PubMed Health⌕ Search

Biomedical subjects

Italo Porto

Publications and source records attributed to Italo Porto.

At least 19 recordsLinked to original sources
PubMed2006

Plaque volume and occurrence and location of periprocedural myocardial necrosis after percutaneous coronary intervention: insights from delayed-enhancement magnetic resonance imaging, thrombolysis in myocardial infarction myocardial perfusion grade analysis, and intravascular ultrasound.

BACKGROUND: Myocardial necrosis can occur during percutaneous coronary intervention (PCI) despite optimal adjunctive pharmacology and careful technique. We investigated the mechanisms of procedural infarction using angiographic analysis, intravascular ultrasound, and delayed-enhancement magnetic resonance imaging. METHODS AND RESULTS: Fifty-two patients (64 vessels) who underwent complex PCI were studied. All patients were preloaded with clopidogrel and received glycoprotein IIb/IIIa inhibitors. "Adjacent" myonecrosis was defined as the presence of an area of new gadolinium hyperenhancement close to the stent. "Distal" myonecrosis was defined as situated at least 10 mm downstream from the stent. Fifteen vessels (23%) had evidence of new hyperenhancement after PCI. Of these, 8 (12%) had the distal type, and 7 (11%) had the adjacent type. Intravascular ultrasound showed a significantly greater reduction in plaque volume (91.6+/-51.5 versus 8+/-14 versus 20+/-35 mm3; P < 0.001) in the group with distal hyperenhancement compared with patients without new hyperenhancement or adjacent hyperenhancement. In the entire sample, a significant correlation was seen between changes in plaque volume (rho = 0.58, P < 0.001) after PCI and the mass of new necrosis measured by magnetic resonance imaging. Thrombolysis in Myocardial Infarction perfusion grade assessment of a closed microvasculature after PCI carried an odds ratio of 8.0 (95% confidence interval, 1.4 to 46.1; P = 0.02) for the occurrence of hyperenhancement, whereas side-branch occlusion was associated with an odds ratio of 16.2 (95% confidence interval, 2.6 to 102.5; P = 0.03). However, a closed microvasculature was associated with distal hyperenhancement (P = 0.02), and side-branch occlusion was associated with adjacent hyperenhancement (P < 0.001). CONCLUSIONS: These data suggest that distal embolization of plaque material occurs in contemporary PCI of native coronary arteries. Efforts to minimize procedural necrosis may require careful review of side branch anatomy and/or use of distal protection during extensive coronary stenting.

Aged↗
PubMed2006

Pharmacological management of no reflow during percutaneous coronary intervention.

Angiographic no reflow is a recognized phenomenon during percutaneous coronary intervention (PCI). It usually follows successful lesion dilation and, by definition, it represents a reduction in epicardial coronary blood flow in the absence of identifiable dissection, obstruction or distal vessel cut off (indicative of distal embolisation). No reflow appears to be more commonly associated with PCI for acute myocardial infarction and PCI for saphenous vein graft occlusions. While the exact mechanism of no reflow is unknown, theoretical causes include local humoral and microembolic effects leading to microcirculatory dysfunction. As the process is multifactorial, various therapeutic strategies are required in different situations. The present day pharmacological management involves the use of vasodilators including nitrates, verapamil, papaverine, adenosine, nicardipine and sodium nitroprusside, but interestingly a vasoconstrictor like epinephrine may also have a role. Glycoprotein IIb/IIIa platelet receptors antagonist have shown a powerful de-thrombotic effect, and the intracoronary administration appears to be particularly promising. We review the pathogenesis of a reduced epicardial flow during PCI and focus on those drugs that have been studied for the treatment of no reflow. Although no double blind, randomized trial has been conducted to assess any of these agents, or to determine the appropriate dosage, we try to identify some useful conclusions from the published evidence.

Angioplasty, Balloon, Coronary↗
PubMed2006

Treatment of spontaneous coronary dissection with drug-eluting stents--late clinical, angiographic and IVUS follow up.

