Mild mitral regurgitation reduces exercise capacity in patients with idiopathic dilated cardiomyopathy.

We evaluated 30 patients with dilated cardiomyopathy (New York Heart Association functional Class II or III with medical treatment) to assess the effect of mild mitral regurgitation (MR) on exercise capacity in patients with congestive heart failure. They were classified into two groups based on results of left ventriculography: MR present (n = 10) and MR absent (n = 20). The severity of the MR by left ventriculography was grade I (mild) in all patients with MR. Steady-state hemodynamic data and angiographic data did not differ significantly between the two groups. Heart rate and systolic blood pressure at rest and in response to symptom-limited exercise testing did not differ between the groups. However, the peak work load was significantly lower in the group with MR than that in the group without MR (101 +/- 32 vs. 142 +/- 29 W, respectively; p < 0.005). Peak oxygen uptake and peak oxygen pulse were also significantly lower in the group with MR than in that without MR (peak oxygen uptake: 18 +/- 23 +/- 5 ml/min/kg; p < 0.05, peak oxygen pulse: 6.6 +/- 2.6 vs. 9.5 +/- 2.7 ml/min/beat: p < 0.01, respectively). Thus, mild MR had a detrimental effect on the exercise capacity in patients with dilated cardiomyopathy.

Attenuated inhibition of adrenergic contraction by nitric oxide in injured guinea pig femoral artery.

The present study aimed to examine the altered modulation of adrenergic contraction by nitric oxide and sensory neuropeptides in balloon-injured muscular artery. A guinea pig femoral artery (GPFA) was injured by a newly developed silastic microballoon catheter. The contralateral GPFA served as the control. The studied GPFAs consisted of six groups; control (C) and injured (I) GPFA, isolated at 0 days, and 2 and 8 weeks after injury (C0, I0, C2, I2, C8, and I8). Isometric tension was measured in the presence of indomethacin (10(-5) M), to exclude effects of cyclooxygenase-generated eicosanoids. Endothelial removal with the catheter was confirmed by histological examination. In each group, except for 10, NG-nitro-I-arginine methyl ester (L-NAME, 10(-6) M) induced significant augmentation of perivascular nerve stimulation (PNS)-evoked adrenergic contraction, which was blocked by L-arginine (3 x 10(-4) M). The degree of L-NAME augmentation in I8 was significantly smaller than that in C8 and I2. Capsaicin (10(-6) M) did not significantly affect PNS-contraction in any group, indicating that there was no sensory neuropeptide involvement in this contraction. In I8, acetylcholine (10(-6) M)-induced relaxation after noradrenaline (10(-5) M)-precontraction was significantly smaller than that seen in the other groups, except for I0, which was lacking in acetylcholine-induced relaxation. Histologically, injured GPFAs showed progressive intimal thickening. The present findings thus showed attenuated nitric oxide-mediated inhibition of adrenergic contraction, accompanying intimal thickening, in balloon-injured muscular artery, 8 weeks after injury.

Comparison of vessel wall morphologic appearance at sites of focal and diffuse coronary vasospasm by intravascular ultrasound.

Coronary vasospasm is manifested by either focal or diffuse pattern in clinical settings. To examine the differences in vessel wall morphologic appearance between the sites of focal and diffuse vasospasm, we studied 29 patients with chest pain at rest, during exertion, or both by intravascular ultrasound. By angiography, focal vasospasm with diameter reduction of 90% +/- 3% (mean +/- SD) was provoked by intracoronary ergonovine (0.01 to 0.04 mg) in 15 patients. Diffuse vasospasm with diameter reduction of 79% +/- 5% (NS) was provoked in seven patients, and the remaining seven patients served as the control group. By ultrasonography, a significantly thickened intimal leading edge with sonolucent zone was observed in 55 sites from 22 coronary arteries with either focal or diffuse vasospasms (0.61 +/- 0.32 mm), although these sites were normal or minimally narrowed by angiography. Seven segments from the control group exhibited a thin intimal leading edge with sonolucent zone (0.23 +/- 0.08 mm, p < 0.01). When the thickness of the intimal leading edge with sonolucent zone was compared between the abnormal sites with focal and diffuse vasospasm, this was significantly greater at focal spasm, 1.01 +/- 0.35 mm (n = 15), than that at diffuse spasm, 0.46 +/- 0.13 mm (n = 40, p < 0.01). At the sites with diffuse spasm, some of the lesions lay scattered along the coronary vessels, although the lesions were localized at the sites of focal vasospasm. These results indicate that atherosclerosis is present at sites with both focal and diffuse vasospasm even in the absence of angiographically significant coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of coronary artery distensibility by intravascular ultrasound. Application of simultaneous measurements of luminal area and pressure.

