PubMed Health⌕ Search

Biomedical subjects

A J Moss

Publications and source records attributed to A J Moss.

At least 19 recordsLinked to original sources
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↗
PubMed1992

Interrelation of left ventricular ejection fraction, pulmonary congestion and outcome in acute myocardial infarction.

The interrelation of different grades of pulmonary congestion evaluated by chest roentgenogram in the coronary care unit, predischarge left ventricular (LV) ejection fraction (EF) and long-term prognosis was studied in 1,850 surviving patients of acute myocardial infarction (AMI). Pulmonary congestion was categorized as: none, mild or moderate, or severe; LVEF was classified as: greater than or equal to 40%, 25 to 39%, or less than 25%. The majority of patients (1,060; 57%) had an LVEF greater than or equal to 40% and no signs of pulmonary congestion. Severe pulmonary congestion was noted in 63 patients (3.4%), 17 with LVEF less than 25% and 16 with LVEF greater than or equal to 40%. One hundred twenty-five patients (6.8%) had an LVEF less than 25%, 49 of whom had no signs of pulmonary congestion. During a mean 2-year follow-up, cardiac mortality occurred in 212 patients (11.5%). The cardiac mortality rate was related to both predischarge LVEF impairment and severity of pulmonary congestion. Cardiac mortality hazard ratios (95% confidence intervals [CI]) for LVEF less than 25%, and 25 to 39% were 5.32 (CI 3.49, 8.13; p less than 0.0001) and 2.91 (CI 2.10, 4.02; p less than 0.0001), respectively, where a referent hazard ratio of 1 was assigned to patients with LVEF greater than or equal to 40% and to those with no pulmonary congestion. Development of pulmonary congestion during AMI significantly increased the cardiac mortality risk derived from LVEF, with a marked mortality effect in patients with severe pulmonary congestion; (hazard ratio 4.20; 95% CI 2.67, 6.62; p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Relation between ventricular repolarization duration and cardiac cycle length during 24-hour Holter recordings. Findings in normal patients and patients with long QT syndrome.

BACKGROUND: The interval from the R wave to the maximum amplitude of the T wave (RTm) contains the heart rate dependency of ventricular repolarization. METHODS AND RESULTS: A computer algorithm was developed to quantify the RTm and preceding RR intervals for each of more than 50,000 beats on 24-hour ambulatory electrocardiographic (Holter) recordings to evaluate the dynamic relation between repolarization duration and cycle length. The relation of RTm to the preceding RR interval (RTm/RR slope) was determined by the best-fit linear regression equation between these two parameters. Eleven normal subjects and 16 patients with long QT syndrome (LQTS) were investigated. Six of the normal subjects had Holter recordings obtained before and after beta-blocker therapy. beta-Blockers were associated with a significant (p = 0.005) reduction in the RTm/RR slope from 0.13 +/- 0.02 to 0.10 +/- 0.02. The mean value of the RTm/RR slope was significantly (p = 0.003) larger in the LQTS patients (0.21 +/- 0.08) than in normal subjects (0.14 +/- 0.03). CONCLUSIONS: These findings indicate that 1) quantification of the dynamic relation between ventricular repolarization and RR cycle length can be obtained on a large number of Holter-recorded heart beats; 2) beta-blockers reduce the RTm/RR slope in normal patients; and 3) LQTS patients have an exaggerated delay in repolarization at long RR cycle lengths.

Adult↗
PubMed1992

Hypolipidemic effect of type Ia antiarrhythmic agents in postinfarction patients.

BACKGROUND: Elevated levels of cholesterol and apoprotein B (apo B), the essential carrier protein for low density lipoprotein, are major lipid risk factors for premature coronary disease. Antiarrhythmic agents are frequently prescribed to patients with coronary heart disease and associated cardiac arrhythmias. As part of another study, we retrospectively investigated the effect of antiarrhythmic agents on blood lipids. METHODS AND RESULTS: The study population consisted of 1,567 postinfarction patients on whom we prospectively collected serial blood samples for lipid and apoprotein determinations and recorded the concomitant medications the patients were receiving at three follow-up time periods. The lipids, analyzed at a central core laboratory, included total cholesterol, triglycerides, high density lipoprotein cholesterol (HDL C), and apoproteins A-I (apo A-I), A-II (apo A-II), and apo B. The difference in the group mean lipid values for patients receiving and not receiving type Ia antiarrhythmic agents (quinidine, procainamide, and disopyramide) was evaluated by the two-sample t test, and multiple linear regression analyses were performed to adjust for relevant covariates. Patients using type Ia antiarrhythmic agents at the 30-month postinfarction contact (n = 76) had 8.6% lower cholesterol (p less than 0.003), 22.3% lower triglycerides (p less than 0.0002), 6.2% lower apo A-I (p = 0.02), 10.1% lower apo A-II (p less than 0.001), and 12.7% lower apo B (p less than 0.0001) levels than patients not on these medications (n = 1,491). These lower lipid levels were found after adjustment for age, sex, diabetes, smoking status, concomitant medications, and a variety of clinical factors relating to the severity of the coronary disease process. The HDL C levels were similar in those receiving and not receiving type Ia agents. CONCLUSIONS: Patients on type Ia antiarrhythmic agents had significantly and meaningfully lower cholesterol, triglyceride, apo A-II, and apo B levels than patients not receiving these agents. The mechanism of this hypolipidemic effect is undefined, but the mechanism may be related to an alteration by these agents of ionic membrane currents at the hepatocyte level.

