Tissue cardiovascular magnetic resonance demonstrates regional diastolic dysfunction in remote tissue early after inferior myocardial infarction.

PURPOSE: To investigate regional diastolic and systolic function using tissue cardiovascular magnetic resonance (CMR), early after transmural myocardial infarction of the inferior wall due to single proximal right coronary artery disease. MATERIALS AND METHODS: Velocity encoded CMR was used to measure early diastolic transmitral flow velocity (E), and regional, longitudinal, myocardial systolic (Sa) and early diastolic (Ea) velocities (tissue CMR) in 15 patients with a recent transmural inferior myocardial infarction and in 15 age and LV-mass index matched control subjects. An unpaired two-tailed t test was used to assess significance of continuous variables. RESULTS: Global systolic (ejection fraction 46 +/- 7% versus 57 +/- 4%, p = 0.000052) and global diastolic LV function (average Ea of infarcted or inferior, remote or anterior, adjacent or septal and lateral myocardium 6.8 +/- 1.7 cm/s versus 10.4 +/- 1.5 cm/s, p = 0.0000012) were impaired in patients as compared to controls. Regional systolic and diastolic LV velocities were impaired in infarcted and adjacent tissue in patients. However, in remote or anterior tissue, systolic velocities were preserved (Sa 6.6 +/- 2.0 cm/s versus 6.8 +/- 1.4 cm/s, p = 0.70), but diastolic velocities were impaired in patients as compared to controls (Ea 7.2 +/- 2.3 cm/s versus 10.2 +/- 2.5 cm/s, p = 0.0026). CONCLUSIONS: Regional diastolic velocities early after inferior myocardial infarction are impaired in the infarcted, adjacent and remote tissue, but regional systolic velocities are preserved in remote tissue.     

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.     

Normal regional right ventricular function and its change with age: a Doppler myocardial imaging study.

BACKGROUND: Doppler Myocardial Imaging (DMI) is a new technique currently being studied for the assessment of regional systolic and diastolic left ventricular (LV) function. No normal values or data on age-related changes in regional myocardial right ventricular (RV) velocities are available. METHODS AND RESULTS: Color DMI was used in 32 healthy volunteers (aged 16-76 years) to derive regional velocities from basal, medial, and apical segments of the RV free wall in the apical 4-chamber view, and from distal segments as well as from the tricuspid annulus in the parasternal long-axis view. Both mitral annular and regional LV velocities (4-chamber, long-axis parasternal view) were also recorded and compared with corresponding RV regional velocities. The M-mode displacement of the cardiac base was measured. Corresponding RV and LV DMI data sets were compared. For longitudinal function, RV free wall systolic velocities were consistently higher than velocities recorded in corresponding LV segments (analysis of variance, P <.05). Older subjects (40-76 years; 13 men, 2 women) had lower RV long-axis regional velocities than younger subjects (16-39 years; 15 men, 2 women), but had higher short-axis RV systolic velocities. For diastolic velocities, a negative correlation between age and the ratio of regional early diastolic to late diastolic velocity was shown for all RV free wall segments (eg, basal segment: r = -0.63, P <.0001). CONCLUSIONS: The right ventricle has higher long-axis regional velocities, a greater excursion of its lateral atrioventricular valve ring, and reduced circumferential shortening velocities compared with the left ventricle. Right ventricular longitudinal shortening is dominant over short-axis function in healthy young subjects. Normal age-related changes of diastolic velocities for each segment of the normal RV free wall have been defined.     

Assessment of regional longitudinal myocardial strain rate derived from doppler myocardial imaging indexes in normal and infarcted myocardium.

Myocardial deformation properties may be characterized by regional strain rates (SRs) calculated from Doppler myocardial velocity data. In 10 control subjects and 12 patients with established transmural infarcts, longitudinal median segmental SR, strain, and myocardial velocity were analyzed and compared with the corresponding wall motion score. All segments in control subjects and normal segments in infarct patients showed no significant difference in either systolic or diastolic SR (systolic: -1.27+/-0.39 s(-1) versus -1.23+/-0.24 s(-1), not significant [NS]; and isovolumic relaxation [IVR]: 1.23+/-0.38 s(-1) versus 1.95+/-0.62 s(-1), NS; respectively) and strain (-0.21+/-0.06 versus -0.19+/-0.06, NS). In infarcted segments, peak systolic SR, systolic strain, and early diastolic SR showed the most pronounced reduction (hypokinetic and akinetic) or even inversion (dyskinetic segments: 0.10+/-0.26 s(-1), 0.00+/-0.03, and -1.78+/-0.67 s(-1), respectively; P<.001). In this study, new myocardial deformation indexes were shown to quantitatively describe the function of normal and chronically infarcted regions.     

