左室舒张性心功能障碍超声左心形态、功能及运动耐量的改变50例分析

对核素心血池扫描证实的５０例左室舒张性心功能障碍（ＬＶＤＤ）病例、２６例左室收缩性心功能障碍（ＬＶＳＨＦ）病例进行Ｍ型、二维、多普勒超声心动图及活动平板运动试验检测，并以２０例正常人为对照组（ＣＧ）。结果表明：（１）左心形态学改变：与ＬＶＳＨＦ组比较，ＬＶＤＤ组左房内径（ＬＡＤ）、左室内径（ＬＶＤ）无明显增加，室间隔厚度（ＩＶＳＴ）、左室后壁厚度（ＰＷＴ）增加。与ＣＧ组比较，ＬＶＤＤ组ＬＡＤ、ＩＶＳＴ、ＰＷＴ增加，但ＬＶＤ差异无显著性。（２）ＬＶＤＤ组收缩功能指标：左室射血分数（ＬＶＥＦ）、心脏指数（ＣＩ）与ＣＧ组比较差异无显著性，ＬＶＳＨＦ组与ＣＧ组比较，ＬＶＳＨＦ组ＬＶＥＦ、ＣＩ减低。与ＣＧ组比较，ＬＶＤＤ组左室舒张功能指标：二尖瓣舒张早期流速峰值（ＥＰＦＶ）、二尖瓣舒张早、晚期流速峰值比（Ｅ／Ａ）、舒张早期减速度（ＤＣ）比ＣＧ组减低，二尖瓣舒张晚期流速峰值（ＡＰＦＶ）、等容舒张时间（ＩＲＴ）较ＣＧ组增高。ＬＶＤＤ组各左室舒张功能指标与ＬＶＳＨＦ组差异无显著性。（３）ＬＶＤＤ组运动时间、运动当量显著低于ＣＧ组，但高于ＬＶＳＨＦ组。     

Decreased adrenergic response in hypertensive patients without left ventricular hypertrophy

To analyze the adrenergic responses and to compare them between hypertensive patients with and without left ventricular hypertrophy (LVH), left ventricular (LV) fractional shortening (FS) and end-systolic wall stress (ESS) were measured by echocardiography and the inotropic response to the infusion of isoproterenol (0.02 μg/kg/min for 5 min) was studied in 25 hypertensive patients without LVH [H(-)] and 30 hypertensive patients with LVH [H(+)]. LVH was determined by echocardiography. Age, gender, heart rate, systolic and diastolic blood pressures, LV end-systolic and end-diastolic diameters, and FS were matched between the groups. The tests were performed before introduction of antihypertensi ve treatment or 4 weeks after its discontinuation. ESS showed a significant inverse linear relation with FS in all the subjects before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of FS corrected for the decrease of ESS (ΔFS/-ΔESS), that is, the slope of the change of the relation between FS and ESS. The change in ΔFS/-ΔESS was significantly smaller (0.49 ± 0.15 cm²/g, mean ± SD) in H(?) than in H(+) patients (1.01 ± 0.57 cm²/g) (p < 0.001). It is concluded that, compared with the H(+) group, adrenergic response is depressed in H (?) patients. This depression might be etioloically related to the phenomenon that LVH did not develop in the H(?) group in spite of the same level of pressure load as in the H(+) group.     

Influence of autonomic neuropathy upon left ventricular dysfunction in insulin-dependent diabetic patients

