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• W2079073774 abstract "The classic strain pattern of lateral ST depression and T-wave inversion on the ECG is a well recognized marker of the presence and severity of anatomic left ventricular hypertrophy (LVH) [1–8]. ECG strain has been associated with adverse prognosis in a variety of populations [9–14], including hypertensive patients [9–11,14], and often implicated as the primary marker of untoward outcomes when ECG LVH criteria have been utilized for risk stratification [9,10,12,14]. Serial assessment of ECG voltage and voltage-duration product criteria for LVH has demonstrated that regression of ECG LVH appears to confer a decreased risk of cardiovascular morbidity and mortality [13–18]. However, the independent predictive value of serial assessment of the ECG strain pattern and whether changes in the ECG strain pattern provide additional prognostic information beyond that provided by changes in ECG LVH have been less extensively evaluated [13,14,19]. In a serial analysis of 274 men and 250 women from the Framingham study with ECG LVH by Framingham criteria [13], development of worsening repolarization abnormalities was associated with statistically significant 1.9-fold and two-fold increased risks of incident cardiovascular disease in men and women, respectively. In contrast, improvement in repolarization findings was associated with only a marginally significant reduction in cardiovascular risk in men but not in women [13]. Although these findings remained similar when additionally adjusted for serial change in systolic pressure, the further impact of serial changes in Cornell voltage on outcome was not evaluated [13]. Among 496 hypertensive patients with ECG LVH by the Perugia score at baseline in the Hypertrophy at ECG and its Regression during Treatment (HEART) survey [14], in-treatment persistence or development of ECG strain was associated with a two-fold increased risk of cardiovascular events, independent of the predictive value of age, sex, diabetes and in-treatment levels of Cornell voltage LVH. However, patients in this study had a high prevalence of ECG strain at baseline (35%) due to the inclusion of strain in the selection criteria for the study, the predictive value of new strain was not examined separately from persistence of strain, the multivariate analyses did not adjust for treatment modalities or blood pressure levels over time and there were modest numbers of patients and events in the study. In 7409 patients from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study who had ECG strain assessed at baseline and year 1 [19], compared with the absence of strain on both ECGs, development of new ECG strain was associated with nearly three-fold to five-fold increased risks of myocardial infarction, stroke, cardiovascular death, the LIFE composite endpoint of these three events, sudden death and all-cause mortality in the setting of antihypertensive therapy associated with substantial decreases in both systolic and diastolic pressure. In contrast, regression of strain between baseline and year 1 was associated with a nonsignificant or marginally increased risk of events, and persistence of strain on both baseline and year 1 ECGs was associated with approximately two-fold higher risks of these endpoints [19]. After adjusting for age, sex, cardiovascular risk factors, in-treatment systolic and diastolic blood pressure, the improved prognosis with losartan therapy in this population [20] and the known predictive value of regression of ECG LVH in LIFE [18,21], development of new strain remained associated with an approximately 2–2.4-fold increased risk of all endpoints, whereas the risk associated with regression or persistence of strain was attenuated and no longer statistically significant [19]. In contrast to the HEART survey [14], regression of ECG LVH by Cornell product and Sokolow–Lyon voltage remained associated with reduced risk for all outcomes, emphasizing the need for serial assessment of both standard ECG LVH criteria and lateral repolarization abnormalities to accurately assess changing risk over time in hypertensive patients. In the present issue of the Journal, Salles et al.[22] extend the evidence for the independent prognostic value of serial changes in the ECG strain pattern to patients with resistant hypertension. In a well defined cohort study of 532 patients with resistant hypertension, ECG strain was present at baseline in 115 patients (21.6%); during follow-up, 17 patients had regression of strain and 22 developed new ECG strain. During median follow-up of 4.8 years, persistence or development of ECG strain was associated with a two-fold increased risk of a composite cardiovascular endpoint and all-cause mortality and with a three-fold increased risk of stroke after adjusting for a number of cardiovascular risk factors, including in-treatment ambulatory blood pressure and ECG LVH treated as time-varying covariates. Importantly, serial evaluation of the combination of ECG strain and ECG LVH criteria further concentrated cardiovascular risk: persistence or development of both ECG strain and ECG LVH by either Sokolow–Lyon voltage, Cornell voltage or Cornell voltage-duration product criteria was associated with more than 2.5-fold increased risks of the composite cardiovascular endpoint compared with the absence of both ECG strain and LVH. Patients who had either ECG strain or LVH had an intermediate risk of cardiovascular morbidity and mortality [22]. The current study has several limitations. First, because this was an observational cohort study, routine follow-up ECGs were not obtained at standardized times during the follow-up period, which could introduce several forms of bias into the study. Patients with more abnormal ECGs at baseline may have been more likely to have additional ECGs during follow-up, increasing the likelihood of observing changes in ECG strain and/or LVH. Perhaps more importantly, because the authors do not provide data on the average time from last in-study ECG to events, we cannot ascertain the proximity of the in-study ECGs used to determine persistence/development vs. absence/regression of ECG strain or LVH, potentially reducing the precision of the relationship between these findings and cardiovascular outcomes compared with routine yearly follow-up. Second, although the authors adjusted for the number of antihypertensive drugs in use during the study, this does not preclude that patients with ECG strain or other high-risk findings may have been treated with higher doses or more effective drugs. Finally, use of the presence or absence of the strain pattern to assess lateral repolarization as opposed to the magnitude of ST depression and/or T-wave inversion may underestimate the ability of small degrees of ST depression in the lateral leads to predict morbidity and mortality, even in conjunction with echocardiographic LVH [23]. Further study of more quantitative measures of lateral repolarization abnormality using computerized electrocardiography will be necessary to more fully elucidate the prognostic value of serial measures of ST depression in these leads. Despite these limitations, these findings raise an important question: does the increased risk associated with development of new strain in LIFE [19] and with persistence or development of strain in the current study [22] warrant more aggressive therapy to reduce risk in hypertensive patients? Would additional antihypertensive treatment in patients who do not regress their ECG strain in response to normal blood pressure lowering further reduce risk in parallel with the greater regression of left ventricular mass index and carotid intimal medial thickness in response to greater lowering of systolic pressure and low-density lipoprotein cholesterol in diabetic patients in the Stop Atherosclerosis in Native Diabetics Study [24]? Or would more aggressive blood pressure lowering expose patients to more serious adverse events with no apparent prognostic benefit as recently observed in diabetic patients enroled in the Action to Control Cardiovascular Risk in Diabetes study [25]? Given the strong relationship of the presence or absence of ECG strain assessed over time to outcome and the evolving evidence that ECG strain is a potentially reversible finding during antihypertensive treatment [14,19,22], development of additional studies that use resolution of ECG strain as an additional treatment endpoint beyond blood pressure lowering is indicated to determine whether regression or prevention of the development of ECG strain is a valid therapeutic goal in patients with hypertension. Only properly designed, prospective trials that randomize patients to blood pressure goal-directed therapy vs. blood pressure reduction and additional therapy in patients whose ECG strain has not regressed or has newly developed will allow these questions to be answered. Acknowledgement P.M.O. has received research support from Merck & Co., Inc." @default.
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• W2079073774 date "2010-08-01" @default.
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• W2079073774 title "Should regression or prevention of development of the electrocardiographic strain pattern be an indication for more aggressive treatment in hypertensive patients?" @default.
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