Quantification of regional left and right ventricular radial and longitudinal function in healthy children using ultrasound-based strain rate and strain imaging.

BACKGROUND: Noninvasive assessment of left (LV) and right (RV) ventricular function in children could benefit from a technique that would characterize local myocardial deformation. Color Doppler myocardial imaging (CDMI) allows the calculation of either local longitudinal or radial Strain Rate (SR) and Strain (epsilon). To determine the clinical feasibility and reproducibility of longitudinal and radial SR and epsilon, the following study was carried out. METHODS: CDMI data were obtained from 33 healthy children (4-16 years). To quantify regional longitudinal and radial function SR and epsilon data were obtained from apical and parasternal views respectively. From the extracted SR curves, peak values for systole, early diastole, and late diastole were calculated. From the extracted epsilon curves the systolic, early and late diastolic epsilon values were calculated. RESULTS: LV longitudinal deformation were homogeneous for LV basal, mid and apical segments (peak systolic SR: -1.9 +/- 0.7 s(-1), systolic epsilon -25% +/- 7%). Longitudinal SR and epsilon values were significantly higher and heterogeneous in the RV (compared with LV walls) and were maximal in the mid part of the RV free wall (peak systolic SR: -2.8 +/- 0.7 s(-1), systolic epsilon -45% +/- 13%). The RV inferior wall showed homogeneous but lower longitudinal SR and epsilon values. The LV systolic and diastolic SR and epsilon values were higher for deformation in the radial direction compared with the longitudinal direction (radial peak systolic SR: 3.7 +/- 0.9 s(-1), radial systolic epsilon 57% +/- 11%; P <.0001). The interobserver variability for radial systolic epsilon and SR was 10.3% and 13.1%, respectively. CONCLUSION: Ultrasound-based Strain SR/epsilon imaging is a practical, reproducible clinical technique, which allows the calculation of regional longitudinal and radial deformation from both LV and RV segments. The combination of regional SR/epsilon indices and the timing of specific systolic or diastolic regional events may offer a new noninvasive approach to quantifying regional myocardial function in congenital and acquired heart disease in children.     

Relationship between longitudinal and radial contractility in subclinical diabetic heart disease

Subclinical left ventricular (LV) dysfunction may be identified by reduced longitudinal contraction. We sought to define the effects of subclinical LV dysfunction on radial contractility in 53 patients with diabetes mellitus with no LV hypertrophy, normal ejection fraction and no ischaemia as assessed by dobutamine echocardiography, in comparison with age-matched controls. Radial peak myocardial systolic velocity (Sm) and early diastolic velocity (Em), strain and strain rate were measured in the mid-posterior and mid-anteroseptal walls in parasternal views and each variable was averaged for individual patients (radial contractility). These variables were also measured in the mid-posterior and mid-anteroseptal walls in the apical long-axis view and each variable was averaged for individual patients (longitudinal contractility). Mean radial Sm, strain and strain rate were significantly increased in diabetic patients (2.9 +/- 0.6 cm/s, 28 +/- 5% and 1.8 +/- 0.4 s(-1) respectively) compared with controls (2.4 +/- 0.7 cm/s, 23 +/- 4% and 1.6 +/- 0.3 s(-1) respectively; all P<0.001), but there was no difference in Em (3.3 +/- 1.2 compared with 3.1 +/- 1.1 cm/s, P=not significant). In contrast, longitudinal Sm, Em, strain and strain rate were significantly lower in diabetic patients (3.6 +/- 1.1 cm/s, 4.3 +/- 1.6 cm/s, 21 +/- 4% and 1.6 +/- 0.3 s(-1) respectively) than in controls (4.3 +/- 1.0 cm/s, 5.7 +/- 2.3 cm/s, 26 +/- 4% and 1.9 +/- 0.3 s(-1) respectively; all P< or =0.001). Thus radial contractility appears to compensate for reduced longitudinal contractility in subclinical LV dysfunction occurring in the absence of ischaemia or LV hypertrophy.     

