运动前后心电时限指标比值的比较

目的 鉴于基于心电R波峰点(Rp)与T波终点(Tn)的心室收缩期与舒张期比率(RSDI)易受Tn定位精度的影响,揭示基于Rp与T波峰点(Tp)的心电时限指标比值(RSD2)能否反映RSDI的趋势.方法 计算Rp至Tp的时限(RpTp)与心室收缩期(RpTn)的相关系数,计算Tp至其后Rp的时限(TpRp)与心室舒张期(...     

Aortic wall elasticity and left ventricular function in hypertensive patients with nonsignificant coronary artery disease

PurposeHypertension is an important cause of nonischemic heart failure. It is important to identify subclinical left ventricular dysfunction in patients with hypertension in an early stage to lower the risk of progression to more severe illness. The aim of our study was to assess the correlation between indices of left ventricular function and aortic stiffness in patients with hypertension.MethodsOur study was a case control study of 42 hypertensive and 40 normotensive patients with nonsignificant coronary artery disease. All the patients underwent echocardiography and left ventricular ejection fraction, global longitudinal strain, post systolic index, pulsed Doppler early transmitral peak flow velocity, early diastolic mitral annular velocity (e′), and aortic elasticity measurements were calculated.ResultsThe hypertensive patients were older (58.47 ± 9.57 vs. 52.94 ± 10.38 years, p = 0.018) and had a higher body mass index (30.09 ± 5.08 vs. 27.48 ± 4.17 kg/m², p = 0.013) and E/e′ ratio (8.16 ± 1.81 vs. 6.56 ± 1.71, p < 0.001) and a lower e′ velocity (8.25 ± 2.28 vs. 9.52 ± 2.34 cm/s, p = 0.015) than normotensives. They also had a lower aortic distensibility (p = 0.008) and a higher aortic stiffness index (p = 0.039) compared with the normotensive group. The hypertensive patients did not show any association between aortic elasticity and stiffness with age or e′ velocity despite significant association in normotensives.ConclusionHypertension is associated with a high prevalence of diastolic dysfunction, elevated left ventricular filling pressure, and increased arterial stiffness, all of which have significant association with adverse outcomes. The measurements found in the hypertensive patients compared with the normotensive group may be due to several age-independent mechanisms.     

高血压患者右室舒张功能72例分析

目的：运用超声心动图，分析高血压患者左室收缩功能衰竭前，右室舒张功能的变化。方法：用多普勒超声心动图测量正常组、高血压组（左室肥厚组、非左室肥厚组）左右室舒张功能参数。统计采用Ｆ检验和ｑ检验。结果：肺动脉流速在高血压左室肥厚组比对照组及非肥厚组块（Ｐ〈０．０１）；高血压非肥厚组与对照组比较，右室舒张早期Ｅ峰较低，Ｄｅｃ１／２Ｔ延长，舒张晚期Ａ峰较高，Ｅ／Ａ比值较小，Ａ波充盈分数增大（Ｐ〈０．０１）     

Atrioventricular Filling Dynamics, Diastolic Function and Dysfunction

Left ventricular diastolic dysfunction is associated with slowing of LV relaxation and a decrease in LV chamber compliance. This impairment of function leads to changes in filling velocities as measured by pulsed wave Doppler echocardiography in the pulmonary veins and across the mitral valve, and in intraventricular flow propagation velocity as measured by color M-mode Doppler. This paper explores some of the physiology of LV filling in a clinical context.     

Effects of chronic β-blockade on rest and exercise hemodynamics in mitral stenosi

β-blocker therapy for mitral stenosis is controversial. This study compares right and left heart hemodynamics at rest and supine submaximal exercise in patients (n = 7) receiving chronic β-antagonists with untreated patients (n = 17) matched for age (mean ± SD = 51 ± 12 years) and valve area (0.7 ± 0.2 cm²/m²). Little benefit was observed with treatment at rest. Although pulmonary capillary wedge pressures (PCWP) were lower during exercise in the β-blocker group (22±4 vs. 31 ± 9 mmHg; P>0.05), exercise performance was not enhanced and cardiac output response during exercise was reduced (control = 41% increase vs. 12% for β-blockade). PCWP rose rapidly when diastolic filling periods were >300 msec in both groups. Pulmonary capillary wedge pressure was found to be a nonlinear functions (P<0.001) of diastolic filling period (PCWP = 15.9 + 5.84 × 10⁵/dfp²). These data suggest that there is a critical heart rate in patients with mitral stenosis above which hemodynamic compromise rapidly occurs. © 1995 Wiley-Liss, Inc.

1 This article is a US Government work and, as such, is in the public domain in the United States of America.

     

Is 'diastolic heart failure' a diagnosis of exclusion? Echocardiographic parameters of diastolic dysfunction in patients with heart failure and normal systolic function

Background: Diastolic heart failure (DHF) is reported to account for 30–50% of heart failure presentations, but its prevalence in the absence of overt coronary disease is unclear. Diastolic heart failure is usually defined by exclusion (heart failure with normal left ventricular (LV) systolic function), and few studies have sought a specific diagnosis of diastolic dysfunction. The objective of the present study was to determine the prevalence of isolated DHF and characterise LV diastolic function in patients without clinical evidence of coronary disease, who were referred for LV function assessment.

Methods: Among 938 consecutive patients referred for assessment of LV function, diastolic dysfunction was sought in patients with clinical heart failure, normal systolic function, and no valvular or coronary disease. The evaluation was based on measurement of early (E) and late (A) transmitral velocities and E wave deceleration time (DT). Pulmonary vein systolic, diastolic and atrial reversal velocities were used to differentiate pseudonormal filling in patients with normal E/A and DT.

