Search PubMed⌕ Search

Biomedical subjects

L Toivonen

Publications and source records attributed to L Toivonen.

At least 19 recordsLinked to original sources
PubMed2002

Heart rate adjustment of magnetic field map rotation in detection of myocardial ischemia in exercise magnetocardiography.

AIMS: We studied the capability of heart rate (HR) adjusted change in multichannel magnetocardiogram (MCG) to detect exercise-induced ischemia. METHODS AND RESULTS: The MCG and 12-lead ECG were recorded simultaneously during supine exercise testing in 17 healthy controls and 24 patients with single vessel coronary artery disease (CAD). In the MCG analysis, we plotted the orientation of the magnetic field map (MFM) against the HR in each cardiac cycle during recovery. A regression line was fitted to the data and the line slope (degrees/bpm) was determined. In the ECG, the ST-segment depression vs HR (ST/HR) slope was evaluated. The HR adjusted MFM rotation was more extensive in the pooled CAD group, and in all subgroups with different stenosed vessel, than in the control group at the ST-segment (1.5 +/- 2.1 degrees/bpm vs 0.29 +/- 0.25 degrees/bpm, p < 0.0005) and at the T-wave apex (0.95 +/- 0.81 degrees/bpm vs 0.24 +/- 0.25 degrees/bpm, p < 0.0005). Areas under the receiver operating characteristic curves of the HR adjusted MFM rotation at the ST-segment (88.5%) and the T-wave (86.0%) were higher than the ones without HR adjustment (75.5% and 68.1%, respectively), and higher than the area of ST/HR slope in the ECG (80.2%). CONCLUSION: HR adjusted MFM rotation detects transient ischemia independent of the stenosed vessel. HR adjustment improves the performance of the MCG in ischemia detection by the analysis of the ST-segment and the T-wave. The MCG was superior to the 12-lead ECG.

Aged↗
PubMed2002

Pre-implant determinants of adequate long-term function of single lead VDD pacemakers.

AIMS: An inherent limitation of single lead VDD pacing is the inability to stimulate the atria. Reprogramming and upgrading the pacemaker system may be required when sinus node dysfunction, atrial undersensing, or atrial fibrillation develop. We evaluated whether routine clinical information is sufficient to select patients to benefit in long-term from VDD pacing. METHODS AND RESULTS: We collected data on 12-lead and monitored electrocardiograms and routine clinical information at implantation of a VDD pacing system in 350 consecutive patients with grade II or III atrioventricular conduction block. The age at implantation was 74.5 +/- 8.0 years, and the follow-up lasted 1.5 +/- 1.5 years. The cumulative maintenance of VDD pacing mode was 91.%. Loss of VDD mode was due to permanent atrial fibrillation in 16 (4.6%), sinus node dysfunction in six (1.7%). atrial undersensing in 11 (3.1%). Chronic atrial fibrillation developed in 23% of patients who had heart enlargement in chest x-ray and a history of paroxysmal atrial fibrillation or flutter. A criterion of normal sinus rate at implantation sufficiently predicted adequate sinus node function. Poor atrial sensing was not predicted by pre-implant characteristics. CONCLUSIONS: According to our data, adequate sinus-driven atrial rate and no history of paroxysmal atrial fibrillation and cardiac enlargement predict maintenance of the VDD pacing mode in elderly patients treated for heart block. Routine information available at implantation is sufficient to guide acceptance of single lead VDD pacing therapy.

Aged↗
PubMed2001

ST-segment level and slope in exercise-induced myocardial ischemia evaluated with body surface potential mapping.

