Job satisfaction and workplace characteristics of primary and specialty care physicians at a bimodal medical school.

PURPOSE: A few medical schools are highly successful in obtaining research funding and producing primary care physicians. The authors compared the job satisfaction of primary and specialty care faculty at one of these bimodal schools. METHODS: In 1998, all full-time physician-faculty (n = 408) in 15 clinical departments at the University of Iowa College of Medicine (a bimodal medical school) were sent a questionnaire based on the Price-Mueller model of job satisfaction. Faculty rated their global job satisfaction and perceptions about 18 workplace characteristics, stressors, and supports. Responses of primary and specialty care physicians were compared in these domains. RESULTS: A total of 71% of surveyed faculty (n = 341) returned usable questionnaires. Primary and specialty care faculty reported similar levels of job satisfaction (p =.20), and similar percentages (51% versus 54%, p =.63) reported overall satisfaction with their jobs at the medical school. However, primary care faculty perceived less opportunity to advance (p <.01), greater professional-role ambiguity (p =.02), less collegiality (p =.02), and less ability to make full use of their clinical skills (p =.01). Primary and specialty care faculty reported similar intentions of leaving the medical school within the coming year (p =.41). CONCLUSIONS: Primary and specialty care physicians at one bimodal medical school reported similar levels of job satisfaction. However, the primary care physicians rated several important job-related domains lower than did their specialty care colleagues, most notably the opportunity to advance within the medical school.

Cigarette smoking increases sympathetic outflow in humans.

BACKGROUND: It is generally accepted that smoking increases blood pressure and inhibits muscle sympathetic nerve activity (SNA). The decrease in muscle SNA with cigarette smoking might be secondary to baroreflex responses to the pressor effect of smoking, thus obscuring a sympathetic excitatory effect of smoking. We tested the hypothesis that smoking increases sympathetic outflow. METHODS AND RESULTS: We examined the effects of sham smoking, cigarette smoking, and cigarette smoking in combination with nitroprusside on muscle (baroreflex-dependent) SNA in 10 healthy habitual smokers. The 3 sessions were performed in random order, each study on a separate day. In an additional study, we also investigated the effects of sham smoking and cigarette smoking on skin (baroreflex-independent) SNA in 9 subjects. Compared with sham smoking, cigarette smoking alone increased blood pressure and decreased muscle SNA. When the blood pressure increase in response to smoking was blunted by nitroprusside infusion, there was a striking increase in muscle SNA. Muscle SNA increased up to 3-fold the levels seen before smoking (P<0.001), accompanied by an increase in heart rate of up to 37+/-4 bpm. Cigarette smoking also induced a 102+/-22% increase in skin SNA (P=0.03). CONCLUSIONS: These data provide the first direct evidence that cigarette smoking increases sympathetic outflow.

Sympathetic and vascular effects of short-term passive smoke exposure in healthy nonsmokers.

BACKGROUND: The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) at rest and during stressful stimuli, including the cold pressor test (CPT), sustained handgrip (SHG), and mental stress (MS). METHODS AND RESULTS: In 17 healthy nonsmokers, blood pressure (BP), heart rate (HR), forearm blood flow (venous occlusion plethysmography), FVR, and MSNA (obtained through direct intraneural recordings) were measured before and during inhalation of sidestream smoke in one session (n = 16) and before and during vehicle (air) inhalation in another session (n = 17) on a separate day. The order of sessions was randomized between subjects. Responses to CPT, SHG, and MS were measured before and after inhalation of smoke or vehicle (ie, twice during each session). After 15 minutes' exposure to sidestream smoke, plasma nicotine and carboxyhemoglobin levels increased to 0.77 +/- 0.11 ng/mL and 0.36 +/- 0.04% (mean +/- SEM, P < .05), respectively. Sidestream smoke, but not vehicle inhalation, increased resting MSNA from 23 +/- 2 to 28 +/- 2 bursts/min (P < .05). FVR increased with passive smoking, but this increase was not significantly different from the change in FVR with vehicle. Plasma norepinephrine and epinephrine, BP, and HR were not changed significantly by sidestream smoke. The responses of MSNNA, BP, HR, and FVR to the stressful stimuli were not potentiated by sidestream smoke, except for an increased BP response to the CPT (P < .05). CONCLUSIONS: Acute short-term passive (sidestream) smoke exposure elicits a modest increase in MSNA in healthy non-smokers but does not change HR, BP, or FVR.

