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Peter M Okin

Publications and source records attributed to Peter M Okin.

30 records · Page 2Linked to original sources
PubMed2004

Electrocardiographic repolarization complexity and abnormality predict all-cause and cardiovascular mortality in diabetes: the strong heart study.

Type 2 diabetes is associated with increased risk of cardiovascular (CV) and all-cause mortality. Although electrocardiographic measures of repolarization abnormality and complexity stratify risk in the general population, their prognostic value in diabetes has not been well characterized. Digital electrocardiogram (ECG) readings were acquired for 994 American Indians with type 2 diabetes. ST segment depression (STD) >/=50 micro V and rate-corrected QT interval (QTc) >460 ms were examined as measures of repolarization abnormality. The principal component analysis (PCA) of the ratio of the second to first eigenvalues of the T-wave vector (PCA ratio) (>32.0% in women and >24.6% in men) was examined as a measure of repolarization complexity on the ECG. After a mean follow-up of 4.7 +/- 1.0 years, there were 56 CV deaths and 155 deaths from all causes. In univariate analyses, STD, QTc, and the PCA ratio predicted CV and all-cause mortality. After multivariate adjustment for age, sex, and other risk factors, STD (hazard ratio 3.68, 95% CI 1.70-7.96) and PCA ratio (2.61, 1.33-5.13) remained predictive of CV mortality and both STD (2.36, 1.38-4.02) and QTc (2.03, 1.32-3.12) predicted all-cause mortality. Computerized ECG measures of repolarization abnormality and complexity predict CV and all-cause mortality in type 2 diabetes, supporting their use to identify high-risk individuals with diabetes.

Analysis of Variance↗
PubMed2003

Albuminuria and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: the LIFE study.

BACKGROUND: Several studies have shown that albuminuria is associated with increased risk for fatal and nonfatal cardiovascular events, independent of conventional risk factors. The partition values for urine albumin-creatinine ratio (UACR) used to identify microalbuminuria have been based on studies that predicted risk in diabetic patients. OBJECTIVE: To determine whether the relation between albuminuria and cardiovascular risk can be used to predict cardiovascular morbidity and mortality in hypertensive patients. DESIGN: Multicenter cohort study derived from a randomized, controlled trial. PATIENTS: 8206 patients with stage II or III hypertension randomly assigned to double-blind therapy with losartan or atenolol. Follow-up was 39 122 patient-years. MEASUREMENTS: Renal glomerular permeability evaluated by UACR. RESULTS: In nondiabetic hypertensive patients with left ventricular hypertrophy, the risk for the composite cardiovascular end point increased continuously as albuminuria increased (P < 0.001 for trend). There was no specific threshold for increased risk. For every 10-fold increase in UACR, hazard ratios in nondiabetic patients increased as follows: composite end point, by 57% (95% CI, 40.6% to 75.0%); cardiovascular mortality, by 97.7% (CI, 66.5% to 235%); all-cause mortality, by 75.2% (CI, 54.0% to 99.4%); stroke, by 51.0% (CI, 28.8% to 76.9%); and myocardial infarction, by 45% (CI, 19.9% to 75.4%) (P < 0.001 for all comparisons). Values were similar in diabetic patients, although for myocardial infarction the trend was weaker and not significant. CONCLUSION: Increased UACR resulted in increasing risk for cardiovascular morbidity and mortality among hypertensive patients with left ventricular hypertrophy. We found no thresholds or plateaus. Risk increases at much lower UACR values than has been reported among diabetic patients.

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PubMed2003

Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: The Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study.

BACKGROUND: Electrocardiographic left ventricular hypertrophy (LVH) predicts cardiovascular morbidity and mortality, and regression of ECG LVH may predict improved prognosis in hypertensive patients. However, uncertainty persists as to how best to regress ECG LVH. METHODS AND RESULTS: Regression of ECG LVH with losartan versus atenolol therapy was assessed in 9193 hypertensive patients with ECG LVH by Sokolow-Lyon voltage or Cornell voltage-duration product criteria enrolled in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study. Patients had ECGs at study baseline and after 6 months, 1, 2, 3, 4, and 5 years of blinded losartan-based or atenolol-based therapy. After 6 months' follow-up, adjusting for baseline ECG LVH levels, baseline and in-treatment systolic and diastolic pressures, and for diuretic therapy, losartan-based therapy was associated with greater regression of both Cornell product (adjusted means, -200 versus -69 mm. ms, P<0.001) and Sokolow-Lyon voltage (-2.5 versus -0.7 mm, P<0.001) than was atenolol-based therapy. Greater regression of ECG LVH persisted at each subsequent annual evaluation in the losartan-treated group, with between 140 and 164 mm. ms greater mean reductions in Cornell product and from 1.7 to 2.2 mm greater mean reductions in Sokolow-Lyon voltage (all P<0.001). The effect of losartan was consistent across subgroups defined by gender, age, ethnicity, and diabetes. CONCLUSIONS: After adjusting for baseline and in-treatment blood pressure and baseline severity of ECG LVH, losartan-based antihypertensive therapy resulted in greater regression of ECG LVH by Cornell voltage-duration product and Sokolow-Lyon voltage criteria than did atenolol-based therapy. These findings support the value of angiotensin receptor blockade with losartan for reversing ECG LVH.

