摘要:

Background To examine prospectively the association between self-reported symptoms of phobic anxiety and subsequent risk of coronary heart disease, a 2-year follow-up study was conducted of a cohort of 33 999 US male health professionals, aged 42 to 77 years in 1988, who were free of diagnosed cardiovascular disease at baseline. Levels of phobic anxiety were assessed using the Crown-Crisp index, a short, diagnostic self-rating scale used for common phobias. Main outcomes were incidents of coronary heart disease consisting of nonfatal myocardial infarction (MI) and fatal coronary heart disease (CHD).Methods and Results One hundred sixty-eight incident cases of CHD occurred during 2 years of follow-up (128 cases of nonfatal MI and 40 cases of fatal CHD). The age-adjusted relative risk of fatal CHD among men with highest levels of phobic anxiety (scoring 4 or higher on the Crown-Crisp index) was 3.01 (95% confidence interval, 1.31 to 6.90) compared with men with the lowest levels of anxiety (scoring 0 or 1 on the phobia index). Risk of fatal CHD increased with levels of phobic anxiety (P trend=.002). When fatal CHD was further categorized into sudden and nonsudden coronary death, the excess risk was confined to sudden death (relative risk among men scoring 3 or higher on the phobia index was 6.08; 95% confidence interval, 2.35 to 15.73). No association was found between phobic anxiety and risk of nonfatal MI. These findings remained essentially unchanged after adjusting for a broad range of cardiovascular risk factors.Conclusions The specificity, strength, and dose-response gradient of the association, together with the consistency and biological plausibility of the experimental and epidemiologic evidence, support a strong causal association between phobic anxiety and fatal CHD. (Circulation. 1994;89:1992-1997.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background An impaired coronary flow reserve in syndrome X has been demonstrated by many studies.Recently, however, a normal coronary flow reserve in response to papaverine was reported, but the number of patients in these studies was small. The aim of this study was to investigate whether coronary flow reserve in response to intracoronary papaverine is really impaired in syndrome X.Methods and Results We investigated 53 syndrome X patients (typical angina, a positive exercise test, and completely normal coronary arteries on angiography) and 26 heart transplant patients with normal coronary arteries (control group).All antianginal medications were stopped 48 hours before the study. A 3.6F intracoronary Doppler catheter was positioned in the proximal left anterior descending coronary artery and was connected to a Millar velocimeter. The coronary blood flow velocity at rest and in response to a hyperemic dose of papaverine was measured. Coronary flow reserve was defined as the ratio of hyperemic coronary blood flow velocity in response to papaverine and resting coronary blood flow velocity. The coronary flow reserve (mean+-SD) in the syndrome X group was 2.72+-1.39. The coronary flow reserve in the control group was significantly higher at 5.22+-1.26 (P<.01). In both groups there was no significant difference in the heart rate or the mean arterial pressure during the study.Conclusions Our study shows that coronary flow reserve in response to intracoronary papaverine is impaired in syndrome X patients.(Circulation. 1994;89:1998-2004.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Practitioners often assume a close relation between angiographic coronary artery stenosis and patient functional capacity.To test this unproven hypothesis, we analyzed the relation between coronary artery stenosis measured by different methods and maximal treadmill exercise tolerance in patients with single-vessel disease before and after intervention by percutaneous transluminal coronary angioplasty (PTCA).