SLICC/ACR damage index independently associated with left ventricular diastolic dysfunction in patients with systemic lupus erythematosus.

Left ventricular (LV) diastolic dysfunction has been reported in both active and inactive systemic lupus erythematosus (SLE) patients without clinical evidence of cardiovascular disease. However, the relationship between the long-term inflammatory burden reflected by the SLICC/ACR damage index and LV diastolic function has not been studied. Eighty-two SLE patients and 82 controls matched for age, sex, body mass index, blood pressure and heart rate underwent echocardiography with tissue Doppler imaging (TDI). LV diastolic function was estimated by the myocardial early diastolic velocity (E') at the lateral annulus. There were 51 patients (62.2%) with nephritis, 23 patients (28.0%) with hypertension, 21 patients (25.6%) with vasculitis, 16 patients (19.5%) with pulmonary hypertension, 4 patients (4.9%) with cerebrovascular disease and 2 patients (2.4%) with diabetes mellitus. Sixty-two patients (75.6%) were taking prednisone and 35 patients (42.7%) used a immunosuppressant. Forty-five patients (54.8%) had active disease and suffered from disease-related end-organ damage. Patients with SLICC/ACR damage index ≥1 had more evidence of LV diastolic dysfunction with lower lateral annulus E' (9.6 ± 3.4 vs 12.9 ± 3.5 cm/s, p < 0.001) than those without. In addition, the proportion of patients with abnormal LV myocardial relaxation (defined as lateral E' < 10.0 cm/s) (51.1% vs 16.2%, χ(2) = 10.8, p = 0.001) were significantly higher. Multivariate analysis showed that the SLICC/ACR damage index ≥1 was independently associated with LV diastolic dysfunction (OR = 3.80, 95%CI: 1.21-11.95, p = 0.023) after adjusting for hypertension, disease duration and medical therapy. This may suggest that the overall inflammatory burden in SLE, as reflected by SLICC/ACR damage index, is associated with the development of diastolic dysfunction in SLE patients.

Effects of rosuvastatin on subclinical atherosclerosis and arterial stiffness in rheumatoid arthritis: a randomized controlled pilot trial.

OBJECTIVE: To ascertain the effect of rosuvastatin on carotid atherosclerosis and arterial stiffness in patients with rheumatoid arthritis (RA). METHODS: Fifty RA patients were randomized in a double-blind placebo-controlled trial to receive 10 mg rosuvastatin (n = 24) or placebo (n = 26). Patients were followed prospectively every 3 months for 12 months. Intima-media thickness (IMT), augmentation index (AIx), and subendocardial viability ratio (SEVR) were measured at baseline, 6 and 12 months. RESULTS: Rosuvastatin resulted in statistically significant reductions of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), and urate levels vs. placebo. However, rosuvastatin had no significant effect on changes in inflammatory markers, including C-reactive protein (CRP) levels [from 2.9 (1.4-11.0) to 3.1 (0.9-13.3) mg/L in the rosuvastatin group compared with from 5.8 (2.6-14.2) to 4.4 (1.2-12.3) mg/L in the placebo group]. Nonetheless, a significant improvement in the Disease Activity Score (DAS) and a reduction in fibrinogen level was observed at 6 and 12 months compared with baseline in the rosuvastatin group. The treatment group exhibited a significant increase in SEVR (from 157 ± 28% to 163 ± 33% in the rosuvastatin group compared with from 143 ± 18% to 143 ± 26% in the placebo group, p = 0.023), but no significant effect was observed in the changes in IMT and AIx. CONCLUSION: Our data suggest that rosuvastatin has a modest anti-inflammatory effect in RA patients with low disease activity in terms of reduction in DAS and fibrinogen level. Rosuvastastin may also improve subendocardial perfusion and lower the urate level.

Cardiovascular complications of severe acute respiratory syndrome.

BACKGROUND AND AIMS: Severe acute respiratory syndrome (SARS) is a virulent viral infection that affects a number of organs and systems. This study examined if SARS may result in cardiovascular complications. METHODS AND RESULTS: 121 patients (37.5 (SD13.2) years, 36% male) diagnosed to have SARS were assessed continuously for blood pressure, pulse, and temperature during their stay in hospital. Hypotension occurred in 61 (50.4%) patients in hospital, and was found in 28.1%, 21.5%, and 14.8% of patients during the first, second, and third week, respectively. Only one patient who had transient echocardiographic evidence of impaired left ventricular systolic function required temporary inotropic support. Tachycardia was present in 87 (71.9%) patients, and was found in 62.8%, 45.4%, and 35.5% of patients from the first to third week. It occurred independent of hypotension, and could not be explained by the presence of fever. Tachycardia was also present in 38.8% of patients at follow up. Bradycardia only occurred in 18 (14.9%) patients as a transient event. Reversible cardiomegaly was reported in 13 (10.7%) patients, but without clinical evidence of heart failure. Transient atrial fibrillation was present in one patient. Corticosteroid therapy was weakly associated with tachycardia during the second (chi(2) = 3.99, p = 0.046) and third week (chi(2) = 6.53, p = 0.01), although it could not explain tachycardia during follow up. CONCLUSIONS: In patients with SARS, cardiovascular complications including hypotension and tachycardia were common but usually self limiting. Bradycardia and cardiomegaly were less common, while cardiac arrhythmia was rare. However, only tachycardia persisted even when corticosteroid therapy was withdrawn.

