Search PubMed⌕ Search

Biomedical subjects

A J Moss

Publications and source records attributed to A J Moss.

At least 109 records · Page 6Linked to original sources
PubMed1994

Cigarette smoking and the age at onset of a first non-fatal myocardial infarction.

BACKGROUND: Smoking is a major risk factor for coronary heart disease. Discontinuance of smoking is associated with a reduction in the risk of coronary disease; this risk approaches the level among non-smokers after stopping smoking for periods ranging from 6 months to several years. We analyzed pertinent prospectively accumulated data from our multicenter postinfarction studies to gain further insight into the complex relationship between cigarette smoking and the premature occurrence of a first myocardial infarction. METHODS: Retrospective analysis of the relationship between the number of cigarettes smoked and the age at onset of patients experiencing their first non-fatal myocardial infarction was investigated in 2445 patients. The intensity of smoking was quantitated in terms of the average number of packs per day smoked during adult years, subcategorized in increments of a half-pack per day up to more than two packs per day. Ex-smokers were identified if they had stopped smoking 1 month before their index infarction. Analysis of variance was used to adjust for the effects of relevant confounding risk factors. RESULTS: The adjusted age for first non-fatal infarction progressively declined with increasing smoking exposure, with an average age reduction of 8.7 years (95% confidence interval; 7.2, 10.2) in those smoking more than two packs per day compared with non-smokers. The graded effect was somewhat more marked in women than in men. The number of cigarettes smoked before infarction had no effect on the severity of the acute infarction or on mortality from cardiac causes during more than 2-year post-hospital follow-up. Those who stopped smoking 1 month or longer before the infarction were significantly older at the time of first infarction than active smokers in all smoking categories. CONCLUSION: This study provides strong evidence that active smoking is associated with an earlier age at onset of first infarctions, with a striking inverse dose-response effect. Stopping smoking appears to reduce the premature occurrence of coronary events.

Age of Onset↗
PubMed1994

Risk of subsequent cardiac events in stable convalescing patients after first non-Q-wave and Q-wave myocardial infarction: the limited role of non-invasive testing. The Multicenter Myocardial Ischemia Research Group.

BACKGROUND: Patients recovering from myocardial infarction are frequently evaluated by non-invasive tests for evidence of myocardial ischemia before returning to work or full activity. The purpose of this study was to evaluate the prognostic significance of clinical and non-invasive ischemic test variables assessed in 549 stable, convalescing patients (median 2 months) after their first Q-wave (n = 363) and non-Q-wave (n = 186) myocardial infarction. METHODS: The ischemic tests performed were resting ECG, exercise ECG, ambulatory ECG, and stress thallium scintigraphy. RESULTS: Cardiac events (unstable angina requiring hospitalization, non-fatal reinfarction, or death from cardiac causes) were observed during a mean 23-month follow-up in 57 patients (15.7%) with Q-wave and in 31 of patients (16.7%) with non-Q-wave infarction. In a step-wise Cox regression model, the only significant independent predictors of subsequent cardiac events (P < 0.001) were post-infarction angina and insulin-dependent diabetes mellitus. The type of infarction did not make a significant contribution to the risk of cardiac events (P = 0.29). However, an interaction between infarct type and post-infarction angina was of borderline significance (P = 0.065), with angina associated with more cardiac events in patients with non-Q-wave than in those with Q-wave infarction. None of the ischemic tests contributed significantly to the Cox model in predicting cardiac events in either infarct type. CONCLUSION: Stable convalescing patients who have recovered from first Q-wave and non-Q-wave myocardial infarction have similar long-term prognoses. The occurrence of post-infarction angina is associated with increased risk of cardiac events in patients with both infarct types, with more marked effect in non-Q-wave than Q-wave infarctions. Ischemia detected by non-invasive tests performed in the convalescing phase after myocardial infarction was not prognostically useful in either infarct type.

Convalescence↗
PubMed1994

Risk of subsequent cardiac events in stable convalescing patients after first non-Q-wave and Q-wave myocardial infarction: the limited role of non-invasive testing.

BACKGROUND: Patients recovering from myocardial infarction are frequently evaluated by non-invasive tests for evidence of myocardial ischemia before returning to work or full activity. The purpose of this study was to evaluate the prognostic significance of clinical and non-invasive ischemic test variables assessed in 549 stable, convalescing patients (median 2 months) after their first Q-wave (n = 363) and non-Q-wave (n = 186) myocardial infarction. METHODS: The ischemic tests performed were resting ECG, exercise ECG, ambulatory ECG, and stress thallium scintigraphy. RESULTS: Cardiac events (unstable angina requiring hospitalization, non-fatal reinfarction, or death from cardiac causes) were observed during a mean 23-month follow-up in 57 patients (15.7%) with Q-wave and in 31 of patients (16.7%) with non-Q-wave infarction. In a step-wise Cox regression model, the only significant independent predictors of subsequent cardiac events (P < 0.001) were post-infarction angina and insulin-dependent diabetes mellitus. The type of infarction did not make a significant contribution to the risk of cardiac events (P = 0.29). However, an interaction between infarct type and post-infarction angina was of borderline significance (P = 0.065), with angina associated with more cardiac events in patients with non-Q-wave than in those with Q-wave infarction. None of the ischemic tests contributed significantly to the Cox model in predicting cardiac events in either infarct type. CONCLUSION: Stable convalescing patients who have recovered from first Q-wave and non-Q-wave myocardial infarction have similar long-term prognoses. The occurrence of post-infarction angina is associated with increased risk of cardiac events in patients with both infarct types, with more marked effect in non-Q-wave than Q-wave infarctions. Ischemia detected by non-invasive tests performed in the convalescing phase after myocardial infarction was not prognostically useful in either infarct type.

