Stenosis severity and risk benefit
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This document discusses several studies on the relationship between stenosis severity and risks of coronary occlusion and acute coronary syndrome: 1) Two studies found that coronary segments with 50-80% stenosis at baseline had higher risks of total occlusion at follow-up than segments with less severe stenosis. 2) Another study found that prior to myocardial infarction, 29% of culprit lesions showed 0-50% stenosis, while 4.1-7.9% showed 50-90% stenosis. 3) A review concluded that the majority of infarcts evolve from angiographically mild to moderate stenoses, not severe stenoses. 4) A study on plaque rupture found that two-thirds of acute coronary disease
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This document summarizes the capabilities of LightLab OCT technology for plaque characterization and precision imaging and therapy. LightLab OCT uses near-infrared light to provide ultra high-resolution imaging down to 12 micrometers. In addition to morphological imaging, it enables spectroscopic, polarization, Doppler, and elastography imaging. These advanced imaging modes allow for a better understanding of microanatomic plaque characteristics such as composition, structure, and orderliness. LightLab OCT technology has applications in selecting appropriate therapies, guiding targeted delivery, and developing new therapeutic approaches.
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The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentiles, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque burden in response to treatment over time.
509 chromosome 6p linked to high hdl
1) A Mexican family with familial hypercholesterolemia (FH) linked to chromosome 1p32 was found to also have elevated HDL-C (high-density lipoprotein cholesterol) linked to chromosome 6p, which protected against atherosclerosis despite FH.
2) The FH trait mapped to chromosome 1p32, a region previously linked to FH, while the elevated HDL-C trait mapped to chromosome 6p, a region not previously linked to FH.
3) This family provides evidence that a locus on chromosome 6p confers an anti-atherogenic effect exceeding its effect on cholesterol levels, and may protect against risk factors beyond FH like hypertension and smoking.
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2) The FH trait mapped to chromosome 1p32, a region previously linked to FH, while the elevated HDL-C trait mapped to chromosome 6p, a region not previously linked to FH.
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The document discusses several studies related to atherosclerosis and cardiovascular disease:
1) A study finds that a polymorphism in the Fas gene promoter region is a genetic risk factor for myocardial infarction by modulating Fas expression.
2) Immunoglobulin treatment suppresses atherosclerosis in mice via its Fc portion by reducing macrophage accumulation in lesions.
3) Inhibition of NF-kB reduces inflammatory molecule expression and attenuates atherosclerosis in mice.
4) MMP-8 may represent a new collagenolytic pathway in acute plaque disruption based on its levels in carotid plaques from patients.
Recent results and findings.
A 71-year-old man with a history of diabetes, coronary artery disease status post myocardial infarction times three, and hypercholesterolemia was found to have an accidental left carotid stenosis and was scheduled for a left carotid endarterectomy. MRI of the carotid arteries was performed using SPIO contrast to better evaluate the extent of disease prior to surgery.
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Vulnerable plaque refers to dangerous forms of atherosclerotic plaques that can rupture or induce thrombosis, disrupting blood flow. The document discusses the history and research around vulnerable plaque, including pioneers in the field and emerging techniques to detect vulnerable plaque such as intravascular ultrasound, optical coherence tomography, and magnetic resonance imaging. It summarizes that vulnerable plaques are typically characterized by a thin fibrous cap, large lipid core, and presence of macrophages.
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The document summarizes research on vulnerable plaques and markers of vulnerability. It finds that ruptured plaques are the most common type of culprit lesion, accounting for around 70% of cases. Major criteria for defining vulnerable plaque include outward remodeling, endothelial dysfunction, and a thin fibrous cap with a large lipid core. Both plaque morphology and activity need to be assessed to identify vulnerability.
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Statins are associated
Statins are associated with a reduced incidence of perioperative mortality in patients undergoing major vascular surgery. In a retrospective case-control study of 2816 patients, statin use was associated with a 78% reduced risk of perioperative mortality. Patients taking statins had over a four-fold lower risk of death compared to non-users. The protective effect of statins was consistent regardless of cardiac risk factors or beta-blocker use.
Preset3
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2) Specific protein structures discussed include truncated forms of MMP9, cellulases from Aspergillus niger and a wood-eating termite, and a C3 serine protease from fire ants. Key structural features of these proteins are highlighted.
3) Structure-based drug design is discussed as a method to use determined protein structures to identify small molecule ligands through docking simulations and molecular dynamics calculations.
Stroes
1. Isolated-low HDL levels in ABCA1 heterozygotes is associated with impaired basal and stimulated endothelial nitric oxide synthase activity.
2. A single rapid infusion of reconstituted HDL completely restored both basal and stimulated endothelial nitric oxide synthase activity in ABCA1 heterozygotes.
3. Impaired lipid trafficking and caveolar disruption caused by dysfunctional ABCA1 profoundly affects endothelial nitric oxide synthase activity.
Esv2n41
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1) Out-of-hospital sudden cardiac death (SCD) remains a major public health challenge, with over 400,000 cases per year in the United States.
2) While there is evidence of slight declines in pre-hospital delay times and more in-hospital treatment, over 60% of cardiac deaths continue to be sudden and outside of a hospital setting.
3) Improving early recognition of heart attack symptoms and rapid intervention through public health initiatives focused on out-of-hospital screening and treatment of patients with cardiac chest discomfort could help reduce the number of sudden cardiac deaths.
