冠心病心室晚电位与左室功能的关系

目的：观察心室晚电位（ＶＬＰ）、心律失常事件（ＡＥ）与左室功能之间的关系。方法：１４５例冠心病患者均进行信号平均心电图（ＳＡ－ＥＣＧ）检测和２４小时ＨＯＬＴＥＲ监测，同期进行冠状动脉造影和左室造影及随访观察。结果：１１４５例冠心病患者（心绞痛５５例、陈旧性心肌梗死９０例），随访１４１±７１（４－３６）月，发生ＡＥ７例。２ＶＬＰ阳性组左室射血分数（ＬＶＥＦ）显著降低（Ｐ＜００５）。３发生ＡＥ组ＬＶＥＦ显著降低（Ｐ＜００５）。结论：左室功能障碍者ＶＬＰ阳性率高、容易发生ＡＥ。     

Relationship between late potentials and left ventricular function in patients with coronary artery disease

We examined the relationship between late potentials and left ventricular function from a hemodynamic point of view in 50 patients with prior myocardial infarction. Late potentials were found in 15 (30%) of 50 patients. A left ventricular aneurysm was found in 28 patients. Late potentials were detected in 14 (50%) of 28 patients with the aneurysm but in 1 (5%) of 22 patients without it (p less than 0.01). In the 50 patients, a hemodynamic data from the late potential positive group (n = 15) were compared to those from the late potential negative group (n = 35). The late potential positive group had a significantly lower ejection fraction, cardiac index and stroke volume than the late potential negative group. We further studied the 28 patients with left ventricular aneurysm in a similar way. The cardiac index and stroke volume were also significantly lower in the late potential positive group. The ejection fraction tended to be lower in the late potential positive group. These results suggest that left ventricular function and left ventricular aneurysm are among the factors that influence the development of late potentials.     

Independent value of signal-averaged electrocardiography and left ventricular function in identifying patients with sustained ventricular tachycardia with coronary artery disease

To determine if the signal-averaged electrocardiographic detection of late potentials is an independent marker of sustained ventricular tachycardia (VT) in patients with documented chronic coronary artery disease (CAD), 57 patients underwent signal-averaged electrocardiography. Mean ejection fraction was 47 +/- 13% in the 14 patients with sustained VT and 56 +/- 19% in the 43 patients without VT (difference not significant). The sensitivity, specificity and accuracy of late potentials for detecting patients with VT were 64% (9 of 14), 79% (34 of 43), and 75% (43 of 57), respectively. Univariate analysis and stepwise logistic regression of angiographic and electrocardiographic variables identified late potentials as an independent marker of the patient with sustained VT. The odds ratio for late potentials to detect patients with prior sustained VT was 2.6. Six-month follow-up revealed a cardiac mortality rate of 11% and an arrhythmia event rate of 22% in patients with late potentials vs a cardiac mortality rate of 3% and an arrhythmia event rate of 13% in patients without late potentials. Thus, signal-averaged electrocardiographic detection of late potentials is useful in identifying patients with prior sustained VT independent of left ventricular function.     

Influence of exercise on QT dispersion in hypertensive patients with left ventricular hypertrophy without coronary artery disease

In hypertensive patients with left ventricular hypertrophy (LVH), the influence of exercise on the regional variations in ventricular repolarization is not well understood. The present study compared dispersions of QT and QT apex (QTD and QTaD), which are indices of regional variations in ventricular repolarization, between hypertensive patients with echocardiographic evidence of LVH and those without LVH. Seventy essential hypertensive patients underwent a modified Bruce protocol exercise test, and QTD and QTaD were measured at rest and at peak exercise level. All subjects had undergone coronary angiography and did not have coronary artery disease. None of them showed ST-segment depression during or after exercise. There were 20 patients with LVH and 50 patients without LVH. The QTD and QTaD at rest were not different between the patients with LVH and those without LVH (56+/-32 vs 57+/-28 ms, 52+/-20 vs 49+/-23 ms). At peak exercise level, QTaD was significantly decreased compared with the baseline in hypertensive patients without LVH (49+/-23 to 42+/-16ms, p<0.05), whereas in patients with LVH QTaD increased (52+/-20 to 67+/-17ms, p<0.05). QTaD at peak exercise level was positively correlated with the left ventricular mass index (r=0.357, p=0.0024). These data were unchanged after correction for heart rate using Bazett's equation. In conclusion, QTaD increased after exercise in hypertensive patients with LVH. Inhomogeneity of repolarization is induced by exercise stress in hypertensives with LVH.     

