Usefulness of isometric hand grip exercise in detecting coronary artery disease during dobutamine atropine stress echocardiography in patients with either stable angina pectoris or another type of positive stress test

Dobutamine atropine stress echocardiography (DASE) detects coronary artery disease (CAD) by increasing myocardial oxygen demand causing ischemia. The sensitivity of the test for detection of CAD is reduced in patients with submaximal stress. We hypothesized that increasing cardiac work load by adding isometric exercise would improve the detection of ischemia during DASE. We studied 31 patients, mean age 57+/-11 years, with angiographically documented CAD. Patients underwent DASE using incremental dobutamine doses from 5 to 40 microg/kg/min, followed by atropine if peak heart rate was <85% of predicted maximal. Hand grip was then performed for 2 minutes at 33% of maximal voluntary contraction, while dobutamine infusion was maintained at the peak dose. The addition of hand grip during dobutamine stress was associated with a significant increase in systolic blood pressure (143+/-21 vs 164+/-24 mm Hg, p = 0.001) and left ventricular end-systolic circumferential wall stress (72+/-30 x 10(3) dynes/cm2 vs 132+/-34 x 10(3) dynes/cm2, p = 0.004). Wall motion score index increased from 1.0 at rest to 1.15+/-0.18 with dobutamine (p = 0.0004 vs rest), and increased further to 1.29+/-0.22 with the addition of hand grip (p = 0.004 vs dobutamine). Ischemia was detected in 19 patients (62%) with dobutamine-atropine stress alone and in 25 (83%) after the addition of hand grip (p <0.05). The addition of hand grip during DASE is feasible, and improves the detection of myocardial ischemia.     

Effects of isoflurane-nitrous oxide and halothane-nitrous oxide anaesthesia on myocardial contractility assessed by transoesophageal echocardiography

In order to evaluate the direct effect of isoflurane-nitrous oxide and halothane-nitrous oxide anaesthesia on cardiac contractility in 20 adults, we have used a method based on left ventricular end-systolic wall stress (LVESWS) vs velocity of circumferential fibre shortening with corrected heart rate (Vcfc), obtained by transoesophageal echocardiography. We found that LVESWS (index of afterload) decreased significantly with isoflurane-nitrous oxide (n = 10) in concentrations of 1.5-1.95 MAC, but there were no significant changes in LVESWS with halothane-nitrous oxide (n = 10). Vcfc decreased significantly with halothane-nitrous oxide in concentrations of 1.5-1.95 MAC, but this index did not change significantly with isoflurane-nitrous oxide. However, there was no significant difference between the two groups in LVESWS or Vcfc. In the analysis of the LVESWS-Vcfc relationship, myocardial contractility associated with isoflurane-nitrous oxide anaesthesia did not differ significantly from that associated with halothane-nitrous oxide anaesthesia at equiMAC concentrations. The results suggest that halothane-nitrous oxide anaesthesia, at 1.5-1.95 MAC, maintained myocardial contractility in similar anaesthetic concentrations to isoflurane-nitrous oxide.     

Acute changes in preload, afterload, and systolic function after superior cavopulmonary connection

BACKGROUND: Superior cavopulmonary connection reduces the volume work of the single ventricle. METHODS: To determine the effects of superior cavopulmonary connection on preload, wall stress (or afterload), and systolic ventricular function, we studied 9 patients before and after operation, and at hospital discharge. Using echocardiography, preload was estimated by the ventricular end-diastolic area, and wall stress was calculated at end-systole and peak-systole. Ventricular function was represented by rate-corrected velocity of circumferential fiber shortening and fractional area change divided by rate-corrected ejection time. RESULTS: End-diastolic area and wall stress decreased postoperatively. Ventricular wall thickness increased with a concomitant decrease in cavity area. There was no change in mean blood pressure or heart rate or in rate-corrected velocity of circumferential fiber shortening or fractional area change divided by rate-corrected ejection time. These findings persisted at hospital discharge. CONCLUSIONS: In single ventricles, superior cavopulmonary correction results in an immediate decrease in preload and afterload. The decrease in afterload results primarily from alterations in ventricular geometry. Although no improvement in systolic function was noted, diminished work related to the reduction in loading conditions may have beneficial long-term effects on preserving myocardial performance.     

