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Biomedical subjects

Francesco Romeo

Publications and source records attributed to Francesco Romeo.

At least 19 recordsLinked to original sources
PubMed2006

Decreased plasma adiponectin concentration in major depression.

Adiponectin is the most abundant adipose-derived plasma protein. Recently adiponectin levels have been linked to most variables of metabolic syndrome and conventional risk factors for cardiovascular disease. However, its relation with major depression is yet unclear. We evaluated plasma adiponectin levels in 32 first-episode drug-naïve major depression (DSM-IV-TR) patients without conventional risk factors for cardiovascular disease and 32 matched healthy subjects. Major depression patients displayed lower adiponectin plasma levels compared to controls (P<0.01). Adiponectin significantly correlated with depression severity, as assessed by HAM-D (rho=0.83, P<0.001). This study shows decreased plasma adiponectin concentrations in major depression patients and relates adiponectinemia reduction to major depression severity.

Adiponectin↗
PubMed2006

Specific changes in the proteomic pattern produced by the BRCA1-Ser1841Asn missense mutation.

BRCA1 is a nuclear phosphoprotein that plays a key role in many cell functions, including DNA repair, control of transcription, recombination and cell cycle homeostasis. Inherited missense mutations in the BRCA1 gene may predispose to breast and ovarian cancer, but the molecular mechanisms underlying BRCA1-induced tumorigenesis are still to be elucidated. Functional studies performed so far have contributed to the characterization of several single-nucleotide variants, mostly located at the BRCT domain, but very little is known about modifications in the protein pattern occurring in cells carrying these mutations. To shed more light in the molecular events triggered by missense mutations affecting breast cancer susceptibility genes, we have analyzed the whole cell proteome of stably transfected HeLa cell lines bearing three distinct single aminoacid changes in the BRCA1 protein (Ser1841Asn, Met1775Arg and Trp1837Arg) by means of liquid chromatography coupled to tandem-mass spectrometry. The results show that the Met1775Arg and the Trp1837Arg do not produce significant changes in the proteomic pattern compared to cells transfected with the wild-type BRCA1 cDNA. On the other hand, a different profile is detected in the BRCA1 Ser1841Asn-bearing cell line. In this particular subset, our attention has been focused on two proteins--the tumor protein D52 (TD52) and the folate receptor alpha (FOL1)--whose expression has been already reported to be upregulated in breast cancer, as well as in other tumors. Our findings indicate that Ser1841Asn BRCA1 mutation is able to activate specific protein pathways that are not triggered by other single aminoacid changes and pinpoint to the role TD52 and FOL1 as potential markers in breast cancer patients carrying this particular BRCA1 gene alteration.

Amino Acid Substitution↗
PubMed2006

Distribution and prognostic significance of QT intervals in the lowest half centile in 12,012 apparently healthy persons.

The presence of an abnormally short QT interval has been noted among survivors of idiopathic ventricular fibrillation and among close relatives of victims of unexplained sudden death. Most reported cases have had rate-corrected QT (QTc) intervals of <300 ms. The prevalence of such values in the community has not been documented. We reviewed the electrocardiograms (ECGs) of 12,012 subjects who underwent routine medical examinations for occupational reasons. The QT interval was measured by 2 physicians in all cases, and QTc interval was calculated. All ECGs with QTc values in the lowest 5% were reviewed by 2 cardiologists expert in QT analysis, and the QT measurement was corrected if necessary. Information about subsequent survival was obtained from the case file or from public records. In the lowest 1/2 centile, the distribution of QTc values continued to follow a normal pattern without evidence of a distinct subpopulation of low values. The shortest QTc encountered was 335 ms. Information about subsequent survival was available for 36 of the 60 subjects with the lowest 1/2 centile of QTc values. None of these subjects died during the 7.9 +/- 4.5 years subsequent to the ECG that demonstrated the short QT interval. In conclusion, a QTc interval of <or=330 ms is extremely rare in healthy subjects, and the presence of a QT interval in the lowest 1/2 centile of the normal range does not imply a significant risk of sudden death.

Adult↗
PubMed2006

Expression of nuclear insulin receptor substrate 1 in breast cancer.