Spontaneous echocardiographic contrast in the true lumen of a dissected aortic aneurysm.

Spontaneous echocardiographic contrast may be seen in the false and true lumens of dissecting aortic aneurysms. Using transesophageal echocardiography, we identified the false lumen as the source of spontaneous echocardiographic contrast in the true lumen of a patient with an aortic dissection.

Percutaneous balloon catheter closure of a patent foramen ovale in a patient with pulmonary disease, profound hypoxemia, and normal right heart pressures.

Right-to-left intracardiac shunting across a patent foramen ovale (PFO) has been reported in patients with pulmonary embolism, right ventricular (RV) infarction, positive pressure ventilation with positive end-expiratory pressure, heart failure with left ventricular assist devices, cardiac tamponade, and unilateral diaphragmatic paralysis. The primary driving force for these shunts is a reduction in the compliance of the pulmonary bed or right ventricle; right atrial pressure is usually elevated and pulmonary hypertension is frequently present. Significant shunting and hypoxemia are unusual in the absence of these diseases. We encountered a patient with normal pulmonary pressures, severe hypoxemia, pulmonary disease, and intracardiac shunting across a PFO in whom it was difficult to determine how great a role intracardiac shunting was playing in his hypoxemia. To assess this, we performed percutaneous balloon catheter occlusion of the PFO, using transthoracic echocardiography with contrast to confirm closure of the PFO. Therapeutic balloon occlusion has been reported in severe hypoxemia due to shunting across a PFO in a patient with RV infarction. Our case is unique, however, in two respects. First, this patient had normal right-sided cardiac pressures and normal RV function and, thus, no obvious driving force for a significant right-to-left shunt. Second, transthoracic echocardiography with contrast was used before and after balloon inflation to confirm closure of the PFO. This technique helped to answer the important clinical question of whether surgical closure of the PFO in this patient with both lung disease and intracardiac shunting would significantly improve his oxygenation.

Adaptive approach to accurate analysis of small-diameter vessels in cineangiograms.

In coronary vessels smaller than 1 mm in diameter, it is difficult to accurately identify lumen borders using existing border detection techniques. Computer-detected diameters of small coronary vessels are often severely overestimated due to the influence of the imaging system point spread function and the use of an edge operator designed for a broad range of vessel sizes, Computer-detected diameters may be corrected if a calibration curve for the X-ray system is available. Unfortunately, the performance of this postprocessing diameter correction approach is severely limited by the presence of image noise. We report here a new approach that uses a two-stage adaption of edge operator parameters to optimally match the edge operator to the local lumen diameter. In the first stage, approximate lumen diameters are detected using a single edge operator in a half-resolution image. Depending on the approximate lumen size, one of three edge operators is selected for the second full-resolution stage in which left and right coronary borders are simultaneously identified. The method was tested in a set of 72 segments of nine angiographic phantom vessels with diameters ranging from 0.46 to 4.14 mm and in 82 clinical coronary angiograms. Performance of the adaptive simultaneous border detection method was compared to that of a conventional border detection method and to that of a postprocessing diameter correction border detection method. Adaptive border detection yielded significantly improved accuracy in small phantom vessels and across all vessel sizes in comparison to the conventional and postprocessing diameter correction methods (p < 0.001 in all cases). Adaptive simultaneous coronary border detection provides both accurate and robust quantitative analysis of coronary vessels of all sizes.

The effect of aminophylline on pharmacological stress with intravenous adenosine.