Body surface potential mapping (BSPM) is superior to 12-lead electrocardiography for detection of acute and old myocardial infarctions (MIs). We used BSPM to examine electrocardiographic criteria for acute reversible myocardial ischemia. BSPM with 123 channels was performed in 45 patients with coronary artery disease (CAD) and 25 healthy controls during supine bicycle exercise testing. Of the 45 patients, 18 patients had anterior, 14 had posterior, and 13 had inferior ischemia documented by coronary angiography and thallium scintigraphy. The ST amplitude was measured 60 ms after the J-point and the ST slope calculated by fitting a regression line from the J-point to 60 ms after it. The optimal locations for detecting ST depression and ST-slope decrease were identified. In the pooled CAD patient group, the optimal location for ST depression was 5 cm below standard lead V(5) (CAD group: -70 +/- 70 microV; controls: 70 +/- 80 microV, p <0.001). Using a cut-off value of -10 microV, the ST depression separated the patients with CAD from controls with a sensitivity of 84% and a specificity of 96%. The ST slope became more horizontal in the patient group than in the control group. The optimal location for ST-slope decrease was over the left side (CAD group: 20 +/- 20 microV/s; controls: 720 +/- 320 microV/s, p <0.001). Using a cut-off value of 320 microV/s, the ST slope separated patients with CAD from controls with a sensitivity of 93% at a specificity level of 88%. The area under the receiver operating characteristic curve of ST slope tended to be higher than the one of ST depression (97% vs 93%; p = 0.097). In conclusion, regions sensitive for ST depression and for ST-slope decrease could be identified in BSPM, despite variation in the location of ischemia and the presence or absence of a history of MI. ST slope is a sensitive and specific marker of transient myocardial ischemia, and might perform even better than ST depression.

Body Surface Potential Mapping↗
PubMed2001

Mutations of the cardiac ryanodine receptor (RyR2) gene in familial polymorphic ventricular tachycardia.

BACKGROUND: Familial polymorphic ventricular tachycardia is an autosomal-dominant, inherited disease with a relatively early onset and a mortality rate of approximately 30% by the age of 30 years. Phenotypically, it is characterized by salvoes of bidirectional and polymorphic ventricular tachycardias in response to vigorous exercise, with no structural evidence of myocardial disease. We previously mapped the causative gene to chromosome 1q42-q43. In the present study, we demonstrate that patients with familial polymorphic ventricular tachycardia have missense mutations in the cardiac sarcoplasmic reticulum calcium release channel (ryanodine receptor type 2 [RyR2]). METHODS AND RESULTS: In 3 large families studied, 3 different RyR2 mutations (P2328S, Q4201R, V4653F) were detected and shown to fully cosegregate with the characteristic arrhythmic phenotype. These mutations were absent in the nonaffected family members and in 100 healthy controls. In addition to identifying 3 causative mutations, we identified a number of single nucleotide polymorphisms that span the genomic structure of RyR2 and will be useful for candidate-based association studies for other arrhythmic disorders. CONCLUSIONS: Our data illustrate that mutations of the RyR2 gene cause at least one variety of inherited polymorphic tachycardia. These findings define a new entity of disorders of myocardial calcium signaling.

Base Sequence↗
PubMed2001

Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias.

BACKGROUND: The congenital long-QT syndrome (LQTS) is caused by mutations on several genes, all of which encode cardiac ion channels. The progressive understanding of the electrophysiological consequences of these mutations opens unforeseen possibilities for genotype-phenotype correlation studies. Preliminary observations suggested that the conditions ("triggers") associated with cardiac events may in large part be gene specific. METHODS AND RESULTS: We identified 670 LQTS patients of known genotype (LQT1, n=371; LQT2, n=234; LQT3, n=65) who had symptoms (syncope, cardiac arrest, sudden death) and examined whether 3 specific triggers (exercise, emotion, and sleep/rest without arousal) differed according to genotype. LQT1 patients experienced the majority of their events (62%) during exercise, and only 3% occurred during rest/sleep. These percentages were almost reversed among LQT2 and LQT3 patients, who were less likely to have events during exercise (13%) and more likely to have events during rest/sleep (29% and 39%). Lethal and nonlethal events followed the same pattern. Corrected QT interval did not differ among LQT1, LQT2, and LQT3 patients (498, 497, and 506 ms, respectively). The percent of patients who were free of recurrence with ss-blocker therapy was higher and the death rate was lower among LQT1 patients (81% and 4%, respectively) than among LQT2 (59% and 4%, respectively) and LQT3 (50% and 17%, respectively) patients. CONCLUSIONS: Life-threatening arrhythmias in LQTS patients tend to occur under specific circumstances in a gene-specific manner. These data allow new insights into the mechanisms that relate the electrophysiological consequences of mutations on specific genes to clinical manifestations and offer the possibility of complementing traditional therapy with gene-specific approaches.