BACKGROUND: Atherosclerotic change in the coronary artery is associated with an impaired vessel wall distensibility. However, there are few data regarding the relation between vessel wall morphology and distensibility. Therefore, with intravascular ultrasound, we assessed coronary artery distensibility in angiographically normal coronary segments of humans. METHODS AND RESULTS: Data were analyzed at 35 angiographically normal coronary sites where circumferential or noncircumferential lesions were demonstrated by ultrasound in 22 patients (mean age, 55 years). After intracoronary injection of 500 micrograms nitroglycerin (NTG), coronary luminal area was measured with intravascular ultrasound (30 MHz, 3.5F to 4.3F, 1800 rpm). Intracoronary pressure was simultaneously measured with a 2F micromanometer-tipped catheter located at the left main coronary artery. The coronary distensibility index was calculated as 10-fold the ratio of luminal area change to intracoronary pressure change during a cardiac cycle. Another pressure-independent vascular stiffness index, beta, was derived by the following formula: beta = [ln(SBP/DBP)]/(dD/diastolic mean diameter), where SBP is systolic intracoronary pressure, DBP is diastolic intracoronary pressure, and dD is the difference between systolic and diastolic diameters. At the sites where luminal areas were measured, thickness of intima-media complex, defined as the distance between the intimal leading edge and the adventitial leading edge, was determined as an index of the severity of atherosclerosis. In seven segments, distensibility index was determined before and after NTG injection to examine the effect of NTG on coronary distensibility. In all examined sites, including circumferential and noncircumferential lesions, the luminal area was 12.6 +/- 5.0 mm2 during systole and 11.6 +/- 4.6 mm2 during diastole, and the calculated coronary distensibility index ranged from 0 to 0.83 mm2/mm Hg. The thickness of the intima-media complex ranged from 0.12 to 1.30 mm, suggesting the presence of various grades of atherosclerosis even in the absence of angiographic lesions. There was a poor inverse correlation between thickness of the intima-media complex and distensibility index (r = .19, y = -0.17x + 0.41, P = .29). However, when noncircumferential lesions were excluded for evaluation, there was a significant inverse correlation between them (r = .58, y = -0.50x + 0.72, P < .01). Under these conditions, the thickness of the intima-media complex also correlated with the value of beta (X10(-1), which ranged from 0.28 to 3.99 (r = .70). After NTG injection, coronary distensibility increased by an average of 71% in the segments with a thin intima-media complex, whereas it did not substantially change in those with a relatively thick intima-media complex. CONCLUSIONS: These results suggest that coronary distensibility is impaired in the coronary sites accompanying occult atherosclerosis, none of which can be detected by the conventional angiography. NTG can augment coronary distensibility in the segments without a markedly thickened intima-media complex. We suggest that thickness of the intima-media complex can contribute to determining the coronary distensibility in clinical settings.

Delayed improvement in exercise capacity with restoration of sinoatrial node response in patients after combined treatment with surgical repair for organic heart disease and the Maze procedure for atrial fibrillation.

BACKGROUND: Although the Maze procedure successfully restores sinus rhythm in patients with heart disease and atrial fibrillation, it is still uncertain whether an addition of the Maze procedure in cardiac surgery is beneficial for exercise performance of the patients after surgery. METHODS AND RESULTS: The Maze procedure was performed in 25 patients (age, 37 to 70 years) during valve surgery (18 patients) or closure of atrial septal defect (7 patients). A cardiopulmonary exercise test using ramp incremental protocol (15 W/min) was performed before and 1 month, 6 months, and 1 year after surgery. Sinus conversion was obtained in 23 of 25 patients 1 month after surgery. However, sinoatrial (SA) node response to exercise was attenuated by surgery: Mean heart rate (HR) was 83 +/- 13/min at rest, 94 +/- 13/min at 60 W, and 107 +/- 17/min at peak exercise. Peak oxygen uptake (PVO2) was unchanged at this period (before, 17.6 +/- 4.5 mL.min-1.kg-1; 1 month after, 17.5 +/- 4.2 mL.min-1.kg-1). Thereafter, SA node response was restored 6 months after surgery: Mean HR was 84 +/- 13/min at rest, 104 +/- 16/min at 60 W, and 130 +/- 20/min at peak exercise (P < .01 versus 1 month). PVO2 was also improved at this period (20.7 +/- 4.0 mL.min-1.kg-1, P < .01). The increase in PVO2 from 1 month to 6 months after surgery was correlated with the increase in peak HR (y = 0.73x +/- 3.6, r = .79). There were no further changes in heart rate response or PVO2 from 6 months to 1 year after surgery. CONCLUSIONS: Atrial fibrillation was successfully treated by combined treatment with surgical repair for organic heart disease and the Maze procedure. However, SA node response to exercise was attenuated early after surgery. Thus, exercise capacity was improved at the late phase after surgery, which was related to the extent of restoration in SA node response.