BACKGROUND: Insulin receptor substrate 1 (IRS-1), a cytoplasmic protein transmitting signals from the insulin and insulin-like growth factor 1 receptors, has been implicated in breast cancer. Previously, it was reported that IRS-1 can be translocated to the nucleus and modulate oestrogen receptor alpha (ERalpha) activity in vitro. However, the expression of nuclear IRS-1 in breast cancer biopsy specimens has never been examined. AIMS: To assess whether nuclear IRS-1 is present in breast cancer and non-cancer mammary epithelium, and whether it correlates with other markers, especially ERalpha. Parallel studies were carried out for the expression of cytoplasmatic IRS-1. METHODS: IRS-1 and ERalpha expression was assessed by immunohistochemical analysis. Data were evaluated using Pearson's correlation, linear regression and receiver operating characteristic analysis. RESULTS: Median nuclear IRS-1 expression was found to be low in normal mammary epithelial cells (1.6%) and high in benign tumours (20.5%), ductal grade 2 carcinoma (11.0%) and lobular carcinoma (approximately 30%). Median ERalpha expression in normal epithelium, benign tumours, ductal cancer grade 2 and 3, and lobular cancer grade 2 and 3 were 10.5, 20.5, 65.0, 0.0, 80 and 15%, respectively. Nuclear IRS-1 and ERalpha positively correlated in ductal cancer (p<0.001) and benign tumours (p<0.01), but were not associated in lobular cancer and normal mammary epithelium. In ductal carcinoma, both nuclear IRS-1 and ERalpha negatively correlated with tumour grade, size, mitotic index and lymph node involvement. Cytoplasmic IRS-1 was expressed in all specimens and positively correlated with ERalpha in ductal cancer. CONCLUSIONS: A positive association between nuclear IRS-1 and ERalpha is a characteristic for ductal breast cancer and marks a more differentiated, non-metastatic phenotype.

Adult↗
PubMed2006

Functional assessment of the collateral-dependent circulation in chronic total coronary occlusion using transthoracic Doppler ultrasound and venous adenosine infusion.

The measurement of collateral flow reserve (CFR; the hyperemic/baseline collateral flow velocity ratio) in patients with chronic total coronary occlusion requires invasive and expensive techniques. Noninvasive transthoracic coronary Doppler echocardiography may be an alternative option. Fifty-one patients with chronic total coronary occlusion were evaluated by transthoracic coronary Doppler echocardiography and venous adenosine infusion to measure CFR in occluded coronary arteries (the left anterior descending artery in 44 patients and the artery supplying the posterior descending artery in 7 patients). CFR data were plotted against 3 angiographic parameters: (1) grade of the epicardial filling of the occluded artery (1=absent, 2=partial, 3=complete), (2) stenosis of the donor artery, and (3) the extent of coronary artery disease (vessels with >or=70% stenosis). Collateral flow was maintained at stress in 34 patients (CFR>or=1, range 1.0 to 2.2) but was withdrawn in 17 patients (CFR<1, range 0.25 to 0.90). CFR increased with the degree of angiographic collateral flow (grade 1: 0.73+/-0.29; grade 2: 1.16+/-0.31; grade 3: 1.34+/-0.49; F=5.31, p=0.008). A multivariate model of CFR prediction showed a direct relation with angiographic collateral grade and the number of diseased vessels and an inverse relation with stenosis of the donor artery. In conclusion, CFR measurement is feasible by transthoracic coronary Doppler echocardiography. One third of the patients with chronic total coronary occlusion had collateral flow withdrawal at stress, which occurs when collateral circulation is poor and when the donor artery is stenotic. CFR correlates with angiographic collateral grade and with the extent of coronary artery disease.

Adenosine↗
PubMed2006

Suppression of atherogenesis by delivery of TGFbeta1ACT using adeno-associated virus type 2 in LDLR knockout mice.