=90% at baseline was associated with shorter exercise duration (7.9 versus 9.2 minutes, P<.04). Similar segregation at baseline was not observed with caliper or computer methods. Regardless of the method of measurement used, correlation between changes of lesion severity and exercise duration from baseline to follow-up was poor. Patients were angiographically classified as "better," "unchanged," or "worse" if follow-up stenosis was below, within, or above 2 SD of mean technical variability from baseline (+-18.8%, caliper; +-14.6%, computer). Exercise duration for PTCA patients improved among those with better lesions (+2.4 minutes, n=50, P=.001) but also among those with unchanged lesions (+1.9 minutes, n=41, P<=.001). Unchanged medically treated patients improved less (+0.5 minutes, n=86, P=.04). Results were similar when patients were angiographically classified by minimum lumen diameter.Conclusions Handheld calipers and quantitative coronary angiography are equivalent techniques for making anatomic measurements.Neither method identified patients having reduced exercise capacity at baseline as well as visual estimation. The relation between changes of coronary stenosis and exercise duration is highly variable, at least in part because of the insensitivity of angiographic methods for detecting small but potentially important changes. Minimal anatomic improvement 6 months after PTCA does not preclude a good functional outcome. Contrary to common belief, angiographic stenosis does not correlate well with functional capacity, even in patients with single-vessel disease. (Circulation. 1994;89:2005-2014.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Survival after coronary artery bypass graft surgery (CABG) and medical therapy in patients with coronary artery disease (CAD) has been studied in both randomized trials and observational treatment comparisons.Over the past decade, the use of coronary angioplasty (PTCA) has increased dramatically, without guidance from either randomized trials or prospective observational comparisons. The purpose of this study was to describe the survival experience of a large prospective cohort of CAD patients treated with medicine, PTCA, or CABG.=75%) left main disease were excluded. Baseline clinical, laboratory, and catheterization data were collected prospectively in the Duke Cardiovascular Disease Databank. All patients were contacted at 6 months, 1 year, and annually thereafter (follow-up 97% complete). Cardiovascular death was the primary end point. Of this cohort, 2788 patients were treated with PTCA (2626 within 60 days) and 3422 with CABG (3080 within 60 days). Repeat or crossover revascularization procedures were counted as part of the initial treatment strategy. Kaplan-Meier survival curves (both unadjusted and adjusted for all known imbalances in baseline prognostic factors) were used to examine absolute survival differences, and treatment pair hazard ratios from the Cox model were used to summarize average relative survival benefits. For the latter, a 13-level CAD prognostic index was used to examine the relation between survival and revascularization as a function of CAD severity. The effects of revascularization on survival depended on the extent of CAD. For the least severe forms of CAD (ie, one-vessel disease), there were no survival advantages out to 5 years for revascularization over medical therapy. For intermediate levels of CAD (ie, two-vessel disease), revascularization was associated with higher survival rates than medical therapy. For less severe forms of two-vessel disease, PTCA had a small advantage over CABG, whereas for the most severe form of two-vessel disease (with a critical lesion of the proximal left anterior descending artery), CABG was superior. For the most severe forms of CAD (ie, three-vessel disease), CABG provided a consistent survival advantage over medicine. PTCA appeared prognostically equivalent to medicine in these patients, but the number of PTCA patients in this subgroup was low.Conclusions In this first large-scale, prospective observational treatment comparison of PTCA, CABG, and medicine, we confirmed the previously reported survival advantages for CABG over medical therapy for three-vessel disease and severe two-vessel disease. For less severe CAD, the primary treatment choices are between medicine and PTCA. In these patients, there is a trend for a relative survival advantage with PTCA, although absolute survival differences were modest. In this setting, treatment decisions should be based not only on survival differences but also on symptom relief, quality of life outcomes, and patient preferences. (Circulation. 1994;89:2015-2025.