Biomedical subjects

I Loschiavo

Publications and source records attributed to I Loschiavo.

4 recordsLinked to original sources

PubMed1995

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.

Adult↗

PubMed1994

[Coronary recanalization: rationale for stents].

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)

Coronary Disease↗

PubMed1993

[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↗

PubMed1991

[Modifications in left atrial function in response to changes in left ventricular filling].

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)

Angina Pectoris↗