ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundTranscatheter occlusion with Gianturco coils has been attempted in a small number of patients with tiny (≤1.5-mm diameter) patent ductus arteriosus, and preliminary results have been encouraging. The present study extends this method to larger ductus sizes and makes recommendations for proper coil size selection.Methods and ResultsCoil occlusion was attempted in 24 consecutive patients with patent ductus arteriosus who did not require other cardiac surgery. Median patient age was 4.2 years (8 months to 30 years), and mean ductus diameter was 1.7±0.8 mm. Two instances of coil embolization occurred in the first 4 patients, with successful coil retrieval. Based on this experience, we proposed that the coil helical diameter should be twice or more the minimum ductus diameter, with coil length sufficient for three or more loops. With these recommendations, coils were successfully implanted in the subsequent 20 consecutive patients. Of the 22 patients with successful coil implantation, 15 (68%) had no residual shunting, and 7 had trace residual shunting by angiography. The continuous murmur was abolished in all 22 patients. No significant complications occurred, and all patients were discharged within 24 hours of successful coil implantation. No change in the systolic pressure gradient between main and left pulmonary artery or ascending and descending aorta was observed.ConclusionsTranscatheter occlusion of patent ductus arteriosus can be safely and effectively achieved in patients with ductus diameters up to 3.3 mm. Coil occlusion does not cause obstruction to flow in the left pulmonary artery or descending aorta. Coils should be selected to provide a helical diameter twice or more the minimum ductus diameter and a length sufficient for three or more loops.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundThe aim of this study was to investigate the association of lipoprotein fractions with the future risk of coronary heart disease (CHD) in patients with non-insulin-dependent diabetes (NIDDM).Methods and ResultsAt baseline, lipoprotein fractions were determined in 313 diabetic patients with NIDDM (153 men and 160 women), and these patients were followed up for 7 years with respect to CHD events (CHD death or all CHD events including CHD death or nonfatal myocardial infarction). Altogether, 56 NIDDM patients (28 men and 28 women) died from CHD and 25 had a nonfatal myocardial infarction (17 men and 8 women) during the follow-up. NIDDM patients having these CHD events during the follow-up had higher levels of total and very-low-density lipoprotein (VLDL) triglycerides and VLDL cholesterol and lower levels of high-density lipoprotein (HDL) and HDL2cholesterol than those without CHD events. The risk for CHD death was fourfold and for all CHD events, twofold higher among diabetics with low HDL cholesterol (<0.9 mmol/L) than among diabetics with HDL cholesterol ≤0.9 mmol/L. High triglyceride level (>2.3 mmol/L) was associated with a twofold increase in the risk of CHD events. In multiple logistic regression analyses, HDL was inversely associated with CHD events and VLDL triglycerides with CHD events in NIDDM patients with low HDL cholesterol level (≤1.12 mmol/L).ConclusionsOur 7-year follow-up study gives evidence that low HDL and HDL2cholesterol, high VLDL cholesterol, and high total and VLDL triglycerides are powerful risk indicators for CHD events in patients with NIDDM.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundObesity in adults is associated with increased left ventricular (LV) mass. The mechanism for this is unclear, however. We tested the hypothesis that insulin resistance is an important independent contributing factor to LV mass in the healthy obese population.Methods and ResultsThe study population consisted of 40 normotensive, nondiabetic, otherwise healthy obese subjects with body mass index (BMI) >25 kg/m2. LV mass was echocardiographically determined according to the Penn convention, using the formula of Devereux and Reichek. Insulin resistance was assessed using indices derived from Intravenous Glucose Tolerance Test (IVGTT): insulin level at baseline, insulin level at 90 minutes of IVGTT (insulin-90), insulin integration over 90 minutes of IVGTT, and rate of glucose disposal (kvalue). Insulin-90 (r=.61,P=.0001),kvalue (r=.55,P=.003), insulin integration over 90 minutes (r=.46,P=.003), basal insulin (r=.44,P=.005), and BMI (r=.59,P=.0001) were all strongly correlated with LV mass by univariate analysis. No significant correlation was found with blood pressure or age. In multivariate regression analysis, only insulin-90 andkvalue correlated significantly with LV mass (P=.03,P=.02, respectively), accounting for 50% of the variance of LV mass, whereas the association with BMI became insignificant (P=.2).ConclusionsLV mass in the normotensive nondiabetic obese population is strongly associated with, and may be mediated by, the degree of insulin resistance and its associated hyperinsulinemia, independent of BMI and blood pressure.