下载免费PDF全文 Design—Retrospective and prospective examination of the jugular venous pulse recording, flow in the superior vena cava, and Doppler echocardiographic studies.
Setting—A tertiary referral centre for both cardiac and pulmonary disease, with facilities for invasive and noninvasive investigation, and assessment for heart and heart-lung transplantation.
Patients—12 patients with primary pulmonary hypertension, most being considered for heart-lung transplantation.
Results—Two distinct patterns of venous pulse and superior vena caval flow were identified: a dominant `a' wave with no `v' wave, an absent or poorly developed `y' descent, and exclusively systolic downward flow in the superior vena cava (group 1, n = 8), and a dominant `v' wave, deep `y' descent and exclusively diastolic downward flow in the superior vena cava (group 2, n = 4). A comparison between the two groups showed age (mean (SD)) 42 (18) ν 36 (7) years, RR interval 700 (65) ν 740 (240) ms, left ventricular end diastolic dimension 3·6 (0·8) ν 3·2 (1·0) cm and end systolic dimension 2·1 (0·5) ν 2·3 (0·3) cm, right ventricular end diastolic dimension 2·6 (0·5) ν 2·8 (0·6) cm, and pressure drop between right ventricle and right atrium 60 (8) ν 70 (34) mm Hg to be similar. Duration of tricuspid regurgitation 520 (30) ν 420 (130) ms and the time interval of pulmonary closure to the end of the tricuspid regurgitant signal 140 (30) ν 110 (40) ms were longer in group 1 compared with group 2, whereas right ventricular filling time was much shorter 180 (70) ν 350 (130) ms. In seven patients from group 1, a single peak of forward tricuspid flow was present, but this pattern was seen in only one patient from group 2.
Conclusions—In patients with primary pulmonary hypertension, the apparent `a' wave seen in the venous pulse is, in fact, a summation wave. It is probably the result of large pressure changes that must underlie rapid acceleration and deceleration of blood across the tricuspid valve when the right ventricular filling time is short.
相似文献 下载免费PDF全文 Design—A treadmill exercise test and 24 hour ambulatory electrocardiographic monitoring were carried out after a period of five days off treatment (control) and at the end of three weeks of each treatment period.
Patients—23 patients with stable angina pectoris, documented coronary artery disease, and a positive exercise test were randomised in a double blind, three way, cross over study.
Results—Compared with the control, nifedipine significantly induced an increase in resting heart rate of (mean (SEM)) 14 (2) beats/min whereas atenolol and the combination significantly reduced it by 24 (2) and 20 (1) beats/min respectively. The number of exercise tests rendered negative after each intervention was five for nifedipine, nine for atenolol, and 11 for the combination. Compared with the control the time to the start of myocardial ischaemia (1 mm ST segment depression) during exercise significantly increased by 3·2 (0·6) min after nifedipine, by 4·6 (0·4) min after atenolol, and by 4·6 (0·5) min after the combination; rate-pressure product (beats/min. mm Hg) at 1 mm ST segment depression increased by 2824 (970) after nifedipine but fell by 4436 (900) and 4501 (719) after atenolol and the combination. The weekly frequency of angina was reduced from a mean of five while taking nifedipine, to three while taking atenolol, and to two while taking the combination. The total ischaemic time during ambulatory monitoring was significantly reduced from 69 (17) min during control to 37·5 (9·8) min during nifedipine, to 15·6 (5·5) min during atenolol, and to 6·5 (2·7) min during the combination.
Conclusion—The undesirable effect of a high basal heart rate induced by nifedipine was neutralised by its combination with atenolol. Whereas atenolol and the combination were equally efficacious in controlling exercise induced ischaemia, the combination was more effective in reducing total ischaemic burden.
相似文献Design—Between group comparison of patients with unstable angina, stable angina, and healthy controls.
Setting—The coronary care unit and cardiac investigation ward of a regional cardiology centre.
