Electrocardiographic left ventricular hypertrophy in patients with suspected acute cardiac ischemia—Its influence on diagnosis, triage, and short-term prognosis
ABSTRACT Objective: To understand the diagnostic and short-term prognostic significance of electrocardiographic left ventricular hypertrophy
(ECG-LVH) for patients who present to the emergency department with symptoms suggesting acute cardiac ischemia, defined as
new or unstable angina pectoris or acute myocardial infarction.
Design: Subgroup analysis of a multicenter, prospective study of coronary care unit admitting practices in the prethrombolytic era.
Setting: The emergency departments of six New England hospitals: two urban medical school teaching hospitals, two medical school—affiliated
community hospitals in smaller cities, and two rural nonteaching hospitals.
Patients: 5,768 patients presenting with symptoms suggesting possible acute cardiac ischemia, including 413 patients who had ECG-LVH
defined by the Romhilt-Estes point score criteria and 5,355 patients who had other electrocardiogram (ECG) findings.
Main results: Only 26% of the 413 patients who had ECG-LVH were ultimately judged to have had acute cardiac ischemia, compared with 72%
of patients who had primary ST-segment and T-wave abnormalities (p<0.001) and 36% of those who had other ECG abnormalities
(p<0.001). Overall, the ECG-LVH patients were one-third less likely than the patients who did not have ECG-LVH to have had
acute cardiac ischemia, after controlling for other predictors of acute ischemia by logistic regression (relative risk=0.66,
95% CI 0.46 to 0.94). The patients who had ECG-LVH were only one-fourth as likely to have had acute myocardial infarctions
as were the patients presenting with primary ST-segment and T-wave changes (12% vs 48%, p<0.001). Instead, a much larger proportion
had had congestive heart failure or hypertension. The admitting physicians had identified ECG-LVH poorly on the admitting
ECGs: only 22% of those who had ECG-LVH had been correctly identified, and for more than 70%, the secondary ST-segment and
T-wave changes of ECG-LVH had been read as being primary. The short-term mortality for the patients who had ECG-LVH was 7.5%.
This was intermediate between the mortality for patients who had primary ST-segment and T-wave abnormalities (10.6%) and those
who had other ECG abnormalities (5.1%). Mortality was not affected by whether the admitting physician had recognized ECG-LVH
Conclusion: ECG-LVH was not a benign ECG finding among the patients who had presented with symptoms suggesting an acute cardiac ischemic
syndrome: short-term mortality among the patients who had ECG-LVH (7.5%) approached that for the patients who had primary
ST-segment and T-wave abnormalities (10.6%, p=0.10). However, the patients who had ECG-LVH were one-thirdless likely to have had any acute cardiac ischemia than were the patients who did not have ECG-LVH, after logistic regression
was used to control for other predictors of acute ischemia. Specifically, acute myocardial infarction was only one-fourth
as likely when LVH was present on the admitting ECG (12%) as it was when primary ST-segment and T-wave abnormalities were
present (48%, p<0.001). Instead, congestive heart failure and hypertensive heart disease were more common. Thus, routine use
of thrombolytic therapy for patients who have ECG-LVH does not seem warranted. ECG-LVH was poorly recognized (in only 22%
of cases) by the physicians in the present study. Better recognition of this common ECG finding may lead to more effective
- SourceAvailable from: Steffen Erhard Petersen
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- "Left ventricular hypertrophy is one of the characteristic cardiac adaptations to obesity. [1-3] As there is now a growing body of literature that has demonstrated a strong relationship between left ventricular hypertrophy and all cause mortality, [4-6] and given the increasing prevalence of obesity, and the fact that obesity is associated with an increased risk of death , understanding the ways in which obesity modulates cardiovascular risk is of increasing clinical importance. Furthermore, identification of the determinants of left ventricular mass in obesity has potentially important implications for prognosis and therapeutic intervention aimed at primary and secondary prevention. "
ABSTRACT: Obesity is linked to increased left ventricular mass, an independent predictor of mortality. As a result of this, understanding the determinants of left ventricular mass in the setting of obesity has both therapeutic and prognostic implications. Using cardiovascular magnetic resonance our goal was to elucidate the main predictors of left ventricular mass in severely obese subjects free of additional cardiovascular risk factors. 38 obese (BMI 37.8 +/- 6.9 kg/m2) and 16 normal weight controls subjects, (BMI 21.7 +/- 1.8 kg/m2), all without cardiovascular risk factors, underwent cardiovascular magnetic resonance imaging to assess left ventricular mass, left ventricular volumes and visceral fat mass. Left ventricular mass was then compared to serum and anthropometric markers of obesity linked to left ventricular mass, i.e. height, age, blood pressure, total fat mass, visceral fat mass, lean mass, serum leptin and fasting insulin level. As expected, obesity was associated with significantly increased left ventricular mass (126 +/- 27 vs 90 +/- 20 g; p < 0.001). Stepwise multiple regression analysis showed that over 75% of the cross sectional variation in left ventricular mass can be explained by lean body mass (beta = 0.51, p < 0.001), LV stroke volume (beta = 0.31 p = 0.001) and abdominal visceral fat mass (beta = 0.20, p = 0.02), all of which showed highly significant independent associations with left ventricular mass (overall R2 = 0.77). The left ventricular hypertrophic response to obesity in the absence of additional cardiovascular risk factors is mainly attributable to increases in lean body mass, LV stroke volume and visceral fat mass. In view of the well documented link between obesity, left ventricular hypertrophy and mortality, these findings have potentially important prognostic and therapeutic implications for primary and secondary prevention.Journal of Cardiovascular Magnetic Resonance 05/2009; 11(1):9. DOI:10.1186/1532-429X-11-9 · 5.11 Impact Factor
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ABSTRACT: Chest pain and other symptoms suggestive of acute cardiac ischemia (ACI, including acute myocardial infarction [AMI] and unstable angina pectoris) account for over 6 million emergency department (ED) visits per year. Of these, the approximately 30% who truly have ACI (just under half of whom will prove to have AMI)  must be quickly and accurately separated from the majority of ED patients who do not have ACI and then promptly treated and admitted to the hospital. This is not an easy task, the environment in which this must be done is not often optimal, and there are no perfect tests that completely handle all possible cases. However, as reviewed in this chapter, there are a number of tests and strategies, that, when combined with good clinical judgement, can be of significant assistance.12/1996: pages 321-331;
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ABSTRACT: Electrocardiographic left ventricular hypertrophy (LVH) and related repolarization changes alter the morphology of the ST segment and/or the T wave. Such electrocardiographic abnormalities--all features that are encountered in patients with acute ischemic heart disease--may confound the early emergency department evaluation of the chest pain patient. In the instance of the chest pain patient demonstrating ST segment/T wave abnormality, the correct electrocardiographic diagnosis must be made not only to offer appropriate management for that particular illness but also to avoid the incorrect application of potentially dangerous therapies such as thrombolysis. This report presents two cases in which the electrocardiogram demonstrated significant repolarization changes consistent with LVH, and focuses on the recognition of the expected ST segment/T waves changes and their differentiation from the primary ST segment/T wave changes associated with acute ischemic heart disease.American Journal of Emergency Medicine 12/1998; 16(7):692-6. DOI:10.1016/S0735-6757(98)90179-6 · 1.15 Impact Factor