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Biomedical subjects

Roberto Corti

Publications and source records attributed to Roberto Corti.

At least 37 records · Page 2Linked to original sources
PubMed2005

Cardiac arrest in a soccer player: a unique case of anomalous coronary origin detected by 16-row multislice computed tomography coronary angiography.

Anomalous origin of the coronary arteries may be present in otherwise normal subjects without clinical significance, but can also be the cause of myocardial ischemia and sudden death in both adults and teenagers. In particular, the origin of the left main coronary artery or left anterior descending artery from the right sinus of Valsalva or right coronary artery may result in compression of the vessel during or immediately after exercise. We present a unique case of coronary anomaly with four separate coronary ostia originating from the right coronary sinus in a soccer player with sudden cardiac arrest. Multislice contrast-enhanced computed tomography has emerged as a valid noninvasive method for the diagnosis of coronary artery anomaly.

Coronary Angiography↗
PubMed2005

Rapid progression of atherosclerotic coronary artery disease in patients with human immunodeficiency virus infection.

We describe the case of a 39-year-old human immunodeficiency virus (HIV)-infected man with angiographically documented rapid progression of coronary artery disease. Over a time course of only 2 months, he developed high-grade stenosis of the left anterior descending coronary artery. The risk of myocardial infarction is increased in patients with HIV infection receiving antiretroviral therapy. However, the absolute risk is small and the marked overall benefits of antiretroviral therapy are evident. Patients receiving HIV protease inhibitors should be screened for hyperlipidemia, hyperglycemia, and hypertension. They may be candidates for lipid-lowering therapies depending on their long-term prognosis and individual risk of cardiovascular disease. Care is need because of possible drug interactions between lipid-lowering drugs and antiretroviral therapy. Invasive treatment of acute myocardial infarction does not differ from that in patients not infected with HIV. The rate of progression of coronary artery disease and the restenosis rate, however, are often unexpectedly high in these patients.

Adult↗
PubMed2005

Cardiovascular effects of coffee: is it a risk factor?

Intake of coffee, one of the most common beverages worldwide, is often reported as a cardiovascular risk factor; however, definitive data are lacking. Acute intake of coffee or beverages containing caffeine can increase blood pressure, heart minute volumes, and cardiac index, as well as activate the sympathetic nervous system in nonhabitual coffee drinkers. Interestingly, this is not observed in habitual coffee drinkers. Restriction of coffee or caffeinated beverages is no longer indicated in the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) guidelines for the treatment of hypertension. In fact, no clear association between coffee and the risk of hypertension, myocardial infarction, or other cardiovascular diseases has been demonstrated. In contrast to early studies, recent research indicates that habitual moderate coffee intake does not represent a health hazard and may even be associated with beneficial effects on cardiovascular health.

Blood Glucose↗
PubMed2004

Effects of percutaneous transluminal angioplasty and endovascular brachytherapy on vascular remodeling of human femoropopliteal artery by noninvasive magnetic resonance imaging.

BACKGROUND: Percutaneous transluminal angioplasty (PTA) of severely stenotic peripheral vascular lesions is hampered by a higher restenosis rate. The effects of PTA on vascular wall as well as the effects of the antirestenotic properties of endovascular brachytherapy (EVBT) remain unclear. MRI allows in vivo noninvasive assessment of the vascular effects of such treatment strategies. We sought to elucidate the vascular effect of PTA and PTA+EVBT by serial MRI. METHODS AND RESULTS: Twenty symptomatic patients with severe stenosis of the femoropopliteal artery were randomly assigned to PTA (n=10) or PTA+EVBT (n=10; 14 Gy by gamma-irradiation source) and imaged by high-resolution MRI before and 24 hours and 3 months after intervention. An independent observer blinded to the procedure analyzed the MRI data. At 24 hours, cross-sectional MRI revealed that lumen area (86% and 67%) and total vessel area (47% and 34%) increased similarly in the PTA and PTA+EVBT groups, respectively. All patients showed severe splitting of the atherosclerotic plaque, resulting in an irregularly shaped lumen. At 3 months, MRI revealed a significant difference in lumen area change between the PTA and PTA+EVBT groups (40% and 106%, respectively; P=0.026) and in the total vessel area (14% and 39%, respectively; P=0.018). At 3 months, plaque disruption was still present in 50% of the patients treated with PTA+EVBT. CONCLUSIONS: After PTA, there is deep disruption of the atherosclerotic plaques and an extensive remodeling process of the arterial wall. Luminal loss after PTA is partially due to inward vessel remodeling. Brachytherapy prevents inward remodeling and induces an increase in lumen area but partially prevents healing of disrupted vessel surface.