Breath-hold dobutamine magnetic resonance myocardial tagging: normal left ventricular response

Analysis of the changes in myocardial deformation produced by adrenergic stress has been limited by the imaging techniques used. We used rapid magnetic resonance imaging (MRI) myocardial tagging to map the dose-dependent response to incremental dobutamine in the normal human left ventricle. Thirteen volunteers underwent breath-hold tagged cine MRI during dobutamine infusion. Images were acquired throughout systole to a peak dose of 20 microg/kg/min. End-systolic percent circumferential shortening (%S) was measured at 3 transmural locations and 4 circumferential locations at 3 long-axis positions. Mean circumferential shortening velocity (CSV) was also calculated at each location and dose. Mean %S reached a maximum of 26 +/- 3% at 10 microg/kg/min compared with 21 +/- 4% at baseline (p <0.003). Peak %S was reached by 10 microg/kg/min before a significant increase in heart rate or blood pressure and was unchanged at higher doses. In contrast, CSV increased linearly with dobutamine dose from 4.4 +/- 0.9 mm/s at baseline to 9.8 +/- 1.4 mm/s at 20 microg/kg/min (p <0.0001). Breath-hold tagged dobutamine MRI is safe and effective in detecting regional and transmural changes in function during incremental dobutamine. CSV increased continuously across the dobutamine dose range. At low dose (< or =10 microg/kg/min) %S increased without any change in blood pressure or heart rate. Maintenance of peak %S beyond 10 microg/kg/min in the presence of decreasing systolic intervals resulted from a continued increase in CSV. Thus, CSV may be the preferred measure of contractile function during dobutamine stimulation in human myocardium.     

Laparoscopic cholangiography: a new technique for difficult cannulation

PURPOSE: To test the hypothesis that rejection could affect the contractility and contractile reserve of left ventricle after heart transplantation. METHODS: Echocardiographic parameters and noninvasive blood pressure end-systolic pressure (ESP), heart rate (HR), end diastolic (EDV) and end-systolic (ESV) volumes, ejection fraction (EF), end-systolic stress (ESS) and the end-systolic relation (ESS/ESV) were recorded in 68 studies in 11 patients, seven days-12 months after heart transplantation. Accordingly with the endomyocardial biopsies results were divided into two groups: group A-with no rejection (53 studies), and group B-with rejection (15 studies). RESULTS: The nitroprusside infusion changed significantly and in the same way, all the parameters except the ESS/ESV ratio (A = 5.5 +/- 1.7 x B = 4.8 +/- 1.5 g/cm2/mL, p = NS); there was a decrease in ESP (A = 107 +/- 15 and B = 109 +/- 12 mmHg, p = NS), EDV (A = 68 +/- 19 and B = 81 +/- 12 mL, p = NS), ESV (A = 12 +/- 5 and B = 18 +/- 12 mL, p = NS) and ESS (A = 59 +/- 13 and B = 82 +/- 20g/cm2, p = NS); there was an increase in HR (A = 94 +/- 9 and B = 93 +/- 16bpm, p = NS) and EF (A = 83 +/- 5 and B = 79 +/- 8%, p = NS). In the dobutamine study it was observed differences for both groups, except for ESP (A = 156 +/- 26 and B = 149 +/- 26mmHg, p = NS). The increase in HR, EF and ESS/ESV ratio was greater in group A (HR-A = 117 +/- 19 and B = 102 +/- 25bpm, p < 0.05; EF-A = 91 +/- 4 and B = 78 +/- 11%, p < 0.05; ESS/ESV-A = 13.1 +/- 6 and B = 6.1 +/- 3.1 g/cm2/mL, p < 0.05). For group A it was smaller the EDV (57 +/- 18 x 94 +/- 35 mL, p < 0.05), ESV (5 +/- 3 x 24 +/- 20 mL, p < 0.05) and ESS (57 +/- 21 x 102 +/- 40 g/cm2, p < 0.05). CONCLUSION: Rejection may not induce changes in resting left ventricular contractility, however, the contractile reserve is depressed during an episode of moderate to severe rejection.     

Preclinical cardiac dysfunction in transfusion-dependent children and young adults detected with low-dose dobutamine stress echocardiography

