The QRS complex—a biomarker that “images” the heart: QRS scores to quantify myocardial scar in the presence of normal and abnormal ventricular conduction☆
Introduction
Acute myocardial infarction (MI) and chronic fibrosis (scar) from ischemic or nonischemic etiology create regions of slowed conduction providing a substrate for reentrant arrhythmias.1 Even in nonischemic cardiomyopathy the scar could be produced by the disruption of blood flow at a microvascular level. In the manuscript, we will review the ability of the QRS complex from the body surface electrocardiogram (ECG) to identify, localize, and quantify (essentially image) MI and chronic fibrosis. This has been documented extensively through specificity2, 3, 4 and necropsy studies4, 5, 6, 7, 8 in the absence of ECG confounders (ie, hypertrophy and conduction defects). In addition, we will lay the theoretical groundwork for how, after taking into account the electrical activation (depolarization) sequence in these confounders, the ECG can potentially be used to quantify MI and fibrosis in any conduction type.4 In the past, it has been difficult to accumulate enough patients in each conduction type to test this hypothesis in rigorous necropsy and specificity studies. However, cardiac magnetic resonance imaging (MRI) with late gadolinium enhancement can now accurately identify and quantify MI and fibrosis in vivo.9, 10
Although not reported in detail in the manuscript, we are currently testing new QRS score criteria to quantify scar for use in all types of ventricular conduction. Ischemic and nonischemic cardiomyopathy patients receive ECG and MRI before implantation of cardioverter-defibrillators. Recent studies have shown that quantification of scar by MRI can identify substrates for reentrant arrhythmias as defined by electrophysiologic testing11, 12 and post-MI mortality.13 In addition, MRI has been used to quantify myocardial scarring/fibrosis in nonischemic cardiomyopathy14, 15 and was associated with inducibility of ventricular arrhythmias16 and increased mortality.17, 18
Although the use of cardiac MRI to risk-stratify patients is promising, it is expensive and currently not widely available. Thus, if QRS scoring can “image” scar size in ischemic and nonischemic cardiomyopathy patients with all types of ventricular conduction, it could have important clinical implications in risk-stratifying patients before implantation of cardioverter-defibrillators.
Section snippets
Traditional ECG criteria for infarction (1920s to 1960s)
In 1918, Smith19 recorded the ECG in dogs after ligating coronary arteries, and in 1920, Pardee20 recorded an ECG of a patient with an acute coronary occlusion. Early studies in the first half of the 20th century comparing ECG diagnosis of MI with postmortem anatomical analysis often involved patients with multiple infarcts, and the ECG was not thought to be reliable at diagnosing MI or determining MI location. In addition, the diagnosis of MI was, and continues to be, confounded by the use of
Technology for quantitative cardiology (1950s to 1970s)
Four major advances occurred in the 1950s to 1970s that laid the groundwork for the development of quantitative electrocardiographic analysis of infarction:
- 1.
the development of the multiterminal intramural needle that could be used to map the spread of electrical depolarization in animal and eventually human hearts26, 27, 28;
- 2.
the introduction of computers into biomedical research to study the relation between experimentally measured activation sequences and simulated body surface ECGs and
Simplified QRS MI size score (1982 version)
In 1977, Savage et al33 performed detailed postmortem histologic analyses of hearts with computer digitization of infarct location in patients with single well-circumscribed infarcts. Before studying the relation between the QRS MI size score and postmortem infarct size, they reported the ability of QRS changes to simply localize infarcts. They showed that anteroseptal MIs were associated with Q waves or markedly diminished R waves in V1 through V3 and inferior MIs were associated with Q waves
QRS MI size scoring in the presence of hypertrophy and conduction defects
According to traditional dogma, fascicular blocks, bundle branch blocks, and hypertrophy simulate or conceal the ECG signs of infarction.60, 61 In contrast, the systematic simulation of combinations of these pathologies suggested that once the correct underlying activation sequence is taken into account, the ECG can in fact detect and quantify infarction.4 QRS scores for use in the presence of these confounders were developed from the simulations and then adjusted after comparison with coronary
Conclusions and future directions
Throughout the first half of the 20th century, numerous studies assessed the association between ECG findings and postmortem anatomical analysis; however, these studies were confounded by the inclusion of the sickest most complex patients who died. It was not possible to unscramble the complex interactions of infarction, hypertrophy, and conduction defects. In the 1950s to 1970s, the development of multiterminal needle (plunge) electrodes led to the determination of the electrical
Acknowledgments
David Strauss thanks Drs Katherine Wu, Håkan Arheden, Galen Wagner, and Peipei Ping for ongoing mentorship and support. The ongoing research is supported by the Donald W. Reynolds Cardiovascular Research Center at Johns Hopkins University, Baltimore, MD. The authors thank Dr Katherine Wu and all the Reynolds investigators for allowing them to present 2 ECG and MRI patient examples. They thank Eric Bergvall for assistance in presentation of the 3-dimensional MRI image.
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David Strauss is supported by the Sarnoff Cardiovascular Research Foundation.