Left atrial and left atrial appendage functional recovery after cardioversion in patients with recent atrial fibrillation: Serial echocardiographic study.

BACKGROUND: The aim of this study is to point out timing of left atrium and its appendage functional recovery after cardioversion (CV) in recent onset atrial fibrillation (AF). METHODS: Fifty patients; 27 within 48-h (group I) and 23 after 48-h (group II), of AF onset, who had successful CV underwent transthoracic echocardiography (TTE), before and immediately after CV, then 15, 30 and 90 days later. Transesophageal echocardiography (TEE) was performed for group II before and for all patients immediately after CV and 1 month later. Mitral peak A velocity and left atrial (LA) reversal (Ar) velocity, tissue Doppler imaging (TDI) of septal mitral annular velocity (A1) and LA free wall velocity (A3) were recorded. Absence or peak A velocity < 50 cm/s was taken as a cut off value for atrial stunning. Intra-atrial conduction time (IACT) was measured. LA appendage late emptying (LAALE) velocity was measured by TEE-pulsed TDI of LA appendage. RESULTS: Post CV, all group II and 34% of group I experienced stunning. In both groups, peak A, Ar, A1, A3 and LAALE velocities increased (p = 0.000), while IACT decreased (p = 0.000) progressively over time. Partial recovery occurred after 15 and 30 days, while full recovery occurred 30 and 90 days post CV in groups I and II, respectively. IACT1 and IACT2 correlated with LA diameter (r = 0.2778 and r = 0.227, respectively, p < 0.01). CONCLUSIONS: Stunning and functional recovery of the LA and its appendage are strongly determined by the duration being in AF. Serial IACT by TDI was a good new parameter for detection of functional recovery of LA and LA appendage.

Optical coherence tomography features of angiographic complex and smooth lesions in acute coronary syndromes.

Plaque rupture (PR) and superimposed thrombosis have been shown as the most frequent underlying substrate in acute coronary syndromes (ACS). Coronary angiography is a luminogram not able to define in vivo features of the culprit plaques. The aim of the study was to use optical coherence tomography (OCT) to investigate the pathology underlying complex (CL) and non-complex angiographic lesions (NCL). We retrospectively enrolled 107 ACS patients admitted to our institution; 83 with non-ST elevation ACS (NSTE-ACS) and 24 with ST-elevation myocardial infarction. Coronary angiography was performed and culprit lesions were classified according to Ambrose criteria into NCL (n = 47) and CL (n = 60). OCT imaging was then performed to better identify plaque morphology; either PR or intact fibrous cap, the presence of superimposed thrombosis, lipid rich plaque, and thin cap fibroatheroma (TCFA). OCT analysis showed that 58 lesions (54.2%) were classified as PR and 48 lesions (44.9%) were associated with thrombi. Lipid rich plaques were identified in 62 lesions (57.9%). PR, intracoronary thrombi, lipid rich plaques and TCFA were more frequent in CL compared with NCL (71.7 vs 31.9%, 63.3 vs 21.3%, 71.7 vs 40.4% and 46.7 vs 21.3% respectively), but PR with superimposed thrombus may be also detected in NCL. OCT demonstrates PR and thrombosis in the majority of ACS patients presenting with CL. However, one-third of NCL show PR by OCT, suggesting that additional intracoronary imaging by OCT may better identify the underlying mechanism of coronary instability than coronary angiography alone.

Mean platelet volume and its relation to insulin resistance in non-diabetic patients with slow coronary flow.

BACKGROUND: Increased mean platelet volume is a central process in the pathophysiology of coronary heart disease. Insulin resistance contributes to increased platelet activation. AIM: To assess the mean platelet volume and its possible relationship with insulin resistance in non-diabetic patients with slow coronary flow. METHODS AND SUBJECTS: The study included 60 patients with slow coronary flow and 20 subjects (controls) with normal coronary arteries. Slow coronary flow patients were divided into 2 groups, insulin resistant (32 patients) and insulin sensitive (28 patients) according to the homeostasis model assessment of insulin resistance index (HOMA-IR). RESULTS: Patients with slow coronary flow had significantly higher mean platelet volume values (7.9±0.47 vs. 7.1±0.5, p<0.01), insulin level (10.8±3.2 vs. 8.2±1.4, p<0.01), and HOMA-IR scores (2.72±0.85 vs. 1.84±0.19, p<0.01). These parameters were significantly higher in insulin-resistant patients than in insulin-sensitive ones. The mean platelet volume was correlated with HOMA-IR (r=0.52, p<0.01) and insulin level (r=0.58, p<0.01). In multivariate analysis, mean platelet volume and HOMA-IR were independent predictors of mean TIMI frame count {(B±SE=0.562±2.95, p<0.01) and (B±SE=0.538±2.46, p<0.01), respectively}. CONCLUSION: Patients with slow coronary flow have increased mean platelet volume which was associated with insulin resistance in non-diabetic slow coronary flow patients. TIMI frame counts correlated with mean platelet volume and increased insulin resistance. Thus, insulin resistance and platelet activity may have a role in the pathogenesis of slow coronary flow. Also, they may have a possible benefit as follow-up markers in non-diabetic patients with slow coronary flow.

Arterial stiffness is associated with tissue Doppler atrial conduction times and P wave dispersion in hypertensive patients.

BACKGROUND: Arterial stiffness is strongly predictive for cardiovascular events in hypertensive individuals and it may increase the risk of stroke. This study was designed to evaluate the possible relationship between arterial stiffness and atrial electromechanical delay and P wave dispersion (PWD), as determinants of AF risk. MATERIALS AND METHODS: The study included 75 hypertensive patients and 45 healthy control subjects. Atrial electromechanical coupling (time interval from the onset of P wave on ECG to the beginning of A wave with tissue Doppler echocardiography [PA]), intraatrial and interatrial electromechanical delay (EMD) and PWD were measured. Stiffness index ß & PWV was measured to assess the arterial stiffness. RESULTS: The interatrial EMD and PWD were prolonged in hypertensive patients compared to controls (p<0.01 for both), There was increased arterial stiffness (PWV and stiffness index ß) in hypertensive patients compared to controls (6.43 ± 1.73 vs. 4.8 ± 1.6 m/sec & 4.9 ± 2.8 vs. 2.63 ± 1.2, p<0.01 for both). By multivariate analysis; PWV and Stiffness index ß were independently correlated with interatrial EMD (B ± SE=0.42 ± 1.87, B ± SE=0.39 ± 0.21 p<0.01 for both) and PWD (B ± SE=0.37 ± 1.93, p<0.01, B ± SE=0.25 ± 0.18, p<0.05 respectively). CONCLUSION: In hypertensive patients arterial stiffness indexes increased and showed a significant correlation with interatrial EMD and PWD independent of other variables. Further research is needed to determine whether interventions that reduce arterial stiffness will limit the growing incidence of AF.

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.