Systolic Coronary Flow Velocity Research Articles

Acceleration Time of Systolic Coronary Flow Velocity to Diagnose Coronary Stenosis in Patients with Microvascular Dysfunction

The aim of this study was to test whether acceleration time of systolic coronary flow velocity could contribute to the diagnosis of coronary stenosis in patients with microvascular dysfunction, on the basis of the hypothesis that systolic coronary flow is less influenced by microvascular function because of compressed myocardium. Coronary flow velocity was assessed in the left anterior descending coronary artery during hyperemia with intravenous adenosine by echocardiography in 502 patients who were scheduled for coronary angiography because of coronary artery disease and significant valvular disease. Coronary flow velocity reserve (CFVR) and the percentage acceleration time (%AT), as the percentage of the time from the beginning to the peak of systolic coronary flow over systolic time during hyperemia, were calculated. The diagnostic ability of CFVR and %AT for angiographic coronary artery stenosis was then analyzed. As invasive substudies, fractional flow reserve and %AT by a dual-sensor (pressure and Doppler velocity) guidewire were measured simultaneously with %AT on transthoracic echocardiography (n= 14). Patients with coronary stenosis had significantly lower CFVR (1.7 ± 0.4) and greater %AT (65 ± 9%) compared with those without stenosis (2.6 ± 0.6 and 50 ± 13%, respectively). Percentage acceleration time by Doppler echocardiography was in good agreement with %AT (r= 0.98) and fractional flow reserve (r= 0.74) invasively measured by dual-sensor guidewire. Cutoff values of CFVR and %AT were determined as 2.0 and 60% in receiver operating characteristic curve analysis. The sensitivity, specificity, and accuracy of CFVR to detect coronary stenosis were 71.1%, 77.3%, and 75.4%, while those of %AT were 83.4%, 71.8%, and 75.4%, respectively. In addition, %AT provided high accuracy to detect coronary stenosis, especially in patients with previous myocardial infarctions, valvular disease, and left ventricular hypertrophy (81.1%, 84.1%, and 73.4%, respectively). The %AT of systolic coronary flow velocity is a promising marker to diagnose coronary stenosis in patients with microvascular dysfunction.

Prompt augmentation in systolic coronary flow velocity and forward coronary wave energy in patients undergoing transcatheter aortic valve implantation

Prompt augmentation in systolic coronary flow velocity and forward coronary wave energy in patients undergoing transcatheter aortic valve implantation

Determinants of coronary flow abnormalities in obstructive type hypertrophic cardiomyopathy: noninvasive assessment by transthoracic Doppler echocardiography

We aimed to visualize the coronary flow velocities (CFV) of patients with hypertrophic obstructive cardiomyopathy by using transthoracic Doppler echocardiography, and to determine the relationship between abnormal CFV patterns and conventional echocardiography indices. Guided by 2-dimensional echocardiography and Doppler color flow mapping, CFV in the distal left anterior descending coronary artery were measured in 21 patients with hypertrophic obstructive cardiomyopathy using a 3.5-MHz transducer. The results were compared with those of 18 control subjects. Abnormal systolic flow patterns were observed in 15 (71%) patients (11 systolic-reversal flow and 4 no systolic flow). For patients and control subjects, peak diastolic velocity and velocity-time integral obtained from distal left anterior descending coronary artery were higher (63 ± 21 cm/s and 18.5 ± 4 cm vs 41 ± 11 cm/s and 14.2 ± 5 cm, respectively; P < .01 for both) whereas peak systolic velocity and velocity-time integral were significantly lower (−17 ± 10 cm/s and 4.5 ± 6 cm vs 24 ± 9 cm/s and 9.5 ± 4 cm, respectively; P < .001 for both). Significant positive and negative correlations between diastolic CFV and septal thickness index ( r = 0.79, P < .0001), and between systolic CFV and septal thickness index ( r = −0.65, P < .005), have been observed. CFV abnormalities that could easily be recorded by a standard Doppler echocardiographic study seem to be related to septal thickness rather than the degree of obstruction in hypertrophic obstructive cardiomyopathy.

