[The use of stress echocardiography in the assessment of results of myocardial revascularizations interventions].
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
A Dagianti
Publications and source records attributed to A Dagianti.
[Effect of antihypertensive treatment on the clinical course of coronary disease].
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Angiotensin-Converting Enzyme Inhibitors↗
Dipyridamole myocardial contrast echocardiography in patients with single-vessel coronary artery disease: perfusion, anatomic, and functional correlates.
The aim of this study was to examine whether myocardial contrast echocardiography (MCE) may be used to study regional myocardial blood flow distribution during dipyridamole-induced hyperemia. MCE was performed before and after dipyridamole infusion in 11 patients with a proximal, significant left anterior descending (LAD) coronary artery stenosis. The relation between contrast-derived parameters and the degree of coronary narrowing and the occurrence of transient regional wall motion abnormalities was also investigated. In the territory supplied by left circumflex coronary artery, mean peak contrast intensity increased after dipyridamole from 50 +/- 18 to 76 +/- 27 IU (p < 0.001). In contrast, a significant reduction in mean peak intensity was observed after dipyridamole in the LAD territory (from 41 +/- 27 to 13 +/- 13 IU, p < 0.01). Similar results were obtained with the use of the area under the time-intensity curve. An increase in peak intensity > or = 10 IU after dipyridamole administration separated normal regions from those supplied by a significant coronary artery lesion with a sensitivity of 91% and a specificity of 91%. Perfusion abnormalities were always detected by contrast echocardiography when septal motion abnormalities developed and, in five patients they were detected in the absence of clinical, electrocardiographic, and echocardiographic signs of ischemia. A weak correlation was found between both peak intensity and area under the curve and percent coronary diameter stenosis and cross-sectional area. In conclusion, dipyridamole MCE can be used during routine coronary angiography to assess myocardial blood flow distribution in patients with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Influence of residual perfusion within the infarct zone on the natural history of left ventricular dysfunction after acute myocardial infarction: a myocardial contrast echocardiographic study.
OBJECTIVES: This study used myocardial contrast echocardiography to investigate the extent of residual perfusion within the infarct zone in a select group of patients with recently reperfused myocardial infarction and evaluated its influence on the ultimate infarct size. BACKGROUND: Limited information is available on the status of myocardial perfusion within postischemic dysfunctional segments at predischarge and on its influence on late regional and global functional recovery. METHODS: Twenty patients with acute myocardial infarction were selected for the study. Patients met the following inclusion criteria: 1) single-vessel coronary artery disease; 2) patency of infarct-related artery with persistent postischemic dysfunctional segments at predischarge; 3) stable clinical condition up to 6 months after hospital discharge. All selected patients underwent coronary angiography and myocardial contrast echocardiography before hospital discharge and repeated the echocardiographic examination 6 months later. Patients were grouped according to the pattern of contrast enhancement in predischarge dysfunctional segments. RESULTS: In nine patients (group I), the length of segments showing abnormal contraction coincided with that of the contrast defect segments. In the remaining 11 patients (group II), postischemic dysfunctional segments were partly or completely reperfused. There was no difference between the two groups in asynergic segment length at predischarge (7.3 +/- 2.5 vs. 7.2 +/- 4.3 cm, p = NS). At follow-up study, asynergic segment length was significantly reduced in group II patients, whereas no changes were observed in group I patients (from 7.2 +/- 4.3 to 4.7 +/- 3.7 cm, p < 0.005; and from 7.3 +/- 2.5 to 7.5 +/- 2.9 cm, p = NS, respectively). CONCLUSIONS: Among patients with a predischarge patent infarct-related artery, further improvement in regional and global function may be expected during follow-up when residual perfusion in the infarct zone is present.
Adult↗
IPO-V2: a prospective, multicenter, randomized, comparative clinical investigation of the effects of sulodexide in preventing cardiovascular accidents in the first year after acute myocardial infarction.