Aged↗
PubMed2004

The selective peroxisomal proliferator-activated receptor-gamma agonist has an additive effect on plaque regression in combination with simvastatin in experimental atherosclerosis: in vivo study by high-resolution magnetic resonance imaging.

OBJECTIVES: We sought to investigate the anti-atherogenic effects of a selective peroxisomal proliferator-activated receptor-gamma (PPAR-gamma) agonist and simvastatin, as well as their combination, over time, in a rabbit model of experimental atherosclerosis. BACKGROUND: The PPARs are nuclear transcription factors that control a variety of cellular functions, with the potential effects required to induce plaque regression and stabilization. METHODS: Atherosclerosis was induced in rabbits (n = 37) by the combination of double-balloon injury and a nine-month high-cholesterol (HC) diet. The rabbits were randomized into a continued HC diet, a normal chow (NC) diet, NC plus simvastatin, NC plus PPAR-gamma agonist, and NC plus simvastatin plus PPAR-gamma agonist. All rabbits underwent magnetic resonance imaging (MRI) at randomization and after six months of treatment and were then sacrificed for histopathologic study. RESULTS: All groups had a similar vessel wall area by MRI (8.45 +/- 0.65 mm(2), p = NS between groups) at randomization. Significant progression was seen in the HC diet group (15 +/- 4%, p < 0.01). In the NC and NC plus PPAR-gamma agonist groups, progression was abolished (-2.5 +/- 3% and -4.5 +/- 5%, respectively; p = NS). The NC plus simvastatin and NC plus simvastatin plus PPAR-gamma agonist groups had significant plaque regression (-12 +/- 4% [p < 0.05] and -22 +/- 4% [p < 0.01], respectively). Regression was independent of plasma lipid levels. All NC groups had similar lipid profiles at the end of treatment. Histopathologic analysis of the NC groups showed a decreased macrophage content and matrix metalloproteinase activity and an increased smooth muscle cell/collagen content of lesions. CONCLUSIONS: Our data indicate that normalization of plasma lipid levels abolishes progression of atherosclerosis. Simvastatin elicits regression of atherosclerotic lesions, and the combination simvastatin plus PPAR-gamma agonist has additive regression effects on plaque. This is paralleled by structural alterations in plaque composition, which may increase plaque stability. These observations support the beneficial effects of statins on atherosclerosis and show additional anti-atherogenic benefits of combining a PPAR-gamma agonist with simvastatin.

Animals↗
PubMed2004

Should standard medical therapy for angina include a statin?

Although a wealth of evidence supports the use of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) in patients with clinically evident coronary artery disease, these agents are still underutilized. Statins are the most effective agents in reducing low-density lipoprotein-cholesterol among lipid-lowering drugs, and studies have recently shown that they improve endothelial function and plaque stabilization, and induce regression of atherosclerotic lesions. This article reviews the most recent evidence and guideline recommendations supporting the use of statins in chronic stable angina pectoris and acute coronary syndromes.

Acute Disease↗
PubMed2004

Shear stress-dependent platelet function after LDL cholesterol apheresis.

BACKGROUND: Platelets play a crucial role in the pathogenesis of acute coronary syndrome (ACS). Thrombus formation with subsequent arterial occlusion is a major determinant in ACS and stroke. Platelets also essentially contribute to the development and progression of atherosclerotic lesions. The aim of the present study was to investigate the effects lipid lowering by LDL apheresis on platelet function in patients with coronary artery disease. METHODS: In six patients with angiographically proven coronary artery disease, venous blood samples were obtained before and after LDL cholesterol apheresis. Citrated whole blood (200 microl) was circulated in polystyrene wells at a shear rate of 1875 s(-1) for 2 min with a rotating teflon cone. Shear-stress dependent platelet adhesion was measured before and after apheresis. RESULTS: After apheresis, there were significant reductions in LDL (-58%) and HDL (-17%) cholesterol, triglycerides (-43%), fibrinogen (-52%), lipoprotein (a) (-57%) and CRP (-57%) levels. LDL apheresis significantly reduced shear-stress dependent platelet adhesion. Bolus administration of heparin significantly prolonged activated clotting time, but had no significant effect on platelet adhesion or aggregates. CONCLUSIONS: In patients with coronary artery disease, shear-stress dependent platelet adhesion is reduced by a single LDL apheresis. In addition to its cholesterol-lowering effect, LDL apheresis reduces circulating levels of fibrinogen and C-reactive protein.