TGFbeta(1) deficiency has been attributed to the development of atherosclerosis. There is, however, little direct evidence for this concept. To examine this hypothesis, low-density lipoprotein receptor knockout (LDLR(-/-)) mice were injected via tail vein with recombinant adeno-associated virus type 2 (rAAV) carrying a bioactive TGFbeta(1) mutant (AAV/TGFbeta1ACT, n=10) or granulocyte-macrophage-colony stimulating factor (AAV/GM-CSF, n=10, a negative control) or saline (n=9, control), and then put on a high cholesterol diet. At 18 weeks, blood lipids were found to be similarly elevated in all LDLR(-/-) mice. TGFbeta1ACT and GM-CSF (DNA, mRNA, and protein) were highly expressed in the tissues of mice given TGFbeta1ACT or AAV/GM-CSF, respectively, showing sustained transfection following gene delivery by the systemic route. Saline-treated and AAV/GM-CSF-treated LDLR(-/-) mice showed extensive areas of atherosclerotic lesion formation. There was evidence of intense oxidative stress (nitrotyrosine staining), inflammation (CD68 staining), and expression of adhesion molecules and the ox-LDL receptor LOX-1 (gene array analysis) in the atherosclerotic tissues. Importantly, atherosclerotic lesion formation was markedly inhibited in the LDLR(-/-) mice given AAV/TGFbeta1ACT. Expression of adhesion molecules and LOX-1, oxidative stress, and inflammatory response all were inhibited in the mice given AAV/TGFbeta1ACT (P<0.05 vs. saline-treated or GM-CSF-treated LDLR(-/-) mice). These data for the first time demonstrate that systemic delivery of TGFbeta1ACT gene via AAV can inhibit formation of atherosclerotic lesions, possibly via anti-inflammatory and anti-oxidant mechanisms. These findings suggest a novel view of TGFbeta(1) in atherogenesis and a potential new gene therapy for treatment of atherosclerosis.

Adenoviridae↗
PubMed2006

Coronary artery restenosis: vascular biology and emerging therapeutic strategies.

Percutaneous coronary intervention with drug-eluting stents is currently the preferred approach to the treatment of obstructive coronary stenoses. Large, randomized trials have demonstrated a significant reduction in the incidence of restenosis after drug-eluting stent placement compared with balloon angioplasty or bare metal stents across a wide range of lesions. Furthermore, these stents have appeared to be effective in maintaining the luminal patency at follow up for up to 2-4 years. Concerns regarding the potential adverse effects of drug-eluting stents, such as aneurysm formation in arteries secondary to drug toxicity or hypersensitivity, as well as the overdependence on antiplatelet therapy for a protracted period to prevent subacute thrombosis, have been raised. However, evidence from large studies has not demonstrated any significant increase in the incidence of such adverse events. Future approaches to treating coronary stenoses involve technical modifications, such as direct stenting, accelerating endothelialization with gene delivery of nitric oxide donors, smooth muscle cell growth inhibitors after stent placement, biodegradable stents and concurrent use of local molecule delivery and oral chemotherapy. Ongoing large-scale postmarketing surveillance studies are expected to provide credible answers to the concerns regarding the safety of these stents.

Animals↗
PubMed2006

Association between enhanced soluble CD40 ligand and proinflammatory and prothrombotic states in major depressive disorder: pilot observations on the effects of selective serotonin reuptake inhibitor therapy.

OBJECTIVE: Major depressive disorder (MDD) is associated with low-grade inflammation, and it is considered a risk factor for coronary artery disease (CAD). CD40 ligand (CD40L) plays an important role in inflammation, platelet activation, and clotting system activation. We investigated soluble CD40L (sCD40L) expression in MDD and assessed whether it may represent a molecular mechanism that links inflammation and a prothrombotic state and whether this condition may be modified by selective serotonin reuptake inhibitor (SSRI) therapy. METHOD: Levels of sCD40L, interleukin-1beta (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble P-selectin (sP-selectin), activated factor VII (FVIIa), and prothrombin fragment 1+2 (F1+2) were measured in 46 drug-naïve, first-episode MDD patients without conventional CAD risk factors and in 46 matched healthy controls. Participants were screened between March 2002 and November 2005. Twenty of the 46 MDD patients were then randomly assigned to either sertraline 100 mg/day (N = 10) or citalopram 20 mg/day (N = 10); the aforementioned variables were measured at baseline and after 6 weeks of treatment. RESULTS: Compared with control subjects, MDD patients had higher baseline levels of sCD40L, IL-1beta, IL-6, TNF-alpha, sP-selectin, FVIIa, and F1+2. In the clinical group, sCD40L levels, HAM-D total scores, and proinflammatory markers were strongly intercorrelated. In contrast, there were no significant correlations in the control group. Mood improvement achieved with SSRI therapy was associated with significant reduction in sCD40L, proinflammatory markers, and prothrombotic markers expression. (All p values < .0001.) CONCLUSIONS: This pilot study shows that CD40/ CD40L pathway up-regulation in MDD patients relates increased levels of sCD40L to a prothrombotic state and, preliminarily, indicates that SSRI therapy may significantly reduce sCD40L and CD40L levels associated with proinflammatory and prothrombotic states.