OBJECTIVES: This study was conducted to assess the efficacy of sulodexide, a glycosaminoglycan compound with antithrombotic properties, in preventing death and thromboembolic events after acute myocardial infarction. BACKGROUND: Antithrombotic therapy has been found to play an important role in the prevention of cardiovascular events and death after acute myocardial infarction. Glycosaminoglycan-containing compounds, including sulodexide, show profibrinolytic and antithrombotic properties that render them suitable for use in patients after infarction. METHODS: A total of 3,986 patients who had recovered from acute myocardial infarction were randomized to receive either the standard therapy routinely administered at each study center, excluding antiplatelet and anticoagulant drugs (control group, 1,970 patients), or the standard therapy plus sulodexide (treated group, 2,016 patients). Between 7 and 10 days after the episode of acute myocardial infarction, sulodexide was administered as a single daily 600-lipoprotein-lipase-releasing unit (LRU) intramuscular injection for the 1st month, followed by oral capsules of 500 LRU twice daily. Patients were evaluated for > or = 12 months. RESULTS: At the end of the study, 140 deaths (7.1%) were recorded in the control group and 97 (4.8%) in the sulodexide group (32% risk reduction, p = 0.0022, chi-square test). A total of 90 patients (4.6%) in the control group had a further infarction, compared with 66 (3.3%) in the sulodexide group (28% risk reduction, p = 0.035). Furthermore, a reduction in left ventricular thrombus formation (evaluated by echocardiography) was observed in the sulodexide group (n = 12; 0.6%), compared with values in the control group (n = 25; 1.3%) (53% risk reduction, p = 0.027). Sulodexide was well tolerated and devoid of significant adverse events. All significant results were confirmed by "actual treatment" analyses. CONCLUSIONS: The study provides evidence that long-term therapy with sulodexide started early after an episode of acute myocardial infarction is associated with reductions in total mortality, rate of reinfarction and mural thrombus formation.
Aged↗
[ACE-inhibitors after infarction: current knowledge and future prospects].
Experimental and clinical findings showing a beneficial effect on ventricular remodelling have led to a widespread use of ACE-inhibitors in myocardial infarction. Recent trials (SAVE, AIRE, GISSI 3, ISIS 4) have clearly demonstrated that in patients with left ventricular dysfunction and/or heart failure the treatment with ACE-inhibitors is mandatory, although several questions remain unanswered. Recent experimental observations on the relationship between ACE and endothelial function, and between ACE and intimal proliferation have gone forward leading to new perspectives on the potential use of ACE-inhibitors in all patients with acute myocardial infarction.
Angiotensin-Converting Enzyme Inhibitors↗
[Supraventricular hyperkinetic arrhythmias in acute myocardial infarct: their prognostic assessment and correlation with the echocardiographic evolution].
To assess the prognostic significance of supraventricular tachyarrhythmias (SVTA) during acute myocardial infarction (AMI), we studied 388 patients with first AMI, without ventricular preexcitation or chronic atrial fibrillation. The prevalence of SVTA was 14% (56/388), including atrial fibrillation (57%), atrial flutter (22%), polyfocal atrial tachycardia (14%), monofocal atrial tachycardia (7%). The arrhythmia appeared within 72 hours from the onset of chest pain in 61% of patients (early SVTA < 72 hours), while in 39% appeared later (late SVTA > 72 hours). Patients with SVTA (Group I n = 56) and without SVTA (Group II n = 232) were similar regarding prevalence of hypertension, dyslipidemia, diabetes, site of infarction and fibrinolysis, but SVTA was associated with a significant increase in death (Group I 18% versus Group II 9%; p < 0.05) and complications as pulmonary oedema and cardiogenic shock (Group I 25% versus Group II 14%; p < 0.05). Left atrial dimensions (LAD), end-diastolic left ventricular volume (EDLVV), end-systolic left ventricular volume (ESLVV) and echo-score, evaluated at admission, were not different between Group I and II (LAD 41.3 +/- 6 mm versus 40.1 +/- 5 mm, NS; EDLVV 181 +/- 34 ml versus 173 +/- 30 ml, NS; ESLVV 80 +/- 21 ml versus 75 +/- 18 ml, NS; echo-score 6.7 +/- 3.1 versus 6 +/- 2.7, NS) while pre-discharge echo-grams in Group I showed a trend towards the increase in volumes and echo-score (EDLVV from 181 +/- 34 ml to 194 +/- 36 ml, p = 0.052; ESLVV from 80 +/- 23 ml to 88 +/- 23 ml, p = 0.051; echo-score from 6.7 +/- 3.1 to 7.8 +/- 3.3, p = 0.070).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Characterization of reversible myocardial dysfunction by magnetic resonance imaging.