Myocardial perfusion imaging with adenosine pharmacological stress may be useful in patients with obstructive lung disease who are unable to exercise. However, these patients are often treated with medications containing theophylline, which is an adenosine antagonist. This study assessed the effect of aminophylline on coronary vasodilation produced by intravenous adenosine as commonly used during cardiac imaging. Changes in coronary flow velocity (measured by intracoronary Doppler catheter) heart rate, arterial pressure and changes in coronary resistance were measured during intravenous infusion of adenosine at 140 micrograms/kg/min before and after aminophylline, 6 mg/kg intravenously in 12 patients. After aminophylline infusion, the theophylline level averaged 14 +/- 1 microgram/mL. The coronary hemodynamic effects of adenosine were markedly attenuated by aminophylline. Adenosine increased coronary blood flow velocity by 192 +/- 39% at control and 78 +/- 16% after aminophylline (P < .05 v control). Adenosine produced a 63 +/- 5% decrease in coronary vascular resistance at control and 40 +/- 6% (P < .05) after aminophylline. The utility of myocardial imaging techniques using coronary vasodilation with intravenous adenosine may be reduced in patients treated with theophylline-containing preparations.

Perforation of saphenous vein graft during coronary stenting: a case report.

We report on a case of coronary perforation during stenting of a saphenous vein graft with a biliary stent. Sealing of the perforation was achieved with another biliary stent deployed within the first stent at the site of the perforation, and with prolonged balloon inflation. This case illustrates that vein graft perforation can occur with coronary stenting, and could potentially be treated with prolonged balloon inflation and/or stenting at the site of the first stent.

Does pharmacologic coronary flow reserve reflect vasodilator responsiveness to increased myocardial demand in humans?

OBJECTIVE: To assess the relationship between maximal pharmacologic coronary flow reserve and metabolic coronary vasodilation in nonstenotic coronary arteries. BACKGROUND: Evaluation of the coronary microcirculation in humans during cardiac catheterization is commonly performed by assessment of coronary hemodynamics during administration of potent coronary vasodilators. However, the relationship between maximal pharmacologic vasodilation and flow increases occurring in response to increased myocardial demand has not been evaluated. METHODS: The coronary blood flow responses to a maximally dilating dose of intracoronary adenosine or papaverine and to a standardized atrial pacing stress were assessed in 49 patients using intracoronary Doppler velocimetry. The blood flow responses to a maximally dilating dose of intracoronary adenosine and to intravenous infusion of dobutamine were determined in 13 patients. RESULTS: The maximal pharmacologic coronary flow reserve averaged 3.2 +/- 0.1 (mean +/- SEM). The coronary blood flow velocity increased by 32 +/- 3% during atrial pacing, and the change in coronary flow velocity was correlated with the change in the mean arterial pressure x heart rate product during pacing. Regression analysis revealed no relationship between the pharmacologic coronary flow reserve and the change in coronary flow velocity during atrial pacing or the response of the flow to pacing normalized with respect to the magnitude of stress reflected by the change in rate x pressure product. The coronary blood flow velocity increased by 135 +/- 16% during dobutamine infusion. Regression analysis revealed no relationship between the pharmacologic coronary flow reserve and the change in coronary flow velocity during dobutamine infusion. CONCLUSIONS: Knowledge of the maximal pharmacologic coronary flow reserve is an inadequate surrogate for assessment of coronary vasodilation in response to increases in myocardial metabolic demand in nonstenotic arteries.

Electron-beam computed tomographic detection of coronary calcification in patients undergoing percutaneous transluminal coronary angioplasty: predictability of restenosis. A preliminary report.

Coronary artery calcification is a recognized marker for coronary atherosclerosis; however, the relationship between calcification and the success of balloon angioplasty at a calcification site has not been determined. The purpose of this study was to evaluate whether the presence of coronary artery calcification, as detected by electron bean computed tomography (EBCT), was predictive of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Site- specific coronary calcification was determined by EBCT in 20 patients with 24 lesions before, immediately after, and 2 to 18 month after PTCA. Calcification was scored using >130 Hounsfield units and >1.02-mm2 area criteria. Coronary calcium at the PTCA site was significantly greater in restenosed versus nonrestenosed patients (109.16 +/- 198.16 mm2 v 4.39 +/- 9.50 mm2) (P < .025). The amount of coronary calcium did not change as a result of the PTCA procedure (+2.72 +/- 22.31 mm2 v -4.81 +/- 7.82 mm2) (P = NS). The rate of progression of calcification was not greater in restenosed versus nonrestenosed patients (1.78 +/- 3.32 mm2/month v 0.09 +/- 0.19 mm2/mo) (P = NS). Site-specific coronary calcification as determined by EBCT appeared to be predictive of patients with an increased likelihood to restenose after PTCA. Further studies are needed to verify these observations in a considerably larger patient population.