Patients—Twenty five consecutive patients admitted to the coronary care unit with unstable angina. Twenty five consecutive patients admitted to the cardiac investigation ward (patients with stable angina undergoing coronary angiography) were used as control for the presence of [ill], drug treatment, and smoking habit. Thirty eight healthy controls (hospital staff and patients admitted for minor surgical procedures who were otherwise healthy) were also studied.
Main outcome
measures—Thiobarbituric acid related substances (TBARS) in plasma and plasma reduced thiol (PSH) as indicators of oxidative damage to lipids and proteins respectively were measured. Coronary angiography was performed in all patients with stable angina and roughly half of those with unstable angina.
Results—Mean (SEM) plasma TBARS in unstable angina and stable angina were 9·95 (0·36) nmol/ml and 9·14 (0·28) nmol/ml respectively (p = 0·08). Mean plasma TBARS in healthy controls were 8·09 (0·21) nmol/ml (p < 0·05 compared with both angina groups). Mean (SEM) PSH concentration in unstable angina was 4·21 (9) nmol/ml and in stable angina was 4·85 (9) nmol/ml (p < 0·05). Mean PSH in healthy controls was 5·64 (8) nmol/ml (p < 0·001 compared with both angina groups). The extent of coronary artery disease, use of medication, and smoking habit were not significantly different between the angina groups.
Conclusions—Biochemical indicators of oxidative stress are more abnormal in unstable than stable angina. This is in keeping with experimental evidence that episodes of ischaemia and reperfusion lead to generation of free radicals and toxic oxygen species and depression of endogenous antioxidant activity. The clinical significance of this finding remains to be determined, although, experimentally, free radicals and toxic oxygen species have adverse effects on myocardial contractile function, myocardial electrical stability, endothelial mediated vasodilatation, and coagulation.
相似文献 下载免费PDF全文 Patients—50 consecutive patients recovering from myocardial infarction. Six patients were excluded because of unsatisfactory recordings or baseline electrocardiographic abnormalities that influenced the diagnostic accuracy of ST segment depression. In 38 patients important ST segment changes were seen before the study recordings.
Main outcome measure—Reproducibility of detecting the electrocardiographic ST segment changes with 12 bipolar leads alone or in combination.
Results—The highest reproducibility rate was found in infarcts involving both the anterior and inferior left ventricular walls (80%). The reproducibility decreased as the extent of ventricular wall involvement decreased and was lowest in inferior infarcts (31%) (p < 0·001). For large infarcts the detection rate was almost equal for the 12 study leads, whereas disparity between leads increased as the infarct size decreased. The highest overall reproducibility was found in a transthoracic lead (V2, V9R) (76%). This lead was significantly better (p = 0·03) than lead CM5 (50%). When the transthoracic lead was combined with an inferior lead, the reproducibility increased (82%) and was significantly better than the combination of CM5 and an inferior lead (58%) (p = 0·02).
Conclusions—Extensive ischaemic electrocardiographic changes are better detected than smaller ones and anterior infarcts better than inferior. A transthoracic lead (V2, V9R) was significantly better than CM5 both alone and when CM5 and the transthoracic lead were combined with an inferior lead.
相似文献 下载免费PDF全文 Design—Prospective study. Immunoturbidimetrically determined myoglobin concentrations were compared with radioimmunoassay results obtained with the same blood samples. The diagnostic performance of myoglobin determination was compared with creatine kinase and creatine kinase MB activity (current standard of routine diagnosis).
Settings—Part 1: coronary care unit. Part 2: emergency room in a university hospital.
Patients—Part 1: 30 patients with acute myocardial infarction admitted not later than four hours (median two hours) after the onset of symptoms. Part 2: 126 patients admitted to the emergency room with chest pain not caused by trauma (51 cases of acute myocardial infarction, 51 cases of angina pectoris, and 24 cases of chest pain not related to coronary artery disease).
Interventions—Part 1: routine treatment including intravenous thrombolytic treatment (28 patients). Part 2: routine emergency treatment without thrombolytic treatment.
Main outcome measures—The analytical quality of the immunoturbidimetric myoglobin assay and a comparison between the myoglobin assay and creatine kinase and creatine kinase MB for diagnostic sensitivity and performance.