Disease chronicity and activity predict subclinical left ventricular systolic dysfunction in patients with systemic lupus erythematosus.

OBJECTIVE: This study investigates parameters that could predict subclinical cardiac dysfunction in systemic lupus erythematosus (SLE) in the absence of valvular, clinical coronary artery and pericardial disease. DESIGN: A case-control trial. SETTING: Rheumatology clinic, a university teaching hospital. PATIENTS: Eighty-two female SLE patients (49 (SD 9) years) and 82 female normal subjects (49 (13) years) matched for age, body mass index, blood pressure and heart rate. INTERVENTIONS: All underwent standard echocardiography and tissue Doppler imaging. MAIN OUTCOME MEASURES: Twenty-two (27%) patients had evidence of impaired left ventricular (LV) long-axis function with mean myocardial peak systolic velocity (Sm) of basal six segments <4.4 cm/s and also subnormal stress-corrected midwall fractional shortening. Thirty-four (42%) patients demonstrated impaired right ventricular (RV) long-axis function. These occurred in the presence of comparable normal LV ejection fraction, cardiac index, and RV fractional area change to the control group. Patients with subnormal mean Sm were older (49 (8) vs 44 (9); p = 0.043) and had a higher prevalence of hypertension (46% vs 22%; p = 0.034), longer disease duration >10 years (82% vs 50%, p = 0.01), higher disease activity score (73% vs 48% for Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)> or =1, p = 0.049) and end-organ damage index (64% vs 47% with Systemic Lupus International Collaborating Clinics Damage Index (SLICC)> or =1, p = 0.049) than those with normal values. Disease duration >10 years, disease activity index and increased arterial stiffness provided additional incremental predictive value of LV long-axis function. CONCLUSION: SLE patients have subclinical long and short-axis dysfunctions. Regular monitoring of cardiac function by tissue Doppler echocardiography may be indicated for patients who had SLE for >10 years, frequent flare or when arterial stiffening is demonstrated.

Increased arterial stiffness correlated with disease activity in systemic lupus erythematosus.

To evaluate the relationships between arterial stiffness, disease activity and end-organ damage in systemic lupus erythematosus (SLE), non-invasive vascular assessments were made on 32 female SLE patients and 32 female normal controls. The patients had significantly increased brachial-ankle pulse wave velocity (PWV) (13.06 +/- 1.79 vs. 11.50 +/- 1.00 m/s; P < 0.001), heart-ankle PWV (8.98 +/- 1.16 vs. 7.88 +/- 0.73 m/s; P < 0.001), carotid augmentation index (AI) (21.6 +/- 17.2% vs. 5.4 +/- 14.0%; P = 0.001) and carotid intima-medial thickness (IMT) (0.753 +/- 0.132 vs. 0.644 +/- 0.092 mm; P = 0.002) when compared with controls. The disease activity and organ damage were evaluated by SLE disease activity index (SLEDAI) and systemic lupus international collaborating clinics (SLICC) damage index. Patients with active disease (SLEDAI > or = 3) had significantly higher carotid AI (34.4 +/- 9.7% vs. 17.8 +/- 17.3%, P < 0.05) than stable ones (SLEDAI < 3) and those with organ damage (SLICC > or = 1) had significantly higher heart-ankle PWV (9.69 +/- 1.13 vs. 8.61 +/- 1.02 m/s, P < 0.05) than those with SLICC = 0. After making adjustments for age, body mass index (BMI) and blood pressure, carotid AI was found to show correlation with SLEDAI and haPWV with SLICC. A carotid AI value of 33.3% identified SLEDAI > or = 3 with a sensitivity of 83% and a specificity of 80%, whereas a heart-ankle PWV value of 9.0 m/s identified SLICC > or = 1 with a sensitivity of 91% and a specificity of 67%. In conclusion, SLE was an independent risk factor of sub-clinical atherosclerosis and arterial stiffness may identify the presence of active disease.

Improvement of left ventricular myocardial short-axis, but not long-axis function or torsion after cardiac resynchronisation therapy: an assessment by two-dimensional speckle tracking.

