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Lasse Oikarinen

Publications and source records attributed to Lasse Oikarinen.

At least 19 recordsLinked to original sources
PubMed2006

Left atrial size and risk of major cardiovascular events during antihypertensive treatment: losartan intervention for endpoint reduction in hypertension trial.

The influence of left atrial size on cardiovascular events during antihypertensive treatment has not been reported previously from a long-term, prospective, randomized hypertension treatment trial. We recorded left atrial diameter by annual echocardiography and cardiovascular events in 881 hypertensive patients (41% women) with electrocardiographic left ventricular hypertrophy aged 55 to 80 (mean: 66) years during a mean of 4.8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Study. During follow-up, a total of 88 primary end points (combined cardiovascular death, myocardial infarction, or stroke) occurred. In Cox regression, baseline left atrial diameter/height predicted incidence of cardiovascular events (hazard ratio: 1.98 per cm/m [95% CI: 1.02 to 3.83 per cm/m]; P=0.042) adjusted for significant effects of Framingham risk score and history of atrial fibrillation. Greater left atrial diameter reduction during follow-up was associated with greater reduction in left ventricular hypertrophy, absence of new-onset atrial fibrillation or mitral regurgitation during follow-up, and losartan-based treatment (B=-0.13+/-0.03 cm/m; P<0.001) in multiple linear regression, adjusting for baseline left atrial diameter/height. However, in time-varying Cox regression analysis, left atrial diameter reduction was not independent of left ventricular hypertrophy regression in predicting cardiovascular events during follow-up. In conclusion, left atrial diameter/height predicts risk of cardiovascular events independent of other clinical risk factors in hypertensive patients with left ventricular hypertrophy and may be useful in pretreatment clinical assessment of cardiovascular risk in these patients.

Aged↗
PubMed2006

Effects of beta-blocker therapy on ventricular repolarization documented by 24-h electrocardiography in patients with type 1 long-QT syndrome.

OBJECTIVES: We tested the hypothesis that in long-QT syndrome (LQT) type 1 (LQT1), beta-blocker therapy may decrease both the diurnal maximal T-wave peak to T-wave end interval (TPE) and the maximal ratio between late and early T-wave peak amplitude (T2/T1 ratio), which are electrocardiographic counterparts of transmural dispersion of repolarization (TDR) and early afterdepolarizations (EA), respectively. BACKGROUND: Ventricular repolarization duration and increased TDR and EAs are the three electrophysiological components generating the high risk of ventricular arrhythmias and sudden death in the inherited LQT. In the most prevalent LQT1 form of LQT, treatment with beta-blockers reduces serious arrhythmia events dramatically without a known influence on QT interval duration. In experimental LQT1 models, beta-blockers decrease TDR and prevent EAs. METHODS: We reviewed 24-h electrocardiographic recordings obtained before and during the treatment with beta-blockers from 24 genotyped LQT1 patients to record maximal TPE intervals and T2/T1 ratios as well as maximal and rate-adapted QT intervals using a computer-assisted program. RESULTS: Treatment with beta-blockers decreased the maximal diurnal T2/T1 amplitude ratio from 3.0+/- 1.0 to 2.2 +/- 0.6 (p = 0.002). Beta-blockers also decreased both maximal TPE intervals and abrupt maximal QT intervals at heart rates higher than 85 beats/min, whereas QT intervals measured at steady-state conditions remained unchanged. CONCLUSIONS: Prevention of abrupt increases of electrocardiographic TDR, EA, and ventricular repolarization duration at elevated heart rates may explain the favorable clinical effects of beta-blockers in LQT1.

Adolescent↗
PubMed2006

Reductions in albuminuria and in electrocardiographic left ventricular hypertrophy independently improve prognosis in hypertension: the LIFE study.