BACKGROUND: Diabetic cardiomyopathy is a well-defined complication of diabetes that occurs in the absence of ischemic, vascular, and hypertensive disease. HYPOTHESIS: The study was undertaken to test the relationship among autonomic neuropathy (AN), 24-h blood pressure (BP) profile, and left ventricular function. METHODS: Nineteen type-1 diabetic patients underwent autonomic tests and echocardiographic examination. Patients were divided according to the presence (AN+) or absence (AN-) of AN. RESULTS: In the AN+ group (n = 8), the E/A ratio at echo was lower than in the AN- group (n = 11) (1.1 +/- 0.3 vs. 1.6 +/- 0.3; p < 0.005). Systolic and diastolic BP reductions during sleep were smaller in the AN+ than in the AN- group (6.6 +/- 6.6 vs. 13.0 +/- 4.3%; p < 0.03 for systolic and 12.8 +/- 6.8 vs. 20.0 +/- 4.0% for diastolic BP reduction; p < 0.03, respectively). Considering all patients, the E/A ratio correlated inversely with awake diastolic BP (r - 0.63; p = 0.005); sleep systolic BP (r - 0.48; p = 0.04), and sleep diastolic BP (r - 0.67; p = 0.002). The AN correlated with diastolic interventricular septum thickness (r 0.57; p = 0.01), sleep systolic BP (r 0.45; p = 0.05), sleep diastolic BP (r 0.54; p = 0.02), and correlated inversely with systolic and diastolic sleep BP reduction (r - 0.49; p = 0.03 and r - 0.67; p = 0.002, respectively). Finally, E/A ratio and AN score correlated between themselves (r - 0.6; p = 0.005). CONCLUSION: Our results suggest that left ventricular diastolic dysfunction may be detected very early in type-1 diabetic patients with AN. Parasympathetic lesion and nocturnal elevations in BP could be the link between AN and diastolic ventricular dysfunction.     

Quantitative Doppler tissue imaging as a correlate of left ventricular contractility

Doppler tissue imaging is a new noninvasive imaging modality that allows quantitation of the low intensity, high amplitude Doppler shifts in the range of myocardial tissue motion. This study was performed to test the hypothesis that Doppler tissue imaging may provide unique information reflecting left ventricular systolic function, and to test the relationship between myocardial tissue velocity and noninvasive measures of ventricular contractility. Nine patients with mild or moderate mitral insufficiency and no regional wall motion abnormality were studied during dobutamine stress echocardiography. Left ventricular ejection fraction and peak systolic velocity of the sub- endocardial left ventricular posterior wall were quantified at baseline and at peak stress and compared with estimated peak dP/dt. During dobutamine infusion, ejection fraction increased from 41.7±22.2 (range 14 to 70) % to 56.6±27.9 (range 17 to 84) % (p=0.001), peak systolic velocity increased from 22.7±4.2 (range 18 to 28) mm/sec to 35.3±10.1 (range 20 to 47) mm/sec (p=0.004), and dP/dt increased from 1050±322 (range 613 to 1574) mm Hg/sec to 1766±768 (range 936 to 3000) mm Hg/sec (p=0.01). Although there were good correlations between left ventricular dP/dt and both ejection fraction (R=0.75) and peak systolic velocity (R=0.81), the correlation between change in dP/dt and change in myocardial velocity (R=0.75) was better than that between change in dP/dt and change in ejection fraction (R=0.36). These data support the hypothesis that myocardial velocity determined with Doppler tissue imaging reflects myocardial contractility, and that catecholamine- induced alteration in contractility is better reflected by changes in myocardial velocity than by changes in ejection fraction.     

Radionuclide assessment of a normal left ventricular response to exercise in patients without evidence of heart disease

The aim of this study was to define normal left ventricularperformance at rest and during supine bicycle exercise withequilibrium radionuclide ventriculography in a normal populationother than young healthy volunteers. Thirty-one patients (meanage 45 years ± 9 SD) with chest pain of varying originandno evidence of heart disease proven by means of noninvasiveand invasive techniques were studied. Left ventricular ejectionfraction (LVEF) at rest averaged 0.64 ± 007 SD and increasedwith peak exercise to 0.73 ± 008 SD (P<0.005). Changein LVEF from rest to maximum exercise ranged within 0–0.19.Six patients (19%) failed to augment LVEF with exercise to morethan 0.05; none of the patients dropped LVEF during exercise.Multivariate analysis revealed no significant predictors ofLVEF response to exercise. However, there was a tendency thatresting LVEF and enddiastolic volume index with exercise mightinfluence LVEF response to exercise. Peak left ventricular ejectionrate (LVER) at rest averaged 3.3s^–1 ± 0.6 SD andincreased to 51 s^–1 ± 11 SD (P<0.005) with exercise.Peak left ventricular early filling rate (LVFR) was 2.8s^–1± 0.6 SD at rest and was measured 5.5 s^–1 ±l.3 SD at maximum exercise (P<0.005). Left ventricular enddiastolicvolume (EDV) did not change significantly from rest to maximumexercise, whereas left ventricular endsystolic volume (ESV)decreased to 79% ± 19 SD (P<0.01) of the value atrest. In conclusion, in a normal population other than healthy youngvolunteers LVEF does not necessarily have to increase with exercise.Moreover, besides an augmentation of heart rate a normal leftventricular response to supine exercise is associated with anincrease of LVER and LVFR, a decrease in ESV and no significantchange in EDV, suggesting augmented contractility and a virtuallynegligible role of the Frank-Starling mechanism during exercise.     