Adrenergic beta-Antagonists↗
PubMed2001

Recording locations in multichannel magnetocardiography and body surface potential mapping sensitive for regional exercise-induced myocardial ischemia.

INTRODUCTION: This study aimed to identify the optimal locations in multichannel magnetocardiography (MCG) and body surface potential mapping (BSPM) to detect exercise-induced myocardial ischemia. METHODS: We studied 17 healthy controls and 24 coronary artery disease (CAD) patients with stenosis in one of the main coronary artery branches: left anterior descending (LAD) in 11 patients, right (RCA) in 7 patients, and left circumflex (LCX) in 6 patients. MCG and BSPM signals were recorded during a supine bicycle stress test. The capability of a recording location to separate the groups was quantified by subtracting the mean signal amplitude of the normal group from that of the patient group during the ST segment and at the T-wave apex, and dividing the resulting amplitude difference by the corresponding standard deviation within all subjects. RESULTS: In MCG the optimal location for ST depression was at the right inferior grid for the RCA, at the mid-inferior grid for the LCX, and in the middle of these locations for the LAD subgroup (mean ST amplitudes: CAD -80 +/- 360fT, controls 610 +/- 660fT; p < 0.001). In BSPM it was on the left upper anterior thorax for the LAD, left lower anterior thorax for the RCA, and on the lower back for the LCX subgroup (mean ST amplitudes: CAD -39 +/- 61 microV and controls 38 +/- 38 microV; p < 0.001). In MCG the optimal site for T-wave amplitude decrease was the same as the one for the ST depression. In BSPM it was on the middle front for the LAD, on the back for the LCX and on the left abdominal area for the RCA group. In accordance with electromagnetic theory, the largest ST segment and T-wave amplitude changes took place in MCG in locations orthogonal to those in BSPM. CONCLUSION: This study identified magnetocardiographic and BSPM recording locations which are sensitive for detecting transient myocardial ischemia by evaluation of the ST segment as well as the T-wave. These locations strongly depend on ischemic regions and are outside the conventional 12-lead ECG recording sites.

Aged↗
PubMed2001

A founder mutation of the potassium channel KCNQ1 in long QT syndrome: implications for estimation of disease prevalence and molecular diagnostics.

OBJECTIVES: We took advantage of the genetic isolate of Finns to characterize a common long QT syndrome (LQTS) mutation, and to estimate the prevalence of LQTS. BACKGROUND: The LQTS is caused by mutations in different ion channel genes, which vary in their molecular nature from family to family. METHODS: The potassium channel gene KCNQ1 was sequenced in two unrelated Finnish patients with Jervell and Lange-Nielsen syndrome (JLNS), followed by genotyping of 114 LQTS probands and their available family members. The functional properties of the mutation were studied using a whole-cell patch-damp technique. RESULTS: We identified a novel missense mutation (G589D or KCNQ1-Fin) in the C-terminus of the KCNQ1 subunit. The voltage threshold of activation for the KCNQ1-Fin channel was markedly increased compared to the wild-type channel. This mutation was present in homozygous form in two siblings with JLNS, and in heterozygous form in 34 of 114 probands with Romano-Ward syndrome (RWS) and 282 family members. The mean (+/- SD) rate-corrected QT intervals of the heterozygous subjects (n = 316) and noncarriers (n = 423) were 460 +/- 40 ms and 410 +/- 20 ms (p < 0.001), respectively. CONCLUSIONS: A single missense mutation of the KCNQ1 gene accounts for 30% of Finnish cases with LQTS, and it may be associated with both the RWS and JLNS phenotypes of the syndrome. The relative enrichment of this mutation most likely represents a founder gene effect. These circumstances provide an excellent opportunity to examine how genetic and nongenetic factors modify the LQTS phenotype.

Adolescent↗
PubMed2001

Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study. Losartan Intervention For End point.

