Left and right ventricular systolic long-axis function and diastolic function in patients with takotsubo cardiomyopathy

Aims: Takotsubo cardiomyopathy is characterized by apical wall motion abnormalities without coronary stenosis. Limited information is available on the genesis of the underlying reversible contractile disorder. Our objective in this prospective study was to investigate biventricular changes in systolic long‐axis function and diastolic parameters in the acute phase and after recovery. Methods and results: Thirteen consecutive patients were examined by echocardiography and coronary angiography at admission and again by echocardiography after 3 months. Amplitudes, systolic and diastolic velocities of the mitral and tricuspid annuli and conventional diastolic parameters were measured. Systolic long‐axis shortening of the left ventricle (LV) and right ventricle (RV) improved from 9·6 ± 2·2 mm to 11·2 ± 1·9 mm (P = 0·02) and from 21·3 ± 3·6 mm to 24·1 ± 2·8 mm (P = 0·02), respectively. LV systolic, early and late diastolic velocities measured by pulsed‐wave tissue Doppler also improved, while additional conventional diastolic parameters of the LV and RV diastolic function were unchanged. Conclusions: Takotsubo cardiomyopathy temporarily affects systolic LV and RV function, while most diastolic parameters remain unchanged.     

Evidence of diminished coronary flow in pulmonary hypertension ‐ explaining angina pectoris in this patient group?

Background: Many patients with pulmonary hypertension (PH) have symptoms of angina without evidence of occlusive coronary artery disease. For the first time, this study addresses the influence of progressively increasing pulmonary artery pressure (PAP) on left anterior descending artery flow in a rat model of PH. The role of pulmonary artery dilatation, septal wall motion abnormality, cardiac output or diastolic blood pressure in determining coronary blood flow (CBF) during PH was determined. Methods: Pulmonary hypertension was induced in 6‐week‐old female nude rats (n = 44) using monocrotaline. Animals underwent right heart catheterization and echocardiography, and blood pressure measurement was taken at baseline, 21 and 35 days. Results: A total of 103 echocardiographic studies were carried out at three fixed time points in rats with variable PAP. CBF decreased from 46·6 ± 14·3 to 24·7 ± 12·3 cm s^?1 (P<0·001) over time. Pulmonary artery diameter increased from 2·30 ± 0·19 to 2·83 ± 0·30 mm (P<0·001), and left ventricular (LV) cardiac output decreased from 143 ± 23 to 78 ± 30 ml min^?1 (P<0·001). Using observed solution estimates of 0·00170 (P = 0·0005) and ?1·75 (P = 0·006) for these variables, we calculated that CBF increased by 5·90 cm s^?1 (15·6%, CI: 14·5–17·1%) or decreased by ?4·86 cm s^?1 (?12·9%, CI: ?14·1–11·9%) for every standard deviation increase in LV cardiac output or pulmonary artery diameter, respectively. CBF decreased significantly with increasing PAP. Pulmonary artery diameter and LV cardiac output appear to be independent determinants of coronary flow in PH. Conclusions: Coronary flow reduction in murine PH has potential to be clinically meaningful and should therefore further studied in a clinical trial.     

A reproducible and stable model of acute ischaemic left ventricular failure in dogs

Summary. A model of acute ischaemic left ventricular (LV) failure is presented. In closed-chest anaesthetized dogs 50 μm plastic microspheres were injected repeatedly into the left main coronary artery over a period of about 40 min. The injections effected stepwise elevations of LV end-diastolic pressure (Lvedp ). Thus, Lvedp could be increased to a desired level, about 20 mmHg, in a very controlled manner. All dogs developed signs of markedly depressed LV performance. Haemodynamic conditions stabilized about 60 min after embolization, and then remained essentially stable for at least 75 min. Lvedp increased from 5·7 ± 0·6 before to 26·1 ± 0·8 mmHg (mean ± SEM) 60 min after embolization. The maximum LVdP/dt decreased from 2696 ± 169 to 1823 ± 98 mmHg·s^-1, cardiac output decreased from 2·81 ± 0·20 to 1·98 ± 0·14 1·min^-1 and mean aortic blood pressure decreased from 144±4 to 127±3 mmHg, while total peripheral resistance increased from 56±3 to 69±3 mmHg·l^-1·min. Myocardial blood flow decreased from 103±7 to 79 ±6 ml·min^-1·100 g^-1 and myocardial oxygen consumption decreased from 12·5±0·9 to 8·3·0·8 ml· min^-1·100 g^-1. Myocardial uptake of lactate and free fatty acids decreased markedly. Electrocardiography showed signs of acute ischaemia. There were no deaths due to ventricular fibrillation. Morphological studies showed multiple small infarcts throughout the entire LV. In conclusion, repeated coronary embolization with 50 μm plastic microspheres, guided by the rise of Lvedp represents a simple and reproducible method for induction of uniform and stable acute LV failure.     