Transfusion-dependent (TD) patients develop cardiac iron overload that will eventually lead to cardiac pump failure. Low-dose dobutamine stress echocardiography may complement resting echocardiography and identify preclinical myocardial dysfunction caused by early cardiac hemosiderosis. Twenty-six iron-overloaded TD patients had stress echocardiography with 5 microg/kg per minute of dobutamine. Indexed left ventricular (LV) mass, LV dimensions, meridional wall stress, and cardiac index were significantly increased. TD patients had similar LV shortening fraction by M-mode (40.5% +/- 5.6% vs 39.4% +/- 4.5%) but had a lower mean LV ejection fraction (53.3% +/- 3.9% vs 46.8% +/- 6.9%, P < .002) and a subnormal increase in cardiac index during dobutamine stress (35% +/- 20% vs 11% +/- 16%, P < .0001). Impairment in LV relaxation was demonstrated by a prolonged isovolumetric relaxation time (0.060 +/- 0.005 vs 0.088 +/- 0.019 seconds, P < .0001), increased peak mitral E wave, and abnormal E/A ratio. Asymptomatic TD patients demonstrate decreased systolic functional reserve and abnormal left ventricular relaxation that may be caused by cardiac hemosiderosis. Low-dose dobutamine stress echocardiography may be useful for detecting and following cardiac dysfunction in patients at risk for cardiac hemosiderosis.     

An in vitro model for adhesion of bacteria to human tooth root surfaces

Using echocardiographic technique, we studied the left ventricular (LV) contractile state in 32 full-term infants within 24 hr after birth. They were divided into 2 groups based on the timing of the examinations; the group 1 (n = 17), < 3 hr after birth; the group 2 (n = 15), > 3 and < 24 hr after birth, and the additional examinations were performed on day 5. The patency of the ductus arteriosus and its internal diameter were determined by pulsed Doppler and two-dimensional echocardiography. The left atrial to aortic root ratio was obtained from M-mode echocardiography, and the LV contractile state was estimated by the relationship between heart rate-corrected velocity of circumferential fiber shortening (mVcfc) and end-systolic meridional wall stress (ESS). The ductus arteriosus was open in all cases of group 1 and in 83% of the cases of group 2, but the ductal diameter and the left atrial to aortic root ratio significantly decreased in group 2. The relationship between mVcfc and ESS showed no significant differences between 2 groups and the control. Afterload, represented as ESS, was significantly lower in group 1 than the control. We suggest that the low afterload condition helps the adequate LV contraction even under the increased preload through the left-to-right ductus arteriosus shunting after birth.     

Limited myocardial contractile reserve and chronotropic incompetence in patients with chronic Chagas' disease: assessment by dobutamine stress echocardiography

OBJECTIVES: To determine whether dobutamine stimulation in patients with Chagas' disease may uncover abnormal contractile responses as seen in ischemic myocardium. BACKGROUND: Segmental left ventricular (LV) dysfunction in the absence of coronary atherosclerosis is frequently seen in patients with chronic Chagas' heart disease. Myocardial ischemia and coronary microcirculation abnormalities have been found in animal models and in humans with Chagas' disease. In addition, chagasic sera may contain autoantibodies against human beta-adrenergic receptors. METHODS: Two groups of patients with Chagas' disease were studied by echocardiography: group 1 (n = 12) without and group 2 (n = 14) with LV segmental wall motion abnormalities (mostly apical aneurysm). Ten normal subjects served as control subjects. We performed qualitative assessment of wall motion and quantitative evaluation of LV cavity under baseline conditions and after dobutamine stimulation. RESULTS: Patients with Chagas' disease exhibited a blunted inotropic and chronotropic response to dobutamine stimulation. After dobutamine, fractional area change in Chagas' group 1 (54.7+/-6.6%; SD) and in group 2 (35.1+/-12.1%) were significantly lower than control group (66.7+/-2.5%; p < 0.001). In addition, in 6 of 14 group 2 patients, dobutamine induced a biphasic response with improvement at low dose and deterioration at peak dose, as seen in patients with coronary artery disease. Although the three groups had similar basal mean heart rates and attained a similar mean peak dobutamine doses, both groups of patients with Chagas' disease had a significantly blunted mean heart rate effect after dobutamine (p < 0.0001). CONCLUSIONS: Thus, dobutamine stimulation unmasks a chronotropic incompetence and a blunted myocardial contractile response in chagasic patients, even in those with no overt manifestation of heart disease.     