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundAn inverse association between height and risk of coronary heart disease (CHD) has been reported in several case-control and cohort studies, but the reasons for the association remain uncertain. We evaluated this association among 22071 male physicians, a population homogeneous for high educational attainment and socioeconomic status in adulthood.Methods and ResultsThe study population was comprised of participants in the Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of low-dose aspirin and β-carotene in the primary prevention of cardiovascular disease and cancer among US male physicians, aged 40 to 84 years, in 1982. Participants were classified into five height categories at study entry, from shortest to tallest, and were followed an average of 60.2 months to determine the incidence of myocardial infarction (MI), stroke, and death from cardiovascular disease. Men in the tallest (≥73 in. or 185.4 cm) compared with the shortest (≤67 in. or 170.2 cm) height category had a 35% lower risk of MI (relative risk, 0.65; 95% confidence interval, 0.44 to 0.99;P=.04), after adjusting for known cardiovascular risk factors. Further, a marginally significant inverse trend (Ptrend=.05) across the height categories was observed. Although the relationship was not strictly linear, for every inch of added height, there was an approximate 2% to 3% decline in risk of MI. In contrast, men in the tallest compared with the shortest height category had only small and nonsignificant decreases in risk of stroke and cardiovascular death. While no significant trend in risks of these end points across the height categories was observed, the numbers of events for these end points were far less than for MI, and thus the confidence intervals were wide.ConclusionsThese data indicate that height is inversely associated with subsequent risk of MI. At this time, a few mechanisms are plausible, but none are convincing. Other epidemiological and basic research efforts are needed to explore a variety of physiological correlates of height that may be responsible for mediating the height-MI association. In the meantime, while height is not modifiable, it is easy to measure and may be useful to evaluate CHD disease risk profiles and target lifestyle interventions.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Conventional risk factors (especially high arterial pressure, elevated cholesterol and glucose levels, and cigarette smoking) are useful predictors of morbid atherosclerotic and hypertensive events, and their control variably reduces the incidence of events. However, both the ability to predict risk and the ability to reduce it by modification of established risk factors are limited. These limitations occur in part because the progression from risk factor exposure to morbid events depends on the variable likelihood that individuals exposed to the same risk factors will progress through two stages: the development of asymptomatic or “preclinical” anatomic and functional cardiovascular disease in response to standard risk factors and other variables, and the precipitation of morbid events by progression of preclinical disease or by the action of additional „triggering” mechanisms in the presence of preclinical disease. Advances in diagnostic methodology now make possible accurate noninvasive detection in many asymptomatic individuals of preclinical disease such as left ventricular hypertrophy, carotid atherosclerosis, and renal dysfunction. Progress in elucidating stimuli to left ventricular hypertrophy and systemic atherosclerosis suggests that focusing research separately on these two stages of disease evolution is a fruitful strategy. The closer relation of measures of preclinical disease than risk factors with the subsequent risk of complications indicates that their detection improves clinical risk stratification. However, critical testing of whether clinical outcome is improved or treatment cost is lowered by basing antihypertensive or antihyperlipidemic treatment decisions in part on the presence of preclinical cardiovascular disease is needed before this strategy is adopted on a widespread scale.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundIt has been well established that arterial stiffness, manifest as an increase in arterial pulse wave velocity or late systolic amplification of the carotid artery pressure pulse, increases with age. However, the populations studied in prior investigations were not rigorously screened to exclude clinical hypertension, occult coronary disease, or diabetes. Furthermore, it is unknown whether exercise capacity or chronic physical endurance training affects the age-associated increase in arterial stiffness.Methods and ResultsCarotid arterial pressure pulse augmentation index (AGI), using applanation tonometry, and aortic pulse wave velocity (APWV) were measured in 146 male and female volunteers 21 to 96 years old from the Baltimore Longitudinal Study of Aging, who were rigorously screened to exclude clinical and occult cardiovascular disease. Aerobic capacity was determined in all individuals by measurement of maximal oxygen consumption ($Vo2max) during treadmill exercise. In this healthy, largely sedentary cohort, the arterial stiffness indexes AGI and APWV increased approximately fivefold and twofold, respectively, across the age span in both men and women, despite only a 14% increase in systolic blood pressure (SBP). These age-associated increases in AGI and APWV were of a similar magnitude to those in prior studies of less rigorously screened populations. Both AGI and APWV varied inversely with $Vo2max, and this relationship, at least for AGI, was independent of age. In endurance trained male athletes, 54 to 75 years old ($Vo2max=44±3 mL · kg-1· min-1), the arterial stiffness indexes were significantly reduced relative to their sedentary age peers (AGI, 36% lower, APWV, 26% lower) despite similar blood pressures.ConclusionsEven in normotensive, rigorously screened volunteers in whom SBP increased an average of only 14% between ages 20 and 90 years., major age-associated increases of arterial stiffness occur. Higher physical conditioning status, indexed by $Vo2max, was associated with reduced arterial stiffness, both within this predominantly sedentary population and in endurance trained older men relative to their less active age peers. These findings suggest that interventions to improve aerobic capacity may mitigate the stiffening ofthe arterial tree that accompanies normative aging. (Ciclation. 1993;88[part 11:1456-1462.)

