[Coronary patency and functional recovery in post-infarction].
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Coronary Disease↗
Biomedical subjects
G Destro
Publications and source records attributed to G Destro.
The left atrial volume curve can be assessed from pulmonary vein and mitral valve velocity tracings.
After instantaneous left atrial volume was defined as the net difference between the forward-flowing blood from the lungs and the blood flowing through the mitral valve, we constructed the left atrial volume curve by sampling the Doppler mitral valve and the right upper pulmonary vein velocity from an apical four-chamber view in eight normal subjects and 11 patients with heart disease. The instantaneous mitral valve flow was estimated as mitral valve velocity x annular area (derived from the same view), whereas the pulmonary venous flow was obtained as right upper pulmonary vein velocity x pulmonary vein area, where pulmonary vein area = mitral valve velocity integral x mitral valve area) divided by pulmonary vein velocity integral. The left atrial volume curve can then be derived as: [(instantaneous pulmonary venous flow - mitral valve flow) + left atrial volume assessed at end diastole by two-dimensional echocardiography]. Biplane angiographic left atrial volume curves, available in four of 11 patients, compared morphologically very closely with the noninvasive curves, whereas the correlation coefficient for maximum (end-systolic) and filling (maximum minus minimum) left atrial volumes obtained from the Doppler-derived curve and the corresponding two-dimensional echocardiographic estimates was 0.95 (p < 0.001, standard error of the estimate = 11.9 ml), the dispersion of the data increased with decreasing volumes. These data demonstrate that combined Doppler mitral valve and pulmonary vein velocities can be used to construct the left atrial volume curve in human beings. The approach described, besides providing a tool for further noninvasive evaluation of the left atrial function, offers the opportunity for relating the continuous pulmonary venous flow to the intermittent filling of the ventricle through the mitral orifice in diastole, underlining the complex role that the left atrial cavity plays in this process.
Adolescent↗
Reperfusion reduces left ventricular dilatation by preventing infarct expansion in the acute and chronic phases of myocardial infarction.
Reperfusion reduces left ventricular dilatation in patients with acute myocardial infarction, but it is unclear to what extent this is a primary effect or only a consequence of the limiting effect of reperfusion on infarct size. To address this issue, 56 consecutive patients were examined by means of two-dimensional echocardiography on day 1, on day 3, before discharge, and at 6 months after an acute myocardial infarction. From this population two groups of 12 patients each, perfectly matched for site of myocardial infarction, extent of ventricular asynergy at two-dimensional echocardiography (akinesis + dyskinesis), and clinical characteristics were identified according to the creatine kinase (CK) time to peak, which was regarded as a marker of spontaneous or induced reperfusion: (1) CK time to peak of 12 hours or less (reperfused patients, n = 12), and (2) CK time to peak of more than 12 hours (nonreperfused patients, n = 12). In these two groups of patients end-diastolic and end-systolic left ventricular volumes and endocardial lengths of asynergic and normal ventricular segments, imaged in a cross-sectional view at the level of the papillary muscles, were then computed. At the first examination end-diastolic volume, end-systolic volume, and endocardial segment lengths of normal and asynergic segments were similar in the two groups of patients. Patients with late CK time to peak, however, showed a progressive increase in left ventricular systolic volumes and in asynergic endocardial segment lengths between the first and third (predischarge) examinations (p < 0.05 for both), with no change in systolic length of the normal myocardium. The left ventricular end-systolic volume and the asynergic endocardial segment length of patients with early CK time to peak, however, did not increase during hospitalization. The increment in end-systolic volume and in systolic infarct segment length from the first to the third examinations was higher in nonreperfused patients (p = 0.018 and p = 0.04, respectively). Changes similar to those detected in systole were found for diastolic volume and diastolic infarcted and noninfarcted segment length in both groups, but they did not reach statistical significance. After 6 months, an increases in volume and endocardial length were found in both groups of patients. Relative to the first examination, however, the increase in systolic volume and in asynergic systolic endocardial lengths remained greater for nonreperfused patients (p = 0.077 and p = 0.01, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
[Endothelial dysfunction in ischemic syndromes].