Percutaneous transvenous mitral commissurotomy immediately restores quick response of VO2 to mild exercise despite insignificant increases in peak VO2.

Percutaneous transvenous mitral commissurotomy (PTMC) increases peak oxygen uptake (VO2) chronically, but not acutely, despite early symptomatic improvements. Analysis of transient VO2 responses to submaximal exercise (an exercise regimen more comparable to the patients' daily activities than that provided by maximal exercise testing), may be sensitive in detecting the acute hemodynamic benefits of PTMC. Since no methods are available to accurately estimate the transient response of VO2, we developed a new technique, using random exercise. In 15 patients who underwent successful PTMC, we repeated the conventional maximal exercise test and the random exercise test before and within a few days after PTMC. For the random exercise test, we intermittently imposed upright bicycle exercise at 50 W, according to a random binary sequence, while measuring breath-by-breath VO2. After determining the transfer function relating workload to VO2, we computed the high resolution VO2 response to a hypothetical step increase in exercise. Despite improvements in resting hemodynamics and New York Heart Association (NYHA) Class, peak VO2 improved insignificantly (952 +/- 271 vs 1,029 +/- 342 ml/min, P = 0.063) shortly after successful PTMC. In contrast, the amplitude of the VO2 step response increased significantly in the early-to-mid portion (28-76s; P < 0.01-0.05). The remaining portion was unchanged. Consequently, the time constant shortened from 64 +/- 26 to 48 +/- 22s (P < 0.05). The maximal Borg scale value during random exercise decreased significantly (13.1 +/- 1.8 vs 11.4 +/- 1.1; P < 0.01). We conclude that the VO2 step response, using the random exercise test, is more sensitive than peak VO2 in detecting the functional improvement that is coupled with the hemodynamic improvement immediately after PTMC.

Progressive decreases in coronary vein flow during reperfusion in acute myocardial infarction: clinical documentation of the no reflow phenomenon after successful thrombolysis.

OBJECTIVES: This study was undertaken to examine the effects of coronary flow dynamics after thrombolysis on infarct size limitation. BACKGROUND: It has been commonly accepted that early thrombolysis does not necessarily salvage infarcted myocardium. Plausible causes for myocardial necrosis include such factors as elapsed time to reperfusion, residual stenosis, collateral vessels, hemodynamic loads, preconditioning and reperfusion injury. Recently, the no reflow phenomenon has been elucidated to be associated with infarct extension in clinical studies employing contrast echocardiography or thallium scintigraphy. METHODS: Nineteen patients with early reperfusion in acute anterior myocardial infarction and comparable clinical background were studied. The patients were classified into two groups on the basis of pattern of thermodilution measurements of great cardiac vein flow after reperfusion: group A, 9 patients with a progressive decrease in great cardiac vein flow during the 1st 24 h of the onset of infarction; and group B, 10 patients without this observation. Left ventricular ejection fraction and thallium perfusion defect were compared between the two groups at follow-up. RESULTS: There were no significant differences in systemic hemodynamic variables between groups A and B, and neither group had recurrent ischemic events suggesting reocclusion or restenosis during the study. In group A, both great cardiac vein flow (mean +/- SD 44 +/- 17% reduction) and oxygen extraction (38 +/- 15% reduction) were progressively decreased after the onset of reperfusion. Compared with group B, this group showed a lower left ventricular ejection fraction (36 +/- 7% vs. 63 +/- 15%, p < 0.01) and a larger thallium-201 defect severity index (1,091 +/- 366 U vs. 247 +/- 261 U, p < 0.01) at follow-up. Although other patient characteristics were comparable between the two groups, antecedent angina occurred in 90% of group B patients in contrast to only 33% of group A patients. CONCLUSIONS: Salvage of myocardium from infarction by successful thrombolysis was not observed in the patients demonstrating progressive decreases in great cardiac vein flow (group A). In those patients, inadequate myocardial reperfusion on a microvascular basis might be associated with a much larger myocardial infarction. Antecedent angina may protect against a progressive decrease in coronary flow and may have beneficial effects on infarct size limitation.