Maximal coronary flow reserve and metabolic coronary vasodilation in patients with diabetes mellitus.

BACKGROUND: Structural and functional abnormalities of the coronary microcirculation have been reported in experimental diabetes mellitus. The purpose of this study was to evaluate coronary microvascular function in human diabetes. METHODS AND RESULTS: Twenty-four diabetic and 31 nondiabetic patients were studied during cardiac catheterization. A Doppler catheter or guidewire was used to measure changes in coronary blood flow velocity in a nonstenotic artery. Maximal coronary blood flow reserve was determined by using intracoronary adenosine or papaverine. Coronary dilation in response to an increase in myocardial metabolic demand was assessed by using rapid atrial pacing. Maximal vasodilator responses to papaverine and adenosine were compared in 12 diabetic patients. Maximal pharmacologic coronary flow reserve was depressed in diabetic (2.8 +/- 0.2, n = 19) compared with nondiabetic (3.7 +/- 0.2, n = 21, P < .001) patients. During atrial pacing, the decrease in coronary vascular resistance was attenuated in the diabetic (-14 +/- 3%) compared with the nondiabetic (-24 +/- 2%, P < .05) patients. Differences in coronary microvascular function between diabetic and nondiabetic patients were not attributable to differences in drug therapy, resting hemodynamics, or incidence of hypertension. In 12 diabetic patients the maximal coronary vasodilator responses to papaverine and adenosine were similar. CONCLUSIONS: This study demonstrates both reduced maximal coronary vasodilation and impairment in the regulation of coronary flow in response to submaximal increases in myocardial demand in patients with diabetes mellitus. These microvascular abnormalities may lead to myocardial ischemia in the absence of epicardial coronary atherosclerosis in some circumstances, and thus contribute to adverse cardiovascular events in diabetic patients.

Robust simultaneous detection of coronary borders in complex images.

Visual estimation of coronary obstruction severity from angiograms suffers from poor inter- and intraobserver reproducibility and is often inaccurate. In spite of the widely recognized limitations of visual analysis, automated methods have not found widespread clinical use, in part because they too frequently fail to accurately identify vessel borders. The authors have developed a robust method for simultaneous detection of left and right coronary borders that is suitable for analysis of complex images with poor contrast, nearby or overlapping structures, or branching vessels. The reliability of the simultaneous border detection method and that of the authors' previously reported conventional border detection method were tested in 130 complex images, selected because conventional automated border detection might be expected to fail. Conventional analysis failed to yield acceptable borders in 65/130 or 50% of images. Simultaneous border detection was much more robust (p<.001) and failed in only 15/130 or 12% of complex images. Simultaneous border detection identified stenosis diameters that correlated significantly better with observer-derived stenosis diameters than did diameters obtained with conventional border detection (p<0.001), Simultaneous detection of left and right coronary borders is highly robust and has substantial promise for enhancing the utility of quantitative coronary angiography in the clinical setting.

Prediction of change in mitral valve area after mitral balloon commissurotomy using cine computed tomography.