BACKGROUND: In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, reduced urine albumin/creatinine ratio (UACR) as well as regression of left ventricular hypertrophy have been associated with lower incidence of cardiovascular events. We wanted to investigate whether these prognostic improvements were independent. METHODS: In 6679 hypertensive patients included in the LIFE study, we measured UACR, left ventricular hypertrophy by electrocardiography, serum cholesterol, plasma glucose and blood pressure after 2 weeks of placebo treatment and again after 1 year of anti-hypertensive treatment with either an atenolol- or a losartan-based regimen. During this first year of treatment, 77 patients encountered a non-fatal stroke or myocardial infarction and were excluded to avoid bias. During the next 3-4 years, 610 composite endpoints [cardiovascular death (n = 228), fatal or non-fatal myocardial infarction or stroke] were recorded. RESULTS: In Cox regression analyses, the composite endpoint was after adjustment for treatment allocation predicted by baseline logUACR [hazard ratio (HR) = 1.16 per 10-fold increase, P < 0.05], 1-year logUACR (HR = 1.29 per 10-fold increase), baseline Sokolow-Lyon voltage (HR = 1.01 per mm, both P < 0.001) and 1-year Cornell product (HR = 1.01 per 100 mm x ms, P < 0.01). Cardiovascular death was predicted by 1-year logUACR (HR = 1.59, P < 0.001), baseline Sokolow-Lyon voltage (HR = 1.01, P = 0.06) and 1-year Cornell product (HR = 1.02, P < 0.001). Both were predicted independent of age, Framingham risk score, current smoking, history of cardiovascular disease and diabetes. Gender, serum cholesterol, plasma glucose and blood pressure did not enter the models. CONCLUSIONS: Baseline UACR and Sokolow-Lyon voltage, as well as in-treatment UACR and Cornell product, added to the risk prediction independent of traditional risk factors, indicating that albuminuria and left ventricular hypertrophy reflect different aspects of cardiovascular damage and are modifiable cardiovascular risk factors.

Aged↗
PubMed2006

Electrocardiographic strain pattern and left ventricular diastolic function in hypertensive patients with left ventricular hypertrophy: the LIFE study.

BACKGROUND: Whether the typical electrocardiographic (ECG) strain pattern (Strain, in leads V5 and/or V6), which is associated with left ventricular hypertrophy (LVH) and LV systolic dysfunction, is independently associated with LV diastolic dysfunction is unknown. METHODS: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study enrolled hypertensive patients with ECG-LVH, of whom 10% underwent Doppler echocardiography. LV diastolic function measures included peak mitral E and A wave velocities and their ratio (E/A); E wave deceleration time (EDT); atrial filling fraction (AFF); and isovolumic relaxation time (IVRT). Normal filling pattern was defined by E/A < 1 with EDT >or= 150 and or=60 ms; abnormal relaxation by E/A < 1 with EDT > 250 ms or IVRT > 100 ms; pseudonormal filling pattern by E/A >or= 1 associated with IVRT > 100 ms or EDT > 250 ms; restrictive pattern by E/A >or= 1 with IVRT < 100 ms and EDT < 250 ms. A combined index of LV systolic-diastolic function was also computed (isovolumic time/ejection time, modified myocardial performance index). Of LIFE echo substudy participants with all needed ECG and Doppler data (n = 791), 110 (14%) had Strain. RESULTS: Strain was associated with male gender, African-American race, diabetes, history of coronary heart disease (CHD), higher systolic blood pressure (BP), LV mass and relative wall thickness, and higher prevalences of echo-LV hypertrophy and wall motion abnormalities, and with slower heart rate (all P < 0.05). Age, diastolic BP and LV ejection fraction were similar in patients with or without Strain. Diastolic parameters, and prevalences of different LV filling patterns, did not differ significantly between patients with versus those without Strain (all P > 0.1), but modified myocardial performance index was higher with Strain (P < 0.05). Findings were consistent in multivariate analyses. The association of Strain with higher modified myocardial performance index was no longer statistically significant after accounting for LV systolic function and wall motion abnormalities. CONCLUSIONS: In hypertensive patients with ECG-LVH, the ECG Strain pattern did not identify independently those with more severe LV diastolic abnormalities.

Aged↗
PubMed2006

Ventricular repolarization and heart rate responses during cardiovascular autonomic function testing in LQT1 subtype of long QT syndrome.