Fibroelastolytic papulosis of the neck: a report of 20 cases

BACKGROUND: Reports of pulmonary edema complicating inhaled nitric oxide therapy in patients with chronic heart failure and pulmonary hypertension have raised the concern that inhaled nitric oxide may have negative inotropic effects. METHODS AND RESULTS: We investigated the effect of multiple doses of inhaled nitric oxide (20, 40 and 80 ppm) on left ventricular contractile state in 10 open-chest pigs. Pressure-volume loops were generated during transient preload reduction to determine the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relation. Inhaled nitric oxide had no effect on systemic vascular resistance, cardiac output, end-systolic pressure volume relationship or stroke work-end-diastolic volume relation under normal conditions. After induction of pulmonary hypertension (intravenous thromboxane A2 analog), inhalation of nitric oxide (80 ppm) resulted in a reduction in pulmonary vascular resistance (mean +/- standard error of the mean) from 10.4 +/- 3 to 6.5 +/- 2 Wood units (p < 0.001) and in pulmonary artery pressure from 44 +/- 4 to 33 +/- 4 mm Hg (p < 0.05). Left ventricular end-diastolic volume rose from 53 +/- 9 ml to 57 +/- 10 ml (p = 0.02). No statistically significant change in cardiac output or systemic vascular resistance was observed. Inhaled nitric oxide had no effect on end-systolic pressure-volume relationship or stroke work-end-diastolic volume relation. CONCLUSIONS: In a porcine model of pulmonary hypertension, inhaled nitric oxide does not impair left ventricular contractile function. Therefore the cause of pulmonary edema observed in some patients receiving inhaled nitric oxide is not due to a negative inotropic action of this therapy.     

Acute phase proteins: alpha-1-acid glycoprotein (AGP) and alpha-1 antichymotrypsin (ACT) in serum of patients with cerebral ischemic stroke

BACKGROUND: Because of methods required for obtaining isolated left ventricular myocytes, evaluation of the contractile function of isolated left ventricular myocytes in normal human patients has been limited. Accordingly, the goal of the present study was to develop a means to isolate human left ventricular myocytes from small myocardial biopsy specimens collected from patients undergoing elective coronary artery bypass operations and to characterize indices of myocyte contractile performance. METHODS: Myocardial biopsy specimens were obtained from the anterior left ventricular free wall of 22 patients undergoing coronary artery bypass operations. Myocytes were isolated from these myocardial samples by means of a stepwise enzymatic digestion method and micro-trituration techniques. Isolated left ventricular myocyte contractile function was assessed by computer-assisted high-speed videomicroscopy under basal conditions and in response to beta-adrenergic receptor stimulation with isoproterenol. RESULTS: A total of 804 viable left ventricular myocytes were successfully examined from all of the myocardial biopsy specimens with an average of 37+/-4 myocytes per patient. All myocytes contracted homogeneously at a field stimulation of 1 Hz with an average percent shortening of 3.7%+/-0.1% and shortening velocity of 51.3+/-1.3 microm/s. After beta-adrenergic receptor stimulation with isoproterenol, percent shortening and shortening velocity increased 149% and 118% above baseline, respectively (P < .05). CONCLUSION: The unique results of the present study demonstrated that a high yield of myocytes could be obtained from human left ventricular biopsy specimens taken during cardiac operations. These myocytes exhibited stable contractile performance and maintained the capacity to respond to an inotropic stimulus. The methods described herein provide a basis by which future studies could investigate intrinsic and extrinsic influences on left ventricular myocyte contractility in human beings.     

Comparison of coronary endothelial dynamics with electrocardiographic and left ventricular contractile responses to stress in the absence of coronary artery disease

Coronary artery endothelial dysfunction has been proposed as a cause of myocardial ischemia and symptoms in patients with angina-like chest pain despite normal coronary angiograms, especially those with ischemic-appearing ST-segment depression during exercise (syndrome X). We measured coronary vasomotor responses to acetylcholine (3 to 300 microg/min) in 42 patients (27 women and 15 men) with effort chest pain and normal coronary angiograms who also had normal electrocardiograms and echocardiograms at rest. All patients underwent treadmill exercise testing and measurement of systolic wall thickening responses to dobutamine (40 microg/kg/min) during transesophageal echocardiography. There were no differences in the acetylcholine-stimulated epicardial coronary diameter (+5+/-13% vs +1+/-13%, p=0.386) and flow (+179+/-90% vs +169+/-96%, p=0.756), or in the systolic wall thickening responses (+134+/-65% vs +118+/-57%, p=0.445) from baseline values in the 12 syndrome X patients compared with the 30 patients with negative exercise test results. In patients in the lowest quartile of coronary flow responses to acetylcholine, dobutamine increased systolic wall thickening by 121+/-73%; 3 had ischemic-appearing ST-segment depression during this stress. This contractile response to dobutamine was no different than the increase in systolic wall thickening (129+/-48%, p=0.777) in patients in the highest quartile of coronary flow responses, 3 of whom also had ischemic-appearing ST-segment depression during this stress. Thus, coronary endothelial dysfunction in the absence of coronary artery disease does not account for ischemic-appearing ST-segment depression in patients with chest pain despite normal coronary angiograms. Further, coronary endothelial dysfunction is not associated with myocardial contractile responses to stress consistent with myocardial ischemia.     

