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A L'Abbate

Publications and source records attributed to A L'Abbate.

At least 19 recordsLinked to original sources
PubMed2003

The effect of lipoproteins on endothelial nitric oxide synthase is modulated by lipoperoxides.

BACKGROUND AND AIM: The effect of low-density lipoproteins (LDLs) on endothelial nitric oxide synthase (eNOS) is debated. By coupling in vivo and in vitro experiments we evaluated the role of oxidized lipid substrates in the modulation of eNOS activity by LDLs. MATERIALS AND METHODS: Plasma lipids, nitrite/nitrates (NO2/NO3), and malondialdehyde (MDA) were measured in 14 controls, and in 13 patients with familial hypercholesterolemia (FH) before and after 12 weeks of treatment with atorvastatin (20 mg u.i.d.). Nitric oxide synthase in cell lysate and NO2/NO3 into the medium were measured in human microvascular (HMEC-1) and umbilical vein (HUVEC) endothelial cells after 24 h of incubation with increasing concentrations of mildly oxidized LDLs with and without atorvastatin and in HMEC-1 with and without vitamin C. In HMEC-1, NO2/NO3 was also determined after exposure to more intensively oxidized LDLs. RESULTS: At baseline, plasma NO2/NO3 (56 +/- 7 vs. 35 +/- 3 micro M) and MDA (5.6 +/- 0.7 vs. 2.9 +/- 0.3 micro M), were significantly (P < 0.02 for both) higher in the FH patients. In the whole study group, NO2/NO3 was more strongly correlated with plasma MDA (Rho = 0.70) than LDL-cholesterol (Rho = 0.57). In the FH patients, atorvastatin induced a significant decline in plasma total and LDL-cholesterol (-3.1 +/- 0.5 and -2.9 +/- 0.5 mM, respectively), NO2/NO3 (-35 +/- 8 microM) and MDA (-3.4 +/- 0.7 microM) (P < 0.001 for all). Changes in plasma NO2/NO3 were related to the concomitant changes in plasma MDA (Rho = 0.79, P < 0.006) and not to changes in LDL-cholesterol. In HMEC-1 and in HUVEC, mildly oxidized LDLs stimulated both e-NOS and NO2/NO3 accumulation; the effect on e-NOS was potentiated by vitamin C in HMEC-1. Atorvastatin had no effect in HMEC-1 while it stimulated eNOS but not NO2/NO3 in HUVEC. The accumulation of NO2/NO3 in HMEC exposed to increasing concentrations of more intensively oxidized-LDLs showed a nonlinear dose-response curve. CONCLUSIONS: In uncomplicated patients with FH, plasma NO2/NO3 concentrations are elevated; the cross-sectional data, intervention study and in vitro experiments indicate that oxidized lipids exert a tonic stimulatory action on e-NOS and NO2/NO3 generation not mediated through superoxide anion formation. Atorvastatin amplify this eNOS response in HUVEC, but not in HMEC, and this effect is not associated with a parallel increased NO2/NO3 generation.

Adult↗
PubMed2003

Influence of chronic aerobic exercise on microcirculatory flow and nitric oxide in humans.

In the present study we assessed the effect of physical training on Laser Doppler skin flux (LDF) and nitric oxide (NO) release, before and after 3 min of brachial artery occlusion. To this end we performed laser Doppler measurements and the venous plasma assay of nitrite/nitrate (NOx) on 10 sedentary healthy subjects and 10 endurance athletes. The sedentary control subjects had lower basal and post reperfusion levels of NOx as compared to athletes (mean +/- SE: 27.8 +/- 3.5 vs. 33.2 +/- 3.4, 48.6 +/- 7.9 vs. 60.1 +/- 10.1 micromol/L; p < 0.05). LDF at baseline was not significantly different in the two groups (157.5 +/- 7.9 and 176.64 +/- 26.7 PU for sedentary subjects and athletes, respectively) while post ischemic LDF was significantly lower in nonathletic subjects than in athletes (209.9 +/- 13 and 343.8 +/- 21.3 PU, p < 0.001). In both groups the hyperaemic stimulus significantly increased LDF and NOx levels (p < 0.01 and p < 0.05, respectively). The flow reserve, estimated as peak/basal LDF, was significantly lower in control subjects than in athletes (1.34 +/- 0.2 and 2.32 +/- 0.9, respectively, p < 0.01). In athletes, as opposed to sedentary subjects, a direct correlation was found between plasma NOx concentration and LDF both in basal conditions (r = 0.92; p < 0.001), and during hyperaemia (r = 0.84; p < 0.01). In conclusion, compared to sedentary subjects, athletes had an enhanced nitric oxide release. Hyperaemia increased LDF and nitric oxide levels both in sedentary subjects and in athletes.