BACKGROUND: In the most prevalent LQT1 form of inherited long QT syndrome symptoms often occur during abrupt physical or emotional stress. Sympathetic stimulation aggravates repolarization abnormalities in experimental LQT1 models. We hypothesized that autonomic function tests might reveal the abnormal repolarization in asymptomatic LQT1 patients. METHODS: We measured heart rates (HRs) and QT intervals in nine asymptomatic carriers of a C-terminal KCNQ1 mutation and 8 unaffected healthy subjects using an approach of global QT values derived from 28 simultaneous electrocardiographic leads on beat-to-beat base during Valsalva maneuver, mental stress, sustained handgrip, and light supine exercise. RESULTS: LQT1 patients exhibited impaired shortening of both QTpeak and QTend intervals during autonomic interventions but exaggerated lengthening of the intervals--a QT overshoot--during the recovery phases. The number of tests with a QT overshoot was 2.4 +/- 1.7 in LQT1 patients and 0.8 +/- 0.7 in unaffected subjects (P = 0.02). Valsalva strain prolonged T wave peak to T wave end interval (TPE) in LQT1 but not in unaffected patients. LQT1 patients showed diminished HR acceleration in response to adrenergic challenge whereas HR responses to vagal stimuli were similar in both groups. CONCLUSIONS: Standard cardiovascular autonomic provocations induce a QT interval overshoot during recovery in asymptomatic KCNQ1 mutation carriers. Valsalva maneuver causes an exaggerated fluctuation of QT and TPE intervals partly explaining the occurrence of cardiac events during abrupt bursts of autonomic activity in LQT1 patients.

Adult↗
PubMed2006

Magnetocardiographic assessment of healed myocardial infarction.

BACKGROUND: We evaluated the capability of multichannel magnetocardiography (MCG) to detect healed myocardial infarction (MI). METHODS: Multichannel MCG over frontal chest was recorded at rest in 21 patients with healed MI, detected by cine- and contrast-enhanced magnetic resonance imaging, and in 26 healthy controls. Of the 21 MI patients, 11 had non-Q wave and 10 Q wave MIs. QRS, ST-segment, T wave and ST-T wave integrals, ST-segment and T wave amplitudes, and QRS and ST-T wave magnetic field map orientations were measured. RESULTS: The MCG repolarization indexes, such as ST segment and ST-T wave integrals, separated the MI group from the controls (ST-T wave integral -1.4 +/- 5.3 vs 1.5 +/- 4.7 pTs, P = 0.034). The abnormalities were more distinct in the Q wave-MI than in the non-Q wave MI subgroup. In the latter, however, a trend similar to the Q wave MI group was found. The relation of QRS area to ST segment and T wave integral improved the detection of healed MIs compared to the ST-T wave indexes alone (QRS-ST-T discordance 14 +/- 10 vs 5.0 +/- 7.1 pTs, P = 0.003). When comparing the MI group to the controls, the orientation of the magnetic field maps differed in the ST-T wave maps (163 +/- 119 degrees vs 58 +/- 17 degrees, P < 0.001) but not in the QRS maps (111 +/- 95 degrees vs 106 +/-93 degrees, P = 0.646). CONCLUSIONS: The MCG repolarization variables can detect healed MI. These ST-T wave abnormalities are more pronounced in patients with Q wave MI than in patients with non-Q wave MIs. Relating the signals of depolarization and repolarization phases improves the detection of healed MI. Repolarization abnormalities are common in healed MI and thus should not always be interpreted as present ongoing ischemia.

Aged↗
PubMed2006

Reproducibility of computerized measurements of QT interval from multiple leads at rest and during exercise.

BACKGROUND: Accurate measurement of the QT interval is important for diagnosing long QT syndrome (LQTS), and in research on determinants of ventricular repolarization time. We tested automatic analysis of QT intervals from multiple ECG leads on chest. METHODS: Eleven healthy volunteers and 10 genotyped LQTS patients were tested at rest and during exercise with a bicycle ergometer twice 1-31 months apart. Electrocardiograms were recorded with the body surface potential mapping system, and 12 precordial channels were selected for analysis. Averaged QT peak and QT end intervals were determined with an automated algorithm, and the difference QT end minus QT peak (Tp-e) was calculated. Repeatability was assessed by coefficient of variation (CV) between measurements. RESULTS: Within one test at rest the QT end intervals were highly repeatable with CV 0.6%. In repeated tests CV was 4.4% for QT end interval and 3.5% when the QT interval was corrected for heart rate. In exercise test at specified heart rates, mean CV was 3.0% for QT end and 2.9% for QT peak interval. The CV of Tp-e interval was 10.2% at rest, and 9.3% in exercise test. Reproducibility was comparable between healthy subjects and LQTS patients. CONCLUSIONS: The BSPM system with automated analysis produced accurate and highly repeatable QT interval measurements. Reproducibility was adequate also over prolonged time periods both at rest and in exercise stress test. The method can be applied in studying duration of ventricular repolarization time in different physiologic and pharmacologic interventions.