The prognosis of spontaneous coronary artery dissection is uncertain and optimal treatment is unknown. We previously described the first reported implantation of drug-eluting stents in spontaneous coronary artery dissection. The immediate angiographic result was good, and we now report the late clinical, angiographic and intravascular ultrasound follow up.

Aortic Dissection↗
PubMed2005

Resting myocardial blood flow is impaired in hibernating myocardium: a magnetic resonance study of quantitative perfusion assessment.

BACKGROUND: Although impairment in perfusion reserve is well recognized in hibernating myocardium, there is substantial controversy as to whether resting myocardial blood flow (MBF) is reduced in such circumstances. Quantitative first-pass cardiovascular magnetic resonance (CMR) perfusion imaging allows absolute quantification of MBF. We hypothesized that MBF assessed at rest by quantitative CMR perfusion imaging is reduced in hibernating myocardium. METHODS AND RESULTS: Twenty-seven patients with 1 or 2-vessel coronary disease and at least 1 dysfunctional myocardial segment undergoing PCI were studied with preprocedure, early (24 hours), and late (9 months) postprocedure CMR imaging. First-pass perfusion images at rest were acquired in 3 short-axis planes by use of a T1-weighted turboFLASH sequence. In each slice, MBF was determined for 8 myocardial segments in mL . min(-1) . g(-1) by deconvolution of signal intensity curves with an arterial input function measured in the left ventricular blood pool. Cine MRI for assessment of global and segmental function and delayed enhancement MRI for detection of viability were also obtained. All coronary lesions were 80% to 95% stenosis in severity. Over all segments, mean MBF normalized by rate-pressure product ("corrected MBF") was 1.2+/-0.3 mL . min(-1) . g(-1) . (mm Hg . bpm/10(4))(-1) in segments without significant coronary stenosis and 0.7+/-0.2 mL . min(-1) . g(-1) . (mm Hg . bpm/10(4))(-1) in segments with coronary stenosis before PCI (mixed model controlling for slice and segment z=-23.9, P<0.001). Early after the procedure, the MBF was 1.2+/-0.2 mL . min(-1) . g(-1) . (mm Hg . bpm/10(4))(-1) in revascularized segments and 1.3+/-0.2 mL . min(-1) . g(-1) . (mm Hg . bpm/10(4))(-1) in nondiseased segments (z=-6.1, P<0.001). Late after PCI, the systolic wall thickening and end-diastolic wall thickness both increased significantly more (both P<0.001) in the myocardial segments subtended by severe coronary stenosis (8+/-17% to 40+/-19% and 6.5+/-1.1 to 9.3+/-2 mm, respectively) than in the myocardial segments supplied by nondiseased vessels. Mean MBF in dysfunctional segments with significantly improved contraction after revascularization was 0.8+/-0.2 mL . min(-1) . g(-1) . (mm Hg . bpm/10(4))(-1) before PCI and 1.2+/-0.2 mL . min(-1) . g(-1) . (mm Hg . bpm/10(4))(-1) after PCI (z=2.0, P=0.04). CONCLUSIONS: CMR perfusion imaging detects impaired resting MBF in hibernating myocardial segments.

Aged↗
PubMed2005

Safety of magnetic resonance imaging one to three days after bare metal and drug-eluting stent implantation.

Despite emerging evidence that magnetic resonance imaging (MRI) is safe within 8 weeks after bare metal coronary stenting, there are limited data on the safety of MRI imaging very early (1 to 3 days) after stent implantation and no published studies to date on the safety of MRI after insertion of drug-eluting stents (DESs). Forty-nine patients underwent cardiovascular MRI (1.5 T) at a median of 1 day after complex percutaneous coronary intervention. The average number of stents per patient was 2.2 +/- 1.1, and the average stent length per patient was 37.8 +/- 19.7 mm. In 15 of these patients > or =1 DES was used: paclitaxel DESs in 14 and sirolimus DESs in 1. In the DES group, the average number of stents was 1.75 +/- 1.0 per patient (3 patients received 3 DESs), and average DES length was 36.5 +/- 14.8 mm per patient. No acute thrombosis was recorded, and at 9-month clinical follow-up only 2 patients (4%) developed adverse events (1 target vessel restenosis and 1 nontarget vessel revascularization); these patients were in the non-DES group.