Results—The immunoturbidimetric myoglobin assay was fast and convenient and gave myoglobin determinations of high analytical quality. The concentration of myoglobin increased, peaked, and returned to the reference range significantly earlier than creatine kinase (p≤ 0·0001) and creatine kinase MB (p≤ 0·0002). Before thrombolytic therapy was started the diagnostic sensitivity of myoglobin was significantly higher than that of creatine kinase MB activity 0–6 h after the onset of chest pain and significantly higher (0·82 ν 0·29) than creatine kinase 2–4 h after the onset of chest pain. In almost all patients (92%) plasma myoglobin concentrations were increased 4–6 h after the onset of chest pain.
Conclusion—Myoglobin was more sensitive in detecting early myocardial infarction than creatine kinase and creatine kinase MB activity. Immunoturbidimetric myoglobin measurements could be useful in the early evaluation of patients with suspected myocardial infarction because this assay takes less than two minutes.
相似文献 下载免费PDF全文 Design—A retrospective and prospective analysis of echocardiographic and Doppler studies.
Setting—A tertiary referral centre for both cardiac and pulmonary disease.
Patients—29 patients with pulmonary hypertension (12 primary pulmonary hypertension, 10 pulmonary fibrosis, five atrial septal defect (ASD), and two scleroderma) were compared with a control group of 10 patients with an enlarged right ventricle but normal pulmonary artery pressure (six ASD, one after ASD closure, one ASD and pulmonary valvotomy, one tricuspid valve endocarditis and repair, and one pulmonary fibrosis). None had clinical or echocardiographic evidence of intrinsic left ventricular disease.
Main Outcome measures—M mode echocardiographic measurements were made of septal thickness, and left and right ventricular internal cavity dimensions. Doppler derived right ventricular to right atrial pressure drop, and time intervals were measured, as were isovolumic relaxation time, and Doppler left ventricular filling characteristics.
Results—The peak right ventricular to right atrial pressure gradient was (mean (SD)) 60 (16) mm Hg in pulmonary hypertensive patients, and 18 (5) mm Hg in controls. The time intervals P2 to the end of the tricuspid regurgitation, and P2 to the start of tricuspid flow were both prolonged in patients with pulmonary hypertension compared with controls (115 (60) and 120 (40) ν 40 (15) and 45 (10) ms, p values <0·001). Pulmonary hypertensive patients commonly had a dominant A wave on the transmitral Doppler (23/29); however, all the controls had a dominant E wave. Isovolumic relaxation time of the left ventricle was prolonged in pulmonary hypertensive patients compared with controls, measured as both A2 to mitral valve opening (80 (25) ν 50 (15) ms) and as A2 to the start of mitral flow (105 (30) ν 60 (15) ms, p values <0·001). The delay from mitral valve opening to the start of transmitral flow was longer in patients with pulmonary hypertension (30 (15) ms) compared with controls (10 (10) ms, p < 0·001). At the time of mitral opening there was a right ventricular to right atrial gradient of 12 (10) mm Hg in pulmonary hypertensive patients, but this was negligible in controls (0·4 (0·3) mm Hg, p < 0·001).
Conclusions—Prolonged decline of right ventricular tension, the direct result of severe pulmonary hypertension, may appear as prolonged tricuspid regurgitation. It persists until after mitral valve opening on the left side of the heart, where events during isovolumic relaxation are disorganised, and subsequent filling is impaired. These effects are likely to be mediated through the interventricular septum, and this right-left ventricular asynchrony may represent a hitherto unrecognised mode of ventricular interaction.
相似文献 下载免费PDF全文 Setting—Coronary care unit, Royal Infirmary, Edinburgh.
Patients—105 patients with acute myocardial infarction (systolic blood pressure >90 mm Hg) were randomised within 24 hours of the start of pain. Unlike previous studies 88% of the patients received thrombolysis.
Methods—Double blind randomised placebo controlled study with either 12·5 mg of captopril three times daily or 20 mg of isosorbide mononitrate three times daily for 28 days.