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundTo determine whether or not a moderate genetic defect of homocysteine metabolism is associated with the development of coronary artery disease, we studied the prevalence of thermolabile methylenetetrahydrofolate reductase, which is probably the most common genetic defect of homocysteine metabolism.Methods and ResultsThree hundred thirty-nine subjects who underwent coronary angiography were classified into three groups: (1) patients with severe coronary artery stenosis (≥70% occlusion in one or more coronary arteries or ≥50% occlusion in the left main coronary artery), (2) patients with mild to moderate coronary artery stenosis (<70% occlusion in one or more coronary arteries or <50% occlusion in the left main coronary artery), and (3) patients with non-coronary heart disease or noncardiac chest pain (nonstenotic coronary arteries). The thermolability of methylenetetrahydrofolate reductase was prospectively determined in all subjects. Plasma homocyst(e)ine levels were then measured in those with thermolabile methylenetetrahydrofolate reductase. The traditional risk factors for coronary artery disease were thereafter ascertained by chart review of all subjects. The prevalence of thermolabile methylenetetrahydrofolate reductase was 18.1% in group 1, 13.4% in group 2, and 7.9% in group 3. There was a significant difference between the prevalence of thermolabile methylenetetrahydrofolate reductase in groups 1 and 3 (P<.04). All individuals with thermolabile methylenetetrahydrofolate reductase irrespective of their clinical grouping had higher plasma homocyst(e)ine levels than normal (group 1, 14.86±5.85; group 2, 15.36±5.70; group 3, 13.39±3.80; normal, 8.50±2.8 nmol/mL). Nonetheless, there was no statistically significant difference in the plasma homocyst(e)ine concentrations of these patients with or without coronary artery stenosis. Using discriminant function analysis, thermolabile methylenetetrahydrofolate reductase was predictive of angiographically proven coronary artery stenosis. The traditional risk factors - age, sex, diabetes, smoking, hypercholesterolemia, and hypertension - were not significantly associated with the presence of thermolabile methylenetetrahydrofolate reductase.Conclsions. Thermolabile methylenetetrahydrofolate reductase is a risk factor for coronary artery disease and is unrelated to other risk factors.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundPrior studies based on autopsy data suggest that infarction of more than 40% of the left ventricle necessitates cardiogenic shock and death.Methods and ResultsTechnetium-99m Sestamibi tomography was used prospectively to measure infarct size at discharge in 166 patients with acute myocardial infarction. Patients with previous myocardial infarction or revascularization were excluded from the trial. Sixteen patients were identified with final infarct sizes >40% of the left ventricle despite acute reperfusion therapy. These 16 patients (13 men) had a mean age of 63±10 years; 44% had a previous history of angina. Ten patients had emergent coronary angioplasty only (mean time to percutaneous transluminal coronary angioplasty [PTCA], 6.0±3.0 hours); 6 had thrombolysis (mean time to tissue plasminogen activator, 4.0±1.5 hours), of which 2 had rescue PTCA (5 and 3 hours from onset of pain). Of 15 patients who had angiograms after therapy, 15 had open infarct-related arteries. The left anterior descending artery was the infarct-related artery in 14 (9 proximal and 5 distal lesions). Half the patients had only single-vessel disease. Infarct size measured 50±7% of the left ventricle (range, 42% to 68%). Ejection fraction by radionuclide angiogram was 0.33±0.09 and 0.38±0.07 at discharge and 6 weeks, respectively. Hospital complications included shock (1 patient), pulmonary edema (2), angina (3), symptomatic nonsustained ventricular tachycardia (1), transient complete heart block (2), and transient bifascicular block (1). At follow-up (13±9 months), the patient with shock had died, but the remaining 15 patients were asymptomatic (1 had late PTCA for angina).ConclusionsIn the interventional and thrombolytic era, patients with large residual myocardial infarctions can survive without heart failure.

ISSN:0009-7322    

出版商:OVID    

年代:1993

数据来源: OVID