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Biomedical subjects

Arthur J Moss

Publications and source records attributed to Arthur J Moss.

At least 19 recordsLinked to original sources
PubMed2004

Use of a wearable defibrillator in terminating tachyarrhythmias in patients at high risk for sudden death: results of the WEARIT/BIROAD.

The automatic ICD improves survival in patients with a history of sudden cardiac arrest. However, some patients do not meet the guidelines for ICD implantation or are unable to receive an implantable device. This study tested the hypothesis that these patients could benefit from a wearable cardioverter defibrillator. Patients with symptomatic heart failure and an ejection fraction of <0.30 (WEARIT Study) or patients having complications associated with high risk for sudden death after a myocardial infarction or bypass surgery not receiving an ICD for up to 4 months (BIROAD Study) were enrolled into two studies. After a total of 289 patients had been enrolled in the trial (177 in WEARIT and 112 in BIROAD), prespecified safety and effectiveness guidelines had been met. Six (75%) of eight defibrillation attempts were successful. Six inappropriate shock episodes occurred during 901 months of patient use (0.67% unnecessary shocks per month of use). Twelve deaths occurred during the study 6 sudden deaths: 5 not wearing and 1 incorrectly wearing the device). Most patients tolerated the device although 68 patients quit due to comfort issues or adverse reactions. The results of the present study suggest that a wearable defibrillator is beneficial in detecting and effectively treating ventricular tachyarrhythmias in patients at high risk for sudden death who are not clear candidates for an ICD and may be useful as a bridge to transplantation or ICD in some patients.

Death, Sudden, Cardiac↗
PubMed2004

Electrocardiographic identification of drug-induced QT prolongation: assessment by different recording and measurement methods.

BACKGROUND: Careful assessment of QT interval prolongation is required before novel drugs are approved by regulatory authorities. The choice of the most appropriate method of electrocardiogram (ECG) acquisition and QT/RR interval measurement in clinical trials requires better understanding of the differences among currently available approaches. This study compared standard and Holter-derived 12-lead ECGs for utility in detecting sotalol-induced QT/QTc and RR changes. Manual methods (digitizing pad and digital on-screen calipers) were compared for precision of QT and RR interval measurement. METHODS AND RESULTS: Sixteen hundred pairs of serial 12-lead digital ECGs were recorded simultaneously by standard resting ECG device and by continuous 12-lead digital Holter over 3 days in 39 healthy male and female volunteers. No therapy was given on the 1st day followed by 160 mg and 320 mg of sotalol on the 2nd and 3rd day, respectively. Holter-derived and standard ECGs produced nearly identical sotalol-induced QT/QTc and RR changes from baseline, as did the manual digipad and on-screen caliper measurements. The variability of on-screen QT measurement in this study was greater than that of digipad. CONCLUSIONS: Digital 12-lead Holter and standard 12-lead ECG recorders, as well as the manual digitizing pad and digital on-screen calipers, are of equal utility for the assessment of drug-induced change from baseline in QT and RR interval, although the variability of the on-screen method in this study was greater than of the digipad.

Electrocardiography↗
PubMed2003

Modulating effects of age and gender on the clinical course of long QT syndrome by genotype.

OBJECTIVES: We aimed to determine whether long QT syndrome (LQTS) genotype has a differential effect on clinical course of disease in male and female children and adults after adjustment for QTc duration. BACKGROUND: Genotype influences clinical course of the LQTS; however, data on the effect of age and gender on this association are limited. METHODS: The LQTS genotype, QTc duration, and follow-up were determined in 243 cases of LQTS caused by the KCNQ1 potassium channel gene mutations (LQT1), 209 cases of LQTS caused by the HERG potassium channel gene mutations (LQT2), and 81 cases of LQTS caused by the SCN5A sodium channel gene mutation (LQT3) gene carriers. The probability of cardiac events (syncope, aborted cardiac arrest, or sudden death) was analyzed by genotype, gender, and age (children < or = 15 years and adults 16 to 40 years). In addition, the risk of sudden death and lethality of cardiac events were evaluated in 1,075 LQT1, 976 LQT2, and 324 LQT3 family members from families with known genotype. RESULTS: During childhood, the risk of cardiac events was significantly higher in LQT1 males than in LQT1 females (hazard ratio [HR] = 1.72), whereas there was no significant gender-related difference in the risk of cardiac events among LQT2 and LQT3 carriers. During adulthood, LQT2 females (HR = 3.71) and LQT1 females (HR = 3.35) had a significantly higher risk of cardiac events than respective males. The lethality of cardiac events was highest in LQT3 males and females (19% and 18%), and higher in LQT1 and LQT2 males (5% and 6%) than in LQT1 and LQT2 females (2% for both). CONCLUSIONS; Age and gender have different, genotype-specific modulating effects on the probability of cardiac events and electrocardiographic presentation in LQT1 and LQT2 patients.

