肥胖对2型糖尿病患者左室舒张功能的影响

目的:通过超声心动图左室舒张功能各项指标的测定,探讨不同程度的肥胖对2型糖尿病患者左室舒张功能的影响。方法:对90例2型糖尿病患者测定身高、体重,计算体重指数(BMI)。根据体重指数的不同,分为三组:正常体重组、超重组、肥胖组。每组病人均测定左室舒张功能指标即左室舒张早期充盈峰值流速(Peak E)、晚期充盈峰值流速(Peak A)、A/E比值、等容舒张时间(IRT)、左房直径(LAD)、二尖瓣半压时间(MV1/2T)。比较各组心脏左室舒张功能情况。结果:BMI与Peak E呈负相关(r=-0.235,P<0.05);BMI与A/E比值呈正相关(r=0.195,P<0.05);BMI与IRT呈负相关(r=-0.163,P<0.05)。2型糖尿病早期亚临床心脏左室舒张功能异常的发生率分别36%;47%;58%。结论:2型糖尿病早期即存在左室舒张功能异常;肥胖加重心脏左室舒张功能异常。     

Effects of catecholamine stimulation on myocardial hibernation.

We have recently shown that low-flow (10%) ischemia in the isolated piglet heart causes an abrupt fall in mechanical function and metabolic activity (acute hibernation), with nearly complete preservation of high-energy phosphates and glycogen after 2 hours of ischemia. We attempted to determine if norepinephrine, as occurs in vivo, would modify the hibernation process. Piglet hearts were perfused at 37 degrees C with red blood cell-enhanced Krebs-Henseleit solution. Performance of the left ventricle was assessed isovolumetrically. With control coronary flow, norepinephrine (40 ng/ml) caused a approximately 50% increase in pressure-rate product and the rate of change of pressure. When coronary flow was reduced to 10%, these measures fell to levels identical to those of ischemic hearts not exposed to norepinephrine. Changes in myocardial O2 metabolism paralleled mechanical function. Lactate release was quantitatively similar in both groups. However, myocardial adenosine triphosphate was reduced from 29 +/- 1 to 13 +/- 2 mumol/gm and glycogen from 300 +/- 46 to 77 +/- 15 mumol/gm by the presence of norepinephrine. Left ventricular compliance was reduced to 51 +/- 5%, compared with 87 +/- 8% in the group without norepinephrine (p less than 0.001). In the norepinephrine group, correlation between left ventricular stiffness and adenosine triphosphate was poor (r = -0.32). Thus hibernating myocardium does not manifest progressive deterioration in the presence of high concentrations of norepinephrine. Diastolic function is less well preserved, however.     

Effects of captopril on left ventricular systolic and diastolic function after acute myocardial infarction.

The left ventricle progressively dilates in some patients after acute myocardial infarction (AMI). Both systolic and diastolic left ventricular (LV) dysfunction can be of significance in the development of heart failure. Captopril has been shown to prevent dilatation, but the effect on LV diastolic function is unknown. In a placebo-controlled double-blind parallel study, 58 AMI patients with heart failure or low ejection fraction, or both, were consecutively randomized at day 7 to either placebo or captopril (25 mg twice daily). No differences were present between the groups at baseline. Fifty-three patients completed the 6-month study period. Both LV diastolic and systolic volume indexes increased significantly in the placebo group (17 and 14%, respectively); in the captopril group there was no change in LV diastolic volume index, but a 13% reduction in LV systolic volume index. Ejection fraction increased significantly in the captopril group. The peak flow velocities of the early and atrial filling phases were measured, and the ratio between the velocities was calculated. A significant reduction was observed during the study period in early peak flow velocity (65 to 52 cm/s) and in the ratio between early and atrial peak flow velocity (1.3 to 0.8) in the placebo group (p less than 0.05), but no significant changes occurred in the captopril group. No correlation was found between dilatation of the left ventricle and reduction in early peak flow velocity or the ratio between early and atrial peak flow velocity. In conclusion, captopril prevented LV dilatation, improved ejection fraction and prevented LV diastolic dysfunction in AMI patients with early signs of LV systolic dysfunction.     