Augmented response in plasma brain natriuretic peptide to dynamic exercise in patients with left ventricular dysfunction and congestive heart failure

OBJECTIVES: We have previously demonstrated that patients with symptomatic congestive heart failure (CHF), but not with asymptomatic left ventricular dysfunction (LVD), have augmented plasma atrial natriuretic peptide (ANP) response to exercise. Plasma brain natriuretic peptide (BNP) response to exercise is less extensively studied. The aim of this study was to determine whether responses of plasma BNP during exercise normalized for exercise workload are altered in patients with LVD and CHF. SUBJECTS AND METHODS: Twenty-nine patients with LVD, 32 patients with CHF (NYHA classes II-III) and 27 age-matched control subjects were studied. Ventilatory, plasma ANP and BNP responses were assessed during symptom-limited cardiopulmonary exercise testing. Plasma natriuretic peptide levels were measured at rest and immediately after peak exercise. The increment in plasma BNP was divided by the increment in oxygen uptake (VO2) from rest to peak exercise, and this ratio [BNP exercise ratio: (peak BNP - rest BNP)/(peak VO2 - rest VO2)] was compared amongst the three groups. RESULTS: Peak VO2 (Control, LVD and CHF: 28.2 +/- 1.7, 21.1 +/- 1.8, 16.2 +/- 0.6 ml, min(-1) kg(-1), respectively), anaerobic threshold and peak workload became smaller as heart failure worsened. Resting and peak plasma ANP levels were significantly higher only in CHF, whilst resting and peak plasma BNP levels displayed a significant and continuous increase from normal subjects to LVD and CHF. The ANP exercise ratio (1.25 +/- 0.36, 2.61 +/- 0.57, 7.72 +/- 1.65, ANOVA P = 0.0002) was significantly higher only in patients with CHF, whilst the BNP exercise ratio (0.35 +/- 0.10, 2.60 +/- 0.69, 4.98 +/- 0.97, ANOVA P = 0.0001) was significantly higher in patients with LVD and became progressively higher in patients with CHF. CONCLUSIONS: These data showed that the BNP exercise ratio, an exercise plasma BNP response normalized with exercise workload, was augmented in patients with LVD, and became progressively higher in CHF, suggesting that an augmented exercise BNP ratio exists early in the course of developing CHF.     

Cardiac correlates of exercise induced pulmonary hypertension in patients with chronic heart failure due to left ventricular systolic dysfunction

BACKGROUND: Patients with chronic heart failure (CHF) due to left ventricular systolic dysfunction (LVSD) may develop pulmonary hypertension at rest and during exercise. The cardiac correlates of pulmonary hypertension have been ascertained in the resting state, but seldom during exercise in these patients. AIMS: We sought to determine the cardiac correlates of exercise induced pulmonary hypertension in patients with LVSD by monitoring the estimated pulmonary artery systolic pressure (PASP) by continuous Doppler echocardiography during semirecumbent bicycle exercise. METHODS: Eighty-five patients (mean age 57 +/- 13 years, 75% male) with CHF due to LVSD (LV ejection fraction [EF] <45%, mean LVEF 26 +/- 8%) were studied. RESULTS: Mitral effective regurgitant orifice area and E-wave were independent predictors of resting PASP. Resting PASP and exercise induced changes in PASP were unrelated (r =-0.08, P = 0.45). Decrease in LV end-systolic volume, increase in left atrial (LA) area, resting LV asynchrony, and decreased tricuspid annular plane systolic excursion (TAPSE) were independent predictors of exercise PASP. CONCLUSIONS: Resting LV asynchrony, impaired LV contractile reserve, and increase in LA dilatation correlate with the severity of exercise induced pulmonary hypertension in patients with CHF due to LVSD, while right ventricular systolic dysfunction is inversely related to the severity of exercise induced pulmonary hypertension.     

Influence of exercise training soon after myocardial infarction on regional myocardial perfusion and resting left ventricular function.