Adolescent↗
PubMed2003

History of hypertension and enhanced thrombogenic activity in postinfarction patients.

Hypertension is a risk factor for coronary thrombosis and death in cardiac patients mediated in part by endothelial damage or dysfunction and increased thrombogenicity. However, there are no data regarding the association between hypertension and thrombogenic activity in stable patients after myocardial infarction and limited data about the prognostic significance of thrombogenic factors in hypertensive patients after infarction. Therefore, levels of thrombogenic, lipid, and inflammatory factors were measured 2 months after an acute myocardial infarction in 461 hypertensive and 582 nonhypertensive patients. Thrombogenic factors included d-dimer, fibrinogen, plasminogen activator inhibitor-1, von Willebrand factor, factor VII, and factor VIIa. Lipid variables included cholesterol (total, HDL, LDL), triglyceride, lipoprotein (a), apolipoprotein-A1, and apolipoprotein-B. The prognostic significance of these factors for predicting cardiac events during a 2-year follow-up was evaluated in hypertensive and nonhypertensive patients. In comparison with nonhypertensive patients, those with hypertension had higher levels of d-dimer (607 versus 453 mg/L, P<0.001), fibrinogen (3.64 versus 3.43 g/L, P<0.001), plasminogen activator inhibitor-1 (29.7 versus 27.3 ng/mL, P=0.01), von Willebrand factor (159 versus 141 IU/dL; P<0.001), and higher levels of inflammatory markers (hsCRP and SAA). In multivariate analysis after adjustment for clinical covariates, elevated d-dimer was the only factor independently associated with a history of hypertension (OR, 1.38, P=0.05). d-Dimer was associated with an increased risk of recurrent cardiac events in both hypertensive (hazard ratio=3.02, P=0.005) and nonhypertensive (hazard ratio=2.42, P=0.02) patients. Thus, patients after infarction with a history of hypertension have enhanced thrombogenic activity, which predisposes them to recurrent cardiac events.

Apolipoproteins↗
PubMed2003

Metabolic syndrome best defines the multivariate distribution of blood variables in postinfarction patients.

The hypothesis was tested that metabolic syndrome (MS) plays a leading role in approximating the multivariate distribution of thrombogenic and metabolic blood variables in a population of postinfarction patients. The multivariate statistical technique of factor analysis was used to determine blood variable clustering 2 months after myocardial infarction. Five clusters resulted in two separate independent factors, dyslipidemia and metabolic, reflecting MS and the remaining interpreted as cholesterol-lipoprotein, vascular-inflammatory, and coagulation. All five factors accounted for 55% of total variance with MS-associated factors accounting for 20% and individual factor contributions as follows: 11.6, 8.6, 12.9, 11.9, and 9.6%, respectively. There were no interactions of metabolic variables with thrombogenic variables or CRP in any factor. Results of subgroup analysis in males and females and in patients on and not on statins were all similar to the total group. We conclude there is no interaction of variables of MS or cholesterol-lipoprotein factors with those of thrombogenic factors. This independence yields the potential for use of factors in evaluating CVD risk. Further, the importance of MS in this group of postinfarction patients is emphasized, as the largest contribution to total variance was from MS factors, meaning that these variables best approximate the original multivariate distribution.

Aged↗
PubMed2003

Noninvasive risk stratification in postinfarction patients with severe left ventricular dysfunction and methodology of the MADIT II noninvasive electrocardiology substudy.

Sudden cardiac death occurs as a result of a complex interplay of changes in myocardial substrate, imbalance of autonomic regulation of the heart, and myocardial vulnerability. Noninvasive electrocardiology serves as a comprehensive tool for investigating factors representing mechanistic pathways leading to cardiac events. Heart rate variability, nonlinear dynamics of heart rate, and heart rate turbulence provide insight into autonomic control of the heart. Prognostic value of these parameters in postinfarction patients is well established for predicting cardiac death, but there is less evidence for their association with sudden death or arrhythmic events. Electrical manifestation of changes in myocardial substrate include QRS and QTc prolongation, presence of conduction disturbances, presence of late potentials, abnormalities of repolarization morphology, and presence of nonsinus rhythm, namely atrial fibrillation. Electrocardiogram (ECG) measures reflecting myocardial vulnerability to arrhythmias include frequent ventricular premature beats, T wave alternans, or QT variability. Prognostic significance of these parameters is documented in studies focused mostly on them as individual markers of risk. The noninvasive electrocardiology substudy of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) allows for simultaneous analysis of several of the above ECG markers of risk and will provide insight about relative contribution of mechanistic pathways leading to cardiac death in postinfarction patients with severe left ventricular dysfunction. Combination of a standard 12-lead ECG and 10-minute high-resolution Holter recordings serves to evaluate the prognostic significance of noninvasive electrocardiology parameters for mortality in patients randomized to conventional treatment and for arrhythmic events in patients randomized to implantable cardioverter defibrillator therapy.