Left ventricular function in patients with hypertrophic cardiomyopathy and its relation to myocardial fibrosis and exercise tolerance

We sought to determine the relation between myocardial extracellular volume (ECV), left ventricular (LV) diastolic function, and exercise tolerance in patients with hypertrophic cardiomyopathy (HCM). Forty five HCM patients with an ejection fraction >50% and no previous septal reduction therapy underwent imaging by CMR and transthoracic echocardiography. CMR was used to quantify LV volumes, mass, EF, LA volumes, scar burden, pre and post contrast T1 relaxation times and ECV. Echocardiography was used to measure outflow tract gradients, mitral inflow and annular velocities, circumferential strain, systolic, early and late diastolic strain rates. Exercise duration and peak oxygen consumption were noted. HCM patients had increased native T1 relaxation time and ECV vs. controls [ECV controls: 24.7 (23.2–26.4) vs. HCM: 26.8 (24.6–31.3)%, P?=?0.014]. Both parameters were significantly associated with LV diastolic dysfunction, circumferential strain, diastolic strain rate and peak oxygen consumption (r?=??0.73, P?<?0.001). Compared to controls, HCM patients have significantly longer native T1 relaxation time and higher ECV. These structural changes lead to worse LV global and segmental diastolic function and in turn reduced exercise tolerance.     

Influence of preload alterations on parameters of systolic left ventricular long-axis function: a Doppler tissue study.

The study examined the influence of preload alterations on parameters of left ventricular (LV) long-axis function during systole. Doppler tissue echocardiography was performed in 32 healthy volunteers at rest who were placed in the Trendelenburg position after administration of 0.8 mg of nitroglycerin sublingually. In a 16-segment LV model, long-axis myocardial strain and systolic velocities were assessed. Isovolumic acceleration was assessed in the lateral mitral annulus. Mean LV strain and systolic velocity were unchanged during the different load conditions. In the mitral annulus, strain was also uninfluenced by preload alterations, whereas the peak systolic velocities seemed influenced by preload reduction. The isovolumic acceleration of the mitral annulus was found to be load dependent (enhanced preload 1.38 +/- 0.50 vs baseline 1.6 m/s2 +/- 0.60, P <.01; and preload reduction 2.18 +/- 0.65 m/s2, P <.01). In conclusion, LV long-axis strain and systolic velocities were not significantly influenced by load alterations, whereas myocardial systolic velocities and isovolumic acceleration in the lateral mitral annulus were significantly load dependent.     

Left ventricular long-axis diastolic function is augmented in the hearts of endurance-trained compared with strength-trained athletes

In order to determine left ventricular global and regional myocardial functional reserve in endurance-trained and strength-trained athletes, and to identify predictors of exercise capacity, we studied 18 endurance-trained and 11 strength-trained athletes with left ventricular hypertrophy (172+/-27 and 188+/-39 g/m(2) respectively), and compared them with 14 sedentary controls. Global systolic (ejection fraction) and diastolic (transmitral flow) function, and regional longitudinal and transverse myocardial velocities [tissue Doppler echocardiography (TDE)], were measured at rest and immediately after exercise. In endurance-trained compared with strength-trained athletes, resting heart rate was lower (59+/-11 and 76+/-9 beats/min respectively; P<0.001), and the increase at peak exercise was greater (+211% and +139% respectively; P<0.001). In addition, exercise duration, workload, maximal oxygen consumption and global systolic functional reserve (but not peak ejection fraction) were higher in the endurance-trained athletes, and resting global diastolic function (E/A ratio 1.62+/-0.40 compared with 1.18+/-0.23; P<0.01) (where E-wave is peak velocity of early-diastolic mitral inflow and A-wave is peak velocity of mitral inflow during atrial contraction) and long-axis diastolic velocities (E(TDE)/A(TDE) ratio 2.2+/-1.2 compared with 1.1+/-0.3; P<0.01) (where E(TDE) and A(TDE) represent peak early- and late-diastolic myocardial or tissue velocity respectively) were augmented. Systolic velocities were similar. Exercise capacity was best predicted from end-diastolic diameter index and E/A ratio at rest, and end-diastolic volume index and diastolic longitudinal velocity during exercise (r=0.74, n=43, P<0.001). In conclusion, endurance-trained athletes had higher left ventricular long-axis diastolic velocities, augmented global early diastolic filling, and greater chronotropic and global systolic functional reserve. Maximal oxygen consumption was determined by diastolic loading and early relaxation rather than by systolic function, suggesting that dynamic exercise training improves cardiac performance by an effect on diastolic filling.     