Mean Myocardial Velocity Mapping in Quantifying Regional Myocardial Contractile Reserve in Patients with Impaired Left Ventricular Systolic Function: Doppler Myocardial Imaging Study

The aim of this study was to use Doppler myocardial imaging–derived mean myocardial velocity (MMV) at baseline and during low-dose dobutamine stress echocardiography (DSE) to quantify regional contractile reserve of the left ventricle (LV). Sixteen patients (mean age 59 ± 7 years) with coronary artery disease and regional left ventricular wall motion abnormalities were studied. During each increment of Dobutamine infusion, 6 2-dimensional transthoracic apical images were acquired in standard gray-scale and Doppler myocardial imaging modes at 30° steps over 180°. For the analysis, the LV was divided into 18 segments. For each segment, both wall motion score and MMV obtained in systole and both early and late diastole were measured at baseline and at each stage of DSE. In viable segments by wall motion score, MMV increased during DSE in systole and in early and late diastole. In contrast, in nonviable segments, MMV did not change during DSE. Mean myocardial velocity mapping is a promising new approach to quantify regional myocardial contractile reserve of the LV. (J Am Soc Echocardiogr 2000;13:96-107.)     

Simultaneous quantification of myocardial perfusion,oxidative metabolism,cardiac efficiency and pump function at rest and during supine bicycle exercise using 1‐11C‐acetate PET – a pilot study

Background: PET using 1‐¹¹C‐acetate (ACE‐PET) applied at rest is used for measuring absolute myocardial blood flow (MBF) and oxidative metabolic rate (k_mono). We evaluated the feasibility of quantitative ACE‐PET during exercise. Methods: Five endurance athletes underwent dynamic PET scanning at rest and during supine bicycle stress. Exercise was maintained at a workload of 120 Watt for 17 min. The rate‐pressure product (RPP) was recorded repeatedly. MBF, k_mono in left (LV) and right (RV) ventricular wall, cardiac output (CO), cardiac efficiency and a lung uptake value reflecting left heart diastolic pressures were calculated from the PET data using previously validated models. Results: MBF increased from 0·71 ± 0·17 to 2·48 ± 0·25 ml min^?1 per ml, LV‐k_mono from 0·050 ± 0·005 to 0·146 ± 0·021 min^?1, RV‐k_mono from 0·023 + 0·006 to 0·087 + 0·014 min^‐1, RPP from 4·7 ± 0·8 to 13·2 ± 1·4 mmHg × min^?1 × 10³ and Cardiac Output from 5·2 ± 1·1 to 12·3 ± 1·2 l min ^?1 (all P < 0·001). Cardiac efficiency was unchanged (P = 0·99). Lung uptake decreased from 1·1 ± 0·2 to 0·6 ± 0·1 ml g^?1 (P < 0·001). Discussion: A number of important parameters related to cardiac function can be quantified non‐invasively and simultaneously with a short scanning protocol during steady state supine bicycling. This might open up new opportunities for studies of the integrated cardiac physiology in health and early asymptomatic disease.     

Myocardial velocities measured during adenosine, dobutamine and supine bicycle exercise: a tissue Doppler study in healthy volunteers

