Rio Salado College
Left ventricular hypertrophy abnormality
Considerations in the Clinical Diagnosis and Efficacy of Electrocardiographic Criteria Versus Anatomical Implications in Left Ventricular Hypertrophy
25 April 2018
Among cardiovascular disorders, heart failure is the only disease with increasing incidence, prevalence, and mortality. Left ventricular hypertrophy is a maladaptive physiological abnormality of the heart that can present anatomically, electrically, or mixed; in response to increased intravascular pressure (also referred to as "pressure overload" and "concentric LVH") or fluid volume overload (also known as "eccentric LVH") from numerous possible factors. In accordance with the multiple forms that LVH is capable of presenting, recent studies have shown that independent risk factors exist within both LVH morphologies, suggesting that clinical diagnosis of LVH cannot be made with a single set of criteria alone. With the modern advancements in electrocardiography and echocardiography, dozens of complex diagnostic criteria specific to both forms of LVH have been developed. This review will attempt to explain the importance of using both sets of criteria in the diagnostic process, in an effort to better enhance the diagnostic efficacy of LVH in the clinical setting. Stress will be placed on the realization that each form of LVH presents with independent diagnostic implications, and that a thorough evaluation of both forms of criteria is crucial to the prognosis of LVH and its successful regression.
There is no argument that left ventricular hypertrophy (LVH) has presented with challenges regarding its diagnostic efficacy and therapeutic management. New advances in research have revealed distinct differences between electrical and anatomic LVH, implicating that they are in fact two separate entities containing certain characteristics that are independent from one another's physiological processes (Aro and Chugh). Additionally, studies have revealed large discrepancies regarding the specificity and sensitivity within the criteria used for both electrical and anatomical LVH, particularly when used alone. This knowledge promotes the need for further research on the methodology being used for LVH diagnosis, with the goal of enhancing the efficacy that current criteria are missing. In order to enhance the clinical efficacy of diagnostic criteria for both electrical and anatomic LVH, it must be considered that each form of the disease is its own entity demonstrating unique effects from external factors in combination with their pre-existing independent characteristics.
Although there are many similarities between both forms of LVH, including their presenting symptoms and long term effects on myocardial function, electrical and anatomic LVH are their own entities; respectively, the factors contributing to their existence are independent, and often do not have influence on each other(Aro and Chugh). The form of LVH that is present, regardless of whether it is electrical or anatomic has different pathological effects on the heart than its counterpart, suggesting the need to test for both forms of the disease prior to making the diagnosis or ruling it out. The pathology of electrical LVH is characterized by principle electrocardiogram (ECG) changes focused on alterations within the myocardial conduction system of the heart and does not necessarily indicate progression to tissue involvement. Morphological abnormalities of the P-wave, ST segment, and T-wave, as well as increases in QRS amplitude and duration such as what is seen in Sokolow-Lyon and Cornell criteria for ECG LVH, have been linked to increased LVH prevalence (Salles et al., 440; Hsieh et al.). These criteria are very specific toward LVH probability and provide good additional clinical information, however, studies have shown that the use of these criteria result in a low yield of sensitivity when compared with diagnostic imaging (Hancock et al.). This in part, is due to the prevalence of underlying ECG patterns and arrhythmias that mimic the criteria used for LVH. Studies involving changes in QRS vectors have indicated increased LVH prevalence. However this criterion is more complex when combined with others by involving cumbersome calculations to determine the result which is impractical (Hsieh et al.).
Little is understood about the processes and risk factors that precede the development of ECG LVH presentation without coexisting anatomic evidence, nor to the regards of the role that it plays in LVH progression. What is known is that electrocardiographic evidence for ECG LVH involves evaluation of different portions of the ECG based on the anatomical position that each lead is representing, making some criteria more reliable than others. This knowledge negatively contributes to the efficacy behind electrical diagnostic criteria for LVH because the specificity and sensitivity of each criterion remains dependent on the locational representation of each lead. Due to these differences in specificity and sensitivity, patients meeting one set of criteria for LVH often do not meet any others (Hancock et al.). The commonality within the most recent clinical research studies, however, is that there is limited reliability behind ECG LVH research due to limitations within the control groups. According to Aro and Chugh, the presence of ECG LVH criteria without corresponding evidence to suggest increased LV mass, makes it improbable that this isolated form of LVH has any myocyte hypertrophy involvement in comparison to the extent seen in anatomical LVH. In light of all of this, there is an extensive amount of research that has yet to be done regarding the development of ECG LVH without tissue involvement. Does ECG LVH without increased LV mass actually effect risk stratification if the patient isn't symptomatic? This is a complex question that will need additional investigation before further discussion can take place.