Several studies have shown evidence of the key role of the endothelium in modulating the tone of epicardial coronary vessels, in the different manifestations of coronary artery disease. Recently, the role of endothelium-dependent vasodilation has been focused, because clinical observations have suggested that myocardial ischemia might be caused or aggravated by inappropriate vasoconstriction of resistance vessels. An abnormal endothelium-dependent vasodilation, either of epicardial and of coronary microvasculature, has been documented in patients with syndrome X and in patients with history of hypertension and left ventricular hypertrophy. Vasoconstriction of the small coronary vessels is probably the mechanism underlying the impaired increase of coronary blood flow during atrial pacing and the wide variations of the ischemic threshold in some patients with chronic stable angina. In patients with variant angina, the endothelial function seems abnormal only in the conductance vessels. It is likely that the endothelial dysfunction of the small coronary arteries be present in many clinical situations in which a discrepancy between a mild atherosclerosis of epicardial coronary artery and signs of ischemia exists, as it has been observed early after successful angioplasty and after coronary artery reperfusion during acute myocardial infarction.
Coronary Vessels↗
Reperfusion of the infarct-related coronary artery limits left ventricular expansion beyond myocardial salvage.
Previous echocardiographic data from the Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto Miocardico (GISSI 1) trial suggest that the relation between left ventricular end-systolic volume and infarct size could be altered by thrombolysis, which would exert a restraining effect on end-systolic volume beyond its reducing effect on infarct size. Thus in 63 patients with one-vessel disease and a recent anterior myocardial infarction, we tested at angiography (1) if perfusion of the anterior descending coronary artery exerts any restraining effect on end-systolic volume above and beyond infarct size reduction and (2) if ejection fraction reflects such an additional, beneficial difference in the ventricular remodeling process. End-systolic volume was calculated using the Dodge method and the right anterior oblique projection, while infarct size was quantified according to the number of ventricular radii whose percent shortening fell below the mean -2 SD of a group of normal individuals. Patients were then divided into two groups according to the perfusion status of the vessel using Thrombolysis in Myocardial infarction (TIMI) criteria (TIMI grade 0 to 1: nonperfused vessel, 27 patients; TIMI grade 2 to 3: perfused vessel, 36 patients). For both groups there was a significant linear relation (p less than 0.001) between end-systolic volume and infarct size; as in our echocardiographic data, the regression lines relating volume to infarct size showed a different slope in the two populations so that, for large and matched infarcts, end-systolic volume was smaller in patients with a perfused vessel (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[The angiographic evaluation of elastic recoil after coronary angioplasty].
Coronary angioplasty is an effective recanalization technique, but is plagued by a high restenosis rate. One of the major effects of balloon dilatation is the stretching of the vessel wall and the subsequent elastic recoil. Although a well known phenomenon, few data have been published on the evaluation of elastic recoil after coronary angioplasty. The purpose of this study was to quantify the acute and short-term elastic recoil after coronary dilatation. Thirty-six patients underwent coronary angioplasty. A digital end-diastolic acquisition of the coronary artery was performed before, immediately after, at 15 min and at 20 hours after dilatation. Elastic recoil was defined as the difference between the diameter of the inflated balloon and the diameter of the vessel after dilatation. It was quantified by a semi-automatic computer-assisted program. Our data show a high elastic recoil immediately after dilatation, equal to 27.9% (p < 0.0001), which continues for the next 20 hours to a final value of 34.1%. No difference was found in the amount of elastic recoil depending on the coronary artery involved, length, severity and eccentricity of the stenosis, time and pressure used during balloon inflation. Elastic recoil was more pronounced (p = 0.002) using balloons with a balloon diameter/vessel diameter ratio > 1.
Angioplasty, Balloon, Coronary↗
Early left ventricular filling: an approach to its multifactorial nature using a combined hemodynamic-Doppler technique.
