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Biomedical subjects

E Picano

Publications and source records attributed to E Picano.

At least 73 records · Page 4Linked to original sources
PubMed1998

Prognostic value of myocardial viability in medically treated patients with global left ventricular dysfunction early after an acute uncomplicated myocardial infarction: a dobutamine stress echocardiographic study.

BACKGROUND: Residual viable myocardium identified by dobutamine stress after myocardial infarction may act as an unstable substrate for further events such as subsequent angina and reinfarction. However, in patients with severe global left ventricular dysfunction, viability might be protective rather than detrimental. The aim of this study was to assess the impact on survival of echocardiographically detected viability in medically treated patients with global left ventricular dysfunction evaluated after acute uncomplicated myocardial infarction. METHODS AND RESULTS: The data bank of the large-scale, prospective, multicenter, observational Echo Dobutamine International Cooperative (EDIC) study was interrogated to select 314 medically treated patients (271 men; age, 58+/-9 years) who underwent low-dose (</=10 microg x kg-1 x min-1) dobutamine for the detection of myocardial viability and high-dose dobutamine for the detection of myocardial ischemia (</=40 microg x kg-1 x min-1 with atropine </=1 mg) performed 12+/-6 days after an acute uncomplicated myocardial infarction and showing a moderate to severe resting left ventricular dysfunction (wall motion score index [WMSI] >1.6). Patients were followed up for 9+/-7 months. Low-dose dobutamine stress echocardiography identified myocardial viability in 130 patients (52%). Dobutamine-atropine stress echocardiography was positive for ischemia in 148 patients (47%) and negative in 166 patients (53%). During the follow-up, there were 12 cardiac deaths (3.8% of the total population). With the use of Cox proportional hazards model, delta low-dose WMSI (the variation between rest WMSI and low-dose WMSI) was shown to exert a protective effect by reducing cardiac death by 0.8 for each decrease in WMSI at low-dose dobutamine (coefficient, -0.2; hazard ratio, 0.8; P<0.03); WMSI at peak stress was the best predictor of cardiac death in this set of patients (hazard ratio, 14.9; P<0.0018). CONCLUSIONS: In medically treated patients with severe global left ventricular dysfunction early after acute uncomplicated myocardial infarction, the presence of myocardial viability identified as inotropic reserve after low-dose dobutamine is associated with a higher probability of survival. The higher the number of segments showing improvement of function, the better the impact is of myocardial viability on survival. The presence of inducible ischemia in this set of patients is the best predictor of cardiac death.

Aged↗
PubMed1998

Relative role of coronary stenosis severity and morphology in determining pharmacologic stress echo positivity.

Angiographically assessed plaque morphology, not only plaque severity, may affect myocardial vulnerability to ischemia during stress testing. The aim of this study was to evaluate directly, in a head-to-head comparison, the relation between coronary stenosis severity and morphology and pharmacologic stress echo response. From our inpatients echo databank, we selected 68 patients (62 men, mean age 57 +/- 9 years) who had undergone high-dose dipyridamole and high-dose dobutamine-atropine echocardiography, performed within 1 week and in random order, before coronary angiography that showed significant coronary artery disease by selection. There were altogether 121 vessels with visually assessed stenosis >50% in 68 patients. Thirty-three had complex-type and 56 simple-type lesions (according to the Ambrose classification), whereas 32 vessels were occluded. During dobutamine echocardiography there were 51 dyssynergic regions of the left ventricle fed by different coronary arteries in 50 patients and dipyridamole stress was able to induce ischemia in 45 separate regions in 44 patients. The overall agreement between the 2 tests in recognizing ischemia was 76%. Induced ischemia was associated with greater quantitatively assessed stenosis severity for both dipyridamole (positive, 70 +/- 12% vs negative, 63 +/- 12% area reduction; p <0.05) and dobutamine (positive, 68 +/- 12% vs negative, 63 +/- 12% area reduction; p <0.05). The simple-type stenosis was more frequently identified with dobutamine (46%) versus dipyridamole (21%, [p <0.01]), whereas the complex-type stenosis was associated with a trend toward more frequent positivity of dipyridamole (55%) versus dobutamine (36%), p = 0.13. Adenosinergic stress positivity is affected not only by plaque severity, but also by plaque morphology, whereas adrenergic stress positivity is affected by plaque severity, not by plaque morphology.