Angina Pectoris↗
PubMed1994

Analysis of HLA and disease susceptibility: chromosome 6 genes and sex influence long-QT phenotype.

The long-QT (LQT) syndrome is a genetically complex disorder that is characterized by syncope and fatal ventricular arrhythmias. LQT syndrome, as defined by a prolonged electrocardiographic QT interval, has a higher incidence in females than in males and does not exhibit Mendelian transmission patterns in all families. Among those families that are nearly consistent with Mendelian transmission, linkage between a locus for LQT syndrome and the H-ras-1 locus on the short arm of chromosome 11 has been reported in some families but not in others. Earlier analyses suggesting that LQT syndrome might be caused by a gene in the HLA region of chromosome 6 were not confirmed by standard linkage analyses. Here, we present an analysis of HLA haplotype sharing among affected pedigree members, showing an excess of haplotype sharing in a previously published Japanese pedigree and possibly also in 15 families of European descent. The haplotypes shared by affected individuals derive from both affected and unaffected parents. In an analysis of independent (unrelated) HLA haplotypes, we also found a nonrandom distribution of HLA-DR genes in LQT syndrome patients compared with controls, suggesting an association between the LQT phenotype and specific HLA-DR genes. Our data indicate that DR2 has a protective effect and, particularly in males, that DR7 may increase susceptibility to the LQT syndrome. Thus, LQT syndrome may be influenced by genes on chromosomes 11 and 6, possibly with a sex-specific effect. These results provide a model for an effect of HLA-region genes inherited from either parent on the expression of an illness that may be determined principally by alleles at loci not linked to HLA.

Chromosomes, Human, Pair 6↗
PubMed1993

Measurement of the QT interval and the risk associated with QTc interval prolongation: a review.

The accurate measurement of the QT interval and its correction or adjustment for cycle length, age, and gender have been topics of increasing interest over the course of the past 70 years. The availability of digitized electrocardiographic recordings on large normal populations together with statistical adjustment for pertinent covariates has provided useful data for defining QT interval prolongation. Data from the International Long QT Syndrome Registry indicate that the probabilistic risk of developing malignant arrhythmias in patients with QT prolongation is exponentially related to the length of the QTc interval. The risk is further accentuated by the development of T-wave alternans, particularly at very prolonged QTc intervals.

Adolescent↗
PubMed1993

Detection and significance of myocardial ischemia in stable patients after recovery from an acute coronary event. Multicenter Myocardial Ischemia Research Group.

OBJECTIVE: To determine the clinical significance of silent and symptomatic myocardial ischemia detected by noninvasive testing in stable postcoronary patients. DESIGN: Cohort study with a mean 23-month follow-up. SETTING: Ambulatory outpatients after recent hospitalization for an acute coronary event. PATIENTS: Nine hundred thirty-six patients (76% male; mean age, 58 years) who were clinically stable 1 to 6 months after hospitalization for acute myocardial infarction or unstable angina. INTERVENTIONS: Noninvasive testing involved rest, ambulatory, and exercise electrocardiograms and stress thallium-201 scintigraphy. MAIN OUTCOME MEASURES: Cox regression analysis was used to evaluate the risk (hazard ratio) of first recurrent primary events (cardiac death, nonfatal infarction, or unstable angina) or restricted events (cardiac death or nonfatal infarction) associated with ischemic noninvasive test results. RESULTS: ST segment depression on the rest electrocardiogram was the only noninvasive test variable that identified a significantly increased risk (P = .05) for first recurrent primary events (hazard ratio; 95% confidence limits): rest electrocardiogram ST depression (1.5; 1.00, 2.25); ambulatory electrocardiogram ST depression (0.86; 0.49, 1.51); exercise electrocardiogram ST depression (1.13; 0.82, 1.56); and stress thallium-201 reversible defects (1.3; 0.96, 1.74). Test results were similar for first recurrent restricted events, and in patients with and without angina. Significantly increased risk (P < .05) was noted when exercise-induced ST depression occurred in patients who also had reduced exercise duration (hazard ratio, 3.4) or when reversible thallium-201 defects occurred in patients who also had increased lung uptake (hazard ratio, 2.8). Each high-risk subset made up less than 3% of the population and contained less than 6% of patients with first primary events. CONCLUSION: Detection of silent or symptomatic myocardial ischemia by non-invasive testing in stable patients 1 to 6 months after an acute coronary event is not useful in identifying patients at increased risk for subsequent coronary events.