Adult↗
PubMed2005

Cytochrome P450 aromatase expression in human seminoma.

BACKGROUND: The enzyme cytochrome P450 aromatase, catalysing the conversion of androgens into estrogens, has been detected in normal human testicular cells suggesting a physiological role of local estrogen biosynthesis on spermatogenesis control. Estrogens, regulating cell growth and apoptosis, can also be involved in tumorigenesis process, but the possible link between estrogens and testicular neoplastic process is, up to now, scarcely known. This study examined aromatase expression in human seminoma, which is the most common germ cell tumour of the testis. METHODS: The tumour-bearing testes were obtained from 20 patients with classic seminoma undergoing to therapeutic orchidectomy. Paraffin embedded tissues were processed for immunohistochemistry using a mouse monoclonal antibody generated against human placental cytochrome P450 arom, as primary antibody, and a biotinylated goat-anti-mouse IgG, as secondary antibody. Furthermore, Western blot analysis of seminoma extracts was carried out. RESULTS: Intense P450 arom immunoreactivity was observed in the seminoma cells and Western blot analysis confirmed the immunodetection. A strong immunostaining was also detected in cells of intratubular germ cell neoplasia (IGCN), adjacent to seminoma. CONCLUSION: The present study demonstrated, for the first time in human, aromatase expression in neoplastic cells of seminoma suggesting a relation between local estrogen biosynthesis and germ cell tumorigenesis. The P450 arom immunolocalization in the cells of IGCN, representing the common precursor of most germ cell tumors, seems to support these findings.

Adult↗
PubMed2005

Lectin-like, oxidized low-density lipoprotein receptor-1 (LOX-1): a critical player in the development of atherosclerosis and related disorders.

LOX-1, a lectin-like 52-kD receptor for oxidized low-density lipoproteins (ox-LDL), is present primarily on endothelial cells. This receptor is upregulated by ox-LDL itself and by angiotensin II, endothelin, cytokines, and shear stress, all participants in atherosclerosis. This receptor is upregulated in the arteries of hypertensive, dyslipidemic, and diabetic animals. Upregulation of LOX-1 has been identified in atherosclerotic arteries of several animal species and humans, not only on the endothelial lining, but also in the neovasculature of the atherosclerotic plaque, and this receptor is often co-localized with apoptotic cells. Recent studies show upregulation of LOX-1 in the ischemic-reperfused myocardium. LOX-1 inhibition is associated with attenuation of atherosclerosis and associated ischemic injury. LOX-1 may be a novel, exciting target for drug therapy.

Apoptosis↗
PubMed2005

In vivo and in vitro studies support that a new splicing isoform of OLR1 gene is protective against acute myocardial infarction.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), encoded by the OLR1 gene, is a scavenger receptor that plays a fundamental role in the pathogenesis of atherosclerosis. LOX-1 activation is associated with apoptosis of endothelial cells, smooth muscle cells (SMCs), and macrophages. This process is an important underlying mechanism that contributes to plaque instability and subsequent development of acute coronary syndromes. Independent association genetic studies have implicated OLR1 gene variants in myocardial infarction (MI) susceptibility. Because single nucleotide polymorphisms (SNPs) linked to MI are located in intronic sequences of the gene, it remains unclear as to how they determine their biological effects. Using quantitative real-time PCR and minigene approach, we show that intronic SNPs, linked to MI, regulate the expression of a new functional splicing isoform of the OLR1 gene, LOXIN, which lacks exon 5. Macrophages from subjects carrying the "non-risk" disease haplotype at OLR1 gene have an increased expression of LOXIN at mRNA and protein level, which results in a significant reduction of apoptosis in response to oxLDL. Expression of LOXIN in different cell types results in loss of surface staining, indicating that truncation of the C-terminal portion of the protein has a profound effect on its cellular trafficking. Furthermore, the proapoptotic effect of LOX-1 receptor in cell culture is specifically rescued by the coexpression of LOXIN in a dose-dependent manner. The demonstration that increasing levels of LOXIN protect cells from LOX-1 induced apoptosis sets a groundwork for developing therapeutic approaches for prevention of plaque instability.

Alternative Splicing↗
PubMed2005

Elevated C-reactive protein levels and coronary microvascular dysfunction in patients with coronary artery disease.