Effect of beta-adrenergic blockade on myocardial function and energetics in congestive heart failure. Improvements in hemodynamic, contractile, and diastolic performance with bucindolol

The hemodynamic effects of beta-adrenergic blockade with bucindolol, a nonselective beta-antagonist with mild vasodilatory properties, were studied in patients with congestive heart failure. Fifteen patients (New York Heart Association class I-IV) underwent cardiac catheterization before and after 3 months of oral therapy with bucindolol. The left ventricular ejection fraction increased from 0.23 +/- 0.12 to 0.29 +/- 0.14 (p = 0.007), and end-systolic elastance, a relatively load-independent determinant of contractility, increased from 0.60 +/- 0.40 to 1.11 +/- 0.45 mm Hg/ml (p = 0.0049). Both left ventricular stroke work index (34 +/- 13 to 47 +/- 19 g-m/m2, p = 0.0059) and minute work (5.5 +/- 2.2 to 7.0 +/- 2.6 kg-m/min, p = 0.0096) increased despite reductions in left ventricular end-diastolic pressure (19 +/- 8 to 15 +/- 5 mm Hg, p = 0.021). There was an upward shift in the peak + dP/dtmax-end-diastolic volume relation (p = 0.0005). These data demonstrate improvements in myocardial contractility after beta-adrenergic blockade with bucindolol. At a matched paced heart rate of 98 +/- 15 min-1, the time constant of left ventricular isovolumic relaxation was significantly reduced by bucindolol therapy (92 +/- 17 versus 73 +/- 11 msec, p = 0.0013), and the relation of the time constant to end-systolic pressure was shifted downward (p = 0.014) with therapy. The slope of the logarithm left ventricular end-diastolic pressure-end-diastolic volume relation was unchanged (p = 0.51) after bucindolol. These data suggest that chronic beta-adrenergic blockade with bucindolol improves diastolic relaxation but does not alter myocardial chamber stiffness. Myocardial oxygen extraction, consumption, and efficiency were unchanged despite improvement in contractile function and mechanical work. Thus, in patients with congestive heart failure, chronic beta-adrenergic blockade with bucindolol significantly improves myocardial contractility and minute work, yet it does not do so at the expense of myocardial oxygen consumption. Additionally, bucindolol improves myocardial relaxation but does not affect chamber stiffness.     

超声心动图评估肥胖对心脏结构和舒张功能的影响

目的:研究肥胖对心脏结构和左室舒张功能的影响以及比较左室舒张功能各项评价指标的敏感性。方法:选择100名健康体检者,根据体质指数分为正常体重组(对照组,25例),超重组(45例),肥胖组(30例)。应用常规超声心动图、组织多普勒成像技术和彩色M型多普勒对其进行检测,并对各组的心脏结构和左室舒张功能参数进行对比分析。结果:与对照组比较,超重组与肥胖组的左房、左室增大,室壁增厚,左室重量指数增加,二尖瓣瓣环舒张早期峰值运动速度(Ea)、Ea/二尖瓣瓣环舒张晚期峰值运动速度比值下降,二尖瓣舒张早期血流峰值速度(E)/Ea比值增加(P<0.05);肥胖组E值、E/二尖瓣舒张晚期血流峰值速度(A)比值下降,A值升高,等容舒张时间延长,舒张早期左室血流传播速度减慢(P<0.05)。与超重组比较,肥胖组心脏结构和舒张功能进一步恶化(P<0.05)。结论:肥胖可引起心脏肥大,左室舒张功能下降,且随体质指数的增加改变更明显。肥胖是亚临床左室舒张功能障碍的独立危险因素,在心肌迟缓型左室舒张功能下降阶段,综合多指标分析可提高左室舒张功能评价的准确性。组织多普勒和E/Ea较常规评价左室舒张功能的方法更敏感、有效。     

Effects of atrial natriuretic peptide on myocardial contractile and diastolic function in patients with heart failure.

Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p less than 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p less than 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p less than 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular diastolic function following myocardial infarction

An acute myocardial infarction causes a loss of contractile fibers which reduces systolic function. Parallel to the effect on systolic function, a myocardial infarction also impacts diastolic function, but this relationship is not as well understood. The two physiologic phases of diastole, active relaxation and passive filling, are both influenced by myocardial ischemia and infarction. Active relaxation is delayed following a myocardial infarction, whereas left ventricular stiffness changes depending on the extent of infarction and remodeling. Interstitial edema and fibrosis cause an increase in wall stiffness which is counteracted by dilation. The effect on diastolic function is correlated to an increased incidence of adverse outcomes. Moreover, patients with comorbid conditions that are associated with worse diastolic function tend to have more adverse outcomes after infarction. There are currently no treatments aimed specifically at treating diastolic dysfunction following a myocardial infarction, but several new drugs, including aldosterone antagonists, may offer promise.     