Changes in left ventricular contractility with the phase of respiration

The end-systolic wall stress (sigma(es))-velocity of circumferential fiber shortening (V(cfsc)) relation was defined during the respiratory cycle, in order to obtain a totally noninvasive measure of left ventricular contractility. Eight young, healthy subjects were studied with echocardiography and calibrated carotid pulse tracings, while performing slow paced breathing. Left ventricular sigma(es) vs. V(efsc) relation was determined by fitting linear regression line to data points obtained at different times during the respiratory cycle. Data are given as mean+/-1SD. Left ventricular sigma(es) and V(efsc) exhibited small but significant changes during the respiratory cycle: sigma(es) was highest in late inspiration (56.9+/-4.8 g/cm2) and lowest in late expiration (49.2+/-3.7 g/cm2); inversely, V(cfsc) was lowest during late inspiration (1.18+/-0.17 circ/s) and highest during late expiration (1.34+/-0.20 circ/s). The relation was significant in each subject (r = -0.64+/-0.13) and remained inverse and significant, when it was determined separately for inspiration and expiration (r = -0.61+/-0.17 and -0.68+/-0.12, respectively). At identical end-systolic wall stress, the velocity of shortening was greater during inspiration then expiration, suggesting that contractility was reduced during the expiratory phase. The reduced expiratory contractility might reflect increased vagal influence on the ventricular myocardium.     

Myotrophic effects of muscle extracts obtained at different intervals after denervation

BACKGROUND: The assessment of return of function within dysfunctional myocardium after acute myocardial infarction (MI) using contractile reserve has been primarily qualitative. Magnetic resonance (MR) myocardial tagging is a novel noninvasive method that measures intramyocardial function. We hypothesized that MR tagging could be used to quantify the intramyocardial response to low-dose dobutamine and relate this response to return of function in patients after first MI. METHODS AND RESULTS: Twenty patients with a first reperfused MI (age, 53+/-12 years; 16 male; 11 inferior MIs) were studied. Patients underwent breath-hold MR-tagged short-axis imaging on day 4+/-2 after MI at baseline and during dobutamine infusion at 5 and 10 microg x kg(-1) x min(-1). At 8+/-1 weeks after MI, patients returned for a follow-up MR tagging study without dobutamine. Quantification of percent intramyocardial circumferential segment shortening (%S) was performed. Low-dose dobutamine MRI was well tolerated. Overall, mean %S was 15+/-11% at baseline (n=227 segments), increased to 16+/-10% at 5 microg x kg(-1) x min(-1) dobutamine (P=NS), 21+/-10% at peak (P<0.0001 versus baseline and 5 microg x kg(-1) x min(-1), and 18+/-10% at 8 weeks (P<0.004 versus baseline and peak). The increase in %S with peak dobutamine was greater in dysfunctional myocardium (103 segments, +9+/-10%) than in normal tissue (124 segments, +4+/-12%, P<0.0001). In dysfunctional regions, %S also increased from 6+/-7% at baseline to 14+/-10% at 8 weeks after MI (P<0.0001). In dysfunctional regions that responded normally to peak dobutamine (> or =5% increase in %S), the increase in %S from baseline to 8 weeks after MI (+9+/-9%) was greater than in those regions that did not respond normally (+5+/-9%, P<0.04). Midmyocardial and subepicardial response to dobutamine were predictive of functional recovery, but the subendocardial response was not. CONCLUSIONS: The response of intramyocardial function to low-dose dobutamine after reperfused MI can be quantified with MR tagging. Dysfunctional tissue after MI demonstrates a larger contractile response to dobutamine than normal myocardium. A normal increase in shortening elicited by dobutamine within dysfunctional midwall and subepicardium predicts greater functional recovery at 8 weeks after MI, but the response within the subendocardium is not predictive.     