Anti-Arrhythmia Agents↗
PubMed1992

Clinical features of the idiopathic long QT syndrome.

Long QT syndrome (LQTS) is an infrequently occurring familial disorder in which affected members have electrocardiographic QT interval prolongation and a propensity to syncope and fatal ventricular arrhythmias. This review of the current literature includes discussions of inheritance, clinical presentation, diagnosis, and treatment of LQTS. At present, there are three modalities of treatment for LQTS patients: beta-blockers, pacemakers, and left cervicothoracic sympathetic ganglionectomy. Because the clinical course of LQTS is quite variable, therapy must be individualized for each patient.

Adrenergic beta-Antagonists↗
PubMed1992

Clues in diagnosing congenital heart disease.

A number of practical office and bedside clues to cardiac disease in infants and children have been passed on through the years. They relate to the history, to the inspection and palpation components of the physical examination, and to knowledge of the specific cardiac defects that are likely to be associated with certain clinical syndromes. With the possible exception of coarctation of the aorta, the clues are not diagnostically specific. In many instances, however, they serve to narrow a broad array of diagnostic possibilities to 2 or 3 and, with the aid of other clues and auscultation, they can often be distinguished from one another. When a primary care physician is confronted with a child who has an incidental murmur that is "probably" innocent but could be organic, useful clues favoring an organic murmur are a history of congenital heart disease in a first-degree relative; a history of maternal rubella syndrome, alcohol use, or teratogenic drug use during pregnancy; a history of inappropriate sweating; a history of syncope, chest pain, or squatting; maternal diabetes mellitus; premature birth; birth at a high altitude; cyanosis; abnormal pulsations; recurrent bronchiolitis or pneumonia; chronic unexplained hoarseness; asymmetric facies with crying; and a physical appearance suggestive of a clinical syndrome.

Child↗
PubMed1991

Effects of diltiazem on long-term outcome after acute myocardial infarction in patients with and without a history of systemic hypertension. The Multicenter Diltiazem Postinfarction Trial Research Group.

The effect of diltiazem on long-term outcome in patients with acute myocardial infarction with and without a history of systemic hypertension was investigated in 2,466 patients using the Multicenter Diltiazem Postinfarction Trial data-base. The baseline variables were comparable in the diltiazem and placebo-treated patients within the groups with and without hypertension. The initial 60-mg dose of diltiazem was associated with a significant (p less than 0.001) but modest (3%) reduction in blood pressure and heart rate in both groups with and without hypertension. Univariate and multivariate analyses revealed a meaningful overall reduction in first recurrent cardiac events (cardiac death or nonfatal reinfarction, whichever occurred first) and cardiac death in patients with hypertension treated with diltiazem compared with results in those treated with placebo. Similar effects were not observed in patients without a history of hypertension. When first recurrent cardiac events were used as the end point, the diltiazem:placebo hazard ratio (95% confidence limits) was 0.77 (0.58, 1.01) for the total hypertension group, and 0.67 (0.47, 0.96) and 1.32 (0.83, 2.10) for patients with hypertension with and without pulmonary congestion during the acute infarction, respectively. Similar results were observed using cardiac death as the end point. Beta blockers had a negligible effect on the hypertension-diltiazem relation. These findings suggest that diltiazem may exert a long-term beneficial effect in most patients with hypertension who do not have pulmonary congestion during an acute infarction, and a detrimental effect in the minority who have pulmonary congestion.

Adult↗
PubMed1991

Treatment of aortic coarctation by axillofemoral bypass grafting in the high-risk patient.

Operative correction of coarctation of the aorta has been performed for 45 years. Reoperation for recurrent coarctation is necessary in as many as 5% to 10% of patients. Repair of recurrent coarctation carries an operative mortality of between 5% and 10%. Coarctation repair involves an increased risk in patients with advanced age, recurrent coarctation, congestive heart failure, and pulmonary disease. We report 3 cases where axillofemoral bypass has been used to treat high-risk patients with aortic coarctation. Two patients had had previous coarctation repair in addition to serious medical problems. Another patient had suffered three myocardial infarctions and had disabling congestive heart failure. All patients had an immediate marked decrease in their preoperative peak systolic pressure gradient across the coarctation. Systemic hypertension and symptoms of congestive heart failure were improved in all patients. The length of follow-up was 15 months, 8.5 years, and 10.5 years. Reassessment with noninvasive vascular segmental pressure studies with and without an exercise component showed no recurrence of the pressure gradient. This procedure should be considered when treating coarctation of the aorta in the high-risk adult.

Aged↗
PubMed1991

Left cardiac sympathetic denervation in the therapy of congenital long QT syndrome. A worldwide report.