It has recently been shown that early left ventricular filling is a multifactorially determined phenomenon, the characteristics of which are highly dependent on relative changes in any of its determinants (left ventricular end-systolic volume, the constant of isovolumic left ventricular pressure decay, left atrial pressure at the onset of mitral valve flow, and left ventricular and left atrial compliance). Thus changes in the pattern of filling do not necessarily reflect changes in diastolic properties; they might instead simply reflect changes in loading conditions. To define a clinically implemented approach where the contribution of each of the covariates of early filling to the filling process and their modification by load manipulation could be assessed, nine patients with ischemic heart disease underwent simultaneous assessment of micromanometer left ventricular pressure and two-dimensional echo-guided Doppler mitral flow velocity before and after administration of nitroglycerin (0.2 mg intravenously). Nitroglycerin induced a significant reduction in the early-filling E wave (from 41 +/- 5 cm/sec to 32 +/- 7 cm/sec; p less than 0.002), whereas the late-filling A wave did not change (from 51 +/- 12 cm/sec to 55 +/- 9 cm/sec; p = 0.15), so that the E/A ratio decreased 27 +/- 16% (p = 0.016). End-systolic volume, the constant of isovolumic left ventricular pressure decay, and left atrioventricular pressure crossover at the onset of mitral flow decreased (from 49 +/- 37 to 43 +/- 38 ml [p = 0.016], from 52 +/- 14 to 47 +/- 13 msec [p = 0.016], and from 19 +/- 10 to 12 +/- 7 mm Hg [p = 0.08], respectively), whereas left atrial compliance (defined as stroke volume/atrioventricular pressure crossover) and left ventricular compliance (computed as change in volume/change in pressure at early and late diastole) did not change (p = 0.15 and p = 0.38, respectively); the diastolic pressure-volume relationship, however, was displaced slightly leftward and markedly downward, suggesting relief of pericardial constraint. A multilinear regression analysis, performed with pooled data at baseline and during infusion of nitroglycerin in each patient, identified left atrioventricular pressure crossover at the onset of mitral flow as the only significant predictor (p less than 0.02) of peak E wave velocity in the circumstances considered. Thus the interaction among covariates of early left ventricular filling and the relationship between filling and diastolic left ventricular and left atrial properties can be addressed with relative ease by means of this clinically implemented approach, in an effort to sort out the contribution of each cofactor to such a complex event.
Echocardiography, Doppler↗
[Intraluminal ultrasound echotomography: a new method in the study of arterial angioplasty. Evaluation of a case].
Intravascular ultrasound angioscopy allows to better define the structure of arterial wall and the effect of angioplasty. We report the case of a patient previously treated by coronary angioplasty, who underwent peripheral angioplasty for a stenosis of the left iliac artery. Intravascular ultrasound imaging performed before and after balloon dilatation clearly identified the plain of dissection and the partial resolution of the stenosis in a better way compared to digital angiography.
Angiography↗
[The role of directional atherectomy in the study of postangioplasty restenosis].
Restenosis is the major limit of arterial recanalization devices. Directional atherectomy has allowed for the first to remove atheroma samples by a percutaneous approach. A group of patients affected by superficial femoral artery disease who underwent directional atherectomy were studied. The patients were treated for primitive stenosis, restenosis after balloon angioplasty and thermal laser angioplasty. Intimal hyperplasia was the distinctive feature of restenosis and the cells were identified by immunohistochemistry and transmission electron microscopy as smooth muscle cells in an active synthetic phenotype. No differences were found in the restenosis process after balloon angioplasty and laser thermal angioplasty. Directional atherectomy is a useful tool to ameliorate our knowledge in the restenosis process after invasive procedure of recanalization.
Aged↗
[Angina due to anatomical anomalies and to functional changes in the epicardial coronary vessels].
Myocardial ischemia with normal coronary arteries can be due to anatomic or functional reasons. The more severe congenital coronary anomalies in the adulthood are the origin of the left main of the left coronary artery from the right aortic sinus, with a course between the aorta and the pulmonary trunk, and the origin of the left main from the pulmonary trunk. Both these anomalies can cause sudden death, usually associated with physical exertion. The coronary vasomotion of epicardial vessels depends on the interaction of several neurohumoral substances. We report the hemodynamic, angiographic and stress test data of 30 patients affected by chest pain, with myocardial ischemia and normal coronary arteries. In 8 patients the response of epicardial coronary arteries to intracoronary infusion of acetylcholine was evaluated.