Atrial Fibrillation↗
PubMed2003

Identification of sotalol-induced changes in repolarization with T wave area-based repolarization duration parameters.

In this study, we investigated the validity of T wave area-based parameters for the identification of drug-induced changes of repolarization. Based on electrocardiograms from 39 healthy patients, we computed the stability of repolarization measurements and compared the sotalol-induced repolarization changes when measured with area-based parameters and traditional QT interval techniques (manual and automatic). Also, we evaluated the effect of different types of heart rate correction on these repolarization measurements. The results show that the stability of the automatic repolarization measurements is higher when measured using computer algorithm than using manual QT measurement. By using a population-based heart rate correction, the area-based parameters reveal significant modification of the overall shape of the T wave in its early, middle, and final part. In conclusion, morphological parameters of T wave are able to identify the changes in repolarization interval induced by sotalol. These parameters are more stable and thus more reliable than the traditional QT interval measurements.

Electrocardiography↗
PubMed2003

MADIT-I and MADIT-II.

The MADIT-I study was a proof-of-principle study, and this randomized trial showed that the implantable cardioverter defibrillator (ICD) saves lives in high-risk patients with coronary heart disease. The MADIT-II study showed that prophylactic ICD therapy was associated with significantly improved survival in patients with ischemic cardiomyopathy, as defined by documented coronary heart disease and advanced left ventricular dysfunction, without requiring screening for ventricular arrhythmias or inducibility by electrophysiologic testing. Taken together, these two trials, as well as the results from several other randomized ICD trials, indicate that ICD therapy is indicated in coronary patients who meet MADIT-I or MADIT-II eligibility criteria and are not excluded by major noncardiac comorbidity.

Cardiac Pacing, Artificial↗
PubMed2003

Implantable cardioverter defibrillator in high-risk long QT syndrome patients.

INTRODUCTION: Implantable cardioverter defibrillators (ICDs) are increasingly being used in high-risk long QT syndrome (LQTS) patients, but there are limited data regarding clinical experience with this therapeutic modality. The aim of this study is to describe the clinical characteristics of 125 LQTS patients treated with ICDs compared with LQTS patients having similar risk indications who were not treated with ICDs. Among 125 LQTS patients with ICDs, there were 54 cardiac arrest survivors, 19 patients who had ICDs implanted due to recurrent syncope despite beta-blocker therapy, and 52 patients with ICDs implanted due to other reasons, including syncope and LQTS-related sudden death in a close family member. Patients with cardiac arrest and those with recurrent syncope despite beta-blocker therapy (n = 73) were compared to 161 LQTS patients who had similar indications (89 cardiac arrest and 72 recurrent syncope despite beta-blocker therapy) but did not receive ICDs. Total mortality was the endpoint of the analysis. There was 1 (1.3%) death in 73 ICD patients followed an average of 3 years, whereas there were 26 deaths (16%) in non-ICD patients during mean 8-year follow-up (P = 0.07 from log rank test from Kaplan-Meier curves). CONCLUSION: ICDs provide an important therapeutic option to prevent sudden arrhythmic death in high-risk LQTS patients. A long-term prospective study is needed to determine the benefit of this therapeutic modality in LQTS patients.

Adolescent↗
PubMed2003

Location of mutation in the KCNQ1 and phenotypic presentation of long QT syndrome.

INTRODUCTION: Recent data showed that long QT syndrome (LQTS) patients with mutations in the pore region of the HERG (LQT2) gene have significantly higher risk of cardiac events than subjects with mutations in the non-pore region. The aim of this study was to determine whether there is an association between the location of mutations in the KCNQ1 gene and cardiac events in LQT1 patients. METHODS AND RESULTS: The study population consisted of 294 LQT1 patients with KCNQ1 gene mutations. Demographic, clinical, and follow-up information was compared among subjects with different locations of KCNQ1 mutations defined as pre-pore region including N-terminus (1-278), pore region (279-354), and post-pore region including C-terminus (>354). Cardiac events observed during follow-up from birth until age of last contact or age 40 years were defined as syncope, cardiac arrest, or sudden death. There were 164 (56%) LQT1 patients with pre-pore mutations, 101 (34%) with pore mutations, and 29 (10%) with post-pore mutations. QTc duration did not differ significantly among the three subgroups (mean QTc = 494, 487, and 501 ms, respectively). There was no significant difference between groups with regard to the risk of cardiac events by age 40 years. CONCLUSION: There are no significant differences in clinical presentation, ECG parameters, and cardiac events among LQT1 patients with different locations of KCNQ1 mutations. These findings indicate that factors other than location of mutation influence clinical phenotype in patients with LQT1 mutations.

Adult↗