Background: Dobutamine stress echocardiography (DSE) quantified by tissue Doppler (TVI) have improved the diagnostic capacity of the procedure. Quantification of other stress modalities, e.g. adenosine stress echo (ASE) and exercise stress echocardiography (ESE) are necessary for assessing any pathophysiological differences in different forms of stress. Methods: Ten healthy individuals underwent ASE, DSE, and ESE during a span of 2–5 days. Left ventricular (LV) apical images at rest and peak stress (max) were postprocessed using TVI on a GE System FiVe equipment. ECG‐derived QRS duration (QRSD, ms), heart rate (HR, bpm), TVI‐estimated basal systolic velocities (S2V, cm s^?1), ejection time (S2T, ms) and strain (S, %) were computed off‐line and compared. Longitudinal displacement imaging, tissue tracking, was also made. Results: Data for ASE, DSE and ESE during peak stress were (HR: 84 ± 12***, 142 ± 19, 137 ± 27; P<0·001) (QRSD: 92 ± 18**, 74 ± 13, 79 ± 9; P<0·05), (S2T: 307 ± 34***, 175 ± 53, 192 ± 25; P<0·001) and (S%: 26·0 ± 3·0, 21·2 ± 7·3, 22·1 ± 5·1; P = n.s.) respectively. Velocity response, registered in the LV septum at max, was lowest during ASE (7·4 ± 1·4) highest during DSE (13·0 ± 2·7; P<0·001 versus ASE) and somewhat intermediate during ESE (11·3 ± 3·5; P<0·001 versus ASE). In contrast, strain and displacement did not differ. Conclusion: ASE evokes significantly less LV systolic response compared with both DSE and ESE. Increased velocity (P<0·05 versus rest) and strain (P>0·05) response at a much lower HR indicates that adenosine has minor effects on contraction presumably secondary to vasodilatation. Powerful chronotropic response to DSE and ESE is probably prerequisite for strong velocity response at the expense of strain and displacement. TVI‐assisted stress echocardiography thereby shows different LV systolic response in healthy individuals, depending on stress modality.     

Abnormal Global Left Ventricular Relaxation Occurs Early During the Development of Pharmacologically Induced Ischemia

In animal and human models, left ventricular (LV) diastolic function has been observed to be highly sensitive to myocardial ischemia. The response of LV diastolic parameters to pharmacologically induced ischemia, however, has not been characterized and might be important in the interpretation of dobutamine stress echocardiography. Eight mongrel dogs, in which were inserted a high-fidelity micromanometer LV catheter, coronary sinus sampling catheter, and ultrasonic coronary artery flow probe, underwent intravenous dobutamine infusion at escalating doses both before (control protocol) and after (ischemia protocol) creation of left anterior descending coronary artery stenosis with a hydraulic cuff occluder adjusted to maintain resting coronary artery flow but attenuate reactive hyperemia. At each dobutamine dose, epicardial short-axis 2-dimensional echocardiographic images and hemodynamic measurements were obtained. LV diastolic function was examined by calculation of peak (–)dP/dt and the time constant of isovolumic relaxation (τ). The dobutamine infusion protocol was terminated on the earliest recognition of an anterior wall motion abnormality. Peak (+)dP/dt normalized for developed isovolumetric pressure was calculated as a relatively load-independent index of global LV contractile function. Dobutamine infusion with and without ischemia resulted in comparable changes in heart rate and (+)dP/dt/IP, with no change in LV end-diastolic or -systolic pressure. The magnitude of peak (-)dP/dt increased less during the ischemia (1231 ± 109 to 1791 ± 200 mm Hg/sec) versus the control (1390 ± 154 to 2432 ± 320 mm Hg/sec) protocol (P < .05). Similarly, the observed decrease in τ was less during the ischemia (53 ± 3 to 38 ± 4 msec) than the control (51 ± 5 to 23 ± 3 msec) protocol, corresponding to a slower rate of relaxation (P < .05). In addition, the smaller decrease in τ was observed at the dobutamine dose before the dose at which an echocardiographic wall motion abnormality was first recognized. Dobutamine-induced ischemia is associated with abnormal LV diastolic function. In addition, these abnormalities seem to occur early in the development of ischemia. These observations extend to pharmacologically induced ischemia prior findings from other models of ischemia, suggesting the high sensitivity of LV diastolic function to the development of myocardial ischemia. (J Am Soc Echocardiogr 1999;12:113-20.)     

Effect of an acute increase in afterload on left ventricular regional wall motion velocity in healthy subjects.

We recorded left ventricular (LV) wall motion velocities before and after angiotensin II infusion by pulsed tissue Doppler imaging in 20 healthy subjects, and evaluated the responses of systolic and diastolic LV function along the long and short axes during an acute increase in afterload. Angiotensin II was administered intravenously to obtain a 30% increase in mean blood pressure. After angiotensin II infusion, LV end-systolic dimension and end-systolic circumferential wall stress increased significantly, and the percentage of LV fractional shortening decreased significantly. Peak first systolic LV wall motion velocity (Sw1 ) along the long axis decreased markedly compared with that along the short axis, and peak second systolic LV wall motion velocity (Sw2 ) along the short axis decreased significantly compared with that along the long axis. Early diastolic LV wall motion velocities along both the long and short axes decreased significantly, whereas atrial systolic LV wall motion velocity did not change. In conclusion, an acute increase in afterload caused a significant decrease in longitudinal fiber shortening during the isovolumic contraction phase (Sw1 along the long axis), circumferential fiber shortening during the ejection phase (Sw2 along the short axis), and LV relaxation during early diastole (early diastolic LV wall motion velocities along both axes) in healthy subjects. Pulsed tissue Doppler imaging may be useful for detecting the effect of various loading conditions on LV wall motion velocities along the long and short axes.     