Some recent cardiovascular applications of nuclear magnetic resonance imaging (MRI) are discussed, on the basis of both literature and personal data. Management of coronary patients has become directed to strategies aiming at salvaging the ischemic myocardium, and MRI can play an important role in providing the necessary data leading to an appropriate assessment. Due to its capability in showing morphofunctional information on wall thickness and thickening, cine-MRI technique can be used to detect myocardial ischemia and infarction, since it allows the acquisition of 16 or more frames of the cardiac cycle which can be displayed in a cine loop format. In an Italian Cooperative Study the role of MRI in discriminating stunned from necrotic areas has been investigated. Comparison of fractional area change by echo versus cine-MR turned out to be almost completely overlapping, but cine-MRI allowed a more accurate measurement of systolic wall thickening due to better visualization of endo- and epicardial borders (more sensitive marker of kinetic damage than wall motion). Other studies have also been performed in order to determine the capability of contrast agents of allowing differentiation between reperfused reversible and irreversible myocardial injury and allowing distinction between reperfused and occlusive myocardial infarction. In a recent study we investigated the MRI possibility of identifying viable myocardium in severely chronic systolic dysfunctioning areas by comparing, in corresponding left ventricular segments, regional perfusion and metabolism at IPPA scintigraphy and regional signal intensity at MR images obtained before and after paramagnetic contrast media administration. The potential role of MRI was shown in the identification of viable myocardium with the use of contrast medium, that is of crucial importance in this respect.
Diagnosis, Differential↗
Influence of reperfusion induced by thrombolytic treatment on natural history of left ventricular regional wall motion abnormality in acute myocardial infarction.
Although several studies have investigated left ventricular (LV) function after reperfusion interventions, it is still unclear whether benefits result from successful therapy or whether such benefits only reflect the natural history of a subgroup of patients with acute myocardial infarction (AMI). This study evaluates the unique effect of thrombolytic therapy on the natural history of regional LV wall motion dysfunction. One hundred seventy-six patients with AMI were studied: 82 patients (group A) underwent conventional treatment and 94 (group B) thrombolytic therapy. LV regional improvement, evaluated by changes in echo score between admission and predischarge examination, was present more frequently in group B (28%) than in group A (17%). Furthermore, improved patients in group B had higher admission echo scores (7.5 +/- 3.5 vs 6.3 +/- 3.1), a prevalence of anterior AMI (68 vs 30.1%) and a higher rate of coronary patency (92 vs 58% in patients who had no improvement). In group A patients the rate of coronary patency was similar in those who did (46.1%) and did not have (36.1%) improvement. Observations at 12 to 18 months showed similar data in group A patients and in group B patients without improvement, whereas a marginal additional improvement was observed in group B patients who had in-hospital improvement. These observations demonstrate that LV function recovery is more frequent and marked in treated than in untreated patients. Follow-up results suggest a prolonged beneficial effect of thrombolytic treatment on LV function. The highest rate of coronary patency in improved group B patients underline the role of reperfusion on natural history of LV dysfunction after AMI.
Coronary Angiography↗
Effectiveness of thrombolysis is associated with a time-dependent increase of malondialdehyde in peripheral blood of patients with acute myocardial infarction.
By using a highly sensitive, high-performance liquid chromatographic technique, plasma values of malondialdehyde (MDA), adenosine and oxypurines were determined in 10 healthy subjects, 10 patients with noncardiac illness, and 20 patients with acute myocardial infarction (AMI) observed within 6 hours from the onset of symptoms. Patients with AMI received fibrinolytic treatment. Peripheral blood was obtained before and serially after thrombolysis (1, 2, 3, 6 and 24 hours). Coronary patency was assessed by timing of peak creatine phosphate kinase and by predischarge angiography. MDA (mean +/- SD) in healthy subjects, noncardiac patients, and immediately before thrombolytic treatment in patients with AMI was 0.051 +/- 0.013, 0.066 +/- 0.020 and 0.397 +/- 0.326 mumol/liter of plasma, respectively. A progressive increase in plasma MDA after thrombolysis was observed only in reperfused patients, whose values at the third, sixth and 24th hours were also significantly greater than those of nonreperfused patients. Time-dependent variations of xanthine and adenosine were also observed in the same group after thrombolysis. The data appear to indicate that a relevant increase in plasma MDA, mostly originating due to phospholipid derangement of postischemic myocytes, occurs only in patients with successful thrombolysis, thus suggesting that if properly assayed, it may represent reliable biochemical evidence of tissue injuries after myocardial reperfusion in humans.