With the use of radiographic imaging such as echocardiography (echo), magnetic resonance imaging (MRI), and computed tomography (CT), anatomical LVH can be objectively diagnosed due to its high sensitivity as opposed to ECG LVH whose evidence is objectively insensitive. Diagnosis of increased left ventricular mass (LVM) with electrocardiography requires that both forms of criteria are met; diagnosis cannot be made by voltage or morphological criteria alone. This is due to the prevalence of underlying ECG patterns and arrhythmias that mimic the criteria used for LVH, attributing to its low sensitivity. Because of the discovery of high sensitivity found in echocardiography in the subsequent years, it has become the gold standard for anatomic LVH diagnosis and monitoring; despite the development of fairly detailed electrocardiographic criteria (Aro and Chugh). All radiographic diagnostic approaches to the identification of anatomical LVH have been developed for the assessment of myocardial tissue remodeling. Diagnostic imaging identifies increased ventricular mass, end diastolic volume (preload), systolic pressure against the heart (afterload), stoke volume, and ejection fraction of the left ventricle to rule out anatomic myocardial involvement.
Due to the high degree of effects that the heart and body have on each other, multiple extra-cardiac factors have been shown to affect the diagnostic results concurrently. Between both electrical and anatomic evidence for LVH, either inhibition or enhancement can play a role in decreased diagnostic specificity and sensitivity (Aro and Chugh; Bacharova et al. 200). This aid in crippled efficacy has shown to be influenced by multiple secondary factors including demographics, pre-existing medical conditions, body composition, and inheritance of certain primary and secondary genetic processes.
Demographic influences on development and diagnosis of LVH include age, gender, race, and ethnic background. A number of these factors have been found to promote increased diagnostic specificity and sensitivity; whereas, others have shown to decrease these measurements. Due to the developmental processes during infancy and early childhood years, there remains to be too much variation within the data to develop an accurate normal range for QRS voltage that can be used clinically for diagnosis or rule out. According to Hancock et al., "QRS voltages tend to decline with increasing age, indicating that current voltage criteria for LVH is more accurate in patients older than 35". Hancock et al. goes on further to explain that the standards for the 16 to 35 year age group are not well established. Studies suggest that amongst the younger populations, LVH is nearly twice as common among men, but as the population ages, it becomes more prevalent among women (Weber, 14).
By the use of randomized control groups, various studies, such as the one performed by Dr. Jan R. Weber at the University of Pennsylvania, have linked gender differences to altered diagnostic outcomes with confirmation by multiple sets of criteria. In a recent study reported by Bacchus et al., the results showed support for the theory that there is increased prevalence within the male population for the development of LVH. This study involved 209 people (124 female, 85 male), 39 of which showed criteria for LVH. Of these, 26 of the male congregation showed non-specific criteria for LVH as opposed to only 13 of the female population (Bacchus et al., 329-30). In a different study, Framingham investigators were able to show in that in a group of 510 men and 855 women, a higher prevalence for LVH development existed in women as opposed to men (Savage et al.) In light of this conflicting evidence, it was noted that multiple conflicting limitations existed between these studies, including, size of the study, age, and previous health history. These inconsistencies support the need for more strict criteria, such as seen in combined use of electrical and anatomic criteria. This will increase both the specificity and sensitivity alike, for greater removal of these limitations.
