Update on mechanical revascularization in acute myocardial infarction: which role and when?

Mechanical revascularization in the acute myocardial infarction by primary angioplasty has several advantages over thrombolytic therapy. The short-term patency rates of the infarct-related artery range from 95 to 99% and a normal flow is achieved in more than 90% of the cases. This prompt and effective reperfusion is probably responsible for the improved prognosis with primary angioplasty. The better outcome after primary angioplasty is observed both in low- and in high-risk patients, in all ages and in patients presenting late (>6 h) after the chest pain. Pooled analysis of randomized studies, show that primary angioplasty as compared to thrombolysis, has a lower incidence of death, stroke and reinfarction. Additional advantages of primary PTCA include the possibility of reperfusion in patients in whom lysis is contraindicated or less effective (e.g. patients in cardiogenic shock, or with prior coronary artery bypass surgery) and the ability to provide prognostic information helpful in the patient triage. Thus, primary PTCA results in better outcome than thrombolysis when performed in centers with success rates comparable to those achieved in the randomized trials. Further studies are still needed to assess its long-term efficacy. Several randomized trials are underway to assess the role of stents and the use of more potent antiplatelet drugs, as the GPIIb/IIIa receptor blockers, in adjunct to balloon angioplasty in the treatment of acute myocardial infarction.

Maximal myocardial perfusion by videodensitometry in the assessment of the early and late results of coronary angioplasty: relationship with coronary artery measurements and left ventricular function at rest.

In the assessment of the acute results of percutaneous transluminal coronary angioplasty (PTCA), myocardial perfusion at maximal vasodilatation theoretically has fewer limitations than the coronary flow reserve measurements and quantitative coronary angiography. The purpose of this study was to compare the myocardial perfusion to the measurements of the severity of the lesion (minimal luminal diameter and percent area stenosis) and to relate it to the changes of left ventricular function after PTCA. Regional myocardial perfusion was assessed during intracoronary papaverine, using the inverse mean transit time of contrast medium (1/Tmn), before, 15 min after, 18-24 hr after, and 6 months after successful single-vessel PTCA in 14 patients with stable angina. Left ventricular angiography (before angioplasty, 18-24 hr after, and 6 months later) was analysed by area-length and centerline methods. Immediately after PTCA, 1/Tmn increased from 0.14 +/- 0.07 sec-1 to 0.21 +/- 0.09 sec-1 (P = .001). Maximal myocardial perfusion remained higher than the pre-PTCA value the day after angioplasty (1/Tmn of 0.23 +/- 0.09 sec-1), while it reduced to near pre-PTCA values at follow-up (1/Tmn of 0.16 +/- 0.05 sec-1). Before PTCA, three out of ten patients had ejection fraction of < 65%, and seven had mild-to-moderate hypokinesis. The day after PTCA the ejection fraction and the regional dysfunction improved significantly. The change in ejection fraction 18-24 hr after PTCA did not correlate with minimal luminal diameter and percent area stenosis and correlated slightly with the improvement of perfusion (r = 0.54, P = .10). At follow-up left ventricular function deteriorated in the whole group, despite the persistence of angiographic success of PTCA, possibly because of changes in the loading condition. Coronary artery stenosis measurements and 1/Tmn failed to correlate with the left ventricular function. Given the difficulties in routine application of the analysis of time-density curves, the measurement of minimal luminal diameter remains a more practical assessment of the results of the intervention. However, the improvement of myocardial perfusion may give more information than coronary artery dimensions of the early recovery of left ventricular function.

[Coronary recanalization: rationale for stents]. / Ricanalizzazione coronarica: il razionale degli stent.

Coronary stenting is a technique complementary to coronary angioplasty, because it is successful in the management of the two major limitations of conventional balloon dilation, i.e. the acute or threatened closure and the restenosis. The currently available intracoronary stents are far from being ideal, mainly for their thrombogenicity. During abrupt closure, the bailout stenting has, in most of the cases, offered a valuable alternative to emergency coronary artery bypass surgery. The major complications after stent insertion are the result of an inadequate stent placement, of persistence of intra and/or poststent obstruction and of the ineffective anticoagulant therapy. The mechanical support (scaffolding) provided by the stent after dilation significantly reduces the amount of elastic recoil, and, improving laminar flow, eliminates arterial wall shear stress that may contribute to an increase in intimal thickening. Moreover, the reduction of arterial cyclical stretching may reduce the rate of neointimal proliferation. By sealing the exposed subintimal spaces, stents may minimise the formation of local thrombi, and thus also limit their later organization and fibrous conversion into part of the restenotic lesion: two recently completed randomized trials (STRESS and BENESTENT) confirm the lower rate of restenosis in patients treated with single stent placement in de-novo lesions as compared with standard balloon angioplasty. The mechanism of stent benefit in reducing restenosis rate seems to be the wider initial lumen, which can accommodate a greater degree of intimal hyperplasia. In the near future, the improvements of the blood and tissue compatibility of the stents, may allow easier management.(ABSTRACT TRUNCATED AT 250 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.

[Endothelial dysfunction in ischemic syndromes]. / La disfunzione endoteliale nelle sindromi ischemiche.

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.

[Modifications in left atrial function in response to changes in left ventricular filling]. / Modificazioni della funzione atriale sinistra in risposta alle alterazioni del riempimento ventricolare sinistro.

In order to investigate the effects of increasing degrees of left ventricular filling impairment on left atrial function, in 9 A-fillers (E/A ratio less than 1, E wave deceleration time greater than 170 ms) and 9 E-fillers (E/A ratio greater than 1, E wave deceleration time less than 150 ms) we constructed the left ventricular and the left atrial volume curves according to a previously validated Doppler 2-dimensional echo method which combines mitral and pulmonary venous flow. Eight normals served as control. The left atrial reservoir (defined as maximum-minimum atrial volume), pump (defined by the volume of blood that enters the left ventricle with the atrial contraction) and conduit functions (defined as left ventricular filling volume--the reservoir and the pump volume) expressed as % of the left ventricular filling volumes, varied significantly between normals (37 +/- 9%, 25 +/- 3%, 37 +/- 11%), A-fillers (48 +/- 9% p less than 0.05, 39 +/- 5% p less than 0.05, 14 +/- 10% p less than 0.001) and E-fillers (27 +/- 6% p less than 0.05, 19 +/- 7% p less than 0.05, 54 +/- 10% p less than 0.01). Also maximum left ventricular and left atrial volumes differed significantly (normals 165 +/- 31 ml, 76 +/- 20 ml; A-fillers 174 +/- 33 ml, 100 +/- 20 ml p less than 0.05; E-fillers 322 +/- 34 ml p less than 0.001, 136 +/- 41 ml p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)