Adult↗
PubMed2005

Electrocardiographic strain pattern and prediction of new-onset congestive heart failure in hypertensive patients: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study.

BACKGROUND: The ECG strain pattern of ST depression and T-wave inversion is strongly associated with left ventricular hypertrophy (LVH) independently of coronary heart disease and with an increased risk of cardiovascular morbidity and mortality in hypertensive patients. However, whether ECG strain is an independent predictor of new-onset congestive heart failure (CHF) in the setting of aggressive antihypertensive therapy in unclear. METHODS AND RESULTS: The relationship of ECG strain at study baseline to the development of CHF was examined in 8696 patients with no history of CHF who were enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study. All patients had ECG LVH by Cornell product and/or Sokolow-Lyon voltage criteria on a screening ECG, were treated in a blinded manner with atenolol- or losartan-based regimens, and were followed up for a mean of 4.7+/-1.1 years. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite the QRS axis in lead V5 or V6. ECG strain was present in 923 patients (10.6%), and new-onset CHF occurred in 265 patients (3.0%), 26 of whom had a CHF-related death. Compared with patients who did not develop CHF, hypertensive patients who developed CHF were older; were more likely to be black, current smokers, and diabetic; were more like to have a history of myocardial infarction, ischemic heart disease, stroke, or peripheral vascular disease; and had greater baseline severity of LVH by Cornell product and Sokolow-Lyon voltage, higher baseline body mass indexes, higher serum glucose levels and albuminuria, similar baseline systolic and diastolic pressures, and reductions in diastolic pressure with treatment but greater reductions in systolic pressure. In univariate Cox analyses, ECG strain was a significant predictor of new-onset CHF (hazard ratio [HR], 3.27; 95% CI, 2.49 to 4.29) and CHF mortality (HR, 4.74; 95% CI, 2.11 to 10.64). In Cox multivariable analyses adjusting for baseline differences between patients with and without new-onset CHF, in-treatment differences in systolic and diastolic pressures, Sokolow-Lyon voltage, and Cornell product, and the impact of treatment with losartan versus atenolol on outcomes, ECG strain remained a significant predictor of incident CHF (HR, 1.80; 95% CI, 1.30 to 2.48) and CHF-related death (HR, 2.78; 95% CI, 1.02 to 7.63). CONCLUSIONS: ECG strain identifies hypertensive patients at increased risk of developing CHF and dying as a result of CHF, even in the setting of aggressive blood pressure lowering.

Aged↗
PubMed2005

Ratio of late to early T-wave peak amplitude in 24-h electrocardiographic recordings as indicator of symptom history in patients with long-QT Syndrome types 1 and 2.

UNLABELLED: We reviewed 24-h electrocardiographic recordings from 214 genotyped subjects--97 with long-QT syndrome type 1 (LQT1), 62 with LQT2, and 55 unaffected--to record maximal diurnal amplitude ratios between late and early T-wave peaks. Maximal amplitude ratios between late and early T-wave peaks were higher in symptomatic than in asymptomatic patients both in LQT1 (3.2 +/- 1.0 vs. 2.3 +/- 0.8; p < 0.001) and in LQT2 patients (2.6 +/- 1.0 vs. 1.7 +/- 0.5; p < 0.001). The maximal amplitude ratio between late and early T-wave peaks was independently associated with symptom history in both LQT1 and LQT2 patients. OBJECTIVES: We tested the hypothesis that in long-QT syndrome types 1 (LQT1) and 2 (LQT2), the diurnal maximal ratio between late and early T-wave peak amplitudes correlates with a history of symptoms better than QT interval durations. BACKGROUND: Genotype and phenotype studies have delineated clinical profiles of the most prevalent LQT1 and LQT2 subtypes of inherited LQT, but prediction of arrhythmia risk remains uncertain, the baseline QTc interval being the best predictor. In experimental long-QT syndrome models, the ratio between late and early T-wave peak amplitude predicts onset of torsade de pointes. METHODS: We reviewed 24-h electrocardiographic recordings from 214 genotyped subjects--97 with LQT1, 62 with LQT2, and 55 unaffected-to record maximal amplitude ratios between late and early T-wave peaks by use of a computer-assisted program. RESULTS: Maximal amplitude ratios between late and early T-wave peaks were higher in symptomatic than in asymptomatic patients both in LQT1 (3.2 +/- 1.0 vs. 2.3 +/- 0.8; p < 0.001) and LQT2 patients (2.6 +/- 1.0 vs. 1.7 +/- 0.5; p < 0.001). Although the QTc interval also was longer in symptomatic patients, only the maximal amplitude ratio between late and early T-wave peaks was independently associated with symptoms in both LQT1 and LQT2 patients. CONCLUSIONS: Maximal diurnal ratio between late and early T-wave peak amplitude improves noninvasive risk assessment both in LQT1 and LQT2 syndromes. We propose this new indicator in clinical evaluation of arrhythmia risk in LQT1 and LQT2.