Additional extra-cardiac factors such as race and ethnicity must also be considered due to their strong genetic influence. This may play a key role in the development of LVH in certain populations. Studies indicate that the racial and ethnical predispositions to LVH are at their highest with African Americans, followed by Hispanics with the lowest, with Euro-Americans in the middle (Schlaich and Schmieder, 1395). The average LV mass index in the African American population is greater than the white population, in both the men and women (Weber, 16). According to more recent research, patients with ECG evidence of LVH were more likely to be African American compared to those without ECG evidence (Hsieh et al.). Likewise, reports from Havranek et al. conclude that "left ventricular hypertrophy by echocardiography was associated with a higher population risk for mortality in African American patients than in whites". In conjunction with mild to moderate hypertension, African Americans have higher sensitivities yet lower specificities to LVH than Euro-Americans when using the Sokolow-Lyon criteria; whereas, the Cornell criteria shows lower sensitivity but higher specificity in the same population (Hancock et al.). Although race and ethnical backgrounds have proven to be factors in LVH development and progression, ECG evidence supporting this is anything but reliable. This is in opposition to greater consistencies with reported anatomic evidence for LVH.
Predisposing health risks including body composition and pre-existing comorbidities have also been found to play an influential role in the development and progression of LVH. Demonstrated by the Framingham study, left ventricular mass compared to the extent of obesity (BMI greater than 30%) has been found to be correlated with each other (Savage et al.). This correlation between LV mass and obesity is consistent between both males and females. Through the comparison of a large number of studies it appears that obesity is not dependent upon age or gender, having only a direct correlation between the degrees of BMI to LVH. Another common observation is the association of increased mass by echocardiography but not increased QRS voltage, possibly due to the insulating effect of adipose tissue and the greater distance between the heart and chest wall electrodes (Hancock et al.). In additional studies involving patient with mild to moderate hypertension, the prevalence of the Cornell criteria was higher in the obese than the non-obese; whereas, the Sokolow-Lyon was less sensitive to the obesity but more sensitive to the non-obese (Nath et al., 128; Abergel et al., 739). This evidence further suggests the need for careful consideration of the patient's body composition in conjunction with diagnostic implications. This patient specific method is critical in determining which form of electrical criteria should be used in conjunction with echocardiography in the clinical setting.
Adding to the influence that obesity has on LVH development and progression is a review regarding the therapeutic approach and regression of LVH. According to Schlaich and Schmieder, the presence of obesity has been shown to increase the risk for LVH 1.5- to 2-fold. Studies correlating weight reduction to decreased blood pressure have been found to indirectly contribute to LVH regression and a decrease in LVM (Schlaich and Schmieder, 1401). In comparison, another study researching the regression of LVH with the use of beta-blockers, found that weight loss in within subjects was directly associated with reduced LVM, regardless of changes in BP (MacMahon et al., 1235). In addition, these studies found that the implementation of routine exercise regimens was proven to have positive results contributing to decreased blood pressure and influence of LVH regression (Schlaich and Schmieder, 1402). Interesting however, is the evidence showing that routine exercise provided no indication for decreases in left ventricular mass. This, in comparison to the weight loss results, is contradictory of one another due to the identical nature of the interventions used for both forms of treatment. The identical influence on biological processes taking place during both treatments is also contradictory to these results; providing suggestion for possible contamination of one or more of the control groups taking place within studies and the need for more detailed evaluation.
Pre-existing medical conditions such as hypertension (HTN) and other cardiovascular diseases have shown to greatly increase the risks for development of LVH. In addition, concurrent presence of these comorbidities also decreases LVH prognosis and increases its rate of mortality. Hypertension is the most common predisposing disease leading to LVH, making it also the highest stressed preventatives for LVH (Deedwania, 280). According to Lovic et al., LVH is initially a transitional phase and compensatory process in response to arterial hypertension; and because so, early detection and treatment of hypertension are of large clinical and practical importance. Other forms of cardiomyopathy have also shown to either mimic or lead to the development of LVH including, aortic stenosis, mitral valve regurgitation, and mitral valve prolapse (To et al.). Another thing to consider in the diagnostic process and clinical efficacy of LVH criteria is that these pre-existent disease processes affect the diagnosis of LVH prior to its actual development. This is due to the effects that their pathological and morphological processes have on the myocardial tissue and its conduction. Because of this, it is also known that existence of these other diseases alongside LVH is also influential in the presentations and diagnosis of both electrical and anatomical forms of LVH.
