patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the o...patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the onset to AD, indicating that AD belongs to the category of effort angina.18 patients were investigated by continuous hemodynamic monitoring. Three patients had significant increase in pulmonary artery diastolic pressure (PADP) before the onset. In the other 15 patients. PADP increased slightly in 12 and remained unchanged in 3 cases before the onset. Left ventriculography showed ejection fraction (EF)>45% in 25 of the 27 patients. These results indicate that left ventricular (LV) systolic dysfunction is not a major factor in the Pathogenesis of AD. The patients with LVEDP>12 mmHg constituted 60% of 25 patients with EF>45%, suggesting that these patients had ohvious LV diastolic dysfunction, which may be the major factor in the pathogenesis of AD.According to the results of our treatment, beta blockers may be used as the major form of tteatment in the patients with AD.展开更多
Objective. To investigate the effect of left ventricular diastolic dysfunction on the pathogenesis of angina decubitus (AD). Methods. The study population consisted of three groups: 20 individuals without cardiovascul...Objective. To investigate the effect of left ventricular diastolic dysfunction on the pathogenesis of angina decubitus (AD). Methods. The study population consisted of three groups: 20 individuals without cardiovascular disease were studied as group Ⅰ.Group Ⅱ included 20 patents with coronary artery disease and without AD. Thirty-one patients with AD and ejection fraction(EF)>50% were studied as group Ⅲ. Group Ⅱ and Ⅲ were matched for age, EF and extent of coronary artery disease. Results. Left ventriculography (LVG) showed that left ventricular (LV) first 1/3 filling fraction(1/3FF) was significantly lower in group Ⅲ than in group Ⅱ and Ⅰ(both P<0001),but LV late 1/3 FF was much higher in group Ⅲ than in group Ⅱ and Ⅰ(P<005, P<001). Left ventricular end-diastolic pressure(LVEDP)was markedly increased before and after LVG in group Ⅱ and Ⅲ as compared with group Ⅰ (both P<005, both P<0001). The difference of LVEDP caused by left atrial contraction (left atrial contraction pressure difference, LACPD)before and after LVG was much higher in group Ⅲ than in group Ⅰ ( P<001, P<0001). Howevere,there were significant differences in LVEDP and in LACPD between before and after LVG only in group Ⅲ (both P<001). Conclusion. The patients with AD have LV diastolic dysfunction, which may be closely related to the pathogenesis of angina decubitus.展开更多
Over the last 20 years, it has emerged that, while surgical revascularisation of extensive ischaemic heart disease may have prognostic advantages, the main issues considered regarding individual management are usually...Over the last 20 years, it has emerged that, while surgical revascularisation of extensive ischaemic heart disease may have prognostic advantages, the main issues considered regarding individual management are usually those of symptomatic improvement only. The major impetus towards invasive intervention is therefore failure of prophylactic anti-anginal therapy. On the other hand, many patients, especially the elderly, now present the clinical problem of ongoing angina without residual invasive options. There is an ongoing need for more effective anti-anginal therapies. Of the currently available major classes of prophylactic anti-anginal agents, neither nitrates, β-blockers nor calcium antagonists generally produce marked improvements in exercise duration. Three areas of new therapeutic development in anti-anginal therapy are worthy of note. These involve the sinus node inhibitor ivabradine, high dose allopurinol (xanthine oxidase inhibitor) and a new class of “metabolic modulators” represented by perhexiline, trimetazidine and probably ranolazine. The current review addresses the therapeutic potential of these agents. Notably, all of these “new” drugs are potentially suitable for management of angina in the setting of impaired left ventricular systolic function, and they may also be utilized in patients with angina independent of the presence of coronary disease (for example in hypertrophic cardiomyopathy). The current evidence for efficacy and potential future development in this area are reviewed.展开更多
Objectives To analyze the changes of vasoactive substances originated from endo- theiium in patients with unstable angina pectoris treated by modified thrombolytic therapy and explore the mech- anisms of the drug to t...Objectives To analyze the changes of vasoactive substances originated from endo- theiium in patients with unstable angina pectoris treated by modified thrombolytic therapy and explore the mech- anisms of the drug to treat unstable angina pectoris. Methods 120 patients with unstable angina pectoris who were not well responsed to common medication were studied. Their ECG stress tests were abnormal and there were ischemic changes in Holter. Urokinase 300,000 U was added in 100 ml normal saline and in- jected within 30 min once a day for 3 days. 300 mg as- pirin was administrated a day before and during uroki- nase applications. Before and after urokinase treat- ments , endothelin-1 , plasma tissue plasminogen activa- tor and its inhibitor-lwere determined. Results Compared with pretreatments, after treatments, the ac- tivities of tissue plasminogen activator increased, endo- thelin-1 and the inhibitor-1 decreased. The changes were significant. Conclusions Modified thrombolytic therapy can regulate the vasoactive substances origina- ted endotheiium in patients with unstable angina pecto- ris . The major substances include endothelin-1, plasma tissue plasminogen activator and inhibitor-1. This mechanism may suggest that urokinase can treat coro- nary heart disease effectively.展开更多
文摘patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the onset to AD, indicating that AD belongs to the category of effort angina.18 patients were investigated by continuous hemodynamic monitoring. Three patients had significant increase in pulmonary artery diastolic pressure (PADP) before the onset. In the other 15 patients. PADP increased slightly in 12 and remained unchanged in 3 cases before the onset. Left ventriculography showed ejection fraction (EF)>45% in 25 of the 27 patients. These results indicate that left ventricular (LV) systolic dysfunction is not a major factor in the Pathogenesis of AD. The patients with LVEDP>12 mmHg constituted 60% of 25 patients with EF>45%, suggesting that these patients had ohvious LV diastolic dysfunction, which may be the major factor in the pathogenesis of AD.According to the results of our treatment, beta blockers may be used as the major form of tteatment in the patients with AD.