Physiological range of mechanical synchronicity of the human heart: comparison between different echocardiographic assessment modalities

Tissue Doppler was performed to assess physiological ranges of mechanical synchronicity in 47 patients aged 38 to 81 y with normal coronary angiograms, ECG recordings and echocardiographic findings. Maximal time delays between two different left ventricular (LV) walls in long axis time-to-peak tissue displacement (TD_D), respectively in time-to-peak strain (TD_S), time-to-peak strain rate (TD_SR), time-to-peak systolic (TD_VS) and early diastolic (TD_VE) velocities of basal and midwall segments were determined as values corrected for heart rate in a 16-segment LV model and in the right ventricle (RV). Strain (TD_S: LV = 212 +/- 108 ms, RV = 195 +/- 15 ms) and strain rate (TD_SR: LV = 183 +/- 67 ms, RV = 120 +/- 60 ms) showed the highest dyssynchrony values (TD_D: LV = 110 +/- 96 ms, RV = 42 +/- 38 ms; TD_VS: LV = 82 +/- 47 ms, RV = 36 +/- 36 ms; TD_VE: LV = 73 +/- 36 ms, RV = 46 +/- 20 ms) in both ventricles. There was no significant association between a certain LV wall and the occurrence of the earliest, respectively latest peak values of any parameter.     

Lisinopril improves arterial function in hyperlipidaemia

Endothelial function is defective in hypercholesterolaemia, and animal models have suggested that angiotensin-converting enzyme inhibitors may prevent arterial damage. We studied the effect of 6 months treatment with lisinopril on endothelial function in a group of patients with hypercholesterolaemia. Forty patients were studied. Forearm blood flow responses to acetylcholine and sodium nitroprusside were assessed by venous occlusion plethysmography. Subjects were then randomized in a double-blind fashion to receive either lisinopril, 20 mg/day (n=20), or placebo (n=20) for 6 months. Plethysmography was then repeated. Baseline variables between groups were comparable. In the lisinopril group blood pressure fell significantly [systolic: 145+/-4 to 128+/-4 mmHg (P<0.001); diastolic: 84+/-2 to 74+/-2 mmHg (P<0.001)]. An improvement was found in the vasodilatory response (expressed as a ratio of the infused/control arm) to acetylcholine, e.g. 3.33+/-0.3 (pre) versus 4.45+/-0.48 (post) at 30 microg/ml (P<0.03), and also to nitroprusside, e.g. 3.0+/-0.2 (pre) versus 3.86+/-0.3 (post) at 3.2 microg/ml (P<0.01). In the placebo group vasodilatation did not change significantly in response to acetylcholine, and nitroprusside responses were unchanged. The data presented suggest that 6 months of lisinopril therapy have a beneficial effect on arterial function in subjects with hyperlipidaemia. Further work should now investigate whether angiotensin-converting enzyme inhibitors are beneficial in reducing mortality and morbidity in hypercholesterolaemia.     

Assessment of regional systolic and diastolic wall motion velocities in highly trained athletes by pulsed wave Doppler tissue imaging.

