Systolic Flow (systolic + flow)

Distribution by Scientific Domains


Selected Abstracts


Comparison of Coronary Flow Velocities Between Patients with Obstructive and Nonobstructive Type Hypertrophic Cardiomyopathy: Noninvasive Assessment by Transthoracic Doppler Echocardiography

ECHOCARDIOGRAPHY, Issue 1 2005
Seden Celik M.D.
Background: We aimed to compare coronary flow velocity (CFV) measurements of patients with nonobstructive (NHCM) and obstructive hypertrophic cardiomyopathy (HOCM) by using transthoracic Doppler echocardiography (TTDE). Methods and Results: In 11 patients with NHCM and 26 with HOCM, CFV in the distal left anterior descending (LAD) coronary was measured by TTDE (3.5 MHz) under the guidance of color Doppler flow mapping in addition to standard 2D and Doppler echocardiography. The results were compared with 24 normal participants who had no evidence of cardiac disease. Peak diastolic velocity of LAD was also higher in NHCM and HOCM than controls (52 ± 14 cm/sec and 54 ± 20 cm/sec vs 41 ± 11 cm/sec, respectively, P < 0.01). The analysis of systolic velocities revealed abnormal flow patterns in 16 (61%) patients with HOCM (12 systolic-reversal flow and 4 no systolic flow) and 6 (54%) (5 reversal flow and 1 zero flow) patients with NHCM (,11 ± 30 cm/sec and ,13 ± 38 cm/sec, vs 24 ± 9 cm/sec, respectively, P < 0.001). Linear regression analysis demonstrated no correlation between intraventricular pressure gradient and coronary flow velocities in HOCM patients. However, there were significant positive and negative correlations between septal thickness and diastolic and systolic velocities, respectively (r = 0.50, P < 0.002, and r =,0.43, P < 0.005). Conclusion: We conclude that the coronary flow velocity abnormalities are independent from the type of hypertrophic cardiomyopathy. [source]


Predictors for Maintenance of Sinus Rhythm after Cardioversion in Patients with Nonvalvular Atrial Fibrillation

ECHOCARDIOGRAPHY, Issue 5 2002
Ökçün M.D.
Recurrence of atrial fibrillation (AF) after cardioversion (CV) to sinus rhythm (SR) is determined by various clinical and echocardiographic parameters. Transesophageal echocardiographic (TEE) parameters have been the focus of clinicians' interests for restoring and maintaining SR. This study determined the clinical, transthoracic, and TEE parameters that predict maintenance of SR in patients with nonvalvular AF after CV. We enrolled 173 patients with nonvalvular AF in the study. TEE could not be performed in 26 patients prior to CV. Twenty-five patients had spontaneously CV prior to TEE. Six patients were excluded because of left atrial (LA) thrombus assessed by TEE. CV was unsuccessful in 6 patients. The remaining 110 consecutive patients (56 men, 54 women, mean age 69 ± 9 years), who had been successfully cardioverted to SR, were prospectively included in the study. Fifty-seven (52%) patients were still in SR 6 months after CV. Age, gender, the configuration of the fibrillation wave on the electrocardiogram, pulmonary venous diastolic flow, and the presence of diabetes, hypertension, coronary artery disease, mitral annulus calcification, and mitral valve prolapse (MVP) did not predict recurrence. Duration of AF, presence of chronic obstructive pulmonary disease (COPD), LA diameter, left ventricular ejection fraction (EF), left atrial appendage peak flow (LAAPF), LAA ejection fraction (LAAEF), pulmonary venous systolic flow (PVSF), and the presence of LA spontaneous echo contrast (LASEC) predicted recurrence of AF 6 months after CV. In multivariate analysis, LAAEF < 30% was found to be the only independent variable (P < 0.0012) predicting recurrence at 6 months after CV in patients with nonvalvular AF. LAAEF more than 30% had a sensitivity of 75% and a specificity of 88% in predicting maintenance of SR 6 months after CV in patients with nonvalvular AF. In conclusion, TEE variables often used to determine thromboembolic risk also might be used to predict the outcome of CV. [source]