Adult↗
PubMed2001

Paradoxical increase in microvascular resistance during tachycardia downstream from a severe stenosis in patients with coronary artery disease : reversal by angioplasty.

BACKGROUND: The pathophysiology of microvascular response to a severe coronary stenosis has not been conclusively identified. The aim of this study was to characterize the human vasomotor response to pacing-induced ischemia of both the stenotic arterial segment and the distal microcirculation. METHODS AND RESULTS: Sixteen patients with stable angina and single-vessel disease were studied. Blood flow velocity and transstenotic pressure gradient were monitored at baseline, after intracoronary adenosine (2 mg), and during ischemia induced by atrial pacing with and without adenosine. At the end of this protocol, the study was repeated after intracoronary phentolamine in 7 patients and after angioplasty in 9. Stenosis resistance was calculated as the ratio between mean pressure gradient and mean flow, and microvascular resistance as the ratio between mean distal pressure and mean flow; values were expressed as percent of baseline. Adenosine decreased (P<0.05) baseline microvascular resistance to 52+/-17%, but not stenosis resistance. Pacing increased both stenosis and microvascular resistances (244+/-96% and 164+/-60% of baseline, respectively, P<0.05). Addition of adenosine to pacing decreased both stenosis (143+/-96% of baseline, P<0.05 versus ischemia) and microvascular (51+/-17% of baseline, P<0.05 versus baseline and ischemia) resistances. Phentolamine did not affect coronary resistance at any step of the protocol. Angioplasty and stenting restored a progressive decline in microvascular resistance during pacing (51+/-19% of baseline, P<0.05 versus baseline). CONCLUSIONS: In patients with coronary artery disease, tachycardia-induced ischemia was associated with elevated resistance of both the stenotic segment and the microvasculature. Revascularization prevents this paradoxical behavior.

Adenosine↗
PubMed2001

Oxygen radical-mediated reduction in basal and agonist-evoked NO release in isolated rat heart.

Oxygen free radicals (OFR) play a primary role in ischemia-reperfusion-mediated vascular dysfunction and this is paralleled by a loss of endothelial nitric oxide synthase (eNOS) activity. The authors tested whether a direct exposure to OFR may affect vascular relaxation by altering nitric oxide (NO) release. Effects of electrolysis(EL)-generated OFR on basal and agonist-evoked NO release were monitored in isolated rat hearts by oxyhemoglobin assay. Electrolysis-induced changes were compared with those obtained after 30 min perfusion with NOS and cyclooxygenase (COX) inhibitors NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) and indomethacin (INDO, 1 m M). Electrolysis-generated hydroxyl radical (.OH) formed by.O2-and H2O2 via the Fenton reaction as revealed by Electron Paramagnetic Resonance (EPR). After EL, basal NO release declined by 60% and coronary perfusion pressure (CPP) increased by approximately 70%. L-NAME/INDO perfusion similarly lowered NO release (-63%) but increased CPP less than EL (56+/-3%P<0.03 v post-EL). In presence of excess substrates and cofactors eNOS activity was not affected by EL. Both acetylcholine (ACh; 1 microM) and bradykinin (BK; 10 n M) had minimal effect in reversing EL-induced vasoconstriction, whereas both partially reversed L -NAME/INDO-mediated constriction. Sodium nitroprusside (SNP, 1 microM) completely reversed L-NAME/INDO constriction and partly countered that after EL (-38+/-2.5, P<0.001). Acetylcholine-evoked NO release was nearly abolished by both treatments whereas BK still elicited partial NO release after eNOS/cyclooxygenase inhibition (P<0.001) but not after EL. In conclusion, OFR severely impair NO-mediated coronary vasorelaxation affecting both basal and agonist-evoked NO release but not eNOS activity. However, EL also significantly blunts NOS/COX-independent vasodilation suggesting alteration of other vasodilatative pathways.