Adult↗
PubMed1998

Acute hemodynamic effects of endogenous adenosine in patients with chronic heart failure.

OBJECTIVE: The objective of this study was to assess the acute hemodynamic effects of endogenous adenosine accumulation in patients with chronic heart failure. Exogenously administered adenosine has been shown to reduce pulmonary vascular resistance and to increase cardiac index in normal subjects and in patients with pulmonary hypertension or end-stage biventricular heart failure. Endogenous adenosine accumulation can be provoked by dipyridamole. METHODS AND RESULTS: Ultra-low-dose dipyridamole (0.07 mg/kg/min for 4 minutes) was administered in 20 patients with either symptomatic idiopathic (n = 12) or ischemic (n = 8) dilated cardiomyopathy and reduced left ventricular ejection fraction (mean 25%+/-5%). Hemodynamic variables were measured before and within 1 minute from the end of dipyridamole infusion. After dipyridamole administration, a mild but significant increase in heart rate (4.5%; p = 0.03) and reduction in mean blood pressure (6.8%; p < 0.001) without changes in right atrial pressure (p = NS) were detected. Dipyridamole increased cardiac output by 26.6% (p < 0.001), cardiac index by 24% (p < 0.001), and stroke volume by 19.8% (p < 0.001), with concomitant 24.6% reduction of systemic vascular resistance (p < 0.001). Moreover, dipyridamole reduced mean pulmonary artery pressure by 8.3% (p < 0.01) and pulmonary vascular resistance by 33.3% (p = 0.001), without changes in pulmonary wedge pressure (p = NS). A significant correlation between percent decrease from baseline in pulmonary and systemic vascular resistance (r = 0.66; p = 0.002) was found after administration of dipyridamole. CONCLUSIONS: Endogenous adenosine accumulation induced by ultra-low-dose dipyridamole infusion acutely improves the hemodynamic profile, decreasing pulmonary and, to a lower extent, systemic vascular resistance and increasing cardiac index in patients with severe chronic heart failure.

Adenosine↗
PubMed1998

European Stroke Prevention Study-2 results: serendipitous demonstration of neuroprotection induced by endogenous adenosine accumulation?

In patients with prior stroke or transient ischaemic attack, anti-platelet treatment with dipyridamole substantially reduced stroke recurrence, with a beneficial effect comparable to and additive with that induced by aspirin (the European Stroke Prevention Study-2). Eugenio Picano and Maria Abbracchio present here a platelet-independent hypothesis, according to which cardiovascular and neuroprotective actions achieved by dipyridamole through chronic elevation of endogenous adenosine levels may have contributed to the therapeutic success of this study.

Adenosine↗
PubMed1998

Value of pharmacologic stress echocardiography in risk stratification of patients with single-vessel disease: a report from the Echo-Persantine and Echo-Dobutamine International Cooperative Studies.

OBJECTIVES: This study sought to verify the effectiveness of pharmacologic stress echocardiography in risk stratification of patients with single-vessel disease. BACKGROUND: Noninvasive prognostic assessment of single-vessel disease is an unresolved issue to date. METHODS: The study evaluated prospectively collected data from 754 patients with angiographic single-vessel disease who underwent either dipyridamole (n = 576) or dobutamine (n = 178) stress echocardiography. Invasive treatment (coronary revascularization within 3 months of stress testing) was performed in 260 patients and medical treatment in 494. RESULTS: Echocardiographic positivity was observed in 421 patients (56%). Patients treated invasively had a higher incidence of stress test positivity (69% vs. 49%, p < 0.001) and left anterior descending coronary artery involvement (60% vs. 46%, p < 0.001) than patients maintained with medical therapy. During a mean follow-up of 37 months, 54 hard cardiac events occurred (14 deaths, 40 nonfatal infarctions): 37 in medically and 17 in invasively treated patients (7.5% vs. 6.5%, p = NS). On Cox analysis, a positive result on stress testing was the only independent prognostic predictor in medically treated patients (relative risk 2.92, 95% confidence interval 1.29 to 6.59). The 4-year infarction-free survival rate was higher for a negative than a positive stress test result in medically (93.9% vs. 87.3%, p = 0.009) but not invasively treated patients (92.7% vs. 97.1%, p = 0.545). Moreover, a significantly higher 4-year infarction-free survival rate was found in invasively versus medically treated patients with a positive (p = 0.012), but not in those with a negative, stress test result (p = 0.853). CONCLUSIONS: Pharmacologic stress echocardiography is effective in risk stratification of single-vessel disease and can accurately discriminate patients in whom coronary revascularization can have the maximal beneficial effect. These findings have a potential favorable impact on the cost-effectiveness of invasive procedures.