Due to the genetic influences taking place at the cellular level, predispositions to prior family history has been found to play a significant role in the development and prognostic implications for LVH. Due to genetics, each person's biological processes work in specific ways, possibly altering the presentations and diagnostic evidence of LVH (Aro and Chugh). According to Mayosi et al. "Genetic factors may explain a significant proportion of variability in quantitative electrocardiographic and echocardiographic measures of left ventricular hypertrophy." Studies show that there is a greater heritability for Sokolow-Lyon voltage than other popular criteria such as Cornell and Romhilt-Estes. In a study involving a genome-wide scan also showed a distinctly stronger genetic link for LVH with the use of the ECG more so than echocardiogram (Mayosi et al., 525). Because of this, ECG phenotypes in the molecular investigation of the genetic susceptibility to LVH may be important (Mayosi et al., 1963). The genetic links that have been found to affect the diagnostic results of both forms of LVH provides only further proof supporting the importance of incorporating all forms of diagnostic criteria into clinical processes.
To compare the efficacy between these extra-cardiac factors certain ones have been found to have greater influence on outcome accuracy than others. At the same time, the degree to which these extra-cardiac factors influence the heart has also shown to be quite inconsistent between multiple studies. Knowing this, the possibility of additional, unknown factors contributing to this inconsistency cannot be ruled out. The possibility of contaminated control groups within past studies should also be considered.
Because of their physical and pathophysiological differences, the criteria for neither electrical LVH nor anatomic LVH can effectively diagnose or rule out ventricular hypertrophy independently. This is because both criterion lack of specificity and sensitivity. The reliance on ECG criteria alone may overlook the presence of other possible life threatening morphologies due to the lack of sensitivity (Hsieh et al.). While, in concentric and eccentric anatomical LVH there are greater effects on the myocardial tissue as opposed to its conduction system, thus increasing sensitivity yet lacking specificity. Composite criteria, when combined with ECG LVH patterns, have been associated with higher adjusted hazard ratios compared to voltage criteria alone (Hsieh et al.). It has also been shown that cases of LVH identified by voltage criteria alone are not all predictive of cardiovascular mortality when certain risk factors are taken into consideration. This was proven during the Framingham study when it was found that excess cardiovascular risk associated with only voltage criteria, was virtually eliminated when adjustment was made for co-existent hypertension (Hsieh et al.). In contrast, studies involving a combination of both voltage and anatomic criteria have shown an increased sensitivity to the prediction of cardiovascular mortality (Larsen et al., 319). The credibility behind this increase in sensitivity is due to a lack of change affecting the results when adjusting for clinical variables. A large number of studies have demonstrated that the risk for cardiovascular events increases depending on the type of LVH (Lovic et al., 390). Criteria in use today contain too much limitation preventing the maintenance of high levels of accuracy independently. For these reasons, no singular criteria can effectively diagnose either form of LVH without supportive evidence from other criteria (Hancock et al.). This evidence further stresses the suggestion for thorough evaluation and attention regarding electrocardiographic evidence for LVH, alongside the use of anatomical diagnostic criteria.
Due to the highly volatile degrees of sensitivity and specificity of diagnostic criteria for both electrical and anatomical LVH, the differential diagnosis must be evaluated through combination of both criteria. Commonly, acute medical conditions can be overlooked or missed due to the resemblance with LVH through either ECG or anatomical presentation, increasing the risk factors for patient mortality in the clinical setting. With ECG LVH, certain leads have more influence and higher specificity than others when evaluating for LVH. Namely, the leads focusing on the left ventricle in the lateral leads of I, aVL, V5, and V6, as well as the septal and anterior leads of V1, V2, V3, and V4. A number of studies have suggested that the presence of similar morphologies in the inferior leads of II, III, and aVF have shown a higher prevalence of acute myocardial ischemia as opposed to LVH. This has not only been found to expand other possible differential diagnosis, but also makes the clinical approach very complex and the therapeutic prognosis difficult.