Acetylcholine↗
PubMed2001

Increased circulating levels of ouabain-like factor in patients with asymptomatic left ventricular dysfunction.

BACKGROUND: Much evidence has been accumulated that human plasma contains digitalis-like factor(s) with Na/K ATPase inhibitor properties. Increased concentrations of ouabain-like factor (OLF) have been reported in patients with moderate to severe hypertension and in patients with overt congestive heart failure due to dilated cardiomyopathy. AIM: The presence of circulating OLF has not been investigated in borderline to mild hypertension or in the early stage of dilated cardiomyopathy. METHODS AND RESULTS: The study population consisted of 18 normal volunteers, 24 patients with borderline to mild hypertension, 47 patients with asymptomatic left ventricular dysfunction (ALVD) due to dilated cardiomyopathy and 26 patients with cardiac arrhythmias but normal left ventricular function. OLF values (pM ouabain equivalent) were assayed in extracted plasma, using a radioimmunoassay for ouabain. OLF was, respectively, 29.4+/-20.6 pM in normal controls, 39.1+/-23.8 pM in hypertensives, 35+/-18 pM in patients with cardiac arrhythmias, 52.3+/-25.8 pM in ALVD patients not treated with digoxin and 64.6+/-29.6 pM in ALVD patients treated with digoxin. Patients with ALVD, both treated and not treated with digoxin, had OLF significantly higher (P<0.05) than all the other groups. In patients with ALVD no correlation between OLF and left ventricular ejection fraction was observed. In the hypertensive group no correlation between OLF and both diastolic and systolic pressure was found. CONCLUSION: Increased concentrations of OLF were observed in patients with left ventricular dysfunction due to dilated cardiomyopathy, before the occurrence of overt heart failure, suggesting that OLF may be an early marker of the disease.

Adult↗
PubMed2001

Relationship between function and perfusion early after acute myocardial infarction.

To assess the relationship between baseline left ventricle function, functional reserve and resting myocardial perfusion in patients with acute myocardial infarction (AMI). After AMI the presence of dysfunctioning but viable myocardium plays a determinant role in clinical outcome. Regional ventricular function was evaluated by echocardiography both in resting conditions and during dobutamine infusion (10 microg/kg/min). Perfusion was assessed by magnetic resonance imaging in a single slice approach where the first pass of an intravenously injected bolus of gadolinium-based contrast agent was followed through six regions of interest within the myocardium. In each patient a region with normal function was used as reference and the cross-correlation coefficient (CCC), which described the myocardial perfusion relatively to the reference region (CCC = 1 means equivalent perfusion), was obtained for the other five myocardial regions. Twenty-two patients were enrolled into the study. Sixty-one segments had normal function and normal perfusion (CCC = 0.92+/-0.23). The perfusion deficit was more marked in the 29 regions with resting akinesia-dyskinesia than in the 20 hypokinetic regions (CCC = 0.71+/-0.45 vs. 0.84+/-0.23; p < 0.05). Out of the 29 regions with resting akinesia-dyskinesia the 13 segments which showed functional improvement following dobutamine had a higher resting perfusion than the 16 segments which were unresponsive to dobutamine (CCC = 0.83+/-0.32 vs. 0.61+/-0.52, p < 0.05). Similarly, out of the 20 regions with resting hypokinesia the 11 segments having functional reserve showed an higher resting perfusion than the segments which did not (0.96+/-0.21 vs. 0.69+/-0.19; p < 0.05). Early after AMI, the perfusion deficit reflects the severity of the mechanical dysfunction. In regions with baseline dyssynergy resting perfusion is, in general, higher when contractile reserve can be elicited by stress-echo.