Cardiovascular response in patients with and without myocardial ischaemia during dobutamine echocardiography stress test for coronary artery disease

Summary. Dobutamine is widely used in cardiac stress testing for coronary artery disease and myocardial viability. To assess the systemic cardiovascular response during dobutamine echocardiography stress testing, we investigated nine patients without myocardial ischaemia (group 1, aged 48 to 72 years) and nine patients with myocardial ischaemia during the test (group 2, aged 53 to 73 years), by use of Doppler/echocardiography and subclavian artery pulse trace calibrated with brachial artery pressures. Peripheral resistance, total arterial compliance, and aortic characteristic impedance were estimated using a 3-element windkessel model of the systemic circulation. During infusion of dobutamine up to 40 μg kg^-1 min^-1, arterial pressure was maintained near baseline levels, whereas heart rate and cardiac index increased, more so in group 1 (mean: 89 and 79%) than in group 2 (58 and 52%; P<0.05 vs. group 1). Peripheral resistance was decreased by ≥32% at peak stress, whereas characteristic impedance was maintained at or above baseline in both groups, and total arterial compliance was not significantly altered. The cardiovascular response in group 2 was not influenced by the wall motion abnormalities. Thus, in these patients the inotropic, chronotropic, and vasodilatory effects of dobutamine balanced the ischaemic impairment of left ventricular function during the stress test.     

Detection of left ventricular dysfunction by Doppler tissue imaging in patients with complete recovery of visual wall motion abnormalities 6 months after a first ST-elevation myocardial infarction

AIMS: The aim of this study was to assess left ventricular (LV) systolic and diastolic function, using Doppler tissue imaging (DTI), in patients with complete recovery of visual wall motion abnormalities six months after a first ST-elevation myocardial infarction (STEMI). METHODS: Out of 90 patients presenting with a STEMI, 68 patients without a history of heart disease were examined by echocardiography before discharge and after 6 months. The patients were compared to 41 age matched healthy subjects (HS). LV function was assessed by visual wall motion and mitral annular velocities using pulsed wave DTI. RESULTS: Sixty-eight patients had visual wall motion abnormalities at baseline. Of these, 19 patients showed complete recovery of wall motion at 6-months follow-up. Patients with complete recovery of wall motion abnormalities had significantly reduced peak systolic and peak early diastolic mitral annular velocities compared to HS at 6 months (8.3 cm s(-1) versus 9.9 cm s(-1), P<0.001 for systolic velocity and 9.3 cm s(-1) versus 13.1 cm s(-1), P<0.001 for diastolic velocity, respectively). CONCLUSION: In patients presenting with a first STEMI, mitral annular systolic and early diastolic velocities assessed by DTI at 6-months follow-up are significantly reduced compared to HS, despite normal standard echocardiographic parameters of LV function. This probably reflects a residual subendocardial damage not detected by conventional echocardiographic methods.     

Left Ventricular Systolic and Diastolic Function in Patients With Apical Ballooning Syndrome Compared With Patients With Acute Anterior ST-Segment Elevation Myocardial Infarction: A Functional Paradox