Blood Component Removal↗
PubMed2004

Evolving concepts in the triad of atherosclerosis, inflammation and thrombosis.

Recent developments into antherothrombosis, the leading cause of morbidity and mortality in Western Society, may help to change our treatment strategy to a more casual approach. The composition of the atherosclerotic plaque, rather than the percent stenosis, appears to be a critical predictor for both risk of plaque rupture and subsequent thrombogenicity. A large lipid core, rich in tissue factor (TF) and inflammatory cells including macrophages, and a thin fibrous cap with compromise of its structural integrity by matrix degrading enzymes, such as metalloproteinases (MMPs), render a lesion susceptible to rupture and subsequent acute thrombosis. Thrombosis may lead to a complete occlusion or, in the case of mural thrombus or intraplaque hemorrhage, to plaque progression. Disruption of a vulnerable or unstable plaque (type IV and Va lesions of the AHA classification) with a subsequent change in plaque geometry and thrombosis may result in an acute coronary syndrome. The high-risk plaque tend to be relatively small, but soft or vulnerable to "passive" disruption because of high lipid content. Inflammatory processes are important components of all stages of atherosclerotic development, including plaque initiation and disruption. As such the early steps in atherosclerotic lesion formation are the over expression of endothelial adhesive protein (i.e. selectins, VCAM and ICAM), chemotactic factors (MCP-1), growth factors (M-CSF), and cytokines (IL-2) that will facilitate the recruitment, internalization and survival of blood-borne inflammatory cells into the vascular wall. Macrophages, following what appears to be a defense mission by protecting the vessel wall from excess lipid accumulation, may eventually undergo apoptosis with release of MMPs and TF. Specific cell recruitment in the vessel wall and build-up of the extracellular matrix are coordinated by a wide variety of stimulators and inhibitors. Active interaction of immune competent cells within the atherosclerotic lesions appears to play a pivotal role in the control of atherosclerotic plaque evolution and, therefore, deserves particular attention from the research community with the ultimate goal of improving preventive and therapeutic medical approaches. Inflammation, thrombosis and atherosclerosis are interdependent and define a triad within the complex pathogenic process of atherothrombosis.

Arteriosclerosis↗
PubMed2004

Vasopeptidase inhibitors: will they have a role in clinical practice?

The human cardiovascular system is regulated by haemodynamic, neurohumoral and structural mechanisms. The endothelium and the neurohumoral system play a key role in modulating both vascular tone and structure by producing vasoactive substances, and in the modulation of blood cell adhesion. Although the neurohormonal systems are essential in vascular homeostasis, they become maladaptive in conditions such as hypertension, coronary disease and heart failure. The clinical success of blocking the renin-angiotensin system by angiotensin converting enzyme (ACE)-inhibitors and the sympathetic nerve system by beta-blockers demonstrates the importance of neurohumoral blockade. The inadequate effect of angiotensin converting enzyme (ACE) or neutral endopeptidase (NEP) inhibitor monotherapy seen in some patients treated for hypertension or congestive heart failure, and the promising effect seen after their combination, led to the development of drugs that simultaneously inhibit both enzyme systems. Neutral endopeptidase, like ACE, is an endothelial cell surface zinc metallopeptidase with similar structure and catalytic site to ACE. NEP is the major enzymatic pathway for degradation of natriuretic peptides. The natriuretic peptide system can be viewed as the endogenous inhibitor of the renin angiotensin system. The dual metalloprotease inhibitors of ACE and NEP, called vasopeptidase inhibitors therefore represent a new and attractive therapeutic strategy for the treatment of cardiovascular disease. The ability to add incremental benefit over already proven therapy, with an acceptable side-effect profile however, is questionable in this new class of agents.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Statins enhance postischemic hyperemia in the skin circulation of hypercholesterolemic patients: a monitoring test of endothelial dysfunction for clinical practice?