Adrenergic beta-Agonists↗
PubMed2001

Personality change as defensive responses of patients evaluated for liver transplant.

Patients affected by endstage liver disease and awaiting liver transplant suffer very stressful conditions. The aim of this study was to evaluate the person ality and behavioral responses of a group of liver transplant candidates, 95 men (M age 50 yr.) and of a group of 18 normal men (M age 49 yr.). The 16 Personality Factor Questionnaire of Cattell, and the PSY Inventory for Behavioral Assessment were administered to assess personality and behavior. On the 16PF Questionnaire, patients had significantly different mean scores from normal subjects on Scale B- (low mental capacity), G (conformity), N (shrewdness), and Q1- (conservatism). They also showed a somewhat lower but not a statistically significant mean on Scale E (submissiveness). In addition, on the four second-order factors of the 16PF (Anxiety, Control, Pathemia, and Extraversion) patients had a significantly higher mean on Control. With respect to PSY Inventors factors, patients showed impairment in energy, sleep, sexual disturbances, and obsessive behaviors. It appears these patients with endstage liver disease, who were evaluated for liver transplant, showed psychological regressive functioning, i.e., high control and dependency on medical staff, submissiveness, which are interpretable as defensive responses to upcoming transplant.

Adult↗
PubMed2000

Coronary atherosclerosis in Type II diabetes: angiographic findings and clinical outcome.

AIMS/HYPOTHESIS: Prevalence and incidence of coronary heart disease (CHD) are increased in patients with Type II (non-insulin-dependent) diabetes mellitus; whether this is entirely due to more extensive coronary atherosclerosis is, however, controversial. METHODS: We analysed the clinical, angiographic and follow-up data of 2253 consecutive patients undergoing coronary angiography over the decade 1983-1992. RESULTS: Abnormal coronary arteries (> or =50% stenosis) were found more frequently in diabetic than in non-diabetic subjects (85 vs 67%, p < 0.0001), the excess being explained by a higher prevalence of three-vessel disease (36 vs 17%, p < 0.0001). The sum of all angiographically detectable lumen stenoses (atherosclerosis score, ATS) was higher in diabetic than in non-diabetic subjects (352 +/- 232 vs 211 +/- 201 units, p < 0.0001). After adjusting for measured cardiovascular risk factors, diabetes was still associated with an excess ATS (114 units in men and 187 units in women, p < 0.0001 for both, p < 0.03 for the interaction ATS x sex). Within the diabetic group, the only variable that was independently (of sex and age) associated with ATS was serum cholesterol, whereas plasma glucose concentration, disease duration and type of treatment were not correlated with the severity of coronary atherosclerosis. In contrast, clinical grade proteinuria was not associated with a more diffuse coronary atherosclerosis either in diabetic (366 +/- 243 vs 354 +/- 233 units) or non-diabetic subjects (231 +/- 201 vs 207 +/- 197 units). Over a mean follow-up period of 88 months, 19% of diabetic patients compared with 10% of non-diabetic patients died of a cardiac cause (age and sex-adjusted odds ratio OR = 1.34 [1.14-1.57]). In a Cox model adjusting for age, sex and all major risk factors, diabetes was still associated with a significant excess risk of dying of a cardiac cause (OR = 1.37 [1.14-1.60]); this excess was similar to, and independent of, that carried by the presence of prior myocardial infarction in the whole population (OR = 1.42 [1.25-1.62]). Proteinuria was associated with a higher risk of cardiac death, particularly in diabetic patients, independently of coronary atherosclerosis (adjusted OR = 1.46 [1.03-1.99]). CONCLUSION/INTERPRETATION: In patients undergoing angiography, diabetes, especially in women, is associated with more severe and diffuse coronary atherosclerosis which is not explained by either the traditional risk factors or the presence of proteinuria. On follow-up, these patients experience an excess of cardiac deaths, to which coronary atherosclerosis and proteinuria make independent, quantitative contributions.