Coronary Artery Bypass↗
PubMed1998

Increased myocardial ultrasonic reflectivity is associated with extreme hypertensive left ventricular hypertrophy: a tissue characterization study in humans.

We assessed myocardial reflectivity pattern in a large spectrum of left ventricular mass values, covering the extremes from absent to severe myocardial hypertensive hypertrophy. Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to the morphometrically evaluated collagen content in humans. We enrolled 88 essential hypertensives. With an echo prototype implemented in our Institute, integrated values of the radiofrequency signal of myocardial walls were obtained and normalized for those of the pericardium (Integrated Backscatter Index, IBI, %). Left ventricular mass index (LVMI) was measured by Devereux formula. There was a weak correlation between septal IBI and LVMI (r = 0.35; P < .001). On the basis of LVMI values, three groups of hypertensives were identified, with absent (Group I, n = 23; LVMI < 125 g/m2), mild to moderate (Group II, n = 44; LVMI from 125 to 174 g/m2), or severe (Group III, n = 21; LVMI > 175 g/m2) left ventricular hypertrophy. The Integrated Backscatter Index in the septum was lower in patients of Group I (IBI = 23.3% +/- 3.6%) and II (IBI = 26.5 +/- 7.6; P = NS v Group I), in comparison with patients of Group III (IBI = 31.1 +/- 5.9; P < .02 v II; P < .0001 v I). An increased myocardial wall reflectivity is detectable only in the presence of extreme forms of hypertensive left ventricular hypertrophy.

Adult↗
PubMed1997

Dipyridamole-induced ischemia as a prognostic marker of future adverse cardiac events in adult patients with hypertrophic cardiomyopathy. Echo Persantine Italian Cooperative (EPIC) Study Group, Subproject Hypertrophic Cardiomyopathy.

BACKGROUND: Myocardial ischemia may play a role in the natural history of hypertrophic cardiomyopathy (HCM). To assess the relative prevalence and the prognostic value of dipyridamole-induced ischemia, 79 patients with HCM and without concomitant coronary artery disease (53 men; mean age, 46+/-15 years) underwent a high-dose (up to 0.84 mg/kg over 10 minutes) dipyridamole test with 12-lead ECG and two-dimensional echo monitoring and were followed up for a mean of 6 years. METHODS AND RESULTS: Twenty-nine patients (37%) showed ECG (ie, ST depression > or = 2 mV) signs of myocardial ischemia during dipyridamole test (group 1), whereas 50 (63%) had a negative test (group 2). No patient had transient wall motion abnormalities during the dipyridamole test. During the follow-up, 16 events (ie, left ventricular or atrial enlargement, unstable angina, syncope, atrial fibrillation, and bundle-branch block) occurred in 29 patients in group 1 and 5 in 50 patients in group 2 (55% versus 10%, P<.001). Patients with a positive dipyridamole test showed worse 72-month event-free survival rates compared with patients with a negative test (36.2% versus 84.2%, P<.001). A forward stepwise event-free survival analysis identified dipyridamole test positivity by ECG criteria (chi2=19.7, P=.0001), rest gradient (chi2=11.3, P=.0008), and age (chi2=4.1; P=.0413) as independent and additive predictors of subsequent events. CONCLUSIONS: ECG signs of myocardial ischemia elicited by dipyridamole are frequent in patients with HCM and identify patients at higher risk of cardiac events, suggesting a potentially important pathogenetic role of inducible myocardial ischemia in determining adverse cardiac events in these patients.

Adult↗
PubMed1997

Chronic oral dipyridamole as a 'novel' antianginal drug: the collateral hypothesis.