Acetylcholine↗
[Myocardial infarct and angiographically normal coronary arteries].
Myocardial infarction and normal coronary arteries is not a rare event in the ischemic heart disease. Even if the patients with acute myocardial infarction and angiographically normal coronary arteries represent a small percentage (reported incidence varies from 1% to 12%) of all patients with acute ischemic attacks, they might be useful to highlight the pathogenetic mechanisms of this syndrome. To improve the understanding of this clinical entity, we reviewed our experience of 18 patients with myocardial infarction and normal coronary arteries. They were compared with a control group of patients with similar clinical characteristics (gender, age, infarct location) and residual coronary artery stenosis. The myocardial damage was less extensive in patients without residual stenosis (peak CK-MB: 56.1 +/- 71.9 vs 126.5 +/- 87.9 IU/I, p < 0.05), with a better left ventricular function either global (ejection fraction: 64 +/- 11 vs 55 +/- 13%, p < 0.05) and regional (SD/chord: -1.36 +/- 1.20 vs -2.42 +/- 1.04, p < 0.02). These findings probably reflect a more prompt and complete reperfusion of the infarct related artery. Myocardial necrosis may occur without obstructive coronary artery disease by the interaction of multiple factors such as abnormal platelet aggregation, thrombus formation and localized or diffuse changes of coronary vascular tone.
Adult↗
Acute anterior myocardial infarction: streptokinase prevents ventricular thrombosis independently of its effect on infarct size.
Left ventricular thrombosis (LVT) is a frequent complication after acute anterior myocardial infarction (AMI). The purpose of this study is to evaluate whether streptokinase (SK) therapy prevents LVT, and whether this effect is due to the preservation of left ventricular function or to the fibrinolytic action of the drug. Sixty-five patients who underwent a left ventricular angiography within 2 months after a first AMI were studied. Twenty-eight patients (SK group) received SK 1,500,000 U i.v. administered over 60 min within 6 h from the onset of symptoms. A lower incidence of LVT was found in the SK group (p = 0.0003). We divided patients into two classes according to the value of akinetic-dyskinetic area (AD): the first group with a lower value of AD, the second group with a higher value of AD. In both groups, a reduced incidence of LVT was associated with SK therapy (p = 0.014, p = 0.015, respectively). Early infusion of SK during AMI seems to prevent the development of LVT, with an effect partly independent from its action on infarct size for small to large myocardial infarction.
Female↗
Increase in plasma digitalis-like activity during percutaneous transluminal coronary angioplasty in patients with coronary stenosis.
Despite the fact that numerous studies have been published regarding the possible presence in plasma of an endogenous Na-K pump inhibitor with a digitalis-like structure in essential hypertension, very little is known about this factor in heart disease in general, and in situations characterized by low cardiac output. We measured the ability of plasma obtained from the femoral vein to inhibit a human renal Na(+)-K+ ATPase before and immediately after percutaneous transluminal coronary angioplasty (PTCA) in 6 patients suffering from angina pectoris and severe coronary stenosis. Intraerythrocyte sodium and potassium concentrations were also measured simultaneously. Na(+)-K+ ATPase inhibition proved significantly greater after angioplasty as compared to basal activity (percentage inhibition: 31.5 +/- 7.8 vs 16.1 +/- 12.2). No significant changes in intraerythrocyte sodium and potassium were detected. Though we are not in a position to define the mechanism underlying the increase in the digitalis-like factor, a plausible hypothesis may be that the reduction in cardiac output during PTCA by raising cardiac pressures may stimulate the production of a factor of compensatory inotropic significance.
Angioplasty, Balloon, Coronary↗
[Evaluation of complications during laser angioplasty with a hot tip system in the treatment of peripheral arteriopathy].