Myocardial contrast echocardiography versus dobutamine echocardiography for predicting functional recovery after acute myocardial infarction treated with primary coronary angioplasty

OBJECTIVES: We sought to compare myocardial contrast echocardiography with low dose dobutamine echocardiography for predicting 1-month recovery of ventricular function in acute myocardial infarction treated with primary coronary angioplasty. BACKGROUND: The relation between myocardial perfusion and contractile reserve in patients with acute myocardial infarction, in whom anterograde flow is fully restored without significant residual stenosis, is still unclear. METHODS: Thirty patients with acute myocardial infarction treated successfully with primary coronary angioplasty underwent intracoronary contrast echocardiography before and after angioplasty and dobutamine echocardiography 3 days after the index infarction. One month later, two-dimensional echocardiography and coronary angiography were repeated in all patients and contrast echocardiography in 18 patients. RESULTS: After coronary recanalization, 26 patients showed myocardial reperfusion within the risk area, although 4 did not. At 1-month follow-up, all patients had a patient infarct-related artery without significant restenosis. Both left ventricular ejection fraction and wall motion score index within the risk area significantly improved in the patients with reperfusion ([mean +/- SD] 38 +/- 8% vs. 48 +/- 12%, p < 0.005; and 2.35 +/- 0.5 vs. 2 +/- 0.6, p < 0.001, respectively), but not in those with no reflow. Of the 72 nonperfused segments before angioplasty, 27 showed functional improvement at follow-up. Myocardial contrast echocardiography had a sensitivity and a negative predictive value similar to dobutamine echocardiography in predicting late functional recovery (96% vs. 89% and 89% vs. 93%, respectively), but a lower specificity (18% vs. 91%, p < 0.001), positive predictive value (41% vs. 86%, p < 0.001) and overall accuracy (47% vs. 90%, p < 0.001). CONCLUSIONS: Microvascular integrity is a prerequisite for myocardial viability after acute myocardial infarction. However, contrast enhancement shortly after recanalization does not necessarily imply a late functional improvement. Thus, contractile reserve elicited by low dose dobutamine is a more accurate predictor of regional functional recovery after reperfused acute myocardial infarction than microvascular integrity.     

Comparison of myocardial contrast echocardiography and low-dose dobutamine stress echocardiography in predicting recovery of left ventricular function after coronary revascularization in chronic ischemic heart disease

BACKGROUND: Dobutamine stress echocardiography (DSE) and myocardial contrast echocardiography (MCE) can predict recovery of left ventricular function after myocardial infarction. DSE also has been shown to predict left ventricular functional recovery after revascularization in chronic ischemic heart disease, whereas MCE has not been evaluated in such patients. This study was performed to compare DSE and MCE in the prediction of left ventricular functional recovery after revascularization in patients with chronic ischemic heart disease. METHODS AND RESULTS: MCE and DSE were performed in 35 patients with chronic coronary artery disease and significant wall motion abnormalities (mean ejection fraction, 0.36 +/- 0.09). Regional wall motion was scored by use of a 16-segment model wherein 1 = normal or hyperkinetic, 2 = hypokinetic, 3 = akinetic, and 4 = dyskinetic. Each segment was evaluated for contractile reserve by DSE and perfusion by MCE. Revascularization (coronary artery bypass graft [n = 13] and percutaneous transluminal coronary angioplasty [n = 10]) was successful in 23 patients. Follow-up echocardiograms were done to assess wall motion 30 to 60 days later. In 238 segments with resting wall motion abnormalities, perfusion was more likely to present than contractile reserve (97% versus 91%, P < .02). Revascularization resulted in functional recovery in 77 of 95 hypokinetic segments (81%) but only 18 of 57 akinetic segments (32%, P < .0001). DSE and MCE were not significantly different in predicting functional recovery of hypokinetic segments. In akinetic segments, DSE and MCE had similar sensitivities (89% versus 94%, respectively) and negative predictive values (93% and 97%, respectively) in predicting functional recovery. However, DSE had a higher specificity (92% versus 67%, P < .02) and positive predictive value (85% versus 55%, P < .02) than MCE in predicting functional recovery. CONCLUSIONS: Both contractile reserve by DSE and perfusion by MCE are predictive of functional recovery in hypokinetic segments after coronary revascularization in patients with chronic coronary revascularization in patients with chronic coronary artery disease. In akinetic segments, myocardial perfusion by MCE may exist in segments that do not recover contractile function after revascularization. Thus, contractile reserve during low-dose dobutamine infusion is a better predictor of functional recovery after revascularization in akinetic segments than perfusion.     