Age Factors↗
PubMed2003

Relation of QT interval and QT dispersion to regression of echocardiographic and electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan Intervention For Endpoint Reduction (LIFE) study.

BACKGROUND: In hypertensive patients, both echocardiographic and electrocardiographic left ventricular hypertrophy (LVH) increase the risk of sudden death, possibly in part because of LVH-induced proarrhythmic repolarization changes. Experimentally, regression of LVH normalizes ventricular electrophysiology. METHODS: To assess the relation of regression of LVH to changes in electrocardiographic measures of ventricular repolarization, we studied 317 hypertensive (61.2% men, mean age 65 +/- 7 years) participants in the Losartan Intervention For Endpoint Reduction (LIFE) study with electrocardiographic evidence of LVH, at study baseline, and after 1 year of blood pressure-lowering treatment with losartan or atenolol and hydrochlorothiatzide as the first adjunct therapy if needed to reach target blood pressure of 140/90 mm Hg. As indexes of LVH, we used echocardiographically determined LV mass as well as the Sokolow-Lyon and Cornell voltages from the electrocardiogram. QT interval duration and QT dispersion from the 12-lead electrocardiogram were used as ventricular repolarization measures. RESULTS: By using tertiles of LV mass change and adjusting for the difference in treatment (losartan or atenolol), shortening of the rate-adjusted QT intervals as well as reduction in QT(apex) dispersion were observed in the tertile showing the greatest decrease in LV mass but not in the tertile without substantial changes in LV mass despite a significant reduction in blood pressure. Similar results were obtained with the use of Sokolow-Lyon and Cornell voltage change tertiles. CONCLUSIONS: In hypertensive patients with electrocardiographic evidence of LVH, regression of echocardiographically determined LV mass and electrocardiographic indexes of LVH may partially reverse the LVH-induced proarrhythmic repolarization changes. This may have a beneficial impact on the increased incidence of sudden death in these patients.

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PubMed2003

Echocardiographic wall motion abnormalities in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE Study.

There is limited information on correlates of left ventricular wall motion (WM) abnormalities in ambulatory patients with hypertension and ECG left ventricular hypertrophy by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria. Therefore, we assessed the prevalence and the correlates of echocardiographic global and segmental left ventricular WM abnormalities in 942 hypertensive patients with hypertrophy enrolled in the Losartan Intervention For End-point reduction in hypertension (LIFE) echo substudy. Patients were separated into groups of those with normal WM or those with segmental or global WM abnormalities. Segmental and global WM abnormalities were mostly of mild degree and were detected in 7% and 6% of the study sample. Compared with subjects with normal motion, those with WM abnormalities were mostly men and had higher prevalences of self-reported coronary heart disease, ECG signs of myocardial infarction, ST-strain pattern, and higher Cornell voltage-duration product, echo-left ventricular mass, and albuminuria, but lower total and high-density lipoprotein cholesterol. Blood pressure was similar among groups. No significant differences were found between patients with global or segmental WM abnormalities. Only half of patients with WM abnormalities had a history or ECG signs of coronary heart disease. Independent correlates of WM abnormalities were higher albuminuria and Cornell voltage-duration product, male gender, and echo-left ventricular hypertrophy, but lower cholesterol. In a subanalysis restricted to patients with WM abnormalities, those with evident cardiovascular disease had a higher prevalence of ST-strain pattern than those with subclinical WM abnormalities, but other clinical, ECG, or echocardiographic parameters were indistinguishable between the 2 groups. Thus, in hypertensives with ECG left ventricular hypertrophy, WM abnormalities, mostly of mild degree, occurred in one eighth of the patients and were associated with male gender, left ventricular hypertrophy, and albuminuria. No significant differences were found between patients with global or segmental wall motion abnormalities.

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PubMed2002

Quantitative assessment of electrocardiographic strain predicts increased left ventricular mass: the Strong Heart Study.