Adult↗
PubMed1993

Dynamic analysis of ventricular repolarization duration from 24-hour Holter recordings.

Evaluation of the influence of the autonomic nervous system on the ventricular repolarization duration was carried out using beat-to-beat analysis of the time intervals between the peaks of the R and T waves (RTm). After pre-processing of digitized Holter ECG's, auto and cross spectrum analyses were applied to heart rate and repolarization duration variability signals. Coherence analysis was used to assess the existence of common spectral contributions. The heart rate variability signal was used as reference of the sympatho-vagal balance at the sinus node. It was found that, in normal individuals, the autonomic nervous system directly influences the ventricular repolarization duration and that this influence is qualitatively very similar to the one that modulates the heart rate. Pathological alteration of these parallel autonomic activities to the heart (on the sinus node and on the ventricle) might cause uncoupling between depolarization and repolarization.

Adrenergic beta-Antagonists↗
PubMed1993

Acquired coronary angiogenesis after myocardial infarction.

Acquired coronary artery microvascular fistulas have been reported in only a few patients after myocardial infarction. We describe 1 patient in whom serial coronary angiography demonstrated the development of coronary angiogenesis at the site of an old myocardial infarction. The area of neovascularity was associated with a large apical left ventricular thrombus. This finding suggests that growth-promoting mitogens are present in myocardium and thrombus and that angiogenesis occurs in some patients following myocardial infarction.

Coronary Angiography↗
PubMed1993

Locus heterogeneity of autosomal dominant long QT syndrome.

Autosomal dominant long QT syndrome (LQT) is an inherited disorder that causes syncope and sudden death from cardiac arrhythmias. In genetic linkage studies of seven unrelated families we mapped a gene for LQT to the short arm of chromosome 11 (11p15.5), near the Harvey ras-1 gene (H ras-1). To determine if the same locus was responsible for LQT in additional families, we performed linkage studies with DNA markers from this region (H ras-1 and MUC2). Pairwise linkage analyses resulted in logarithm of odds scores of -2.64 and -5.54 for kindreds 1977 and 1756, respectively. To exclude the possibility that rare recombination events might account for these results, we performed multipoint linkage analyses using additional markers from chromosome 11p15.5 (tyrosine hydroxylase and D11S860). Multipoint analyses excluded approximately 25.5 centiMorgans of chromosome 11p15.5 in K1756 and approximately 13 centiMorgans in K1977. These data demonstrate that the LQT gene in these kindreds is not linked to H ras-1 and suggest that mutations in at least two genes can cause LQT. While the identification of locus heterogeneity of LQT will complicate genetic diagnosis, characterization of additional LQT loci will enhance our understanding of this disorder.

Chromosome Mapping↗
PubMed1992

Instantaneous cardiac death in the posthospital period after acute myocardial infarction.

Sudden arrhythmic cardiac death is a major unresolved health problem, yet there is no agreement on the chronologic definition of sudden death. This retrospective study investigates the frequency distribution of the chronology of the terminal cardiac event in a large postinfarction population and identifies factors associated with instantaneous (< 1 minute) cardiac death. This study involved 229 patients enrolled in the Multicenter Diltiazem Post-infarction Trial who died during 2-year follow-up and had quantitative information on the chronology of the terminal event. Thirty-two percent of the cardiac deaths occurred instantaneously. Patients who died instantaneously were more likely (p < 0.05) to be men, to have a baseline ejection fraction < 0.40, and to have frequent (> or = 10/hour) and repetitive (> or = 3 in a row) ventricular ectopic complexes (VECs) on an ambulatory electrocardiogram than those who did not die instantaneously. Patients who died instantaneously received more digitalis and class IA antiarrhythmic agents and less beta blockers in the week before death than those dying noninstantaneously. Logistic regression analysis identified 3 independent factors that differentiated instantaneous from noninstantaneous death (relative risk; 95% confidence interval): frequent VECs (2.15; 1.11 to 4.17); digitalis (2.57; 1.31 to 5.06); and no beta blocker medication (2.90; 1.09 to 7.75). Instantaneous death (within 1 minute) was responsible for almost one third of the cardiac deaths that occurred in this postinfarction population. Frequent VECs, digitalis, and absence of beta-blocker therapy distinguished patients who died instantaneously from those who died noninstantaneously.

Adrenergic beta-Antagonists↗
PubMed1992

Prevention of sudden cardiac death.

Since the vast majority of these deaths are triggered by arrhythmias, the first step in prevention is to understand the risk factors for malignant rhythms. The second is to identify patients who may benefit from preventive intervention. Finally, who should get drugs, who automatic cardioverter-defibrillator implantation. The determinants of that choice remain to be elucidated.

Anti-Arrhythmia Agents↗