Taylor.aeha cac imt progression talk.1
This document discusses using measurements of carotid intima-media thickness (CIMT) and coronary artery calcium (CAC) to monitor atherosclerosis and cardiovascular risk. It finds that progression in these measures is associated with increased risk of cardiovascular events. However, accurately detecting progression with CIMT is challenging due to measurement reproducibility. While CAC progression over 15% per year also indicates higher risk, determinants are uncertain and statins may paradoxically increase CAC while reducing events. More research is still needed to clarify using progression of atherosclerosis to monitor risk.
Vascular interventions atalar- johns hopkins
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1) Early experiments with intravascular MRI to image arteries and plaques.
2) The technical challenges of MRI-guided balloon angioplasty and stent placement, such as developing MRI-compatible devices and monitoring procedures.
3) Examples of MRI-guided balloon angioplasty, stent placement, and plaque imaging in human studies.
4) The potential for MRI to guide new treatments like gene therapy delivery to diseased arteries.
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1) The study examined 92 hearts from patients with severe coronary artery disease who died suddenly. The hearts were sectioned and plaque types were classified.
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3) If results of the RAVEL clinical trial showing "zero" restenosis out to 5 years
Vp watch2002
I. This document discusses various animal models that have been used to study atherosclerosis and plaque rupture, including quail, pigeons, chickens, dogs, monkeys, pigs, rats, rabbits, and mice. It provides details on the types of lesions developed and similarities to human disease for each model.
II. The double knockout LDL/apoE mice are highlighted as offering improvements in studying clinical complications of atherosclerosis like human heart disease. However, it is unclear how closely they model vulnerable plaques.
III. Questions are raised about how closely the coagulation systems of these animal models resemble humans and whether any model fully captures repeated plaque ruptures and the role of aging in natural history as seen in humans.
Vp symposium31602
Trans-Blood Vision is a patented infrared technique that uses short-wave infrared wavelengths to see directly through blood. It has the potential to find vulnerable plaque lesions without first entering them, determine their size and surface characteristics in high resolution, and look at their material constituents both on and below the surface. While it cannot provide direct visual guidance for therapy or penetrate as deeply as ultrasound, combining it with augmentative technologies could allow for real-time multi-mode detection, analysis, and therapy guidance of vulnerable plaque lesions. The document concludes that Trans-Blood Vision warrants significant investigation, possibly in combination with other emerging technologies.
Vpschoenhagen
This study used intravascular ultrasound to examine arterial remodeling and plaque characteristics in 131 patients with either stable angina or recent unstable symptoms. Patients with unstable presentations had greater plaque burden at the culprit lesion despite similar luminal narrowing, and a greater extent of positive arterial remodeling compared to those with stable angina. The culprit lesions in unstable patients also showed a higher rate of echolucent plaque morphology. This suggests that bulky, remodeled plaques may be more vulnerable to rupture, leading to acute coronary syndromes. Further prospective study is needed to better understand the relationship between clinical presentation and plaque features.
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Stenosis severity and risk benefit
- 1. Stenosis Severity & Risk of Coronary Occlusion 0 10 20 30 40 50 60 70 80 90 100 1st Qtr 2nd Qtr 3rd Qtr 4th Qtr East West North 0 50 100 150 200 250 300 350 400 2161 None 5-49% 50-80% 81-95% 52 21 1% 2% 10% 24% Stenosis Severity at Baseline CoronarySegments(n) Occlusions at 5-Year Follow-Up Alderman et al, JACC 1993;22:1141-1154
- 2. Stenosis Severity and Associated Risk of MI 0 10 20 30 40 50 60 70 80 90 100 1st Qtr 2nd Qtr 3rd Qtr 4th Qtr East West North 0 100 200 300 2674 0% 2% 50% 75% 90-99% 29 10 0.3% 3.5% 4.1% 7.9% Stenosis Severity Prior to MI CoronarySegments(n) MI Culprit Lesions at Follow-Up Nobuyoshi et al, JACC 1991;18:904-910 8.7%
- 3. Majority of Infarcts Evolve from Angiographically Mild to Moderate Stenoses Falk et al, Circulation 1995;92:657-671 0 10 20 30 40 50 60 70 80 90 100 1st Qtr 2nd Qtr 3rd Qtr 4th Qtr East West North 0 10 20 30 40 50 60 70 80 90 100 MIPatients(n) Ambrose 1988 Little 1988 Nobuyoshi 1991 Giroud 1992 All Stenosis Prior to MI >70% 50-70% <50% 0 20 40 60 80 100 120 140 160 180 200 68% 18% 14%
- 4. 235 103 18 237 108 18 313 101 16 0 50 100 150 200 250 300 350 Niacin + resin, n=27 Lovastatin + resin, n=32 Diet + resin, n=53 Mild stenosis <40% Moderate stenosis 40-70% Severe stenosis >70% Coronarysegments(n) 4 41 2 1 1 4/785 5/312 4/52 Stenosis Severity and Associated Risk of ACS Insights from FATS
- 5. •Severely stenotic plaques progress to total occlusion and myocardial infarction more frequently than mildly stenotic plaques Key Points
- 6. •Two-thirds of acute CAD syndromes evolve from mildly obstructive plaques because they by far outnumber the severely obstructive lesions Key Points
- 7. • Ruptured plaques have: Large lipid cores Thin fibrous cap Increased inflammation and MMPs Increased neovascularity Reduced collagen and SMCs Key Points