We studied the relationship between left ventricular (LV) function and the increased LV mass in 18 highly trained rowing athletes (14 men, 4 women; mean age 20.7 +/- 4.5 years) using pulsed wave Doppler tissue imaging (PWDTI). Thirteen untrained volunteers, matched for age and body mass index, acted as control participants. Peak systolic, early diastolic (Ev), and late diastolic (Av) myocardial velocities (cm/s); Ev/Av ratio; and isovolumic relaxation time (ms) were measured at the level of basal lateral wall and basal posterior interventricular septum (bas-IVS) segments. In comparison with control participants, athletes showed a greater LV cavity size (P <.05), wall thickness (IVS, P <.001; posterior wall, P <.01), and mass index (P <.001). In athletes, systolic velocity of bas-IVS had increased (P <.001) and was positively correlated with IVS thickness (r = 0.66, P <.005) and LV mass index (r = 0.71, P <.001). Of the PWDTI-measured diastolic indexes, Ev/Av ratio significantly increased in athletes in comparison with control participants in both the examined segments (bas-IVS, P <.05; basal lateral wall, P <.05). When Ev and Av were separately considered, a different behavior was found in the 2 segments: Ev significantly increased in the basal lateral wall (P <.005); Av significantly decreased in the bas-IVS. The increase in the systolic velocity of bas-IVS suggests that septum greatly contributes to the longitudinal LV systolic shortening and increase of stroke volume in athletes compared with untrained participants. Moreover, the behavior of PWDTI diastolic velocities suggests a more effective relaxation activity in the longitudinal axis at the level of lateral wall. This study suggests therefore the usefulness of PWDTI in the assessment of functional properties of "athlete's heart" and differentiation from pathologic cardiac conditions.     

Assessment of left ventricular systolic and diastolic function by Doppler tissue imaging in patients with preinfarction angina.

BACKGROUND: The aim of this study was assessment of left ventricular (LV) systolic and diastolic function by pulsed wave Doppler tissue imaging (DTI) in patients with or without preinfarction angina in acute myocardial infarction. METHODS: We prospectively evaluated 31 consecutive patients (4 women, 27 men; age 58 +/- 10 years) with a first acute myocardial infarction. LV systolic and diastolic function was assessed by classic methods and DTI on the third day during acute myocardial infarction. Patients were divided into 2 groups according to the presence (group 1; n = 10) or absence (group 2; n = 21) of preinfarction angina. Mitral inflow velocities and early diastolic mitral annular velocity (Em), late diastolic mitral annular velocity (Am), peak systolic mitral annular velocity, Em/Am, the ratio of early diastolic mitral inflow velocity (E) to Em, and myocardial performance index were calculated by DTI. RESULTS: Group 1 had significantly higher Em and Em/Am than group 2 (11.3 +/- 3.34 cm/s vs 7.4 +/- 2.07 cm/s, P <.0001; 1.01 +/- 0.38 cm/s vs 0.6 +/- 0.2 cm/s, P =.001, respectively). The E/Em ratio and myocardial performance index were significantly lower in group 1 than in group 2 (5.1 +/- 2.92 vs 8.10 +/- 3.15, P=.018; 0.49 +/- 0.15 vs 0.65 +/- 0.24, P =.042, respectively). Wall-motion score index was lower in those with preinfarction angina than in those without (1.6 +/- 0.36 vs 1.9 +/- 0.39; P =.04, respectively). Peak systolic mitral annular velocity and Am were not statistically different between groups (9.4 +/- 1.84 vs 8.3 +/- 2.03, P =.172; 11.7 +/- 3.07 vs 12.1 +/- 3.34, P =.72, respectively). There were no significant differences between the 2 groups regarding transmitral E velocity, atrial contraction mitral inflow velocity (A), E/A ratio, isovolumetric relaxation time, and deceleration time of the mitral E wave (P =.91, P =.08, P =.58, P =.81, and P =.71, respectively). CONCLUSION: LV diastolic function was better in patients with preinfarction angina than in patients without. This condition could not be detected by conventional mitral inflow Doppler velocities, but could be detected by DTI. This preliminary evidence shows that DTI is better than conventional mitral Doppler indices in the assessment of a favorable LV diastolic function in patients with preinfarction angina.     

Treatment of post resuscitation myocardial dysfunction: aortic counterpulsation versus dobutamine

BACKGROUND: Post resuscitation myocardial stunning is well described and recognized as a significant contributor to poor long-term outcome following cardiac arrest. Optimal strategies for treatment have not been determined. METHODS: Ten domestic swine (49+/-3 kg) underwent 15 min of untreated ventricular fibrillation before being successfully resuscitated. Left ventricular systolic and diastolic function was measured at pre-arrest baseline, at 30 min and at 6 h post resuscitation. Five animals were treated immediately after resuscitation with intra-aortic balloon counterpulsation (IABP) and five were given dobutamine (5 mcg/kg per min). RESULTS: No baseline differences were found. At 30 min post resuscitation pulmonary capillary wedge pressure and LVEDP were significantly higher (16+/-3 vs. 7+/-1 and 20+/-2 vs. 11+/-1 mmHg) while LV isovolumic relaxation ('Tau') was significantly longer (34+/-2 vs. 20+/-2 ms) in the IABP treated versus the dobutamine treated animals. Likewise, at 6 h post resuscitation LV ejection fraction was significantly less (21+/-6 vs. 39+/-4%), and LVEDP significantly higher (18 vs. 10 mmHg) in the IABP group. Heart rate was not different between the groups at any time post resuscitation. CONCLUSION: Dobutamine was superior to IABP for treatment of post resuscitation left ventricular systolic and diastolic dysfunction. The hypothesized advantage of IABP for treatment of post resuscitation myocardial stunning without excessively raising the heart rate like dobutamine was not realized.     