Adult↗
PubMed2005

Left main and saphenous vein graft spasm: an unusual association.

We present a case of left main spasm which was associated with spasm of a saphenous vein graft. This case emphasizes the importance of excluding an excessive vasoconstrictory response in patients treated with percutaneous coronary interventions.

Coronary Vasospasm↗
PubMed2005

Troponin elevation after percutaneous coronary intervention directly represents the extent of irreversible myocardial injury: insights from cardiovascular magnetic resonance imaging.

BACKGROUND: Although troponin elevation after percutaneous coronary intervention (PCI) is common, uncertainties remain about the mechanisms of its release and its relationship to the volume of myocardial tissue loss. Delayed-enhancement MRI of the heart has been shown to reliably quantify areas of irreversible myocardial injury. To investigate the quantitative relationship between irreversible injury and cardiac troponin release, we studied the incidence and extent of new irreversible injury in patients undergoing PCI and correlated it to postprocedural changes in cardiac troponin I. METHODS AND RESULTS: Fifty patients undergoing PCI were studied with preprocedural and postprocedural (24 hours) delayed-enhancement MRI for assessment of new irreversible myocardial injury. Cardiac troponin I measurements were obtained before PCI and 24 hours after PCI. Of these 50 patients, 24 underwent a further third MRI scan at a median of 8 months after the procedure. Mean patient age was 64+/-12 years. After the procedure, 14 patients (28%) had evidence of new myocardial hyperenhancement, with a mean mass of 6.0+/-5.8 g, or 5.0+/-4.8% of total left ventricular mass. All of these patients had raised troponin I levels (range 1.0 to 9.4 mug/L). Thirty-four patients (68%) had no elevated troponin I and no evidence of new myocardial necrosis on MRI. There was a strong correlation between the rise in troponin I measurements at 24 hours and mean mass of new myocardial hyperenhancement, both early (r=0.84; P<0.001) and late (r=0.71; P<0.001) after PCI, although there was a trend for a reduction in the size of PCI-induced myocardial injury in the late follow-up scan (P=0.07). CONCLUSIONS: In the setting of PCI, patients demonstrating postprocedural elevation in troponin I have evidence of new irreversible myocardial injury on delayed-enhancement MRI. The magnitude of this injury correlates directly with the extent of troponin elevation.

Angioplasty, Balloon, Coronary↗
PubMed2005

Interplay of platelet polymorphisms, risk factors, and von [corrected] Willebrand factor [corrected] in determining collagen-adenosine diphosphate PFA-100 results in patients with coronary artery disease.

Platelets play a pivotal role in thrombus formation in patients with coronary artery disease (CAD), since the high shear generated in the presence of severe coronary stenoses can increase platelet reactivity (PR) and trigger thrombogenesis. Several reports have suggested a functional effect of human platelet antigen (HPA)-1 and HPA-2 gene polymorphisms on PR. However, the true determinants of high-shear PR in CAD patients taking their usual medications are still incompletely understood. In 104 patients with stable CAD we analyzed the possible clinical, biochemical and genetic factors affecting high-shear PR, measured by the ex vivo platelet function analyzer (PFA-100) collagen-adenosine diphosphate method. In univariate analysis, a lower PR was associated with decreased plasma von Willebrand factor-ristocetin cofactor activity, increased blood levels of triglycerides, female sex, use of thienopyridines, lower platelet count, and HPA-1b carriership. All variables, except HPA-1b, remained associated with lower PR in multivariate analysis. However, the introduction in the model of the HPA-1 and HPA-2 genotypes as interaction terms led to a significant improvement in the prediction of PR, although the quantitative effect was small (about 3% improvement, P=0.046).Thus, in CAD patients, there seems to be only a mild effect of the platelet glycoprotein HPA-1 and HPA-2 polymorphisms on collagen-adenosine diphosphate-stimulated PR after the effect of well-established clinical and biochemical determinants are considered.