RATIONALE AND OBJECTIVES: Mitral balloon commissurotomy (MBC) can successfully increase the mitral valve area (MVA) in mitral stenosis, but the outcome is variable. In multicenter studies, qualitative echocardiographic scores obtained before MBC are only weakly predictive of the increase in MVA after MBC. METHODS: To evaluate whether the change in MVA after MBC can be predicted by evaluating mitral valve morphology using cine computed tomography (CT), we studied 12 women with mitral stenosis and 11 female control subjects. RESULTS: In the patients with mitral stenosis, MVA increased from 1.13 +/- 0.24 to 1.93 +/- 0.56 cm2 (P < .0001) after MBC. A standard echocardiographic score assessment of mitral valve morphology before MBC was not associated with the change in MVA after MBC in these patients (P > .20). However, the total mitral valve morphology score evaluated by cine computed tomography was strongly associated with the change in MVA after MBC (r = -.87; P < .0005). In addition, the individual morphologic characteristics of mitral valve mobility (P < .0025), leaflet thickness (P < .05), and subvalvular disease (P < .05) were significant predictors of the change in MVA after MBC. CONCLUSION: Cine computed tomography may be useful for predicting immediate increases in MVA in patients after MBC and may be helpful for preoperative assessment of these patients.

Assessment of cardiac volumes and left ventricular mass by cine computed tomography before and after mitral balloon commissurotomy.

We used cine computed tomography (CT) to determine whether decreased mitral valve gradients and pulmonary artery pressures resulted in decreased right ventricular and atrial volumes after percutaneous mitral balloon commissurotomy (MBC). In patients treated for severe mitral stenosis, previous studies have shown that after the mitral valve gradient decreases, the left atrial volume is reduced and left ventricular stroke volume is increased. The effects of commissurotomy on right heart chamber sizes have been difficult to assess with angiography and echocardiography. Moreover, in follow-up studies performed after surgery, changes in cardiac chamber volumes occurring after the mitral valve gradient and pulmonary pressure are reduced are confounded by the effects of thoracotomy. Our group has previously demonstrated that cine CT can accurately measure both left and right cardiac chamber volumes. We studied 11 female patients before, immediately after, and at 1 year after MBC, and 9 female control subjects of comparable age. To assess cardiac chamber volumes, we used cine CT. To assess the effects of MBC, we used cardiac catheterization and Doppler echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

Lumen centerline detection in complex coronary angiograms.

We have developed a method for lumen centerline detection in individual coronary segments that is based on simultaneous detection of the approximate positions of the left and right coronary borders. This approach emulates that of a clinician who visually identifies the lumen centerline as the midline between the simultaneously-determined left and right borders of the vessel segment of interest. Our lumen centerline detection algorithm and two conventional centerline detection methods were compared to carefully-defined observer-identified centerlines in 89 complex coronary images. Computer-detected and observer-defined centerlines were objectively compared using five indices of centerline position and orientation. The quality of centerlines obtained with the new simultaneous border identification approach and the two conventional centerline detection methods was also subjectively assessed by an experienced cardiologist who was unaware of the analysis method. Our centerline detection method yielded accurate centerlines in the 89 complex images. Moreover, our method outperformed the two conventional methods as judged by all five objective parameters (p < 0.001 for each parameter) and by the subjective assessment of centerline quality (p < 0.001). Automated detection of lumen centerlines based on simultaneous detection of both coronary borders provides improved accuracy in complex coronary arteriograms.

Effect of adenosine antagonism on metabolically mediated coronary vasodilation in humans.

OBJECTIVES: This study was performed to assess the importance of adenosine in mediating metabolic coronary vasodilation during atrial pacing stress in humans. BACKGROUND: Numerous animal studies have examined the role of adenosine in the regulation of coronary blood flow, with inconsistent results. METHODS: The effect of the adenosine antagonist aminophylline (6 mg/kg body weight intravenously) on coronary functional hyperemia during rapid atrial pacing was determined in 12 patients. The extent of inhibition of adenosine vasodilation was assessed using graded intracoronary adenosine infusions before and after aminophylline administration in seven patients. Coronary blood flow changes were measured with a 3F intracoronary Doppler catheter. RESULTS: After aminophylline administration, the increase in coronary flow velocity during adenosine infusions was reduced from 84 +/- 48% (mean +/- SD) to 21 +/- 31% above control values (p < 0.001) at 10 micrograms/min and from 130 +/- 39% to 59 +/- 51% above control values (p < 0.001) at 40 micrograms/min. During rapid atrial pacing under control conditions, coronary blood flow velocity increased by 26 +/- 16%. The flow increment during paced tachycardia after aminophylline (23 +/- 10%) was unchanged from the control value, despite substantial antagonism of adenosine coronary dilation by aminophylline. CONCLUSIONS: These data suggest that adenosine does not play an important role in the regulation of coronary blood flow in response to rapid atrial pacing in humans.