Effect of cardiac resynchronization therapy on left ventricular diastolic filling pattern in responder and nonresponder patients

BACKGROUND: The aim of this study was to investigate the short- and long-term effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) diastolic filling pattern and the relation between the diastolic filling pattern and the response to CRT. METHODS: Twenty-three patients with systolic heart failure and complete left bundle-branch block underwent implantation of biventricular pacemaker devices. In order to follow the changes in diastolic function, mitral inflow, pulmonary venous flow, and LV flow propagation (Vp) velocities were measured with pulsed-wave and color M-mode Doppler echocardiography 1 week before and 1 and 6 months after pacemaker implantation. At the 6-month follow-up, patients were divided into two groups according to their response to CRT defined as a relative increase in LV ejection fraction (LVEF) > or =25% versus baseline. RESULTS: After biventricular pacemaker implantation, significant clinical improvement was observed in all patients. Compared to baseline, the ratio of early-to-late peak velocities (E/A) decreased significantly at the 6th month (E/A ratio: from 1.5 +/- 0.9 to 0.8 +/- 0.5 at the 6th month (P = 0.02)). Pulmonary systolic flow to diastolic flow ratio (PVs/PVd) increased with CRT after 6 months (PVs/PVd ratio: from 0.9 +/- 0.4 to 1.3 +/- 0.7 at the 6th month (P = 0.02)). E/Vp ratio decreased significantly at the 1st and 6th month (E/Vp ratio: from 2.7 +/- 0.8 to 2 +/- 0.8 at the 1st (P < 0.002) and to 1.9 +/- 0.7 at the 6th month (P < 0.02)). In responders (n: 17, 74%), E wave and PVra velocity decreased, E-wave deceleration time increased, and E/Vp ratio improved significantly, whereas in nonresponders, changes in LV diastolic parameters remained insignificant. However, diastolic filling pattern improved significantly at the 1st and 6th month of CRT in both responders and nonresponders. CONCLUSION: CRT enhances diastolic filling patterns in both responder and nonresponder patients. This may be related to improvement in symptoms even in nonresponders who have a relative increase in LVEF <25%.     

Pulsed tissue Doppler imaging of left ventricular systolic and diastolic wall motion velocities to evaluate differences between long and short axes in healthy subjects.

Our objective was to evaluate in healthy subjects the left ventricular (LV) wall motion velocities along the long and short axes by means of pulsed tissue Doppler imaging (TDI) to clarify the differences in the LV systolic and diastolic function between both axes. Wall motion velocities were recorded at the mid-wall portion of the middle site of the LV posterior wall in the parasternal long-axis view, and at the subendocardial portion of the middle site of the LV posterior wall in the apical long-axis view by pulsed TDI in 35 healthy subjects (mean age 26 +/- 10 years, mean heart rate 72 +/- 7 bpm). In all subjects, the LV pressure curve, its first derivative (dP/dt), the LV wall motion velocity, the phonocardiogram, and the electrocardiogram were simultaneously recorded. The systolic wave of the LV posterior wall motion velocity exhibited 2 peaks: the first and second systolic waves (Swl and Sw2, respectively). The diastolic wave also exhibited 2 peaks, the early diastolic and atrial systolic waves. The Swl along the long axis was greater than either the Sw1 and Sw2 along the short axis or the Sw2 along the long axis. The peak Sw1 along the long axis coincided with the peak dP/dt and was slightly earlier than the peak Swl along the short axis. The onset of Sw1 along the long axis coincided with the onset of the first heart sound. The Sw2 along the short axis was greater than that along the long axis. The early diastolic wave along the short axis was greater than that along the long axis, whereas the atrial systolic wave along the long axis was greater than that along the short axis. Thus, in healthy subjects, shortening of the longitudinal fibers predominated over that of the circumferential fibers during early systole, whereas shortening of the circumferential fibers predominated over the longitudinal fibers during the ejection phase. During diastole, the circumferential fibers predominated in the LV wall expansion at early diastole, whereas the longitudinal fibers predominated at atrial systole. In conclusion, pulsed TDI provided information that is useful in understanding the characteristics of LV wall motion along the long and short axes.     