Aged↗
PubMed2000

Interaction between coronary artery stenosis and coronary microcirculation in ischemic heart disease.

The hallmark of ischemic heart disease is the presence of focal obstructions in the major coronary arteries. Classically, epicardial stenoses are thought to exert their pathogenetic role mainly through a limitation on maximal flow capacity in the distal vascular bed. Ischemia is thus thought to occur whenever oxygen consumption exceeds the flow availability. Although a number of experimental studies confirmed these assumptions, the adherence of this experimental model with the clinical observations is still far from being convincing. Evidence now exists that atherosclerosis causes more profound alterations in the regulation of myocardial perfusion, besides the hydraulic effects of epicardial obstructions. These alterations affect endothelial regulation of coronary vasomotor tone both in the large arteries and in the distal microcirculation. In agreement with this experimental evidence, an abnormal response to endothelium-mediated vasodilators has been reported in patients with coronary artery disease. Moreover, several studies also reported an abnormal response of atherosclerotic coronary microcirculation to atrial pacing tachycardia and dipyridamole, which are thought to be largely endothelium independent. An even more striking observation is the finding of an intense microvascular constrictor response in the myocardium, supplied by a severely stenotic coronary artery, to pacing-induced ischemia. This observation strongly suggests that coronary microcirculation might aggravate the flow reduction imposed by the epicardial stenosis, thus playing some role in the pathogenesis of ischemia. This phenomenon might reflect the presence of a primary abnormality of coronary microcirculation in patients with coronary artery disease or the existence of a pressure-oriented regulation of vascular tone which prevent trans-stenotic pressure drop by means of a heterogeneously distributed microcirculatory vasoconstriction.

Adaptation, Physiological↗
PubMed2000

Coronary microcirculatory vasoconstriction during ischemia in patients with unstable angina.

OBJECTIVE: To verify the behavior of coronary microvascular tone during spontaneous ischemia in patients with unstable angina (UA). BACKGROUND: In UA, the pathogenetic role of vasoconstriction is classically confined at the stenotic coronary segment. However, microcirculatory vasoconstriction has been also suggested by previous experimental and clinical studies. METHODS: The study included 10 patients with UA (recent worsening of anginal threshold and appearance of angina at rest) and single-vessel CAD. Blood flow velocity was monitored by a Doppler catheter in the diseased artery. Transstenotic pressure gradient was monitored by aortic and distal coronary pressure monitoring. Stenosis resistance was calculated as the ratio between pressure gradient and blood flow, microvascular resistance as the ratio between distal pressure and blood flow. Measurements were obtained at baseline, following intracoronary adenosine (2 mg) and during transient ischemia. Aortic and distal coronary pressures were also measured during balloon coronary occlusion. RESULTS: Adenosine did not affect stenosis resistance, while it decreased (p < 0.05) microvascular resistance to 52 +/- 22% of baseline. Angina and ischemic ST segment shift were associated with transient angiographic coronary occlusion in 7 of 10 patients; however, in no case was ischemia associated with interruption of flow. Despite markedly different flow values, distal coronary pressure was similar during adenosine and during spontaneous ischemia (48 +/- 15 vs. 46 +/- 20 mm Hg, respectively, NS). During ischemia, a marked increase in the resistance of both coronary stenosis and coronary microcirculation was observed (to 1,233% +/- 1,298% and 671% +/- 652% of baseline, respectively, p < 0.05). Distal coronary pressure was markedly reduced during balloon coronary occlusion (14 +/- 7 mm Hg, p < 0.05 vs. both adenosine and ischemia), suggesting the absence of significant collateral circulation. CONCLUSIONS: In patients with UA, transient myocardial ischemia is associated with vasoconstriction of both stenotic arterial segment and downstream microcirculation.

Adenosine↗
PubMed2000

Early impairment of coronary flow reserve and increase in minimum coronary resistance in borderline hypertensive patients.