Abnormal transoesophageal Doppler coronary flow reserve in patients with dilated cardiomyopathy: relationship to exercise capacity.

1. In patients with dilated cardiomyopathy, abnormal myocardial blood flow may contribute to poor myocardial function. 2. The aim of this study was to investigate the possible contribution of abnormal myocardial blood flow to the limitation of exercise capacity in patients with dilated cardiomyopathy. 3. Coronary flow reserve was assessed in 16 patients with dilated cardiomyopathy and 9 matched normal control individuals. All participants had angiographically normal coronary arteries. At rest and after dipyridamole infusion (0.56 mg/kg intravenously), peak systolic and diastolic coronary flow velocities were measured in the proximal left anterior descending coronary artery using transoesophageal pulsed Doppler echocardiography, guided by colour flow imaging. Coronary flow reserve was calculated as the ratio of hyperaemic to basal diastolic and systolic peak coronary flow reserve. 4. Baseline diastolic and systolic coronary flow velocities were significantly higher in patients (50 +/- 6 and 30 +/- 4 cm/s respectively) compared with control individuals (37 +/- 3 and 20 +/- 1 cm/s respectively) (mean +/- S.E.M.) (P < 0.05). Diastolic and systolic peak coronary flow reserve were significantly lower in patients (1.60 +/- 0.14 and 1.40 +/- 0.09 respectively) compared with control individuals (2.89 +/- 0.15 and 2.17 +/- 0.17 respectively) (P < 0.001). Although peak VO2 and exercise time were significantly lower in patients compared with control individuals, coronary flow reserve did not correlate to exercise capacity in patients with dilated cardiomyopathy. 5. These results confirm the abnormalities of coronary flow reserve previously observed in patients with dilated cardiomyopathy, but suggest that such abnormalities do not contribute to the limitation of exercise capacity in these patients.

Abnormal coronary flow velocity pattern in patients with left ventricular hypertrophy, angina pectoris, and normal coronary arteries: A transesophageal Doppler echocardiographic study

Previous invasive studies have suggested that coronary flow reserve is impaired in patients with left ventricular hypertrophy (LVH) and symptoms of ischemia. We tested whether transesophageal Doppler, a semiinvasive technique, can detect altered characteristics of baseline coronary blood flow velocity in such patients. Thirty patients with LVH (hypertrophic cardiomyopathy in 4, aortic stenosis in 17, hypertension in 9) were studied. Fourteen patients had asymptomatic LVH. Sixteen patients had clinical symptoms of ischemia with angiographically normal epicardial coronary arteries. Ten subjects with no cardiovascular disease were studied as a control group. Peak diastolic and systolic coronary flow velocities were recorded in the proximal part of the left anterior descending artery (LAD) with the use of pulsed Doppler guided by color flow imaging. Patients with symptomatic LVH had higher diastolic peak coronary flow velocity (81 ± 10 cm/sec, p = 0.0001) compared with normal subjects (41 ± 8 cm/sec) and patients with asymptomatic LVH (44 ± 8 cm/sec). In patients with asymptomatic LVH the diastolic coronary flow velocity/indexed ventricular mass ratio was lower (0.28 ± 0.09 cm/gm/m 2, p = 0.0001) compared with symptomatic patients (0.52 ± 0.12 cm/gm/m 2) and compared with controls (0.47 ± 0.16 cm/gm/m 2). Patients with symptomatic LVH but no aortic stenosis also had higher peak systolic coronary flow velocity (38 ± 9 cm/sec) compared with the other groups ( p = 0.0001). In the group of patients with aortic stenosis a significant inverse linear relation was found between peak systolic coronary flow velocity and peak pressure gradient ( r = −0.60, p = 0.01). In conclusion, patients with symptomatic LVH have abnormally high baseline coronary flow velocities resulting in magnified intimal shear stress. Because flow velocity equals flow/vessel cross-sectional area, it is suggested that high coronary flow velocities in patients with symptomatic LVH result from both augmented coronary flow and failure of the vessel to enlarge commensurately with the increase in LV mass (relative functional stenosis). In patients with aortic stenosis, peak systolic coronary flow velocity appears to be influenced by transvalvular pressure drop.