Adenosine↗
Silent ischemia in unstable angina is related to an altered cardiac norepinephrine handling.
BACKGROUND: Inferential evidence suggests that silent ischemia might be related to sympathetic activity. Study of [3H]norepinephrine kinetics is a suitable tool to assess the regional sympathetic activity. This method was applied to investigate whether silent myocardial ischemia in unstable angina is related to and depends on cardiac sympathetic overactivity. METHODS AND RESULTS: Patients with active unstable angina were compared with patients with inactive unstable angina, stable effort angina, and controls. Silent myocardial ischemia was evaluated by three 24-hour Holter monitoring periods on alternate days, and [3H]norepinephrine kinetics was assessed under rest conditions and following the cold pressor test. Simultaneously, catecholamine concentrations were measured in the aortic, coronary sinus, and peripheral venous blood. Different than the other groups (p = 0.0013), in patients with active unstable angina, the majority of silent ischemic episodes occurred without increase in heart rate. These patients had a positive coronary sinus-aorta norepinephrine gradient, both at rest and following the cold pressor test. [3H]Norepinephrine kinetics demonstrated an increased selective cardiac spillover, both at rest and, even more, after the cold pressor test. Reduced cardiac [3H]norepinephrine extraction also was found. A significant relation was found between the number of ischemic episodes or the overall duration of silent ischemia and norepinephrine spillover, both at rest and following cold application. CONCLUSIONS: During the acute phase of unstable angina (but not in the quiescent phase or in stable effort angina), a disorder in cardiac norepinephrine handling occurs. This results in a reflex cardiac sympathetic overactivity that plays a major role in the occurrence of silent myocardial ischemia.
Angina, Unstable↗
[Myocardial protection: a look to the future].
Three main types of damage induced by ischemia and reperfusion have been identified: lethal reperfusion injury, microvascular and macrovascular reperfusion injury, and myocardial stunning. Pathophysiological and therapeutic aspects of these ischemia/reperfusion sequelae are reviewed and discussed on the light of recent experimental and clinical results.
Adrenergic beta-Antagonists↗
[Role of the endogenous opioid system in the modulation of anginal pain].
The Authors make an analysis of the complex interactions occurring between peripheral and central factors in the regulation of anginal pain. As for the role of the endogenous opioid system, results obtained in a study using a particular methodological approach have demonstrated that patients with asymptomatic ischemic heart disease have a higher endogenous opioid tone at the level of the central nervous system.
Angina Pectoris↗
Rheological features of erythrocytes in acute myocardial infarction.
There is evidence that oxidative insult plays a role in the development of acute myocardial infarction. Significance has also been attributed to changes in viscosity of the blood and in the deformability and aggregation of erythrocytes affecting their rheological behavior. In a group of patients with myocardial infarction we found a decreased erythrocyte filtration and an increased blood viscosity with no significant change in plasma viscosity. These changes were accompanied by alterations in the microviscosity of the erythrocyte membrane assessed by measuring the polarization of specific fluorescent molecules. From our data it is evident that there is an increase in the rigidity of the membrane at the lipid/protein boundary, with an associated increase in the fluidity of the deep lipid core of the membrane, while no changes were observed in the dynamic behavior of the membrane proteins. These physico-chemical perturbations in the membrane could be the basis for the decreased filtration of erythrocytes. We found, however, no evidence of lipid peroxidation in the erythrocyte membrane.
Adenosine Triphosphate↗
[Coronary morphometry in essential arterial hypertension].