Adult↗
PubMed2004

Temporal repolarization lability differences among genotyped patients with the long QT syndrome.

The investigators sought to test whether certain long QT syndrome (LQTS) mutations are associated with increased repolarization lability and whether repolarization lability (quantified by the QT variability index [QTVI]) is increased in patients with LQTS compared with controls. In 32 genotyped patients with LQTS type 1 (LQT1), 32 genotyped patients with LQTS type 2 (LQT2), and 32 controls, the QTVI was increased in patients with LQT2 (-0.973 +/- 0.394, p = 0.01 vs controls) and in patients with LQT1 with mutations other than KCNQ1-FIN (-0.942 +/- 0.264, p = 0.04 vs controls) but was similar between the KCNQ1-FIN group and controls.

Adult↗
PubMed2004

Electrocardiographic strain pattern and prediction of cardiovascular morbidity and mortality in hypertensive patients.

The ECG strain pattern of lateral ST depression and T-wave inversion is a marker for left ventricular hypertrophy (LVH) and adverse prognosis in population studies. However, whether ECG strain is an independent predictor of cardiovascular (CV) morbidity and mortality in the setting of aggressive antihypertensive therapy is unclear. ECGs were examined at study baseline in 8854 hypertensive patients with ECG LVH who were treated in a blinded manner with atenolol- or losartan-based regimens. Strain was defined by the presence of a downsloping convex ST segment with an inverted asymmetrical T wave opposite to the QRS axis in leads V5 and/or V6 and was present in 971 patients (11.0%). The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study composite end point of CV death or nonfatal myocardial infarction or stroke occurred in 1035 patients (11.7%). In Cox analyses adjusting only for treatment effect, ECG strain was a significant predictor of CV death (hazard ratio [HR] 2.26, 95% confidence interval [CI] 1.78 to 2.86), fatal/nonfatal myocardial infarction (HR 2.16, 95% CI 1.67 to 2.80), fatal/nonfatal stroke (HR 1.76, 95% CI 1.39 to 2.21), and the composite CV end point (HR 1.99, 95% CI 1.70 to 2.33). After further adjusting for standard CV risk factors, baseline blood pressure, and severity of ECG LVH, ECG strain remained a significant predictor of CV mortality (HR 1.53, 95% CI 1.18 to 2.00), myocardial infarction (HR 1.55, 95% CI 1.16 to 2.06), and the composite CV end point (HR 1.33, 95% CI 1.11 to 1.59). Thus, ECG strain is a marker of increased CV risk in hypertensive patients in the setting of aggressive blood pressure lowering, independent of baseline severity of ECG LVH.

Aged↗
PubMed2004

QRS duration and QT interval predict mortality in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention for Endpoint Reduction in Hypertension Study.