Coronary-artery vasoconstriction induced by cocaine, cigarette smoking, or both.

BACKGROUND: In humans, the use of cocaine and cigarette smoking each increase the heart's metabolic need for oxygen but may also decrease the supply of oxygen. As cocaine abuse has proliferated, cocaine-associated chest pain, myocardial infarction, and sudden death have occurred, especially among smokers. We assessed the influence of intranasal cocaine and cigarette smoking, alone and together, on myocardial oxygen demand and coronary arterial dimensions in subjects with and subjects without coronary atherosclerosis. METHODS: In 42 smokers (28 men and 14 women; age, 34 to 79 years; 36 with angiographically demonstrable coronary artery disease), we measured the product of the heart rate and systolic arterial pressure (rate-pressure product) and coronary arterial diameters before and after intranasal cocaine at a dose of 2 mg per kilogram of body weight (n = 6), one cigarette (n = 12), or intranasal cocaine at a dose of 2 mg per kilogram followed by one cigarette (n = 24). RESULTS: No patient had chest pain or ischemic electrocardiographic changes after cocaine use or smoking. The mean (+/- SE) rate-pressure product increased by 11 +/- 2 percent after cocaine use (n = 30, P < 0.001), by 12 +/- 4 percent after one cigarette (n = 12, P = 0.021), and by 45 +/- 5 percent after both cocaine use and smoking (n = 24, P < 0.001). As compared with base-line measurements, the diameters of nondiseased coronary arterial segments decreased on average by 7 +/- 1 percent after cocaine use (P < 0.001), by 7 +/- 1 percent after smoking (P < 0.001), and by 6 +/- 2 percent after cocaine use and smoking (P < 0.001). The diameters of diseased segments decreased by 9 +/- 2 percent after cocaine use (n = 18, P < 0.001), by 5 +/- 5 percent after smoking (n = 12, P = 0.322), and by 19 +/- 4 percent after cocaine use and smoking (n = 12, P < 0.001). The increase in the rate-pressure product and the decrease in the diameters of diseased segments caused by cocaine use and smoking together were greater (P < 0.001 and P = 0.037, respectively) than the changes caused by either alone. CONCLUSIONS: The deleterious effects of cocaine on myocardial oxygen supply and demand are exacerbated by concomitant cigarette smoking. This combination substantially increases the metabolic requirement of the heart for oxygen but simultaneously decreases the diameter of diseased coronary arterial segments.

Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels.

OBJECTIVES: This study was performed to determine the acute effect of cigarette smoking on proximal and distal epicardial conduit and coronary resistance vessels. BACKGROUND: Cigarette smoking causes constriction of epicardial arteries and a decrease in coronary blood flow in patients with coronary artery disease, despite an increase in myocardial oxygen demand. The role of changes in resistance vessel tone in the acute coronary hemodynamic effect of smoking has not been examined. METHODS: Twenty-four long-term smokers were studied during cardiac catheterization after vasoactive medications had been discontinued. The effect of smoking one cigarette 10 to 15 mm long on proximal and distal conduit vessel segments was assessed before and immediately after smoking and at 5, 15 and 30 min after smoking (n = 8). To determine the effect of smoking on resistance vessels, coronary flow velocity was measured in a nonobstructed artery with a 3F intracoronary Doppler catheter before and for 5 min after smoking (n = 8). Eight patients were studied without smoking to control for spontaneous changes in conduit arterial diameter (n = 5) and resistance vessel tone (n = 3). RESULTS: The average diameter of proximal coronary artery segments decreased from 2.56 +/- 0.12 mm (mean +/- SEM) before smoking to 2.41 +/- 0.09 mm 5 min after smoking (-5 +/- 2%, p < 0.05). Distal coronary diameter decreased from 1.51 +/- 0.07 to 1.39 +/- 0.06 mm (-8 +/- 2%, p < 0.01). Marked focal vasoconstriction after smoking was observed in two patients. Coronary diameter returned to baseline by 30 min after smoking. There was no change in vessel diameter in control patients. Despite a significant increase in the heart rate-mean arterial pressure product, coronary flow velocity decreased by 7 +/- 4% (p < 0.05) and coronary vascular resistance increased by 21 +/- 4% (p < 0.01) 5 min after smoking. There was no change in these variables in the control subjects. CONCLUSIONS: Smoking causes immediate constriction of proximal and distal epicardial coronary arteries and an increase in coronary resistance vessel tone, despite an increase in myocardial oxygen demand. These acute coronary hemodynamic effects may contribute to the adverse cardiovascular consequences of cigarette smoking.