Main outcome measures—Clinical outcome and left ventricular size and function assessed by echocardiography, radionuclide ventriculography, and magnetic resonance imaging.
Results—There was no difference in left ventricular size or function in either treatment group as measured one week after the end of the trial. Even the placebo group tended to decrease left ventricular diameter over the four week study period (one week: 5·0 (0·1) ν, five weeks: 4·8 (0·1) cm, NS). Four patients had an adverse clinical outcome in the placebo group whereas no adverse outcome was seen in the captopril group.
Conclusions—Vasodilator treatment may be of limited value or of no benefit for most infarct patients, particularly those treated with thrombolytic agents. Captopril, however, may benefit patients at high risk.
相似文献Methods—Two donor hearts meeting the requirements for heart transplantation and 11 diseased hearts were removed during a transplantation procedure and were studied in a horizontal 2·35 T superconducting magnet. Spectra were obtained at 0°C about 30 minutes after the excision. The areas of the inorganic phosphate peak (Pi) and of the phosphocreatine peak (PCr) were summed and expressed as a ratio with respect to the area of the β ATP peak.
Results—The ratio (Pi + Pcr)/β ATP was found to be significantly lower in five hearts with a myocardial infarct (0·77 (0·18)) than in hearts with dilated cardiomyopathy (1·25 (0·29)) and in normal hearts (1·69 (0·11)). The area of the phosphodiester peak was expressed as a ratio with respect to the area of the β ATP peak: no differences were found between the three groups.
Conclusions—These results suggest that the phosphocreatine concentration is lower in ischaemic heart disease than in dilated cardiomyopathy and that the phosphodiester peak is probably not useful in distinguishing between these two types of heart disease.
相似文献Design—Isovolumic and total relaxation times and left atrial and left ventricular dP/dt were identified from high fidelity (micromanometer) pressure recordings in the left ventricle and left atrium during percutaneous transluminal angioplasty of the left anterior descending coronary artery.
Patients—20 patients with isolated disease of the left anterior descending artery and normal left ventricular function.
Results—The isovolumic relaxation time lengthened during the first seven to nine seconds of ischaemia; then it shortened by an average of 15% up to the twentieth second, initially as a result of increased left atrial contractility and subsequently because of impaired ventricular relaxation. Ventricular ischaemia resulted in impaired left ventricular diastolic compliance, as shown by an increase in the total relaxation time, before there was evidence of systolic impairment. Minimum dP/dt decreased progressively (by −37% at the twentieth second of ischaemia), whereas maximum dP/dt fell only after 20 seconds of ischaemia (by −11%).
Conclusions—Relaxation and filling of the left ventricle (indices of diastolic function) are more sensitive to myocardial ischaemia than myocardial contractility and systolic function. Left atrial contractility increases during left ventricular ischaemia.
相似文献 下载免费PDF全文 Design—Prospective study. Coronary flow reserve was measured with an intracoronary Doppler flow probe in the proximal left anterior descending coronary artery in each patient. A dose of intracoronary papaverine producing maximal vasodilation was then administered.
Setting—A regional cardiothoracic centre and a supraregional transplant unit.
Patients—Seven patients with chest pain but normal coronary anatomy (controls), and 61 cardiac transplant patients between three months and 10 years after operation (median 4·5 years). Twenty one cardiac transplant patients had angiographic evidence of minor coronary occlusive disease (mean (SD) percentage stenosis diameter 23% (6%)) in a primary or secondary coronary vessel (group 1), with 12 of these in the left anterior descending coronary artery (stenosis diameter (mean (SD) 24% (8%)). The remaining 40 transplant patients had normal coronary angiograms (group 2).
Main outcome measure—Coronary flow reserve was defined as the ratio of the peak flow velocity after papaverine to the resting flow velocity.