OBJECTIVES: The present study aims to investigate whether laser Doppler flowmetry can be used to monitor improvements in vascular function during statin therapy. BACKGROUND: Endothelial dysfunction is an early feature of atherosclerosis in hypercholesterolemic patients and can be improved by statins. There are several methods to assess endothelial function in vivo, none of them being feasible in everyday practice. METHODS: Skin perfusion, measured by laser Doppler flowmetry, was assessed at rest and during reactive hyperemia. Nineteen hypercholesterolemic patients (age 42 to 73 years, total cholesterol 5.4 to 9.6 mmol/l) were studied before and during statin therapy. To further investigate the mechanisms, postischemic skin hyperemia was measured before and after intradermal injection of the nitric oxide synthase inhibitor L-NAME and its inactive isoform D-NAME (0.5 micromol/10 microl each). On a separate day, the healthy volunteers were reexamined before and 2 h after 1,000 mg aspirin. RESULTS: Postischemic skin blood flow was markedly reduced in hypercholesterolemic patients (45 +/- 11%) compared with healthy controls (238 +/- 20%, p < 0.0001) and improved after statin therapy (113 +/- 15%, p = 0.0005 vs. pre-treatment). In the healthy volunteers, the hyperemic responses were not significantly different after L-NAME and D-NAME. Aspirin reduced hyperemia from 274 +/- 49% to 197 +/- 40% (p = 0.025). CONCLUSIONS: Reactive hyperemia of the skin microcirculation can be easily and reproducibly assessed by laser Doppler flowmetry. Vasodilator prostaglandins are the major mediators of postischemic skin hyperemia, which is impaired in hypercholesterolemic patients and can be enhanced by cholesterol-lowering therapy. Thus, laser Doppler flowmetry may represent a tool to assess and monitor vascular function during therapy in everyday practice.

Adult↗
PubMed2003

Aspirin and clopidogrel in acute coronary syndromes: therapeutic insights from the CURE study.

Platelet adhesion, activation, and aggregation are central to thrombus formation, which follows atherosclerotic plaque disruption and causes acute coronary syndromes. Aspirin and clopidogrel exert their antiplatelet effects by inhibiting thromboxane A2 production and adenosine diphosphate-induced platelet aggregation pathways, respectively. Aspirin has proven benefits in primary and secondary prevention of coronary artery disease. Clopidogrel, an alternative antiplatelet agent used in patients with aspirin intolerance, is especially useful in combination with aspirin after coronary stent procedures. The CURE (Clopidogrel in Unstable Angina to Prevent Recurrent Events) study demonstrates for the first time the benefit of adding clopidogrel to aspirin rather than using aspirin alone in patients having acute coronary syndromes without ST-segment elevation myocardial infarction. Patients who are resistant to aspirin (up to 10%) have higher rates of cardiovascular events and may derive special benefit from the combination therapy. Aspirin resistance can be assessed through platelet aggregometry testing, measurement of urinary thromboxane metabolites, and, possibly, genomic testing in the future.

Acute Disease↗
PubMed2003

Dysfunctional baroreflex regulation of sympathetic nerve activity in patients with vasovagal syncope.

BACKGROUND: The interplay of resting muscle sympathetic nerve activity (MSA) and the baroreceptor reflex in patients with vasovagal syncope remains elusive. Hence, the aim of the present study was to investigate MSA, baroreceptor sensitivity, heart rate, and blood pressure under resting conditions and during orthostatic stress in patients with a history of vasovagal syncope. METHODS AND RESULTS: MSA was measured using microneurography at rest and during lower body negative pressure (LBNP) to mimic orthostatic stress in patients with a history of vasovagal syncope (n=10) and in age-matched healthy controls (n=8). Heart rate and blood pressure were simultaneously recorded. Cardiac baroreceptor sensitivity was calculated with the spectral technique (alpha coefficient). Resting MSA in the patients with syncope was significantly increased as compared with controls (42.4+/-2.3 versus 26.5+/-3.6 bursts/min, P=0.001), whereas activation of MSA during orthostatic stress in the patient group was significantly blunted (5.1+/-1.6 versus 15.2+/-2.1 bursts/min at LBNP -50 mm Hg, P=0.002). In the patients with syncope, cardiac baroreceptor sensitivity was significantly reduced under supine resting conditions (8.5+/-0.7 versus 13.0+/-1.1 ms/mm Hg, P=0.001), as well as under orthostatic stress (7.3+/-0.7 versus 13.4+/-1.5 ms/mm Hg, P=0.003). CONCLUSIONS: This study shows that in patients with vasovagal syncope, resting MSA is increased and baroreflex regulation during orthostatic stress is blunted, thus leading to impaired MSA adaptation. These results provide new insights into mechanisms of vasovagal syncope and suggest that pharmacological modulation of baroreceptor sensitivity may represent a promising treatment of neuromediated syncope.

Adult↗
PubMed2003

Pathogenetic concepts of acute coronary syndromes.