There is scant information regarding the effect of exercise training begun soon after hospital discharge for myocardial infarction (MI) with respect to subsequent improvement in exercise tolerance, enhancement of regional myocardial perfusion, or left ventricular function. Accordingly, 19 post-MI patients (mean age 53 +/- 7 years) underwent treadmill exercise quantitative thallium-201 (Tl-201) scintigraphy and rest radionuclide angiography (RNA) prior to and after 12 weeks of thrice-weekly exercise training which was targeted to 70-85% of maximum exercise heart rate achieved. Training was begun at 25 +/- 3 days after hospital discharge. Eight Tl-201 scan segments were each scored from 1-6 points based upon uptake and washout criteria with 6 being the most severe defect (greater than 50% reduction in Tl-201 events with no delayed redistribution). When matched to the pretraining peak workload on exercise testing, 12 weeks of training significantly lessened heart rate (120 +/- 4 to 97 +/- 4, p less than 0.001), peak systolic blood pressure (142 +/- 6 to 129 +/- 5 mmHg, p less than 0.01), and significantly reduced double product [17.2 +/- 10.8 to 12.7 +/- 9 (x10(3), p less than 0.001]. Training was associated with a reduction of exercise-induced ST depression or angina (42 to 16%) which was not statistically significant. The mean resting by RNA ejection fraction was 50 +/- 3% prior to training and 51 +/- 3% after training. There was no significant change in overall Tl-201 defect score or the number of defect regions per patient scan comparing pre- and post-training scintigrams.(ABSTRACT TRUNCATED AT 250 WORDS)     

Emergency coronary angioplasty in patients with severe left ventricular dysfunction or cardiogenic shock after acute myocardial infarction

Emergency percutaneous transluminal coronary angioplasty (PTCA) was performed during an acute myocardial infarction (AMI) after either systemic or intracoronary thrombolytic therapy in six patients with severe ischaemic left ventricular dysfunction or cardiogenic shock, among 37 patients (17%) who were treated with PTCA during AMI over a 13-month period. Thrombolytic therapy with streptokinase (1.5 x 10 Units) was initiated after a mean (+/- SD) time delay of 5.5 +/- 1.3 h from the onset of symptoms. The infarct-related artery was found to be occluded (TIMI grade 0-1) in three patients and partially reperfused (TIMI grade 2) in the remaining patients at baseline coronary angiography. Intracoronary administration of urokinase (100-200,000 Units) was ineffective in those patients failing systemic thrombolysis and resulted in only a slight increase of residual lumen in three patients. The coronary artery could be opened by a guidewire mechanical technique in patients with persistent coronary artery occlusion and coronary dilation could be done in all patients. The mean percentage diameter stenosis of the infarct-related vessel was reduced from 98.8 +/- 2% to 27 +/- 11% (P less than 0.005). After the procedure, left ventricular ejection fraction increased from 27 +/- 8% to 41 +/- 7% (P less than 0.02), systemic blood pressure and cardiac index increased respectively from 86 +/- 10 to 126 +/- 14 mmHg (P less than 0.005) and from 2.2 +/- 0.6 to 3.3 +/- 0.6 (P less than 0.01). Left ventricular end-diastolic pressure decreased from 26 +/- 8 to 18 +/- 3 mmHg (P less than 0.05). Severe mitral regurgitation was relieved in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular diastolic filling in patients with left ventricular dysfunction

The pattern of abnormal left ventricular diastolic filling and its specificity in coronary disease patients with severe left ventricular dysfunction has received little attention. We evaluated the left ventricular diastolic filling curve derived from gated blood pool scans in 21 normals, 61 coronary disease patients with ejection fractions less than or equal to 30%, and 51 congestive cardiomyopathy patients with ejection fraction less than or equal to 30%. The peak filling rate (PFR), peak ejection rate (PER), PFR/PER and the % stroke volume filled at 1/3 of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined for each group. The PFR and PER were reduced in both coronary disease and congestive cardiomyopathy groups. The PFR/PER was increased in the coronary disease group (1.19 +/- 0.28) and congestive cardiomyopathy group (1.21 +/- 0.32) as compared to normals (0.93 +/- 0.20, P less than 0.001). A greater %SV-1/3 DT and %SV-RFP were noted in both coronary disease and congestive cardiomyopathy groups. Coronary disease and congestive cardiomyopathy patients with a mean pulmonary capillary pressure (PCP) greater than or equal to 18 mm Hg had a greater PFR/PER, %SV-1/3 DT, and %SV-RFP than patients with a PCP less than 18 mm Hg. An abnormal and nonspecific pattern of left ventricular diastolic filling is present in both coronary disease and congestive cardiomyopathy patients and is characterized by an increased PFR/PER, a greater %SV-1/3 DT, and a greater %SV-RFP. This pattern may be related to elevated PCPs.     

Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy

The aim this study was to evaluate systolic and diastolic function in volume overload induced myocardial hypertrophy in rats. Volume overload myocardial hypertrophy was induced in thirteen male Wistar rats by creating infrarenal arteriovenous fistula (AVF). The results were compared with a SHAM operated group (n=11). Eight weeks after surgery, tail-cuff blood pressure was recorded, then rats were sacrificed for isolated heart studies using Langendorff's preparation. AVF rats presented increased left and right ventricular weights, compared to controls. The increased normalized ventricular volume (V0/LVW, 0.141+/-0.035 mL/g vs. 0.267+/-0.071 mL/g, P<0.001) in the AVF group indicated chamber dilation. Myocardial hydroxyproline concentration remained unchanged. There was a significant decrease in +dP/dt (3318+/-352 mm Hg s(-1) vs. 2769+/-399 mm Hg s(-1); P=0,002), end-systolic pressure-volume relation (246+/-56 mm Hg mL(-1) vs. 114+/-63 mm Hg mL(-1); P<0,001), and -dP/dt (1746+/-240 mm Hg s(-1) vs. 1361+/-217 mm Hg s(-1), P<0.001) in the AVF group, which presented increased ventricular compliance (DeltaV(25): SHAM=0.172+/-0.05 mL vs. AVF=0.321+/-0.072 mL, P<0.001) with preserved myocardial passive stiffness (Strain(25): SHAM=13.5+/-3.0% vs. AVF=12.3+/-1.9%, P>0.05). We conclude that volume-overload induced hypertrophy causes myocardial systolic and diastolic dysfunction with increased ventricular compliance. These haemodynamic features help to explain the long-term compensatory phase of chronic volume overload before transition to overt congestive heart failure.     

Left ventricular response to exercise in aortic stenosis: an exercise echocardiographic study

BACKGROUND: While normal at rest, left ventricular (LV) systolic function may become abnormal during exercise in patients with aortic stenosis. Once contraindicated in patients with aortic stenosis, exercise testing is now recommended in asymptomatic patients with aortic stenosis to elicit symptoms and thereby ascertain the need for aortic valve replacement. However, the clinical significance of an abnormal LV response to exercise in asymptomatic patients with aortic stenosis remains unknown. OBJECTIVE: The aim of this study was to evaluate the clinical implications of an abnormal LV response during exercise in the setting of aortic stenosis. METHODS: We monitored the LV response to exercise by 2D-Doppler echocardiography during a symptom limited semirecumbent bicycle exercise in 50 patients with tight aortic stenosis (aortic valve area < or = 1.0 cm(2)) and a normal LV systolic function (LV ejection fraction, EF > or = 50%) and followed them for an average of 11 months. RESULTS: Twenty patients had an abnormal LV response to exercise with a mean decrease in LV EF from 64 +/- 10 to 53 +/- 12% while 30 patients had a normal LV response to exercise with a mean increase in LV EF from 62 +/- 7 to 70 +/- 8%. Patients with an abnormal LV response during exercise were more likely to develop symptoms during exercise than patients with a normal LV response: 80% versus 27% (P< 0.0001). The survival free of cardiac events was significantly lower in patients with abnormal LV response to exercise than in patients with a normal response (P = 0.03). CONCLUSION: Exercise echocardiography provides objective data that facilitate interpretation of exercise elicited symptoms in asymptomatic patients with severe aortic stenosis. In addition, an abnormal LV response to exercise may predict a poor outcome.     