AIMS: It is still unknown whether elevated C-reactive protein levels are responsible for coronary microcirculatory dysfunction in patients with coronary artery disease (CAD). This study was aimed at evaluating the association between C-reactive protein levels and endothelium-dependent and endothelium-independent coronary blood flow (CBF) responses in non-culprit arteries of patients with CAD. METHODS AND RESULTS: We studied 28 patients (14 with normal and 14 with elevated C-reactive protein levels, >5 mg/L) with single-vessel disease and otherwise angiographically normal coronary arteries undergoing percutaneous transluminal coronary angioplasty (PTCA). CBF was measured in the non-PTCA vessel using an intracoronary Doppler guide wire and quantitative coronary angiography at baseline, after intracoronary infusion of substance P and of adenosine, and expressed as per cent change from baseline. The increases in CBF during infusion of substance P and of adenosine were lesser in patients with elevated than in those with normal C-reactive protein levels (34+/-22 vs. 61+/-34%, P=0.04 and 131+/-53 vs. 189+/-89%, P=0.03, respectively). Multivariable analysis identified elevated C-reactive protein level as the only independent predictor of reduced response to substance P (P=0.01) and adenosine (P=0.02). CONCLUSION: In patients with CAD, evidence of systemic inflammation is independently associated with endothelium-dependent and endothelium-independent coronary microvascular dysfunction, which, in turn, may be critical to precipitate myocardial ischaemia, in particular, in unstable patients.

Adenosine↗
PubMed2005

The effects of PPAR-gamma ligand pioglitazone on platelet aggregation and arterial thrombus formation.

BACKGROUND: It has been suggested that peroxisome proliferator-activated receptor (PPAR)-gamma ligands reduce the development of atherosclerosis and myocardial ischemia-reperfusion injury; both of these phenomena are associated with platelet activation. We postulated that PPAR-gamma activation would inhibit platelet activation and intra-arterial thrombus formation. METHODS AND RESULTS: Sprague-Dawley rats were fed chow mixed with pioglitazone (1 or 10 mg/kg/day) for 7 to 10 days. A filter soaked in 30% FeCl(3) was applied around the abdominal aorta to study the patterns of arterial thrombogenesis. The aortic blood flow was continuously monitored using an ultrasonic Doppler flow probe. ADP and arachidonic acid-induced platelet aggregation and the expression of constitutive nitric oxide synthase (cNOS) and thrombomodulin in aorta were measured. Pioglitazone feeding delayed the time to occlusive thrombus formation by 40% (P<0.01 vs. control, n=9) without affecting the weight of the thrombus. ADP- as well as arachidonic acid-induced platelet aggregation was also inhibited by pioglitazone feeding (P<0.01 vs. control, n=9). Pioglitazone feeding also upregulated the aortic expression of cNOS and thrombomodulin; both are considered important factors in platelet aggregation and thrombus formation in vivo. The effect of a high dose (10 mg/kg/day) of pioglitazone was not more potent than that of a low dose (1 mg/kg/day). CONCLUSION: These results indicate that pioglitazone administration decreases platelet aggregation and delays intra-arterial thrombus formation in rats, at least partially, by an increase in the expression of cNOS and thrombomodulin.

Animals↗
PubMed2005

Evaluation of flow in the left anterior descending coronary artery but not in the left internal mammary artery graft predicts significant stenosis of the arterial conduit.

OBJECTIVES: The purpose of this study was to evaluate which Doppler-derived flow index best predicts new distal left anterior descending coronary artery (LAD) stenosis in patients with left internal mammary artery (LIMA) graft. BACKGROUND: The LIMA flow measurement has been proposed to assess graft function, but it may be misleading in case of new distal LAD stenosis and/or competitive flow from native LAD. Distal LAD coronary flow reserve (CFR: hyperemic/baseline peak flow velocity ratio) may be more appropriate. METHODS: The LIMA and distal LAD flow was measured by transthoracic Doppler echocardiography in 96 patients undergoing diagnostic/therapeutic coronary angiography, 7 +/- 4 years after cardiac bypass surgery. The LIMA flow indexes (systolic-to-diastolic peak velocity ratio [SDPVr] >1, diastolic time velocity integral fraction [DTVIf] <0.5, and CFR <2) and LAD CFR <2 were used to predict > or =70% new LAD stenosis. RESULTS: The LAD CFR <2 predicted new LAD stenosis, found in 21 of 77 patients without competitive flow from native LAD, with significantly higher diagnostic accuracy (98%) than LIMA flow indexes (SDPVr >1 = 61%, DTVIf <0.5 = 69%, and CFR <2 = 72%). The LIMA flow indexes were abnormal in 17 of 19 patients with competitive graft flow, but only 5 had graft restriction, and none had significant LAD stenosis. In a multivariate model of new distal LAD stenosis prediction, competitive flow from native LAD reduced the predictive role of LIMA but not of LAD CFR. CONCLUSIONS: In patients without competitive flow from native LAD, LAD CFR is more accurate for the detection of LAD stenosis than LIMA CFR. In patients with competitive graft flow, abnormal LIMA flow patterns and blunted LIMA CFR do not reflect downstream LAD flow as LAD CFR does.