Consequence of diseases in aorta on evaluation of aortic regurgitation by aortic flow velocity profiles.

The aim of the study was to investigate whether flow velocity profiles of the aorta are related to the severity of aortic valve regurgitation (AR) in patients with diseases of the aorta. Aortic root angiography, abdominal aortic flow velocity measurements by pulsed Doppler method, and regurgitant jet measurements by color Doppler echocardiography were performed in 62 patients with various etiologies of AR and 13 patients without AR. The regurgitant fraction of abdominal aortic flow velocity profiles was related to the angiographic severity of AR except for the patients with Takayasu's arteritis and those after thoracic aorta grafting who showed large regurgitant fraction regardless of AR. Color Doppler evaluation was also correlated well with angiographic findings, but it was not possible in 13 of 62 patients with AR because of the inadequate color Doppler images. Although the observation of abdominal aortic flow profiles is clinically of value in noninvasive evaluation of AR, it could not be applied in patients with Takayasu's arteritis and those after graft surgery.

[Correlation of serial MRI and histological findings following intra-tumor local chemotherapy for malignant brain tumor].

Serial magnetic resonance imaging (MRI) studies on patients with malignant brain tumor after postoperative adjuvant therapy have been rarely reported. Leukoencephalopathy after such treatment is a well-known serious adverse effect, which we studied by serial MRI after postoperative adjuvant therapy in 15 patients with malignant brain tumors (anaplastic glioma 6, astrocytoma Grade III 5, astrocytoma Grade II 2, and metastatic brain tumor 2) (Table 1). All patients were examined by MRI, more than twice postoperatively. Adjuvant therapy was as follows: adriamycin (ADM) (0.5 mg) was injected through Ommaya reservoir into the tumor bed at the craniotomy. The usual total dose of ADM was 5.0 mg. In three of 15 patients, local methotrexate chemotherapy was added. Fourteen patients received a course of local irradiation 58 Gy on average combined with local ADM chemotherapy. Histological findings of three autopsy cases and ten reoperated ones were correlated with the serial MRI. Consecutive MRI were examined one and three months after adjuvant therapy. The results were as follows: One month after adjuvant therapy, thin and high signal intensity areas could be seen in the marginal zone of the tumor cavity on the gadolinium-enhanced T1-weighted MRI. High signal intensity areas could also be seen in the operative cavity on the T1-weighted MRI, which were suspected to be residual hematomas. In one patient, a high, diffuse and widespread signal area could be seen on T2-weighted MRI, suggesting leukoencephalopathy. Three months after adjuvant therapy, a high thick signal intensity area could be seen in the marginal zone of the tumor cavity and along the route of the Ommaya tube on the gadolinium-enhanced T1-weighted MRI, but there was no mass effect in these space taking lesions. In five cases, a low signal intensity area could be seen in the porencephalic cystic lesion, in one of which septum formation of cystic cavity was detected on the gadolinium-enhanced T1-weighted MRI. Morphologically, there was massive coagulation necrosis in the tumor cavity, but in the vicinity of the cystic wall abundant fibrous connective tissue was found to correspond with the high and thick signal intensity area on the above-mentioned gadolinium-enhanced T1-weighted MRI.(ABSTRACT TRUNCATED AT 400 WORDS)

Intravascular ultrasound detection of atherosclerosis at the site of focal vasospasm in angiographically normal or minimally narrowed coronary segments.