Long-Term Mechanical Consequences of Permanent Right Ventricular Pacing: Effect of Pacing Site

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2010
DARRYL P. LEONG M.B.B.S.
Optimal Right Ventricular Pacing,Introduction: Long-term right ventricular apical (RVA) pacing has been associated with adverse effects on left ventricular systolic function; however, the comparative effects of right ventricular outflow tract (RVOT) pacing are unknown. Our aim was therefore to examine the long-term effects of septal RVOT versus RVA pacing on left ventricular and atrial structure and function. Methods: Fifty-eight patients who were prospectively randomized to long-term pacing either from the right ventricular apex or RVOT septum were studied echocardiographically. Left ventricular (LV) and atrial (LA) volumes were measured. LV 2D strain and tissue velocity images were analyzed to measure 18-segment time-to-peak longitudinal systolic strain and 12-segment time-to-peak systolic tissue velocity. Intra-LV synchrony was assessed by their respective standard deviations. Interventricular mechanical delay was measured as the difference in time-to-onset of systolic flow in the RVOT and LV outflow tract. Septal A' was measured using tissue velocity images. Results: Following 29 ± 10 months pacing, there was a significant difference in LV ejection fraction (P < 0.001), LV end-systolic volume (P = 0.007), and LA volume (P = 0.02) favoring the RVOT-paced group over the RVA-paced patients. RVA-pacing was associated with greater interventricular mechanical dyssynchrony and intra-LV dyssynchrony than RVOT-pacing. Septal A' was adversely affected by intra-LV dyssynchrony (P < 0.05). Conclusions: Long-term RVOT-pacing was associated with superior indices of LV structure and function compared with RVA-pacing, and was associated with less adverse LA remodeling. If pacing cannot be avoided, the RVOT septum may be the preferred site for right ventricular pacing. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1120-1126) [source]


Prospective analysis of carotid artery flow in breast cancer patients treated with supraclavicular irradiation 8 or more years previously,

CANCER, Issue 2 2008
No increase in ipsilateral carotid stenosis after radiation noted
Abstract BACKGROUND. To the authors' knowledge, the effects of supraclavicular fossa radiation on the carotid artery are not well described. In the current study, the authors performed a prospective study to examine the long-term risk of carotid artery stenosis after supraclavicular irradiation for breast cancer. METHODS. A total of 46 breast cancer patients who were treated with adjuvant radiation to the supraclavicular fossa with >8 years of follow-up underwent bilateral Doppler imaging of the carotid artery. Two independent cardiologists interpreted each ultrasound study with no knowledge of which side was treated. RESULTS. The median follow-up from the date of diagnosis was 14.6 years and the mean patient age at the time of ultrasound was 55 years. The median prescribed dose to the supraclavicular fossa was 50 grays. Four patients were found to have clinically relevant, asymptomatic carotid stenosis, for which a cardiology referral was necessary. Only 1 of these 4 patients had stenosis involving the irradiated carotid artery only; 1 patient had bilateral stenosis and 2 patients had only contralateral stenosis. There was no difference noted with regard to isolated ipsilateral versus contralateral medial intimal thickening of the carotid artery (5 patients vs 6 patients, respectively). Furthermore, there were no differences noted with regard to ipsilateral versus contralateral peak systolic flow in the internal (83.5 vs 85.6 cm/seconds; P = .522 by the Student t test and P = .871 by the signed rank test) or common (74.4 vs 77.0 cm/seconds; P = .462 by the Student t test and P = .246 by the signed rank test) carotid artery. CONCLUSIONS. In this prospective study of breast cancer patients with long follow-up, there was no evidence of late, clinically relevant stenosis, increased intimal thickening, or increased peak systolic carotid artery flow secondary to supraclavicular irradiation. Cancer 2008. © 2007 American Cancer Society. [source]