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background The endothelium synthesizes and releases a relaxing factor with the physiochemical properties of nitric oxide (NO).However, the role of endothelium-derived NO in the basal regulation of systemic and pulmonary vascular resistance in humans is not known. Our primary objectives were to determine the effects of inhibiting NO synthesis on blood pressure and systemic vascular resistance and to establish the role of endothelium-derived NO in the regulation of normoxic pulmonary vascular tone.Methods and Results We studied the systemic and pulmonary hemodynamic effects of NG-monomethyl-l-arginine (L-NMMA, 0.03 to 1.0 mg x kg-1x min-1IV), an NO synthase inhibitor, in 11 healthy volunteers, aged 33+-2 years. An arterial cannula and a pulmonary artery catheter were placed in each subject to measure blood pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure. Cardiac output was determined by the Fick technique, and systemic and pulmonary vascular resistances were calculated. Serum NO levels (free and protein bound) were measured by chemiluminescence in 5 subjects. Six of the subjects also received phenylephrine (25 to 100 micrograms/min IV) to compare the cardiac hemodynamic effects of L-NMMA with those of a direct-acting vasoconstrictor. L-NMMA caused dose-dependent increases in both blood pressure and systemic vascular resistance. At the highest dose of L-NMMA, there was a 15.5+-1.3% increase in mean blood pressure and a 63.4+-8.2% increase in systemic vascular resistance (each P<.01). Pulmonary vascular resistance increased 39.8+-9.4% (P<.01), whereas mean pulmonary artery pressure did not change. Administration of L-NMMA also reduced cardiac output by 27.8+-2.9% and stroke volume by 15.4+-3.5% (each P<.01). Serum NO levels decreased 65+-10% from basal values (P<.05), confirming inhibition of endogenous NO production. Phenylephrine increased blood pressure to a level comparable to that observed with L-NMMA. The decline in stroke volume was greater with L-NMMA than with phenylephrine (P<.01).Conclusions This study demonstrates that basal release of endothelium-derived NO is directly involved in the determination of systemic vascular resistance and, therefore, blood pressure in healthy humans. In addition, NO regulates basal normoxic pulmonary vascular tone. The complex hemodynamic effects of NO are composite properties of its actions on systemic and pulmonary vascular resistance and cardiac function. (Circulation. 1994;89:2035-2040.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Resting vascular tone is low in the normal pulmonary circulation, and experimental studies have suggested that this may be due to the continuous release of endothelium-derived nitric oxide (NO), a locally acting vasodilator. We have investigated whether NO contributes to the normal control of pulmonary vascular tone and resistance in children.Methods and Results We studied the hemodynamic effects of NG-monomethyl-l-arginine (L-NMMA), a specific inhibitor of NO synthesis, on the pulmonary circulation of six children 2 to 17 years old (mean, 9 years) with congenital heart disease but normal pulmonary blood flow, pressure, and resistance (all had isolated left heart obstructive lesions). The diameter of a segmental pulmonary artery and pulmonary blood flow velocity were measured by quantitative angiography and intra- arterial Doppler catheters. There was a consistent, dose-dependent fall in pulmonary blood flow velocity in response to three increasing doses of L-NMMA (compared with baseline, flow velocity fell to 75+-7%, 62+-8%, and 40+-10%, P<.01). Flow velocity returned to control values with subsequent infusion of l-arginine, the substrate for NO. Thereafter, acetylcholine, an endothelium-dependent dilator, produced an increase in flow velocity (56+-10% greater than baseline, P<.01). Arterial diameter was unchanged during L-NMMA and l-arginine infusions, indicating that the major effect of each agent is to alter vascular tone distal to the segmental pulmonary arteries.Conclusions The dilator action of endothelium-derived NO contributes to the maintenance of low resting pulmonary tone in normal children. Impairment of NO production may contribute to the elevated pulmonary vascular resistance that complicates some cases of congenital heart disease. (Circulation. 1994;89:2041-2044.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Noninvasive cardiac-specific analysis of contractile function in patients with dilated heart failure remains problematic. This study tests whether maximal power divided by the square of end-diastolic volume (PWRmx/EDV2, or preload-adjusted PWRmx) can provide such assessment.Methods and Results To validate the load insensitivity of the PWRmxindex and determine its response to contractile change, 24 subjects with chronic dilated cardiomyopathy underwent invasive pressure-volume catheterization study using the conductance catheter technique. Preload was transiently reduced by 30% using balloon occlusion of the inferior vena cava, and afterload impedance was lowered by 50%, induced by a bolus