冠心病患者左心功能的改变

目的:观察不同程度冠心病患者左心功能的变化。方法;78例冠心病患者分成稳定性心绞痛(SA)、不稳定性心绞痛(UA)、急性心肌梗死(AMI)和陈旧性心肌梗死(OMI)4组,并与30例健康成人(对照组)比较。采用无创伤自动检测仪及彩色多普勒血流显像仪测定心功能指标;心排血指数(CI),外周阻力(TPR),左室射血前期(PEP)及左室射血时间(LVET);左室收缩功能:射血分数,每搏量,心搏出量;左室舒张功能:A峰,E峰,峰值速度比值,峰值充盈,标准化充盈速度。结果:AMI和OMI组心功能明显减低(P<0.01):CI减少,TPR增高,PEP延长,LVET缩短,左室收缩功能减弱,舒张功能降低;UA和SA组心功能减低(P<0.05～<0.01);AMI和OMI组比UA和SA组心功能减低有显著差异(P<0.05)。结论;冠心病随病情加重,心功能明显恶化。     

Prognostic significance of ventricular late potentials in coronary artery disease

By means of high-gain ECG and signal-averaging techniques, we tried to determine the prevalence and prognostic significance of ventricular late potentials (VLPs) in coronary artery disease (CAD). No VLPs were detected in normal subjects (n = 25) or in patients with various noncoronary cardiopathies with sustained ventricular tachycardia and/or fibrillation (VT/VF) (n = 10). Among 92 CAD patients, VLPs were apparent in 35% (32 of 92) at the beginning of the study. The prevalence of VLPs increased to 48% (19 of 40) in the presence of ventricular aneurysm (VA) and to 82% (14 of 17) in the presence of a history of previous sustained VT/VF. To determine the prognostic significance of VLPs, a prospective analysis was conducted during a mean of 7.4 months (range 1 to 22 months). During the follow-up period, 11 patients (12%) presented with an episode of sustained VT/VF, and six of them died from documented VT/VF. Three other patients died from cardiogenic shock. An episode of sustained VT/VF occurred in 31% (10 of 32) of the patients with VLPs vs 2% (1 of 58) of the patients without VLPs (p less than 0.001), and six patients with VLPs died from sustained VT/VF vs none in the group of patients without VLPs (p less than 0.01). This VLP-related increase in arrhythmic risk was still present in the particular subgroup of patients with a history of previous sustained VT/VF (n = 17) and in patients with VA (n = 40). The risk of developing sustained VT/VF was also influenced by the length of the VLP and by a low mean ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of digoxin on left ventricular function in coronary artery disease patients

To assess whether digitalis modifies or prevents the deterioration of the left ventricular ejection fraction and wall motion during acute ischemia, we performed gated blood pool radionuclide ventriculograms in 15 patients with angiographically documented coronary artery disease. All patients were studied in the resting state and during maximal supine bicycle exercise, both before and 1 hour after 1 mg intravenous digoxin.There was no significant difference, pre-digoxin vs post-digoxin, in exercise tolerance (415 ± 84 vs 418 ± 107 seconds), number of segments with abnormal resting wall motion (12 vs 11) or exercise wall motion (21 vs 19). Ten patients developed angina during the same exercise load, irrespective of digoxin administration. Twelve patients had subnormal left ventricular ejection fraction during exercise pre-digoxin, vs 13 patients post-digoxin (P = ns). In the resting state, the left ventricular ejection fraction was higher after digoxin (53 ± 14% pre vs 58 ± 14% post, P < 0.05). During exercise, however, the left ventricular ejection fraction was not significantly improved after digoxin (50 ± 16% pre vs 53 ± 17% post, P = ns).These data indicate that although acute administration of digoxin improves the resting left ventricular function, it does not improve exercise tolerance to angina. Furthermore, intravenous digoxin does not appear to prevent the deterioration of left ventricular wall motion and ejection fraction during exercise induced ischemia.     