OBJECTIVES: This study was designed to examine the relation of computer-measured ST depression (STdep) in the lateral precordial leads to the presence of left ventricular hypertrophy (LVH). BACKGROUND: Qualitative abnormalities of repolarization in the lateral precordial leads of the electrocardiogram, as manifested by the strain pattern of T-wave inversion and STdep, are markers for LVH and adverse prognosis. However, the independent relationship of increased left ventricular (LV) mass to quantitative measures of STdep in these leads remains unclear. METHODS: Electrocardiograms and echocardiograms were examined in the second Strong Heart Study examination in 1,595 American Indian participants without evident coronary disease. The absolute magnitude of ST segment deviation above or below isoelectric baseline was measured by computer in leads V(5) and V(6), and participants were grouped according to gender-specific quartiles of maximal STdep. Left ventricular hypertrophy was defined by indexed LV mass >49.2 g/m(2.7) in men and >46.7 g/m(2.7) in women. RESULTS: Increasing STdep was associated with older age, greater pulse pressure, serum fibrinogen levels and urinary albumin/creatinine ratios, and with stepwise increases in LV mass (145 +/- 28 vs. 150 +/- 33 vs. 156 +/- 36 vs. 164 +/- 43 g, p < 0.001), indexed LV mass (38.2 +/- 7.7 vs. 39.3 +/- 8.7 vs. 40.5 +/- 9.4 vs. 44.0 +/- 11.0 g/m(2.7), p < 0.001), and prevalence of LVH (11.6 vs. 19.1 vs. 21.5 vs. 31.2%, p < 0.001). After controlling for clinical differences, increasing STdep remained strongly associated with increased prevalence of LVH (p = 0.0001). CONCLUSIONS: In the absence of evidence of coronary disease, increasing STdep in the lateral precordial leads is associated with increasing LV mass and increased prevalence of anatomic LVH.

Electrocardiography↗
PubMed2002

Principal component analysis of the T wave and prediction of cardiovascular mortality in American Indians: the Strong Heart Study.

BACKGROUND: Increased QT interval dispersion (QTd) is a proposed ECG marker of vulnerability to ventricular arrhythmias and of cardiovascular (CV) mortality. However, principal component analysis (PCA) of the T-wave vector loop may more accurately represent repolarization abnormalities than QTd. METHODS AND RESULTS: Predictive values of QTd and PCA were assessed in 1839 American Indian participants in the first Strong Heart Study examination. T-wave loop morphology was quantified by the ratio of the second to first eigenvalues of the T-wave vector by PCA (PCA ratio); QTd was quantified as the difference between maximum and minimum QT intervals. After 3.7+/-0.9 years mean follow-up, there were 55 CV deaths. In univariate analyses, an increased PCA ratio predicted CV mortality in women (chi2=7.8, P=0.0053) and men (chi2=9.5, P=0.0021). In contrast, increased QTd was a significant predictor of CV mortality in women (chi2=30.6, P<0.0001) but not in men (chi2=2.0, P=NS). In multivariate Cox analyses controlling for risk factors and rate-corrected QT interval, the PCA ratio remained a significant predictor of CV mortality in women (chi2=4.0 P=0.043) and men (chi2=6.4, P=0.011); QTd was a significant predictor in women only (chi2=11.0, P=0.0009). PCA ratios >90th percentile (32% in women and 24.6% in men) identified women with a 3.68-fold increased risk of CV mortality (95% CI, 1.54 to 8.83) and men with a 2.77-fold increased risk (95% CI, 1.18 to 6.49). CONCLUSIONS: Abnormalities of repolarization measured by PCA of the T-wave loop predict CV death in men and women, supporting use of PCA for quantifying repolarization abnormalities.

Arizona↗
PubMed2002

Ethnic differences in electrocardiographic criteria for left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint.

BACKGROUND: African Americans have greater precordial QRS voltages than whites, with concomitant higher prevalences of electrocardiographic (ECG) left ventricular hypertrophy (LVH) and lower specificity of ECG LVH criteria for the identification of anatomic hypertrophy. However, the high mortality associated with LVH in African American patients makes more accurate ECG detection of LVH in these patients a clinical priority. METHODS: Electrocardiograms and echocardiograms were obtained at study baseline in 120 African American and 751 white hypertensive patients enrolled in the Losartan Intervention For Endpoint (LIFE) echocardiographic substudy. The ECG LVH was determined using Sokolow-Lyon, 12-lead sum, and Cornell voltage criteria. Echocardiographic LVH was defined by LV mass indexed to height(2.7) >46.7 g/m(2.7) in women and >49.1 g/m(2.7) in men. RESULTS: After adjusting for ethnic differences in LV mass, body mass index, sex, and prevalence of diabetes, mean Sokolow-Lyon and 12-lead sum of voltage were significantly higher, but Cornell voltage was lower, in African Americans than in whites. As a consequence of these differences, when identical partition values were used in both ethnic groups, Sokolow-Lyon and 12-lead voltage criteria had lower specificity in African Americans than whites (44% v 69%, P = .007 and 44% v 59%, P = .10) but had greater sensitivity in African Americans (51% v 27%, P < .001 and 62% v 45%, P = .003). In contrast, Cornell voltage specificity was higher (78% v 62%, P = .09) but sensitivity was slightly lower (49% v 57%, P = 0.16) in African Americans. However, when overall test performance was compared using receiver operating curve analyses that were independent of partition value selection, ethnic differences in test performance disappeared, with no differences in accuracy of any of the ECG voltage criteria for the identification of LVH between African American and white hypertensive individuals. CONCLUSIONS: When standard, non-ethnicity-specific thresholds for the identification of LVH are used, Sokolow-Lyon and 12-lead voltage overestimate and Cornell voltage underestimates the presence and severity of LVH in African American relative to white individuals. However, these apparent ethnic differences in test performance disappear when ethnic differences in the distribution of ECG LVH criteria are taken into account. These findings demonstrate that ethnicity-specific ECG criteria can equalize detection of anatomic LVH in African American and white patients.