文摘Objective. To investigate the effect of left ventricular diastolic dysfunction on the pathogenesis of angina decubitus (AD). Methods. The study population consisted of three groups: 20 individuals without cardiovascular disease were studied as group Ⅰ.Group Ⅱ included 20 patents with coronary artery disease and without AD. Thirty-one patients with AD and ejection fraction(EF)>50% were studied as group Ⅲ. Group Ⅱ and Ⅲ were matched for age, EF and extent of coronary artery disease. Results. Left ventriculography (LVG) showed that left ventricular (LV) first 1/3 filling fraction(1/3FF) was significantly lower in group Ⅲ than in group Ⅱ and Ⅰ(both P<0001),but LV late 1/3 FF was much higher in group Ⅲ than in group Ⅱ and Ⅰ(P<005, P<001). Left ventricular end-diastolic pressure(LVEDP)was markedly increased before and after LVG in group Ⅱ and Ⅲ as compared with group Ⅰ (both P<005, both P<0001). The difference of LVEDP caused by left atrial contraction (left atrial contraction pressure difference, LACPD)before and after LVG was much higher in group Ⅲ than in group Ⅰ ( P<001, P<0001). Howevere,there were significant differences in LVEDP and in LACPD between before and after LVG only in group Ⅲ (both P<001). Conclusion. The patients with AD have LV diastolic dysfunction, which may be closely related to the pathogenesis of angina decubitus.
文摘Over the last 20 years, it has emerged that, while surgical revascularisation of extensive ischaemic heart disease may have prognostic advantages, the main issues considered regarding individual management are usually those of symptomatic improvement only. The major impetus towards invasive intervention is therefore failure of prophylactic anti-anginal therapy. On the other hand, many patients, especially the elderly, now present the clinical problem of ongoing angina without residual invasive options. There is an ongoing need for more effective anti-anginal therapies. Of the currently available major classes of prophylactic anti-anginal agents, neither nitrates, β-blockers nor calcium antagonists generally produce marked improvements in exercise duration. Three areas of new therapeutic development in anti-anginal therapy are worthy of note. These involve the sinus node inhibitor ivabradine, high dose allopurinol (xanthine oxidase inhibitor) and a new class of “metabolic modulators” represented by perhexiline, trimetazidine and probably ranolazine. The current review addresses the therapeutic potential of these agents. Notably, all of these “new” drugs are potentially suitable for management of angina in the setting of impaired left ventricular systolic function, and they may also be utilized in patients with angina independent of the presence of coronary disease (for example in hypertrophic cardiomyopathy). The current evidence for efficacy and potential future development in this area are reviewed.
文摘Objectives To analyze the changes of vasoactive substances originated from endo- theiium in patients with unstable angina pectoris treated by modified thrombolytic therapy and explore the mech- anisms of the drug to treat unstable angina pectoris. Methods 120 patients with unstable angina pectoris who were not well responsed to common medication were studied. Their ECG stress tests were abnormal and there were ischemic changes in Holter. Urokinase 300,000 U was added in 100 ml normal saline and in- jected within 30 min once a day for 3 days. 300 mg as- pirin was administrated a day before and during uroki- nase applications. Before and after urokinase treat- ments , endothelin-1 , plasma tissue plasminogen activa- tor and its inhibitor-lwere determined. Results Compared with pretreatments, after treatments, the ac- tivities of tissue plasminogen activator increased, endo- thelin-1 and the inhibitor-1 decreased. The changes were significant. Conclusions Modified thrombolytic therapy can regulate the vasoactive substances origina- ted endotheiium in patients with unstable angina pecto- ris . The major substances include endothelin-1, plasma tissue plasminogen activator and inhibitor-1. This mechanism may suggest that urokinase can treat coro- nary heart disease effectively.