Left ventricular diastolic filling in patients with coronary artery disease and normal left ventricular function

Abnormal left ventricular diastolic filling (DF) has been noted in coronary disease (CD) patients with normal left ventricular function (NLVF). Inclusion of patients with regional wall disease, hypertension, and left ventricular hypertrophy may be responsible for abnormal DF. We evaluated left ventricular DF curves derived from gated blood pool scans in 21 normals (group 1), in 38 CD patients with NLVF specifically defined (group 2), and in 28 CD patients with ejection fractions greater than 50% and regional disease (group 3). The peak filling rate (PFR), mean filling rate (MFR), the percentage of stroke volume filled at one third of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined. Groups 1 and 2 had similar DF parameters. Group 2 patients with 75% obstructive left anterior descending disease (LAD) had a reduced %SV-RFP and PFR (2.56 +/- 0.56 end-diastolic volumes/sec [EDV/S]) as compared to normals (3.11 +/- 0.65 EDV/S, p less than 0.01). Group 3 patients had a reduced PFR (2.14 +/- 0.53 EDV/S, p less than 0.001), MFR, %SV-1/3 DT, and %SV-RFP. DF in CD patients with NLVF was similar to normals in a select group of patients but was abnormal in patients with regional disease and greater than 75% LAD disease with NLVF.     

Modification of left ventricular response to pacing tachycardia by nifedipine in patients with coronary artery disease

The calcium blocking agent nifedipine was shown to protect the isolated left ventricle against the development of altered diastolic compliance during severe global ischemia. To assess the influence of nifedipine during myocardial ischemia in human subjects, we studied the effect of nifedipine (20 mg sublingually) on the hemodynamic response to pacing tachycardia (heart rate 66 ± 4 to 143 ± 4 beats per minute) in 17 patients with multivessel coronary artery disease. Typical anginal pain occurred in all patients during pacing tachycardia before nifedipine, but in only 3 of 17 patients during pacing after nifedipine. In 11 patients a significant (≥ 5 mm Hg) increase in postpacing left ventricular end-diastolic pressure (LVEDP, 15 ± 2 mm Hg to 28 ± 2 mm Hg, p < 0.01) developed, and was associated with an upward shift of the left ventricular diastolic pressure-volume curve. In these patients, pretreatment with nifedipine did not alter resting LVEDP or aortic pressure, but did attenuate or abolish the increase in LVEDP and the shift in left ventricular diastolic pressure-volume curves after pacing tachycardia to the same rate and for the same duration. The antianginal effect of nifedipine was not associated with a reduction in contractility, because there was no change in LV + dp/dt after nifedipine. However, the increase in left ventricular systolic pressure achieved in response to pacing tachycardia was less after nifedipine. We conclude that nifedipine favorably modifies the symptomatic and hemodynamic response to pacing tachycardia in patients with coronary artery disease. The mechanism is uncertain and could involve a direct myocardial effect, peripheral vasodilation, coronary vasodilation or a combination of these effects.     

冠心病持续性室性心动过速患者的Q—T离散度

为评价Q-T_d对冠心病患者发生室性心动过速的预测价值,观察18例冠心病持续性室性心动过速患者和20例对照组的Q-T_d。结果显示持续型室性心动过速组Q_(Td)(104±28ms)明显大于对照组(61±19ms,P<0.01)。表明Q-T_d的增加可作为预测室性心动过速发生的重要指标。     

Prevalence of late potentials in patients with and without ventricular tachycardia: Correlation with angiographic findings

Late potentials occurring at the end of or after the QRS complex were searched for from the body surface using high gain amplification and signal averaging techniques with filter settings between 100 and 300 hertz. The number of repetitions of the averaging process ranged between 150 and 300. Two hundred thirty-six patients were studied. In 27 control subjects, no late potentials were recorded. Among 146 patients without ventricular tachycardia or fibrillation, late potentials were present in 49 (34 percent). The mean duration of late potentials was 31 ± 15.3 ms (median 25). Of 63 patients with documented ventricular tachycardia or fibrillation, 45 (71 percent) had late potentials (mean duration 51 ± 31.5 ms; median 50) (probability [p] < 0.001). There was a close correlation between the detection of late potentials and left ventricular function. Late potentials occurred more frequently in patients with than in those without ventricular akinesia or aneurysm and in patients with than in those without ventricular tachycardia or fibrillation.

In conclusion, late potentials are a frequent finding in patients with regional contraction abnormalities, both in patients with and in those without documented ventricular tachycardia. The greater prevalence and longer duration of these signals in patients with ventricular tachycardia or fibrillation might be responsible for the greater susceptibility to ventricular tachycardia. Long-term follow-up studies will be necessary to assess the possible prognostic significance of late potentials in patients without previously documented ventricular tachycardia or fibrillation.     