OBJECTIVES: This study was designed to assess the relation of electrocardiographic (ECG) strain to increased left ventricular (LV) mass, independent of its relation to coronary heart disease (CHD). BACKGROUND: The classic ECG strain pattern, ST depression and T-wave inversion, is a marker for left ventricular hypertrophy (LVH) and adverse prognosis. However, the independence of the relation of strain to increased LV mass from its relation to CHD has not been extensively examined. METHODS: Electrocardiograms and echocardiograms were examined at study baseline in 886 hypertensive patients with ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage enrolled in the Losartan Intervention For End point (LIFE) echocardiographic substudy. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite to the QRS axis in leads V5 and/or V6. RESULTS: Strain occurred in 15% of patients, more commonly in patients with than without evident CHD (29%, 51/175 vs. 11%, 81/711, p < 0.001). When differences in gender, race, diabetes, systolic pressure, serum creatinine and high density lipoprotein cholesterol were controlled, strain on baseline ECG was associated with greater indexed LV mass in patients with (152 +/- 33 vs. 131 +/- 32 g/m2, p < 0.001) or without CHD (131 +/- 24 vs. 119 +/- 22 g/m2, p < 0.001). In logistic regression analyses, strain was associated with an increased risk of anatomic LVH in patients with CHD (relative risk 5.14, 95% confidence interval [CI] 1.16 to 22.85, p = 0.0315), without evident CHD (relative risk 2.91, 95% CI 1.50 to 5.65, p = 0.0016), and in the overall population when CHD was taken into account (relative risk 2.98, 95% CI 1.65 to 5.38, p = 0.0003). CONCLUSIONS: When clinical evidence of CHD is accounted for, ECG strain is likely to indicate the presence of anatomic LVH. Greater LV mass and higher prevalence of LVH in patients with strain offer insights into the known association of the strain pattern with adverse outcomes.

Aged↗
PubMed2001

Plasma and pericardial fluid natriuretic peptide levels in postinfarction ventricular dysfunction.

AIMS: In the present study we examined plasma and pericardial fluid ANP and BNP concentrations in postinfarction ventricular dysfunction. The association of peptide levels to left ventricular (LV) dysfunction and to the localization of the myocardial infarction (MI) was studied. METHODS AND RESULTS: Plasma and pericardial fluid samples were obtained from 37 patients undergoing coronary bypass surgery. According to the ECG and preceding coronary angiography, the patients were divided into three groups: previous anterior myocardial infarction (MI) (n=12), previous inferior/posterior MI (n=15) and no history of MI (n=10). When compared to the control group with no MI, the patients with anterior MI had elevated plasma ANP and BNP (134+/-13 vs. 81+/-15 pg/ml, P<0.01 and 95+/-10 pg/ml vs. 26+/-8 pg/ml, P<0.01, respectively) and pericardial fluid BNP (473+/-60 pg/ml vs. 57+/-8 pg/ml, P<0.001) levels. The plasma natriuretic peptide concentrations were not increased in the patients with inferior/posterior MI, but the pericardial fluid BNP concentrations were greater than in the patients with no history of MI (129+/-35 pg/ml vs. 57+/-8 pg/ml, P<0.05). Six of the 12 patients with previous anterior MI had LVEF> or =45%. Despite their normal LV systolic function, these patients had increased plasma and pericardial fluid BNP levels when compared to the group with no history of MI (68+/-18 pg/ml vs. 26+/-8 pg/ml, P<0.05 and 534+/-258 pg/ml vs. 57+/-8 pg/ml, P<0.01, respectively). CONCLUSIONS: Previous anterior myocardial infarction was associated with increased cardiac BNP production even if the LV systolic function was normal (LVEF> or =45%). The high pericardial fluid BNP concentrations in postinfarction patients suggest that the BNP synthesis and release are augmented in the ventricular myocardium independent from the LVEF.

Adult↗
PubMed2001

Magnetocardiographic intra-QRS fragmentation analysis in the identification of patients with sustained ventricular tachycardia after myocardial infarction.