Because the dozens of different electrical criteria for LVH is highly specific yet very insensitive, differential diagnoses with similar morphologies need to be considered. Due to the almost exact morphology, acute myocardial ischemia is the biggest diagnostic differential in suggestive electrical LVH (Carey et al.). This includes acute anterior myocardial infarctions, and acute coronary syndromes. Anterior infarcts are nearly hidden entirely with LVH voltage (Pipberger et al.). Because of this, blood testing in addition to diagnostic imaging is imperative in the suspicion for acute infarct. Acute coronary syndrome is the most common form of acute ischemia and can mimic the electrical patterns of LVH when it is present in congruent leads (Pollehn et al.).
Left ventricular "strain pattern" is the most recognized marker for LVH on ECG, however its diagnostic sensitivity is of little reliability. This is because the "strain pattern" seen on ECG can also be indicative of other forms of cardiomyopathy including aortic stenosis, mitral valve prolapse, and mitral regurgitation (Ogah et al.). Evidence suggests that the presence of "strain pattern" type ST-T morphology with increased QRS voltage is associated with larger values for LV mass and higher risks for cardiovascular complications (Kannel et al, 815.; Okin et al., 50). However Hancock et al. goes further to explain that "this evidence is an insufficient indication whether this pattern has more clinical implication than lesser ST-T abnormalities". An opposing argument to this from a case study involving middle-aged individuals without prior cardiovascular disease concluded that ECG strain was in fact associated with higher risks. These increased risks included death, incidental heart failure, myocardial infarction, and cardiovascular disease (Inoue et al.). This is in addition to the risk of the development of LV concentric remodeling. In response to these conflicting data sets is the argument that because of the identical nature of ventricular strain pattern to other forms of myocardial ischemia and cell death, the use of this criteria should not be considered for use in the clinical setting (Hancock et al.).
Anatomical diagnostic criteria for LVH is highly sensitive to hypertrophic cardiomyopathy, however lacks a great deal of sensitivity; making the differential diagnosis of anatomical LVH crucial to determine the exact disease process (Aro and Chugh). Obstructive cardiomyopathy without hypertrophy has a common resemblance to left ventricular wall structure consistent on consistent to LVH on echocardiogram imaging. Aortic stenosis has been shown to be the most prevalent contributor to this form of cardiomyopathy miming anatomic LVH. Rudolph et al., explains the prevalence of aortic stenosis and myocardial fibrosis, in that, they have been shown be highly prevalent (up to 50%) in accompany of anatomical LVH. However, this statistic was only applied to patients with advanced stages of LVH and/or aortic stenosis. This data shows the difficulty involved in the differentiation of these diseases with only non-invasive techniques. Diagnosis in the athletic population is especially difficult, yet crucial. Hypertrophic cardiomyopathies, namely LVH, account for nearly one third of all exercise related sudden cardiac deaths (Basavarajaiah et al., 729). Studies involving athletic heart syndrome (AHS), have shown that this exercise induced cardiomegaly mimics the anatomic physiology of LVH with mild enlargement of the left ventricular cavity (To et al.). The studies found that the distinguishing factor characteristic to AHS is the anatomic symmetry of LV wall thickening accompanied by normal diastolic function, indicated increased muscle and not pathologic compensation.
There are many different disease processes, many of which need emergency intervention. This puts into perspective the possible consequences that can ensue if the appropriate diagnostic algorithms and criteria not used. This fact alone is more than enough reason to make the appropriate changes to the diagnostic processes for LVH for the enhancement of the diagnostic efficacy for clinical LVH. This review of diagnostic LVH criteria has proven that, in order to successfully enhance the clinical efficacy of diagnostic criteria for both electrical and anatomic LVH, acknowledgment that each form of the disease are separate entities demonstrating unique effects from external factors in combination with pre-existing independent characteristics. The data shows that no single criteria can be used for the clinical diagnosis of LVH. There must be supporting evidence by verified criterion to accurately and safely diagnose LVH in the clinical setting. Furthermore, implementation of diagnostic criteria fueled by patient-specific factors may also prove to be influential in the diagnostic efficacy of clinical LVH.
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