老年左心室功能不全患者行冠状动脉内支架术

目的　评价左心室功能不全对老年冠心病患者选择性冠状动脉内支架术安全性和远期预后的影响。方法　4 76例老年冠心病患者行选择性冠状动脉内支架术 ,其中 73例左心室射血分数 <4 0 % (左心室功能不全组 ) ,4 0 3例左心室射血分数≥ 4 0 % (对照组 )。分析两组患者手术结果和远期预后。结果　两组支架术成功率 (95 .8%和95 .9% )和手术并发症相似 (2 .2 %和 2 .7% ,P >0 .0 5 )。在 (16± 8.4 )个月随访期中 ,左心室功能不全组死亡率较对照组显著增高 (14 .1%和 3.2 % ,P =0 .0 0 1)。多因素分析显示 ,左心室射血分数是老年患者冠状动脉内支架术后远期死亡的独立预测因素 (RR 0 .95 0 ,95 %CI0 .919～ 0 .981,P =0 .0 0 2 )。结论　左心室功能不全的老年冠心病患者选择性冠状动脉内支架术安全 ,但远期死亡风险较高     

Left ventricular function and exercise capacity in patients with slow coronary flow

Background: Endothelial and microvascular dysfunction have been implicated in slow coronary flow (SCF). How and to what extent do these etiological factors affect left ventricular (LV) function and exercise capacity? Aim: The aim of the study was to evaluate LV systolic and diastolic function by pulsed tissue Doppler imaging (TDI) in SCF patients and their effects on exercise capacity. Subjects and methods: Sixty SCF patients and 20 control subjects were included in the study. Echocardiographic examination, treadmill exercise test, and TDI were performed. Isovolumic myocardial acceleration (IVA) and myocardial performance index (MPI) were measured. Results: TDI mean parameters for systolic and diastolic LV function were significantly impaired in SCF group with decreased Sa, IVA, Ea/Aa, and increased MPI (0.31 ± 0.06 vs. 0.26 ± 0.04, P < 0.01) compared to control. There was significant correlation between thrombolysis in myocardial infarction (TIMI) frame count and TDI mean parameters for LV systolic function (Sa & IVA, r =?0.53, P < 0.01 & r =?0.36, P < 0.05, respectively). Mean TIMI frame count was correlated with MPI and E/Ea. SCF patients had poorer peak exercise capacity than the controls (9.9 ± 1.9 METs vs. 12.7 ± 2.3, P < 0.01) with significant negative correlation with mean TIMI frame count (r =?0.46, P < 0.01). Conclusion: There is impairment of LV systolic and diastolic function in SCF patients with clinical impact on exercise capacity which emphasizes the importance of close follow‐up of these patients for risk stratification. (Echocardiography 2012;29:158‐164)     

Left ventricular dysfunction in normotensive Type 1 diabetic patients: the impact of autonomic neuropathy.

AIMS: The pathophysiological mechanisms responsible for increased cardiovascular mortality in diabetic autonomic neuropathy (AN) are largely unknown. The aim was to determine the relative role of AN in the pathogenesis of cardiac diastolic dysfunction and left ventricular hypertrophy in Type 1 diabetes. METHODS: Ten Type 1 diabetic patients with AN, defined by cardiovascular tests (AN+) and 10 age- and sex-matched patients without neuropathy (AN-) as well as 10 healthy subjects (C) participated in the study. Left ventricular diastolic function was assessed by Doppler echocardiography, whilst systolic function was evaluated by cine magnetic resonance (MR) imaging. RESULTS: Doppler echocardiography showed a significant decrease in E/A ratio, i.e. the ratio between peak Early transmitral filling velocity during early diastole (E-wave) and peak transmitral Atrial filling velocity during late diastole (A-wave), in AN+ compared with C (P < 0.01) [0.95 +/- 0.08 (mean +/- sem) (AN+); 1.19 +/- 0.09 (AN-); 1.33 +/- 0.10 (C)]. The E-wave deceleration time was significantly shorter in AN+ compared with AN- and C (P < 0.02) [178 +/- 7 ms (AN+); 203 +/- 9 ms (AN-); 205 +/- 9 ms (C)]. Cine MR imaging showed a significantly greater left ventricular mass index in AN+ compared with C [103 +/- 4 g/m(2) (AN+) vs. 98 +/- 7 (AN-) and 92 +/- 4 g/m(2) (C), P < 0.05]. CONCLUSION: Autonomic neuropathy is associated with left ventricular hypertrophy and diastolic dysfunction in Type 1 diabetic patients.     