OBJECTIVE: To evaluate relations between coronary flow velocity and myocardial oxygen demand at rest, as well as coronary vasodilator capacity and flow reserve, in asymptomatic subjects with borderline hypertension as compared to normotensive controls and patients with sustained high blood pressure (HBP) and without left ventricular hypertrophy (LVH). SUBJECTS AND METHODS: Forty-two asymptomatic males were studied: 13 healthy normotensive volunteers; 12 subjects with borderline HBP and 17 asymptomatic subjects with sustained systemic hypertension. Coronary flow velocity in left anterior descending artery and coronary flow reserve were assessed by transesophageal echo-doppler at baseline and during intravenous adenosine infusion. Left ventricular mass, peak systolic wall stress (PSWS; Pa), and midwall fractional shortening (MFS; %) were obtained from M-mode images of the left ventricle in transthoracic long-axis view and in transesophageal transgastric view. RESULTS: Coronary flow velocity at baseline was not significantly different in the three groups, despite significantly higher rate-pressure product (RPP) in the hypertensive groups as compared with controls. Only in control subjects, was resting coronary flow velocity significantly correlated with RPP (y = 4279 + 200x, r = + 0.58, P < 0.05) and PSWS (y = 17.2 + 5.1 x, r = + 0.62, P < 0.05). Coronary reserve was 3.5 +/- 0.65 in controls and significantly lower (P < 0.05) in borderline hypertensive (2.87 +/- 0.46) and in sustained hypertensive subjects (2.66 +/- 0.56). Minimum coronary resistance was significantly increased in both hypertensive groups (1.30 +/- 0.29 and 1.39 +/- 0.48 mmHg/s per cm) as compared to normotensive controls (0.93 +/- 0.20 mmHg/s per cm, P < 0.01). CONCLUSIONS: In asymptomatic subjects with borderline hypertension and without LVH, a significant reduction in coronary flow reserve is already detectable and appears almost entirely related to an impaired coronary vasodilator capacity rather than to an increased myocardial oxygen demand.

Adenosine↗
PubMed2000

Adenosine and angiotensin system interact in the regulation of renal microcirculation in humans.

We sought to evaluate the possible interaction between the adenosine and angiotensin systems in the regulation of renal microcirculation in humans. Twenty normotensive patients entered the study. Ten patients (group 1) were pretreated with 50 mg of captopril, an inhibitor of angiotensin-converting enzyme, whereas 10 patients (group 2) were pretreated with placebo. Incremental doses of adenosine (from 10(-5) to 1 mg) were injected into a renal artery to all patients at 5-min intervals. Adenosine injection reduced mean renal blood flow velocity in both groups (from 17.3+/-2.8 and 16.7+/-2 cm/s to 5.1+/-1.1 and 3.8+/-0.8 cm/s, in groups 1 and 2, respectively). The decrease in flow velocity was immediate after adenosine, and its duration was proportional to dosage (y = 3.05 x -2.7; R2 = 0.46; p < 0.01). However, group 1 had a slope of regression lower than group 2 (2.37 vs. 3.82 s; p < 0.03). The index of renal resistance (mean arterial pressure/mean blood flow velocity) increased linearly in both groups with adenosine, but group I showed a lower slope of increment (2.77 vs. 5.57 mm Hg/cm/s; p < 0.01). Adenosine administration induced a marked and transient increase in human renal resistance. This vasoconstrictive effect of adenosine was blunted by captopril pretreatment.

Adenosine↗
PubMed2000

Effects of long-term treatment with verapamil on left ventricular function and myocardial blood flow in patients with dilated cardiomyopathy without overt heart failure.