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PubMed2002

Improved electrocardiographic detection of left ventricular hypertrophy.

We studied the echocardiographic measurements and the digital electrocardiograms (ECGs) of 3378 participants in the Cardiovascular Health Study and divided the subjects into a Learning Set of 1678 subjects and a demographically matched Test Set of 1700 subjects. We defined left ventricular hypertrophy (LVH) as values of the echocardiographic left ventricular mass index (LVMI) >116 g/m(2) in men or >104 g/m(2) in women. We performed univariate linear regression separately on the male and female subjects in the Learning Set to find all the ECG parameters that correlated significantly with LVMI. We then applied multivariate linear regression (MLR) to these parameters to identify the 4 variables for each sex that discriminated best between the subjects with and without LVH. We then applied the resultant sex-specific linear regressions to the subjects in the Test Set. We found that the diagnostic performances for LVH of the new MLR equations were superior to those of three commercial computerized ECG diagnostic algorithms in both men and women. We also found that for the new MLR and for all three commercial algorithms, the diagnostic sensitivities at matched specificities were superior in the men compared to those in the women. We conclude that the new MLR equation identifies patients with echocardiographically determined LVH more reliably than do 3 commercial computerized diagnostic algorithms and that the sensitivities of each of these modalities is greater in men than it is in women.

Echocardiography↗
PubMed2002

Microalbuminuria in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study.

OBJECTIVES: Left ventricular hypertrophy and albuminuria have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiac and renal glomerular damage has not been evaluated in a large hypertensive population with target organ damage. The present study was undertaken to determine whether albuminuria is associated with persistent electrocardiographic (ECG) left ventricular hypertrophy, independent of established risk factors for cardiac hypertrophy, in a large hypertensive population with left ventricular hypertrophy who were free of overt renal failure. METHODS: Patients with stage II-III hypertension were enrolled in the study if they had left ventricular hypertrophy on a screening ECG by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria, and clinic blood pressures between 160 and 200/95-115 mmHg and plasma creatinine < 160 mmol/l. A second ECG and morning spot urine were obtained after 14 days of placebo treatment. Renal glomerular permeability was evaluated by urine albumin/creatinine (UACR, mg/mmol). Microalbuminuria was present if UACR > 3.5 mg/mmol and macroalbuminuria if UACR > 35 mg/mmol. RESULTS: The mean age of the 8029 patients was 66 years, 54% were women. Microalbuminuria was found in 23% and macroalbuminuria in 4% of patients. Microalbuminuria was more prevalent in patients of African American (35%), Hispanic (37%) and Asian (36%) ethnicity, heavy smokers (32%), diabetics (36%) and in patients with ECG left ventricular hypertrophy by both ECG-criteria (29%). Urine albumin/creatinine was positively related to Sokolow-Lyon voltage criteria and Cornell voltage-duration product criteria. In multiple regression analysis, higher UACR was independently associated with older age, diabetes, higher blood pressure, serum creatinine, smoking and left ventricular hypertrophy. Patients smoking > 20 cigarettes/day had a 1.6-fold higher prevalence of microalbuminuria and a 3.7-fold higher prevalence of macroalbuminuria than never-smokers. ECG left ventricular hypertrophy by Cornell voltage-duration product or Sokolow-Lyon criteria was associated with a 1.6-fold increased prevalence of microalbuminuria and a 2.6-fold increase risk of macroalbuminuria compared to no left ventricular hypertrophy on the second ECG. CONCLUSIONS: In patients with moderately severe hypertension, left ventricular hypertrophy on two consecutive ECGs is associated with increased prevalences of micro- and macroalbuminuria compared to patients without persistent ECG left ventricular hypertrophy. High albumin excretion was related to left ventricular hypertrophy independent of age, blood pressure, diabetes, race, serum creatinine or smoking, suggesting parallel cardiac damage and albuminuria.

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