Results—Group 1 patients had a noticeably impaired coronary flow reserve (2·6 (1·1)) compared with control patients (3·9 (0·4), p = 0·05) and, after adjusting for year after operation, compared with group 2 patients (3·8 (1·0), p < 0·001). No other variables were associated with a reduction in coronary flow reserve. Mean resting flow velocity was similar in all three groups (controls, 7·4 (4·6) cm/s; group 1, 7·5 (5·9) cm/s; and group 2, 7·3 (3·9) cm/s). Mean peak flow velocity response to papaverine was reduced in group 1 patients (18·1 (13·5) cm/s) relative to group 2 patients (27·5 (15·4) cm/s, p = 0·05) but not controls (28·4 (15·1) cm/s, p = 0·1).
Conclusions—Coronary flow reserve and the peak flow response to the coronary vascular smooth muscle relaxant papaverine are impaired in cardiac transplant patients with minor coronary occlusive disease. This disturbance of cardiac microvascular function may contribute to the late morbidity and mortality seen in cardiac transplant patients with coronary occlusive disease.
相似文献 下载免费PDF全文 Design—Retrospective and prospective study of 50 patients with dilated cardiomyopathy, by electrocardiography, echocardiography, and Doppler cardiography.
Setting—Tertiary cardiac referral centre.
Patients—50 patients (mean age (SD) 58 (16)) with dilated cardiomyopathy, all with functional mitral regurgitation.
Results—The values of QRS duration ranged widely, from 70 to 190 ms with a mean value of 110 ms, and were unimodally distributed. The overall duration of mitral regurgitation correlated positively with QRS time (r=0·65) over the entire range of values. When the duration of mitral regurgitation was divided into contraction, aortic ejection, and relaxation times, increased QRS duration prolonged contraction (r=0·51) and relaxation (r=0·52) times. Aortic ejection time was affected by RR interval (r=0·74). Duration of QRS correlated negatively with peak rate of rise in left ventricular pressure (+dP/dt) (r=−0·48), and positively with the time intervals from Q to peak pressure (r=0·49) and to peak +dP/dt (r=0·72), and also with those from the start of mitral regurgitation to peak pressure (r=0·49) and to peak +dP/dt (r=0·76). Duration of QRS did not directly affect the peak rate of left ventricular pressure fall (−dP/dt), or the isovolumic relaxation period.
Conclusions—Values of QRS duration are unimodally distributed in patients with dilated cardiomyopathy, without evidence of a discrete group of patients with left bundle branch block. Prolonged QRS duration reduces peak +dP/dt, prolongs overall duration of the pressure pulse, the time to peak +dP/dt, and relaxation time. Duration of QRS must therefore be taken into account in assessing standard measurements of myocardial function in patients with dilated cardiomyopathy.
相似文献 下载免费PDF全文 Design—The commonly used electrocardiographic related tests of autonomic function were studied. Two repeat measurements of all tests were made on all subjects on four separate days over a four week period.
Subjects—Ten normal subjects with no known autonomic dysfunction were investigated.
Main outcome measures—These were deep breathing (subject seated and supine), Valsalva manoeuvre, standing up from lying position, and normal relaxed breathing (subject supine). During the tests the electrocardiogram and respiratory pattern were recorded by computer. Beat to beat RR intervals were measured automatically from the electrocardiogram, and from these the results of the tests were calculated.
Results—Variance analysis showed significant between subject variability for all tests (p < 0·005), but some tests showed a much smaller relative within subject variability than others. Average repeatability data (within subject SD) for each test were calculated, and included deep breathing sitting (maxmin) RR (46 ms), Valsalva ratio (0·17), and lying to standing RR ratio (0·11). These compare with between subject SDs of 65 ms, 0·38, and 0·13 respectively, at mean values of 305 ms, 1·92, and 1·15 respectively. The data highlighted one subject with the poorest repeatability, whose electrocardiogram turned out on closer inspection to be under atrial rather than sinus control at times. Poor repeatability in the other subjects was related to variability in the respiratory pattern, and in the deep breathing test, repeat variability was significantly correlated (r = 0·79) with variability in the respiratory amplitude (p < 0·05).
Conclusions—Repeatability data should be available to each laboratory carrying out autonomic function tests. The data provided in this study could be used as a baseline. Poor repeatability highlights the need to re-examine the test procedures, or the test data from specific subjects. Variability of respiratory pattern is associated with poor repeatability, and so careful instructions on respiration should be given to each subject before the tests.