The aim of this study was to investigate if magnetocardiographic (MCG) analysis of cardiac micropotentials within the QRS complex can identity patients prone to ventricular arrhythmias, and to compare it to MCG time-domain, late-field analysis. The study population consisted of 136 patients with remote MI, 53 with and 83 without a history of VT. After averaging and high pass filtering of multichannel MCG signals, time-domain parameters describing the end-QRS activity and fragmentation index M and score S describing the whole QRS complex were computed. Fragmentation and time-domain parameters differed between the VT and control groups: fragmentation index M was 12 +/- 3 versus 9 +/- 2 (P <0.001), fragmentation score S was 83 +/- 42 versus 56 +/- 21 (P < 0.001), and filtered QRS duration was 144 +/- 32 versus 114 +/- 19 ms (P < 0.001) in VT and control groups, respectively. A combination of fragmentation parameters yielded 87% sensitivity and 61% specificity in VT identification. Corresponding figures for a time-domain parameter combination were 81% and 72%. Sensitivity of time-domain analysis was 88% and specificity was 75% in a subgroup with anterior MI. In multivariate analysis, fragmentation and time-domain analyses discriminated VT patients from controls independently of the extent of coronary artery disease or left ventricular dysfunction. MCG in postinfarction patients reveals pathology associated with propensity to ventricular arrhythmias inside and not only at the end of the QRS complex. MCG seems most accurate in the anterior infarct location.

Aged↗
PubMed2001

Repolarization abnormalities detected by magnetocardiography in patients with dilated cardiomyopathy and ventricular arrhythmias.

INTRODUCTION: Abnormal repolarization is one of the acknowledged mechanisms leading to malignant ventricular arrhythmias. We used a novel magnetocardiographic technique to investigate the role of inhomogeneous repolarization in patients with nonischemic dilated cardiomyopathy prone to sustained ventricular arrhythmias. METHODS AND RESULTS: Forty-nine dilated cardiomyopathy patients were studied, 18 with a history of sustained ventricular tachycardia (n = 6) or ventricular fibrillation (n = 12) and 31 with no ventricular arrhythmias. The magnetocardiogram was registered and QT apex and QT end intervals were determined by a computer algorithm. Inhomogeneity of repolarization was characterized with indices describing QT apex and QT end dispersion, and T wave end duration. In addition, time-domain late fields of the QRS complex in magnetocardiography and QT dispersion in 12-lead ECG were determined. T wave end was longer in the arrhythmia group in patients with sinus rhythm (87 +/- 15 msec vs 73 +/- 12 msec; P = 0.005) and in those not having bundle branch block. Magnetocardiographic late fields of the QRS complex were not different between groups. QT apex and end dispersion on magnetocardiography or 12-lead ECG showed no difference. CONCLUSION: Prolongation of the end part of the T wave revealed by magnetocardiography is related to malignant ventricular arrhythmias in dilated cardiomyopathy. The results suggest that abnormal repolarization rather than delayed conduction underlies the arrhythmias in this disease.

Adult↗
PubMed2001

Postmyocardial infarction patients susceptible to ventricular tachycardia show increased T wave dispersion independent of delayed ventricular conduction.

INTRODUCTION: Experimentally, both delayed ventricular conduction and nonhomogeneous ventricular repolarization contribute to reentrant arrhythmias. We tested the hypothesis that increased T wave dispersion is independent of delayed ventricular conduction associated with arrhythmia vulnerability in postmyocardial infarction (post-MI) patients. METHODS AND RESULTS: We studied 32 post-MI patients with clinical or inducible monomorphic ventricular tachycardia (VT group), 28 post-MI patients without arrhythmias (MI group), and 13 healthy controls, using magnetocardiographic (MCG) mapping with signal averaging. Twelve-lead ECG was the reference. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE) were used as measures of ventricular conduction and nonhomogeneity in ventricular repolarization, respectively. In MCG, the VT group showed the longest fQRS (135+/-34 msec vs 114+/-22 msec in the MI group; P = 0.012). Mean TPE and maximum TPE in VT versus MI groups were 78+/-9 msec versus 70+/-6 msec (P < 0.001) and 117+/-23 msec versus 104+/-19 msec (P = 0.020), respectively. Maximum TPE did not correlate with fQRS in the VT group (r = 0.063; P = NS) but did correlate in the MI group (r = 0.396; P = 0.037). For identification of post-MI patients prone to VT, selection of cutoff values for fQRS >140 msec and mean TPE >81 msec gave sensitivity and specificity of 41% and 89%, and 31% and 96%, respectively. Their combination increased sensitivity to 63% while maintaining 89% specificity. CONCLUSION: Post-MI patients susceptible to VT show increased T wave dispersion independent of delayed ventricular conduction.