Adenosine Diphosphate↗
PubMed2005

Intravascular ultrasound to guide stenting of an anomalous right coronary artery coursing between the aorta and pulmonary artery.

We report on a case of anomalous right coronary artery with interarterial course which caused severe symptoms and was treated percutaneously after failed bypass surgery. Using intravascular ultrasound (IVUS) guidance, a drug eluting stent was placed at the ostium of the anomalous artery, correcting both the baseline narrowing and the phasic, systolic arterial compression.

Adult↗
PubMed2004

Inflammation, genetics, and ischemic heart disease: focus on the major histocompatibility complex (MHC) genes.

BACKGROUND: Increasing data suggest that ischemic heart disease (IHD) shares several characteristics with common inflammatory diseases (such as rheumatoid arthritis), in which the pathogenetic role of inflammatory gene polymorphisms is well established. Variants in the genes for the major histocompatibility complex (MHC) molecules on the short arm of chromosome 6 show profound "linkage disequilibrium", leading to the formation of "haplotypes", i.e., frozen blocks of alleles travelling together through generations. DESIGN: We performed a review of published studies linking IHD with gene polymorphisms of the MHC molecules tumor necrosis factor (TNF)-alpha and -beta, the class II DR human leukocyte antigens, heat shock protein 70-1, hemochromatosis related gene, and complement C4. RESULTS: The emerging data are quite conflicting and do not provide definitive evidence for a role of these gene variants in the pathogenesis of IHD; a possible exception is the G252A and polymorphism in the TNF-beta gene (also known as lymphotoxin-alpha) which, in a comprehensive genome-scan linkage analysis of unrelated Japanese, but not in a smaller German population, was linked to myocardial infarction. However, some important biases appear, e.g. different study design and variable linkage disequilibrium among different populations. CONCLUSIONS: Preliminary positive results should encourage future studies to focus on clinical models of IHD with well-codified inflammatory components, using novel methods (such as haplotype analysis) to assess gene polymorphisms and their clinical effect.

Alleles↗
PubMed2004

Intravascular ultrasound to guide the management of intracoronary thrombus: a case report.

Percutaneous coronary intervention can be associated with distal embolization of thrombotic material causing myocardial necrosis and infarction. We discuss the role of intravascular imaging to guide the use of a distal protection device by describing the outcome of a young woman presenting with non-ST elevation myocardial infarction. Coronary angiography demonstrated an isolated minor stenosis in the proximal left anterior descending coronary artery with slight haziness beyond the lesion. Intravascular ultrasound confirmed an extensive thrombus overlying a bulky atherosclerotic plaque. A distal filter wire was therefore successfully used to reduce the risk of distal embolization. The use of intravascular ultrasound in patients presenting with acute coronary syndrome may reveal large thrombi that are difficult to image using conventional angiographic techniques. Intravascular ultrasound can therefore be used as a tool to select lesions requiring distal protection.

Adult↗
PubMed2004

Usefulness of high-pressure post-dilatation to optimize deployment of drug-eluting stents for the treatment of diffuse in-stent coronary restenosis.

Drug-eluting stents (DESs) may represent a simple, effective treatment for in-stent restenosis (ISR); however, the underexpansion of stents is a significant cause of target vessel failure. It was hypothesized that high-pressure postdilatation would be necessary to optimize DES expansion and minimize the risk for restenosis when treating patients with ISR. Fifteen patients with diffuse ISR were treated by predilatation (including cutting balloons), DES deployment, and high-pressure postdilatation, with the measurement of luminal and stent dimensions by intravascular ultrasound after each intervention. After initial deployment, DES underexpansion was present in 10 of 15 patients (66%); after high-pressure postdilatation, there was a significant increase in luminal dimensions, including minimum luminal area (4.3 +/- 0.3 to 5.6 +/- 0.4 mm(2), p <0.001) and a doubling in the proportion of patients with optimal stent expansion. At long-term follow-up (median 11 months), target lesion revascularization occurred in 1 patient (7%) because of edge restenosis; there was no restenosis within the DES.

Aged↗