The propensity of plaque to disrupt is a major determinant of future ischemic events. Although they are distinct from one another, the atherosclerotic and thrombotic processes appear to be interdependent and may be integrated under the term "atherothrombosis." It is now clear that plaque composition, rather than the percent stenosis, is a major determinant of plaque vulnerability. Plaque disruption seems to depend on both passive and active phenomena and is not purely mechanical. Inflammation (activation of monocytes/macrophages) is a major determinant of both plaque vulnerability and thrombogenicity as they relate to plaque disruption. In one-third of acute coronary syndromes, there is, however, no plaque disruption but only superficial erosion of a markedly stenotic, fibrotic plaque. In these cases, thrombus formation may be exacerbated by a hyperthrombogenic state present in patients with certain systemic risk factors. The endothelium plays a pivotal role in vascular homeostasis and hemostasis. This dynamic organ regulates blood thrombogenicity as well as contractile, secretory, and mitogenic activities in the vessel wall. Some classic risk factors induce endothelial dysfunction by reducing the bioavailability of nitric oxide, increasing tissue endothelin-1, and activating pro-inflammatory signaling pathways. Vascular hemostasis, which is the maintenance of blood fluidity and vascular integrity, is achieved by counter-balancing the intrinsic clotting tendency of blood. As a consequence of the central role of endothelial cells in hemostatic control, a dysfunctional endothelium will generate a pro-thrombotic environment favoring development of atherosclerotic lesions and thrombotic complications.

Acute Disease↗
PubMed2003

New understanding, diagnosis, and prognosis of atherothrombosis and the role of imaging.

Despite crucial advances in our knowledge of the pathologic mechanisms and the availability of effective diagnostic and treatment modalities, coronary atherothrombosis remains the most frequent cause of ischemic heart disease. Plaque disruption with superimposed thrombosis is the main cause of unstable angina, myocardial infarction, and sudden death. New findings have recently introduced exciting concepts that could have major impact on the treatment of the atherothrombotic disease. We will discuss the mechanisms that lead to the development of atherothrombosis and those responsible for the acute coronary syndromes, as well as some of the concepts derived from in vivo observations using new imaging technologies (eg, high-resolution magnetic resonance imaging).

Arteriosclerosis↗
PubMed2003

Emerging importance of HDL cholesterol in developing high-risk coronary plaques in acute coronary syndromes.

Cardiovascular disease is the principal cause of death in industrialized countries. Hyperlipidemia, with high low-density lipoprotein cholesterol and triglycerides, and low high-density lipoprotein cholesterol levels (<40 mg/dL in men and <45 mg/dL in women), is a known major cardiovascular risk factor. Statins are considered the most potent and effective agents to reduce low-density lipoprotein cholesterol, but they have a variable effect on high-density lipoprotein cholesterol and triglycerides. Different clinical trials with statins have shown a decrease in low-density lipoprotein cholesterol by 35% and a reduction of the incidence of coronary events by as much as 30%. However, 60 to 70% of events still occur, despite remarkable reduction of low-density lipoprotein cholesterol concentration. Recent National Cholesterol Education Program guidelines highlighted the importance of high-density lipoprotein cholesterol concentration in the prevention and treatment of cardiovascular disease. High-density lipoprotein cholesterol is considered an independent risk factor and has an inverse relation with coronary events. The association of low levels of high-density lipoprotein cholesterol with an increased incidence of cardiovascular events implies a critical role of high-density lipoprotein in the protection against atherosclerotic disease and in the progression of coronary atherosclerotic disease. High-density lipoprotein cholesterol appears to exert this protective effect through multiple mechanisms. High-density lipoprotein is not only involved in reverse cholesterol transport, but also prevents endothelial dysfunction; inhibits the homing of monocytes, apoptosis, platelet activation, and factor X activation; and has antioxidant properties. In this article the authors review the available experimental and clinical evidence supporting the importance of high-density lipoprotein cholesterol as a protective factor in coronary artery disease, and the strategies developed to increase high-density lipoprotein cholesterol.

Animals↗
PubMed2003

Statins and plaque stability.

3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are now the standard of care for patients with hypercholesterolaemia. This class of inhibitors, known as 'statins', has been shown to reduce cardiovascular morbidity and mortality. Accumulating data demonstrates a variety of mechanisms in which HMG-CoA reductase inhibition benefits the cardiovascular system. This review will discuss the pharmacology, clinical trials, and mechanisms, besides lipid lowering, of statin therapy.

Arteriosclerosis↗