Dipyridamole is an adenosine transport blocker that produces elevation of tissue adenosine levels. The oral formulation has long been used as a 'coronary vasodilator', but inappropriate vasodilation can lead to a pro-ischemic effect. However, available evidence linking adenosine to angiogenesis raises the possibility of a therapeutically relevant anti-ischemic effect of the drug. Molecular biology data show that in a hypoxic milieu, increased interstitial adenosine increases proliferation of endothelial cells in culture by stimulating A1 and A2 adenosine receptors and induces vascular endothelial growth factor which leads to angiogenesis. Morphologic data indicate that chronic, intermittent dipyridamole administration increased endomyocardial capillary length density by 33% in hypertensive and 11% in normotensive rabbits. Experimental data suggest that chronic treatment with dipyridamole increases collateral flow and decreases exercise-induced left ventricular dysfunction in the territory dependent upon a critical coronary stenosis. Clinical data indicate that the meta-analysis of all published double-blind, placebo-controlled, randomized trials assessing the effect of dipyridamole as an antianginal agent showed a highly significant drug benefit (odds ratio = 0.299, confidence intervals = 0.202-0.443). Treatment duration (log time in days) was significantly correlated to the observed benefit (log odds) (r = -75, P = 0.0031), consistently with a structural change in the collateral coronary circulation requiring time to emerge. The available data support the 'adenosine collateral hypothesis' (i.e., a beneficial angiogenetic effect of chronic endogenous adenosine accumulation). The angiogenetic effect would be different from the coronary vasodilator effect in several respects: coronary anatomical target (mainly capillaries instead of arterioles); cellular target (mainly endothelium rather than smooth muscle cell); receptor target (A1 and A2 rather than A2 adenosine receptors); time required for effect (weeks or months rather than minutes or hours); clinical use (possibly therapeutic for angiogenesis; mainly diagnostic for vasodilator stress testing). Prospective, properly designed trials are needed to assess convincingly the efficacy of a drug used for 40 years and yet possibly prematurely discarded as an effective antianginal treatment.

Adenosine↗
PubMed1997

Prognostic value of dobutamine-atropine stress echocardiography early after acute myocardial infarction. Echo Dobutamine International Cooperative (EDIC) Study.

OBJECTIVES: The aim of this multicenter, multinational, prospective, observational study was to assess the relative value of myocardial viability and induced ischemia early after uncomplicated myocardial infarction. BACKGROUND: Dobutamine-atropine stress echocardiography allows evaluation of rest function (at baseline), myocardial viability (at low dose) and residual ischemia (peak dose, up to 40 micrograms with atropine up to 1 mg) in one test. METHODS: Dobutamine-atropine stress echocardiography was performed 12 +/- 5 days (mean +/- SD) after a first uncomplicated acute myocardial infarction in 778 patients (677 men; mean age 58 +/- 10 years) with technically satisfactory rest echocardiographic study results. Patients were followed-up for 9 +/- 7 months. RESULTS: Dobutamine-atropine stress echocardiographic findings were positive for myocardial ischemia in 436 of patients (56%) and negative in 342 (44%). During follow-up, there were 14 cardiac-related deaths (1.8% of the total cohort), 24 (2.9%) nonfatal myocardial infarctions and 63 (8%) hospital readmissions for unstable angina. One hundred seventy-four patients (22%) underwent coronary revascularization (bypass surgery or coronary angioplasty). Spontaneous events occurred in 61 of 436 patients with positive and 40 of 342 patients with negative findings on dobutamine-atropine stress echocardiography (14% vs. 12%, p = 0.3). When only spontaneously occurring events were considered, the most important predictor was myocardial viability (chi-square 9.7). Using the Cox proportional hazards model, only the presence of myocardial viability (hazard ratio [HR] 2.0, p < 0.002) and age (HR 1.03, p < 0.001) were predictive of spontaneously occurring events. When only hard cardiac events were considered, age was the strongest predictor (chi-square 3.6, p = 0.056), followed by wall motion score index (WMSI) at peak dose (chi-square 3.3, p = 0.06) and remote ischemia (chi-square 2.25, p = 0.1). When cardiac death was considered, WMSI at peak dose was the best predictor (HR 9.2, p < 0.0001). CONCLUSIONS: During dobutamine stress, echocardiographic recognition of myocardial viability is more prognostically important than echocardiographic recognition of myocardial ischemia for predicting unstable angina, whereas WMSI at peak stress was the best predictor of cardiac-related death. Different events can be recognized with different efficiency by various stress echocardiographic variables.

Adult↗
PubMed1997

Flow-function relation in patients with chronic coronary artery disease and reduced regional function. A positron emission tomographic and two-dimensional echocardiographic study with coronary vasodilator stress.

