Gianni Destro

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)

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.

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.

Increased intensity of contrast material immediately after late angioplasty of infarct-related coronary artery is associated with reduced ventricular volumes at six months

To assess the contribution of residual muscle perfusion in the infarcted territory to prevent ventricular remodeling, 24 patients with 1-vessel disease underwent coronary angiography and angioplasty of a critical left anterior descending coronary stenosis 18+/-11 days after a first anterior myocardial infarction. The degree of stenosis was assessed using biplane quantitative angiography, whereas ventricular volumes, together with regional wall motion, were computed from single-plane ventriculography. Patients were reevaluated at 6 months after they had been subdivided according to the videointensity of the territory of the culprit vessel, as assessed from images obtained during main stem dye contrast injections before and immediately after angioplasty using a subtraction technique (group A, increased intensity [n= 15]; group B, no change [n=9]), assuming that higher peak intensities reflect greater myocardial blood volume. There was a significant time group interaction for ventricular volumes (diastolic, -13+/-12% for group A vs +20+/-24% for group B, p=0.008; systolic, -15+/-19% for group A vs +18+/-36% for group B, p=0.017), although no interaction was evident for the degree of resolution of coronary stenosis or the extent of recovery of regional dysfunction. The effects on volumes were paralleled by changes in ventricular end-diastolic pressure (-3+/-7 mm Hg in group A vs +5+/-6 mm Hg in group B, p=0.006), although baseline clinical characteristics and medical regimen over the 6-month period were quite comparable between the 2 groups. In conclusion, despite late angioplasty of the culprit vessel, ventricular remodeling is prevented mainly when the procedure guarantees improved perfusion at the muscular level. The result is not necessarily mediated by recovery of regional systolic function.

Three years experience with thermal and excimer lasers in the treatment of peripheral artery disease

Laser angioplasty is an effective tool to revascularize peripheral artery disease, but the major limitation is a high restenosis rate. Our experience with the hot tip laser system has shown a high primary success, 59–73% of the arteries were patent at 18 months, although 21% resulted in severe restenosis. The excimer laser seems to have a better long-term patency. Histology of restenosis specimens removed by atherectomy, shows the key role of the smooth muscle cells in this process.

Acetylcholine test in patients with angina pectoris and normal coronary angiography

Angina pectoris with normal coronary artery on the coronary angiography is an intriguing issue. Intracoronary infusion of acetylcholine has recently been used to test the integrity of endothelial cells. We studied 16 patients with this syndrome. A relationship has been found between the acetylcholine test and the exercise stress test in normotensive patients. The presence of hypertension makes the evaluation of the test more unpredictable, probably because of the damage on the endothelial cells related to systemic hypertension.

Restenosis after hot-tip laser-balloon angioplasty: histologic evaluation of the samples removed by Simpson atherectomy

Laser balloon angioplasty has been used in recent years to treat peripheral artery disease. Despite a primary success the technique is plagued by a high restenosis rate. Directional atherectomy was performed in a small group of patients affected by primitive stenosis or restenosis after an invasive procedure. Light microscopy, immunohistochemistry, and transmission electron microscopy have identified the cellular component of intimal hyperplasia as smooth muscle cells in an active synthetic phenotype. The arterial healing process after invasive procedures seems to develop similarly independently of the device employed.