OBJECTIVES: The purpose of this study was to use intravascular ultrasound imaging to examine the presence of occult atherosclerosis at the site of focal vasospasm in angiographically normal or minimally narrowed segments, testing the role of atherosclerosis in the development of vasospasm. BACKGROUND: Previous clinical and experimental studies have suggested that early atherosclerosis is present at the site of focal vasospasm. However, no clinical data exist demonstrating occult disease at the site of vasospasm at angiographically insignificant stenoses. METHODS: Twenty-two patients with chest pain at rest or during exertion, or both, were studied. Vasospasm was provoked by intracoronary administration of ergonovine maleate (0.01 to 0.04 mg). After relief of vasospasm by nitroglycerin administration, intravascular ultrasound imaging was performed with a 32- or 64-element, 20-MHz, synthetic aperture array ultrasound device. RESULTS: Focal vasospasm (arterial diameter reduction > or = 90%) with ST-T segment elevation was provoked in 15 patients: in the left anterior descending coronary artery in 8 patients and in the right coronary artery in 7. The remaining seven patients (control group) showed diffuse narrowing, averaging 22 +/- 12% (mean +/- SD) in diameter from the baseline angiograms after ergonovine administration. Atherosclerosis, defined as a significantly thickened intimal leading edge (0.42 +/- 0.07 mm) associated with an increased sonolucent zone (0.57 +/- 0.30 mm), was detected by ultrasound at all 15 sites with focal vasospasm, although these sites were normal or minimally narrowed by angiography. In contrast, seven segments from the control group exhibited a thin intimal leading edge (0.14 +/- 0.04 mm, p < 0.01) and sonolucent zone (0.10 +/- 0.07 mm, p < 0.01), indicating the absence of localized atherosclerotic lesions. CONCLUSIONS: These results indicate that atherosclerosis is present at the site of focal vasospasm, even in the absence of angiographically significant coronary disease. We suggest that the existence of such atherosclerotic lesions is related to the occurrence of focal vasospasm in the clinical settings.

Diastolic suction in the human ventricle: observation during balloon mitral valvuloplasty with a single balloon.

Diastolic suction has been demonstrated experimentally as a ventricular negative pressure when the ventricle is allowed to relax completely in the absence of filling, but it has not been extensively studied in the in vivo human heart. In balloon mitral valvuloplasty with a single balloon, the mitral orifice is occluded and inflow is considered to be completely obstructed during a balloon inflation. To demonstrate diastolic suction in the human ventricle, we measured left ventricular pressure during valvuloplasty with a high-fidelity catheter tip manometer in 17 patients. Left ventricular pressure fell below zero during a balloon inflation in all patients (-2 to -12 mm Hg). The peak negative diastolic pressure showed significant correlations with end-systolic volume index (r = 0.53, p = 0.03) and with the ejection fraction (r = 0.80, p = 0.0001). Thus diastolic suction was demonstrated in the human beating heart, and the sucking effect was potent in the heart with small end-systolic volume and high-ejection fraction.

Increase in peak oxygen uptake by restoration of atrial contraction in patients after percutaneous transvenous mitral commissurotomy.

The aim of the present study was to determine the effect of sinus conversion after mitral commissurotomy on the exercise performance of patients with mitral stenosis (MS) and atrial fibrillation (Af). Electric cardioversion was attempted 10 days after successful balloon mitral commissurotomy in 32 patients with MS and Af. Both symptom-limited exercise tests with respiratory gas analysis and constant workload exercise tests with echo-Doppler examinations were performed before, five days and three months after mitral commissurotomy, and five days after successful sinus conversion. The balloon commissurotomy attenuated the increase in transmitral pressure gradient during exercise. However, no significant increase either in peak oxygen uptake (PVO2) or stroke volume were observed even three months after commissurotomy in patients with persistent Af. Sinus conversion was successful in 17 patients and PVO2 increased from 21.4 +/- 4.1 to 23.4 +/- 4.0 ml/min/kg (p < 0.01). The extent of the increase in PVO2 was related to the atrial contribution in transmitral flow (R2 = 0.39, y = 0.81x + 1.2). Sinus rhythm was maintained for three months in 14 of 17 patients. Increased PVO2 was also preserved in these patients. These results suggest that the sinus conversion after mitral commissurotomy has an effect on the exercise performance of patients with MS and Af.

Left ventricular diastolic pressure-volume response immediately after successful percutaneous transvenous mitral commissurotomy.

The left ventricular (LV) diastolic pressure-volume response after percutaneous transvenous mitral commissurotomy (PTMC) was investigated to determine whether it was related to the baseline conditions of the left ventricle. Left ventriculography was performed, and the measurements of LV pressure were obtained in 32 patients before and after PTMC. Mitral valve area increased from 1.0 +/- 0.3 to 1.9 +/- 0.4 cm2 (p < 0.005) after PTMC, which caused a decrease in left atrial mean pressure (14.8 +/- 5.9 to 7.4 +/- 2.7 mm Hg; p < 0.005). LV end-diastolic pressure increased in all patients 5 minutes after PTMC. However, patients could be divided into 2 groups according to the following changes in LV end-diastolic pressure 20 minutes after PTMC: In 22 patients, LV end-diastolic pressure returned to the near-baseline level 20 minutes after PTMC (before 5.0 +/- 2.2, 5 minutes after 8.6 +/- 3.1, and 20 minutes after 6.3 +/- 2.5 mm Hg) with a significant increase in LV end-diastolic volume index (64 +/- 12 to 74 +/- 14 ml/m2; p < 0.001) and augmentation of LV stroke volume index (39 +/- 9 to 47 +/- 11 ml/m2; p < 0.001). However, in the remaining 10 patients with a larger LV volume (> 80 ml/m2) and reduced ejection fraction (< 50%) at baseline, LV end-diastolic pressure further increased 20 minutes after PTMC (before 5.5 +/- 2.8, 5 minutes after 7.8 +/- 2.7, and 20 minutes after 11.0 +/- 2.9 mm Hg) without significant changes in LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)