OBJECTIVES: We sought to elucidate the flow-function relation in chronic postischemic dysfunction during vasodilator stress. BACKGROUND: In patients with ischemia and regional dysfunction, stress echocardiography can elicit three responses in the dysfunctioning segments: no change, improvement or worsening. The physiology underlying these responses is unclear. METHODS: Seventeen patients with ischemia and left ventricular dysfunction underwent evaluation of regional function by two-dimensional echocardiography and myocardial blood flow by positron emission tomography and 13N-ammonia. Flow (ml/min per g) and function (regional wall motion score [RWMS] from 1 = normal to 4 = dyskinetic) were evaluated both at rest and after dipyridamole (0.56 mg/kg body weight over 4 min). RESULTS: In 45 normal segments, rest to dipyridamole flow increased from 0.83 +/- 0.22 (mean +/- 1 SD) to 1.87 +/- 0.90 (p < 0.01) with a hyperkinetic contraction pattern. Among dysfunctioning segments, responders (n = 11) showed an upsloping flow-function curve during stress (i.e., increased function [RWMS rest 2.5 +/- 0.5 vs. dipyridamole 1.2 +/- 0.4] and increased flow [rest 0.69 +/- 0.30 vs. dipyridamole 1.89 +/- 1.43, p < 0.01]); nonresponders (n = 20) had a flat flow-function curve during dipyridamole (i.e., fixed function [RWMS rest and dipyridamole 2.6 +/- 0.5] and no flow increase [rest 0.64 +/- 0.24 vs. dipyridamole 0.87 +/- 0.51, p = NS): Ischemic segments (n = 9) exhibited a downsloping flow-function curve during dipyridamole (i.e., worsened function [RWMS rest 2 +/- 0.5, dipyridamole 3.1 +/- 0.6] and no significant flow change [rest 0.67 +/- 0.29 vs. dipyridamole 0.79 +/- 0.23, p = NS]). CONCLUSIONS: Myocardial segments with rest dysfunction and a contractile reserve elicitable by a vasodilator stress more often exhibit residual flow reserve, whereas segments with a fixed or worsening mechanical response during stress show a flat flow response.

Aged↗
PubMed1997

Increased myocardial echo density in left ventricular pressure and volume overload in human aortic valvular disease: an ultrasonic tissue characterization study.

Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to morphometrically evaluated collagen in human beings. Our objective was to assess myocardial reflectivity pattern of patients with severe left ventricular hypertrophy caused by either aortic stenosis (AS) or aortic regurgitation (AR). Ten patients with AS, 10 patients with AR, and 10 closely age- and gender-matched healthy controls were studied by two-dimensional Doppler echocardiography. By using an echocardiographic prototype, we performed a radiofrequency analysis to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall (integrated backscatter index: IBI, expressed in percentage). All patients with stenosis or aortic insufficiency showed a normal regional and global resting systolic function (fractional shortening: AS = 36.0 +/- 6.6 versus AR = 40.3 +/- 6.2 versus control = 40.2 +/- 8.7; p = not significant [NS]) Left ventricular mass index (Devereux's formula) was markedly increased in patients with stenosis or aortic insufficiency (AS = 199.3 +/- 18 versus AR = 208.8 +/- 60 versus control = 97.3 +/- 11 g/m2; p < 0.0001). Myocardial echo density was increased in patients with stenosis or aortic insufficiency in comparison with controls, both in the septum (IBI%: AR = 40.7 +/- 7.9 versus AS = 33.4 +/- 4.2 versus control = 23.0 +/- 6.2; p < 0.0001) and in the posterior wall (IBI%: AR = 27.1 +/- 4.3 versus AS = 23.0 +/- 2.6 versus control = 15.0 +/- 4.2; p < 0.0001). No significant correlations were found between septal and posterior wall IBI and their thickness. Abnormally increased myocardial echo density--possibly related to disproportionate collagen deposition--can be detected in patients with pressure or volume overload caused by aortic valve disease and without overt systolic dysfunction.

Aged↗
PubMed1997

The elusive link between coronary lesion morphology and dobutamine stress echocardiography results. The EDIC (Echo Dobutamine International Cooperative) Study Group.