injection of nitroglycerin. Contractile state was varied by intravenous dobutamine, verapamil, or esmolol. PWRmxwas calculated from the simultaneous product of ventricular pressure and rate of volume change (dV/dt), the latter derived from the volume catheter signal. PWRmxvaried directly with preload but was minimally influenced by afterload. However, PWRmx/EDV2was not significantly altered by either loading change. PWRmx/EDV2did vary with contractility, correlating closely with changes in the end-systolic pressure-volume relation (r=.91, P<.001). To test the noninvasive application of this index, 12 additional patients were studied, with PWRmx/EDV2derived from nuclear ventriculography combined with a novel method to measure central arterial pressures. Subjects received intravenous nitroprusside or dobutamine in random order. Ejection fraction increased similarly with both agents (+42.9+-8.9% for dobutamine and +29.4+-5.3% for nitroprusside, both P<.01). In contrast, PWRmx/EDV2did not significantly change with nitroprusside but increased by 126+-16.1% with dobutamine (P<.01).Conclusions Preload-adjusted PWRmxis a steady-state index of ventricular systolic function that is sensitive to inotropic state and minimally influenced by physiological changes in afterload impedance or volume load. It appears useful for noninvasive cardiac-specific analysis of acute drug effects. (Circulation. 1994;89:2045-2053.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background The clinical relevance of myocardial cell damage in dilated cardiomyopathy is uncertain.Myocardial uptake of Indium-111 monoclonal antimyosin antibodies (MAA) was used to study myocardial damage in patients with idiopathic (IDC) and alcoholic (ADC) dilated cardiomyopathy and to assess its prognostic implications.1.87 were associated with increased risk of death or transplantation.Conclusions In patients with IDC, variations of MAA uptake are detected in patients who present acutely but not in those with chronic stable disease.In patients with ADC, MAA uptake mainly depends on alcohol consumption. In both situations, reduction of uptake correlates with improvement of ventricular function. Higher intensities of MAA uptake are associated with a worse outcome. The intensity of antibody uptake, along with other clinical and functional variables, may be helpful in risk stratification of patients with dilated cardiomyopathy. (Circulation. 1994;89:2054-2061.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Right ventricular function may be an important determinant of exercise capacity, peak oxygen consumption (Vo2), and the ventilatory response to carbon dioxide production (Ve/Vco2relation) in patients with chronic heart failure (CHF).Methods and Results We studied the role of right ventricular function in CHF and also investigated the effects of absent right ventricular reserve in patients previously operated on with Fontan's procedure by measuring metabolic gas exchange during exercise in five groups of patients:(1) 10 patients who had previously undergone Fontan's procedure for congenital heart disease in whom the right ventricle is not functional; (2) 11 age-matched control subjects with dilated cardiomyopathy (DCM); (3) 15 age-matched normal subjects; (4) 42 patients with CHF; and (5) 16 age-matched control subjects. Left and right ventricular ejection fractions (LVEF and RVEF) were measured by radionuclide ventriculography in group 4. In the young subjects, the Ve/Vco2slope was lower in the control subjects than in the other two groups, being 24.4+-4.3 against 33.3+-6.6 in group 1 (P<.001) and 29.6+-8.1 in group 2 (P<.05). The correlation between peak Vo2and Ve/Vco2was -0.80 (P=.005) in group 1 and -0.76 (P=.007) in group 2. In the older age groups, the Ve/Vco2slope was significantly greater (38.0+-14.9 versus 25.4+-3.7; P<.001) in the heart failure group (group 4). In neither control group was there a significant relation between peak Vo2and Ve/Vco2slope. In group 4, the relation between peak Vo2and Ve/Vco2was similar to that seen for groups 1 and 2. LVEF was 24.3+-14.1%, and RVEF was 32.5+-13.1%. There was no correlation between either RVEF or LVEF and peak Vo2or Ve/Vco2slope in the heart failure group.Conclusions The relation between excessive ventilation and reduction in peak oxygen consumption is present in patients with no functioning right ventricle.RVEF is not a determining feature of either exercise capacity or the excessive ventilatory response in CHF. (Circulation. 1994;89:2062-2069.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID