity adjustment altered pathways enriched in downregulated genes. Non-negative matrix factorization identified 3 HFpEF transcriptomic subgroups with distinctive pathways and clinical correlates, including a group closest to HFrEF with higher mortality, and a mostly female group with smaller hearts and proinflammatory signaling. These groupings remained after sex adjustment. Weighted gene coexpression analysis yielded analogous gene clusters and clinical groupings.ConclusionsHFpEF exhibits distinctive broad transcriptomic signatures and molecular subgroupings with particular clinical features and outcomes. The data reveal new signaling targets to consider for precision therapeutics.

Dataset Information

Temporal changes of noninvasive electrocardiographic risk factors for sudden cardiac death in post-myocardial infarction patients with preserved ejection fraction: Insights from the PRESERVE-EF study.

Publications

Temporal changes of noninvasive electrocardiographic risk factors for sudden cardiac death in post-myocardial infarction patients with preserved ejection fraction: Insights from the PRESERVE-EF study.

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