Impact of left ventricular ejection fraction on endothelial function in patients with coronary artery disease

BACKGROUND: Endothelial dysfunction is present in patients with coronary artery disease (CAD) or with congestive heart failure. HYPOTHESIS: This study was performed to evaluate the impact of systolic heart function on endothelial function in patients with CAD. METHODS: The study population consisted of 283 consecutive patients (mean age 59 years, 176 men) undergoing coronary angiography. Endothelial function was assessed by measuring flow-mediated vasodilation (FMD) of the brachial artery. RESULTS: Patients (n = 236) with an ejection fraction (EF) > or = 55% on routine echocardiogram were younger (mean age 58 vs. 62 years), showed a lower prevalence of diabetes (15 vs. 38%) and myocardial infarction (13 vs. 66%), and showed a higher FMD (4.8 +/- 2.4 vs. 4.0 +/- 2.0%, p < 0.05) than patients (n = 47) with an EF < 55%. The correlation coefficient between FMD/endothelial function and EF/systolic heart function was 0.149 (p < 0.02) in the overall study population. Multivariate analysis showed that of age, gender, frequency of diabetes mellitus, myocardial infarction, and CAD extent, EF was the only significant independent parameter correlating with FMD in patients with CAD. CONCLUSIONS: Compared with the other tested risk factors, EF surprisingly was the only significant independent parameter correlating with endothelial function in patients with CAD. Our results support the view that endothelial function is an independent prognostic factor in patients with CAD.     

Effect of gender on left ventricular function during exercise in patients with coronary artery disease

This study evaluated the effect of gender on left ventricular (LV) function in 84 men and 20 women with coronary artery disease (CAD) (greater than or equal to 50% luminal narrowing of one or more of the major coronary arteries). All patients underwent rest and upright exercise radionuclide ventriculography on a bicycle ergometer. There were no differences between men and women in age, hypertension, medications, and extent of CAD disease (number of diseased vessels or CAD score). Although men exercised for a longer duration than women, both achieved similar exercise heart rates and blood pressures. Angina pectoris or ST depression during exercise occurred in similar proportion in both groups. The LV ejection fraction and the systolic pressure-to-end-systolic volume ratio at rest and during exercise were similar in both men and women. Thus, men and women with comparable extent of CAD demonstrate similar manifestations of myocardial ischemia and LV dysfunction during exercise. Gender does not appear to influence LV function independent of the extent of CAD.     

Effect of age on left ventricular function during exercise in patients with coronary artery disease

The purpose of this study was to assess the effect of age on left ventricular performance during exercise in 79 patients with coronary artery disease (greater than or equal to 50% narrowing of one or more major coronary arteries). Fifty patients under the age of 60 years (group I) and 29 patients 60 years or older (group II) were studied. Radionuclide angiograms were obtained at rest and during symptom-limited upright bicycle exercise. The history of hypertension, angina or Q wave myocardial infarction was similar in both groups. Multivessel coronary artery disease was present in 30 patients (60%) in group I and in 19 patients (66%) in group II (p = not significant). There were no significant differences between the two groups in the hemodynamic variables (at rest or during exercise) of left ventricular ejection fraction, end-diastolic volume, end-systolic volume and cardiac index. Exercise tolerance was higher in group I than in group II (7.8 +/- 0.4 versus 5.7 +/- 0.4 minutes, p = 0.009), although the exercise heart rate and rate-pressure product were not significantly different between the groups. There was poor correlation between age and ejection fraction, end-diastolic volume and end-systolic volume at rest and during exercise. Abnormal left ventricular function at rest or an abnormal response to exercise was noted in 42 patients (84%) in group I and in 25 patients (86%) in group II (p = not significant). Thus, in patients with coronary artery disease, age does not influence left ventricular function at rest or response to exercise. Older patients with coronary artery disease show changes in left ventricular function similar to those in younger patients with corresponding severity of coronary artery disease.     