HMG CoA reductase inhibition and left ventricular mass in hypertrophic cardiomyopathy: a randomized placebo-controlled pilot study

BACKGROUND: Statins reduce cardiomyocyte hypertrophy in animal models of hypertrophic cardiomyopathy, aortic banding and heart failure after myocardial infarction. We investigated the effect of the hydroxymethylglutaryl coenzyme A reductase inhibitor atorvastatin on left ventricular (LV) mass in patients with hypertrophic cardiomyopathy in a randomized placebo-controlled double-blind pilot study. MATERIALS AND METHODS: Patients with hypertrophic cardiomyopathy were randomized to be treated once daily by atorvastatin 80 mg or placebo for nine months. LV mass was assessed by serial cardiac magnetic resonance imaging. LV systolic and diastolic function was determined by echocardiography. Markers of collagen metabolism and inflammation were also assessed. RESULTS: Out of 78 screened patients with hypertrophic cardiomyopathy 28 (2 x 14) patients were eligible for randomization. Eleven patients in each group completed the study with cardiac magnetic resonance imaging assessments meeting the evaluation standards at baseline and at follow-up. Low-density lipoprotein cholesterol levels in the atorvastatin group decreased from 3.24 +/- 1.14 mmol L(-1) (125 +/- 44 mg dL(-1)) at baseline to 1.37 +/- 0.49 mmol L(-1) (53 +/- 19 mg dL(-1)) at follow-up (P < 0.001), but were unchanged in the placebo group. Baseline LV mass was 228 +/- 51 g in the placebo and 232 +/- 67 g in the atorvastatin group. The primary endpoint of change in LV mass from baseline to follow-up was 2 +/- 10% in the atorvastatin group versus 0 +/- 13% in the placebo group (P = NS). Parameters of LV volumes and diameters, systolic and diastolic function, and markers of collagen metabolism were also unchanged in both groups. CONCLUSION: In patients with hypertrophic cardiomyopathy, this randomized placebo-controlled double-blind pilot study did not demonstrate an effect of 9-month treatment with atorvastatin 80 mg on LV mass reduction.     

Decreased left ventricular longitudinal contraction in normotensive and normoalbuminuric patients with Type II diabetes mellitus: a Doppler tissue tracking and strain rate echocardiography study

Type II diabetes mellitus is associated with congestive heart failure with preserved ejection fraction. This group of patients has been assumed to have isolated diastolic dysfunction; however, the longitudinal systolic contraction of the left ventricle has not been studied previously. The objective of the present study was to investigate the longitudinal contraction of the left ventricle in normotensive Type II diabetes mellitus patients with normal ejection fraction. We examined 32 normotensive patients with Type II diabetes mellitus with ejection fraction >0.55 and fractional shortening >0.25. Exclusion criteria were angina pectoris, cardiac valve disease, albuminuria, retinopathy or neuropathy. Normal subjects (n =32) served as controls. A 16 segment model of motion amplitude assessed left ventricular longitudinal contraction and the average of the segments was calculated as the tissue tracking score index. Peak systolic velocity and strain rate was also obtained in each segment. Patients with Type II diabetes mellitus had a significantly lower tissue tracking score index compared with normal subjects (5.8+/-1.6 mm compared with 7.7+/-1.1 mm; P <0.001). Mean peak systolic velocity was also significantly lower (4.3+/-1.5 cm/s compared with 5.4+/-1.0 cm/s; P <0.001), as well as peak systolic strain rate (-1.2+/-0.3 s(-1) compared with -1.6+/-0.4 s(-1); P <0.001). Patients with Type II diabetes mellitus and preserved diastolic function had a significantly lower tissue tracking score index compared with normal subjects (6.6+/-1.5 mm; P <0.001), but patients with diastolic dysfunction had an even more profound decrease in tissue tracking score index compared with patients without diastolic dysfunction (4.9+/-0.9 mm; P <0.01). In conclusion, the longitudinal systolic contraction was significantly decreased in normotensive patients with Type II diabetes mellitus with normal ejection fraction, which was most profound in patients with concomitant diastolic dysfunction.     

