Relationship between histopathological features of aspirated thrombi and long-term left ventricular function in patients with ST-segment elevation myocardial infarction.

OBJECTIVE: This study was an investigation of the severity of inflammation (SOI) in aspirated material and thrombus age to examine any association with pre-discharge and long-term left ventricular (LV) function after ST-elevation myocardial infarction (STEMI). METHODS: The study group comprised 25 patients with STEMI from whom an occlusive thrombus was aspirated from the infarct-related artery with a 7-F catheter. The SOI in the aspirate was determined according to the mean leukocyte count in 5 high-power magnification fields and graded as mild in the presence of ≤100 leukocytes per field or significant if there were >100 leukocytes per field. The thrombi were categorized as fresh or lytic/organized (L/O) using predefined criteria. Echocardiographic assessment was performed prior to discharge and at 1 year. Adverse left ventricular remodeling (LVR) was defined as a 20% increase in LV end-diastolic volume in comparison with baseline values. RESULTS: LVR was observed in 8 patients. The mean leukocyte count of the aspirate (127.5±86.0 vs 227.2±120.7; p=0.026) and frequency of significant inflammation (35% vs 75% p=0.046) were significantly higher in the group with LVR. The serum high-sensitivity C-reactive protein (hsCRP) level was significantly correlated with the leukocyte count of the aspirate (r=0.532; p=0.006). An L/O thrombus was related to better pre-discharge and long-term LV volumes and ejection fraction values compared with a fresh thrombus. CONCLUSION: A significant increase in the leukocyte count in the aspirate and a fresh thrombus might predict long-term LV functional deterioration irrespective of the clinical and procedure-related characteristics. In addition, serum markers of inflammation, like hsCRP, might also reflect the intensity of the local inflammatory response at the site of occlusion.

Assessment of repolarization abnormalities in baseline electrocardiograms of patients with myocarditis

Background/aim: Myocarditis in the acute phase usually presents with sinus tachycardia but many other arrhythmias might be seen as well. In this study we aimed to investigate repolarization abnormalities in baseline ECG of patients with myocarditis for the first time.Materials and methods: Thirty patients diagnosed with myocarditis and 25 healthy age-matched controls were included. Two different cardiologists measured corrected QT (QTc), QT dispersion (QTd), QT peak (QTp), T wave peak to T wave end (TpTe), TpTe/QT ratio, and TpTe/QTc ratio in 12-lead ECG.Results: When compared with the control group, QTp (P: 0.021), QT (P: 0.003), TpTe (P < 0.001), TpTe/QTc ratio (P < 0.001), and TpTe/QT ratio (P: 0.005) were significantly higher in patients with myocarditis. A comparison of receiver operating characteristic (ROC) curves was conducted using the Hanley and McNeil method. The area under the curve (AUC) of the electrocardiographic characteristics QT (AUC: 0.736; 95% CI [0.600-0.846]), QTP (AUC: 0.680; 95% CI [0.540-0.799]), and TpTe (AUC: 0.771; 95% CI [0.638-873]) and TpTe/QTc (AUC: 0.774; 95% CI [0.641-0.876]) and TpTe/QT (AUC: 0.726; 95% CI [0.589-0.838]) in myocarditis were not significantly different from each other but all of them were different from 0.5.Conclusion: Baseline ECGs of patients with myocarditis were associated with repolarization abnormalities. These novel findings may be one of the reasons underlying arrhythmic events in patients with myocarditis.

Evaluation of atrial conduction features with tissue Doppler imaging in patients with chronic obstructive pulmonary disease.

BACKGROUND: The electrical activity of atria can be demonstrated by P waves on surface electrocardiogram (ECG). Atrial electromechanical delay (AEMD) measured with tissue Doppler imaging (TDI) echocardiography can be a useful non-invasive method for evaluating atrial conduction features. We investigated whether AEMD is prolonged in patients with chronic obstructive pulmonary disease (COPD). PATIENTS AND METHODS: Study consisted of 41 (15 female, 26 male, mean age 62 + 12 years) patients with COPD and 41 healthy subjects. Pulmonary function tests,12 lead surface ECG and echocardiographic examination were performed and recorded. P wave changes on surface ECG, minimum (P (min)) and maximum (P (max)) duration of P wave and its difference as P wave dispersion (P (wd)) were measured and recorded. Atrial electromechanic delay (AEMD) was calculated from colored-TDI recordings. RESULTS: Pulmonary functions were significantly lower in COPD group than the control group as expected. Right atrial areas and pulmonary arterial systolic pressures (PAP) were significantly higher in COPD group than the controls (right atrial area: 11.9 ± 3.4 cm(2) and 8.2 ± 2.2 cm(2), p < 0.0001 and PAP: 38.4 ± 12.2 and 19.0 ± 3.2 mmHg p < 0.0001, respectively). P wave intervals on surface ECG were significantly increased in COPD patients than the control group (P (max): 105 ± 11 and 90 ± 12 ms, p < 0.0001; P (min): 60 ± 12 and 51 ± 10 ms, p = 0.003 and P (wd): 39 ± 10 and 31 ± 7 ms, p < 0.0001). According to the AEMD measurements from different sites by TDI, there was a significant delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave in patients with COPD when compared with controls measured from tricuspid lateral septal annulus (TAEMD) (COPD: 41.3 ± 9.8 ms, control: 36 ± 4.5 ms; p = 0.005). There was a positive correlation between TAEMD and right atrial area (r = 0.63, p < 0.0001) and also between TAEMD and PASP (r = 0.43, p < 0.0005) and a negative correlation between TAEMD and forced expiratory volume (FEV1) (r = -0.44, p = 0.04). CONCLUSIONS: Right atrial electromechanical delay is significantly prolonged in patients with COPD. The right atrial area, PAP and FEV1 levels are important factors of this prolonged delay. Also the duration of atrial depolarization is significantly prolonged and propagation of depolarization is inhomogeneous in patients with COPD. These may be the underlying mechanisms to explain the atrial premature beats, multifocal atrial tachycardia, atrial flutter and fibrillation often seen in patients with COPD secondary to these changes.