Predictors of sustained ventricular tachycardia inducibility in patients with nonsustained ventricular tachycardia and chronic coronary artery disease

To assess the likelihood of inducing sustained ventricular tachycardia, we analyzed a cohort of 58 retrospective and 18 prospective patients with chronic coronary artery disease who underwent electrophysiologic study because of spontaneous nonsustained ventricular tachycardia (three or more beats, lasting less than 30 seconds, at a rate greater than 100/min). In 24 of the 58 retrospective patients (41%) sustained ventricular tachycardia was inducible. Stepwise logistic regression identified two "major" variables--left ventricular aneurysm/dyskinesis/akinesis (p = 0.0001; relative risk = 11.88) and ejection fraction less than 40% (p = 0.0002; relative risk = 9.69)--and one "minor" variable--nonsustained ventricular tachycardia longer than 10 beats (p = 0.0151; relative risk = 4.21)--as significant predictors of inducibility. Nineteen patients with both major variables had a high probability of inducibility (greater than 90%). Nineteen patients with neither major variable had a low probability of inducibility (less than 5%). The remaining 20 patients with only one of the major variables had an intermediate probability of inducibility (14% to 75%). The significance of the third minor factor, nonsustained ventricular tachycardia longer than 10 beats, was confined to this intermediate group, in which it could be used to segregate relatively high (65% to 75%) and relatively low (14% to 20%) probability of inducibility. Prospective application of the predictor function stratified 18 additional patients into three groups with high (six patients), intermediate (seven patients), and low (five patients) probability of inducibility. The observed rate of inducibility in each group was 5 of 6 (83%), 2 of 7 (29%), and 0 of 5 (0%), respectively. These data suggest that patients with nonsustained ventricular tachycardia and chronic coronary artery disease can be stratified into subgroups with high, intermediate, and low probability of inducibility of sustained ventricular tachycardia on the basis of ejection fraction and regional ventricular wall motion defects alone.     

血运重建对冠心病合并心功能不全患者心肌收缩功能和心室重构的影响

目的探讨血运重建对冠心病合并左心功能不全患者心肌收缩功能和心室重构的影响。方法86例冠心病合并心功能不全患者术前应用超声心动图进行心功能、左心室(左室)几何形态和心肌活性评定,分为有存活心肌组和无存活心肌组,两组分别行血运重建或药物治疗。随访(13±5)个月后重新评价上述指标。结果57例有存活心肌的患者中行血运重建者较药物治疗者左室射血分数(LVEF)、存活节段数、左室球状指数(LVSI)明显提高;左室舒张末容积(LVEDV)、左室收缩末容积(LVESV)、左室重量(LVM)明显降低(P值均<0.01)。29例无存活心肌的患者中上述指标两种治疗间无显著性差异(P值均>0.05)。结论血运重建能改善冠心病合并左心功能不全但有存活心肌患者的心肌收缩功能和几何形态。     

Association of obesity with left ventricular remodeling and diastolic dysfunction in patients without coronary artery disease

Obese patients frequently complain of dyspnea. Deconditioning and altered left ventricular (LV) systolic or diastolic function with elevated filling pressures may contribute to dyspnea. This study analyzed 4,281 patients who underwent diagnostic coronary angiography from January 1, 1995, to December 31, 2000. No patients had coronary artery stenoses >50% of the luminal diameter, and all underwent echocardiography within the same 6-year period. The association between body mass index (BMI) and LV structure and systolic and diastolic function was examined. All analyses controlled for age and gender, with the effect size for BMI expressed using a standardized coefficient (SC). A higher BMI was associated with greater LV mass (SC 0.18, p <0.001), wall thickness (SC 0.17, p <0.001), and end-diastolic diameter (SC 0.07, p <0.001). Stroke volume increased with a higher BMI (SC 0.12, p = 0.001), but there was no association between BMI and the ejection fraction (SC 0.003, p = 0.81). Hemodynamic data from invasive studies showed an association between a higher BMI and increased LV end-diastolic pressure (mean 17 mm Hg for BMI <25 kg/m(2) vs 24 mm Hg for BMI >or=40 kg/m(2); SC 0.18, p <0.001), which persisted after controlling for end-diastolic volume (SC 0.22, p <0.001). Obesity was associated with ventricular remodeling, which may normalize wall stress while increasing stroke volume to match metabolic demand. Obesity was not associated with decreased systolic function. However, obesity was associated with increased LV end-diastolic pressure, which suggests an association between obesity and diastolic dysfunction. In conclusion, ventricular remodeling, LV diastolic dysfunction, and elevated filling pressures may contribute to the prevalence of heart failure in obese patients.