To evaluate the prevalence and pathophysiological significance of I and II order coronary arteries with a tortuous course we reviewed 1530 coronaroventriculographies. Tortuosity was identified by the finding of 4 bendings at least, with an angle less than 60 degrees, present both in systole and in diastole. Morphologic alteration was found in 64% of hypertensives and in 13% only of non hypertensive coronaropathic patients; the prevalence was 58% in valvular aortic stenosis (being 16% in the remaining valvulopathies) and 100% in hypertrophic cardiomyopathy. No normal subject showed coronary tortuosity. A retrospective analysis of patients' echocardiograms pointed out a significant association between tortuosity and concentric left ventricular hypertrophy, expressed by mass/volume ratios clearly above the normal values (1 +/- 0.2): 1.6 +/- 0.17 in hypertensives, 2.1 +/- 0.2 in aortic stenoses and 2.6 +/- 0.2 in hypertrophic cardiomyopathy. Among hypertensive subjects, we selected a group with essential systemic hypertension and no coronary stenoses nor dysmetabolic diseases: this group was divided into 2 subgroups on the basis of presence or absence of coronary tortuosity. A comparison of these subgroups for age, echocardiographic parameters (left ventricular mass index, mass, mass/volume ratio, end systolic stress) and hemodynamic data (end diastolic left ventricular pressure, gradient: mean aortic pressure--end diastolic left ventricular pressure) showed no significant difference between patients with or without tortuosity. Moreover those patients were evaluated by ergometric test, echo stress, cold pressor test and dipyridamole stress test: a significantly higher prevalence of myocardial ischemia was found in the subgroup with tortuous vessels (63% versus 11%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Chi-Square Distribution↗
[A non-Q wave myocardial infarct with an up or down shift of the ST segment in the acute phase: the clinical, echocardiographic, ergometric and coronary angiographic correlates].
To assess the significance of ST segment shift during the acute phase of non-Q myocardial infarction we studied the clinic echocardiographic, ergometric and coronarographic findings of 46 patients with a first non-Q wave myocardial infarction. The study population was subdivided in 2 subgroups on the basis of acute electrocardiographic change (Group I with ST elevation, Group II with ST depression). Patients with ST elevation had little myocardial infarction with enzymatic (early CPK peak) and coronarographic (low prevalence of coronary occlusion) signs of early spontaneous fibrinolysis. The second group had more diffuse myocardial infraction, higher prevalence of multivessel coronary disease and positive stress test. The ECG changes in this subgroup an probably due to subendocardial necrosis for the presence of collateral flow. The worse intrahospital prognosis of patients with ST segment depression may be related to cardiac function and age.
Aged↗
[The role of compromised regional function of the left ventricle in the evolution of postinfarct ventricular thrombosis].
Five hundred twenty-nine patients with acute myocardial infarction (AMI) underwent clinical, enzymatic and echocardiographic evaluation. Two-dimensional echocardiography identified 71 patients with left ventricular thrombus (LVT): 63 males and 8 females; mean age 54 +/- 12 years; 70 with anterior AMI and 1 with inferior AMI. The incidence of LVT was 13.8% and 27.7% among anterior AMI. At admission to Coronary Care Unit the patients with LVT showed more extensive left ventricular dysfunction than patients without LVT: Killip classification > or = 2 was 54.5% versus 41.4%, p < 0.05; peak of creatinphosphokinase was 1337 UI/L versus 951 UI/L, p < 0.05; echo-score was 7.2 +/- 2.8 versus 4.7 +/- 3.5, p < 0.01. Serial echocardiograms showed disappearance of LVT in 24 patients. Regarding regional wall motion abnormalities, patients with LVT disappearance showed lower pre-discharge echo-scores than patients with LVT persistence (6.7 +/- 2.2 versus 8.4 +/- 2.9; p < 0.01) although echo-scores at admission were similar in the 2 groups (7.1 +/- 1.1 versus 7.3 +/- 3.4, NS). These results suggest: the importance of extension of myocardial infarction and left ventricular dysfunction in LVT evolution; the importance of treatment limiting infarct size and improving left ventricular function, such as thrombolytic therapy. Anticoagulant therapy could be limited to patients with higher risk of embolization (as the protruding shape of LVT).
Chi-Square Distribution↗
[The efficacy of slow-release diltiazem in the treatment of stable angina of effort: a comparison between diltiazem and placebo].
The efficacy of a new slow release (SR) diltiazem preparation was assessed in 10 patients with stable effort angina. A double-blind, placebo controlled, randomized, crossover protocol was carried out comparing the effects of diltiazem 60 mg tid and diltiazem SR 120 mg bid on clinical and ergometric parameters. Exercise test was carried out 3 and 12 hours after the last dose of diltiazem or diltiazem SR respectively. Both drug preparations reduced the incidence of positive test, increased the exercise time and the time of onset of ischemic ST depression. The beneficial effects of the drugs appeared to be due to a reduction in myocardial oxygen consumption at the same workload as shown by the lesser value of pressure rate product at submaximal exercise. In conclusion, diltiazem SR at 12 hours after the last administration has the same effectiveness of diltiazem 60 mg at 3 hours.
Aged↗