AIMS: To evaluate whether short-axis function plays a part in determining left ventricular (LV) geometric and functional improvement after cardiac resynchronisation therapy (CRT). METHODS AND RESULTS: 39 patients who received CRT were enrolled. 2D speckle tracking echocardiography was performed at baseline and three months after CRT to assess mean systolic circumferential (epsilon-circum), radial (epsilon-radial) and longitudinal (epsilon-long) strain and torsion. Responders of reverse remodelling (n = 21) had higher baseline mean epsilon-circum than non-responders (p<0.05), who also had improvement in mean epsilon-circum and mean epsilon-radial (both p<0.05) after CRT. Also, the increase in mean epsilon-circum correlated with increase in ejection fraction (r = 0.57, p<0.001) and decrease in mid-cavity width (r = -0.52, p = 0.001). A baseline mean epsilon-circum of >or=6.5% predicted a gain in ejection fraction >or=5%, with a sensitivity of 73% and a specificity of 71%. The baseline epsilon-long was not different between the two groups, and remained unchanged after CRT. The torsion did not improve in responders, but was worsened in non-responders (p<0.05). CONCLUSIONS: The improvement of LV short-axis function but not long-axis function or torsion contributes to the improvement in LV global function and geometry at three-month follow up. A relatively preserved mean epsilon-circum of >or=6.5% might be useful to predict favourable responses after CRT.

The Hong Kong diastolic heart failure study: a randomised controlled trial of diuretics, irbesartan and ramipril on quality of life, exercise capacity, left ventricular global and regional function in heart failure with a normal ejection fraction.

BACKGROUND: Although heart failure with a preserved or normal ejection fraction (HFNEF or diastolic heart failure) is common, treatment outcomes on quality of life and cardiac function are lacking. The effect of renin-angiotensin blockade by irbesartan or ramipril in combination with diuretics on quality of life (QoL), regional and global systolic and diastolic function was assessed in HFNEF patients. METHODS: 150 patients with HFNEF (LVEF >45%) were randomised to (1) diuretics alone, (2) diuretics plus irbesartan, or (3) diuretics plus ramipril. QoL, 6-minute walk test (6MWT) and Doppler echocardiography were performed at baseline, 12, 24 and 52 weeks. RESULTS: The QoL score improved similarly in all three groups by 52 weeks (-46%, 51%, and 50% respectively, all p<0.01), although 6MWT increased only slightly (average +3-6%). Recurrent hospitalisation rates were equal in all groups (10-12% in 1 year). At 1 year, LV dimensions or LVEF had not changed in any group, though both systolic and diastolic blood pressures were lowered in all three groups from 4 weeks onwards. At baseline both mean peak systolic (Sm) and early diastolic (Em) mitral annulus velocities were reduced, and increased slightly in the diuretic plus irbesartan (Sm 4.5 (SEM 0.17) to 4.9 (SEM 0.16) cm/sec; Em 3.8 (SEM 0.25) to 4.2 (SEM 0.25) cm/sec) and ramipril (Sm 4.5 (SEM 0.24) to 4.9 (SEM 0.20) cm/sec; Em 3.3 (SEM 0.25) to 4.04 (SEM 0.32) cm/sec) groups (both p<0.05). NT-pro-BNP levels were raised at baseline (595 (SD 905) pg/ml; range 5-4748) and fell in the irbesartan (-124 (SD 302) pg/ml, p = 0.01) and ramipril (-173 (SD 415) pg/ml, p = 0.03) groups only. CONCLUSIONS: In this typically elderly group of HF patients with normal LVEF, diuretic therapy significantly improved symptoms and neither irbesartan nor ramipril had a significant additional effect. However, diuretics in combination with irbesartan or ramipril marginally improved LV systolic and diastolic longitudinal LV function, and lowered NT-proBNP over 1 year.

Tissue Doppler velocity is superior to displacement and strain mapping in predicting left ventricular reverse remodelling response after cardiac resynchronisation therapy.

OBJECTIVE: To compare the values of three different forms of tissue Doppler imaging (TDI) processing in predicting left ventricular (LV) reverse remodelling-namely, tissue velocity, displacement and strain mapping. DESIGN: Standard echocardiography with TDI was performed before and 3 months after cardiac resynchronisation therapy (CRT). SETTING: University teaching hospital. PATIENTS: 55 patients with heart failure who received CRT and were followed up for at least 3 months were recruited. INTERVENTIONS: During off-line analysis, the time to peak systolic velocity in the ejection phase, time to peak positive displacement and time to peak negative strain were measured in the six basal, six mid-segmental model. Parameters of systolic asynchrony derived by velocity, displacement and strain mapping were correlated with percentage reduction in LV end systolic volume (LVESV) and absolute gain in ejection fraction (EF). RESULTS: Among the three TDI processing technologies, all parameters of tissue velocity correlated with LV reverse remodelling (r = -0.49 to r = -0.76, all p < 0.001), but the predictive value was strongest in models with 12 LV segments. For displacement mapping, only the two parameters that included 12 LV segments correlated modestly with reduction in LVESV (r = -0.36, p < 0.05) and gain in EF. However, none of the strain mapping parameters predicted a favourable echocardiographic response. The receiver operating characteristic (ROC) curve areas were higher for parameters of tissue velocity based on 12 LV segments (ROC areas 0.88 and 0.94) than the corresponding areas derived from displacement mapping (ROC areas 0.72 and 0.71). CONCLUSION: Tissue velocity parameters of systolic asynchrony are superior to those of displacement and strain mapping in predicting LV reverse remodelling response after CRT.