Adult↗
PubMed2005

Pharmacogenomics in cardiovascular disease: the role of single nucleotide polymorphisms in improving drug therapy.

Pharmacogenomics is the study of how an individual's genetic inheritance affects the body's response to drugs. Pharmacogenomics holds the promise that drugs might one day be tailor-made for individuals and adapted to an individual's genetic makeup. Several studies have shown that both adverse and beneficial responses to cardiovascular drugs can be influenced by single nucleotide polymorphisms in genes coding for metabolising enzymes, drug transporters and drug targets. Despite the large amount of data about gene-drug interactions, the translation of pharmacogenomics in clinical practise is slow. To improve this, there is a need of new technology and large prospective trials allowing for simultaneous analysis of multiple genetic variants in molecular pathways that could affect drug disposition and action.

Animals↗
PubMed2005

Electrical cardioversion of atrial fibrillation: different methods for a safe and effective technique.

Atrial fibrillation is the most common cardiac arrhythmia observed in clinical practice. Many different therapeutic approaches are available at present but none may be considered the gold standard treatment. Antiarrhythmic drugs are not very effective agents to cardiovert persistent atrial fibrillation and, therefore, the technique most frequently used to restore sinus rhythm is external direct current cardioversion, which has proved to be safe and very effective. Esophageal cardioversion is an alternative method that could obviate some of the limitations of the external technique, such as the high energy required, need for anesthesia and longer hospital stay. Another technique performed during the last two decades is internal cardioversion, but at present, the advantage of this technique is limited to the small proportion of cases of unsuccessful external cardioversion.

Atrial Fibrillation↗
PubMed2004

Coronary flow reserve of the angiographically normal left anterior descending coronary artery in patients with remote coronary artery disease.

Coronary artery disease (CAD) has been suggested to alter coronary flow reserve (CFR; the ratio between hyperemic and baseline coronary flow velocities) not only in territories supplied by stenotic arteries but also in angiographically normal, remote regions. However, few data exist regarding the left anterior descending (LAD) coronary artery as the normal index artery. The influence of remote CAD on CFR of the angiographically normal LAD was evaluated with transthoracic Doppler ultrasound to measure CFR in the LAD during 90 seconds of venous adenosine infusion (140 microg/kg/min) in 122 subjects who were assigned to 1 group; group 1 comprised 49 controls without angiographically detectable CAD, and group 2 consisted of 73 patients with an angiographically normal LAD and remote CAD. Group 2 was divided into 4 subgroups: 16 patients with previous remote percutaneous coronary intervention (group 2A); 13 patients with significant remote stenosis (group 2B); 23 patients with previous remote myocardial infarction and percutaneous coronary intervention (group 2C); and 21 patients with previous remote myocardial infarction but no percutaneous coronary intervention (group 2D). CFR in the LAD was not significantly different in groups 1 and 2 (3.08 +/- 0.61 and 3.03 +/- 0.69, respectively, p = NS). Decreased ejection fraction and increased wall motion score index in patients with remote CAD (p < 0.00001) and multivessel CAD did not affect CFR in the LAD (group 2A 3.18 +/- 0.77; group 2B 3.05 +/- 0.65; group 2C 3.07 +/- 0.79; group 2D 2.86 +/- 0.50, respectively; F = 0.63, p = NS). In conclusion, CFR of an angiographically normal LAD is preserved in patients with remote CAD, even in the presence of previous remote myocardial infarction and wall motion abnormalities.

Adult↗