Midwall fractional shortening is an independent predictor of left ventricular diastolic dysfunction in asymptomatic patients with systemic hypertension

Conventional measures of left ventricular (LV) systolic performance suggest that diastolic dysfunction precedes the development of systolic dysfunction in hypertension. Midwall fractional shortening is a new measure of systolic function that identifies hypertensive patients who have evidence of target-organ damage, impaired contractile reserve, and increased mortality. We therefore sought to determine whether depressed midwall fiber shortening is associated with abnormal diastolic function. Echocardiograms were obtained in 102 otherwise healthy hypertensive patients without treatment with normal conventional measures of systolic function. Of these, 15 had depressed midwall shortening based on previously described normative relations. Patients with depressed midwall shortening had slightly higher blood pressure. Abnormal diastolic function, defined as late (A) LV inflow velocity greater than early (E) velocity, was observed in 33% of those with normal midwall shortening but in 60% of those with depressed shortening (p <0.05). Patients with A/E >1 had lower absolute midwall fiber shortening (15 +/- 3% vs 18 +/- 3%, p <0.0001) but similar endocardial shortening. Patients with abnormal midwall shortening had higher A/E and longer isovolumic relaxation times (both p <0.05). In multivariate analysis, midwall fractional shortening, age, and heart rate were independent predictors (p <0.01) of A/E in a model including blood pressure, LV mass, and endocardial shortening. We conclude that subnormal midwall shortening predicts LV diastolic abnormalities in this population of hypertensive patients with otherwise normal measures of LV systolic function. Contrary to our previous understanding, depressed LV systolic performance, when identified with this newer method, occurs coincidentally with impaired diastolic function.     

Resection of the metatarsal head for diabetic foot ulcers

Dobutamine-induced hypotension has been disregarded as a marker of more severe functional abnormalities in patients with suspected coronary artery disease. However, its functional significance in patients with myocardial infarction has not been studied. The aim of this study was to define the predictors of systolic blood pressure (SBP) response to dobutamine in patients with previous myocardial infarction. Dobutamine stress (up to 40 microg/kg per minute) echocardiography was performed in 326 patients with prior myocardial infarction referred for evaluation of myocardial ischemia. A 16-segment, four-grade score model was used to assess left ventricular function. Wall motion score index was derived by summation of wall motion score divided by 16. SBP and heart rate increased from rest to peak dobutamine stress (127 +/- 22 vs 134 +/- 27 mm Hg and 72 +/- 14 vs 122 +/- 24 bpm, p < 0.00001 in both). An increase of SBP > or = 30 mm Hg occurred in 50 patients (15%). By multivariate analysis, independent predictors of failure of SBP increase were higher peak wall motion score index (p < 0.001), higher resting SBP (p < 0.01), and medication with calcium channel blockers (p < 0.05). SBP drop > or = 20 mm Hg occurred in 54 patients (17%). Independent predictors of SBP drop were higher resting wall motion score index (p < 0.001), higher resting SBP (p < 0.0001), and older age (p < 0.05). In patients with myocardial infarction, left ventricular function and baseline systolic blood pressure are powerful predictors of SBP response to dobutamine stress testing.     

Changes of endothelin-1 and atrial natriuretic peptide during dobutamine stress echocardiography

The aim of this study was to test the hypothesis that plasma endothelin-1 (ET-1) and atrial natriuretic peptide (ANP) concentrations in patients with ischemic heart disease are related either to myocardial ischemia or left ventricular (LV) dysfunction during dobutamine stress echocardiography. Plasma concentrations of ET-1 and ANP were measured in three patient groups. Group I (n = 21) patients had normal stress echocardiography and a resting LV ejection fraction (LVEF) of 40% or more. Group II (n = 32) had positive stress echocardiography and a resting LVEF of more than 40%. Group III (n = 18) had positive stress echocardiography with a resting LVEF of less than 40%. All three groups were subjected to thallium 201 scintigraphy and coronary angiography studies. The resting LV end-diastolic pressure was significantly higher in groups II and III than in Group I. The LVEF decreased significantly in group III compared to groups I and II. In the resting state, groups II and III had higher ET-1 concentrations than Group I (p = 0.021 and p = 0.039, respectively). The plasma ANP concentration was higher in group III than in groups I and II (p = 0.005 and p = 0.054, respectively). During peak dobutamine infusion, the ET-1 concentration dropped 8.7% from the baseline in group I, 10.2% in group II, and 10.5% in group III. The ANP concentrations were increased in all three groups but only the increase in Group II reached statistical significance. In conclusion, in patients with suspected ischemic heart disease, the concentrations of ET-1 and ANP may predict significant anatomic and functional coronary artery disease. However, ET-1 does not play a pathophysiologic role during an ischemic attack.     