BACKGROUND: Coronary lesion angiographic morphology of the complex type is associated to enhanced susceptibility to ischemia during vasodilator adenosinergic stress testing and attributed to the reduced vasodilatory capacity of the damaged endothelium. Whether coronary lesion morphology can also influence the results of adrenergic pharmacologic stress test remains unknown. The aim of our study was to assess the relationship between coronary plaque morphology and dobutamine-atropine stress echocardiography (DASE) results. METHODS AND RESULTS: We analyzed DASE (up to 40 mcg/kg/min plus atropine) and coronary angiography data of 42 patients with single vessel disease and no totally occluded vessel at angiography. 7 patients had angina, 35 had previous infarction. A diagnostic DASE was performed in all patients within 1-10 (mean 4.7 +/- 3.4) days before coronary angiography. An angiographic lesion was considered complex when irregular borders and/or intraluminal lucencies, suggestive of ulcer and/or thrombus were present. According to the angiographic lesion morphology (Ambrose classification), 2 groups were identified: Group I, with simple lesion; Group II with complex lesion. The two groups were similar for number of patients (n = 21), age (I = 55 +/- 11 vs II = 53 +/- 7 years, p = ns), coronary stenosis severity expressed as % diameter reduction (I = 77 +/- 14 vs II = 78 +/- 15%, p = ns), presence of previous infarction (I = 17 vs II = 18 pts, p = ns). No difference was found in the prevalence of positivity between the two groups (I = 72 vs II = 62%, p = ns). The two groups achieved a similar peak dobutamine dose (I = 32 +/- 9 vs II = 33 +/- 9 mcg/kg/min, p = ns) and peak Wall Motion Score Index (I = 1.5 +/- 0.26 vs II = 1.45 +/- 0.28, p = ns). CONCLUSIONS: In patients with non occlusive single vessel disease, coronary morphology of complex type is not associated with greater vulnerability to dobutamine induced ischemia.

Adult↗
PubMed1997

Dipyridamole stress echocardiography: state of the art 1996. EPIC (Echo Persantin International Cooperative) Study Group.

Dipyridamole stress is the forerunner and prototype of pharmacological stress echo tests in the diagnosis of coronary artery disease. Among the various stress echo tests, it is probably the least technically demanding to perform and the easiest to interpret. Its accuracy is similar to dobutamine stress echocardiography but its feasibility is higher. The prognostic impact of dipyridamole stress echo has also been proven for presentation of hard end-points such as cardiac death. The safety and prognostic value of this test has been conclusively demonstrated as a result of extensive experience in large scale multicentre projects. Dipyridamole stress is many different tests in one: dipyridamole atropine is best for diagnosis; dipyridamole dobutamine or dipyridamole-exercise is highly sensitive for the detection of minor forms of coronary artery disease; low and high dose dipyridamole is best suited for prognostic stratification; infra-low dipyridamole with low dose dobutamine administration is probably best suited for selective myocardial viability identification. Each patient should have their own test, tailored on the basis of the clinical picture and the diagnostic issue.

Coronary Disease↗
PubMed1997

Role of stress echocardiography in risk stratification early after an acute myocardial infarction. EPIC (Echo Persantin International Cooperative) and EDIC (Echo Dobutamine International Cooperative) Study Groups.

Resting and stress echocardiography is a 'one-stop shop', which enables a wide range of information to be collected on resting function, myocardial viability, and induced ischaemia, all of which are useful for prognostic stratification. Large scale, multicentre, prospectively collected data show the prognostic failure of resting function and inducible ischaemia, both independently and combined, which are especially effective in predicting cardiac death. The GISSI data show that the increment of risk as a result of reduction in ventricular function has a hyperbolic trend, with a relatively moderate increase in mortality for ejection fraction values between 50 and 30%, but with marked increases below 30%. The EPIC data show that the 1-year risk of cardiac death is as low as 2% in patients with negative dipyridamole stress echocardiography: it doubles if the test is positive at a high dose, and is almost four times higher if it is positive at a low dose. In the field of prognostic stratification, in the absence of carefully controlled studies, the choice between coronary angiography as the only essential study, or use of a non-invasive test to discriminate access to catheterization currently reflect alternate philosophical approaches rather than scientifically based decisions. In the invasive approach, stress echocardiography offers relief from the vicious circle of chest pain-coronary angiography revascularization. In the non-invasive and physiological approach, stress echo is capable of offering, in one sitting, an insight into the main determinants of survival: function, viability, and ischaemia.