Results: Normal LV systolic function was present in 331 patients (35%), of whom 53 (6%) met criteria for a clinical diagnosis of DHF. Diastolic dysfunction was confirmed by echocardiography in 38 patients (72% of clinical DHF patients), of whom 27 had impaired LV relaxation, 10 had pseudonormal filling, and one had restrictive filling. Diastolic function was normal in 13 and indeterminate in two patients. Pseudonormal or restrictive LV filling were more prevalent in patients with acute heart failure (7/20, P < 0.05).

Conclusions: Carefully defined, isolated DHF is uncommon, but most of these patients demonstrate echocardiographic evidence of diastolic dysfunction.     

Myocardial contractile effects of nitric oxide

Recent experimental and clinical research solved some of the controversies surrounding the myocardial contractile effects of NO. These controversies were: (1) does NO exert a contractile effect at baseline? (2) is NO a positive or a negative inotrope? (3) Are the contractile effects of NO similar when NO is derived from NO-donors or from the different isoforms of NO synthases (NOS)? (4) Does NO exert the same effects in hypertrophied, failing or ischemic myocardium? Transgenic mice with cardioselective overexpression of NOS revealed NO to produce a small reduction in basal developed LV pressure and a LV relaxation-hastening effect mainly through myofilamentary desensitization. Similar findings had previously been reported during intracoronary infusions of NO-donors in isolated rodent hearts and in humans. The LV relaxation hastening effect was accompanied by increased diastolic LV distensibility, which augmented LV preload reserve especially in heart failure patients. This beneficial effect on diastolic LV function always overrode the small NO-induced attenuation in LV developed pressure in terms of overall LV performance. In most experimental and clinical conditions, contractile effects of NO were similar when NO was derived from NO-donors or produced by the different isoforms of NOS. Because expression of inducible NOS (NOS2) is frequently accompanied by elevated oxidative stress, NO produced by NOS2 can lead to peroxynitrite-induced contractile impairment as observed in ischemic or septic myocardium. Finally, shifts in isoforms or in concentrations of myofilaments can affect NO-mediated myofilamentary desensitization and alter the myocardial contractile effects of NO in hypertrophied or failing myocardium.     

Olmesartan attenuates the development of heart failure after experimental autoimmune myocarditis in rats through the modulation of ANG 1-7 mas receptor

Angiotensin-converting enzyme 2 (ACE-2) is a membrane-associated carboxy-peptidase catalyzes the conversion of the vasoconstrictor angiotensin (ANG)-II to the vasodilatory peptide ANG 1-7. In view of the expanding axis of the renin angiotensin system, we have investigated the cardioprotective effects of olmesartan (10mg/kg/day) in experimental autoimmune myocarditis. Olmesartan treatment effectively suppressed the myocardial protein expressions of inflammatory markers in comparison to the vehicle-treated rats. However, the protein and mRNA levels of ACE-2 and ANG 1-7, and its receptor Mas were upregulated in olmesartan treated group compared to vehicle-treated rats. Olmesartan medoxomil treatment significantly decreased the expression levels of phospho-p38 mitogen-activated protein kinase (MAPK), phospho-JNK, phospho-ERK and phospho-(MAPK) activated protein kinase-2 than with those of vehicle-treated rats. Moreover, vehicle-treated rats were shown to be up-regulated protein expressions of NADPH oxidase subunits (p47phox, p67phox and Nox-4), myocardial apoptotic markers and endoplasmic reticulum stress markers in comparison to those of normal and all these effects are expectedly down-regulated by an olmesartan. In addition, attenuated protein levels of phosphatidylinositol-3-kinase (PI3K) and phospho-Akt in the vehicle-treated EAM rats were prevented by olmesartan treatment. Our results suggest that beneficial effects of olmesartan treatment was more effective therapy in combating the inflammation, oxidative stress, apoptosis and signaling pathways associated with heart failure at least in part via the modulation of ANG 1-7 mas receptor.     

Right ventricular diastolic dysfunction in arterial systemic hypertension: analysis by pulsed tissue Doppler.

AIMS: This study analyses right ventricular longitudinal function in arterial systemic hypertension by pulsed tissue Doppler. METHODS AND RESULTS: Thirty normotensives and 30 hypertensives, free of cardiac drugs, underwent standard Doppler echocardiography and pulsed tissue Doppler of right ventricular lateral tricuspid annulus and left ventricular lateral mitral annulus. By tissue Doppler, systolic and diastolic measurements were obtained. Hypertensives had higher left ventricular mass and impaired Doppler diastolic indexes, without changes of global systolic function. Tissue Doppler showed reduction of right ventricular E/A ratio and prolongation of relaxation time in comparison with controls (both P<0.00001). In the overall population, the length of tissue Doppler derived right ventricular relaxation time was positively related to right ventricular anterior wall thickness while right ventricular E/A ratio was positively related to E/A ratio of left ventricular mitral annulus (both P<0.00001). These relations remained significant even after adjusting for clinical and echocardiographic confounders by separate multivariate models. CONCLUSIONS: Arterial systemic hypertension is associated to right ventricular longitudinal diastolic dysfunction. This dysfunction involves the prolongation of active relaxation, which is independently associated with the degree of right ventricular hypertrophy and the impairment of passive wall properties, which is mainly due to ventricular interaction occurring under left ventricular pressure overload conditions.