OBJECTIVE: To compare left ventricular (LV) systolic and diastolic function in patients with apical ballooning syndrome (ABS) and those with acute myocardial infarction (AMI) using 2-dimensional Doppler echocardiography and strain rate imaging (SRI).PATIENTS AND METHODS: We prospectively enrolled patients with newly diagnosed AMI and ABS who had akinetic apical walls. Both 2-dimensional Doppler echocardiography and SRI were performed on hospital day 1 or within 24 hours of primary percutaneous coronary intervention.RESULTS: Twenty-four patients with AMI and 13 patients with ABS (mean ± SD age, 63±15 vs 73±12 years; P=.03) were prospectively enrolled in the study from October 3, 2005 through July 12, 2006. The mean ± SD LV end-diastolic volume was larger (58.1±9.1 vs 45.2±10.6 mL/m²; P<.001) and the mean ± SD LV ejection fraction was lower (35%±6% vs 43%±9%; P=.006) in patients with ABS compared with patients with AMI. The early diastolic mitral annular velocity was similar (0.06±0.02 vs 0.06±0.02 m/s; P=.85) in both groups, but the ratio of early diastolic mitral valve inflow velocity to early diastolic mitral annulus velocity was higher in patients with AMI than in patients with ABS (16.3±6.9 vs 12.2±3.2; P=.05). The systolic strain rate was decreased at the apex in both groups (P=.98). Both the early diastolic strain rate of the apex (0.64±0.24 vs 0.48±0.30 s^-1; P=.04) and the postsystolic shortening index of the apex (61%±15% vs 45%±23%; P=.006) were higher in the patients with ABS than in those with AMI. However, early diastolic SR was higher in the akinetic apical walls of patients with AMI with recovery than those with no recovery (0.64±0.35 vs 0.43±0.25 s^-1; P=.04) and was similar between akinetic apical walls of patients with AMI with recovery and the akinetic apical walls of ABS.CONCLUSION: Compared with patients with AMI, those with ABS showed the functional paradox of worse initial LV systolic function with larger LV size but better LV diastolic function. The early systolic strain rate and postsystolic shortening were greater in patients with ABS than in those with AMI; hence, these measurements can be helpful in distinguishing ABS from AMI and in detecting myocardial viability.ABS = apical ballooning syndrome; AMI = acute myocardial infarction; CAG = coronary angiography; E = early diastolic mitral valve inflow velocity; Ea = early diastolic mitral annulus velocity; E/Ea = ratio of early diastolic mitral valve inflow velocity to early diastolic mitral annulus velocity; ECG = electrocardiography; LV = left ventricular; LVEF = LV ejection fraction; PCI = percutaneous coronary intervention; SR = strain rate; SRI = SR imaging; STEMI = ST-segment elevation myocardial infarction; WMSI = wall motion score indexThe clinical presentation of apical ballooning syndrome (ABS) mimics that of acute myocardial infarction (AMI). Both conditions are characterized by acute onset of chest pain, electrocardiographic (ECG) changes, and increases in cardiac enzymes and apical or midventricular wall motion abnormalities, which often make it difficult to differentiate ABS from AMI, especially during the acute stage. However, management and prognosis of these conditions are different because left ventricular (LV) wall motion abnormalities and LV systolic function in patients with ABS almost always recover in a period of days to weeks compared with patients with AMI, who frequently experience residual wall motion abnormalities even after timely acute reperfusion therapy.The early improvement in LV wall motion abnormalities in patients with ABS is consistent with myocardial viability despite significant LV wall motion abnormalities during the initial event. Therefore, we speculate that ABS is a good clinical model of viable apical myocardium, and comparison of LV systolic and diastolic function between patients with ABS and those with AMI can provide a unique opportunity to assess systolic and diastolic parameters associated with myocardial viability.Strain rate imaging (SRI) is a new tissue Doppler-based method that can quantify regional myocardial deformation.¹ Early experimental and clinical studies have shown that SRI can not only differentiate abnormal from normal myocardial contractility during the initial phase of an infarction but can also demonstrate subsequent recovery of transient ischemia.^1-5 The objectives of this study were to compare 2-dimensional Doppler echocardiographic and SRI features of patients with ABS and AMI and to evaluate systolic and diastolic parameters associated with myocardial viability.     

Preserved vasodilator response to adenosine in insulin-dependent diabetes mellitus