Age-related variation in left ventricular myocardial contractile state expressed by the stress velocity relation

The assessment of ventricular function plays an important role in the pre- and postoperative management of many congenital heart abnormalities. Normal ranges in left ventricular systolic function indices have been defined during childhood and age-related alterations in left ventricular myocardial contractile state have recently been reported. This study was carried out to investigate the developmental changes in left ventricular contractile state expressed by the endsystolic meridional stress (ESS)/rate-corrected velocity of circumferential fiber shortening (VCFc) relation, calculated by echo in normal children and young adults. We examined 146 healthy subjects (80 males and 66 females), mean age 70.85 +/- 63.89 months (range 0.5-228) and body surface area (BSA) 0.807 +/- 0. 47 (range 0.18-2.01) with no clinical and echocardiographic evidence of cardiac disease and with normal blood pressure. The subjects were divided into three groups according to age: <6 months (group 1, n = 32), 6-36 months (group 2, n = 34), and >36 months (group 3, n = 80). Enddiastolic volume and mass (M) of the left ventricle were measured by M-mode Echo. ESS was considered as an index of afterload and the VCFc as an index of systolic ventricular function. The left ventricular ejection time used for the calculation of VCFc was measured from aortic flow obtained by PW-Doppler. The ESS/VCFc relation was used to assess left ventricular contractility. Systolic blood pressure, volume, and mass of the left ventricle increase with age. The gradual increase in pressure despite a stable mass/volume ratio [M/V = 0.900 + (0.0007 x age); r = 0.27, p < 0.005] resulted in a substantial increase of afterload [ESS = 29.78 + (0.116 x age); r = 0.58, p < 0.0001]. VCFc showed an inverse hyperbolic regression with afterload [VCFc = 1.01 + (7.598/ESS); r = 0.59, p < 0.0001]. The regression lines (best linear fit) between VCFc and ESS are significantly different in the three groups. The Y intercept was higher and the slope steeper in group 1 [VCFc = 1.74 - (0.017 x ESS); r = 0.65, p < 0.0005] vs group 2 [VCFc = 1.54 - (0.008 x ESS); r = 0.58, p < 0.001] and group 3 [VCFc = 1.52 - (0.007 x ESS); r = 0.57, p < 0.0001]. These data indicate that, in children, the volume and mass of the left ventricle increase, whereas the M/V ratio remains relatively constant; the progressive increase in arterial blood pressure explains the increase of afterload. The VCFc is higher in the first few years of life compared to that seen in older children due to reduced afterload and increased contractile state. Left ventricular contractility, expressed as ESS/VCFc relation, is thus inversely proportional to age. In the first months of life the left ventricular myocardium exhibits a higher basal contractile state and a greater sensitivity to changes in afterload. For obtaining an accurate assessment of left ventricular function, the ESS/VCFc relation in different age groups should be measured.     

Left ventricular contractile performance, ventriculoarterial coupling, and left ventricular efficiency in hypertensive patients with left ventricular hypertrophy

Contractile performance of hypertrophied left ventricle may be depressed in arterial hypertension. Ventriculoarterial coupling is impaired when myocardial contractile performance is reduced and when afterload is increased. The left ventricular contractile performance and the ventriculoarterial coupling were evaluated in 30 hypertensive patients with moderate left ventricular hypertrophy and 20 control subjects. Left ventricular angiography coupled with the simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress/volume index, the slope of end-systolic pressure-volume relationship, ie, end-systolic elastance, effective arterial elastance, external work, and pressure-volume area. In hypertensive patients, left ventricular contractile performance, as assessed by end-systolic elastance/ 100 g myocardial mass, was depressed (4.35 +/- 1.13 v 5.21 +/- 1.89 mm Hg/mL/100 g in control subjects P < .02), when end-systolic stress-to-volume ratio was comparable in the two groups (3.85 +/- 0.99 g/cm2/mL in hypertensive patients versus 3.51 +/- 0.77 g/cm2/mL in control subjects). Ventriculoarterial coupling, evaluated through effective arterial elastance/end-systolic elastance ratio, was slightly higher in hypertensive patients (0.53 +/- 0.08 v 0.48 +/- 0.09 mm Hg/mL in control subjects, P < .05), and work efficiency (external work/pressure-volume area) was similar in the two groups (0.78 +/- 0.04 mm Hg/mL in hypertensive patients versus 0.80 +/- 0.03 mm Hg/mL in control subjects). This study shows that despite a slight depression of left ventricular contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with left ventricular hypertrophy. Thus, it appears that left ventricular hypertrophy might be a useful means of preserving the match between left ventricle and arterial receptor with minimal energy cost.