"Hot tip" laser angioplasty has been used in the treatment of peripheral artery disease. The purpose of our study (the largest in Italy) is to evaluate the complications during the recanalization of stenotic and occluded iliac and femoro-popliteal arteries, using a hot tip laser system coupled to an Argon or Nd Yag laser. One hundred twenty-three patients have been treated. The complications were: arterial spasm in 2 patients; distal embolizations in 6 patients; arterial dissections in 35 patients; vessel wall perforations in 20 patients. Vessel wall perforation is the more severe complication and did never allow to complete the procedure. The presence of intravascular calcified deposits increases the risk of perforation, due to the loss of the coaxial position of the probe. Only the development of a guided laser system could allow a safer delivery of laser radiation, reducing the risk of arterial wall perforation.
Adult↗
[Effects of magnesium pidolate on cardiovascular hemodynamics].
Aim of this study is to define the hemodynamic effects of magnesium (Mg) in patients with ischemic heart disease. Thus, the effects of 1 g of Mg pidolate injected over 3 min iv were evaluated in 10 patients by analysis of pressure data from a micromanometer catheter in the left ventricle and of volume data derived from Doppler and 2-dimensional echocardiography. Recordings were made before and immediately after the injection, at 3, 5, and 8 min. At 5 min, Mg induced a significant reduction in left ventricular peak systolic pressure (from 132.4 +/- 19.4 to 122.7 +/- 17.5 mmHg, p = 0.015, with early filling notably augmented (E wave of Doppler curve; from 39.4 +/- 8.5 to 43.9 +/- 9.7 cm/s, p = 0.013) and a slight increase in cardiac output (from 6.23 +/- 1.4 to 6.9 +/- 1.7 l/min, p = 0.092). Heart rate increased (from 75.9 +/- 9.6 to 78.13 +/- 8.4 b/min, p = 0.062) and the constant of isovolumetric pressure decay decreased (from 48.9 +/- 13.2 to 45.7 +/- 14.9 ms, p = 0.065), probably as a final effect of aortic pressure reduction. The diastolic pressure-volume relationship was insignificantly displaced downward (p = 0.11) and to the right (p = 0.62). In conclusion, Mg unloads the ischemic left ventricle through a reduction of systemic aortic pressure, with a secondary increase in early filling; this increase may derive from a rise in the atrioventricular diastolic gradient, subsequent to an improvement in ventricular emptying. Active relaxation is improved, and passive diastolic properties are not affected, in spite of the reported calcium-antagonist action of the drug.
Adult↗
[Doppler-hemodynamic evaluation of variations in left ventricular filling due to reduction of external mechanical compression].
It has been recently shown that preload reduction affects the pattern of left ventricular (LV) filling in a way that mimics those Doppler changes that have been associated with impaired LV diastolic function. In order to better relate changes of mitral flow velocity profile to changes of the diastolic properties of the ventricle, in 11 ischemic patients diastolic pressure-volume relations from micromanometer LV pressure and LV volume derived from Doppler and 2D-echocardiography were constructed before and after TNT (0.2 mg iv). TNT induced a significant reduction in LV peak pressure (% change: -13 +/- 7%, p: 0.0003), end-diastolic pressure (EDP) (-62 +/- 45%, p: 0.0006), and constant of isovolumic pressure decay (T) (-8.4 +/- 6.6%, p: 0.012). The left atrial pressure at the time of mitral valve opening (PCO: defined as the pressure at the time of initial transvalvular flow assessed by Doppler) decreased 5.3 +/- 9.6 mmHg (p: 0.11). The early filling E wave of the Doppler velocity profile was significantly reduced by TNT (-20.1 +/- 12.7%, p: 0.0003), while the atrial contribution to total filling increased by 21.3 +/- 29.7% (p: 0.03). The E/A ratio decreased from 0.87 +/- 0.31 to 0.66 +/- 0.22 (p: 0.016), and the change correlated with changes in EDP (p less than 0.05) and PCO (p less than 0.01). The diastolic pressure-volume relationship was displaced downward (p: 0.0007) and minimally leftward (p: 0.45), suggesting relief of external constraint.(ABSTRACT TRUNCATED AT 250 WORDS)
Coronary Disease↗
[A case of adenoameloblastoma].
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Adolescent↗