Effect of increases in heart rate and arterial pressure on coronary flow reserve in humans.

OBJECTIVES: The objective of this study was to determine the effect of increases in heart rate and arterial pressure on maximal pharmacologic coronary blood flow reserve. BACKGROUND: Coronary flow reserve measurements are useful in assessment of the physiologic significance of coronary lesions. However, animal studies suggest that alterations in hemodynamic status may influence coronary flow reserve independent of coronary stenosis. METHODS: Coronary flow reserve was measured during cardiac catheterization with the use of a 3F coronary Doppler catheter and intracoronary papaverine. Flow reserve was measured under control conditions and during increases in heart rate produced by atrial pacing (18 patients) or during elevation of arterial pressure by intravenous phenylephrine infusion (9 patients) with intracoronary alpha-adrenergic blockade by phentolamine. RESULTS: Coronary flow reserve progressively decreased from 3.7 +/- 0.9 (mean +/- SD) at the rate of 71 +/- 8 beats/min at rest to 3.0 +/- 0.6 during pacing at 100 beats/min and to 2.6 +/- 0.5 during pacing at 120 beats/min. Flow reserve decreased because of a progressive increase in rest coronary flow velocity during pacing (122 +/- 16% of control value at 100 beats/min, 139 +/- 16% of control value at 120 beats/min), whereas papaverine hyperemia peak velocity remained unchanged. Flow reserve decreased with pacing tachycardia whether the initial flow reserve was normal or depressed. Mean arterial pressure increased from 95 +/- 12 mm Hg to 130 +/- 8 mm Hg during intravenous phenylephrine infusion and to 123 +/- 10 mm Hg during combined intravenous phenylephrine and intracoronary phentolamine infusions. Coronary flow reserve was not affected by the blood pressure increases (control value 4.3 +/- 1.0, phenylephrine 4.4 +/- 1.5, phenylephrine and phentolamine 4.4 +/- 2.0). CONCLUSIONS: Sudden increases in heart rate but not mean arterial pressure lead to a substantial reduction in maximal coronary blood flow reserve. These data suggest that the diagnostic utility of all flow reserve measurement techniques might be improved by standardization of heart rate during measurement or extrapolation of the measured flow reserve to that expected at a reference heart rate.

Simultaneous detection of both coronary borders.

A method for simultaneous detection of both coronary borders that is based on three-dimensional graph searching principles is presented. The simultaneous method and the authors' previously reported conventional method were applied to 29 coronary images, of which 19 were selected because conventional methods might be expected to have difficulty. Coronary borders identified by the two methods were visually compared. In the 19 difficult images, simultaneous border detection yielded superior results in 7 images and equivalent results in 12 images. Superior or equivalent results were obtained in the remaining 10 typical images. In a set of 43 uncomplicated images, minimal lumen diameters derived using simultaneous border detection correlated well with diameters derived using conventional border detection (r=0.97), diameters obtained from observer-defined borders (r=0.91), and diameters obtained using the Brown-Dodge quantitative coronary arteriography method (r=0.85). Thus simultaneous detection of left and right coronary borders provides improved accuracy in the detection of vessel borders in difficult coronary angiograms.