Relation of Death Within 90 Days of Non-ST-Elevation Acute Coronary Syndromes to Variability in Electrocardiographic Morphology

Syed, Zeeshan; Scirica, Benjamin M.; Mohanavelu, Satishkumar; Sung, Phil; Michelson, Eric L.; Cannon, Christopher P.; Stone, Peter H.; Stultz, Collin M.; Guttag, John V.

doi:10.1016/j.amjcard.2008.09.099

Cited by 19 publications

(28 citation statements)

References 8 publications

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“…The derivation cohort consisted of 765 patients, with 14 deaths within 90 days. The derivation cohort was used to derive parameters for a new MV risk metric (morphologic variability in beat‐space [MVB], described below) and was the same population that the original MV metric was derived from …”

Section: Methodsmentioning

confidence: 99%

“…The risk metric, MVB, quantifies beat‐to‐beat variability in ECG signals and is an evolution of a previously described metric, MV . Unlike TWA, which only considers alternating morphologic changes in the ST segment or T wave, MV quantifies morphologic changes in the entire beat, including the TP segment.…”

Section: Methodsmentioning

confidence: 99%

“…There are data to suggest that heart‐rate–based metrics, such as heart rate variability (HRV), deceleration capacity (DC), heart rate turbulence (HRT), severe autonomic failure (SAF), and heart rate motifs, measure autonomic modulation of heart rate. Morphology‐based metrics include T‐wave alternans (TWA), which is designed to measure specific alternating changes in cardiac repolarization, morphologic variability (MV), which is designed to quantify the beat‐to‐beat morphologic variability in ECG signals, and symbolic mismatch, which is designed to uncover anomalous patterns of beats.…”

Section: Introductionmentioning

confidence: 99%

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ECG Morphological Variability in Beat Space for Risk Stratification After Acute Coronary Syndrome

Liu

Syed

Scirica

et al. 2014

JAHA

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BackgroundIdentification of patients who are at high risk of adverse cardiovascular events after an acute coronary syndrome (ACS) remains a major challenge in clinical cardiology. We hypothesized that quantifying variability in electrocardiogram (ECG) morphology may improve risk stratification post‐ACS.Methods and ResultsWe developed a new metric to quantify beat‐to‐beat morphologic changes in the ECG: morphologic variability in beat space (MVB), and compared our metric to published ECG metrics (heart rate variability [HRV], deceleration capacity [DC], T‐wave alternans, heart rate turbulence, and severe autonomic failure). We tested the ability of these metrics to identify patients at high risk of cardiovascular death (CVD) using 1082 patients (1‐year CVD rate, 4.5%) from the MERLIN‐TIMI 36 (Metabolic Efficiency with Ranolazine for Less Ischemia in Non‐ST‐Elevation Acute Coronary Syndrome—Thrombolysis in Myocardial Infarction 36) clinical trial. DC, HRV/low frequency–high frequency, and MVB were all associated with CVD (hazard ratios [HRs] from 2.1 to 2.3 [P<0.05 for all] after adjusting for the TIMI risk score [TRS], left ventricular ejection fraction [LVEF], and B‐type natriuretic peptide [BNP]). In a cohort with low‐to‐moderate TRS (N=864; 1‐year CVD rate, 2.7%), only MVB was significantly associated with CVD (HR, 3.0; P=0.01, after adjusting for LVEF and BNP).ConclusionsECG morphological variability in beat space contains prognostic information complementary to the clinical variables, LVEF and BNP, in patients with low‐to‐moderate TRS. ECG metrics could help to risk stratify patients who might not otherwise be considered at high risk of CVD post‐ACS.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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ECG Morphological Variability in Beat Space for Risk Stratification After Acute Coronary Syndrome

Liu

Syed

Scirica

et al. 2014

JAHA

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“…In MERLIN-TIMI 36, 20% of 6,355 patients experienced at least 1 episode of ischemia on cECG within 7 days of NSTE-ACS, and such patients experienced a nearly 3-fold increase in mortality and 2-fold increase in recurrent myocardial infarction (MI) over the next year (27). Furthermore, high morphologic variability in the shape of the entire heart beat signal on 24-h cECG monitoring within 48 h post NSTE-ACS in DISPERSE-2 TIMI 33 trial was associated with a marked increase in the risk of death at 90 days (adjusted hazard ratio [HR]: 6.9, p ϭ 0.001) (28).…”