Experimental data derived from animal models suggest that the endogenous nucleoside adenosine has important cardioprotective properties. The potent vasodilator effects of adenosine may contribute to this cardioprotection as ischaemia-induced release of endogenous adenosine has been suggested to adjust local blood flow to the metabolic demands of the tissue. Interestingly, the vascular effects of adenosine appeared to be impaired in animal models for diabetes mellitus. This observation may be of importance with respect to the increased cardiovascular mortality in diabetes. Therefore, the authors investigated the in vivo vasodilator effects of adenosine in insulin-dependent diabetic patients. In 12 uncomplicated insulin-dependent male diabetic patients and 12 healthy male age-matched subjects, the brachial artery was cannulated for infusion of adenosine (0.15, 0.5, 1.5, 5, 15 and 50 μg 100^?1 mL min^?1) and for measurement of mean arterial pressure (MAP). Forearm blood flow (FBF) was measured by venous occlusion mercury-in-silastic strain gauge plethysmography. Maximal vasodilatation was assessed by standardized post occlusive reactive hyperaemia (PORH). Baseline forearm blood flow was 2.7 ± 0.4 and 1.8 ± 0.2 0.2 mL 100^?1 mL min^?1 for the diabetic patients and control group respectively. In the diabetic patients, adenosine infusion raised forearm blood flow to 2.4 ± 0.4, 2.6 ± 0.4, 4.4 ± 0.7, 6.3 ± 1.0, 9.8 ± 1.5 and 14.2 ± 2.1 mL 100^?1 mL min^?1 for the respective dosages. In the control group these values were 1.7 ± 0.21, 1.9 ± 0.3, 3.2 ± 0.8, 6.0 ± 1.2, 10.9 ± 2.1 and 17.1 ± 3.4 mL 100^?1 mL min^?1 respectively (P > 0.1 for between group comparison). Forearm blood flow at the contralateral side was not significantly affected by the placebo and adenosine infusions. Similar results were obtained when results were expressed as changes in forearm vascular resistance or forearm blood flow ratio (FBF infused arm/FBF control arm). Maximal vasodilatation did not differ between the two groups. The authors conclude that the forearm vasodilator response to adenosine is preserved in uncomplicated insulin-dependent diabetic patients. This observation argues against a primary role of a reduced adenosine responsiveness in the cardiovascular sequelae of diabetes.     

超声心动图评价左室部分切除成形术的血流动力学变化

目的应用超声心动图评价左心室部分切除成形术治疗终末期扩张型心肌病血流动力学变化。方法自1998年4月至12月,12例经末期扩张型心肌病患者接受了左心室部分切除术治疗。术前及术后1个月内行经胸超声心动图,术中行经食管超声心动图检查,取左室长轴切面测量左室内径,以双面面积长轴法测量左室收缩功能,用9段记分法定量评价室壁运动。结果左室心肌平均切除重量44.8±12.5g。超声心动图检查左室舒张末期、收缩末期内径显著减少(81.5±11.53至65.9±10.29mm);(72.67±11.28至58.16±10.27mm),P<0.05。左心射血分数增加(19.4%±7.4%至29.73%±8.17%),P<0.01;每搏量和左室整体及局部室壁运动得分无明显改变,P>0.05。结论左室部分切除治疗晚期扩张型心肌病近期能显著减少心腔内径、心室容积,每搏量无增加,室壁运动幅度无明显改变,远期效果并不象人们所期盼的那样,心功能改善不明显。射血分数的提高可能仅仅依赖于舒张末期容积的减低和二尖瓣返流的矫正。     

Improvement of left ventricular relaxation as assessed by tissue Doppler imaging in fluid-responsive critically ill septic patients

Purpose

Left ventricular (LV) diastolic function is often impaired in critically ill septic patients. The peak velocity of the mitral annulus early wave during diastole (E′), measured by Doppler echocardiography, is a major tool to evaluate LV relaxation, the ATP-dependent part of diastole. The authors hypothesized that if volume expansion (VE) is followed by an increase in stroke volume (SV) (“adequate” VE), LV relaxation and consequently E′ may be increased.

Methods

This was a prospective study in which 83 mechanically ventilated septic patients with circulatory failure were enrolled. Doppler echocardiography was performed before and after the infusion of 500?ml of saline over 20?min. Patients were then classified into two groups according to their response to VE: responders (R) were those in whom SV increased by at least 15?%; all others were considered to be non-responders (NR). SV, mitral flow early wave velocity (E), E′ and the E/E′ ratio were measured before and after VE. VE-induced variations (?) in all parameters were compared in R and NR. Patients with an E′?Results Fifty-nine patients (71?%) were R and 24 (29?%) were NR. Fifty-six percent of R patients and 58?% of NR patients had LV diastolic dysfunction. For patients with LV diastolic dysfunction (n?=?47), ?E′ was significantly higher in the R group (29?±?5 vs. 5?±?8?%; p?=?0.01) whilst ?E/E′ was higher in the NR group (35?±?9 vs. 2?±?6?%; p?=?0.02).

Conclusions

E′ maximal velocity increased with adequate VE, suggesting an improvement of LV relaxation with the correction of hypovolaemia in patients with septic shock.     