[Comparison of exercise capacity evaluated by cardiopulmonary exercise test and hemodynamic parameters in patients with atrial septal defect].

We evaluated the maximal exercise tolerance using cardiopulmonary exercise testing, and investigated the relation of the hemodynamic parameters such as mean pulmonary artery pressure (PAm) and pulmonic-to-systemic flow ratio (Qp/Qs) to exercise tolerance in 18 adult patients consecutively. All the patients had atrial septal defect (ASD). Maximal oxygen uptake (VO2 max) averaged only 21.6 +/- 5.6 ml/min/kg and 63.5 +/- 16.2% of the predicted values (VO2max). And anaerobic threshold averaged 12.5 +/- 2.3 ml/min/kg and 56.7 +/- 12.4% of the predicted values. There were 2 patients who had marked pulmonary hypertension (PH, PAm more than 44 mmHg). Maximal exercise tolerance of these patients was severely impaired, and %VO2max was only 45.9% and 46.2% respectively. In patients without PH (PAm less than 20 mmHg), however %VO2 max ranged widely from 100.3 to 44.7% and PAm correlated with %VO2max weakly (r = -0.53, p less than 0.05). But there was a significant inverse relationship between Qp/Qs and %VO2max(r = -0.85, p less than 0.01). In 16 patients without PH, maximal O2-pulse during exercise was also inversely correlated with Qp/Qs (r = -0.76, p less than 0.01). The relation between PAm and %VO2max suggests that afterload on the right ventricle may be an important determinant of exercise capacity in patients with PH. And the relation between Qp/Qs and %VO2max or Qp/Qs and % maximal O2-pulse suggests that Qp/Qs may also be a very important determinant factor of exercise capacity in patients without PH.

Quantitative assessment of coronary artery stenosis by intravascular Doppler catheter technique. Application of the continuity equation.

BACKGROUND: Quantitative assessment of coronary artery stenoses plays a central role in clinical decision making. According to the continuity equation, the ratio of the time-velocity integral of prestenotic to stenotic flow velocities represents the ratio of the cross-sectional area of the stenotic to prestenotic segments. However, no data exist regarding the application of this method to clinical assessment of human coronary artery diseases. Therefore, we attempted to determine the severity of coronary artery stenoses by applying the continuity equation to the coronary circulation. METHODS AND RESULTS: Nineteen patients with a stenosis of the proximal left anterior descending coronary artery (LAD) and one patient with a stenosis in an aortocoronary bypass graft to the LAD were studied. Coronary flow velocities at the prestenotic and stenotic segments were measured with an end-mounted Doppler catheter (3F, 20 MHz), and the time-velocity integral ratio was calculated. Percent area stenosis was calculated as (1-time-velocity integral ratio) x 100. In three patients with severe stenosis (greater than 90% in area stenosis), velocity at the stenosis could not be determined because of aliasing of Doppler signals, and in four, Doppler signals at the stenosis were not measurable because of technical difficulties. The stenotic flow velocity was successfully recorded in 13 patients (65%) with mild to moderate stenosis. The diastolic peak flow velocity at the stenosis was 90 +/- 36 cm/sec (mean +/- SD), and was significantly greater than the velocity at the prestenotic segment, 48 +/- 18 cm/sec (p less than 0.01). Percent area stenosis determined by Doppler continuity equation correlated closely with that by biplane coronary angiography (r = 0.83, y = 0.92x-0.45, p less than 0.01). CONCLUSIONS: Application of the continuity equation to Doppler catheter measurement of coronary flow velocity can be used to successfully compute the severity of coronary stenoses. This may be a useful alternative method to estimate functional severity of coronary artery disease, although further technical developments will be necessary to improve the sensitivity.