Myocardial blood flow (MBF) abnormalities are present in early stage dilated cardiomyopathy (DCM) and have been attributed to coronary microvascular abnormalities. The favorable effects of verapamil on coronary microcirculation might indicate its use in early stage DCM. We assessed the safety of long-term combination therapy of verapamil and enalapril and its effects on both left ventricular function and myocardial perfusion compared with enalapril alone in 18 patients with DCM (15 men, 3 women; mean age, 50+/-9 years) without overt heart failure (NYHA class I-II). At baseline and after 6 months of randomized treatment with either enalapril (10-20 mg) (nine patients, group 1) or enalapril (10-20 mg) and verapamil (120-240 mg) (nine patients, group 2), left ventricular function was assessed at rest, during handgrip, and during bicycle exercise by equilibrium radionuclide angiography. Mean MBF was measured at rest and after dipyridamole by positron emission tomography (PET) and 13N-ammonia as a flow tracer. At baseline, the two groups had reduced left ventricular ejection fraction at rest, which was further impaired during isometric exercise, but increased at peak bicycle exercise. MBF was similarly reduced in the two groups at rest and during dipyridamole. During treatment, no adverse events occurred in either group. After 6 months there was no significant difference in the main study variables either between the two groups or within each group before and after treatment. Long-term combination therapy with verapamil and enalapril is safe in patients with DCM without overt heart failure. Despite no favorable effect on myocardial perfusion, combined treatment prevented deterioration of left ventricular function, similarly to enalapril alone.

Calcium Channel Blockers↗
PubMed2000

Clinical experience with SonoVue in myocardial perfusion imaging.

Ultrasound-enhancing agents have the potential to evaluate myocardial perfusion, adding a new dimension to echocardiography. This article summarizes the clinical studies involving SonoVue, a new intravenous ultrasound contrast agent, in assessing myocardial perfusion. Safe and well tolerated, SonoVue coupled with echocardiography has the capability to identify perfusion abnormalities, as confirmed by scintigraphic imaging. While the optimal modalities for ultrasound perfusion assessment are not yet determined, numerous technical advances have been introduced: continuous infusion or slow intravenous administration of the agent, harmonic intermittent imaging, pulse inversion, background subtraction, color coding, and others. SonoVue is a promising new agent in the booming field of myocardial contrast echocardiography.

Angioplasty, Balloon, Coronary↗
PubMed2000

Clinical evidence for myocardial derecruitment downstream from severe stenosis: pressure-flow control interaction.

To verify the interaction between coronary pressure (CP) and blood flow (CBF) control, we studied nine candidates for angioplasty of an isolated lesion of the left anterior descending coronary artery [i.e. , percutaneous transluminal coronary angioplasty (PTCA)]. CBF (i.e., flow velocity x coronary cross-sectional area at the Doppler tip) and CP were monitored during washout of 2-5 mCi of (133)Xe after bolus injection into the left main artery before and after PTCA. Xe mean transit time (MTT) was calculated as the area under the time-activity curve, acquired by a gamma camera, divided by the dose obtained from a model fit of the Xe curve in the anterior wall. CBF response to intracoronary adenosine (2 mg) was also assessed. PTCA increased baseline CBF (from 14.5 +/- 9.4 to 20 +/- 8 ml/min, P < 0.01), coronary flow reserve (from 1.52 +/- 0.24 to 2.33 +/- 0.8, P < 0.01), and CP (from 64 +/- 9 to 100 +/- 10 mmHg, P < 0.05). MTT decreased from 89 +/- 32 to 70 +/- 19 s (P < 0.05) after PTCA; however, MTT and CBF changes were not correlated (r = -0.09, not significant). Inasmuch as MTT is the ratio of distribution volume to CBF, MTT x CBF was used as an index of perfused myocardial volume. Volume increased after PTCA from 23 +/- 18 to 56 +/- 30 ml. A direct correlation was observed between the percent increase in distal CP and percent increase in perfused volume (r = 0.91, P < 0.01). Thus low CP was not associated with exhaustion of flow reserve but, rather, with reduction of perfused myocardial volume. These data suggest that, in the presence of a severe coronary stenosis, derecruitment of vascular units occurs that is proportional to the decrease in driving pressure. Residual perfused units maintain a vasomotor tone, thus explaining the paradoxical persistence of coronary reserve.

Angioplasty, Balloon, Coronary↗