Forearm metabolism during infusion of adrenaline: comparison of the dominant and non‐dominant arm

Human skeletal muscle metabolism is often investigated by measurements of substrate fluxes across the forearm. To evaluate whether the two forearms give the same metabolic information, nine healthy subjects were studied in the fasted state and during infusion of adrenaline. Both arms were catheterized in a cubital vein in the retrograde direction. A femoral artery was catheterized for blood sampling, and a femoral vein for infusion of adrenaline. Forearm blood flow was measured by venous occlusion strain‐gauge plethysmography. Forearm subcutaneous adipose tissue blood flow was measured by the local ¹³³Xe washout method. Metabolic fluxes were calculated as the product of forearm blood flow and a‐v differences of metabolite concentrations. After baseline measurements, adrenaline was infused at a rate of 0·3 nmol kg^?1 min^?1. No difference in the metabolic information obtained in the fasting state could be demonstrated. During infusion of adrenaline, blood flow and lactate output increased significantly more in the non‐dominant arm (8·12 ± 1·24 versus 6·45 ± 1·19 ml 100 g^?1 min^?1) and (2·99 ± 0·60 versus 1·83 ± 0·43 μmol 100 g^?1 min^?1). Adrenaline induced a significant increase in oxygen uptake in the non‐dominant forearm (baseline period: 4·98 ± 0·72 μmol 100 g^?1 min^?1; adrenaline period: 6·63 ± 0·62 μmol 100 g^?1 min^?1) while there was no increase in the dominant forearm (baseline period: 5·69 ± 1·03 μmol 100 g^?1 min^?1; adrenaline period: 4·94 ± 0·84 μmol 100 g^?1 min^?1). It is concluded that the two forearms do not respond equally to adrenaline stimulation. Thus, when comparing results from different studies, it is necessary to know which arm was examined.     

Influence of propranolol infusion on cyclic variation of myocardial integrated backscatter in hypertrophic obstructive cardiomyopathy

It has been demonstrated that cyclic variation, assessed by myocardial integrated backscatter, reflects regional myocardial contractile function. The aim of this study was to investigate the influence of administration of β-blocker propranolol on cyclic variation in patients with hypertrophic cardiomyopathy and persistent left ventricular (LV) pressure gradient and to test the hypothesis that the reduction of LV pressure gradient would be related to the change in regional contractile function. Before and after 2 mg propranolol infusion, transthoracic echocardiography with integrated backscatter analysis was performed on 11 patients (8 men and 3 women, mean age 54 ± 12 years old). Integrated backscatter curves were obtained from the ventricular septum and LV posterior walls. With propranolol infusion, there was a significant reduction of LV fractional shortening (0.39 ± 0.08 to 0.34 ± 0.09, P < .01) and LV pressure gradient (83 ± 40 mm Hg to 42 ± 32 mm Hg, P < .001). In the posterior wall, the magnitude of cyclic variation significantly decreased (7.1 ± 2.2 dB to 5.6 ± 1.8 dB, P < .01), whereas in the septum, no apparent change in this parameter was observed (5.8 ± 2.1 dB to 4.7 ± 1.9 dB). Our findings suggest that in this form of cardiomyopathy, (1) the posterior wall myocardium is more susceptible to negative inotropic effects than the septum; (2) the reduction of LV pressure gradient is not related to that of regional wall motion; and (3) poor response of the ventricular septum is possibly because of more severe myocardial disarray and hypertrophy. (J Am Soc Echocardiogr 2002;15:1251-55.)     

Pulsed tissue Doppler evaluation of mitral annulus motion: a new window to assessment of diastolic function

Diastolic dysfunction is an important cause of cardiac heart failure. To date detailed assessment of diastolic left ventricular (LV) function has required invasive methods which are impractical in the clinical routine. The prevailing non-invasive method has been Doppler echocardiography with use of mitral inflow and pulmonary vein inflow parameters, measurements providing no direct assessment of either ventricular relaxation or compliance, and influenced by multiple haemodynamic factors. We sought to determine the tissue Doppler pattern from the mitral annulus motion in normals and in patients with expected LV-diastolic dysfunction. Using pulsed tissue Doppler we recorded peak velocities from the mitral annulus motion in 16 young normals, 10 older normals and in two groups of patients expected to have an LV-diastolic relaxation abnormality, i.e. 15 patients with systemic hypertension and 10 patients with significant aortic stenosis. The peak early diastolic (E) annulus velocity was significantly (P < 0·001) lower in older normals compared with young, and the late diastolic velocity (A) was higher (P < 0·01). Compared with the older normals, patients showed significantly lower E-velocities (P < 0·05 hypertensive patients), more pronounced in the patients with aortic stenosis (P < 0·001), but the A-velocities were not higher. In systole a decrease in peak velocity was noted with increasing age and in patients with aortic stenosis. In conclusion, pulsed tissue Doppler measurement of annulus motion seems to provide valuable and easily obtainable information about LV-diastolic function, and furthermore there is a striking change in velocity pattern with increasing age which necessitates age-matched reference values.     