Aged↗
PubMed2001

Current-density estimation of exercise-induced ischemia in patients with multivessel coronary artery disease.

Magnetocardiographic and body surface potential mapping data measured in 6 patients with multivessel coronary artery disease were used in equivalent current-density estimation (CDE). Patient-specific boundary-element torso models were acquired from magnetic resonance images. Positron emission tomography data registrated with anatomical magnetic resonance imaging data provided the gold standard. Discrete current-density estimation values were computed on the epicardial surface of the left ventricle from difference (stress-rest) ST-segment maps. The ill-posed inverse problem was regularized with 3 different methods (Tikhonov regularization with an identity or a surface Laplacian operator and a maximum a posteriori estimator). Comparisons with positron emission tomography studies showed that the maximum a posteriori estimator is superior to other regularizations, provided that a suitable a priori information is available. In general, good correspondence was found for segments of high and low amplitude in current-density estimations, and the viable and scar areas in positron emission tomography, respectively.

Body Surface Potential Mapping↗
PubMed2001

Beat-to-beat analysis method for magnetocardiographic recordings during interventions.

Multichannel magnetocardiography (MCG) during exercise testing has been shown to detect myocardial ischaemia in patients with coronary artery disease. Previous studies on exercise MCG have focused on one or few time intervals during the recovery period and only a fragment of the data available has been utilized. We present a method for beat-to-beat analysis and parametrization of the MCG signal. The method can be used for studying and quantifying the changes induced in the MCG by interventions. We test the method with data recorded in bicycle exercise testing in healthy volunteers and patients with coronary artery disease. Information in all cardiac cycles recorded during the recovery period of exercise MCG testing is, for the first time, utilized in the signal analysis. Exercise-induced myocardial ischaemia was detected by heart rate adjustment of change in magnetic field map orientation. In addition to the ST segment, the T wave in the MCG was also found to provide information related to myocardial ischaemia. The method of analysis efficiently utilizes the spatial and temporal properties of multichannel MCG mapping, providing a new tool for detecting and quantifying fast phenomena during interventional MCG studies. The method can also be applied to an on-line analysis of MCG data.

Coronary Disease↗
PubMed2001

Relation of QT interval and QT dispersion to echocardiographic left ventricular hypertrophy and geometric pattern in hypertensive patients. The LIFE study. The Losartan Intervention For Endpoint Reduction.

OBJECTIVE: In hypertensive patients, left ventricular hypertrophy (LVH) predicts increased mortality, in part due to an increased incidence of sudden death. Repolarization-related arrhythmogenesis may be an important mechanism of sudden death in hypertensive patients with LVH. Increased QT interval and QT dispersion are electrocardiographic (ECG) measures of ventricular repolarization, and also risk markers for ventricular tachyarrhythmias. We assessed the relation of QT intervals and QT dispersion to echocardiographically determined left ventricular (LV) mass and geometry in a large population of hypertensive patients with ECG evidence of LVH. METHODS: QT intervals and QT dispersion were determined from baseline 12-lead ECGs in 577 (57% male; mean age 65 +/- 7 years) participants in the LIFE study. LV mass index (LVMI) and geometric pattern were determined by echocardiography and QT interval duration and QT dispersion were assessed in relation to gender-specific LVMI quartiles. RESULTS: In both genders, increasing LVMI was associated with longer rate-adjusted QT intervals. QT dispersion measures showed a weaker association with LVMI quartiles. Both concentric and eccentric LVH were associated with increased QT interval duration and QT dispersion. These relations remained significant after controlling for relevant clinical variables. CONCLUSIONS: In hypertensive patients with ECG evidence of LVH, increased LVMI and LVH are associated with a prolonged QT interval and increased QT dispersion. These findings suggest that an increased vulnerability to repolarization-related ventricular arrhythmias might in part explain the increased risk of sudden death in hypertensive patients with increased LV mass.

Aged↗