Section: Noninvasive Assessmentsmentioning

confidence: 99%

The Year in Non–ST-Segment Elevation Acute Coronary Syndrome

Giugliano

Braunwald

2009

Journal of the American College of Cardiology

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EpidemiologyMortality following acute myocardial infarction has declined by approximately 30% over the past 2 decades (1), although the burden of coronary heart disease (CHD) remains high. This year, it is estimated, on average, approximately 1 American will have an acute coronary event every 25 s, resulting in 1 death per minute (2). The prevalence of NSTE-ACS is increasing relative to ST-segment elevation myocardial infarction (STEMI) due to changes in the distribution of risk factors in the population (e.g., older age, predominance of females, higher rate of diabetes) (1), use of preventative medications (3), and increasingly sensitive troponin assays (4). Two risk factors heading in opposite directions are smoking and obesity. Smoke-free legislation appears to have reduced hospitalization for ACS (5), whereas the obesity-diabetes pandemic has resulted in a disproportionate increase in non-ST-segment elevation myocardial infarction (NSTEMI) among young patients (each 5 kg/m 2 increase of body mass index is associated with a 3-year decrease in age of first NSTEMI) (6). PathophysiologyOur understanding of the pathophysiology of ACS continues to improve, particularly with advances in imaging techniques and biomarkers. Two invasive imaging techniques-optical coherence tomography and intravascular ultrasound-can identify vulnerable plaques with thin-capped fibroatheromas (TCFA) and positive remodeling in patients with ACS (7). These plaque morphologies have been associated with subsequent adverse cardiac events (8). Interestingly, different stressors may cause a plaque to rupture in different locations (e.g., exertion: thick shoulder [9], diabetes: thin midportion [10]). This raises the hope that information regarding plaque morphology could be helpful in prioritizing risk factors and setting treatment goals.In addition to the well-known risk factors leading to lipid-rich vulnerable plaques, a number of intriguing studies have linked nontraditional factors such as panic disorder (11), physical distress (12), and insufficient sleep (13) to incident CHD. Evaluation of both pharmacologic (e.g., with serotonin reuptake inhibitors [14]) and nonpharmacologic therapies (e.g., use of music [15] and patient information sheets [16]) directed at reducing anxiety, depression, and stress are needed.Although plaque rupture and intraluminal obstruction are the most common mechanisms underlying an ACS, in the CASPAR study (17), nearly 25% of patients with ACS prospectively undergoing coronary angiography did not have a culprit lesion. Furthermore, nearly one-half of these patients without culprit lesions exhibited ischemic ST changes after administration of intracoronary acetylcholine, suggesting that these patients may benefit from therapies (e.g., calciumblockers, nitrates) directed at preventing spasm. Although the notion of coronary artery spasm serving as one of the important mechanisms underlying ACS is not new (18), the findings of the CASPAR study remind us that coronary artery endothelial function, in addition to vessel m...

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“…In the Dose confirmation Study assessing anti-Platelet Effects of AZD6140 vs. clopidogrel in non–ST-segment Elevation myocardial infarction-2 (DISPERSE-2) trial, patients with high morphologic variability showed an increased risk of death during follow-up (hazard ratio 8.46; p <0.001). [44] The relationship between high morphologic variability and death could be observed even after adjusting for baseline clinical characteristics and heart rate variability measures (adjusted hazard ratio 6.91; p = 0.001).…”

Section: Introductionmentioning

confidence: 99%

The Clinical Significance of Continuous ECG (Ambulatory ECG or Holter) Monitoring of the ST-Segment to Evaluate Ischemia: A Review

Wimmer¹,

Scirica²,

Stone³

2013

Progress in Cardiovascular Diseases

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Silent ischemia is a common manifestation of coronary artery disease (CAD). Continuous ECG (cECG) monitoring is an effective tool for assessing the frequency and duration of silent ischemic episodes for patients with CAD and for risk stratifying asymptomatic patients or those after an acute coronary syndrome by identifying those at increased risk for future cardiovascular events or death. cECG also allows monitoring of the effectiveness of therapy in patients with CAD. Treatment strategies targeted toward the elimination of silent ischemia have shown that revascularization was better than medical therapy in eliminating silent ischemia, but large scale, prospective studies targeting silent ischemia as a treatment endpoint are still lacking. Future research is warranted to study the effects of newer medical agents or the selected use of revascularization in those patients with persistent silent ischemia despite current medical regiments.

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Relation of Death Within 90 Days of Non-ST-Elevation Acute Coronary Syndromes to Variability in Electrocardiographic Morphology

Cited by 19 publications

References 8 publications

ECG Morphological Variability in Beat Space for Risk Stratification After Acute Coronary Syndrome

ECG Morphological Variability in Beat Space for Risk Stratification After Acute Coronary Syndrome

The Year in Non–ST-Segment Elevation Acute Coronary Syndrome

The Clinical Significance of Continuous ECG (Ambulatory ECG or Holter) Monitoring of the ST-Segment to Evaluate Ischemia: A Review

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