整体长轴收缩期峰值应变率指标评价心肌梗死患者左室收缩功能

目的 探讨整体长轴收缩期峰值应变率指标在评价心肌梗死患者左室整体收缩功能中的应用价值.方法 对14例心肌梗死患者与20例健康对照者,采集心尖两腔、四腔及左室长轴切面二维超声图像,应用VVI技术测量左室各节段收缩期长轴峰值应变率(SRs)并取平均值得出左室整体长轴收缩期峰值应变率(GSRs).以常规二维超声心动图评价左室壁节段运动,计算室壁运动积分指数(WMSI),并应用Simpson双平面法计算左室射血分数(LVEF).应用脉冲波组织多普勒显像(PDTI)技术测量并计算二尖瓣环平均收缩期峰值速度(Sm).比较两组间各指标,评价GSRs指标与WMSI指标、Sm指标及LVEF指标的关系.结果 心肌梗死患者组及正常对照组GSRs、WMSI、Sm及LVEF分别为(-0.57±0.21)%和(-1.02±0.09)%、(1.90±0.80)和(1.10±0.30)、(6.20±1.50)cm/s和(9.80±1.30)cm/s、(32.90±7.10)%和(65.50±5.70)%,差异均有统计学意义(P<0.05),且GSRs与WMSI、Sm及LVEF均呈高度相关(r=0.97,-0.98,-0.93, P<0.0001).结论 GSRs是客观评价左室整体收缩功能的新指标.     

超声评价缺血心肌骨髓基质细胞移植后疗效

目的:采用超声评价骨髓基质细胞(MSCs)移植前后兔缺血心肌局部运动及心功能,探讨骨髓基质细胞移植对缺血心肌的影响。方法:20只日本大耳白兔开胸结扎左冠状动脉前降支建立心肌梗死模型后随机分成2组,即对照组、移植组。分别在心肌梗死前1天、心肌梗死后1周、移植后4周行超声检查,测量左室前壁厚度(AW)、左室舒张末期内径(LVDd)、射血分数(EF),左室前壁收缩期峰值速度(Vs)、舒张早期峰值速度(VE)、舒张晚期峰值速度(VA)。结果:MSCs移植后4周,移植组较对照组LVDd缩小(P<0.05),EF、Vs和VE则增高(P<0.05)。结论:超声能够检测到兔梗死心肌MSCs移植后心肌局部运动与心脏功能的变化。     

Parametric quantification of myocardial ischaemia using real‐time perfusion adenosine stress echocardiography images,with SPECT as reference method

Background: Real‐time perfusion (RTP) adenosine stress echocardiography (ASE) can be used to visually evaluate myocardial ischaemia. The RTP power modulation technique, provides images for off‐line parametric perfusion quantification using Qontrast^® software. From replenishment curves, this generates parametric images of peak signal intensity (A), myocardial blood flow velocity (β) and myocardial blood flow (Axβ) at rest and stress. This may be a tool for objective myocardial ischaemia evaluation. We assessed myocardial ischaemia by RTP‐ASE Qontrast^®‐generated images, using 99mTc‐tetrofosmin single‐photon emission computed tomography (SPECT) as reference. Methods: Sixty‐seven patients admitted to SPECT underwent RTP‐ASE (SONOS 5500) during Sonovue^® infusion, before and throughout adenosine stress, also used for SPECT. Quantitative off‐line analyses of myocardial perfusion by RTP‐ASE Qontrast^®‐generated A, β and Axβ images, at different time points during rest and stress, were blindly compared to SPECT. Results: We analysed 201 coronary territories [corresponding to the left anterior descendent (LAD), left circumflex (LCx) and right coronary (RCA) arteries] from 67 patients. SPECT showed ischaemia in 18 patients. Receiver operator characteristics and kappa values showed that A, β and Axβ image interpretation significantly identified ischaemia in all territories (area under the curve 0·66–0·80, P = 0·001–0·05). Combined A, β and Axβ image interpretation gave the best results and the closest agreement was seen in the LAD territory: 89% accuracy; kappa 0·63; P<0·001. Conclusion: Myocardial isachemia can be evaluated in the LAD territory using RTP‐ASE Qontrast^®‐generated images, especially by combined A, β and Axβ image interpretation. However, the technique needs improvements regarding the LCx and RCA territories.