Echocardiography↗
PubMed1997

Effects of antianginal therapy with a calcium antagonist and nitrates on dobutamine-atropine stress echocardiography. Comparison with exercise electrocardiography.

BACKGROUND: Anti-ischaemic therapy with nitrates and/or calcium channel blockers profoundly affects the results of pharmacological stress echocardiography with coronary vasodilators but the influence on catecholamine stress testing remains unsettled. AIMS: The present study aimed to assess the effects of non-beta-blocker antianginal therapy on dobutamine (up to 40 micrograms.kg-1.min-1)-atropine (up to 1 mg) stress. echo-cardiography and to evaluate whether drug-induced changes in the dobutamine atropine stress echocardiography response may predict variations in exercise tolerance. METHODS: Twenty six patients with angiographically assessed coronary artery disease (seven patients with single-, 10 with double-, and nine with triple-vessel disease) performed a dobutamine atropine stress echocardiography and an exercise electrocardiography test in random order both off and on antianginal drugs (nitrates and calcium antagonists). In doubtamine-atropine stress echocardiography, we evaluated: dobutamine time (i.e. the time from initiation of the dobutamine infusion to obvious dyssynergy), wall motion score index (in a 16-segment model of the left ventricle, each segment ranging from 1 = normal, to 4 = dyskinetic), and rate-pressure product at peak stress. RESULTS: Dobutamine-atropine stress echocardiography positivity occurred in 26 out of 26 patients off and in 23 patients on therapy (100 vs 88%, P = ns). Atropine coadministration was needed to evoke echo positivity in no patient off and in five out of 26 on therapy (0 vs 19% P < 0.01). The achieved rate pressure product during dobutamine-atropine stress echocardiography was comparable on and off therapy (17 +/- 4 vs 19 +/- 5 x 10(3) mmHg x heart rate. min-1, P = ns). Therapy induced an increase in dobutamine time (on = 16 +/- 3 vs of = 13 +/- 3 min, P < 0.01) and a decrease in peak wall motion score index (on = 1.3 +/- 0.2 vs off = 1.5 +/- 0.3, P < 0.01). The therapy induced changes in exercise time during the exercise electrocardiography test were not significantly correlated to dobutamine-atropine stress echocardiography variations in either dobutamine time (r = 0.07, P = ns), or peak rate pressure product (r = 0.24, P = ns), or peak wall motion score index (r = 0.02, P = ns). CONCLUSIONS: (1) non-beta-blocker antianginal therapy only modestly reduces dobutamine-atropine stress echocardiography sensitivity, although atropine coadministration is more often required to reach stress echo positivity under therapy; (2) therapy reduces the severity of dobutamine atropine stress echocardiography ischaemia stratified in the time and space domain, but these changes are only poorly correlated to variations in exercise tolerance.

Atropine↗
PubMed1997

The coronary angiogenetic effect of heparin: experimental basis and clinical evidence.

Heparin is a highly sulfated polysaccharide consisting of a repeating disaccharide structure as found in other glycosaminoglycanes. The intravenous and subcutaneous formulation of the drug is routinely used for its well-known, time-honored antithrombotic effect. However, available evidences linking heparin to angiogenesis raise the possibility of a therapeutically relevant antiischemic effect of the drug. Molecular biology data show that in a hypoxic milieu heparin could facilitate angiogenesis through interactions with a family of polypeptide growth factor mitogens that stimulate endothelial cell proliferation. Experimental data suggest that heparin can augment collateral circulation when combined with other potentially angiogenetic factors, such as repeated ischemia, coronary occlusion, or physical exercise. Clinical data, although very initial, encompassing a total of only 41 heparin-treated patients with coronary artery disease, suggest that heparin facilitates collateral development stimulated by exercise-induced myocardial ischemia in humans. According to the heparin-collateral hypothesis, the mechanism of action of heparin as an antiischemic medication would be independent of its anticoagulant action. The molecular targets of heparin are Factor Xa and IIa for antithrombotic action, heparin-binding growth factors (including fibroblast growth factor and vascular endothelial growth factor) for angiogenesis. The antithrombotic effect is not linked to a cellular target, whereas the angiogenetic effect directly stimulates endothelial cells. The molecular cofactor required for effect is antithrombin III for antithrombosis, and possibly endogenous adenosine for angiogenesis. The therapeutic effect is achieved within minutes or hours for antithrombosis, and within weeks or months for angiogenesis.

Angina Pectoris↗