The relationship between flow-mediated dilatation and left ventricular function in type 2 diabetic patients with microalbuminuria

Objective The aim of this study was to assess the relationship between flow-mediated dilatation (FMD) and left ventricular (LV) systolic and diastolic function in type 2 diabetic patients with or without microalbuminuria. Research Design and Methods We prospectively evaluated 68 consecutive patients (36 women, 32 men; mean age 57±11 yr) with type 2 diabetes mellitus (DM). Patients were divided into two groups according to whether or not they had microalbuminuria: group 1 (n=29, mean age 58±10 yr) with microalbuminuria and group 2 (n=39, mean age 56±10 yr) without microalbuminuria. LV function was assessed by classical methods and Doppler tissue imaging (DTI). Left ventricular ejection fraction (EF), interventricular (IVS) and posterior wall (PW) thickness, peak early (E) and late (A) transmitral filling velocities, their ratio (E/A) and deceleration time of the mitral E wave (DT), LV isovolumetric relaxation time (IVRT), flow propagation of velocity (Vp), and E/Vp were evaluated by conventional echocardiography. Early diastolic (Em), late diastolic (Am), and peak systolic (Sm) mitral annular velocities were measured. Em/Am and the ratio of early diastolic mitral inflow velocity to Em (E/Em), which is a reasonably good index for predicting elevated LV filling pressure, were calculated by DTI. Endothelial function, measured as flow-mediated dilatation of the brachial artery using ultrasound, was calculated in two groups. Results FMD was lower in those with microalbuminuria than those without (8.8±6.44% vs 12.6±7.24%, p=0.03). Group 1 had longer DT (223±39 ms vs 199±37 ms, p=0.01) and longer IVRT (109±13 ms vs 100 ±13 ms, p=0.03) than that of group 2 with conventional echocardiography. Group 1 had significantly lower Em/Am (0.79±0.27 cm/s vs 1.02±0.44 cm/s, p=0.01), lower Vp (40.4±9.98 vs 50.4±19.01 cm/s, p=0.01) than that of group 2. Group 1 had significantly higher serum creatinine (1±0.33 mg/dL vs 0.7±0.19, p=0.001). In logistic regression analysis, FMD was the only variable independently related to microalbuminuria. FMD was positively correlated with EF (r=0.43, p=0.02) and E/A (r=0.40, p=0.03), and negatively correlated with E/Em (r=0.41, p=0.04) and E/Vp (r=0.41), p=0.04) only in patients with microalbuminuria. Conclusion It was found that left ventricular diastolic function and FMD are impaired in type 2 diabetic patients with microalbuminuria. FMD may be related to LV diastolic dysfunction only in patients with microalbuminuria.     

ACE inhibition with ramipril improves left ventricular function at rest and post exercise in patients with stable ischaemic heart disease and preserved left ventricular systolic function.

AIMS: To assess the effects of 6 months intervention with +ramipril on resting and post exercise left ventricular function in patients with stable ischaemic heart disease and preserved left ventricular systolic function. METHODS and RESULTS: Patients (n=98, age 65+/-9 years, 37% women) were randomized to double-blind treatment with ramipril 5 mg. day(-1)(n=32), ramipril 1.25 mg. day(-1)(n=34), or placebo (n=32). Resting and post maximum exercise echocardiography/Doppler examinations were performed at baseline and after 6 months. Changes over 6 months in resting transmitral E-wave deceleration time (Edt) and Edt adjusted for heart rate (Edt/RR) differed between the ramipril 5 mg, ramipril 1.25 mg, and placebo groups: Edt 24+/-82, -1+/-69, and -29+/-64 ms, respectively, P=0. 012; Edt/RR 30+/-105, 2+/-61, and -28+/-69 ms, respectively, P=0.015. Changes in the difference between resting and post exercise Edt/RR also varied between groups: -53+/-137, -28+/-118, and 35+/-101 ms, respectively, P=0.029. No differences in E/A indices were noted. Resting atrioventricular plane displacement improved in the combined ramipril groups vs the placebo group: 0.2+/-0.8 vs -0.2+/-1.3 mm, P<0.05.Conclusion Six months ramipril treatment in patients with stable ischaemic heart disease and preserved left ventricular systolic function improved resting left ventricular function and reduced the exercise induced diastolic filling abnormalities usually seen in these patients.