Effects of amrinone on myocardial energetics in severe congestive heart failure

Animal and human studies suggest that amrinone can cause significant improvement in the systemic hemodynamics of patients with severe congestive heart failure (CHF), and do so without increasing myocardial oxygen consumption. Because patients with CHF appear to be vulnerable to any further worsening of the myocardial oxygen supply-and-demand balance, amrinone may have a distinct advantage over catecholamine agents that tend to increase myocardial oxygen demand.     

Effects of nicardipine on left ventricular function and energetics in man

The effects of nicardipine, a new dihydropyridine calcium antagonist, on left ventricular function and energetics were studied in 13 patients. Nicardipine was administered as a 2 mg bolus (i.v.) followed by an infusion titrated to maintain a 10–20 mm Hg decrease in systolic pressure. Nicardipine increased heart rate 19% (P < 0.001) while left ventricular end-diastolic pressure was not significantly changed and stroke volume (ml) increased 13% (P < 0.01). Peak values for the first and second time derivatives of left ventricular pressure were increased by 26% (P < 0.01) and 50% (P < 0.02) respectively. Peak aortic blood flow, peak aortic blood acceleration, and the peak rate of change of ejection power were increased 86% (P < 0.001), 123% (P < 0.01), and 113% (P < 0.001), respectively. Stroke work was not changed during nicardipine infusion. External power increased by 40% (P < 0.01); however, the ratio of oscillatory to total power was not significantly different. Although the product of heart rate and systolic aortic pressure was not significantly altered with nicardipine, myocardial oxygen consumption increased 18% (P < 0.02) with a disproportionate increase in coronary blood flow of 41% (P < 0.001) and decrease in coronary resistance of 39% (P < 0.001). The time constant for left ventricular isovolumic relation decreased 22% (P < 0.001) during nicardipine infusion while the minimum value of dP/dt was unchanged. Thus, when administered intravenously in man, nicardipine is a potent coronary and systemic vasodilator producing reflex tachycardia, increased indices of myocardial contractile state, and improved isovolumic relaxation with an associated increase in myocardial oxygen consumption.     

Sex-specific associations of obesity with exercise capacity and diastolic function in Koreans

Background and aimsWomen with obesity are highly predominant among patients with heart failure with preserved ejection fraction (HFpEF). We aimed to elucidate sex-specific associations of obesity with exercise capacity and diastolic function.Methods and resultsHealthy individuals without known cardiovascular diseases undergoing cardiopulmonary exercise test and echocardiography (n = 736) were included and categorized into 4 groups according to their sex and obesity. Exercise capacity was lower in women than men. Obesity was associated with a lower exercise capacity in women (23.5 ± 7.3 vs. 21.3 ± 5.4 ml/kg/min, p < 0.05) but not in men (28.2 ± 7.8 vs. 28.0 ± 6.6 ml/kg/min, p > 0.10). Overall, women had a higher E/e′ than men. Women without obesity had a similar E/e′ to men with obesity (8.2 ± 1.8 vs. 8.4 ± 2.1, p > 0.10), and women with obesity had the highest E/e′. Among 5 risk factors (aging, obesity, elevated blood pressure, elevated heart rate, and elevated fasting glucose), obesity was a significant determinant of exercise intolerance in women but not men. Furthermore, obesity was associated with a greater risk of diastolic dysfunction in women than men (women, adjusted odds ratio 4.35 [95% confidence interval 2.44–7.74]; men, adjusted odds ratio 2.91 [95% confidence interval 1.42–5.95]).ConclusionObesity had a more deleterious effect on exercise capacity and diastolic function in women than men, even in a healthy cohort. These subclinical changes might contribute to the development of a female predominance among HFpEF patients, particularly among individuals with obesity.     

Abnormal systolic and diastolic myocardial function in obese asymptomatic adolescents

Structural and functional cardiac changes are known in obese adults. We aimed to assess the relationship between body mass index (BMI) and cardiac function in overweight and obese asymptomatic adolescents.