Subendocardial motion in hypertrophic cardiomyopathy: assessment from long- and short-axis views by pulsed tissue Doppler imaging.

BACKGROUND: Tissue Doppler imaging (TDI) is a recently developed technique that allows the instantaneous measurement of intrinsic regional myocardial motion velocity. Pulsed TDI is capable of separately assessing left ventricular (LV) regional motion velocity caused by circumferential and longitudinal fiber contraction. This particular feature of function is still controversial in patients with hypertrophic cardiomyopathy (HC). METHODS: To better characterize intrinsic circumferential and longitudinal LV systolic myocardial function in HC, we used pulsed TDI to measure short- and long-axis LV motion velocities, respectively. The subendocardial motion velocity patterns at the middle of the LV posterior wall (PW) and ventricular septum (IVS) in LV parasternal and apical long-axis views were recorded by pulsed TDI in 19 patients with nonobstructive HC and in 21 normal controls (NC). RESULTS: Peak short- and long-axis systolic subendocardial velocities in both the LV PW and IVS were significantly smaller in the HC group than in the NC group, and the time to peak velocity was significantly delayed. Furthermore, peak PW systolic velocity was significantly greater along the long axis than along the short axis in the NC group (8.8 +/- 1.5 cm/s vs 8.2 +/- 1.4 cm/s, P <.05), whereas the opposite was observed in the HC group (6.1 +/- 1.2 cm/s vs 7.5 +/- 1.0 cm/s, P <.0001). No significant differences were found in either group between the long- and short-axis IVS velocities (HC: 5.9 +/- 1.4 cm/s vs 5.5 +/- 1.3 cm/s; NC: 7.8 +/- 1.3 cm/s vs 7.9 +/- 1.6 cm/s). CONCLUSIONS: By using the capability of pulsed TDI for the evaluation of intrinsic myocardial velocity instantaneously in a specific region and direction, we found impairment of LV myocardial systolic function in patients with HC not only in the hypertrophied IVS but also in the nonhypertrophied LV PW. We also found a greater decrease in LV PW velocities along the long axis than the short axis, suggesting greater impairment of long-axis contraction in patients with HC. Because our HC patients did not appear to have excessive intracavitary pressure, these results suggest that the relatively normal-appearing PW is directly affected by the HC pathologic process.     

Differences in left ventricular hypertrophy and dysfunction between patients with cerebral hemorrhage and those with cerebral infarction

Left ventricular (LV) hypertrophy and dysfunction due to hypertension have been established as risk markers for stroke in hypertensive patients. The purpose of this study was to examine the differences in LV hypertrophy and dysfunction between patients with cerebral hemorrhage and those with cerebral infarction. The study enrolled 23 hypertensive patients with cerebral infarction, 25 hypertensive patients with cerebral hemorrhage, and 24 normotensive controls (controls). Standard echocardiography was performed; LV mass index was measured to evaluate LV hypertrophy, and conventional diastolic transmitral flow velocities were measured to assess LV diastolic function, which was also evaluated by measuring mitral annular velocities using tissue Doppler echocardiography. The Tei index, which reflects both the diastolic and systolic function of LV, was also calculated. The LV mass index and Tei index were significantly higher in cerebral hemorrhage (116 +/- 38 g/m(2) and 0.57 +/- 0.13) than those in controls (92 +/- 20 g/m(2) and 0.46 +/- 0.10) (p < 0.05). In contrast, the LV mass index and Tei index in cerebral infarction (100 +/- 27 g/m(2) and 0.46 +/- 0.12) were not different from those in controls. Thus, the Tei index was significantly worse in the patients with cerebral hemorrhage than in those with cerebral infarction (p < 0.05). On the other hand, the parameters, which reflect diastolic function, showed no significant differences between cerebral hemorrhage and cerebral infarction. These results indicate that LV hypertrophy and dysfunction due to hypertension are more apparent in patients with cerebral hemorrhage than in those with cerebral infarction.