BACKGROUND: Long QT syndrome (LQTS) is a congenital disorder accompanied by a high incidence of sudden cardiac death. beta-Adrenergic blockade is the therapy of choice, and it is successful in 75-80% of patients. For those in whom cardiac events (syncope or cardiac arrest) are not prevented by beta-blockade, experimental studies suggest that left cardiac sympathetic denervation (LCSD) may be useful. METHODS AND RESULTS: We identified 85 LQTS patients worldwide who underwent LCSD, and we provide here the first large-scale evaluation of its efficacy. The time interval between the first cardiac event and LCSD and the follow-up period after LCSD were similar (5.6 +/- 6.1 versus 5.9 +/- 5.7 years). The mean age of the patients at surgery was 20 +/- 13 years. LCSD was followed by highly significant (p less than 0.0001) decreases in the number of patients with cardiac events (from 99% to 45%), in the number of cardiac events per patient (from 22 +/- 32 to 1 +/- 3), and in the number of patients with five or more cardiac events (from 71% to 10%). There were seven sudden deaths (8%), and the 5-year survival rate was 94%. The marked reduction in the incidence of tachyarrhythmic syncope suggests that LCSD has also reduced the risk for sudden death in this high-risk population. CONCLUSIONS: The present findings demonstrate that for LQTS patients who continue with syncope or cardiac arrest despite the use of beta-blockers, LCSD is a very effective therapy.

Adolescent↗
PubMed1991

The long QT syndrome. Prospective longitudinal study of 328 families.

BACKGROUND: The Long QT Syndrome (LQTS) is an infrequently occurring familial disorder in which affected individuals have electrocardiographic QT interval prolongation and a propensity to ventricular tachyarrhythmic syncope and sudden death. We prospectively investigated the clinical characteristics and the long-term course of 3,343 individuals from 328 families in which one or more members were identified as affected with LQTS (QTc greater than 0.44 sec1/2). METHODS AND RESULTS: The first member of a family to be identified with LQTS, the proband, was usually brought to medical attention because of a syncopal episode during childhood or teenage years. Probands (n = 328) were younger at first contact (age 21 +/- 15 years), more likely to be female (69%), and had a higher frequency of preenrollment syncope or cardiac arrest with resuscitation (80%), congenital deafness (7%), a resting heart rate less than 60 beats/min (31%), QTc greater than or equal to 0.50 sec1/2 (52%), and a history of ventricular tachyarrhythmia (47%) than other affected (n = 688) and unaffected (n = 1,004) family members. Arrhythmogenic syncope often occurred in association with acute physical, emotional, or auditory arousal. The syncopal episodes were frequently misinterpreted as a seizure disorder. By age 12 years, 50% of the probands had experienced at least one syncopal episode or death. The rates of postenrollment syncope (one or more episodes) and probable LQTS-related death (before age 50 years) for probands (n = 235; average follow-up 54 months per patient) were 5.0% per year and 0.9% per year, respectively; these event rates were considerably higher than those observed among affected and unaffected family members. CONCLUSIONS: Among 232 probands and 1,264 family members with prospective follow-up, three factors made significant independent contributions to the risk of subsequent syncope or probable LQTS-related death before age 50 years, whichever occurred first (Cox hazard ratio; 95% confidence limits): 1) QTc (1.052; 1.017, 1.088), 2) history of cardiac event (3.1; 1.3, 7.2), and 3) heart rate (1.017; 1.004, 1.031). The findings from this prospective longitudinal study highlight the clinical features, risk factors, and course of LQTS.

Adult↗
PubMed1991

Efficacy of permanent pacing in the management of high-risk patients with long QT syndrome.

BACKGROUND: From the international long QT syndrome (LQTS) study, 30 patients with corrected QT interval (QTc) of more than 0.44 second 1/2 were identified who had permanent pacemakers implanted for management of recurrent syncope or aborted cardiac arrest. METHODS AND RESULTS: Pacemakers were implanted on average 7 years after the onset of the first syncopal episode. Most of the patients were female (87%), the average age at implantation was 19 +/- 13 years, the mean QTc was 0.55 +/- 0.08 second, and 57% were receiving antiadrenergic treatment for LQTS when the pacemaker was placed. Using birth as the time origin, the median cardiac event rate was significantly (p less than 0.001) reduced by pacing from 0.5 to 0 events per patient per year, with 21 patients experiencing no cardiac events during an average pacemaker follow-up of 49 months per patient. In 10 patients in whom the demand atrial pacing rate was faster than the intrinsic sinus rate, the average heart rate was increased 23 beats/min (from 58 to 81 beats/min) with pacing with reduction in the QT interval from 0.59 seconds to 0.46 seconds. CONCLUSIONS: The beneficial effects of pacing in high-risk LQTS patients probably relate to the prevention of bradycardia, pauses, and the shortening of long QT intervals--factors that are known to be arrhythmogenic in this syndrome. Permanent cardiac pacing reduces the rate of recurrent syncopal events in high-risk LQTS patients, but it does not provide complete protection.

Adult↗