Left ventricular hypertrophy is a risk factor for cardiovascular mortality, including sudden cardiac death. Experimentally, left ventricular hypertrophy delays ventricular conduction and prolongs action potential duration. Electrocardiographic QRS duration and QT interval measures reflect these changes, but whether these measures can further stratify risk in patients with electrocardiographic left ventricular hypertrophy is unknown. We measured the QRS duration and QT intervals from the baseline 12-lead electrocardiograms in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study, which included hypertensive patients with electrocardiographic evidence of left ventricular hypertrophy randomized to either losartan-based or atenolol-based treatment to lower blood pressure. In the present study, we related study baseline electrocardiographic measures to cardiovascular and all-cause mortality. There were 5429 patients (male 45.8%; mean age 66+/-7 years) included in the present analyses. After a mean follow-up of 4.9+/-0.8 years, there were 417 deaths from all causes, including 214 cardiovascular deaths. In separate univariate Cox regression analyses, QRS duration and several QT measures were significant predictors of cardiovascular mortality and all-cause mortality. However, in multivariate Cox analyses including all electrocardiographic measures and adjusting for other risk factors as well as treatment strategy, only QRS duration and maximum rate-adjusted QT(apex) interval remained as significant independent predictors of cardiovascular (P=0.022 and P=0.037, respectively) and all-cause mortality (P=0.038 and P=0.002, respectively). In conclusion, in a hypertensive risk population identified by electrocardiographic left ventricular hypertrophy, increased QRS duration and maximum QT(apex) interval can further stratify mortality risk even in the setting of effective blood pressure-lowering treatment.

Aged↗
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.

Aged↗
PubMed2002

Ambulatory electrocardiographic evidence of transmural dispersion of repolarization in patients with long-QT syndrome type 1 and 2.

BACKGROUND: Transmural dispersion of repolarization (TDR) may be related to the genesis of torsade de pointes (TdP) in patients with the long-QT (LQT) syndrome. Experimentally, LQT2 models show increased TDR compared with LQT1, and beta-adrenergic stimulation increases TDR in both models. Clinically, LQT1 patients experience symptoms at elevated heart rates, but LQT2 patients do so at lower rates. The interval from T-wave peak to T-wave end (TPE interval) is the clinical counterpart of TDR. We explored the relationship of TPE interval to heart rate and to the presence of symptoms in patients with LQT1 and LQT2. METHODS AND RESULTS: We reviewed Holter recordings from 90 genotyped subjects, 31 with LQT1, 28 with LQT2, and 31 from unaffected family members, to record TPE intervals by use of an automated computerized program. The median TPE interval was greater in LQT2 (112+/-5 ms) than LQT1 (91+/-2 ms) or unaffected (86+/-3 ms) patients (P<0.001 for all group comparisons), and the maximal TPE values differed as well. LQT1 patients showed abrupt increases in TPE values at RR intervals from 600 to 900 ms, but LQT2 patients did so at RR intervals from 600 to 1400 ms (longest RR studied). Asymptomatic and symptomatic patients showed similar TDRs. CONCLUSIONS: TDR is greater in LQT2 than in LQT1 patients. LQT1 patients showed a capacity to increase TDR at elevated heart rates, but LQT2 patients did so at a much wider rate range. The magnitude of TDR is not related to a history of TdP.

Adult↗
PubMed2002

Differentiation between LQT1 and LQT2 patients and unaffected subjects using 24-hour electrocardiographic recordings.

This study assesses the use of 24-hour ambulatory electrocardiographic recordings in distinguishing patients with long-QT1 syndrome (LQT1) from those with LQT2, and for distinguishing affected from unaffected patients. The diagnoses of the congenital LQT syndrome and its most common types LQT1 and LQT2 are made difficult because of the limitations of the electrocardiogram as a diagnostic tool. With an automated computerized program, Holter recordings from 15 LQT1 and 15 LQT2 patients and 43 healthy subjects (training set) were reviewed to select the best criteria using QT duration and rate dependence as well as the difference between QT end and QT apex to separate the 3 groups. Fixed criteria were then applied in blinded fashion to separate a different group of 32 genotyped patients and 16 unaffected subjects (test set). In the training set, the RR interval (100 ms), a slope value for median QT/RR curves of -0.016 separated 25 of 30 (83%) and a minimal QT end - QT apex value of 80 ms, separated 26 of 30 (87%) LQT1 patients from LQT2 patients. When all selected criteria were applied to differentiate LQT1 from LQT2 versus unaffected genotypes in the test set, 38 of 48 cases (79%) were correctly identified, whereas using the electrocardiogram alone, 60% of patients were correctly classified into 3 genotypes (p = 0.03). Combining measures for QT duration, rate dependence, and QT end - QT apex interval, derived from Holter recordings, complements the clinical differentiation between LQT1 versus LQT2 patients and between affected and unaffected persons for genotype screening purposes.

Adolescent↗
PubMed2002

Correlates of left atrial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all, P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all, P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.

Aged↗
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.

Aged↗