相似文献Design—Blinded histological analysis.
Setting—Hospital medical school.
Patients—Six hearts of children with the Noonan phenotype and isolated ventricular hypertrophy were compared with age and sex matched controls.
Methods—Histological analysis was performed with an image analyser under light microscopy. Representative sections from the entire left ventricular free wall were examined. Results were expressed as the percentage of fields showing disarray related to the number of fields evaluated: 100 fields were examined for each patient.
Results—In the patients with Noonan syndrome myocardial disarray was present in the ventricular septum in 24 (5·7)% (mean (SD)) of fields and in the free wall in 22·2 (6·8)%. In the controls disarray was present in the septum in 3·8 (2·3)% of fields and in the free wall in 2·4 (2·8)%. In both regions the extent of disarray was significantly greater in patients with Noonan syndrome (p < 0·0005; 95% confidence interval 14 to 26·3 for the septum: p < 0·005, 95% confidence interval 11·4 to 28·2 for the free wall).
Conclusions—The ventricular hypertrophy associated with Noonan syndrome is histologically similar to hypertrophic cardiomyopathy but whether the two diseases are the expression of the same genetic defect remains to be determined.
相似文献 下载免费PDF全文 Setting—University hospital specialising in internal medicine.
Participants—14 healthy male volunteers 10 of whom were studied.
Intervention: Transoesophageal atrial pacing.
Main outcome measures—At paced rates of 70, 80, and 90 ppm the ratio of early to late peak transmitral flow velocity (E/A) was 1·97 (0·28), 1·49 (0·21), and 0·95 (0·11) respectively; the ratio of early to late time-velocity integrals of transmitral flow (Ei/Ai) was 3·03 (0·51), 2·11 (0·24), and 1·14 (0·30) respectively; and the atrial filling fraction (AFF) was 0·17 (0·03), 0·21, (0·04), and 0·24 (0·04) (mean (SD)).
Results—Heart rate showed a linear correlation with E/A (r2 = 0·806), Ei/Ai (r2 = 0·838), and AFF (r2 = 0·343). Neither the peak aortic flow velocity or the mean aortic flow acceleration showed significant changes during pacing at rates of 70, 80, 90, and 100 ppm.
Conclusions—E/A and Ei/Ai can be expected to decrease by 0·5 and 0·9 for each increase of 10 beats/min in heart rate.
Knowledge of this relation may be useful for the development of algorithms to correct for heart rate when diastolic function is assessed.
相似文献METHODS—ERP and monophasic action potential duration (MAPD) were measured from a single left ventricular epicardial site in 26 patients undergoing coronary artery surgery. Cardiopulmonary bypass was instituted and normothermia maintained. Refractory period was determined by the extrastimulus technique at a basic cycle length of 500 ms, at four times (group 1, 15 patients) or two times (group 2, 11 patients) the preischaemic diastolic threshold. A three minute period of ischaemia was instituted by aortic cross clamping between the input from the pump oxygenator and the heart.
RESULTS—After three minutes of ischaemia, mean (SEM) ERP lengthened from 232 (5) ms (control) to 246 (7) ms (p < 0.005) in group 1, and from 256 (10) ms (control) to 348 (25) ms (p < 0.005) in group 2. In the same time MAPD shortened from 256 (5) ms (control) to 189 (9) ms (p < 0.001) with no difference between groups. Thus postrepolarisation refractoriness developed during ischaemia. Before ischaemia, ERP showed a good correlation with APD (R2 = 0.64) but by one minute of ischaemia the correlation was poor (R2 = 0.29).
CONCLUSIONS—These results show that during the first three minutes of global ischaemia in patients with coronary artery disease: (1) ERP lengthened in response to both a low and a high stimulus strength; and (2) there was a good correlation between ERP and APD before ischaemia, which was lost by one minute as APD decreased and ERP increased. These findings may have important implications in arrhythmogenesis.
Keywords: refractoriness; ischaemia; repolarisation 相似文献
下载免费PDF全文 Design—Prospective direct comparison of paired measurements by both techniques in each patient.
