Gunnar Smith

Mechanical Dispersion Assessed by Myocardial Strain in Patients After Myocardial Infarction for Risk Prediction of Ventricular Arrhythmia

OBJECTIVES The aim of this study was to investigate whether myocardial strain echocardiography can predict ventricular arrhythmias in patients after myocardial infarction (MI). BACKGROUND Left ventricular (LV) ejection fraction (EF) is insufficient for selecting patients for implantable cardioverter-defibrillator (ICD) therapy after MI. Electrical dispersion in infarcted myocardium facilitates malignant arrhythmia. Myocardial strain by echocardiography can quantify detailed regional and global myocardial function and timing. We hypothesized that electrical abnormalities in patients after MI will lead to LV mechanical dispersion, which can be measured as regional heterogeneity of contraction by myocardial strain. METHODS We prospectively included 85 post-MI patients, 44 meeting primary and 41 meeting secondary ICD prevention criteria. After 2.3 years (range 0.6 to 5.5 years) of follow-up, 47 patients had no and 38 patients had 1 or more recorded arrhythmias requiring appropriate ICD therapy. Longitudinal strain was measured by speckle tracking echocardiography. The SD of time to maximum myocardial shortening in a 16-segment LV model was calculated as a parameter of mechanical dispersion. Global strain was calculated as average strain in a 16-segment LV model. RESULTS The EF did not differ between ICD patients with and without arrhythmias occurring during follow-up (34 +/- 11% vs. 35 +/- 9%, p = 0.70). Mechanical dispersion was greater in ICD patients with recorded ventricular arrhythmias compared with those without (85 +/- 29 ms vs. 56 +/- 13 ms, p < 0.001). By Cox regression, mechanical dispersion was a strong and independent predictor of arrhythmias requiring ICD therapy (hazard ratio: 1.25 per 10-ms increase, 95% confidence interval: 1.1 to 1.4, p < 0.001). In patients with an EF >35%, global strain showed better LV function in those without recorded arrhythmias (-14.0% +/- 4.0% vs. -12.0 +/- 3.0%, p = 0.05), whereas the EF did not differ (44 +/- 8% vs. 41 +/- 5%, p = 0.23). CONCLUSIONS Mechanical dispersion was more pronounced in post-MI patients with recurrent arrhythmias. Global strain was a marker of arrhythmias in post-MI patients with relatively preserved ventricular function. These novel parameters assessed by myocardial strain may add important information about susceptibility for ventricular arrhythmias after MI.

Echocardiographic left ventricular geometry in hypertensive patients with electrocardiographic left ventricular hypertrophy: The LIFE Study.

Aim: To assess the prevalence of echocardiographic left ventricular hypertrophy (LVH) and concentric remodeling in hypertensive patients with electrocardiographic (ECG)-LVH and to estimate the costeffectiveness of echocardiography and ECG for detection of LVH.Design: Echocardiographic LV measurements and the prevalence of abnormal LV geometric patterns were compared between 964 hypertensive patients with ECG-LVH (Cornell voltage-duration product > 2440 and/or SV1

Albuminuria predicts cardiovascular events independently of left ventricular mass in hypertension: a LIFE substudy

We wanted to investigate whether urine albumin/creatinine ratio (UACR) and left ventricular (LV) mass, both being associated with diabetes and increased blood pressure, predicted cardiovascular events in patients with hypertension independently. After 2 weeks of placebo treatment, clinical, laboratory and echocardiographic variables were assessed in 960 hypertensive patients from the LIFE Echo substudy with electrocardiographic LV hypertrophy. Morning urine albumin and creatinine were measured to calculate UACR. The patients were followed for 60±4 months and the composite end point (CEP) of cardiovascular (CV) death, nonfatal stroke or nonfatal myocardial infarction was recorded. The incidence of CEP increased with increasing LV mass (below the lower quartile of 194 g to above the upper quartile of 263 g) in patients with UACR below (6.7, 5.0, 9.1%) and above the median value of 1.406 mg/mmol (9.7, 17.0, 19.0%***). Also the incidence of CV death increased with LV mass in patients with UACR below (0, 1.4, 1.3%) and above 1.406 mg/mmol (2.2, 6.4, 8.0%**). The incidence of CEP was predicted by logUACR (hazard ratio (HR)=1.44** for every 10-fold increase in UACR) after adjustment for Framingham risk score (HR=1.05***), history of peripheral vascular disease (HR=2.3*) and cerebrovascular disease (HR=2.1*). LV mass did not enter the model. LogUACR predicted CV death (HR=2.4**) independently of LV mass (HR=1.01* per gram) after adjustment for Framingham risk score (HR=1.05*), history of diabetes mellitus (HR=2.4*) and cerebrovascular disease (HR=3.2*). *P<0.05, **P<0.01, ***P<0.001. In conclusion, UACR predicted CEP and CV death independently of LV mass. CV death was predicted by UACR and LV mass in an additive manner after adjustment for Framingham risk score and history of CV disease.

Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study)

To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan- or atenolol-based treatment. Patients ⩾65 years (older group) included more women and patients with isolated systolic hypertension or albuminuria (all P<0.05). Compared to patients <65 years, older patients had higher pulse pressure, LV mass, and prevalence of concentric hypertrophy at baseline (78 vs 69 mmHg, 234 vs 224 g, and 28 vs 16%, respectively, all P<0.01), while the mean blood pressure did not differ. Over 4 years, reductions in LV mass and the mean blood pressure were similar in both groups, but older patients more often had residual hypertrophy (31 vs 15%, P<0.001) with a preponderance of eccentric geometry. In multivariate analysis of 4-year change in LV mass controlling for baseline mass, larger hypertrophy reduction was associated with losartan treatment, while age, gender, body mass index, and 4-year change in pulse pressure and albuminuria did not enter (Multiple R 2=0.40, P<0.001). Thus, in up-to-80-year-old hypertensive patients with left ventricular hypertrophy, age did not significantly attenuate hypertrophy reduction during antihypertensive treatment, although residual hypertrophy was more prevalent in older patients as a consequence of higher initial LV mass.

Is albuminuria a cardiovascular risk factor independent of left ventricular hypertrophy in hypertension? A LIFE study

Background: Albuminuria and left ventricular (LV) hypertrophy are strong cardiovascular risk factors perceived to be Interrelated. In the LIFE study we investigated the predictive value of albuminuria for the composite endpoint (CEP) of cardiovascular death, nonfatal stroke or non-fatal myocardial infarction controlling for, respectively, echocardiographic LV mass, end-diastolic LV posterior wall thickness (PWTd) and relative wall thickness (RWT). Methods: After two weeks of placebo treatment, clinical, laboratory, and echocardiographic varrables were assessed in 960 hypertensive patients from the LIFE Echo substudy, aged 55-80 (mean 66+7) years, with electrocardiographic LV hyperlrophy. Morning urine albumin and creatinine were measured, and urine albumincreatinine ratlo (UACR) was calculated. Macroand microalbuminuria were defined as UACR235 and 3.5<UACRc35, respectively. Results: Macroand microalbuminuria were found I” 23 (2.7%) and 146 (17.2%) patients respectively, and were both associated with higher incidence of CEP (22%, 15.1% vs. 9.9%‘). PWTD above the median value of about 10.1 mm added significantly to the risk of CEP in patients with albuminuria (19.8% vs. 7.3%*), but not in patients without albuminuria (10.8 vs. 9.4%). In Cox regression analyses controlling for LV mass index, log UACR remaned significantly predictive of the CEP (odds ratio [OR] = 1,5) as was history of peripheral vascular disease (1.9’), diabetes (2.1”). cerebral vascular disease (2.3”): smoking (1.8’): and low hioh densitv lipoprotein _. . cholesterol (0.5’). Log UACR significantly predicted the CEP I” alternative models adiustina for RWT or PWTd (ORs=lS and 1.4). independent of the same clinical covariates. go.05, ** P<O.Ol. Conclusions: Albuminuria strongly predicts cardiovascular morbidity and mortality I” hypertensive patients with electrocardiographic LV hypertrophy Independent of LV mass and geometry. Thus, despite the known relation of albuminuria with LVH. the predictive value of albuminma for cardiovascular events is independent of that of LV hyperlrophy.