Setting—Intensive care unit in a cardiovascular centre.
Patients—65 patients after open heart surgery (mean (SD) age 53 (12) years).
Interventions—Cardiac output was measured simultaneously by the transoesophageal Doppler and thermodilution techniques. Cardiac output was measured again after a mechanical intervention or volume loading.
Results—The limits of agreement were −2·53 to +0·83 1·min−1 for cardiac output measured by the Doppler and thermodilution techniques. This suggests that the Doppler method alone would not be suitable for clinical use. The second measurement of cardiac output by thermodilution was compared with cardiac output estimated from the first and second Doppler measurements and the first thermodilution measurement. The limits of agreement (−0·55 to +0·51 1·min−1) were good enough for clinical use.
Conclusions—After cardiac output had been measured simultaneously by both the Doppler and thermodilution techniques, subsequent transoesophageal Doppler alone gave a clinically useful measurement of cardiac output.
相似文献 下载免费PDF全文 Design—Platelet function was assessed by measurement of the in vivo synthesis of thromboxane by gas chromatography-mass spectrometry of thromboxane's major urinary metabolite, 2,3-dinor-thromboxane-B2.
Setting—Coronary care unit of Huddinge University Hospital.
Subjects—30 patients with acute myocardial infarction given either streptokinase 1·5 million units intravenously over one hour + 500 mg aspirin (n = 10), 500 mg aspirin (n = 10), or neither thrombolysis nor aspirin (n = 10).
Results—Patients treated by thrombolysis had a 20-fold increase in thromboxane formation during thrombolysis compared with control patients not treated by thrombolysis (p = 0·0001). Until two days after thrombolysis thromboxane production in patients treated with streptokinase did not decrease to a value comparable with patients treated with aspirin but not given thrombolysis.
Conclusions—Thromboxane production increased considerably during thrombolysis, possibly reflecting greatly enhanced platelet activation. The slow decrease in thromboxane formation after treatment with aspirin suggests that the efficacy of thrombolysis might be improved by more efficient antiplatelet treatment.
相似文献Design—Prospective study; analysis of numbered plasma samples performed blind with respect to clinical data.
Setting—Regional paediatric cardiothoracic unit.
Patients—Nine patients, median age 4, range 2 to 9 years, five males. Patients under the age of 1 year were excluded because of the frequent blood sampling involved.
Main outcome measures—Plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin, plasma renin activity, aldosterone, noradrenaline and adrenaline, and urinary concentrations of cyclic guanosine monophosphate (cGMP) as measured by radioimmunoassay.
Results—After 30 minutes of cardiopulmonary bypass plasma atrial natriuretic peptide (ANP) decreased from (mean (SEM)) 151 (71) pg/ml to 52 (44) pg/ml (NS), and urinary production of its second messenger cyclic guanosine monophosphate (cGMP) decreased from 1286 (600) pmol/ml to 151 (414) pmol (p < 0·05). Other plasma concentrations of hormones studied did not change significantly although arginine vasopressin, adrenaline, and noradrenaline increased whereas aldosterone and plasma renin activity decreased. After cardiopulmonary bypass stopped there was an immediate and significant rise in plasma ANP, but within the next 24 hours plasma ANP declined significantly (p < 0.05), decreasing from 294 (49) pg/ml to 64 (29) pg/ml at 22 hours. In the postoperative period there was a significant correlation between plasma ANP and both mean fluid balance (r = 0·96, p < 0·001) and mean urine output (r = 0·97, p < 0·001). Plasma aldosterone peaked (p < 0·05) at 22 hours after operation, and argine vasopressin peaked (p < 0·05) at two hours and then declined (p < 0·05) to a trough at 24 hours. Plasma renin activity, adrenaline, noradrenaline, and urinary cGMP concentrations, and mean central venous pressure did not change significantly in the postoperative period.
Conclusion—The changes documented show the differing pattern of release of water balance hormones invoked by cardiopulmonary bypass. The central role of ANP is shown by its strong correlation with urinary output and its similarly strong relation to fluid balance.
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